text:
10 WWE Superstars Who Need A New Finisher
by Kevin Pantoja
A finishing move needs to be something special. It has to be worthy of ending a grueling match against your opponent. It also should be a signature move that is fitting of the wrestler performing it. Some finishers are iconic like Randy Orton's RKO, Ric Flair's Figure Four, or Stone Cold Steve Austin's Stunner.
Unfortunately, that's far from the case with a lot of finishers. There are some incredibly talented performers out there who have matches that end with a whimper due to a lame finisher. Even if the move belongs to someone successful, you can't help but not get the right reaction when their matches end. With that in mind, we've chosen ten WWE Superstars in dire need of a need finisher.
10 Dolph Ziggler
Honestly, almost everything about Dolph Ziggler could use a change. He's been a constant staple of WWE programming since 2009. That's a decade of Raw, Smackdown, and pay-per-views where he's mostly been the same guy. At this point, fans find it difficult to care about him.
RELATED: 10 Finishing Moves That Everyone Should Kick Out Of
One thing that he should change is his finisher. When he uses the superkick, it's a tired move done by a lot of wrestlers. When he uses the Zig Zag, it leaves a lot to be desired. We're not sure what would be a good replacement, but almost anything different would be worth it at this point.
9 Alexa Bliss
Alexa Bliss has taken WWE by storm since moving to the main roster in 2016. Bliss has won the Raw, Smackdown, and Tag Team Women's Titles while becoming one of the most successful ladies on the roster. Despite all of those accomplishments, her finisher needs work.
The Twisted Bliss is a solid match ender that plays off of Alexa Bliss' gymnastics background. However, she has chosen to adopt the DDT as a more consistent finisher. That move was awesome when Jake Roberts made it famous in the 80s. Now, it's something everyone does so it has lost all appeal as a finishing move.
8 EC3
During his time with TNA, EC3 rose to the top of the company. He was one of the best heels in any promotion from 2013 until 2015. When he joined NXT in 2018, many predicted he'd make an impact. Instead, EC3 was often forgotten about in NXT and has all but disappeared on the main roster.
EC3 could certainly do with a new finisher. His current fireman's carry neck breaker variation just isn't all that interesting. It's a move that almost anyone could pull off in the middle of the match. There's no feeling like it could end a match so when it happens, it's lackluster. It won't be the change to get him on TV a ton, but it couldn't hurt.
7 Zack Ryder
We've come a long way from the crowd chanting for Zack Ryder while The Rock was in the ring back in 2011. Ryder was red hot back then, but his star has waned and he barely appears on television these days. Even when he won the United States Title in 2011, he did so with a weak finishing move.
RELATED: 10 Times Superstars Were Beaten By Their Own Finishers
The Rough Ryder is ultimately nothing more than a leg lariat. Yes, his finisher is pretty much just a clothesline with your leg. There's almost no way to make it look impactful. Unfortunately, Ryder's attempts at stuff like a 450 splash haven't gone all that well, so he might be stuck with the Rough Ryder for a while.
6 Natalya
Here's someone who does have a good finishing move. The Sharpshooter is a legendary move done by the likes of Bret Hart and Sting in the past. That's pretty good company. That's also a major reason why Natalya needs to update it. Her connection to the move is simply the fact that her uncle made it famous.
It's sweet that Natalya wants to pay homage to Bret Hart. But far too much of her gimmick is based on being a member of the Hart family. From the colors she wears to her theme music to her catchphrase to her finisher. She's busted out a sweet lariat and powerbomb variations in the past. Using one of those would help her distinguish herself more instead of just being a Hart family member.
5 Tyler Breeze
There has been an obvious problem with Tyler Breeze's finishing move since he first began getting shine in NXT. Breeze had plenty of tools to be a major player in the industry. He could put on good matches, talked a good game, and he absolutely nailed his character in a way that most people can't.
But at the end of even his best matches, you'd see him hit the Beauty Shot and groan. The name of the move is fitting, but the fact that it's just a simple spinning heel kick is so disappointing. For a guy as creative with his character as Breeze is, he should be able to come up with something better to wrap up a victory.
4 Braun Strowman
Braun Strowman may seem like an odd choice for this list. Since becoming a singles star in 2016, he's mostly been unstoppable and has recorded one of the best winning percentages in all of wrestling. But that doesn't mean his finisher is anything special. It's a basic running powerslam.
RELATED: The 10 Worst Finishers In WWE Today
We're not doubting its effectiveness, but Braun Strowman is capable of so much more. He has lifted trucks and showed off some absurd feats of strength on TV, so a simple move where he runs and slams a guy doesn't cut it. Braun Strowman is a larger than life character, so not having a finisher fitting of that persona is a missed opportunity.
3 Rusev
Who doesn't love Rusev? The guy has become quite popular and has gotten every gimmick over. He's even a highlight when he appears alongside Lana on Total Divas. As much as we'd love for Rusev to get the world, a first step in getting there might be improving his finishing move. It's ridiculously outdated.
When Rusev first arrived as an anti-American Bulgarian brute, the Accolade was a fine choice. It's a powerful hold that calls back to similar characters of the past. But the more Rusev changes his character, the less we like his camel clutch. He is so likable that he needs a finisher that will get the crowd up and out of their seats.
2 Big E
Big E is one of the most impressive specimens in all of wrestling. He may act goofy with his dancing, gyrating, and pancake throwing, but he's an incredible athlete. For the most part, his signature move fails to capitalize on any of those qualities. The Big Ending sees Big E hoist his opponent over his shoulder and drop them down onto his chest.
The problem is that landing on someone's chest doesn't hurt all that much. In fact, some wrestlers have gone on record by calling that the best move to get hit with because of the soft landing on Big E's massive pecs. His tandem stuff with New Day is much better than what Big E has in his arsenal on his own.
1 Naomi
Like Big E, Naomi is an unbelievable athlete. But unlike Big E, her finishers utilize that skill. The split-legged moonsault is an impressive sight, while the Rear View sees her leap high into the air. Unfortunately, neither one of those moves is all that good.
The split-legged moonsault looks fine but is a move that often misses the mark in terms of impact. The Rear View is just a goofy looking move where Naomi attacks opponents with her butt. It can be difficult to take someone seriously when they're fighting you with their rear end. Naomi desperately needs something new to cap off her offense.
NEXT: 5 Best (& 5 worst) Finishing Moves In WWE Today
10 Stupidest Babyface Moments In WWE History
Ranking Every SmackDown Women's Champion (So Far)


13th September 2012 by Burren Smokehouse.
It is National Organic Week in Ireland, with many places like our own offering tastings of organic food. It is also the week, when Bord Bía is holding their annual National Organic awards ceremony.
Today the winner in the different organic categories was announced, and we are very happy to announce that the Burren Smokehouse was the winner of the "Best Organic Prepared Food" category with the Burren Smoked Irish Organic (cold) Smoked Salmon.
Birgitta and Peter Curtin's daughter Róisín attended the ceremony and is pictured here with Minister Shane McEntee and Tara McCarthy from Bord Bía.


text:
Pisarz polny, łac. notarius campestris – urząd wojskowy w I Rzeczypospolitej. Na Litwie był pisarz polny litewski, a w Koronie pisarz polny koronny.

