text:
Robin Ørnsrud
Klinisk institutt 1
Se også NIFES
E-postRobin.Ornsrud@uib.no
Nordnesboder 5, 5005 Bergen
Post:Postboks 2029 Nordnes, 5817 Bergen
Vis forfatter(e) (2021). Assessing mineral availability in fish feeds using complementary methods demonstrated with the example of zinc in atlantic salmon. Journal of Visualized Experiments. 1-16.
Vis forfatter(e) (2020). The microbial safety of seaweed as a feed component for black soldier fly (Hermetia illucens) larvae. Food Microbiology. 9 sider.
Vis forfatter(e) (2020). Mercury, lead, arsenic, and cadmium in Norwegian seafood products and consumer exposure. Food Additives & Contaminants. 99-106.
Vis forfatter(e) (2020). In vitro digestion method to evaluate solubility of dietary zinc, selenium and manganese in salmonid diets. Journal of Trace Elements in Medicine and Biology. 152-159.
Vis forfatter(e) (2020). A ranking method of chemical substances in foods for prioritisation of monitoring, based on health risk and knowledge gaps. Food Research International. 1-13.
Vis forfatter(e) (2019). Tolerance and dose-response assessment of subchronic dietary ethoxyquin exposure in Atlantic salmon (Salmo salar L.). PLOS ONE. 36 sider.
Vis forfatter(e) (2019). Seaweed-fed black soldier fly (Hermetia illucens) larvae as feed for salmon aquaculture: Assessing the risks of pathogen transfer. Journal of Insects as Food and Feed. 15-27.
Vis forfatter(e) (2019). Replacing fish meal with insect meal in the diet of Atlantic salmon (Salmo salar) does not impact the amount of contaminants in the feed and it lowers accumulation of arsenic in the fillet. Food Additives & Contaminants. 1191-1205.
Vis forfatter(e) (2019). Identification of ethoxyquin and its transformation products in salmon after controlled dietary exposure via fish feed. Food Chemistry. 259-268.
Vis forfatter(e) (2019). Feed-to-fillet transfer of selenite and selenomethionine additives to plant-based feeds to farmed atlantic salmon fillet. Journal of Food Protection. 1456-1464.
Vis forfatter(e) (2019). Effect of levels and sources of dietary manganese on growth and mineral composition of post-smolt Atlantic salmon fed low fish meal, plant-based ingredient diets. Aquaculture. 1-9.
Vis forfatter(e) (2019). Apparent availability of zinc, selenium and manganese as inorganic metal salts or organic forms in plant-based diets for Atlantic salmon (Salmo salar). Aquaculture. 562-570.
Vis forfatter(e) (2018). Zinc uptake in fish intestinal epithelial model RTgutGC: Impact of media ion composition and methionine chelation. Journal of Trace Elements in Medicine and Biology. 377-383.
Vis forfatter(e) (2018). Utilization of H2SO4-hydrolysed phosphorous from herring bone by-products in feed for Atlantic salmon (Salmo salar) 0+ postsmolt. Aquaculture Nutrition. 348-365.
Vis forfatter(e) (2018). Subchronic dietary exposure to ethoxyquin dimer induces microvesicular steatosis in male BALB/c mice. Food and Chemical Toxicology. 608-625.
Vis forfatter(e) (2018). Selenium and selenium species in feeds and muscle tissue of Atlantic salmon. Journal of Trace Elements in Medicine and Biology. 124-133.
Vis forfatter(e) (2018). Safe limits of selenomethionine and selenite supplementation to plant-based Atlantic salmon feeds. Aquaculture. 617-630.
Vis forfatter(e) (2018). Erucic acid (22:1n-9) in fish feed, farmed, and wild fish and seafood products. Nutrients. 1-12.
Vis forfatter(e) (2017). Sensitivity and toxic mode of action of dietary organic and inorganic selenium in Atlantic salmon (Salmo salar). Aquatic Toxicology. 116-126.
Vis forfatter(e) (2017). Lower levels of Persistent Organic Pollutants, metals and the marine omega 3-fatty acid DHA in farmed compared to wild Atlantic salmon (Salmo salar). Environmental Research. 49-59.
Vis forfatter(e) (2017). Comprehensive characterization of ethoxyquin transformation products in fish feed by traveling-wave ion mobility spectrometry coupled to quadrupole time-of-flight mass spectrometry. Analytica Chimica Acta. 72-82.
Vis forfatter(e) (2016). Utilization of acid hydrolysed phosphorous from herring bone by-products in feed for Atlantic salmon (Salmo salar) start-feeding fry. Aquaculture. 173-184.
Vis forfatter(e) (2016). Lead intoxication in dogs: risk assessment of feeding dogs trimmings of lead-shot game. BMC Veterinary Research. 8 sider.
Vis forfatter(e) (2016). Increased dietary phosphorous prevents vertebral deformities in triploid Atlantic salmon (Salmo salar L.). Aquaculture Nutrition. 72-90.
Vis forfatter(e) (2016). Dietary vitamin A supplementation ameliorates the effects of poly-aromatic hydrocarbons in Atlantic salmon (Salmo salar). Aquatic Toxicology. 171-183.
Vis forfatter(e) (2014). Transcriptional responses in Atlantic salmon (Salmo salar) exposed to deltamethrin, alone or in combination with azamethiphos. Comparative Biochemistry and Physiology - Part C: Toxicology & Pharmacology. 23-33.
Vis forfatter(e) (2013). Establishing an upper level of intake for vitamin A in Atlantic salmon (Salmo salar L.) postsmolts. Aquaculture Nutrition. 651-664.
Vis forfatter(e) (2013). Cross-generational feeding of Bt (Bacillus thuringiensis)-maize to zebrafish (Danio rerio) showed no adverse effects on the parental or offspring generations. British Journal of Nutrition. 2222-2233.
Vis forfatter(e) (2012). Zebrafish (Danio rerio) as a model for investigating dietary toxic effects of deoxynivalenol contamination in aquaculture feeds. Food and Chemical Toxicology. 4441-4448.
Vis forfatter(e) (2012). Dietary phosphorus does not reduce the risk for spinal deformities in a model of adjuvant-induced inflammation in Atlantic salmon (Salmo salar) postsmolts. Aquaculture Nutrition. 12-20.
Vis forfatter(e) (2012). Continuous light induces bone resorption and affects vertebral morphology in Atlantic salmon (Salmo salar L.) fed a phosphorous deficient diet. Aquaculture Nutrition. 610-619.
Vis forfatter(e) (2011). Investigations on the Metabolism and Potentially Adverse Effects of Ethoxyquin Dimer, a Major Metabolite of the Synthetic Antioxidant Ethoxyquin in Salmon Muscle. Journal of Food Protection. 1574-1580.
Vis forfatter(e) (2010). Vitamin K-dependent gamma-glutamylcarboxylase in Atlantic salmon (Salmo salar L.). Fish Physiology & Biochemistry. 627-635.
Vis forfatter(e) (2010). Dietary fatty acids and inflammation in the vertebral column of Atlantic salmon, Salmo salar L., smolts: a possible link to spinal deformities. Journal of Fish Diseases. 957-972.
Vis forfatter(e) (2009). Supplementation of dietary minerals during the early seawater phase increase vertebral strength and reduce the prevalence of vertebral deformities in fast-growing under-yearling Atlantic salmon (Salmo salar L.) smolt. Aquaculture Nutrition. 366-378.
Vis forfatter(e) (2009). Retinoic acid cross-talk with calcitriol activity in Atlantic salmon (Salmo salar). Journal of Endocrinology. 473-482.
Vis forfatter(e) (2009). Differential gene expression of bgp and mgp in trabecular and compact bone of Atlantic salmon (Salmo salar L.) vertebrae. Journal of Anatomy. 663-672.
Vis forfatter(e) (2009). Dietary menadione nicotinamide bisulphite (vitamin K-3) does not affect growth or bone health in first-feeding fry of Atlantic salmon (Salmo salar L.). Aquaculture Nutrition. 638-649.
Vis forfatter(e) (2007). The vitamin D receptor and its ligand 1 alpha,25-dihydroxyvitamin D-3 in Atlantic salmon (Salmo salar). Journal of Endocrinology. 459-471.
Vis forfatter(e) (2004). Teratogenic interaction between elevated egg incubation temperature and egg vitamin A status in Atlantic salmon (Salmo salar L.). Journal of Fish Diseases. 213-223.
Vis forfatter(e) (2004). Tailoring of a cardioprotective muscle fatty acid composition of Atlantic salmon (Salmo salar) fed vegetable oils. Food Chemistry. 567-580.
Vis forfatter(e) (2004). Influence of egg vitamin A status and egg incubation temperature on subsequent development of the early vertebral column in Atlantic salmon (Salmo salar L.) fry. Journal of Fish Biology. 399-417.
Vis forfatter(e) (2003). Seasonal changes in selected muscle quality parameters in Atlantic salmon (Salmo salar L.) reared under natural and continuous light. Aquaculture Nutrition. 161-168.
Vis forfatter(e) (2003). Determination of carotenoid and vitamin A concentrations in everted salmonid intestine following exposure to solutions of carotenoid in vitro. Comparative Biochemistry and Physiology - Part A: Comparative Physiology. 683-692.
Vis forfatter(e) (2002). Hypervitaminosis A in first-feeding fry of the Atlantic salmon (Salmo salar L.). Aquaculture Nutrition. 7-13.
Vis forfatter(e) (2002). Bioavailability of selenium from raw or cured selenomethionine- enriched fillets of Atlantic salmon (Salmo salar) assessed in selenium-deficient rats. British Journal of Nutrition. 13-20.
Vis forfatter(e) (2021). Program for overvåking av fiskefôr - Årsapport for prøver innsamlet i 2020. 2021 - 28. 2021 - 28. .
Vis forfatter(e) (2021). Challenges that prevent an increased utilization of marine residual raw materials and marine species in Norway. 29/2021. 29/2021. .
Vis forfatter(e) (2020). Protocol for risk assessment of "other substances". The Norwegian Scientific Committee for Food and Environment. .
Vis forfatter(e) (2020). Program for overvåking av fiskefôr - Årsrapport for prøver innsamlet i 2019. 2020 - 34. 2020 - 34. .
Vis forfatter(e) (2020). Program for fremmedstoffer i fôrmidler av fisk - Rapport for innsamlede prøver 2019. 2020 - 40. 2020 - 40. .
Vis forfatter(e) (2020). HØRINGSUTTALELSE VEDRØRENDE REGULERINGSPLAN MED KONSEKVENSUTREDNING FOR UTVINNING AV GULL I BOGADALENKOLSVIK I BINDAL KOMMUNE. .
Vis forfatter(e) (2019). Ranking of substances for monitoring in foods, drinks and dietary supplements - based on risk and knowledge gaps. Scientific Opinion of the Scientific Steering Committee of the Norwegian Scientific Committee for Food and Environment. 2019:13. 2019:13. .
Vis forfatter(e) (2019). Program for fremmedstoffer i fôrmidler av fisk : Surveillance project on undesirable substances in feed ingredients of fish origin Rapport for innsamlede prøver 2018 : report 2018. 2019 - 36. 2019 - 36. .
Vis forfatter(e) (2019). Oksidativt stress, vårdropp i pigmentering og produksjonslidelser hos laks. 2019 - 16. 2019 - 16. .
Vis forfatter(e) (2019). Risk assessment of cadmium in mineral fertilisers – fate and effects in the food chain and the environment in Norway. Scientific Opinion of the Panel on Animal Feed of the Norwegian Scientific Committee for Food and Environment. 2019:07. 2019:07. .
Vis forfatter(e) (2018). Program for overvåking av fiskefôr. 25-2018. 25-2018. .
Vis forfatter(e) (2018). Miljøgifter i hubro i Norge 1994-2014 - Rottegifter, klororganiske forbindelser og toksiske metaller. 18. 18. .
Vis forfatter(e) (2018). Evaluation of the maximum limits for selenium in Atlantic salmon feeds. 13-2018. 13-2018. .
Vis forfatter(e) (2017). Nivåer av tungmetaller, rottegifter og organiske miljøgifter i norske hubroer fra 1998-2014 . 9. 9. .
Vis forfatter(e) (2016). Sjømat i Oslofjorden – Uønskede stoffer i torsk, makrell og taskekrabbe Overvåking av forurensede havner og fjorder 2013-2015. .
Vis forfatter(e) (2015). The risk of development of antimicrobial resistance with the use of coccidiostats in poultry diets. Opinion of the Panel on Animal Feed of the Norwegian Scientific Committee for Food Safety. 2015:30. 2015:30. .
Vis forfatter(e) (2014). Økt utnyttelse av næringsstoffer fra marint restråstoff. 11/2014. 11/2014. .
Vis forfatter(e) (2014). Zinc and copper in pig and poultry production – fate and effects in the food chain and the environment VKM Report. Opinion of the Panel on Animal Feed of the Norwegian Scientific Committee for Food Safety. 2014:28. 2014:28. .
Vis forfatter(e) (2014). Utnyttelse av P fra sildeavskjær som alternativ P kilde i fôr til laksesmolt (Salmo salar L.). 8/2014. 8/2014. .
Vis forfatter(e) (2014). Nye marine ingredienser fra sildeavskjær som P ingrediens i fôr til lakseyngel (Salmo salar L.). 9/2014. 9/2014. .
Vis forfatter(e) (2013). Risk evaluation - triploid fish. .
Vis forfatter(e) (2013). Risk assessment of mycotoxins in cereal grain in Norway. Opinion of the Scientific Steering Committee of the Norwegian Scientific Committee for Food Safety. 2013:21. 2013:21. .
Vis forfatter(e) (2013). Risk assessment of lead exposure from cervid meat in Norwegian consumers and in hunting dogs. .
Vis forfatter(e) (2013). Program for overvåkning av fiskefôr - årsrapport 2012. .
Vis forfatter(e) (2013). Overvåkning forurensede havner og fjorder - undersøkelse av fremmedstoffer i torsk fra Salten i Nordland. .
Vis forfatter(e) (2012). Risk assessment regarding processing requirements of by-products from aquaculture for use in fish feed. Opinion of the Panel on Animal Feed of the Norwegian Scientific Committee for Food Safety. 2012:14. 2012:14. .
Vis forfatter(e) (2012). Overvåkning forurensede havner og fjorder - undersøkelse av fremmedstoffer i fisk og sjømat fra Ølenfjorden. .
Vis forfatter(e) (2011). Description of the processes in the value chain and risk assessment of decomposition substances and oxidation products in fish Oils. Opinion of Steering Committee of the Norwegian Scientific Committee for Food Safety. 2011:19. 2011:19. .
Vis forfatter(e) (2018). The Norwegian monitoring program for fish feed -Metals and minerals in feed and feed ingredients.
Vis forfatter(e) (2018). Methods for analyzing selenium in fish feed.
Vis forfatter(e) (2016). Miljøgifter i hubro.
Vis forfatter(e) (2014). Dietary impacts of marine P ingredients from herring byproducts on growth, mineralization and skeletal development in Atlantic salmon (Salmo salar L.) fry.
Vis forfatter(e) (2009). Deformations of the spinal column in Atlantic salmon.
Vis forfatter(e) (2019). Subchronic dietary exposure to ethoxyquin dimer induces microvesicular steatosis in male BALB/c mice.
Vis forfatter(e) (2019). Selenium supplementation to salmon feeds; speciation, toxic mode of action, and safe limits.
Vis forfatter(e) (2019). Safe limits of selenomethionine and selenite supplementation to plant-based Atlantic salmon feeds.
Vis forfatter(e) (2018). Tolerance and dose-response assessment of subchronic dietary exposure to ethoxyquin in Atlantic salmon .
Vis forfatter(e) (2018). Spesiering og biotilgjengelighet av selen og sink i laksefôr.
Vis forfatter(e) (2018). Hazard Characterization of ethoxyquin and ethoxyquin dimer.
Vis forfatter(e) (2018). A study of selenoproteins in Atlantic salmon (salmo salar) using hyphenated mass spectrometry and bioinformatics. Nordic conference on Plasma spectrochemistry.
Vis forfatter(e) (2018). A possible connection between oxidative stress and production related diseases in Atlantic salmon (Salmo salar L).
Vis forfatter(e) (2017). Characterization of Atlantic salmon (Salmo salar) selenoproteins using bioinformatics and hyphenated analytical techniques.
Vis forfatter(e) (2016). Levels of undesirable substances in marine feed ingredients, commercial Norwegian fish feed and farmed Atlantic salmon in the last 13-15 years.
Vis forfatter(e) (2016). Evaluation of the maximum limit for selenium in feed for salmonids.
Vis forfatter(e) (2016). A short story on feed additives in Norwegian fish feed and farmed fish.
Vis forfatter(e) (2015). Feeding for fish welfare and robustness.
Vis forfatter(e) (2013). Vertebral columns of Atlantic salmon (Salmo salar) show alterations in protein abundance due to variable dietary P levels.
Vis forfatter(e) (2013). Changes in protein abundance in the vertebral column of Atlantic salmon (Salmo salar) fed variable dietary P levels.
Vis forfatter(e) (2012). Lock Improved phosphorus utilization in Atlantic salmon (Salmo salar L.) by H2SO4 hydrolysis of minerals in fish bones.
Vis forfatter(e) (2010). Farmed fish as a vitamin K source, limitations of menadione in fish feed.
Vis forfatter(e) (2010). Continuous light induces bone resorption and affects vertebral morphology in Atlantic salmon (Salmo salar L.) fed a phosphorous deficient diet.
Vis forfatter(e) (2009). Dietary Fatty Acids and Inflammation in the vertebral column of Atlantic salmon (Salmo salar) smolts: A possible link to spinal deformities.
Vis forfatter(e) (2008). Roles of fat soluble vitamins in bone development and mineral metabolism.
Vis forfatter(e) (2008). Interference of retinoic acid in the vitamin D endocrine system in Atlantic salmon (Salmo salar).
Vis forfatter(e) (2008). Establishing an upper level of vitamin A in Atlantic salmon (Salmo salar).
Vis forfatter(e) (2006). Fettløselige vitaminers rolle i beinutvikling og mineralmetabolisme.
Vis forfatter(e) (2005). Elevated retinol levels do not cause spinal deformities in the developing salmon embryo.
Vis forfatter(e) (2002). Endogenous vitamin A status and deformities in Atlantic salmon eggs and juveniles reared at two temperatures.
Vis forfatter(e) (2001). Hypervitaminosis A in first-feeding fry of the Atlantic salmon (Salmo salar L.).
Vis forfatter(e) (2012). Selèn til fisk og folk. FiskeribladetFiskaren.
Hovedfagsoppgave
Vis forfatter(e) (1998). Bioavailability of selenium from selenomethionine-enriched ("tailor-made") fillets of Atlantic salmon.
Vis forfatter(e) (2012). Triploid laks – en kandidat for kommersielt oppdrett? Havforskningsrapporten.
Vis forfatter(e) (2007). Optimal fôrsammensetning i tidlig sjøvannsfase kan redusere innslaget av ryggradsdeformasjoner hos høstsmolt. Kyst og havbruk. 164-165.
Vis forfatter(e) (2004). Forskning innen fiskeernæring og helse ved NIFES i Bergen. Fiskehelse.
Vis forfatter(e) (1999). Karotenoider som vitamin A kilde i fisk. Norsk Fiskeoppdrett. 34-35.
Vis forfatter(e) (2015). Trygt fôr, trygg mat. FiskeribladetFiskaren.
Vis forfatter(e) (2013). Risikabel risiko. FiskeribladetFiskaren.
Vis forfatter(e) (2019). Development of novel methods to evaluate availability of zinc, selenium and manganese in Atlantic salmon (Salmo salar).
Vis forfatter(e) (2003). Retinoids in salmonid aquaculture with special emphasis on development deformities. -.
Vis forfatter(e) (2013). Changes in protein abundance in the vertebral column of Atlantic salmon (Salmo salar) fed variable dietary P levels. 4 sider.
Vis forfatter(e) (2018). Tolerance and dose-response of subchronic dietary ethoxyquin (EQ) exposure in Atlantic salmon (Salmo salar L.).
Vis forfatter(e) (2018). Selenium speciation in fish feed by HPLC-ICPMS.
Vis forfatter(e) (2018). Analysis of selenoproteins in Atlantic salmon (salmo salar) fed selenium supplemented feeds.
Vis forfatter(e) (2014). Environmental contaminants in mother and child - Is there a correlation between mothers seafood intake and levels of environmental persistent organic contaminants in mother and child at 3, 6 and 12 months post partum.
Vis forfatter(e) (2013). Vertebral columns of Atlantic salmon (Salmo salar) show alterations in protein abundance due to variable dietary P level.
Vis forfatter(e) (2013). The use of triploid salmon in Norwegian Aquaculture.
Vis forfatter(e) (2013). Radiological studies on vertebral deformities in triploid Atlantic salmon (Salmo salar).
Vis forfatter(e) (2013). Phosphatase activities in Atlantic salmon (Salmo salar) vertebral bone and scales: our findings from the past years.
Vis forfatter(e) (2008). Inflammation as a risk factor for spinal deformities in farmed Atlantic salmon underyearling smolts.
Vis forfatter(e) (2008). Dietary menadione nicotinamide bisulphite (vitamin K) does not affect growth or bone health in first feeding Atlantic salmon (Salmo salar).
Vis forfatter(e) (2007). Investigations on first feeding fry of Atlantic salmon (Salmo salar L.) fed diets with different levels of menadione nicotinamide bisulphite (MNB).
Vis forfatter(e) (2006). Workshop innen beindeformiteter hos laks og torsk i intensivt oppdrett.
Vis forfatter(e) (2004). The effect of 1;25-dihydroxyvitamin D3 and 24r,25-dihydroxyvitamin D3 on the activity of osteoblasts on tilapia (Oreochromis mossambicus) scales in primary culture.
Vis forfatter(e) (1999). Bioavailability of selenium from selenomethionine-enriched (tailor made) fillets of Atlantic salmon (Salmo salar) assessed in a rat model.
Vitenskapelig oversiktsartikkel/review
Vis forfatter(e) (2015). Polyaromatic hydrocarbons in aquafeeds, source, effects and potential implications for vitamin status of farmed fish species: A review. Aquaculture Nutrition. 257-273.
Vis forfatter(e) (2012). Vertebral deformities in farmed Atlantic salmon (Salmo salar L.) - etiology and pathology. Journal of Applied Ichthyology. 433-440.
Vis forfatter(e) (2011). Vitamin K in fish nutrition. Aquaculture Nutrition. 585-594.
Vis forfatter(e) (2019). Modelling of the feed-to-fillet transfer of ethoxyquin and one of its main metabolites, ethoxyquin dimer, to the fillet of farmed Atlantic salmon (Salmo salar L.). . Food Additives & Contaminants. 1042-1054.
Næringsstoffer
Fiskeernæring
Matvarekunnskap
Næringsmiddeltoksikologi


