Rubber Monkey was founded in the Winter of 1993. We built our first puppet stage and performed a traditional hand puppet show called "An Puppet Show" as part of a performance art event on the North side of Chicago. The show featured little vignettes entitled Kitty's Cooking, Contract Renegotiations at Puppetco, The Boat, Princess Faints, The Ballerina, The Puppet Critic, and more. The show also included a shadow puppet performance as the Intermission.
In 1994 we were asked to perform as part of a large Halloween Ball in an abondoned warehouse in downtown Chicago. Intriqued by shadow puppetry, we built a new stage specifically for that purpose. The show included original live music as well as shadow puppetry. We called it "7" after the number of scenes in the play.
Later that year we were asked to perform "7" at a banquet held upstairs at Morseland in Chicago. This gave us the opportunity to improve upon the design of our stage and the portability of our sound system.
Over the course of the next few months we were asked to provide the visuals via shadow puppetry for a couple of band performances at the Double Door and at the Metro.
In 1995 we were commissioned to create and perform a new play specifically for a fundraiser in Chicago. We redesigned the stage from the ground up, wrote an entire music score and created "The Haunted Toaster".
Later that year we were asked to do a double feature of both "7"and "The Haunted Toaster" at Poop Studios in Wicker Park.
While writing "Circus Politique" Patrick McCarthy, the founder of The Rubber Monkey Puppet Company, invented a mechanism that casts three dimensional shadows. During a traditional shadow puppet show there is a plain white screen separating the audience from the puppeteers. The audience simply watches the shadows cast on the screen by the puppets. During a Rubber Monkey Puppet Company show the shadows appear to leave the screen and project into the audience.
After performing for fundraisers, banquets, parties, bars, coffee shops, and galleries we decided to create our own permanent puppet theater.


text:
Kemfert ist der Familienname folgender Personen:
 Beate Kemfert (* 1964), deutsche Kunsthistorikerin
 Claudia Kemfert (* 1968), deutsche Wirtschaftswissenschaftlerin