Historia urzędu
Powstał prawdopodobnie około 1570 roku w celu odciążenia hetmanów odnośnie do prac administracyjnych. Od 1633 pisarz nie mógł sprawować żadnego urzędu senatorskiego. W XVII wieku pisarz polny razem ze strażnikiem wielkim, strażnikiem polnym i oboźnym utworzyli ścisły sztab hetmański, do którego należały sprawy skarbowo-wojskowe, ewidencja i sprawozdanie dotyczące stanu liczebnego wojsk zaciężnych. Zadaniem tego sztabu była ponadto kontrola jakości uzbrojenia i wyposażenia na podstawie przepisów i zawartych umów. Sztab zajmował się także kompletowaniem stanu armii.

Po znaczącej redukcji wojska w 1717 pozycja pisarza polnego zmalała. Od czasu utworzenia w 1775 Departamentu Wojskowego Rady Nieustającej był już właściwie niepotrzebny, gdyż sprawami fiansowania i zaopatrzenia wojsk zajmowały się Komisje Wojskowe, Departament Wojskowy Rady Nieustającej oraz Kancelaria Wojskowa króla, wchodził jednak jako niższy urzędnik do Departamentu Wojskowego. Pobierał jednocześnie bardzo wysoką pensję - pisarz polny koronny otrzymywał rocznie 30 000 złotych, a pisarz polny litewski 15 000 złotych.

W latach 1764-1792 urząd pisarza polnego sprawowany był już tylko formalnie, a pozostając ciągle w rękach magnackich należał do jednej z wielu synekur. W czasie reform Sejmu Czteroletniego w 1790 sejm przywrócił pozycję tego urzędu, awansując pisarzy polnych koronnego i litewskiego do rangi generałów-lejtnantów (najwyższy stopień wojskowy ówczesnych wojsk Rzeczypospolitej) i zlecając im przeprowadzenie inspekcji armii na obszarze całego państwa. Powierzona pisarzom polnym czynność związana była z planowanym powiększeniem stanu liczebnego armii.

Pierwszym pisarzem polnym był Wacław Baworowski, a jednym z ostatnich, uważanym za najbardziej zasłużonego, był pisarz polny koronny Kazimierz Rzewuski.

Kompetencje urzędu
Pisarz polny wchodził w skład "sztabu" hetmana. Do jego kompetencji należała administracja wojskowa (wyręczał w tym hetmana), prowadził ewidencję armii, którą przedstawiał na początku każdej kadencji sejmu, przeprowadzał przeglądy oddziałów wojskowych, wypłacał żołnierzom żołd. Dbał o wyposażenie oddziałów, pilnował jakości uzbrojenia, a o wszelkich niedociągnięciach miał obowiązek informować króla bądź hetmana. Przeprowadzał inspekcje zamków na Ukrainie i Podolu (obowiązek ten przejął po dowódcach obrony potocznej). Oczywiście musiał brać udział we wszystkich wyprawach wojennych.

Pisarz polny, tak samo jak inni urzędnicy, przed objęciem urzędu musiał złożyć przysięgę. Bez tego wszystkie podejmowane przez niego czynności, a także składane sejmowi raporty, uważane były za nieważne.

W pułkach pisarzy polnych wspomagali pisarze pułkowi.

Przypisy

Bibliografia
 Mała Encyklopedia Wojskowa, 1967, Wydanie I
 Zbigniew Góralski, Urzędy i godności w dawnej Polsce, Ludowa Spółdzielnia Wydawnicza, Warszawa, 1988, , str. 176-179

Urzędy wojskowe

redpajama_set_name: RedPajamaWikipedia


Decision Women comprises of all women from 26 years and above. Decision Women believes in serving the Lord with love, total commitment, righteousness and managing their home with respect and dignity.
They use their entrepreneurial abilities to trade and do businesses to break the cycle and power of poverty.
Decision Women holds quarterly prayer meetings to discuss issues pertaining to women, children, family, spirituality, business, prosperity and good living with clear conscience.
The annual meeting for Decision Women is held every October for spiritual empowerment, household management and networking.
Decision Women organises fashion, beauty, cooking and catering training and workshops.
10 An excellent woman [one who is spiritual, capable, intelligent, and virtuous], who is he who can find her?
Her value is more precious than jewels and her worth is far above rubies or pearls…..


Maybe you're just getting started turning, or maybe you've been at it a while and are just trying to decide what wood to use for a specific project. Whatever the case, it can be daunting to try and select a wood from the extreme variety available. Hopefully, this brief guide will aid you in selecting the best wood for your next project, wherever you are in your journey.
This may be a little obvious, but it is a sensible place to start. Regardless of your woodworking knowledge, you know what are able to spend on the project this can knock out a lot of options that you don't need to consider in the first place. Now, you may be thinking, "but I have no idea what different woods cost?!?" That's fine, while I advocate for supporting your local wood shops when possible, you can use online retailers as a resource even if you don't buy from them (and sometimes you have to because your local supplier doesn't have what you need). Go to a site like WoodWorkersSource.com or BellForestProducts.com and search for the size blank you need within a given price range. This will give you an idea of what woods you should be looking into. Once you have a list of hardwoods in your price range, you can start to narrow further.
I'll go ahead and address before you ask, yes you can just stain a piece of light wood. However, this will not give you the same look as a true colored wood, and will show up light if your piece ever gets scratched, but it can be a way to get a nice looking piece at a lower cost when you're starting out.
Burning: A darkening process where wood is scorched by a torch, then the black ash on the outside is brushed off, revealing a significantly darker piece of wood underneath.
Ebonizing: This process uses household ingredients. The solution is made from vinegar which has had steel wool sitting in it for a number of weeks. When applied to a piece, it reacts to the tannins in the wood to produce a dark color.
I am not an expert on these darkening methods, and I would assume they each work better on certain woods than others. Each method also has its own associated risks, so be sure to do your research into each method to ensure you know how to do it safely and effectively before attempting.
Some of the characteristics associated with durability are hardness/density, rot resistance, and insect resistance. One thing to note is that the hardness of a wood doesn't actually have anything to do with the the classification of ''hardwood". That classification actually comes from the trees seeds, so don't assume that a hardwood is, well.. hard. The most famous example is balsa wood which is one of the softest woods in the world, and yet it's considered a hardwood. Now that we have that cleared up, lets take a look at these characteristics.
In general, the harder the wood the denser it is. However, though hardness and density are related, they are not directly proportional (as you can see above). An even more extreme case: Bois D'arc (osage orange) has a Janka hardness of 2620 lb-ft while black palm only has a hardness of 2020 lb-ft. However, Bois D'arc only has a density of 54 lb/ft, while the 'softer' black palm has a density of 61 lb/ft.
Using a denser wood will give more weight to your piece, which can give it a feel of higher quality. Using a harder wood will give your piece a little extra resistance to dents and dings, which may be very beneficial if the piece is functional rather than decorative.
Keep in mind, the harder a wood, the harder it will be to work with, and the more wear it will cause on your tools. In the images above I experimented with woods on both ends of the spectrum. The rolling pin was made from a piece of poplar, a very soft wood of only 540 lb-ft. The candle holder was made from a piece of Spanish cedar of nearly equal softness at 600 lb-ft. On the other end, the two pens and pencil were made from Honduran rosewood which comes in at 2,200 lb-ft.
Some woods do better with moisture and insect resistance than others, thus making them more suitable for outdoor and marine applications. While a great deal of protection can be acquired through various finishing techniques, having a wood that is more naturally suited to these situations is never a bad thing. As far as these two criteria go, you will simply have to do a little research for each wood you are considering. They can be a great help in selecting the right wood for a specific project to ensure it will last a long time.
There are many great resources for all of this info including books, websites, and magazines. One specific resource I have found helpful is wood-database.com. It has information on hundreds of woods with most of the types of info we've covered here as well as estimated prices, CITES appendix listings, toxicity, etc.
As I mention previously, the harder the wood, the more difficult it is to work with. Here are the results of the few turnings I have pictured: The soft woods were easier to turn and did not dull the tools as quickly. However, even on little slip would put a deep gouge in the wood. Additionally, the final projects mar much easier due to their softness. Lastly, you cannot turn these woods down to as small of a diameter as the hardwoods because they are weaker. The hardwood, despite being ~4x harder than the other woods, was still pleasant to turn (if you are using carbide tools, dulling isn't really an issue), and I was definitely happier with the final results. In general, I think I would recommend staying above the 1,000 lb-ft mark.
Get a notebook and every time you turn something, write down what kind of wood it was and what you thought about it: How did it turn? Any issues like chipping or tear out? What kind of finish did you use, and did you like it on this particular wood? Etc.
I'm kind of nerdy and I love making spreadsheets, so I cataloged all of my wood species and their associated specs so that whenever I have a project in mind, I can go to that spreadsheet, see what I have on hand, filter by specific criteria, and hopefully pick out a good wood for the job.
If you would like to see other projects we've been working on, check out our new Instagram @LakeCitiesCraft for weekly posts!