Management, and front desk are terrible!
Our family has stayed here several times each time the the customer service got worse.
The rooms are small but, decent, the location is perfect we have a daughter that lives walking distance and we like being close to the shopping.
We will not be staying there again which is a loss for them since we come every couple of months and usually get 2 rooms one for our other daughter.
On our last visit I accidentally left my favorite items of clothing in one of the drawers in the room. I called immediately when I realized this and was sent to housekeepings voicemail I left several messages including one for the hotel manager and never heard back. finally 4 days later I was able to get through to the manager of housekeeping he was rude, didn't speak enough english to get my name right after repeating it and spelling it over and over he finally figured it out just to tell me that my clothes were not there because the housekeepers would have put it in the log book. I begged him to please just look in lost and found and described my items and he refused. I lost about 1500.00 worth of non replaceable items. Yes, I know it's my fault for leaving them I am just so sad about it.
Okay hotel. I felt service was lacking, check in was minimal and I was left to my own devices a bit.
Room tiny but okay for one. Decor was odd, I didn't get the blue tinted mirror taking up a whole wall, made the room feel cold.
Food very good, breakfast nice.
I had issues with the shower and had to get handyman in.
I don't think I would stay again.
We appreciate the feedback, Hollie.
We're disappointed your time with us was less than ideal. We care deeply about the satisfaction of our guests so we regret that our service and amenities didn't meet your expectations. Thank you again for your feedback. We'll be sure to address your concerns with our team moving forward.
I stayed for the second time this year at the Nomo Soho Hotel came back because the the previous experience I had - back in February this year, was excellent. The location of the hotel is probably one of the best - in the heart of Soho (the hippest place to be in NYC), everything is close by, the trains station is a block away, great restaurants & bars all around (even a karaoke place right across the Lafayette entrance), and amazing stores at every meter. And it has a nice terrace right in front!
The staff was very nice, in particular the Manager of the hotel- Mr. Pablo - who was incredibly attentive, always eager to meet the needs of its customers. The room i stayed in, 2001, was a great one, just a bit noisy from overseeing Lafayette street. I asked if I could change the room and immediately i was offered more options.
As well, Jeffrey, the front desk agent, such a respectful man, always smiling and eager to be of service.
There was a free wine tasting every day at 5 PM in the hotel's lobby, sometimes fresh fruits or other treats awaited at the entrance of the hotel- making one's stay feel so much closer to home. I have stayed here over the past years many times, and I have to say that in the last years I was quite disappointed with the staff and the fact that I had booked through a third party - Hotels.com, that had hidden taxes...So, this year, when i was back , I was a bit reluctant, but the place had changed so, so much for the better. I was amazed. I stayed in total this year over three weeks here and I don't think I could have made a better decision. I highly recommend it!
Thank you for the outstanding review, Ala!
It's a design hotel,very nice, but the rooms are very small and the bathrooms really tiny.
I don't think I will stay again in the future in this hotel.
Dear Guest, we appreciate the feedback.
We regret to hear that you were unsatisfied with your room. We aim to provide our guests with the most comfortable experience possible, and we'd love to help you reserve a room that better suits your individual needs of space and comfort in the future.
We hope for the opportunity to share a more positive experience with you soon.