Siehe auch:
 Kaempfert
 Kempfert

redpajama_set_name: RedPajamaWikipedia


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Objectives: To determine the LD50 and organ toxicity of monosodium glutamate (MSG). Materials and Methods: A total of 30 adult albino Wistar rats of both sexes were used in this study. Fifteen of them were used for acute toxicity test. The second stage of the experiment was performed with 15 rats which received 500 mg/kg, 750 mg/kg, 1000 mg/kg, and 1250 mg/kg of MSG thoroughly mixed with the feeds, respectively, with unlimited supply of drinking water on daily basis for 8 weeks. Group E, which was the control, received an equal amount of feeds without MSG. The animals' weights were measured weekly, constantly observed daily for systemic effects and later sacrificed at the end of 8 weeks in a desiccator under anesthesia with ether following an overnight fast. Blood was obtained by left ventricular cardiac puncture for biochemical analysis. The kidneys, heart, lungs, spleen, liver, and testis were dissected and fixed in 10% formal saline for histological examination using hematoxylin and eosin (Hand E) methods. Results: There was a significant increase in the mean weight of the animals and controls (P < 0.05). There was a significant decrease in the mean serum cholesterol levels, a significant increase in the mean fasting plasma glucose, and plasma alanine transferase levels of the experimental animals when compared with the controls (P < 0.05). The histological finding revealed a reduction in spermatocytes in testes of animals fed with 1000 mg/kg MSG plus necrosis and scanty seminiferous tubules. There was massive necrosis on the liver and lungs, fatty change in the spleen and degenerative changes of heart muscle cells. There were also irregular spaces of various shapes and sizes and necrosis in the kidney. Conclusion: The study demonstrated that consumption of MSG has deleterious effects in virtually all organs which will apparently affect their functions.
Noxious substances abound in our environment. We come in contact with them every day, either directly or indirectly. In either way, they may have an effect on our organs in particular and health in general. Few of these noxious substances such as carbon monoxide are inhaled; some such as are alcohol and tobacco are consumed, and much of these substances are added to our food in the form of additives. Most food additives act either as preservatives or enhancers of palatability. One of such food additive is monosodium glutamate (MSG). It is sold in most open markets and stores in Nigeria as "Ajinomoto," marketed by West African Seasoning Company Limited, as "Vedan" or "white magi" marketed by Mac and Mei (Nig) Limited.
The flavor-enhancing power of MSG was discovered to be glumate by Dr. Kikunae Ikeda in 1908. Glutamate is one of the most commonly occurring amino acids. It plays a crucial role in a broad variety of metabolic process, such as in the detoxification of drugs. It is also responsible for 75% of the excitatory neurotransmission in the brain. MSG is readily utilized by glutamate receptors throughout the mammalian body. These receptors could be found in the brain, spinal cord, conducting system; nerve terminals, kidney, liver, testis, lungs, spleen, and heart. Therefore, advocates of food safety should consider these organs as potential sites of damage. Neural injury associated with trauma, stroke, epilepsy, and many neurodegenerative diseases such as Alzheimer's, Huntington's, Parkinson's disease, and Amyotrophic lateral sclerosis was reported to have been mediated by excessive activation of the glutamate receptors. Thus, the free glutamic acid can get into the brain injuring and frequently killing neurons.
Adverse systemic reactions associated with consumption of MSG include: Arrhythmias, hypertension, angina, myalgia, arthritis, depression, dizziness, anxiety, hyperactivity, insomnia, numbness, seizures, diarrhea, nausea and vomiting, shortness of breath, nocturia, oligozoospermia.
Food containing MSG can be identified in the market with the following names: Enzyme modified, anything protein fortified or fermented, autolyzed yeast, broth, bouillon, natural flavoring, gelatin, olyzed protein, pectin, soy protein, sauce, stock, whey protein, yeast extract, and yeast food.
MSG has been used in newborn laboratory mice to induce adult obesity. This is because of the lesion it provokes in the arcuate nucleus of the hypothalamus, resulting in increased caloric intake above utilization of calories. MSG has been shown to trigger epileptic convulsions in rats. The severity of the convulsions and death incidence increased progressively with age.
MSG has a toxic effect on the testis by causing significant oligozoospermia and increased abnormal sperm morphology in a dose-dependent fashion in adult male Wistar rats. It has been implicated in male infertility, by causing testicular hemorrhage, degeneration, and alteration of sperm cell population and morphology.
It has been reported that MSG has neurotoxic effects resulting in brain damage, retinal degeneration, endocrine disorder, and some pathological conditions such as addiction, stroke, epilepsy, brain trauma, neuropathic pain, schizophrenia, anxiety, Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis.
Thirty adult Wistar rats of both sexes with average weight 160–200g were used for the study. Fifteen rats were used for acute toxicity test and the remaining 15 for the second stage of the experiment.