text:
MTHFR A1298C polymorphisms reduce the risk of congenital heart defects: a meta-analysis from 16 case-control studies
Di Yu1,
Zhulun Zhuang1,
Zhongyuan Wen2,
Xiaodong Zang1 &
Xuming Mo1
Italian Journal of Pediatrics volume 43, Article number: 108 (2017) Cite this article
Methylenetetrahydrofolate reductase (MTHFR) plays a crucial role in the hyperhomocysteinemia, which is a risk factor related to the occurrence of congenital heart defect (CHD). However, the association between MTHFR polymorphism and CHD has been inconclusive.
We conducted an updated meta-analysis to provide comprehensive evidence on the role of MTHFR A1298C polymorphism in CHD. Databases were searched and a total of 16 studies containing 2207 cases and 2364 controls were included.
We detected that a significant association was found in the recessive model (CC vs. AA + AC: OR = 1.38, 95% CI: 1.10–1.73) for the overall population. Subgroup analysis showed that associations were found in patients without Down Syndrome in genetic models for CC vs. AA (OR = 1.47, 95% CI: 1.01–2.14), CC vs. AC (OR = 1.29, 95% CI: 1.00–1.66) and recessive model (OR = 1.44, 95% CI: 1.14–1.82). We conducted a meta-regression analysis, Galbraith plots and a sensitivity analysis to assess the sources of heterogeneity.
In summary, our present meta-analysis supports the MTHFR 1298C allele as a risk factor for CHD. However, further studies should be conducted to investigate the correlation of plasma homocysteine levels, enzyme activity, and periconceptional folic acid supplementation with the risk of CHD.
Congenital heart disease (CHD) is the most common defect in newborns, affecting approximately 8 to 10 per 1000 live births and causing 5%–10% of spontaneously aborted pregnancies [1, 2]. In addition, CHD is the leading cause of infant death all over the world, with mortality of 24.1% [3]. It has been proven that CHD is influenced by both genetic and environmental factors [4, 5]. Several genomewide association studies (GWASs) were conducted to identify the genetic factors in the development of CHD in the past decades [6, 7]. However, the etiology of CHD is still not fully known.
The methylenetetrahydrofolate reductase (MTHFR) gene, as one of the most crucial enzymes for the metabolism of folate/homocysteine, is located on chromosome 1p36.3. Specifically, this enzyme catalyzes the conversion of 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate, which participates in the remethylation of homocysteine to methionine [8]. The lack of folic acid is known to result in hyperhomocysteinemia, which has been described as a possible risk factor for the occurrence of CHD [5, 7, 9, 10]. The MTHFR gene has 2 common mutations, C677T and A1298C, which result in the conversion of alanine to valine and glutamate to alanine, respectively. Moreover, these two mutations have been proved to decrease MTHFR enzyme activity, increase the level of homocysteine and eventually decrease the plasma concentration of folic acid.
Since Wenstrom first confirmed that MTHFR C677T polymorphism increased plasma homocysteine levels and the occurrence of CHD, several studies have been conducted to test this viewpoint. Several meta-analyses were also performed and suggested that MTHFR C677T polymorphism was associated with a susceptibility to CHD. However, few studies were carried out to investigate the association between MTHFR A1298C polymorphism and the risk of CHD. Xuan et al. conducted a correlation meta-analysis and found that the 1298C allele is a risk factor in the Caucasian population [11]. However, the included articles were published before Jun 2014. Therefore, we conducted an updated meta-analysis of all the available published data to integrate the results from case-control studies to provide comprehensive evidence on the role of MTHFR A1298C polymorphism in CHD.
Identification of relevant studies
We conducted an electronic search for relevant articles published before May 2016 in PubMed and Web of Science databases with the combination of the following terms: "methylenetetrahydrofolate reductase OR MTHFR", "polymorphism OR snp OR variant" and "CHD OR congenital heart defect OR Malformation of heart OR Heart Abnormality OR Birth Defect OR Deformity OR Congenital Abnormality". To expand the coverage of our searches, we further carried out searches in the Chinese National Knowledge Infrastructure (CNKI) and Wanfang databases with the translation of all English search terms. We also scanned for more qualifying studies from the reference lists of the retrieved articles.
Eligibility of relevant studies
We included case-control studies with human subjects that investigated the association between MTHFR A1298C polymorphism and CHD risk in both the English and the Chinese language. All phenotypes of CHDs, such as atrial septal defect, ventricular septal defect, patent formen ovale, patent ductus arteriosus, trilogy of fallot, coaratation of the aorta, and pulmonary valve stenosis, were included in this meta-analysis. Reviews, animal studies, simple commentaries, case reports and unpublished reports were excluded. Moreover, the studies that did not offer original data of allele frequencies in the initial publication were excluded after unsuccessful attempts to obtain this information by correspondence with the authors. Additionally, we usually retained the study with the most extensive data for the meta-analysis to avoid overlap in the information.
All data was extracted independently by two authors, and any disagreement was adjudicated by the corresponding author. The following information was extracted from each study: first author, year of publication, country of origin, ethnicity, type of CHD, and number of cases and controls, besides counts of alleles in case and control groups, and Hardy-Weinberg equilibrium were calculated (Table 1).
Table 1 The main characteristics of all included studies for MTHFR A1298C polymorphism
STATA (version 12.0; StataCorp, College Station, Texas, USA) was used for meta-analysis. All genotype models for the MTHFR A1298C polymorphisms were evaluated. The association between the A1298C polymorphism and CHD was compared using the odds ratio (OR) corresponding to a 95% confidence interval (95% CI). The pooled ORs were performed for C vs. A, CC vs. AA, AC vs. AA, CC vs. AC, dominant model (CC + AC vs. AA) and recessive model (CC vs. AA + AC). We used Q-test and the I 2 test to quantify the proportion of the total variation due to heterogeneity. I 2 ranges from 0 to 100%. A value of 0% means no observed heterogeneity, and larger values reflect increasing heterogeneity, with 25% regarded as low, 50% as moderate, and 75% as high heterogeneity. The pooled odds ratio (OR) was estimated with models based on fixed-effects or random-effects assumptions. If the effects were assumed to be heterogeneity (P < 0.1, I2 > 50%), the random-effects model was then used. Otherwise, a fixed-effect model was selected. And we used the Hardy–Weinberg equilibrium (HWE) to check the distributions of genotypes in the controls. Additionally, the stability of the results was assessed by sensitivity analysis and the influence of the individual study on the pooled ORs was reflected by deleting the single study involved in the meta-analysis each time.
