Download Dear Students,

Dear Students,
We are pleased to announce the NYU School of Medicine's NIDDK-funded
summer research fellowships for the Summer 2015. The award from the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) T35 training
grant will provide summer research opportunities to medical students at NYU and
in the New York City area. The grant provides fellowships for students doing
basic research with an NYU faculty mentor in diabetes, digestive disorders, and
kidney diseases. These fellowships, of up to 8 weeks in duration, will provide
students with a summer stipend of approximately $3,750. This fellowship is NOT
contingent on your eligibility for work-study funding.
If you are interested in pursuing this exciting opportunity, please review the
attached program requirements and list of mentors and research projects available,
and then contact the mentor to schedule an appointment to meet with them. Note
that this is not an exhaustive list of project titles. In consultation with your
mentor, there may be opportunities for other NIDDK projects based on your
interests and current work in the mentors' labs. Mentors will then select one
student for each available project and ask the student to submit a formal
application to the program directors. If you are selected to apply for a project,
please submit a completed application to Erin Hazard ([email protected]).
While this is an NYU grant and preference will be given to NYU students, careful
review will be given to all applications. The application form is attached in this
email, and the deadline for submitting your application is February 1, 2015.
Students will be notified of final decisions in mid-March and asked to confirm
their participation in this program.
If you have any questions about the NIDDK summer research fellowships, please
contact Erin Hazard, NYU School of Medicine, Office of Medical Education at
[email protected].
NYU School of Medicine
NIDDK T35 Medical Student Training Program Application for Summer 2015
Personal Information
Name:
Class:
Medical School:
Gender: _____ F ______ M
Ethnicity: ______ Hispanic or Latino _______ Not Hispanic or Latino _______ Unknown or not reported
Race: ______ American Indian/Alaska Native _____ Asian ______ Native Hawaiian or Pacific Islander
_____ Black or African American ______ White ______ More than one race _____ Unknown or not reported
Undergraduate Institution:
Year of Graduation:
Graduate Institution (if applicable, and degree):
Past Research Involvement (yes/no):
If “Yes”
Title of Research:
Mentor:
Institution:
Publications:
Project Information
Mentor Name:
Mentor Department and Division (if applicable):
Summer 2015 Research Start Date:
Project Title:
(A good title is brief and informative. The research hypothesis should be the basis of the title.)
Project Abstract:
(The abstract should include the research question, the rationale for study, the hypothesis, method, and
expected main findings. It should be no more than 300 words.)
Project Proposal
Background and Significance:
(State the fundamental problem motivating this area of research and the importance of the project. 500 words
maximum).
Hypothesis:
(State the research question, or the concept to be tested. 3-4 sentences).
Specific Aims:
(Concisely state the specific aims of the project. One or two specific aims is recommended. Do not propose
more than can be accomplished.)
Research Design:
(Describe the overall strategy, methodology, and analyses to be used to accomplish the specific aims of the
project.)
Potential Pitfalls and Alternate Plans:
(Consider potential problems in your approach. List strategies you will use to address these problems if they
arise.)
References:
(In the main text of your proposal, annotate references and provide a list of these references here. We suggest
using the format in the journal Cell to cite references.)
Approval
Mentor Signature ________________________ Date: _________________
I approve of the trainee’s proposal.
T35 Program Signature ____________________Date: _________________
On behalf of the Advisory Committee, I approve of the trainee’s proposal.
Your completed application should be no longer than 4 pages, exclusive of references.
If you are a medical student from outside of NYU, please also provide one letter of reference along with
your application.
NYU School of Medicine
NIDDK T35 Medical Student Training Program
Mentors and Projects for Summer 2015
Mentor Name
Mentor Email Address
Project Title
Description of Project
Blaser, Martin
[email protected]
Digestive hormones after H. pylori eradication
Assessment of the response of digestive hormones to Helicobacter pylori eradication from healthy young adults.
From on-going clinical trials, we have archived serum specimens for examination of gastric, pancreatic, and intestinal
hormones.
Effect of antibiotic treatment on oxalate metabolic gene
expression
We have established murine models of antibiotic exposures that lead to alterations in adiposity. Intestinal bacteria can
metabolize oxylate, preventing its absorption, and the subsequent risk to the host of oxalate nephrolithiasis. From
specimens from our antibiotic-treated and control mice, we will assess oxalate levels in bodily fluids.