They were each assigned into five groups: Treatment group A, B, C, and D of n = 12 and control group of n = 3. The animals were obtained and bred at uniform conditions in the animal house of the Department of Pharmacology, College of Medicine, Abia State University, Uturu, Nigeria. They were acclimatized for 7 days before the study. The animals had free access to standard animal feeds purchased from a local commercial supplier and water adlibitum and housed under standard conditions of temperature (25°C ± 20°C), under 12 h light-darkness cycles. The MSG (3 g/satchet containing 99% MSG) was obtained from a grocery store at New Market, Aba in Abia State.
The rats in the treatment group A, B, C, and D were given, respectively, 500 mg/kg, 750 mg/kg, 1000 mg/kg, and 1250 mg/kg of MSG thoroughly mixed with their feeds, respectively, on a daily basis for 8 weeks. The control group E received equal amounts of feeds without MSG. The animals were sacrificed at the end of 8 weeks under anesthesia with ether after an overnight fast. About 3 ml of blood was obtained by left ventricular cardiac puncture from the rat and placed in a container for biochemical analysis. The kidneys, heart, lungs, spleen, liver, and testis were quickly dissected and fixed in 10%, formal saline for routine histological technique.
The tissues were dehydrated in ascending grade of alcohol (ethanol), cleared in xylene and embedded in paraffin wax. Serial sections of 6 microns thick were obtained using a rotatory microtome. The deparaffinized sections were stained routinely with hematoxyline and eosin (H and E). Photomicrographs of the desired sections were made for further observations.
Blood collected from the rats was used for fasting plasma glucose, cholesterol, and serum Alanine transaminase (ALT) estimation. Plasma glucose was assayed by Trinder (oxidase-peroxidase system). The serum cholesterol was determined by the method of enzymatic hydrolysis and oxidation. The serum ALT activity was assayed by a method of Reitman and Frankel. All determinations were performed within 24 h of a collection of sample.
Data were analyzed for mean, standard deviation, and compared for significance between the control and experimental groups using Chi-square. The level of significance for all experiment was P < 0.05.
The median lethal dose LD50 was found to be 500 mg/kg. This is the median of 200 mg/kg which did not kill any of the animals so administered and 800 mg/kg that killed all its animals.
Two weeks into the study, most of the animals in the experimental group became hyperactive. Four weeks later, one of the animals in the group fed with 1250 mg/kg of MSG developed bulging of eyeballs (exophthalmos), blurred vision, and had several bouts of seizures before its demise six days later. Most of the animals gained maximal weight in the course of the study.
Consumption of MSG worldwide with its attendant toxic effects still remains a concern to medical and food scientists.
A significant increase in weight was observed in rats fed with MSG. This was comparable to a similar study carried out to induce obesity in laboratory mice. This is probably because of the effect that it provokes in the arcuate nucleus of the hypothalamus, resulting in increased caloric intake above utilization. MSG also increases appetite and improves the palatability of the poor quality diet. There was a significant decrease in the mean cholesterol compared with the control. This is in contrast with the work of Savastanon et al. where the cholesterol level of the experimental group was higher than control. This could be attributed to the activation of the enzyme, 3-hydroxy-3-methoxyglutamyl-CoA reductase, which catalyzed the rate-limiting step of cholesterol synthesis.
Concerning glucose level, a significant increase was observed in the treated group compared to the controls. This result compares favorably with the work of Negata et al., where MSG was used to induce obesity in type 2 (noninsulin-dependent) diabetes mellitus in mice due to elevated blood glucose.
A significant increase in the serum ALT was observed in the MSG-treated rats compared to the control [Table 4].
This study was necessitated by the observed indiscriminate use of MSG in Nigeria for seasoning and flavor enhancing purposes without taking into consideration the possible adverse effects from its use over time, even at low concentrations. The ALT enzyme is a sensitive marker of liver damage. Therefore, the increase in serum ALT activity by 1%, 10.7%, and 28.1% in rats fed with MSG of 750 mg/kg, 1000 mg/kg, and 1250 mg/kg respectively, may perhaps be an indication of liver damage.
Thus MSG may be hepatotoxic at 750 mg/kg and above, hence should be avoided during the treatment of liver disorders. Since ALT was found to be a positive indicator of insulin resistance, diabetes mellitus and obesity, which are risk factors for coronary disease, the use of MSG at even low dose should not be encouraged because of the possible untoward implications.
The results of the H and E staining of the test is showed reduction in spermatocytes, vacuolations, patchy areas of necrosis and scanty seminiferous tubules of the group treated with 1000 mg/kg of MSG compared to the control. The vacuolations observed may be due to MSG interference.
In the liver, with increasing dose of MSG there was massive necrosis in the central vein and distortion of its cytoarchitecture compared to the control section. This distortion could be associated with functional changes that may be detrimental to health and may affect the hemopoietic function of the liver resulting in cell death. This occurs as a controlled event involving a genetic program in which caspase enzymes are activated.