The publication bias was estimated by Begg and Egger's test (the significance was set at P < 0.05). Moreover, we used Egger's plot of the MTHFR A1298C polymorphism to search for evidence of publication bias. The asymmetric funnel plots caused publication bias and the symmetric one did not.
Subgroup analyses were carried out by region (Asia, Europe, America or Africa), sample size (case number > 100 vs. <100), Down syndrome (without vs. with), HWE (consistent vs. inconsistent).
Characteristics of eligible studies
The search strategy identified 3907 potentially relevant studies. Based on the inclusion criteria, a total of 16 relevant case-control [12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27] studies concerning MTHFR A1298C polymorphism and CHD, involving 2207 cases and 2364 controls, were included in this meta-analysis. The flow chart of the selected study is summarized in Fig. 1. Of these 16 articles, 6 were conducted in Asia [12, 15,16,17, 19, 20, 24, 25], 6 in Europe [21,22,23, 27], 3 in America [13, 14, 18] and 1 in Africa [12]. The distribution of the genotypes in the control groups was consistent with HWE except for 4 studies [12, 16, 20, 26]. The patients in 2 cases included studies accompanied by Down syndrome (DS) [27] [18]. The main characteristics of the included studies are presented in Table 1.
Flow chart of article screening and selection process
Results of the meta-analysis
We examined all genetic models of MTHFR A1298C polymorphism and the risk of CHD. Significant association was found in the recessive model (CC vs. AA + AC: OR = 1.38, 95% CI: 1.10–1.73; P heterogeneity = 0.289) when all eligible studies were pooled in the fixed-effect model (Fig. 2). In the subgroup analysis of region, obvious associations were found in Europe when relevant studies were pooled with the fixed-effect model for CC vs. AC (OR = 1.48, 95% CI: 1.05–2.09; P heterogeneity = 0.846) (Fig. 3) and recessive model (OR = 1.40, 95% CI: 1.01–1.94; P heterogeneity = 0.594) (Fig. 2). Moreover, remarkable associations were also found when the patients without DS were pooled with random- or fixed-effect models for CC vs. AA (OR = 1.47, 95% CI: 1.01–2.14; P heterogeneity = 0.021) (Fig. 4), CC vs. AC (OR = 1.29, 95% CI: 1.00–1.66; P heterogeneity = 0.461) (Fig. 5) and recessive model (OR = 1.44, 95% CI: 1.14–1.82; P heterogeneity = 0.308) (Fig. 6). The results of the subgroup analysis of the associations between MTHFR A1298C polymorphism and CHD are shown in Table 2.
Pooled OR (recessive model) for the association between the MTHFR A1298C polymorphism and CHD in the overall and subgroups population
Pooled OR (CC vs. AC) for the association between the MTHFR A1298C polymorphism and CHD in the European population
Pooled OR (CC vs. AA) for the association between the MTHFR A1298C polymorphism and CHD in the non-Down Syndrome population
Pooled OR (CC vs. AC) for the association between the MTHFR A1298C polymorphism and CHD in the non-Down Syndrome population
Pooled OR (recessive model) for the association between the MTHFR A1298C polymorphism and CHD in the non-Down Syndrome population
Table 2 Subgroup analysis of the association between MTHFR A1298C polymorphism and CHD
Sensitivity analysis was carried out to detect the influence of the individual study on the pooled ORs by omitting a single study involved in the meta-analysis each time. The results showed that the corresponding pooled ORs were not substantially altered, except for one study for CC vs. AC [15], indicating the relatively stability of the results. The main results of the sensitivity analysis are shown in Table 3.
Table 3 Sensitivity analysis of the association between MTHFR A1298C and CHD by omitting a single study each time
Heterogeneity analysis
Significant heterogeneity was detected in models of C vs. A (Q = 55.60; P = 0.000; I 2 = 73.0%), CC vs. AA (Q = 28.62; P = 0.012; I 2 = 51.1%), AC vs. AA (Q = 51.05; P = 0.000; I 2 = 70.6%) and CC + AC vs. AA (Q = 58.86; P = 0.000; I 2 = 74.5%), while no heterogeneity in models of CC vs. AC (Q = 12.047; P = 0.569; I 2 = 0.0%) and CC vs. AA + AC (Q = 16.42; P = 0.289; I 2 = 14.7%). Subsequently, a subgroup analysis was performed while obvious heterogeneity still existed. Therefore, we carried out a meta-regression with a Knapp-Hartung modification to identify the sources of heterogeneity and we found that inconsistencies with HWE in the control group may contribute to the heterogeneity in CC vs. AA (P = 0.002) and CC vs. AA + AC (P = 0.014). The main results of the heterogeneity analysis are shown in Table 4.
Table 4 Heterogeneity analysis of the association between MTHFR A1298C polymorphism and CHD
Furthermore, we created Galbraith plots to graphically assess the sources of heterogeneity in models of C vs. A, CC vs. AA, AC vs. AA and CC + AC vs. AA (Additional file 1: Figure S1). A total of 5, 1, 5, and 6 studies were identified as the main sources of heterogeneity, respectively. After the outlier studies were omitted, the heterogeneity was effectively removed in models of C vs. A (Q = 11.78; P = 0.300; I 2 = 15.1%), CC vs. AA (Q = 20.56; P = 0.082; I 2 = 36.8%), AC vs. AA (Q = 13.57; P = 0.194; I 2 = 26.3%) and CC + AC vs. AA (Q = 11.71; P = 0.230; I 2 = 23.1%). Meanwhile, the corresponding ORs did not change substantially (C vs. A: OR = 0.97, 95% CI: 0.87–1.08; CC vs. AA: OR = 1.23, 95% CI: 0.95–1.59; AC vs. AA: OR = 0.96, 95% CI: 0.83–1.11; CC + AC vs. AA: OR = 0.95, 95% CI: 0.82–1.09).
Publication bias
Publication bias was assessed by Begg and Egger's test (Additional file 2: Table S1). No publication biases for MTHFR A1298C polymorphism were detected in all genetic models. Egger's funnel plots are shown in Additional file 3: Figure S2.
According to statistics, nearly 18 million newborns come into the world each year and in China, about 0.9 million are born with a birth defect. Among them, up to 200,000 newborns are born with CHD, which has been the major birth defect for decades on the mainland of China. This is a serious problem, as the natural mortality rate of infants is 30 to 40% for one year without treatment. However, the etiology of CHD has not yet been fully understood and no effective interventions can be delivered. In most cases, surgery is the only way to save life, with this treatment costing tens of billions of dollars. Therefore, the prevention of CHD has great significance for public health.
