No data available that match "Models, Genetic"

*  Project: Mouse genetic model of a dysregulated serotonin transporter variant associated with autism
Project: Mouse genetic model of a dysregulated serotonin ... Detail. Mouse genetic model of a dysregulated serotonin ... Projects. Mouse genetic model of a dysregulated serotonin ... project mouse genetic model of a dysregulated serotonin transporter variant associated with autism projects home project detail mouse genetic model of a dysregulated serotonin transporter variant associated with autism project description unavailable funder autism speaks fiscal year funding project number principal investigator veenstra vanderweele jeremy strategic plan question question how can i understand what is happening biology strategic plan objective o not specific to question objectives federal or private private institution vanderbilt university state country tennessee web link no url available web link no url available web link no url available new history related projects mouse genetic model of a dysregulated serotonin transporter variant associated with autism mouse genetic model of a dysregulated serotonin tr...
*  Wilms Tumor-Aniridia-Genital Anomalies-Retardation Syndrome disease: Malacards - Research Articl
Context Animal Models Compounds Drugs & Therapeutics ... Expression Genes Genetic Tests GO Terms Pathways Products ... Context Animal Models Compounds Drugs & Therapeutics ... Wilms Tumor-Aniridia-Genital Anomalies-Retardation Syndrome disease: Malacards - Research Articles, Symptoms, Drugs, Genes, Clinical Trials. . Search. Advanced. Home. User Guide. What's in a MalaCard. Search Guide. Our Sources. Analysis Tools. GeneCards. GeneAnalytics. GeneAlaCart. PathCards. VarElect. News and Views. Disease Lists/Categories. About. About MalaCards. Our Publications. Academic Licensing. Weizmann Institute. LifeMap Discovery. User feedback. Terms of Use. MalaCards Team. Feedback. Log In / Sign Up. MCID: WLM004 MIFTS : 5. Wilms Tumor-Aniridia-Genital Anomalies-Retardation Syndrome malady Genetic diseases common, Cancer diseases categories. Gene Related disease Download this MalaCard Expand all tables. Jump to section Aliases & Classifications Anatomical Context Animal Models Compounds Drugs & Therapeutics Expression ...
*  GPS in your DNA: Genetics can reveal your geographic ancestral origin -
GPS in your DNA: Genetics can reveal your geographic ancestral ... GPS in your DNA: Genetics can reveal your geographic ancestral ... a probabilistic model of genetic traits for every coordinate...
*  Microbial Identification & Strain Typing | Charles River
Research + Find a Model Rodent Surgery Health Monitoring & ... Diagnostic Services Genetically Engineered Model Services Genetic...
*  Transposagen Biopharmaceuticals Inc Announces New Product Offering TGEMTM Genetically Modified Ra
Offering TGEMTM Genetically Modified Rat Models. Employer:. ... Offering: TGEM TM Genetically Modified Rat Models. Tweet. 4/22/ ... it has added 170 genetically modified rats and related...
*  Genetics Selection Evolution | Abstract | Genomic breeding value estimation using nonparametric addi
Genetics Selection Evolution. Abstract. ... additive regression models. ... this journal. My Genetics Selection Evolution. Genetics...
*  Genetics firm weaves history and DNA for predicting diseases - Tech Chronicles
Genetics firm weaves history and DNA for ... Tech Chronicles. Genetics firm weaves history and DNA for ... lean on genetics to predict our health in the future....
*  Genetic Testing May Help Avoid Unnecessary Surgery in Detecting Thyroid Cancer, Study Says | news@JA
Genetic Testing May Help Avoid Unnecessary ... Diseases. Genetic Testing May Help Avoid Unnecessary ... , Study Says. Genetic Testing May Help Avoid Unnecessary ... Genetic Testing May Help Avoid Unnecessary Surgery in Detecting Thyroid Cancer, Study Says. news@JAMA. news@JAMA. Genetic Testing May Help Avoid Unnecessary Surgery in Detecting Thyroid Cancer, Study Says. Genetic Testing May Help Avoid Unnecessary Surgery in Detecting Thyroid Cancer, Study Says. September 7, 2012. New research shows that testing gene expression levels could help clinicians distinguish between malignant and benign thyroid tumors. New genetic testing developed in Italy may boost the accuracy of thyroid cancer detection while reducing unnecessary diagnostic thyroidectomies by nearly 50%. Investigators at the University of Pisa developed models to measure gene expression levels in 93 thyroid tumor cell samples obtained with fine-needle aspiration. In evaluating whether gene expression levels could accurately predict thyroid mal...
*  IMPC | International Mouse Phenotyping Consortium
Human Disease Mouse Models Rare diseases links. News and Events ... The fundamental genetic similarity between mice and humans...
*  Genetic forms of hypopituitarism and their manifestation in the neonatal period - UCL Discovery
Genetic forms of hypopituitarism and their ... Bookmark Share. . Genetic forms of hypopituitarism and their ... , MT ; 2009. Genetic forms of hypopituitarism and their ... Genetic forms of hypopituitarism and their manifestation in the neonatal period - UCL Discovery. UCL Discovery. UCL home » Library Services » Electronic resources » UCL Discovery Enter your search terms. Advanced search. UCL Theses. About UCL Discovery. For UCL authors Deposit your research. UCL e-theses guidelines. Genetic forms of hypopituitarism and their manifestation in the neonatal period. Genetic forms of hypopituitarism and their manifestation in the neonatal period. Abstract The anterior pituitary gland is a central regulator of growth, reproduction and homeostasis. The development of the pituitary gland depends on the sequential temporal and spatial expression of transcription factors and signalling molecules. These include the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, PITX1, PITX2, OTX2, SOX2 and SOX3. Mutatio...