Rolling Meadows | Attorneys' Title Guaranty Fund, Inc.
Final water and sewer bills must be paid. Copy of deed and PTAX required.
Deed will not be recorded. Lien will be recorded. 1% interest per month and penalty of 10% of tax amount. $200 late fee will apply on the 31st of each month.


text:
Q: Query table and return values with the highest confidence only and remove duplicates I want to find a Microsoft SQL query to only get the maximum customer_confidence for a specific customer.

Scenario 1
In the example table you will see that number 454 for customer 2603396 has two confidence percentages, one at 75% and one at 50%, I would only like the 75% to be returned.
Scenario 2
For number 918 I have two customer numbers 2744398 and 4866968, I only want the highest customer_confidence customer result to be returned, in the example table it should be 2744398 with 75% confidence.
How can I achieve this in Microsoft SQL?
Here is what I have tried:
select
        distinct no, customer
        ,max(customer_confidence) as 'customer_confidence'
from (Table)

redpajama_set_name: RedPajamaStackExchange


Konecranes will publish its January-March 2019 Interim Report on Friday, April 26, 2019 at 9.00 a.m. Finnish time. The report will be available on the company's website at www.konecranes.com after publishing.
An analyst and press conference will be held at restaurant Savoy's Salikabinetti (address Eteläesplanadi 14) at 11.00 a.m. Finnish time. The Interim Report will be presented by Konecranes' President and CEO Panu Routila and CFO Teo Ottola.
The link is accessible from a smart phone or a computer. The link becomes active 15 minutes prior to start time.
After the event it is possible to ask questions.


Matthieu Brucher has announced the update of ATKSidechainCompressor, his dual channel compressor plug-in, and ATKSideChainExpander, his dual channel expander plug-in, for 64-bit Mac OS X (10.8 minimum) and Windows (32 and 64-bit) in VST2, VST3 and AU plug-in formats.
These new versions have more parameters than the previous ones, which means that the parameters used in a project with the former version won't be loaded in the same way for these new versions.
These stereo plugins can work on two channels, left/right or middle/side, possibly in linked mode (only one set of parameters), and can be set up to mix the input signal with the compressed signal (serial/parallel compression). The side chain channels can be used to steer the gain stage (the same setup will be used, right/left or middle/side), depending on the switch on the top right of the plugins. The same coloration stage from ATKColoredCompressor and ATKColoredExpander are used here.


In only a relatively short time since learning how to dive with tiger sharks, the industry may be on its way out due to lack of tiger sharks. What has happened to these animals?
In this first segment from the hour long interview, Walter tells Skyler about the early days of tiger shark diving, how it came to be, the learning process, and what the current state is. There was a time when you could see tiger sharks year-round...now, even during peak season, it is a special event to see even one rather than a regular event. Why?


NOTE: THIS PRODUCT IS ON HOT SALE. DUE TO THE SHORTAGE OF STOCK, WE RECOMMEND YOU TO STORE 5 OR MORE FOR YOUR CONTINUOUS USE AND MAXIMUM RESULTS.
Modern medical experts point out that, gold contact to the skin will release negative ions, positive ions, and human interaction, to promote blood flow between ions in the organization, producing new energy, so as to improve blood circulation, accelerate skin.


Firefighters and paramedics are on scene following a crash in Warwick. A car and motorcycle were involved in the incident on Harbour Road near Morgan Road at about 4.45pm.
Police have been contacted for information.


text:
Q: Show hide form fields in react using onFocus and onBlur I'm working on a form that initially only shows one input field and when it is focused, it shows other inputs and the submit button.
I also want to hide all those extra fields if the form loses focus while they are empty. And this is the part that I'm not being able to implement.
This is my code: I use a controlled form and a state to handle focus.
const FoldableForm = () => {
  const [formState, setFormState] = useState(defaultFormState);
  const [hasFocus, setFocus] = useState(false);

  const handleOnBlur = () => {
    if (!formState.message.trim() && !formState.other_input.trim()) {
      setFocus(false);
    }
  };

  return (
    <form
      onFocus={() => setFocus(true)}
      onBlur={handleOnBlur}
    >
      <textarea
        name="message"
        onChange={(e) => setFormState({ ...formState, message: e.target.value })}
      />
      {hasFocus && (
        <>
          <input
            type="text" name="other_input"
            onChange={(e) => setFormState({ ...formState, message: e.target.other_input })}
          />
          <button type="button">Post comment</button>
        </>
      )}
    </form>
  );
}

Currently, if I type something in the text area, setFocus(false) is never invoked, so it works as intended.
Otherwise, if I leave it empty and click on the other input field, the handleOnBlur function is called, it sets focus to false, so the form is 'minimized'.
This is expected because the blur event (from the textarea) is triggered before the focus event (from the new input field). So I tried to use setTimeout to check, after a fraction of a second if the focus event had already occurred.
To do so, I used a second state (shouldShow) that is updated in a setTimeout inside the handleOnBlue function.
setTimeout(() => {
  if(!hasFocus) {
    setShouldShow(false); // this should cause the form to minimize
  }
}, 100);

However, according to the react lifecycle, the value of hasFocus that is passed to the setTimeout function is at the invocation time, not at execution. So setTimeout here is useless.
I also tried to use references, but I couldn't make it work.

A: This behavior is because of closures in JavaScript. The value of hasFocus is not the value of the variable at the moment your callback inside setTimeout is executed. It's the value when the onBlur callback is executed.
One solution would be to use functional updates.
Define a state which holds both hasFocus and shouldShow inside:
  const [state, setState] = useState({ hasFocus: false, shouldShow: false });

When you try to access the previous state using functional updates, you get the most recent value:
setTimeout(() => {
    setState((state) => {
        if (!state.hasFocus) {
            return { ...state, shouldShow: false };
        }

        return state;
     });
}, 100);

codesandbox
Another solution would be to debounce a function which sets the hasFocus state to false, which imo is way better.

A: In your case i think that the usage of the shouldShow state is redundant and you can also avoid using a timeout which may lead to bugs.
You can take advantage of the FocusEvent.relatedTarget attribute and prevent hiding the extra fields when blur from an input and focus to another happens simultaneously.
The handleOnBlur function should look like this:
  const handleOnBlur = (e) => {
    if (e.relatedTarget && e.relatedTarget.name === "other_input") return;

    if (!formState.message.trim() && !formState.other_input.trim()) {
      setFocus(false);
    }
  };

You can find a working example in this code sandbox.
The problem with this approach is that if you have multiple fields appearing you need to check if any of those is focused like below:
["other_input", "another_input"].includes(e.relatedTarget.name)


Kentucky basketball has been at its best when John Calipari has had a rim protector anchoring his defense.
And the Wildcats could have another elite rim protector in freshman Nick Richards, who was profiled by CoachCal.com as part of its 'Meet the Wildcats' series.
But Richards wasn't always destined for basketball stardom, spending time as a skateboarder and a soccer player before entering high school at 6 foot 10 and somewhere between 180 and 190 pounds.
It wasn't easy early on.
And he's well aware of what his role is, and willing to be that kind of star noting that "if it takes 'three points, 20 rebounds and seven blocks' to win a game," he'll take it.
Kentucky fans are happy that he is Brad Calipari Jersey, with the former No. 17 player in the 247Sports Composite ready to put on show for Big Blue Nation.


text:
Хорас Маккой () е американски журналист, драматург, сценарист и писател на произведения в жанра трилър, криминален роман и драма.

Биография и творчество
Хорас Стенли Маккой е роден на 14 април 1897 г. в Пеграм, Тенеси, САЩ. Израства в Тенеси и Тексас. От малък е запален читател. По време на Първата световна война служи във въздушния корпус на Съединените щати. Има няколко мисии като фотограф зад вражески линии на бомбардировачи и разузнавачи. Ранен е и получава Военен кръст за заслуги към Франция от правителството на Франция.

След войната, в периода 1919 – 1930 г. работи като спортен редактор на "Далас джърнал" в Тексас. През 1924 г. става и радиокоментатор на бейзболни срещи. В края на 20-те години започва да пише криминални истории за различни пълп-списания. Публикува първия си разказ през 1927 г.

Участва и като актьор в Малкия театър в Далас. Когато режисьорът на театъра, Оливър Хиндел, отива да работи в MGM в Холивуд, Маккой го последва, за да стане филмов актьор. Участва в един филм, след което се включва към сценаристите. За да се издържа работи и на различни други временни места.

Работата му в киното го вдъхновява да пише романи. Първият му роман "Уморените коне ги убиват, нали?" е издаден през 1935 г. Той представя историята на един танцов маратон от епохата на депресията. Романът е успешен и през 1969 г. е екранизиран в едноименния филм с участието на Джейн Фонда.