In the spleens of the treated group, there was generalized fatty change, tissue hypertrophy, and massive infiltration of inflammatory cells. Histological features in the control group were normal. The fatty change reported in this study may have been induced by the toxic level of MSG. This can also be seen in the liver, muscle, and kidney. Other causes of fatty change (steatosis) include protein malnutrition, diabetes mellitus, obesity, and anoxia. In industrialized nations, alcohol abuse is so far the most common cause of fatty change, especially in the liver.
In the heart, there were degenerative changes of the cardiac muscles and necrosis. The mechanism by which MSG does this needs further investigation.
In the kidney, there was necrosis, reduction in the number of renal corpuscles and irregular shapes of various sizes in the treated group which was at variance with the control.
The necrosis observed may have been due to high doses of MSG on the kidney. Pathological or accidental death is regarded as necrotic and could result from extrinsic insults to the cell as osmotic, thermal, toxic, and traumatic effects.
Our study demonstrates that consumption of MSG has deleterious effects on virtually all the organs which will apparently affect their functions. Such negative effects call for caution in its use as a flavor enhancer and in industries.
It is, therefore, recommended that further studies be carried out to establish the mechanism by which effects its deleterious effects in the body.
1 Ikeda K. New seasonings. Chem Senses 2002;27:847-9.
2 Meister A. Biochemistry of glutamate. Glutamine and glutathione. In: Filer LJ Jr, Garattini S, Kare MR, Reynolds WA, Wurtman RJ, editors. Glutamic Acid: Advances in Biochemistry and physiology, Raven, New york; 1979. p. 69-84.
3 Ganong W. Review of Medical Physiology. 22nd ed. Singapore: Appleton and Lange, Lange Medical Publication; 2005. p. 107-8, 235.
4 Gill S, Mueller RW, McGuire PF, Pulido OM. Potential target sites in peripheral tissues and excitatory neurotransmission and excitotoxicity. Bureau of chemical safety. Health protection branch Canada, Ottawa. Toxicol Pathol 2000;28:26-8.
5 Beal MF. Mechanisms of excitotoxicity in neurologic diseases. FASEB J 1992;6:3338-44.
6 Tindwel J. Monosodium Glutamate (MSG). Available from: http//www.allergies. About.com/cs/MSG/a/aa022100a.htm. [Last accesed on 2008 Jul 15].
7 NOHA. Reactions to Free Glutamic Acid in Sensitive People. Available from: http://www.nutritionandhealth.org/nohanews/NNSPOO_MSGhtm. [Last accessed on 2008 Jul 15].
8 MSG. Available from: http://www.drtindal.org/monosodium%20glutamate.htm. [Last accessed on 2009 Apr 16].
9 Wikipedia. The Free Encyclopedia. Available from: http://www.enwikipedia.org/wiki/monosodiumglutamate. [Last accessed on 2006 Oct 13].
10 Arauz-Contreras J, Feria-Velasco A. Monosodium-L-glutamate-induced convulsions – I. Differences in seizure pattern and duration of effect as a function of age in rats. Gen Pharmacol 1984;15:391-5.
11 Onakewhor JU, Oforofuo IA, Singh SP. Chronic administration of monosodium glutamate induced oligozoospermia and glycogen accumulation in Wistar rat testes. Afr J Reprod Health 1998;2:190-7.
12 Oforofuo IA, Onakewhor JU, Idaewor PE. The effect of chronic administration of MSG on the histology of the adult Wistar rat testes. Biosci Res Commun 2002;9:26-8.
13 Eweka AO, Adjene JO. Histological studies of the effects of monosodium glutamate on the medial geniculate body of adult Wistar rat. Electron J Biomed 2007;2:9-13.
14 Samuels A. The toxicity/safety of processed free glutamic acid (MSG): A study in suppression of information. Account Res 1999;6:259-310.
15 Trinder P. Determination of blood glucose using an oxidase-peroxidase system with a non-carcinogenic chromogen. J Clin Pathol 1969;22:158-61.
16 Reitman S, Frankel S. A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases. Am J Clin Pathol 1957;28:56-63.
17 Colucci PE, Grovum WL. Factors affecting the voluntary intake of food by sheep 6. The effect of monosodium glutamate on the palatability of straw diets by sham-fed and normal animals. Br J Nutr 1993;69:37-47.
18 Savastano S, Di Somma C, Belfiore A, Guida B, Orio F Jr, Rota F, et al. Growth hormone status in morbidly obese subjects and correlation with body composition. J Endocrinol Invest 2006;29:536-43.
19 Nagata M, Suzuki W, Iizuka S, Tabuchi M, Maruyama H, Takeda S, et al. Type 2 diabetes mellitus in obese mouse model induced by monosodium glutamate. Exp Anim 2006;55:109-15.
20 Al-Mamary M, Al-Habori M, Al-Aghbari AM, Baker MM. Investigation into the toxicological effects of Catha edulis leaves: A short term study in animals. Phytother Res 2002;16:127-32.
21 Chung RT, Casson DR, Murray G, Song S, Grinspoon S, Hadigan C. Alanine aminotransferase levels predict insulin resistance in HIV lipodystrophy. J Acquir Immune Defic Syndr 2003;34:534-6.
22 Grundy SM. Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. Am J Cardiol 1999;83:25F-9F.
23 Waters CM, Moser W, Walkinshaw G, Mitchell IJ. Death of neurons in the neonatal rodent and primate globus pallidus occurs by a mechanism of apoptosis. Neuroscience 1994;63:881-94.
24 Lee RJ, editor. Fatty change and steatohepatitis. In: Diagnostic Liver Pathology. St. Louis: Mosby Year Book; 1994. p. 167.
25 Farber JL, Chien KR, Mittnacht S Jr. Myocardial ischemia: The pathogenesis of irreversible cell injury in ischemia. Am J Pathol 1981;102:271-81.