No data available that match "Models, Genetic"

(1/26926) A genetic model of substrate deprivation therapy for a glycosphingolipid storage disorder.

Inherited defects in the degradation of glycosphingolipids (GSLs) cause a group of severe diseases known as GSL storage disorders. There are currently no effective treatments for the majority of these disorders. We have explored a new treatment paradigm, substrate deprivation therapy, by constructing a genetic model in mice. Sandhoff's disease mice, which abnormally accumulate GSLs, were bred with mice that were blocked in their synthesis of GSLs. The mice with simultaneous defects in GSL synthesis and degradation no longer accumulated GSLs, had improved neurologic function, and had a much longer life span. However, these mice eventually developed a late-onset neurologic disease because of accumulation of another class of substrate, oligosaccharides. The results support the validity of the substrate deprivation therapy and also highlight some limitations.  (+info)

(2/26926) A computational screen for methylation guide snoRNAs in yeast.

Small nucleolar RNAs (snoRNAs) are required for ribose 2'-O-methylation of eukaryotic ribosomal RNA. Many of the genes for this snoRNA family have remained unidentified in Saccharomyces cerevisiae, despite the availability of a complete genome sequence. Probabilistic modeling methods akin to those used in speech recognition and computational linguistics were used to computationally screen the yeast genome and identify 22 methylation guide snoRNAs, snR50 to snR71. Gene disruptions and other experimental characterization confirmed their methylation guide function. In total, 51 of the 55 ribose methylated sites in yeast ribosomal RNA were assigned to 41 different guide snoRNAs.  (+info)

(3/26926) Familial antiphospholipid antibody syndrome: criteria for disease and evidence for autosomal dominant inheritance.

OBJECTIVE: To develop diagnostic criteria for a familial form of antiphospholipid antibody syndrome (APS), identify families with >1 affected member, examine possible modes of inheritance, and determine linkage to potential candidate genes. METHODS: Family members of probands with primary APS were analyzed for clinical and laboratory abnormalities associated with APS. Families with > or =2 affected members were analyzed by segregation analysis and typed for candidate genetic markers. RESULTS: Seven families were identified. Thirty of 101 family members met diagnostic criteria for APS. Segregation studies rejected both environmental and autosomal recessive models, and the data were best fit by either a dominant or codominant model. Linkage analysis showed independent segregation of APS and several candidate genes. CONCLUSION: Clinical and laboratory criteria are essential to identify the spectrum of disease associated with APS. We believe a set of criteria was developed that can precisely define affected family members with APS. Modeling studies utilizing these criteria strongly support a genetic basis for disease in families with APS and suggest that a susceptibility gene is inherited in an autosomal dominant pattern. However, in these families, APS was not linked with HLA, Fas, or other candidate genes, including beta2-glycoprotein 1, HLA, T cell receptor beta chain, Ig heavy chain, antithrombin III, Fas ligand, factor V, complement factor H, IgK, and Fas.  (+info)

(4/26926) Telomere length dynamics and chromosomal instability in cells derived from telomerase null mice.