Следващият му роман "Саванът няма джобове" е с главен герой героичен и неразбран репортер. През 1948 г. е публикуван романът му в стил ноар, "Прости се с утрешния ден", който е разказан от името на аморалния герой, Ралф Котър. През 1950 г. е екранизиран в едноименния филм с участието на Джеймс Кагни.

Романът му "I Should Have Stayed Home" (Трябваше да остана у дома) е история за преживяванията на млад актьор от южна страна, който се опитва да намери работа през 30-те години на Холивуд.

Произведенията на Маккой документират трудностите, с които американците се сблъскват по време на депресията и следвоенните периоди. Макар и недооценен по свое време, той е признат за значим автор като Дашиъл Хамет и Джеймс Кейн.

Хорас Маккой умира от инфаркт на 15 декември 1955 г. в Бевърли Хилс, Холивуд.

Произведения

Самостоятелни романи
 They Shoot Horses, Don't They? (1935)Уморените коне ги убиват, нали?, София: "Народна култура", (1990), изд.: ИК "Бард", София (2014), прев. София Василева
 No Pockets in a Shroud (1937)Саванът няма джобове
 Kiss Tomorrow Goodbye (1948)Прости се с утрешния ден
 I Should Have Stayed Home (1951)
 Scalpel (1953)
 Corruption City (1959)

Сборници
 Thrillers (1983)

Екранизации и сценарии

Източници

  Биография и библиография във "Fantasticfiction"
  Биография и библиография в "Goodreads"
  Биография и библиография във "Venetian Vase"

Външни препратки

Американски писатели
Американски сценаристи
Американски писатели на трилъри
Автори на криминални романи
Американски драматурзи
Американски журналисти
Починали в Холивуд
Починали от инфаркт на миокарда

redpajama_set_name: RedPajamaWikipedia


text:
Gitelman syndrome combined with complete growth hormone deficiency
Se Ra Min, Hyun Seok Cho, Jeana Hong, Hae Il Cheong, Sung Yeon Ahn
Min, Cho, Hong, Cheong, and Ahn: Gitelman syndrome combined with complete growth hormone deficiency
Se Ra Min, MD1, Hyun Seok Cho, MD1, Jeana Hong, MD1, Hae Il Cheong, MD2,3,4, Sung Yeon Ahn, MD1
1Department of Pediatrics, Kangwon National University School of Medicine, Chuncheon, Korea.
2Department of Pediatrics, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
3Research Coordination Center for Rare Diseases, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
4Kidney Research Institute, Medical Research Center, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
Address for correspondence: Sung Yeon Ahn, MD. Department of Pediatrics, Kangwon National University Hospital, 156, Baengnyeong-ro, Chuncheon 200-701, Korea.
Tel: +82-33-258-9136, Fax: +82-33-258-2418, ahn74@kangwon.ac.kr
Received February 04, 2013 Revised March 14, 2013 Accepted March 18, 2013
Gitelman syndrome is a rare autosomal recessive hereditary salt-losing tubulopathy, that manifests as hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutations in the solute carrier family 12(sodium/chloride transporters), member 3 (SLC12A3) gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT) in the distal convoluted tubule of the kidney. It is associated with muscle weakness, cramps, tetany, vomiting, diarrhea, abdominal pain, and growth retardation. The incidence of growth retardation, the exact cause of which is unknown, is lower than that of Bartter syndrome. Herein, we discuss the case of an overweight 12.9-year-old girl of short stature presenting with hypokalemic metabolic alkalosis. The patient, on the basis of detection of a heterozygous mutation in the SLC12A3 gene and poor growth hormone (GH) responses in two provocative tests, was diagnosed with Gitelman syndrome combined with complete GH deficiency. GH treatment accompanied by magnesium oxide and potassium replacement was associated with a good clinical response.
Keywords: Gitelman syndrome, Sodium Chloride Symporters, Growth hormone
Gitelman syndrome is a rare autosomal recessive renal tubular disorder1). Characteristic laboratory abnormalities are hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is usually caused by mutations in the SLC12A3 gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT) in the distal convoluted tubule of the kidney2). Diagnosis is most often made incidentally during adolescence or early adulthood. Although Gitelman syndrome is sometimes asymptomatic, it can present with clinical symptoms such as fatigue, muscle weakness, cramps, tetany, vomiting, diarrhea, and abdominal pain. Growth retardation and poor weight gain are common features, but are less severe than in Bartter syndrome3). Although potassium depletion may have some negative effect on growth, the exact cause of growth retardation in Gitelman syndrome is unknown. Reports of Gitelman syndrome combined with growth hormone (GH) deficiency are quite rare. Here, we report on a girl with Gitelman syndrome, diagnosed by molecular evaluation, combined with GH deficiency.
A 12.9-year-old girl visited our department of pediatrics complaining of chronic abdominal pain and diarrhea. She had also experienced tetany of the hand and foot for several months. At her full-term birth, her weight was 2.75 kg. Her family history had no history of renal, endocrinologic, or cardiovascular disease. Her father's height was 170 cm, her mother's 155 cm, and the midparental height, 156 cm. She had no history of diuretics use. Her height was 138.4 cm (<3rd percentile, -2.33 standard deviation score [SDS]); her weight was 43.3 kg (25th-50th percentile, -0.23 SDS); her body mass index was 22.7 kg/m2 (85th-90th percentile). The puberal stage was breast II and pubic hair I, and her bone age, according to the Greulich-Pyle method, was 11 years. Her blood pressure was 100/60 mmHg. Initial biochemical analysis revealed, on the basis of the following values, metabolic alkalosis with hypokalemia: sodium 139 mEq/L, potassium 2.4 mEq/L, chloride 98 mEq/L, blood urea nitrogen 5.8 mg/dL, creatinine 0.4 mg/dL, aspartate aminotransferase 48 U/L, alanine aminotransferase 67 U/L, pH 7.467, PCO2 47.4 mmHg, HCO3- 34.5 mmol/L (normal range, 22 to 26 mmol/L), base excess 9.6 mmol/L (-4 to 2 mmol/L), total calcium 9.9 mg/dL, phosphorus 4.7 mg/dL. Further laboratory investigation showed the following: magnesium 1.48 mg/dL (1.5 to 2.3 mg/dL), serum osmolality 218 mOsmol/kg (275 to 295 mOsmol/kg), renin 32.66 ng/mL/hr (<4.2 ng/mL/hr), and aldosterone 361.28 pg/mL (20 to 220pg/mL). Urine test results were as follows: Na+ 61 mEq/L, K+ 29.0 mEq/L, Cl- 57 mEq/L, osmolality 641 mOsmol/kg (50 to 1400 mOsmol/kg), spot urine calcium/creatinine ratio <0.02 mg/mg (0.03 to 0.2 mg/mg), 24 hours urine calcium 0.62 mg/kg (1.0 to 4.0 mg/kg/day), 24 hours urine magnesium 0.74 mg/kg (2.82±0.79 mg/kg/day). The calculated transtubular potassium gradient (TTKG) had increased to 8.078.
The patient had normal thyroid and parathyroid function. Abdominal ultrasound showed normal kidneys and diffuse mild fatty infiltration of the liver. GH stimulation tests for short stature revealed complete deficiency (Table 1). Magnetic resonance imaging of the brain revealed no remarkable findings. Her intelligence quotient as measured by the Korean Wechsler Intelligence Scale for Children III test was 67. Whole-blood DNA sequencing showed heterozygous mutation in the SLC12A3 gene (Fig. 1). Although her sister and brother were not genetically evaluated, they showed normal electrolyte and blood gas readings.
The patient was treated with 0.7 IU/kg/wk of GH and administered oral replacement of magnesium oxide (MgO, 1 g) and potassium chloride (KCl, 1.8 g). Serum photassium and magnesium level increased to 3.0 mEq/L and 1.85 mg/dL. She showed a 5.6 cm height gain over seven months. The frequency of abdominal pain and diarrhea markedly decreased, and the tetany and muscle-cramping symptoms were eliminated.
The patient, aged 12.9 years, presented with hypokalemia, metabolic alkalosis, and hyperreninemic hyperaldosteronism accompanied by short stature, obesity, and mild mental retardation. She was diagnosed with Gitelman syndrome by detection of heterozygous mutation in the SLC12A3 gene.
Gitelman syndrome results from various inactivation mutations in the SLC12A3 gene on chromosome 16q, which encodes the thiazide-sensitive sodium chloride cotransporter channel in the distal convoluted tubule. 172 distinct phenotype-variable mutations in the SLC12A3 gene have been reported4). Defects in the thiazide-sensitive NCCT impair Na+ and Cl- reabsorption, causing natriuresis and leading to volume contraction, which activates the renin-angiotensin-aldosterone axis. Increased aldosterone leads to secretion of K+ and H+, which causes hypokalemia and alkalosis5). Bartter syndrome also results from congenital renal tubule defects, the site of which is the thick ascending limb of the loop of Henle. Patients with Bartter syndrome present with symptoms in early childhood, and suffer a more severe failure to thrive. Patients with Gitelman syndrome, by contrast, are mostly asymptomatic or become fully symptomatic only in adolescence or adulthood6). Gitelman syndrome is associated with less severe growth retardation.
There are many factors that may contribute to growth retardation in Bartter or Gitelman syndrome. However, factors such as prematurity, significant salt loss in the antenatal-neonatal period, and marked polyuria are not present in Gitelman syndrome. Hypokalemia and metabolic alkalosis may have some effect on growth. Although hypokalemia can play key role in growth retardation, some patients still have growth problems after the normalization of serum electrolytes. Experimental studies, which found that rats fed a potassium-poor diet exhibited significant body-length reduction and weight gain, along with low levels of serum GH and insulin-like growth factor 1 (IGF-1), suggested that potassium depletion could have a negative effect on pituitary GH secretion7,8). Partial or complete GH deficiency has been found in several patients with either Bartter syndrome9-12) or Gitelman syndrome13-15). In all of the corresponding reports, growth response to GH treatment was generally good. In four reported cases of Gitelman syndrome with GH deficiency, growth velocity rose to 10.2-12 cm/yr during the first year of GH treatment. The girl in this report exhibited a 5.6 cm height gain during 7 months of GH treatment (growth velocity, 9.6 cm/yr). The reason for the association between hypokalemic tubulopathies and GH deficiency is not clear. GH treatment seemed to be helpful for the correction of hypomagnesemia. GH treatment has markedly increased magnesium absorption and retention in growing pigs16) and restored the serum magnesium levels in children with Gitelman syndrome13). In our case, as the patient was treated with MgO and GH simultaneously, the effect of GH on serum magnesium level could not be evaluated.
GH and IGF-1 treatment has been shown to not stimulate longitudinal growth unless to correct hypokalmeia in hypokalemic rats17,18). Experimental study demonstrated that potassium depletion leads to tissue-specific alteration in GH and IGF-1 metabolism in rats fed a potassium-deficient diet19).
Pubertal delay seems not to correlate with Gitelman syndrome symptoms. In this case, pubertal stage was delayed relative to chronologic age, but pubertal responses of LH and FSH to GnRH were observed.
If a child with Gitelman syndrome shows marked growth retardation, the GH-IGF-1 axis should be checked. GH treatment as well as the correction of serum potassium level is important for optimal growth. Further clinical research on Gitelman syndrome patients is required for more comprehensive analysis of the relations among growth retardation, abnormal GH-IGF-1 axis, and response to GH treatment.
This case report was supported by a grant (A120017) from the Korea Healthcare technology R&D Project, Ministry for Health, Welfare and Family Affairs, Republic of Korea.
1. Gitelman HJ, Graham JB, Welt LG. A new familial disorder characterized by hypokalemia and hypomagnesemia. Trans Assoc Am Physicians 1966;79:221–235. PMID: 5929460.
2. Abuladze N, Yanagawa N, Lee I, Jo OD, Newman D, Hwang J, et al. Peripheral blood mononuclear cells express mutated NCCT mRNA in Gitelman's syndrome: evidence for abnormal thiazide-sensitive NaCl cotransport. J Am Soc Nephrol 1998;9:819–826. PMID: 9596079.
3. Fremont OT, Chan JC. Understanding Bartter syndrome and Gitelman syndrome. World J Pediatr 2012;8:25–30. PMID: 22282380.
4. Vargas-Poussou R, Dahan K, Kahila D, Venisse A, Riveira-Munoz E, Debaix H, et al. Spectrum of mutations in Gitelman syndrome. J Am Soc Nephrol 2011;22:693–703. PMID: 21415153.
5. Graziani G, Fedeli C, Moroni L, Cosmai L, Badalamenti S, Ponticelli C. Gitelman syndrome: pathophysiological and clinical aspects. QJM 2010;103:741–748. PMID: 20650971.
6. Sinha A, Lnenicka P, Basu B, Gulati A, Hari P, Bagga A. Gitelman syndrome: novel mutation and long-term follow-up. Clin Exp Nephrol 2012;16:306–309. PMID: 21964762.
7. Flyvbjerg A, Dorup I, Everts ME, Orskov H. Evidence that potassium deficiency induces growth retardation through reduced circulating levels of growth hormone and insulin-like growth factor I. Metabolism 1991;40:769–775. PMID: 1861625.
8. Gil-Pena H, Garcia-Lopez E, Alvarez-Garcia O, Loredo V, Carbajo-Perez E, Ordonez FA, et al. Alterations of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment. Am J Physiol Renal Physiol 2009;297:F639–F645. PMID: 19587145.
9. Ruvalcaba RH, Martinez FE. Case report: familial growth hormone deficiency associated with Bartter's syndrome. Am J Med Sci 1992;303:411–414. PMID: 1605173.
10. Boer LA, Zoppi G. Bartter's syndrome with impairment of growth hormone secretion. Lancet 1992;340:860–860. PMID: 1357289.
11. Akil I, Ozen S, Kandiloglu AR, Ersoy B. A patient with Bartter syndrome accompanying severe growth hormone deficiency and focal segmental glomerulosclerosis. Clin Exp Nephrol 2010;14:278–282. PMID: 20127383.
12. Buyukcelik M, Keskin M, Kilic BD, Kor Y, Balat A. Bartter syndrome and growth hormone deficiency: three cases. Pediatr Nephrol 2012;27:2145–2148. PMID: 22707176.
13. Ko CW, Koo JH. Recombinant human growth hormone and Gitelman's syndrome. Am J Kidney Dis 1999;33:778–781. PMID: 10196023.
14. Bettinelli A, Rusconi R, Ciarmatori S, Righini V, Zammarchi E, Donati MA, et al. Gitelman disease associated with growth hormone deficiency, disturbances in vasopressin secretion and empty sella: a new hereditary renal tubular-pituitary syndrome? Pediatr Res 1999;46:232–238. PMID: 10447120.
15. Slyper AH. Growth, growth hormone testing and response to growth hormone treatment in Gitelman syndrome. J Pediatr Endocrinol Metab 2007;20:257–259. PMID: 17396444.
16. Pointillart A, Denis I, Colin C, Lacroix H. Influence of exogenous porcine growth hormone on magnesium metabolism in intact pigs receiving normal magnesium intakes. Magnes Res 1994;7:39–42. PMID: 8054259.
17. Dorup I, Flyvbjerg A. Effects of IGF-I infusion on growth and muscle Na(+)-K+ pump concentration in K(+)-deficient rats. Am J Physiol 1993;264(5 Pt 1):E810–E815. PMID: 8388640.
18. Hochberg Z, Amit T, Flyvbjerg A, Dorup I. Growth hormone (GH) receptor and GH-binding protein deficiency in the growth failure of potassium-depleted rats. J Endocrinol 1995;147:253–258. PMID: 7490555.
19. Hsu FW, Tsao T, Rabkin R. The IGF-I axis in kidney and skeletal muscle of potassium deficient rats. Kidney Int 1997;52:363–370. PMID: 9263991.
Heterozygous mutations were detected in exon 3 and 15 of SLC12A3 gene. (A) a heterozygous c.494A>T (p.Gln165Leu) in exon 3, (B) a heterozygous c.1868T>C (p.Leu623Pro) in exon 15.
GnRH and GH stimulation tests showed normal pubertal response and complete GH deficiency
GnRH LH (mIU/mL) 0.1 12.52 10.18 6.88 3.98
FSH (mIU/mL) 2.71 15.94 18.36 16.38 14.16
Estradiol (ng/dL) 1.55
L-dopa GH (ng/mL) 0.18 0.37 0.88 0.3 3.5
Clonidine GH (ng/mL) 0.18 0.12 0.11 0.55 0.71
IGF-1 (ng/mL)a) 161.33
GnRH, gonadotropin releasing hormone; GH, growth hormone; LH, luteinizing hormone; FSH, follicle stimulating hormone; IGF-1, insulinlike growth factor 1.
a) Normal range for age: 191 to 462 ng/mL.
Efficacy of growth hormone therapy in adults with childhood-onset growth hormone deficiency2014 March;19(1)
Growth hormone treatment in non-growth hormone-deficient children2014 March;19(1)
Genetic syndromes associated with overgrowth in childhood2013 September;18(3)
Psychosocial Adaptation in Children with Growth Hormone Deficiency.2000 June;5(1)
Management of Young Adults with Childhood Growth Hormone Deficiency.2003 December;8(2)