From metagenomic sequencing of fecal specimens obtained from antibiotic-treated and control mice, we have 300
Alterations in choline gene expression in antibiotic-treated mice GB of sequence. We will perform informatic searches of bacterial genes involved in choline metabolism to determine
whether antibiotic treatments affect the major pathways.
Boeke, Jef
[email protected]
Engineering Designer Yeast Chromosomes to Make Small
Molecules
Designer mammalian neochromosomes for xenotransplantation
Cadwell, Ken
Chao, Moses
[email protected]
[email protected]
[email protected]
We seek to humanize yeast cells to make them effective models for a wide range of human disorders. This works
well for disorders affecting a gene system that is conserved between human and yeast, such as metabolic systems.
We are currently assembling a neochromosome with over 25 huan genes to reconstruct the "purine metabolome”
which includes many genes responsible for perplexing human genetic disorders.
Mechanisms of Paneth cell abnormalities in Atg16L1 mutant
mice
We previously found that a norovirus induces Paneth cell abnormalities in the small intestine of mice deficient in the
IBD gene Atg16L1 develop. The student will determine the mechanism of this pathology, which we have shown
occurs in IBD patients that carry the Atg16L1 risk variant.
Nod2 control of commensal bacteria
We have found that mutation of the IBD gene Nod2 in the hematopoietic compartment leads to an overgrowth of a
commensal bacterium that induces intestinal disease. The student will determine how Nod2 functions in white blood
cells to prevent this adverse change in the gut microbiota.
Transactivation of Trk tyrosine kinase receptors by GPCR
ligands
Cross-talk between adenosine and the BDNF receptor, TrkB, occurs by a process called receptor transactivation. We
are interested in identifying other GPCR ligands that are capable of transactivation.
Hypermethylation as a microbiome-mediated epigenetic
phenomenon in CIMP(+) colorectal cancers
Microbiome-mediated metabolism of common oral
anticoagulants
Updated 12.2.14
We seek to design and construct synthetic systems to build mammalian neochromosomes with an ultimate eye to
reducing the risks associated with xenotransplantation. We are exploring ways to deliver such molecules to a wide
variety of mammalian cells, including pig cells, which could lead to new ways to make xenotransplantation safer.
Neochromosomes to model human disease
Mechanisms of obesity from a lack of BDNF
Cho, Ilseung
Synthetic neochromosomes can be designed and built up from standardized parts to produce a wide variety of small
molecules and metabolites that may be of clinical relevance. We have built toy systems that produce carotenoids and
violaceins which produce visual pigments, making it easier to optimize the systems. We seek to improve the
technology and use it to tap the tremendous chemico/biological richness of the microbiome to produce a vast array of
small molecules.
Convit, Antonio
[email protected]
Obesity, insulin resistance, and the brain in adolescence
Cronstein, Bruce
[email protected]
Role of adenosine and its receptors in steatosis and
steatohepatitis
BDNF is involved in the control of appetite and body weight and mutations in BDNF and its receptor TrkB result in
obesity. The signaling mechanisms by TrkB receptors that lead to food intake and obesity are unknown.
We are assessing whether the gut microbiome is associated with hypermethylation in CIMP+ colorectal cancers.
Microbe-mediated hypermethylation as a carcinogenesis pathway has been described in other malignancies but has
not been studied in colon cancer.
We are studying the specific taxonomic and functional characteristics of the gut microbiome that can affect the
metabolism of commonly used oral anticoagulations such as warfarin.
The goal of this work is to carefully evaluate the nature of the brain abnormalities that may be related to obesity and
insulin resistance among adolescents.
We have previously demonstrated that increased adenosine release, stimulating A1 and A2B receptors, mediates
alcohol-induced hepatic steatosis. We will determine the role of adenosine receptors in other forms of hepatic
steatosis.