To study the effect of continued telomere shortening on chromosome stability, we have analyzed the telomere length of two individual chromosomes (chromosomes 2 and 11) in fibroblasts derived from wild-type mice and from mice lacking the mouse telomerase RNA (mTER) gene using quantitative fluorescence in situ hybridization. Telomere length at both chromosomes decreased with increasing generations of mTER-/- mice. At the 6th mouse generation, this telomere shortening resulted in significantly shorter chromosome 2 telomeres than the average telomere length of all chromosomes. Interestingly, the most frequent fusions found in mTER-/- cells were homologous fusions involving chromosome 2. Immortal cultures derived from the primary mTER-/- cells showed a dramatic accumulation of fusions and translocations, revealing that continued growth in the absence of telomerase is a potent inducer of chromosomal instability. Chromosomes 2 and 11 were frequently involved in these abnormalities suggesting that, in the absence of telomerase, chromosomal instability is determined in part by chromosome-specific telomere length. At various points during the growth of the immortal mTER-/- cells, telomere length was stabilized in a chromosome-specific man-ner. This telomere-maintenance in the absence of telomerase could provide the basis for the ability of mTER-/- cells to grow indefinitely and form tumors.  (+info)

(5/26926) Plasmid replication initiator protein RepD increases the processivity of PcrA DNA helicase.

The replication initiator protein RepD encoded by the Staphylococcus chloramphenicol resistance plasmid pC221 stimulates the helicase activity of the Bacillus stearothermophilus PcrA DNA helicase in vitro. This stimulatory effect seems to be specific for PcrA and differs from the stimulatory effect of the Escherichia coli ribosomal protein L3. Whereas L3 stimulates the PcrA helicase activity by promoting co-operative PcrA binding onto its DNA substrate, RepD stimulates the PcrA helicase activity by increasing the processivity of the enzyme and enables PcrA to displace DNA from a nicked substrate. The implication of these results is that PcrA is the helicase recruited into the replisome by RepD during rolling circle replication of plasmids of the pT181 family.  (+info)

(6/26926) Transplacement mutagenesis: a novel in situ mutagenesis system using phage-plasmid recombination.

Site-specific mutagenesis provides the ability to alter DNA with precision so that the function of any given gene can be more fully understood. Several methods of in vitro mutagenesis are time-consuming and imprecise, requiring the subcloning and sequencing of products. Here we describe a rapid, high fidelity method of in situ mutagenesis in bacteriophage lambda using transplacement. Using this method, mutations are transferred from oligonucleotides to target phages using a plasmid interface. A small (50 bp) homology region bearing a centred point mutation is generated from oligonucleotides and subcloned into a transplacement plasmid bearing positive and negative phage selectable markers. Following a positive/negative selection cycle of integrative recombination and excision, the point mutation is transferred precisely from plasmid to phage in a subset ( approximately 25-50%) of recombinants. As the fidelity of both oligonucleotide synthesis and phage-plasmid recombination is great, this approach is extremely reliable. Using transplacement, point mutations can be accurately deposited within large phage clones and we demonstrate the utility of this technique in the construction of gene targeting vectors in bacteriophages.  (+info)

(7/26926) Rapid modification of bacterial artificial chromosomes by ET-recombination.

We present a method to modify bacterial artificial chromosomes (BACs) resident in their host strain. The method is based on homologous recombination by ET-cloning. We have successfully modified BACs at two distinct loci by recombination with a PCR product containing homology arms of 50 nt. The procedure we describe here is rapid, was found to work with high efficiency and should be applicable to any BAC modification desired.  (+info)

(8/26926) Amplification of cDNA ends based on template-switching effect and step-out PCR.

A new method for amplifying cDNA ends is described which requires only first-strand cDNA synthesis and a single PCR to generate a correct product with very low or no background. The method can be successfully applied to total RNA as well as poly A+ RNA. The same first-strand cDNA can be used to amplify flanking sequences of any cDNA species present in the sample.  (+info)

What kind of modeling agencies accept glamour models?

What I mean is, when I look at playboy models and video models, they don't look like fashion models.  What kind of agency accepts glamour models that are shorter than the high fashion model?

From what ive seen there isnt a particular big glam agency, you more so try to make direct contact with a publication and send them pics.  Glam models arent your usual fashion models like you said they are shorter then most models.  Start off by finding a photographer you are comfortable with and get a portofolio together.  Once you have a variety of poses you are willing to take use that to shop yourself around with any magazines in the area.