redpajama_set_name: RedPajamaCommonCrawl


text:
You are at:Home»Columns»Google is trying to bully Bixby out of Samsung products
Google is trying to bully Bixby out of Samsung products
By Marce on	 29th Jul 2020 Columns, Industry News, News
It's strange to think that Google can easily trade with Samsung, a South Korean company, but its neighbours in China aren't allowed Google services on its devices. But does Google want Samsung to replace its beloved digital assistant Bixby? We're not sure.
According to a report by Bloomberg, Samsung and Google are in discussions to integrate more of its software — specifically looking at its digital assistant offerings. Google has the brilliant Google Assistant, that's by far the most advanced in the sector, while Samsung has Bixby, which is more of a nuisance than an assistant if you ask anyone in the Stuff office.
But this proposed deal will supposedly give the "…US tech giant's services more prominence on Samsung phones at the expense of those from the Korean manufacturer," as The Verge states it. That sounds like… Samsung is considering dropping Bixby? Which is hard to believe considering the company has been pushing its own assistant on mobile phone and TV users since it rolled out.
Apparently, this deal would also include promoting the Google Play Store in lieu of Samsung's own app store, which is fair. Because who uses the Galaxy App Store anyway?
Overlord Google?
Although we're convinced Bixby should be laid to rest already, we can't help but question Google's absolute power when it comes to the mobile space. Some competition is always good, because it gives the consumer a choice. There's not much choice when your only options are the Google Play Store and Google Assistant.
Speaking from personal experience, I can't fault Google's Assistant tech. Our smart home runs completely on Google and it just works. But a the same time, since using Huawei's Google-less devices, it's become clear that more choice is sometimes a good thing.
Because Huawei's phones are sans-Google Play Store, we've been introduced to the fantastic world of third-party downloaders. These give you all the options you'll get from Google and Apple's stores, and then some. Also, because you don't use your Google account to sign in to each and every app you download and log into, Google can't track your every move anymore. It's an oddly satisfying and freeing feeling.
It's also interesting that this comes as Google, and a bunch of other tech giants are trying to convince US lawmakers that they aren't abusing their powers. Hmmm. "The Play Store and Google's mandatory service bundling on Android phones have received heightened antitrust scrutiny, and a deal with Samsung could undermine Google's argument that the Android platform enables strong competition," The Verge reports. I tend to agree with them on this.
But convincing Samsung to drop its assistant baby won't be an easy task. Samsung has invested a lot of money and marketing budget in building its own ecosystem and driving people toward it. Samsung opting for Google Assistant would bolster Google's ecosystem, not its own.
We'll have to wait and see how these talks pan out because if there's one thing I've learnt from tech, is that you can't trust rumours and hearsay. And the most shocking news… generally comes as a surprise.
Google and Samsung join forces to conquer the world…not really, but maybe
Apple vs. Samsung: Samsung takes a hit before patent trial even restarts
Light Start: Takealot shells out millions, WhatsApp goes dark, the PS5 will be "affordable" and Google buys Fitbit
Light Start: Samsung closes factory, Westworld gets sneaky, Google warns against sideloading and we'll finally see Baldur's Gate 3


text:
World / Africa
Protesters march on Omar al-Bashir's residence amid calls to step down
Demonstrators mark second day of sit-in outside Sudanese president's compound
07 April 2019 - 18:11 Agency Staff
Sudanese armed forces watch protesters during a demonstration outside the military headquarters in the capital, Khartoum, April 7 2019. Picture: ASHRAF SHAZLY/AFP
Khartoum — Thousands of protesters held a sit-in outside Sudanese President Omar al-Bashir's residence in central Khartoum on Sunday, having camped there overnight, following the biggest demonstration in months of protests against his 30-year rule, witnesses said.
At least one person died on Saturday during "rioting" in Omdurman, Khartoum's twin city, state news agency Suna said.
Sudan has seen months of mostly small but sustained protests in which dozens of demonstrators have been killed dissenting against Bashir's rule. Security forces have used tear gas, stun grenades and live ammunition to disperse protests.
Bashir has refused to step down, saying that his opponents need to seek power through the ballot box.
Since the sit-in began on Saturday, security forces tried several times to clear the protesters from the compound's vicinity using tear gas, including on Sunday morning, but thousands remained.
Sudanese activists called for Saturday's protests to mark the anniversary of the 1985 military coup that overthrew autocratic president Jaafar Nimeiri following mass protests against his rule. The protesters urged the military to side with them once more in their bid to push Bashir out of power.
Apart from Bashir's residence, the compound, the most heavily guarded in Sudan, also houses the defence ministry and the headquarters of the national intelligence and security service.
Get our news and views in your inbox
Thousands of protesters also gathered in the Burri neighbourhood of Khartoum on Sunday, where they blocked several main roads, witnesses said.
The person killed on Saturday was a laboratory doctor who died of his injuries, according to a statement from an opposition doctors' committee. Medical staff have played a prominent role in the protests.
Suna said other civilians and police officers were wounded on Saturday in Omdurman.
Police and security forces on Saturday blocked all bridges leading to the capital's centre from Khartoum North and Omdurman, across the River Nile to the north and west respectively, in what appeared to be a bid to prevent the sit-in from swelling.
The bridges remained closed on Sunday, causing traffic jams.
Sudan protest demands are legitimate but caused deaths, says president
Omar al-Bashir admits in parliament the economic crisis that triggered the demonstrations has affected a wide section of the country
Sudan journalists protest over jailed editor, say witnesses
Osman Mirghani was seized by security agents in February after commenting on President Omar al-Bashir's decision to implement a state of emergency
Sudan protesters rally as new cabinet is sworn in
Anti-Bashir demonstrators take to the streets in Khartoum
Women lead protest against Bashir
Protests initially erupted on December 19 after a government decision to triple the price of bread.
US judge slashes Roundup jury award to $25m from ...
World / Americas
Almost 20-million children not vaccinated in 2018
Pro-China mayor is the face of the opposition in ...
World / Asia