NYU School of Medicine
NIDDK T35 Medical Student Training Program
Mentors and Projects for Summer 2015
Mentor Name
Mentor Email Address
Project Title
Description of Project
Darwin, Andrew
[email protected]
Activation of the Yersinia enterocolitica Psp response
The Psp stress response system is essential for virulence of the intestinal pathogen Yersinia enterocolitica. This
project will use genetic and biochemical techniques to understand the signal transduction mechanisms that lead to its
transcriptional upregulation.
Stress relief by the Yersinia enterocolitica Psp response
The Psp stress response system is essential for virulence of the intestinal pathogen Yersinia enterocolitica. The goal
of this project is to investigate how two of its components, the PspB and -C membrane proteins, can prevent bacterial
cell death being caused during production of a critical virulence factor known as a type three secretion system.
The Psp stress response system is essential for virulence of the intestinal pathogen Yersinia enterocolitica. To help us
Isolation and characterization of envelope stress suppressors in
understand its physiological function, this project will use a genetic screen to identify and characterize bacterial genes
Yersinia enterocolitca
that can compensate for its loss, or in other words can suppress a Psp null phenotype.
Ding, Yu-Shin
The norepinephrine transporter: a novel target for imaging
brown adipose tissue (brown fat)
Learn how to analyze the PET and CT data obtained from this grant study. The experience gained from this project
will be applied to future proposed imaging study of brown fat using the NYU newly acquired PET/MR combined
scanner with simultaneous acquisition.
The dramatic increase in obesity in the U.S. has fueled growing interest in the role of the “food environment,” defined
as the availability of both healthy and unhealthy food in a geographic community. Studies have found that low-income
and minority neighborhoods have less access to supermarkets, and neighborhoods with fewer supermarkets have
higher obesity rates. However, there are significant limitations to this research, and correlation may not indicate
causation. Food choice and consumption patterns are deeply ingrained, and it is possible that the causal arrow goes
both ways, or that food choice and proximate food resources are not as related as many assume. The relationship
between them may be overestimated (or underestimated) due to other weaknesses in the current research, such as
failure to address spatial autocorrelation – the extent to which adjoining areas are similar and may produce spillover
effects -- and the “modifiable areal unit problem” – the fact that area boundaries are arbitrary and can be redrawn in a
way that alters area-level measures.
We are analyzing existing administrative data to address this gap in knowledge regarding the impact of the
food environment on body mass index (BMI). Our dataset is large and comprehensive, consisting of repeated BMI
measurements from almost all New York City public school children across multiple years. Our data also include the
exact residential and school location of each student. When we combine these data with available data on the
locations of food sources, we have a unique and powerful resource for answering key questions regarding the impact
of food availability on the BMI of children and youth.
Elbel, Brian
[email protected]
Impact of the Food Environment on Child Body Mass Index
Feske, Stefan
[email protected]
CRAC channels in Th1 and Th17 cells as mediators of colitis
and therapeutic targets
The overall goal of this project is to understand the role of Ca2+ influx mediated by Ca2+ release activated Ca2+
(CRAC) channels in the proinflammatory function of Th17 and Th1 cells and how they control autoimmunity in IBD.
Elucidating how SOCE regulates the colitogenic function of T cells will allow us to assess the benefits and risks
associated with CRAC channel inhibition as a potent immunosuppressive treatment for IBD.
Fisher, Edward
[email protected]
VLDL overproduction in insulin resistance and the role of the
insulin-mediated degradation of apoB100 via autophagy
The overall goal of the project is to obtain detailed understanding of dyslipidemia in insulin resistance (IR) and
diabetes (DM). People with IR and DM oversecrete VLDL from the liver, which leads to high triglyceride and low HDL
levels. Specifically, the student will extend our recent discovery that under normal circumstances, insulin can promote
the autophagic degradation of partially assembled VLDL particles prior to their secretion by the liver. If this
degradation pathway is impaired in IR/DM, it would result in VLDL oversecretion.
Froemke, Robert
Updated 12.2.14
[email protected]
[email protected]
Diabetes and atherosclerosis
Diabetics have increased rates of coronary artery disease. We have found in mouse models of diabetes that
hyperglycemia increases the level of leukocytes, some of which enter atherosclerotic plaques and become
cholesterol-laden macrophages. Diabetics tend to have low levels of HDL. Other people have found that HDL can
reduce leukocyte counts in hypercholesterolemic mice, and we have found in a mouse model of diabetes that
correction of low HDL reduces the elevated counts caused by hyperglycemia. We are now pursuing the mechanism
by which HDL does this and what is in common between the hypercholesterolemic and hyperglycemic metabolic
settings.