As we known, MTHFR is a crucial regulatory enzyme in the metabolic pathway of folate/homocysteine and lack of it may cause hyperhomocysteinemia, which is one of the proven risk factors related to the occurrence of CHDs [28, 29]. MTHFR A1298C polymorphism results in the conversion of glutamate to alanine, which leads to a high level of homocysteine and low plasma concentration of folic acid. What is more, our previous meta-analysis demonstrated a positive association between maternal folate supplementation and a decreased risk of CHD [30]. From that date forward, many studies have explored the association between MTHFR A1298C polymorphism and the risk of CHD, yet the results are still controversial.
Recently, a meta-analysis for association between A1298C polymorphism and CHD was conducted and it was found that CC vs. AC (OR = 1.354, 95% CI: 1.022–1.793) and the recessive model (OR = 1.322, 95% CI: 1.015–1.732) increased the risk of CHD in the overall pediatric population. However, due to the lack of the analysis of the source of the heterogeneity and small sample size (1834 cases and 1744 controls), we believe that the results of the meta-analysis might not be stable. Thus, we performed an updated meta-analysis to integrate the same kinds of studies to increase the sample size and statistical power (2207 cases and 2364 controls), and then obtain a more authentic result.
Our results indicate that the CC homozygote increased susceptibility to CHD by 38% compared with AA + AC (95% CI: 1.10–1.73) in the overall population. Patients with DS are always accompanied by CHD and might be interfering with the results. Therefore, we excluded relevant studies and the results showed that the CC homozygote had a 47%, 29% and 44% elevated risk of CHD, when compared with AA (95% CI: 1.01–2.14), AC (95% CI: 1.00–1.66), or AA + AC (95% CI: 1.14–1.82) in children without DS, respectively. Meanwhile, compared with AC or AA + AC, CC homozygote also increased by 48% (95% CI: 1.05–2.09) and 40% (95% CI: 1.01–1.94) the risk of CHD to children in Europe, respectively. We conducted heterogeneity analyses, such as subgroup analysis, meta-regression, sensitivity analysis and Galbraith plots, to detect the source of heterogeneity, and found that the corresponding ORs did not change substantially after excluding the relevant studies. Therefore, our results are relatively reliable and stable; namely, CC homozygote is a risk factor for CHD, especially in children without DS or children in Europe.
However, there were still some limitations in our meta-analysis. First, all the data from studies were collected only in Chinese and English, which means that relevant studies performed in other languages, may be missed. Additionally, we extracted all our raw data from case-control studies, which were prone to information biases. Although no publication bias was found, heterogeneity existed, which may confuse the overall results. Therefore, we conducted meta-regression, Galbraith plots and sensitivity analysis to explore the sources of heterogeneity and proved that our results are stable. Second, almost all studies did not definitively classify the CHDs and used different types of heart defects in their papers. Thus, we have not included enough studies to perform a subgroup analysis with different CHD subtypes, which may have various etiologies. Third, the subjects of all the studies were from different countries and races, with different living environments, physical conditions and diet. Moreover, folate intake was the most crucial factor. Studies have demonstrated that periconceptional use of multivitamins containing folic acid can reduce the incidence of CHDs [31, 32]. Additionally, our previous meta-analysis showed that moderate supplementation with folic acid is associated with a significantly decreased risk of CHDs [30]. Thus, periconceptional folic acid supplementation and food fortification with folic acid should be taken in consideration. Finally, the number of case-controls is still not enough to draw a definite conclusion.
In conclusion, the results of this meta-analysis demonstrate that MTHFR A1298C polymorphism is significantly associated with CHD susceptibility. However, further larger sample studies are warranted to enable definitive conclusions, especially in plasma homocysteine levels, enzyme activity, and periconceptional folic acid supplementation. What is more, gene-gene and gene-environment interactions should be taken into account to further investigate the association between the MTHFR A1298C polymorphisms and CHD risk.
Hoffman JI. Incidence of congenital heart disease: I. Postnatal incidence. Pediatr Cardiol. 1995;16:103–13.
Hoffman JI. Incidence of congenital heart disease: ii. Prenatal incidence. Pediatr Cardiol. 1995;16:155–65.
Gilboa SM, Salemi JL, Nembhard WN, Fixler DE, Correa A. Mortality resulting from congenital heart disease among children and adults in the united states, 1999 to 2006. Circulation. 2010;122:2254–63.
Burn J, Brennan P, Little J, Holloway S, Coffey R, Somerville J, Dennis NR, Allan L, Arnold R, Deanfield JE, Godman M, Houston A, Keeton B, Oakley C, Scott O, Silove E, Wilkinson J, Pembrey M, Hunter AS. Recurrence risks in offspring of adults with major heart defects: results from first cohort of british collaborative study. Lancet. 1998;351:311–6.
Fredriksen A, Meyer K, Ueland PM, Vollset SE, Grotmol T, Schneede J. Large-scale population-based metabolic phenotyping of thirteen genetic polymorphisms related to one-carbon metabolism. Hum Mutat. 2007;28:856–65.
Cordell HJ, Bentham J, Topf A, Zelenika D, Heath S, Mamasoula C, Cosgrove C, Blue G, Granados-Riveron J, Setchfield K, Thornborough C, Breckpot J, Soemedi R, Martin R, Rahman TJ, Hall D, van Engelen K, Moorman AF, Zwinderman AH, Barnett P, Koopmann TT, Adriaens ME, Varro A, George AL Jr, Dos Remedios C, Bishopric NH, Bezzina CR, O'Sullivan J, Gewillig M, Bu'Lock FA, Winlaw D, Bhattacharya S, Devriendt K, Brook JD, Mulder BJ, Mital S, Postma AV, Lathrop GM, Farrall M, Goodship JA, Keavney BD, et al. Nat Genet. 2013;45:822–4.
Hu Z, Shi Y, Mo X, Xu J, Zhao B, Lin Y, Yang S, Xu Z, Dai J, Pan S, Da M, Wang X, Qian B, Wen Y, Wen J, Xing J, Guo X, Xia Y, Ma H, Jin G, Yu S, Liu J, Zhou Z, Wang X, Chen Y, Sha J, Shen HA. Genome-wide association study identifies two risk loci for congenital heart malformations in han chinese populations. Nat Genet. 2013;45:818–21.