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text:
Callum Hudson-Odoi can fi...	Callum Hudson-Odoi can finally start for Maurizio Sarri
Callum Hudson-Odoi can finally start for Maurizio Sarri
by Nick Metcalfe Published April 2, 2019 Published Apr 2, 2019
MAURIZIO SARRI says Callum Hudson-Odoi is likely to be handed his first Premier League start in one of Chelsea's next two matches.
Sarri has come in for criticism for his reluctance to play the 18-year-old England international, who has impressed while coming off the bench for his club and during his starts in the Europa League, and was the subject of interest from German giants Bayern Munich in January.
Blues fans chanted the winger's name during Sunday's unconvincing league win at Cardiff. 'First of all, in pre-season after four or five training sessions, I realised Callum was really a player with very great potential,' said Chelsea boss Sarri, whose side host Brighton tonight and West Ham on Monday.
'In my opinion, in that moment, he wasn't ready to play at this level. But during this season he has improved and now he's ready. In my opinion, he is our future and now he is ready to play. Probably he will start tomorrow or in the next match.'
Sarri also again insisted he is unmoved by criticism from Blues fans. 'I am not happy, of course, but I am not concerned,' he added.
'It can happen. I can understand very well the frustration of our fans. But, in the end, we are not doing so badly.'

redpajama_set_name: RedPajamaCommonCrawl


A dynamic performance exploring the experiences of the people who dreamed of and built Niagara's Welland Canal, from William Hamilton Merritt to the present day. Told through story, music, movement and video, this visually arresting theatre piece embodies our local history and animates the mayhem, tragedies and triumphs of this national waterway.
ECT celebrates Canada's 150th anniversary of Confederation with this original play about the canal that helped to shape the Niagara Region.
Doors will be open at 1:30pm, show starts at 2pm. Tickets will be also available at the door.
Essential Collective Theatre presents: The Welland Canal Play will be at The Sanctuary - Centre for the Arts in Ridgeway, ON on Sunday, October 29, 2017. Doors at 1:30PM, and the Show Starts around 2:00PM. Essential Collective Theatre presents: The Welland Canal Play line-up includes The Welland Canal Play. The Sanctuary - Centre for the Arts is located at 209 Ridge Road , Ridgeway, ON.
Cutoff is Sunday, October 29, 2017 10:59 am EST unless it sells out earlier.