Metabolic sensors for sucrose preference in the mammalian
brain
Animals can sense both the rewarding (hedonic) value of food as well as the nutritive (caloric) value, depending on
their metabolic needs. In this study we explore the metabolic sensors in the mouse hypothalamus that compute the
hedonic and caloric values of various sugars in real-time.
Neural circuitry of feeding behavior in the mammalian brain
Two regions of the mammalian brain are important for food-seeking behavior: the frontal cortex (where behavioral
choices are computed) and the ventral tegmental area (which releases dopamine when rewarding stimuli such as
food are presented). As it is unclear how these two regions communicate with each other, we will perform anatomical
studies to assess the dopaminergic input to the frontal cortex, and behavioral studies to determine the consequences
of activating or inactivating these inputs on food seeking.
NYU School of Medicine
NIDDK T35 Medical Student Training Program
Mentors and Projects for Summer 2015
Mentor Name
Mentor Email Address
Project Title
Goldberg, Ira
[email protected]
Lipid metabolism and macrophage polarization
Hubbard, E. Jane
[email protected]
Description of Project
We will create mice with deletion of two genes required for uptake of lipid into macrophages. We will then test
whether loss of lipid uptake prevents macrophage to an alternatively activated (M2-like) phenotype.
Cardiac fatty acid uptake
We have deleted a fatty acid transporter, CD36, in endothelial cells. We will study how this deletion affects uptake of
fatty acids in the heart.
Molecular mechanisms that regulate germ line stem cell
plasticity
Altering nutritional input or the activity of nutritionally-sensitive signal transduction pathways impacts germ line stem
cell quiescence and activation. We are using the powerful genetic tools in C. elegans to uncover in an unbiased
manner the molecular mechanisms that underlie this regulation.
Components of the TOR pathway that regulate germline
response to nutrition
Our lab showed that components of the TOR signaling pathways regulate germ cell accumulation during development
in response to nutritional cues. We are exploring the effects of this pathway on cell cycle and cell fate.
How does nutrition interface with insulin/IGF-like ligands to
influence germline development?
We have defined a role for the C. elegans insulin/IGF-like signaling pathway in germline cell cycle control during
development. We are investigating the connection to nutrition: What cues regulate key ligand production and/or
activity?
We have defined a germline-autonomous role for the C. elegans insulin/IGF-like signaling pathway and its
How do FOXO targets in the germ line in respond to insulin/IGFdownstream transcription factor FOXO in germline cell cycle control during development. Using functional in vivo
like pathway signaling?
assays, we are investigating which FOXO targets are relevant.
Kong, Xiangpeng
[email protected]
Epitopes of UPEC adhesin FimH
Type 1-piliated uropathogenic E. coli is the major causative agent for UTI and FimH is its adhesion molecule.
Identifying its epitopes will help to design vaccine to prevent UTI.
Mechanism of invasion of UPEC
Use the single molecule method to visualize the invasion of uropathogenic E. coli (UPEC), so we may gain an
understanding of the invasion mechanism.
Structure-based HIV/AIDS vaccine development
Littman, Dan
[email protected]
Human T cell immunity to luminal microbiota
Visualization of microbial specific Th17 cells in the intestine
Determination of Th17 cell fate
Loke, P'ng
[email protected]
[email protected]
Role of C-type lectin receptors in liver inflammation
Role of hepatic dendritic cell lipid content on their immune
phenotype
Role of RIP3 Kinase in liver injury and regeneration
Updated 12.2.14
Changes in microbiota are associated with metabolic and inflammatory disease in humans including obesity,
inflammatory bowel disease, and rheumatoid arthrtitis. Our lab identified the ability of segmented filamentous
bacteria to induce intestinal Th17 and drive autoimmune arthritis in mouse models, however, the role of microbial
derived antigens in shaping the intestinal and systemic CD4+ T cell repertoire is unknown. In this rotation, the
student will prepare CD4+ T cell clones from peripheral blood and intestinal tissue and identify clones that specifically
respond to naturally processed antigens derived from intestinal bacteria. This work will help develop tools to identify
and define the role of microbiota-specific T cells in human disease.