Goyette P, Pai A, Milos R, Frosst P, Tran P, Chen Z, Chan M, Rozen R. Gene structure of human and mouse methylenetetrahydrofolate reductase (mthfr). Mamm Genome. 1998;9:652–6.
Hobbs CA, James SJ, Parsian A, Krakowiak PA, Jernigan S, Greenhaw JJ, Lu Y, Cleves MA. Congenital heart defects and genetic variants in the methylenetetrahydroflate reductase gene. J Med Genet. 2006;43:162–6.
Huhta JC, Hernandez-Robles JA. Homocysteine, folate, and congenital heart defects. Fetal Pediatr Pathol. 2005;24:71–9.
Xuan C, Li H, Zhao JX, Wang HW, Wang Y, Ning CP, Liu Z, Zhang BB, He GW, Lun LM. Association between mthfr polymorphisms and congenital heart disease: a meta-analysis based on 9,329 cases and 15,076 controls. Sci Rep. 2014;4:7311.
Chao CS, Wei J, Huang HW, Yang SC. Correlation between methyltetrahydrofolate reductase (mthfr) polymorphisms and isolated patent ductus arteriosus in taiwan. Heart Lung Circ. 2014;23:655–60.
Christensen KE, Zada YF, Rohlicek CV, Andelfinger GU, Michaud JL, Bigras JL, Richter A, Dube MP, Rozen R. Risk of congenital heart defects is influenced by genetic variation in folate metabolism. Cardiol Young. 2013;23:89–98.
Galdieri LC, Arrieta SR, Silva CM, Pedra CA, D'Almeida V. Homocysteine concentrations and molecular analysis in patients with congenital heart defects. Arch Med Res. 2007;38:212–8.
Huang J, Mei J, Jiang L, Jiang Z, Liu H, Ding F. Mthfr rs1801133 c>t polymorphism is associated with an increased risk of tetralogy of fallot. Biomed Rep. 2014;2:172–6.
Koshy T, Venkatesan V, Perumal V, Hegde S, Paul SF. The a1298c methylenetetrahydrofolate reductase gene variant as a susceptibility gene for non-syndromic conotruncal heart defects in an indian population. Pediatr Cardiol. 2015;36:1470–5.
Li D, Yu K, Ma Y, Liu Y, Ji L. Correlationship between congenital heart disease and polymorphism of mthfr gene. Wei Sheng Yan Jiu. 2015;44:933–8.
Locke AE, Dooley KJ, Tinker SW, Cheong SY, Feingold E, Allen EG, Freeman SB, Torfs CP, Cua CL, Epstein MP, MC W, Lin X, Capone G, Sherman SL, Bean LJ. Variation in folate pathway genes contributes to risk of congenital heart defects among individuals with down syndrome. Genet Epidemiol. 2010;34:613–23.
Obermann-Borst SA, van Driel LM, Helbing WA, de Jonge R, Wildhagen MF, Steegers EA, Steegers-Theunissen RP. Congenital heart defects and biomarkers of methylation in children: a case-control study. Eur J Clin Investig. 2011;41:143–50.
Sahiner UM, Alanay Y, Alehan D, Tuncbilek E, Alikasifoglu M. Methylene tetrahydrofolate reductase polymorphisms and homocysteine level in heart defects. Pediatr Int. 2014;56:167–72.
Sayin Kocakap BD, Sanli C, Cabuk F, Koc M, Kutsal A. Association of mthfr a1298c polymorphism with conotruncal heart disease. Cardiol Young. 2015;25:1326–31.
Storti S, Vittorini S, Iascone MR, Sacchelli M, Collavoli A, Ripoli A, Cocchi G, Biagini A, Clerico A. Association between 5,10-methylenetetrahydrofolate reductase c677t and a1298c polymorphisms and conotruncal heart defects. Clin Chem Lab Med. 2003;41:276–80.
van Driel LM, Verkleij-Hagoort AC, de Jonge R, Uitterlinden AG, Steegers EA, van Duijn CM, Steegers-Theunissen RP. Two mthfr polymorphisms, maternal b-vitamin intake, and chds. Birth Defects Res A Clin Mol Teratol. 2008;82:474–81.
Wang B, Liu M, Yan W, Mao J, Jiang D, Li H, Chen Y. Association of snps in genes involved in folate metabolism with the risk of congenital heart disease. J Matern Fetal Neonatal Med. 2013;26:1768–77.
Xu J, Xu X, Xue L, Liu X, Gu H, Cao H, Qiu W, Hu Z, Shen H, Chen Y. Mthfr c.1793g>a polymorphism is associated with congenital cardiac disease in a chinese population. Cardiol Young. 2010;20:318–26.
Zidan HE, Rezk NA, Mohammed D. Mthfr c677t and a1298c gene polymorphisms and their relation to homocysteine level in egyptian children with congenital heart diseases. Gene. 2013;529:119–24.
Bozovic IB, Vranekovic J, Cizmarevic NS, Mahulja-Stamenkovic V, Prpic I, Brajenovic-Milic B. Mthfr c677t and a1298c polymorphisms as a risk factor for congenital heart defects in down syndrome. Pediatr Int. 2011;53:546–50.
Gueant-Rodriguez RM, Gueant JL, Debard R, Thirion S, Hong LX, Bronowicki JP, Namour F, Chabi NW, Sanni A, Anello G, Bosco P, Romano C, Amouzou E, Arrieta HR, Sanchez BE, Romano A, Herbeth B, Guilland JC, Mutchinick OM. Prevalence of methylenetetrahydrofolate reductase 677t and 1298c alleles and folate status: a comparative study in mexican, west african, and european populations. Am J Clin Nutr. 2006;83:701–7.
Kapusta L, Haagmans ML, Steegers EA, Cuypers MH, Blom HJ, Eskes TK. Congenital heart defects and maternal derangement of homocysteine metabolism. J Pediatr. 1999;135:773–4.
Feng Y, Wang S, Chen R, Tong X, Wu Z, Mo X. Maternal folic acid supplementation and the risk of congenital heart defects in offspring: a meta-analysis of epidemiological observational studies. Sci Rep. 2015;5:8506.
Smedts HP, Rakhshandehroo M, Verkleij-Hagoort AC, de Vries JH, Ottenkamp J, Steegers EA, Steegers-Theunissen RP. Maternal intake of fat, riboflavin and nicotinamide and the risk of having offspring with congenital heart defects. Eur J Nutr. 2008;47:357–65.
Verkleij-Hagoort AC, de Vries JH, Ursem NT, de Jonge R, Hop WC, Steegers-Theunissen RP. Dietary intake of b-vitamins in mothers born a child with a congenital heart defect. Eur J Nutr. 2006;45:478–86.
The work was fully supported by grants from the National Natural Science Foundation of China (No. 81370277 & 81,370,279) and Jiangsu Provincial Special Program of Medical Science (BL2013003).
All data generated or analyzed during this study are included in PubMed and Web of Science databases.
Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, 210008, China
Di Yu, Zhulun Zhuang, Xiaodong Zang & Xuming Mo
Department of Cardiovascular Center, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210008, China
Zhongyuan Wen
Di Yu
Zhulun Zhuang
Xiaodong Zang
Xuming Mo
XMM and DY conceived and designed the experiments. DY, ZLZ and XMM performed the experiments. DY, ZLZ and ZYW analyzed the data. XDZ contributed analysis tools. DY, ZLZ and ZYW wrote the paper. All authors reviewed the manuscript. All authors read and approved the final manuscript.
Correspondence to Xuming Mo.
The authors declare that they have no competing interests
Galbraith plots for models of C vs. A, CC vs. AA, AC vs. AA and CC + AC vs. AA. (TIFF 1442 kb)
Publication bias for MTHFR A1298C polymorphism. (DOCX 15 kb)
Egger's funnel plots in all genetic models for MTHFR A1298C polymorphism. (TIFF 1828 kb)
Yu, D., Zhuang, Z., Wen, Z. et al. MTHFR A1298C polymorphisms reduce the risk of congenital heart defects: a meta-analysis from 16 case-control studies. Ital J Pediatr 43, 108 (2017). https://doi.org/10.1186/s13052-017-0425-1
Methylenetetrahydrofolate reductase
Neurology, Behaviour and Development