text:
2021 NBA All-Star Game Betting Picks – Team LeBron vs. Team Durant
Posted by underdog | Mar 5, 2021 | Basketball Betting Picks, Sports Betting Picks | 0 |
Now that the two team captains completed their draft for the 2021 NBA All-Star Game, we will analyze both teams and determine which team has the edge to cover the odds for the match.
LeBron James leads one team and picked eleven players. On the other hand, Kevin Durant picked twelve players because he can't participate in the game due to an injury. Handicappers are leaning towards Team LeBron. Thus, his team is 3.5-point favorites over the other team.
Analysis and Predictions for 03/07/2021
It is the fourth year that the NBA All-Star went for the format. LeBron won the first three games. In 2021, King James enlisted several former NBA MVPs in his lineup. According to sportsbook pay per head reports, he picked Steph Curry and Giannis Antetokounmpo. James said he based his selection on what the players have done lately.
According to basketball news, James got four of the top seven scoring leaders in league with Curry, Damian Lillard, Antetokounmpo, and Luka Doncic. Also, he got five players of the top 11 assist leaders, including Chris Paul, Doncic, Nikola Jokic, Lillard, and Ben Simmons. He also got rebound kings in his roster, including Rudy Gobert, Antetokounmpo, Domantas Sabonis, and Jokic.
On the other hand, Durant picked five of the top ten scoring leaders, including Bradley Beal, Joel Embiid, Zach Lavine, Kyrie Irving, and Kawhi Leonard. Also, he got two former MVPs in James Harden and Leonard. However, Harden is the only assist leader in Durant's lineup.
2021 NBA All-Star Game Betting Picks
Game time: 03/07/2021 at 8 PM ET
Bet on team Lebron at -3.5
Our free sports betting picks are for Team LeBron. King James will win his fourth All-Star game in a row. He won by an average of 6 points, which would cover the spread.
PreviousSimplebet Raises Millions for New Sports Betting Service
NextNewcastle United vs Aston Villa Betting Pick – Premier League Predictions
Jaguars vs Ravens Betting Pick – NFL Week 15 Predictions
Giants vs Mariners Betting Pick – MLB Predictions
Newcastle United vs Aston Villa Betting Pick – Premier League Predictions


text:
SACSETI
SACSETI Mission Statement
SACSETI Philosophy
UNIVERSAL MEMBERSHIP
SACSETI EVENTS
SIRIUS SCREENING 15th June 2013
The Citizens Hearing On Disclosure
The Disclosure Project
Whistle Blowers Testimony
The CE-5 Initiative
Self Investigations –
Famous Cases
Report a close encounter
CE-5 Research Group
Documentaries –
THE THRIVE MOVEMENT
SIRIUS DISCLOSURE
OUT OF THE BLUE – HD FEATURE FILM
THE FRIENDSHIP CASE
FORBIDDEN ARCHEOLOGY: Secret Discoveries of Early Man
THE SILENT REVOLUTION OF TRUTH – UFOs and Prophecies from Outer Space
Intriquing Quotes
Mainstream Hints
The Phoenix Lights – An Historic Event
On October 13th 1997, Residents of Phoenix in Arizona witnessed an enormous triangular ship that hovered motionless for 106 minutes and made no sound whilst 'hovering' above the densely populated city. Over 10,000 people claim to have witnessed this mysterious sighting including various military and police personnel and even then governor Fife Symington who described the event as other worldly.
Since then, major grass roots effort have been carried out to explore, research and bring out this valuable information to the general public and the world.
"THE PHOENIX LIGHTS – WE ARE NOT ALONE"
Producers Lynne D. Kitei, M.D. and Steve Lantz present their Internationally award-winning film, an in-depth examination of the mile-wide, V-shaped light formations and craft witnessed by thousands of people in Phoenix and throughout Arizona on March 13th 1997. UFO buffs call it "the most documented unexplained mass sighting ever recorded."
Dr Lynne D. Kitei who was one of the key witnesses of the event has since then pushed aside her successful medical career as an acclaimed physician and health educator to pursue the Phoenix Lights Book and internationally award-winning documentary project.
To support the Phoenix Lights Documentary and project, please visit their website and start your journey of exploration into the most witnessed and talked about sightings of our modern era.
http://www.thephoenixlights.net/
By Ashley Epstein | July 29, 2014 | Blog, Education, Investigations | No Comments |
← John E. Mack.
Ariel School Sighting in Ruwa, Zimbabwe →
"It now seems quite clear that Earth is not the only inhabited planet. There is evidence that the bulk of the stars in the sky have planetary systems. Recent research concerning the origin of life on Earth suggests that the physical and chemical processes leading to the origin of life occur rapidly in the early history of the majority of planets within our Milky Way galaxy–perhaps as many as a million–are inhabited by technical civilizations in advance of our own. Interstellar space flight is far beyond our present technical capabilities, but there seems to be no fundamental physical objections to preclude, from our own vantage point, the possibility of its development by other civilizations."
Carl Sagan, Ph.D. (Late Professor of Astronomy and Space Sciences, Cornell University)
Join The Global Awakening
Federal Aviation Administration Chief John Callahan -The Anchorage Incident August 23, 2014
VALLEE, JACQUES – ( French Scientist & UFO Investigator ) August 17, 2014
Ancient Aliens on the Moon? August 13, 2014
Astronaut Edgar Dean Mitchell – Sixth Man on the Moon August 10, 2014
The Collective Awakening of Mankind August 6, 2014
Cynthia Hind ( South African Ufologist ) July 29, 2014
Copyright © 2019 | Theme by: Theme Horse | Powered by: WordPress


text:
Sheboygan County reports 7 more COVID-19 deaths; more than half of the county's deaths have come since Nov. 1
Matt Piper
Sheboygan Press
SHEBOYGAN — COVID-19 has contributed to the deaths of seven more Sheboygan residents, the county health department reported Tuesday.
It's the second-most deaths reported in a single day, after nine on Nov. 10. Of the 61 deaths in the county since the start of the pandemic, 32 have come since the start of November, and 10 have been reported already this week.
Of deaths reported Tuesday, one person was in their 40s, one was in their 50s, one was in their 70s and four were 80-plus.
The health department doesn't provide other details about those who died, except that COVID-19 was either the cause or a significant contributor in their deaths. (They didn't die for non-COVID reasons, like an accident or an overdose.)
A record 107 COVID-19 deaths were announced statewide Tuesday, after smaller increases over the weekend. Seventy-three deaths were announced in the previous four days combined.
Both Sheboygan County and the state Department of Health Services note that it can take several days to confirm a COVID-19 death, so the date they're reported doesn't always reflect the actual date of death.
Of those who've died in the county since the pandemic began, two have been in their 30s, three in their 40s, five in their 50s, 10 in their 60s, 15 in their 70s, and 26 were 80-plus.
The county health department's Tuesday report also included 57 positive results out of 216 new tests, or about 26% positivity.
That marked the fewest new cases reported in a day since Oct. 11, after the county on Monday reported 391 cases since Thanksgiving.
Twenty-four people were hospitalized with COVID-19 Tuesday, up two from Monday.
Testing is still available on Wednesdays and Fridays at the Sheboygan County Aging and Disability Resource Center parking lot in Sheboygan Falls through Dec. 9. The health department recommends registering ahead of time at www.register.covidconnect.wi.gov.
If you have questions or immediate needs related to COVID-19, you can text COVID19 to 211-211, visit 211Wisconsin.org or call 211.
Contact Matt Piper at (920) 810-7164 or mpiper@gannett.com. Follow him on Twitter at @matthew_piper.


text:
Time to compromise for climate: French FM
French Foreign Minister Laurent Fabius speaks to the press outside the Palais Coburg Hotel in Vienna, Austria on July 13, 2015
French Foreign Minister Laurent Fabius urged top diplomats from 45 nations Monday to "start looking now for compromise" in forging a global climate rescue pact.
"Our negotiators are being stymied by political questions they can't always resolve at their level" of authority, he told foreign and environment ministers gathered in Paris to give a boost to the flagging process.
"We ministers have to start looking now for compromise on the big political issues," he added.
"That's how the negotiations are going to move forward."
Paris will host a 195-nation UN climate conference from November 30 to December 11 which will be tasked with hammering out a worldwide deal to hold dangerous global warming in check.
The current draft of the accord is an unwieldy, 80-page laundry list of sticking points and options, France's top negotiator, Laurence Tubiana, told journalists last week.
Underscoring the urgency of the task, the US National Oceanic and Atmospheric Administration (NOAA) reported Monday that the first half of 2015 was the hottest on record.
Fabius urged ministers and senior officials to narrow the gap on two issues in particular, starting with the level of ambition—a term meaning the scale of curbs in carbon emissions.
The UN has enshrined a goal of limiting average global warming to two degrees Celsius (3.6 degree Fahrenheit) over pre-industrial levels. Scientists say disastrous climate impacts can be avoided at this threshold.
But many countries, especially poorer ones, say this is not ambitious enough.
Another issue that has bedevilled the UN climate talks almost since they started more than 20 years ago, is how to share responsibility for curbing carbon emissions.
Developing countries want rich nations, which have polluted for longer, to bear more of the burden.
But the United States and others point the finger to developing states like China and India burning through vast carbon stocks to fuel their fast-growing populations and economies.
The two Asian giants now account for more emissions than the United States and European Union together.
Ministers in Paris to boost flagging climate talks
Citation: Time to compromise for climate: French FM (2015, July 20) retrieved 18 January 2020 from https://phys.org/news/2015-07-compromise-climate-french-fm.html
Pace of climate talks far too slow: UN chief
Periled by climate change, Marshall Islands makes carbon pledge
World Bank urges 'substantial' pre-2020 climate funds
UN climate talks stall despite G7 push on carbon
Final week of climate talks start with new draft text
Race to save animals on Australia's fire-ravaged 'Galapagos'
Oceans were hottest on record in 2019
New climate models suggest Paris goals may be out of reach
Study weighs deep-sea mining's impact on microbes