How microbial-specific Th17 cell generation occurs in the intestine is not clear. Using a novel Th17-prone, SFB
specific TCRTg mouse, we will study how these cells interact with antigen presenting cells microscopically.
We have shown that segmented filamentous bacteria (SFB), a commensal microbe, can induce Th17 helper T cell
differentiation in the gut. To find the mechanism of how SFB can skew T helper cell differentiation into Th17, we will
examine the fate of "Th17 wanna be" cells in the absence of RORgt after exposure to SFB, by combining RORgt-GFP
reporter knock-in mice, RORgt conditional knockout mice, and transgenic mice specific for SFB antigen.
The effects of vitamin A deficiency on the intestinal microbiota Fecal samples will be collected from vitamin A deficient mice for deep sequencing analysis.
The effects of helminth infection on the intestinal microbiota
Miller, George
We will determine the atomic structures of monoclonal antibodies derived from human patients and use its epitope
information for immunogen design.
Mice will also be infected with helminths to determine the combined effects of vitamin A deficiency and helminth
infection.
We are investigating whether ligation C-type lectin receptors exacerbates hepatic fibro-inflammatory disease after
liver injury using mouse models and human liver specimens.
We are investigating how lipids are acquired by intra-hepatic dendritic cells and the mechanism by which lipids
modulate dendritic cell phenotype and immune stimulatory function.
Rip3 Kinase regulates necro-apoptosis. We postulate that Rip3 Kinase would have a critical role in hepatocyte injury
and regulation of hepatocyte regeneration.
NYU School of Medicine
NIDDK T35 Medical Student Training Program
Mentors and Projects for Summer 2015
Mentor Name
Mentor Email Address
Moore, Kathyrn
[email protected]
Nance, Jeremy
[email protected]
Project Title
The increased accumulation of macrophages and lymphocytes in adipose tissue during obesity propagates chronic
inflammation, which is closely associated with systemic insulin resistance, and the development of metabolic
syndrome and type 2 diabetes (T2D). Recent studies have explored the mechanisms by which these immune cells
arerecruited. However, the signals that cause macrophages to persist in adipose, promoting chronic inflammation, are
not understood. We recently uncovered a novel role for the neuronal guidance cue, Netrin-1, in inducing macrophage
(Mø) chemostasis and thus blocking their emigration from atherosclerotic plaques. Our preliminary data indicate that
Netrin-1 is also increased in adipose tissue from obese mice and humans compared to lean controls. Lethally
Role of netrin-1 in adipose inflammation and insulin resistance
irradiated wild-type mice reconstituted with Ntn1 null bone marrow display protection against diet-induced adipose
inflammation and insulin resistance compared to mice with wild-typemarrow. Based on these data we hypothesize
that Netrin-1 critically regulates immune cell trafficking and accumulation in WAT and metabolic dysfunction in HFD
feeding, thereby leading to insulin resistance and diabetes. To test this hypothesis, we will determine (1) the
mechanisms of Netrin-1 regulation in WAT, (2) the contribution of Mø and Treg derived netrin-1 on WAT inflammation
in mouse models of tissue-specific or conditional deletion of netrin1, and (3) whether Netrin-1 targeting using a
nanoparticle delivery system improves metabolic parameters in obese mice.
Regulation of epithelial junction formation
Lumenogenesis in the C. elegans renal tubule
Nudler, Evgeny
[email protected]
Sensor mechanisms of HSF activation
NO signaling in C.elegans
Pei, Zhiheng
[email protected]
Philips, Mark
[email protected]
Rindler, Michael
[email protected]
Ryoo, H. Don
[email protected]
Updated 12.2.14
[email protected]
This project will use genetic and cell biological approaches to determine how junctions assemble in epithelial cells in
the model organism C. elegans.
This project examines how the lumen forms in the C. elegans excretory cell, which is analogous to the mammalian
kidney.
The major goal of this project is to understand the molecular mechanism of the heat shock response activation.