What is modeling,who is a model and how do models make money?What do modeling agents do?

What is modeling,who is a model and how do models make money?What do modeling agents do?

A model is a person who appears in magazines, ad campaigns, catalogues, fashion shows, billboards, etc often selling a product or representing a designer. The agent is the one who finds the work for models. Models get paid by the clients who book them and the agent takes a 10-15% commission

So Vogue magazine needs models to wear the clothes on the page, They call various agencies and have a bunch of models come to the office and decide which one they want for the shoot. Then they pay the agency, and the agency takes their commission and pays the model

What is the link between atheletes/models/etc and binge-eating disorders?

I read somewhere that atheletes and models- or any other professionals whose bodies are on "public display on a frequent basis"- notably struggle with binge-eating disorders where they rapidly and excessively consume foods at certain periods of time, usually due to depression, anxiety, boredom, etc. 

It seems sort of odd to me that this is the case, considering atheletes and models are usually very slender. 

What do you guys think are some of the links?

You are asking about two very different groups of people. 

When it comes to elite level athletes, yes, there are certain sports where eating disorders are a big problem. It has less to do with "bodies on display" than with "if I lose 5 kg I'll shave 5 seconds off my time" or similar. You can, for example, look into ski jumping, where a minimum BMI has been set due to  jumpers losing as much weight as they can - to unhealthy low lovels - to be able to fly further on their jumps. 

Models are on public display, but they also have to maintain a certain body type as their role is a living hanger for the clothes. Unlike with (most) athletes, models can and do use illicit drugs to keep their weight down.

Now there will be binging and purging in both groups, but I do not know to what extent it exists.

What are the names of the abercrombie and fitch models in Hawaii?

Recently while shopping, I saw some male models at the front of both the womens and mens store at the Ala Moana Shopping centre in Hawaii. Are they workers or models?


What do modeling agencies look at in models?

When a model applies to a modeling agency, do they care about the colour of the eyes and hair? I've noticed that the majority of models are either blonde with blue eyes or brown hair with blue or green eyes. Also, for runway models, is the body more important than the looks?

No, however say an agency has mainly blonde/blue eyed models, then they will likely be looking for brown/black eyed/hair models to expand their selection. In general, the modeling industry doesn't really favor a specific eye or hair color. (Eastern Europeans are very popular, they have light eyes and hair but to balance that Brazilians are also very popular who mainly have dark eyes and hair)!

What do modeling agencies look for in aspiring fashion models?

I'm talking about models who end up in shows such as fashion week. I would particularly like to know how much the models are supposed to weigh. Do modeling agencies really care about how much they weigh, or is it just as long as they're skinny?

Agencies look for, firstly, a girl who has the right measurements; ideally 32-24-24 and 5'10". Weight doesn't matter so long as they fit these parameters. If you are looking for specific weight, I would say most runway models are weighing between 55-65kg. Model scouts also look for interesting faces— models such as Kelly Mittendorf and Marie Piovesan are successful newcomers who have features outside of the norm. 

Celebrities and socialites sometimes are able to break into modelling because of their "connections" and wealth, which is why they're able to get away with being heavier/curvier or shorter. For an average model, it's all about measurements.

What is the difference between centerfolds and fashion models?

Are centerfolds considered to be models? I say no because they model for lust, whereas fashion models are used to sell or market clothes through campaigns, runways, and magazines. Can anyone provide a clear explanation between these professions?

They are both considered models.

One models for the fashion industry to sell clothes. The other models for the adult entertainment industry to sell its products.They both model to sell some sort of product. Although the fashion model usually has clothes on, and the other models nude usually, but sometimes the roles are reversed and the fashion model can sometimes model nude, but they are still selling some sort of fashion item. 

I think the main different is the fashion model, models to sell a fashion item. While the centerfold model, models to sell nude images of themselves which is the actual product, and not usually an item outside of that (at least most of the time).

What kind of a diet do male models and actors have?

I'm talking about male movie stars, male models, and male adult film stars.  I know they spend a lot of time in the gym, but what about their diet?

Can they never eat any fatty foods or just limit the bad food they eat?

Or do they only work out a lot when they have an upcoming movie or photoshoot and just kind of let themselves go a little when they are not working?

Sex, Alchol and Parties. I have a male model friend - he's all about that. I keep annoying him with "stop, you are harming yourself" comments! ==>>Don't do it!