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Church Pension Group | Beyond the Pandemic
The Good Steward
Beyond the Pandemic: Preparing for the Coming Year
The COVID-19 pandemic has changed the way we live and how we interact with each other. The Episcopal Church has faced its own challenges—and has overwhelmingly responded to the difficulties with an outflowing of creativity and connection.
Future Gathering
Looking forward to a post-pandemic time, thought leaders from the Episcopal community have penned essays that have been gathered in We Shall Be Changed: Questions for the Post-Pandemic Church. This collection of thoughtful reflections will be available in September through Church Publishing Incorporated (CPI).
The essays address such questions as how to manage the recent upset to church finances, work with the people in your community who may have faced devastating losses, and bring people back together in a supportive way in a new world.
They were written to encourage community conversation about current and future events, all while facing difficult truths, embracing gifts, and anticipating new challenges.
Structure may be especially important now. Enter CPI's 2020-2021 edition of Planning for Rites and Rituals: A Resource for Episcopal Worship.
This liturgical season planner for worship can provide a jumping-off point for any events in the coming year. You can make preparation easier for Sundays and Feast Days by consulting this resource's suggestions for worship and formation. They include rites, readings, prayers, litanies, blessings, pageants, hymns, and checklists for each season.
Acting as a leader in the church is a position of great responsibility regardless of world events. Both We Shall Be Changed and Planning for Rites and Rituals can give you inspiration and ideas as you continue to provide solace and support to Church members in uncertain times.


text:
Biografia
Al termine degli studi a Bologna, Bartolomeo Averoldi aderì all'Ordine degli Umiliati, e a soli 23 anni e a capo della prepositura di Contignaga. Passa poi alla parrocchia di Gambara, ed è poi chiamato a ricoprire la carica di vicario dell'Ordine. Stava allora cercando di ottenere la guida dell'abbazia di Sant'Eufemia a Brescia, quando invece il papa stesso, nel 1451, lo chiamò a presiedere la bene più ricca Badia Leonense. Il monastero di Leno era, a quel tempo, in grosse difficoltà e andava prendendo piede l'ipotesi di aggregarlo alla riformata Congregazione Cassinese che faceva capo a Santa Giustina di Padova. L'Averoldi nel 1471 infatti stipulò l'ingresso dell'abbazia di Leno nella Congregazione, come per altro avevano già fatto molti altri istituti benedettini, ma non se ne fece nulla. Così otto anni più tardi il vescovo di Spalato, Pietro Foscari, avanzò la proposta di scambiare la sede vescovile dalmata con la cessione in commenda del monastero lenese. L'Averoldi, persona più interessata all'avanzamente carrieristico piuttosto che al benessere della comunità benedettina di Leno, accettò la richiesta del Foscari, ricevendo così la cattedra episcopale. Ma l'ambizioso carattere di Averoldi non poté accontentarsi della periferica Spalato e profuse tutto il suo impegno per ottenere diocesi più rilevanti come Treviso e soprattutto Brescia, ma senza risultato. La morte lo colse a Verona nel 1503.

Note

Voci correlate
Abbazia di Leno
Arcidiocesi di Spalato-Macarsca

Collegamenti esterni

Bartolomeo
Vescovi di Spalato
Umiliati
Averoldi


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redpajama_set_name: RedPajamaGithub


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package org.opengroup.osdu.ingest.provider.gcp.config;

import org.opengroup.osdu.ingest.provider.gcp.IGcpPackageMarker;
import org.springframework.cloud.gcp.data.datastore.repository.config.EnableDatastoreRepositories;
import org.springframework.context.annotation.Configuration;

@Configuration
@EnableDatastoreRepositories(basePackageClasses = IGcpPackageMarker.class)
public class GcsConfiguration {
}