redpajama_set_name: RedPajamaCommonCrawl


text:
3531 Fiesta Dr
$66,000 (Estimated Value)
3531 Fiesta Dr is a single family residence located in Greensboro, NC 27406. Built in 1953, this property features 2 bedrooms, 2 bathrooms, 8,276 sq ft lot, and 1,122 sq ft of living space. The estimated market value for 3531 Fiesta Dr is $66,000.
For the surrounding community of Greensboro, NC 27406, the average sale price for similar homes to 3531 Fiesta Dr is $87,616. The nearby schools are below average and include Julius I Foust Elementary, Allen Middle and Ben L Smith High School. The overall crime risk for this area is moderately high with 18 criminal and sex offenders residing within 1 mile. The natural disaster risk for this area includes very low earthquake risk, medium tornado risk, and minimal flood risk.
$66,000 estimated value
Property Details: 3531 Fiesta Dr
Subdivision: LAKE PROP SEC B
Zoning: RS-9
BuiltUp (Layered Asphalt) Roof
10/25/2004 Sold $50,252 $45 Public Records
2017 $577 (+1.36%) $15,000 $27,400 $42,400
2014 $594 (+1.4%) $10,000 $32,400 $42,400
2009 $625 $11,000 $34,600 $45,600
3533 Fiesta Dr, Greensboro, NC 27406
3522 Ravendale Dr, Greensboro, NC 27406
This home $66,000 Estimated Value
Comparable Sales$87,616 AVG SALES Price
The average sales price of homes similar to 3531 Fiesta Dr is $87,616 ($72/sq.ft.)
363 E Montcastle Dr Unit B $78,500 01/03/2020 $61 1,290 sq.ft. 3 Bed, 3 Bath 1.8 mi away
1324 Kirkman St $52,000 12/31/2019 $52 1,008 sq.ft. 2 Bed, 1 Bath 1.1 mi away
2117 McKelvey Dr $62,500 12/31/2019 $56 1,121 sq.ft. 3 Bed, 2 Bath 0.6 mi away
1415 Vance St $70,000 12/31/2019 $56 1,248 sq.ft. 3 Bed, 2 Bath 2.5 mi away
818 Valley Oak Dr $130,000 12/30/2019 $103 1,260 sq.ft. 3 Bed, 2 Bath 1.3 mi away
1303 W Vandalia Rd $136,000 12/23/2019 $103 1,321 sq.ft. 3 Bed, 2 Bath 0.7 mi away
3605 Jerome Dr $96,000 12/18/2019 $79 1,212 sq.ft. 3 Bed, 2 Bath 1.9 mi away
520 Jonathan Ln $94,000 12/17/2019 $80 1,168 sq.ft. 3 Bed, 2 Bath 0.7 mi away
525 Jonathan Ln $120,000 12/17/2019 $98 1,225 sq.ft. 3 Bed, 2 Bath 0.6 mi away
3421 Winchester Dr $45,000 12/10/2019 $36 1,250 sq.ft. 3 Bed, 2 Bath 1.2 mi away
This 2 bedroom and 2.0 bathroom home was built in 1953. 3531 Fiesta Dr has approximately 1,122 square feet of living space.
During the month of 12/2019, a total of 23 properties had foreclosure filings in the 27406 zip code surrounding 3531 Fiesta Dr, with one in every 1,160 housing units receiving a foreclosure filing. In Guilford County, where 3531 Fiesta Dr, Greensboro, NC 27406 is located, there were 156 properties with foreclosure filings documented during the month of 12/2019, a foreclosure rate of one in every 1,442 housing units. In North Carolina, one in every 2,375 housing units had a foreclosure filing in 12/2019, while one in every 2,541 housing units had a foreclosure filing nationwide.


Blog > Dear Dr. Z, Why is my internet so slow?
Dear Dr. Z, Why is my internet so slow?
Dear Dr. Z, I have Windows 8. My internet browser is moving so sluggish! It was working fine, but over the past few months it's become so slow. Just trying to read my favorite news sites is a chore. What can I do?
Larry, check your internet connection. Are you using DSL? If so, examine your wiring. Sometimes bad telephone lines will fray and effect your internet speed. If you're using a wi-fi connection, be sure that you're not in close quarters with many other devices using radiation. Wireless networks operate on similar frequencies to devices like microwaves and cordless phones.
Beyond the external possibilities, it may just be an old windows install. If you're using a Windows computer, you should definitely try to reinstall your software at least once a year. Windows computers get bogged down by so many registry errors and junk files that it can slow down the user experience. Along with laggy programs, the slow internet surfing you speak of is a a tale-tell sign of just that.
How long has your Windows OS has been installed? Do you think it's time to reboot it or even upgrade? Windows 10 is currently free for Windows 8 users for the first year.
If you don't think that could be the issue though, you may have some malware creeping around your system. Have you been surfing any new sites lately? Have you downloaded files from an untrustworthy source? Most importantly, have you opened any spam emails or their attachments? Those are the prime methods malicious people use to infiltrate your system with viruses, spyware and adware.
These viruses, along with stealing your personal info, can slow your computer function to a crawl. I once had a bad virus and it took me nearly 5 minutes just for any page to load. At that point, I decided to be proactive and have new surfing habits. I've never opened any strange emails, but I also decided to only download files from reputable sites. Torrents and the like are not only illegal, they're simply no good for your computer. Who wants to download a bad movie and a virus along with that?
A Sharknado and a virus to boot?
In the meantime, try out CC Cleaner. This program cleans out your temporary internet files and a bunch of other junk that's hindering your web experience. If you use this and your surfing speed returns to normal, just thank me later Larry!


Euphoric Misery introduce their latest collection of streetwear staples, tracksuits and butterfly prints.
Euphoric Misery is a UK streetwear brand which is based around the idea that everything exists as contrasting and inseparable opposites. Light & dark, good & bad etc. Drawing inspiration from 90s streetwear and classic sportswear the brand now introduces its latest collection for the current spring/summer 2019 season. Shot on 35mm film the lookbook is themed around work. Shot in an abandoned factory and based on the idea that a lot of people are unhappy with their jobs. A lot of people work jobs they hate and clothes are their escape, they work to buy new clothes.
Highlights from the latest Euphoric Misery SS19 drop include football inspired graphic tees, butterfly prints, hoody and track pants combos in classic 90s colour blocking style and baggy fit velour tracksuits.
The Euphoric Misery SS19 collection is available now from euphoricmisery.com. In other recent streetwear news you can also check out our feature exploring 5 French streetwear brands that should be on your radar.


Hagerstown is a city in Washington County, Maryland, and is also the county seat of Washington County. Hagerstown is Maryland's sixth largest incorporated city.
A German immigrant named Jonathan Hager purchased 200 acres in 1739 known as the Great Appalachian Valley between the Blue Ridge and Allegheny Mountains in Maryland and called it Hager's Fancy. Soon after, Jonathan Hager and his wife, Elizabeth, officially founded the town of Elizabethtown which was named after Jonathan's wife, Elizabeth. Fourteen years later, Jonathan Hager became known as the "Father of Washington County" after his efforts helped Hagerstown become the county seat of newly created Washington County which Hager also helped create from neighboring Frederick County, Maryland.
Hagerstown's strategic location at the border between the North and the South made the city a primary staging area and supply center for four major campaigns during the Civil War. Throughout the Civil War, private physicians and citizens of Hagerstown gave assistance or aid to men from both the North and South in a number of locations. Hagerstown's nickname of the "Hub City" came from the large number of railroads (and roads) that served the city. Hagerstown was the center of the Western Maryland Railway. One of the most recognizable symbols of Hagerstown is the weathervane known as "Little Heiskell". It was named after the German tinsmith Benjamin Heiskell who crafted it in 1769 in the form of a Hessian soldier.
Hagerstown, Maryland offers public as well as private schools including a Washington County Technical High School.
Hagerstown, Maryland, is host to many events including The "Interstate BBQ Festival", the Hagerstown Duathlon, and a semi-pro baseball team, The Hagerstown Suns. An annual tradition in Hagerstown, "The Western Maryland Blues Fest held on the first weekend following Memorial Day in City Center and the City Park in Hagerstown among many other events held throughout the year.