Brian Wilson & Jeff Beck Announce their Rock 'N' Roll Fantasy Camp April 18-21 in Las Vegas!
Legendary Rock and Roll Hall of Famers Revered Singer/Songwriter Brian Wilson and Renowned Guitarist Jeff Beck Announce their Rock 'n' Roll Fantasy Camp April 18-21 in Las Vegas!
Learn, write, record, and perform alongside "one of the greatest living songwriters of the 20th century" and "one of the most influential guitarists in the history of rock music".
Los Angeles, CA - February 27, 2013 - For only four days this spring Rock 'N' Roll Fantasy Camp is presenting a once-in-a-lifetime musical experience dedicated to two Rock and Roll Hall of Fame living legends. Join the 2013 Grammy Award-winning, renowned singer/songwriter and co-founder of The Beach Boys Brian Wilson and eight-time Grammy Award-winning, revered guitar virtuoso Jeff Beckin Las Vegas this April 18-21 for an exclusive music camp. Hosted at the MGM Grand Hotel & Casino and the camp's facility located west of the Las Vegas Strip, this is your chance to attend a music camp that will take you up close and behind the scenes teaching you the songwriting skills to perfect your compositions and learn the inside musical performance techniques of Wilson and Beck.Registration is open now. Please call 1-888-762-2263 or visit www.rockcamp.comonline for further details, up-to-date camp information and to make your reservation - spaces are limited!
Named "one of the greatest living songwriters of the 20th century," Brian Wilson will be bringing his personal longtime team of professional musicians including musical director and guitarist Jeffrey Foskett, band members Darian Sahanaja on keyboards, Probyn Gregory on bass, and Scott Bennett on drums to teach you everything about one of the great American songbooks. Additional session players and touring band members will be joining the camp alongside special guestsand rock star counselors.
Dubbed by Rolling Stone as "one of the most influential guitarists in the history of rock music," Jeff Beck has been a pioneer of sound spanning across nearly every genre of music. As a member of the Yardbirds, the Jeff Beck Group, and as a solo artist, Beck has recorded and performed alongside a musical A-list for over five decades creating a masterful and timeless canon of work.
Rock 'N' Roll Fantasy Camp is an event unlike any other. All experience levels are welcome regardless of musical ability, fans and musicians alike wanting to participate in this one-of-a-kind experience will be able to learn, sing and perform alongside all of Wilson's and Beck's songs.
Campers that attend will play in a band led by one of Rock 'n' Roll Fantasy Camp's Rock Star counselor like: Billy Hinsche (Dino, Desi & Billy), Danny Seraphine (Chicago), Jeff Foskett (Brian Wilson Band), Teddy Andreadis (Guns N' Roses), and MANY more! Attendees will join in master classes with world-class professional musicians, write and record an original song, and take part in live rehearsals. Even if you aren't interested in picking up an instrument, camp counselors will be conducting in-depth vocal lessons and mentoring sessions to help shape your vocal chords into something you only hear on the radio. At the culmination, campers will perform a live concert at theRouge Lounge inside the MGM Grand in front of family and friends, with everyone to enjoy their very own intimate, private concert by Brian Wilson and the band, making this four-day experience priceless!
Attendees will be given the option to bring their own instruments, or use the camp musical equipment provided by Roland, Boss, DW Drums, JamHub, Newtek, Four Star Wire and Cable, Fender, Gibson, My Star Sound, Zildjian, Cakewalk, and Electro-Voice. All backline is provided including amps, drum kits, PA, and keyboards. This is the ultimate fan experience.
Past rock star camp counselors have included Gene Simmons (KISS), Warren Haynes (Allman Brothers, Gov't Mule), Bill Wyman (The Rolling Stones), Slash, Bret Michaels (Poison), Brian Wilson (The Beach Boys), Cheap Trick, Dr. John, George Thorogood, Jack Bruce (Cream), Mark Farner (Grand Funk Railroad), Jane Wiedlin (The Go-Go's), Joe Satriani, Joe Walsh, Meatloaf, Mickey Hart (The Grateful Dead), Lita Ford (The Runaways), Steve Vai, Todd Rundgren, Vince Neil (Motley Crue), Duff McKagan and Matt Sorum (Guns N' Roses, Velvet Revolver), Michael Anthony (Van Halen) and Rudy Sarzo (Ozzy Osbourne, Quiet Riot), among others.
Upcoming Rock 'N' Roll Fantasy Camps include March 5-9: Sammy Hagar, Steve Vai, Eddie Trunk and many more; and April 4-7: the Def Leppard Fantasy Camp. Please call 1-888-762-2263 or visitwww.rockcamp.comonline for further details, up-to-date camp information and to make your reservation.
The recent recipient of a 2013 Grammy Award for his "long-lost" but not forgotten masterpiece The SMiLE Sessions, Brian Wilson is a world-renown singer and performer named "one of the greatest living songwriters of the 20th century." This past summer, the hottest concert ticket the world over was the Beach Boys 50th Anniversary Reunion Tour with sold out shows across the globe. Recently,River Road Entertainment and John Wells Productions announced they are in development on the Wilson biopic titled Love & Mercy. Academy Award nominated producer Bill Pohlad is set to direct with Paul Dano (Looper, Ruby Sparks, There Will Be Blood) to star as Wilson in his early years.
FROM RECORDING THE BEATLES (MAGICAL MYSTERY TOUR AND THE "WHITE ALBUM"), TO PRODUCING FOUR DAVID Bowie albums (including Ziggy Stardust) and two by Supertramp, to working with Elton John, Pink Floyd, Procul Harum, Jeff Beck, Duran Duran, Harry Nilsson, the Rolling Stones, Lou Reed, Devo, Kansas, the Tubes, and more, Ken Scott may well have shaped more of the sonic landscape of modern music than any other one person.


In the Gospel, Jesus extends a paradoxical invitation: Take up a "yoke" to find rest. What did He mean?
Today's reading is best understood in its context within Matthew's Gospel. In the preceding verses, Jesus upbraids some of the cities of Galilee for refusing to repent and believe in Him as Israel's Messiah, even though they had seen Him perform many "mighty works." Their proud resistance to Jesus, the carpenter's Son, brought them spiritual blindness. Because He had revealed so much to them without a response of repentance and faith, He warned them: "…it shall be more tolerable on the day of judgment for the land of Sodom than for you" (Mt 11:24).
It was "at that time" that Jesus turned to His Father with praise and gratitude: "I give praise to You, Father, Lord of heaven and earth, for although You have hidden these things from the wise and learned, You have revealed them to little ones." Jesus here contrasts the "wisdom" and "learning" of the religious leaders of the people, the scribes and Pharisees, to the simplicity of "little ones." Opposition to Jesus always came from the ones who prided themselves on their knowledge of Scripture and the tradition of the Jews in the Mosaic Law. Their knowledge, sadly, didn't lead them to humility. The power they derived from their privileged positions corrupted them, so much so that Jesus once told the people: "The scribes and the Pharisees sit on Moses' seat; so practice and observe whatever they tell you, but not what they do; for they preach but do not practice. They bind heavy burdens, hard to bear, and lay them on men's shoulders; but they themselves will not move them with their finger" (Mt 23:2-3). The Law of Moses was meant to be a joy for God's people, showing them the path to life. It was to be an escape from sin, into which all of us are born, that was even more liberating than their escape from physical slavery in Egypt (see CCC 2057). However, through pride and hard hearts, the "wise" and "learned" manipulated and added so much to the Law that it became a crushing burden on the very people it was meant to free.
Jesus says He will be the One to reveal God to those seeking Him, but not in an arbitrary, selective way: "Come to Me, all…" His invitation to share the intimate knowledge of the Father that is His through Sonship goes out to all who have the humility to accept it. Jesus knew that religion that did not lead to a relationship with God left its practitioner with a heavy burden—the weight of his own sin, as well as the unfulfilled longing of his heart to know his Creator. To that weary soul, Jesus promised rest, but in a paradoxical way. The rest would not come in cessation of activity but in taking on the "yoke" of Jesus. A yoke always forms a communion—a farmer yokes an animal to a plough, and together they dig up the soil. One animal is yoked to another, and together they share the burden of the work. When we take the yoke of Jesus upon ourselves and learn from Him, we discover that He has perfectly fulfilled God's Law for us. As St. Paul tells us, Jesus "emptied Himself, taking the form of a servant, being born in the likeness of men…He humbled Himself and became obedient to death, even death on a cross" (Phil. 2:7-8). When we are yoked to Jesus, we are yoked to His humble obedience. At long last, we "find rest" for ourselves. We are no longer alone. The yoke of Jesus, although it requires self-denial, is "easy" and His "burden light," because we share it with Him.
Who would turn down an invitation like this?
Possible response: Lord Jesus, I have often made my burdens in life heavier by trying to bear them alone. Help me yoke myself to You today.
Zechariah was a prophet during the time when a remnant of Jews who had been in exile in Babylon (punishment for their serious covenant unfaithfulness) were allowed to return to Judah and to re-establish the life they had lost as God's people (about 520 B.C.). Zechariah sought to stir up desire and commitment to re-build the Temple in Jerusalem, the center of religious life. Through him, the LORD gave prophetic visions of a future Messianic king who would rule over a restored kingdom of David.
This prophecy helps us understand why Jesus, hundreds of years after it was written, would describe Himself as "meek and humble of heart," offering "rest" to the weary. The humble Messiah had finally arrived, and only the humble could "see" Him.
Possible response: Lord Jesus, help me remember that victories in Your kingdom are won through humility, not might.
St. Paul gives us a practical application of what happens in our lives when we respond to Jesus' call to take His yoke upon ourselves. The "rest" He offers is our "rest" from the weight of sin. St. Paul tells us that, as believers, we now have God's own Spirit living in us. The work of the Spirit is to free us from the death-producing power of our "flesh." St. Paul uses this term to describe the sin that seeks to rule us as we dwell in our mortal bodies (concupiscence). Our bodies, made in God's image and likeness, are good, but our rebellious self-love always tries to subvert them. Jesus' victory over sin, death, and the devil means that believers, through baptism, have the gift of the Holy Spirit to disrupt and destroy the power of sin over us. That is why Jesus said, "My yoke is easy, and My burden light" in our Gospel reading. As St. Paul says, the "yoke" of Jesus will mean death to our flesh—mortification—but we are not alone in this work of liberation. The Spirit enables us to "put to death the deeds of the body" so that we "will live." The heavy mastery of our own sin over us, experienced as our crushing inability to be the people we know we ought to be, is now broken. Finally, we can find rest.
Possible response: Holy Spirit, help me do battle with the self-love that so easily besets me. I know all it can offer is death.


text:
The following is a list of county roads in Palm Beach County, Florida.  Roads are maintained locally by the Palm Beach County Engineering and Public Works Department. Nearly every route in this list is a former state road since decommissioned by the Florida Department of Transportation. Most routes are signed using standard county road shields, but some are unsigned on streets.

County Road A1A

County Road A1A is a former routing of SR A1A through Juno Beach and Jupiter. It serves as a paralleling alternate route to Federal Highway (US 1), running parallel to the Atlantic Ocean. CR A1A is often signed as "SR A1A" in green street signs despite county designation shields and maintenance. The road is known as Ocean Drive in Juno Beach and Ocean Boulevard in Jupiter, and is closed to through trucks.

Major intersections

County Road 700

County Road 700 is Connors Highway from an intersection with US 98 / US 441 / SR 80 and SR 700 to CR 880 in Twentymile Bend.

The road is a former routing of US 98, US 441, and SR 700. It has a posted speed limit of .

Major intersections

County Road 702

County Road 702 is 45th Street from Jog Road to US 1. The road was formerly designated SR 702.

Major intersections

County Road 704A

County Road 704A is Australian Avenue in West Palm Beach. The road is an extension of Congress Avenue (SR 807), and begins just north of an interchange with Southern Boulevard (US 98 / SR 80).  The road terminates at an intersection with Blue Heron Boulevard (SR 708) in Riviera Beach. The road was formerly designated SR 704A.

County Road 706

County Road 706 exists along two sections of Indiantown Road in and around Jupiter. The western segment was formerly designated SR 706, while the eastern segment is an extension of the current state road.

County Road 707

County Road 707 is South Beach Road from US 1 / SR 811 to the Martin County line in Tequesta. It was formerly designated SR 707.

County Road 711

County Road 711 is Pratt Whitney Road from SR 710 west of Palm Beach Gardens north to the Martin County line west of Jupiter. It was formerly designated SR 711.

Major intersections

County Road 717

County Road 717 exists in two segments. The first is a northwestern extension of SR 717 in Belle Glade, connecting SR 715 (Southwest 16th Street) with the Lake Okeechobee Scenic Trail and the Torry Island campground. The second segment begins at SR 729 in Pahokee and travels on Muck City Road east to SR 700 south of Bryant.

Both routes were formerly designated SR 717.

Major intersections

County Road 782

County Road 782 is the unsigned designation for Linton Boulevard in Kings Point and Delray Beach. CR 782's western terminus is at Jog Road (former SR 845) and it travels east to Ocean Boulevard (SR A1A).

The road was formerly designated SR 782.

Major intersections

County Road 792

County Road 792 is the unsigned designation for part of Woolbright Road around Boynton Beach. CR 792 begins at an intersection with Military Trail, which itself is a state-turned-county road. The road's eastern terminus is SR A1A. CR 792 was formerly designated SR 792.