A new version (v2) of the case has been released. Fixes some alignment issues Optimised for better printing Reviewed for easier installation on wall See all v2 files (3 pieces) in 3D view here.
Forum user dexterp37 just won a FREE HestiaPi Touch! Thank you all for your very valuable input and help! We will get in touch with you directly.
Preorders for the 65EUR Kit are now OPEN!
For those who prefer more insight (like us) rather than blindly installing an image file here are some very rough steps. Please read the warning: Under User Manual: Documentation Please help us making it better if you find mistakes by posting here.
New HestiaPi Touch for 65EUR?
Happy New Year! We got new clothes (UI) !
Win a FREE HestiaPi Touch in 20 seconds!
Answer 5 questions to get a chance to win this perfect Xmas toy: === CLICK TO WIN === We want to get to know you better and this is our way to say thank you!
Not your average Black Friday newsletter!
Take control of your home in the next 2 weeks and save 20% ! Free shipping anywhere on earth. Simple as that.
It was actually a very good day as all planets aligned and we got both a major UI update *and* a complete 3D printable set of files for the case, all on the same day! Now that we woke up from that long night its time to tell the world!


text:
Putin Is Angry: Ukraine Is Getting Thousands of Javelin and Stinger Missiles
Javelin anti-tank missile. Image Credit: Creative Commons.
Ukraine Set to Receive More Javelin and Stinger Missiles – Ukrainian National Security and Defence Council Secretary Oleksiy Danilov announced on Saturday that Ukraine is expecting a new shipment of weapons, including Stinger missiles and Javelins within a matter of days.
"The weapons will be on the territory of our country in the nearest future," he said. "We are talking about days."
What Are Javelin and Stinger Missiles?
The Javelin is an American-made missile launcher that uses an infrared-seeking missile. The weapon has been used heavily by Ukrainian soldiers to destroy Russian tanks. Thousands have already been deployed to Ukraine.
2,000 Javelin missiles were pledged by the United States before this latest delivery was announced.
The Stinger missile, officially the FIM-92 Stinger, is a portable air-defense system that utilizes an infrared-seeking surface-to-air missile. The missile uses IR and UV sensors to track targets and is also effective at tracking and destroying drones and aircraft.
Stinger missiles were used successfully by the mujahedeen's ground troops during the 1980s Soviet-Afghanistan war.
Ukraine Receives Additional Anti-Tank Weapons from Europe
On top of missiles from the United States, Ukraine continues to receive large numbers of both guided and unguided anti-tank weapons from Europe. The missiles have proven essential for the Ukrainian military, allowing Ukrainian fighters to hold off Russian invaders from several major population centers, including Kyiv.
Ukrainian fighters have so far been able to hold off a 40-mile convoy of Russian military vehicles that arrived in Kyiv last week and dispersed around the city. 500 Stinger missiles were pledged to Ukraine by Germany.
Image of Javelin anti-tank weapon. Image Credit: US Department of Defense.
Javelin Missile. Image Credit – Creative Commons.
Javelin anti-tank weapon. Image Credit: Creative Commons.
Germany also pledged to supply 1,000 anti-tank weapons from its arsenal. Sweden has already delivered 5,000 anti-tank weapons and Norway has pledged 2,000.
Is Russia Running Low on Ammunition?
Several experts have warned over the last week that Russia is coming close to running out of ammunition – perhaps revealing why Russian President Vladimir Putin recently appealed for military assistance from China.
Ben Hodges, a retired United States Army officer who previously served as commanding general for United States Army Europe, told CNN on March 14 that Russia may be just 10 days away from running out of troops and ammunition.
"I believe that we are probably about 10 days away from Russia culminating. In other words, running out of time, running out of people, and running out of ammunition," he said.
Ivan Ingraham, who served as a Special Operations Officer for the United States Marin Corps, for 24 years, also said in an opinion piece published on March 10 that Russia's lack of progress in Ukraine was not surprising.
"Many Russian units are running short on fuel and ammunition. A forty-mile convoy on single-lane roads is a combined arms engagement dream. I can only imagine artillery instructors at Fort Sill, where the U.S. military trains its artillery forces rolling their sleeves with glee to set up sand table training, never mind free and open engagement areas for aerial-delivered munitions from platforms like the A-10 Warthog, which would be well-suited to striking a long-sprawling convoy," he wrote in Task & Purpose.
Unless Russia shifts to new military tactics or receives assistance from China – and unless Russian troops successfully destroy more ammunition depots in Ukraine – the Russian forces may find themselves forced to retreat within a matter of days.
Jack Buckby is a British author, counter-extremism researcher, and journalist based in New York. Reporting on the U.K., Europe, and the U.S., he works to analyze and understand left-wing and right-wing radicalization, and reports on Western governments' approaches to the pressing issues of today. His books and research papers explore these themes and propose pragmatic solutions to our increasingly polarized society.
In this article:Anti-Tank Missile, Javelin, Missiles, Russia, Stinger Missile, Ukraine, War in Ukraine
All these complexes will help Dnbass. Donbass takes them away from Bandera Nazis. The Slavs of Donbass thank you for your support.
The hit of a tank but by a missile is subject to lethal metal splinters, not to mention lethal temperatures. This may explain a separate article I read about numerous bodies returned over the border to the russians slot in crime. Someone did video the body train, so Much so that the russians changed body loading to night time to hide the extent of Russian losses. The Russians lost 15,000 in Afghanistan in 10 years. If the Ukrainian advice of Russian losses is accepted, Russia is going to lose more than afghanistan within 3 weeks. Effectively Russian losses are a factor of over 170x afghanistan.
Oh, those tens of thousands of dead Russian soldiers. The real figure is known only in Russia. Even the US represents between 4,000 and 7,000 people. And this should at least be divided by 5. It is immediately clear that the Ukrainian troll is writing. Either a green man, then a red one, then a blue one … More fantasy, Bandera Nazi! 🙂
Sam McGowan
Sending weapons to Ukraine then actually getting them to the troops are two different things. They have to be trucked from the supply bases and trucks are subject to air attack. Not to mention the Russians are now hitting the Ukrainian supply and training bases in Western Ukraine. There is a lot of speculation and few facts being tossed around by various people. I don't know if 1945 pays for submissions or not but they probably do. If they pay, people are writing stuff for money.
So where are the a-10s and artillery batteries? Where are the MIGs, SAMs and anti-ship missiles?
They don't have them.


Two years ago my New Year's Resolution was to make the cleaning products in my home as natural as possible and homemade (Because I am ALL ABOUT SAVING MONEY). Laundry detergent is a MUST and I was paying ~ $12 each month for the 7th Generation brand. I am spending ~$4 now for a 5 gallon bucket full of laundry detergent that lasts me 2-3 months, depending on the time of the year ( Remember that I am doing laundry for 3 boys and 1 farm Momma :), lots and lots of laundry!).
I've been making this for 2 years now and have made adjustments and feel very confident in this recipe. Our clothes are clean and smell good. Give yourself time to adjust to not smelling the "Mountain Breeze" or "Lavender Fields" or whatever the heck they call all the stuff they put in Laundry Detergent these days.
Reduce to simmer and add grated bar of soap. Stir mixture until soap is dissolved.
Add 4 cups of water/soap mix to the bucket and stir well.
Add essential oil of choice ( I love rosemary for laundry!) and enough water to fill bucket without overfilling.