Major intersections

County Road 794

County Road 794 is an unsigned extension of SR 794 along Yamato Road within incorporated and unincorporated Boca Raton.

County Road 798

County Road 798 is Palmetto Park Road in unincorporated and incorporated Boca Raton. The road was formerly designated SR 798. CR 798 forms the north–south boundary in the Boca Raton street numbering grid.

The road begins at an intersection with Glades Road (CR 808) outside the city limits and terminates at Ocean Boulevard (SR A1A) within Boca Raton.

Major intersections

County Road 806A

County Road 806A is a short segment of George Bush Boulevard in Delray Beach. The road, formerly SR 806A, begins at an intersection with Federal Highway (US 1) and heads east, bridging the Intracoastal Waterway, to terminate at Ocean Boulevard (SR A1A).

Major intersections

County Road 807

County Road 807 is a southern extension of SR 807 along Congress Avenue. It was formerly designated SR 807.

County Road 808

County Road 808 is a western extension of SR 808 along Glades Road in unincorporated Boca Raton.

County Road 809

County Road 809 is split into two segments of Military Trail that sandwich SR 809. The southern section was formerly a state-maintained road, while the northern is always a county-maintained extension.

County Road 809A

County Road 809A is the designation for Northlake Boulevard in the vicinity of Palm Beach Gardens. It was formerly designated SR 809 west of Military Trail and SR 809A east of it.

County Road 811

County Road 811 comprises a portion of Dixie Highway in West Palm Beach, which itself is a historic auto trail. This segment of the trail was formerly designated SR 811.

County Road 812

County Road 812 is the designation for Lantana Road from southeast of Wellington into Lantana, just south of Lake Worth. The road was formerly designated SR 812.

Major intersections

County Road 827

County Road 827 is the designation for three former segments of SR 827: an unnamed segment south of Belle Glade, Browns Farms Road east of Belle Glade, and Loxahatchee Road near the northern border of Parkland. The original route has since been bisected by the Loxahatchee National Wildlife Refuge.

County Road 827A

County Road 827A is an unnamed road south of Belle Glade, serving as an alternate route to US 27 along with CR 827. The road was formerly designated SR 827A.

Major intersections

County Road 880

County Road 880 is a signed route from Belle Glade to Twentymile Bend. It is a former routing of SR 80 (which now uses the Hooker Highway).

References

External links
FDOT General Highway Map, Palm Beach County

County


"Get a job, you racists, and stop playing the victim! Don't you remember the '80s?"
Does that sound like a successful political program to you? Does it sound like an adequate response when perhaps one-fourth or more of your party's voters are staging a minor revolt? Of course not. And yet, that is effectively the message the Republican elite is delivering to Donald Trump's disaffected white working-class supporters.
I recently suggested that the Republican Party, and the conservative movement, offer next to nothing to working-class Trump supporters. There are no obvious conservative policies that will generate the sort of growth needed to raise the standard of living for these working-class voters. Instead, the GOP's Powers That Be make a great show of obedience and deference to the center-right donor class, even when that donor class' preferred policies — endless war, unlimited immigration, and slashing tax burdens on the wealthy — have almost no relation to conservative ideas or even popular opinion.
Several columnists have responded critically to my original piece. They claimed to argue with me. Instead, they confirmed my thesis.
My friend Kevin Williamson implies in National Review Online that I am indulging in "racial identity politics to help poor whites feel better about dependency." Tom Nichols writes in The Federalist that I want to play the "bitter card of victimhood and entitlement that liberals use."
Williamson says that he'd rather poor whites "took the necessary steps to improve their condition in life." Nichols outlines some of these necessary steps, saying these men need "to stop fleecing the disability system, to kick their addiction, to be fathers to their children, to get a job no matter how low or unappealing it is, and to stick with it until you get a better one." He implies that I'm against this kind of virtue. That's wrong.
In fact, this is all great life advice. I would happily repeat it to anyone. But it illustrates rather than rebuts the problem I described. Issuing godly financial advice is the job of parents and pastors and personal-finance gurus. It is not a substitute for politics or government. It is not the conservative movement's nor the Republican Party's job to tell voters to keep their fingernails trimmed and to proofread their resumes, wise as those things may be. And it should be plain as day that such tut-tutting is certainly not going to win the loyalty of the party's down-on-their-luck base.
It is not enough to say, "Stop bothering us with your economic problems, and be more virtuous; we're too busy addressing the complicated problems of our rich patrons, and using the levers of the state to make it easier for them to invest in foreign work forces instead of the whiny entitled American worker." Which, is, of course, the message that has come through to Trump voters over the last two decades.
The conservative movement can no longer repeat its old formulas as if they were a magisterium given divine authority to guard the deposit of faith in 19th century's economic liberalism. "Get a job!" is an insufficient response to the problems faced by poor Americans.
I presume that most of the working-class whites who support Trump do want jobs. I doubt that, like Williamson, they see hard work in industries that are ringed by some tariff protections as the same kind of "dependency" as a straight welfare payment. (Do Lockheed employees suffer some stigma and self-doubt from this kind of dependency on government, I wonder?) But I am not yet even arguing for protective tariffs.
Despite a natural desire to work and to create, we've seen working-age men dropping out of the workforce at alarming rates for decades. Many of these men do some work, but remain underemployed in the service industries. And the overall picture of the decline of this once-middle class is not one of living high and happy on the dole; it's far more depressing than that. Some of them do stay on Social Security Disability, and some of them abuse it, because it is competitive with some of the low-paid service work that is relatively easy to find but hard for formerly proud men to take.
At the same time as this decline of work, the returns are starting to come in on the post-Cold War policies that elite conservatives have championed, namely free trade and liberal-to-uncontrolled low-skill immigration.
We also see better now than before that mass immigration of low-skilled workers does actually interact with the laws of supply and demand as you would expect; it lowers the wages of low-skilled American workers. Yes, technology has played a role in displacing workers. And yes, some forms of trade liberalization were obviously coming after the fall of the Iron Curtain. But economists did not expect the costs of these policies to be this concentrated.
America's elites, however, have won astounding gains during these decades with their ability to more easily invest in the development of foreign workforces, and to hire recent immigrants who don't share the typical American's democratic revulsion at entering into low-status service jobs at their great homes. The stock market proved resilient in the face of an economic crash, recovering and surpassing its previous value, even as real median household income is still almost $4,000 below the pre-recession level. Williamson says the answer is growth driven by investment. Growth is here, but it is captured at the top. Investors are getting gains. Why aren't others?
Without trying to hand working-class Americans a permanent victim card, we should allow ourselves to notice that following some of the bootstrapping advice that Williamson and Nichols offer as a substitute for political reflection is more difficult now than in the past. Why? The bootstrapping solution also requires resources — spiritual, social, habitual, familial, and cultural. These resources sometimes well forth from a man who has hit rock bottom in life; many callers into Dave Ramsey's radio show will testify to that. But for others these resources are usually "loaned," so to speak, from what conservatives used to treasure as the mediating institutions of our society — namely, families, churches, ethnic clubs, paternalistic employers, schools, and even unions. Collectively we might refer to these institutions as a kind of treasury of resources. My intuition, confirmed faintly by statistics on declining church attendance, rising divorce and cohabitation and illegitimacy, and the shortening terms of employment, suggest that these institutions have abandoned their paternalistic roles, or partly disintegrated, especially among working-class Americans. In other words, this treasury of resources is close to bankruptcy.
By their nature, the networking, emotional support, and loyalty traditionally delivered by these institutions to working people is almost invisible to policy wonks. These institutions push and pull. Men are much more urgent job-seekers and better job-keepers when they are living with a wife and children. Americans have slowed their pace of internal migration to find work, perhaps because moving to find work is more difficult when you are divorced and would leave children behind. Perhaps it is more difficult when you tried participating in George W. Bush's ownership society and over-invested in an inflated home that you can no longer afford to sell. Or perhaps it is more difficult because the institutions that you would seek out for social stimulation and solidarity in new places, like your denomination's local church or an Italian-American club, mean little to you now or have ceased to exist. That societal treasury, if it were full, could supply people with motivation, resources, and unofficial patronage networks to make difficult changes in life, like moving for work.
This state of affairs should be a frightening thing for any civic-minded American, particularly those who call themselves conservative. Long before American conservatives pledged themselves to the free-market tenets of Manchester liberalism in economics, the people defined by a conservative political persuasion dedicated themselves to protecting and defending those mediating institutions. If these institutions are in as much disrepair as I see, do conservatives have any idea how to regenerate them?
It is true that I manifestly do not have the answers yet, nor do I believe Donald Trump has them. My aim in trying to understand and explain Trumpism and generate sympathy for the people who find themselves supporting Donald Trump is not to ratify dependency or a sense of victimhood in working-class people; it's to slap conservatives out of a torpor, to tell them that they are not victims of this Trump-led populist revolt, but the authors of it. And to warn them that they make Trumpism inevitable by enabling the American elite and the political class in its cultural and economic secession from the rest of the American nation. And ultimately, my aim is to recruit men like Kevin Williamson and Tom Nichols into the incredibly inconvenient work of stripping away the policy ideas and political formulas that have grown stale over the last 20 years, and to revivify the American right, and the bonds that hold our nation together.


text:
Christian Church /
General /
Deep and Wide
Creating Churches Unchurched People Love to Attend
By Andy Stanley
Andy Stanley's bestselling and award-winning vision for the local church is now available in softcover. New bonus content includes a study guide, church staff helps, and an interview with Andy on the most frequently asked questions about Deep and Wide.
With surprising candor and transparency pastor Andy Stanley explains how one of America's largest churches began with a high-profile divorce and a church split.
But that's just the beginning...
Deep and Wide provides church leaders with an in-depth look into North Point Community Church and its strategy for creating churches unchurched people absolutely love to attend.
For the first time, Andy explains his strategy for preaching and programming to "dual audiences" mature believers and cynical unbelievers. He argues that preaching to dual audiences doesn't require communicators to "dumb down" the content. According to Stanley, it's all in the approach.
You'll be introduced to North Point's spiritual formation model: The Five Faith Catalysts. Leaders responsible for ministry programing and production will no doubt love Andy's discussion of the three essential ingredients for creating irresistible environments. For pastors willing to tackle the challenge of transitioning a local congregation, Andy includes a section entitled: Becoming Deep and Wide.
If your team is more concerned with who you are reaching than who you are keeping, the expanded edition of Deep & Wide will be more than a book you read; it will be a resource you come back to over and over
"Couldn't be prouder of my son, Andy. And I couldn't be more excited about the content of this book. I wish a resource like this existed when I was starting out in ministry."
- Dr. Charles Stanley, Founder, In Touch Ministries
"Deep and Wide pulls back the curtain for all of us to see what is required behind the scenes to build a prevailing church. I was both challenged and inspired by this book."
- Bill Hybels, author of Just Walk Across the Room
"The most common question I get from pastors is, 'How do I get the people in my church to be open to change?' From now on my answer will be, 'Read Deep and Wide by Andy Stanley'. Thanks Andy. Great book "
- Craig Groeschel, Pastor, LifeChurch.TV, author, It: How Churches and Leaders Can Get It and Keep It
"It is completely false that churches must sacrifice quality to get quantity, must artificially choose between evangelism and discipleship, or cannot have depth and growth at the same time. Few prove this fact better than the ministry of Andy Stanley, who has grown North Point Community Church on purpose and with passion. No Christian leader can afford to miss this book."
- Rick Warren, pastor, Saddleback Church; author, The Purpose Driven Church
Manufacturer: Zondervan
Author: Andy Stanley