The goal of this project is to identify and characterize new genes that control aging and stress resistance.
Foregut microbiome in development of esophageal
adenocarcinoma
This is a NIH Roadmap Initiative grant with a goal to demonstrate that there is a change in the foregut microbiome at
various stages of reflux disorder developing toward esophageal adenocarcinoma. If reflux disorder represents a
microbiome-related disease, it could be possible to design new antibiotic or probiotic treatment strategies to prevent
GERD and reverse the current trend of increasing rate of esophageal adenocarcinoma.
The oral microbiome and upper aerodigestive squamous cell
cancer
This is an innovative study to examine whether the oral microbiome is associated with risk of upper aerodigestive cell
cancers (UADSCC: oral, pharyngeal, laryngeal and esophageal squamous cell cancers). The goals of our study are
to relate the oral microbiome to UADSCC risk and to identify the impact of alcohol and tobacco use on the oral
microbiome, in the first epidemiologic investigation of this topic.
Subcellular localization and trafficking of Rheb, a small GTPase
Rheb, the Ras related GTPase that activates mTor and is therefore important in diabetes.
that activates mTor in response to insulin
Synthesis, assembly, and targeting of uroplakins
The aims of the project are to investigate the biosynthesis and intracellular trafficking of uroplakins, which form
crystalline arrays in the apical membrane of the bladder and are also stored in fusiform vesicles recruited to the
membrane during bladder distension. The studies take advantage mutant mouse models to elucidate the molecular
mechanisms of fusiform vesicle formation and fusion.
We have recently found that a stress response pathway known as the Unfolded Protein Response is required for the
Unfolded protein response in drosophila intestine development normal development of the Drosophila intestine. We plan to identify the precise underlying mechanism, focusing on
and function
the idea that unfolded protein-related stress occurs in healthy tissues that express large amounts of secretory
proteins.
The role of ATF4 in the amino acid starvation response.
Segal, Leopoldo
Description of Project
Amino acid deprivation activates a stress response pathway mediated by the transcription factor ATF4. We plan to
determine the precise role of ATF4 and its downstream effectors in mediating the effects of reduced amino acid
intake, which includes enhanced stress resistance of cells and extension of lifespan.
Topographical analysis of the aero-digestive microbiome in
children with chronic cough
Gastroesophageal reflux and microaspiration occurs more frequently among children with chronic cough. In this
project, we will examine the microbiome in the lower/upper airway mucosa as well as the microbiome in the upper GI
tract in children with various degrees of gastroesophageal reflux.
Evaluation of regional lower airway microbiome in NTM
bronchiectasis
We have observed that enrichment of the lung microbiome with anaerobes (possible though microaspiration) is
associated with a blunted TNF alpha production to TLR stimulation, an innate immune response commonly impaired
in nontuberculous mycobacteria (NTM) disease. In this project, we will examine regional differences in microbiome
and host immune response comparing areas of NTM bronchiectasis with airways without significant disease.
NYU School of Medicine
NIDDK T35 Medical Student Training Program
Mentors and Projects for Summer 2015
Mentor Name
Mentor Email Address
Project Title
Description of Project
Schmidt, Ann Marie
[email protected]
The role of RAGE in diet induced obesity
RAGE and its ligands are highly expressed in the adipose and liver tissue of mice fed for two weeks with high fat diet,
that is, a time prior to the development of obesity, and RAGE null mice are protected from diet induced obesity. The
goal of the project is to use mice with conditional cell specific deletion of RAGE to test the hypothesis that both
inflammatory and adipocyte specific signals mediate RAGE-dependent development of obesity and metabolic
dysfunction in mice fed high fat diet.
The role of mDia1 in diabetic nephropathy
The cytoplasmic domain of RAGE binds to the formin mDia1 and mDia1 is required for the actions of RAGE in
contributing to the pathogenesis of diabetic nephropathic changes in mice. The goal of the project is to dissect the
effects of podocyte RAGE and mDia1 in the development of glomerular disease in diabetic mice.
The development of small molecule antagonists that block
RAGE signaling
Sigmund, Eric
[email protected]
This project is devoted to applying a comprehensive model to diffusion-weighted MRI contrast in the kidney,
Advanced diffusion-weighted MRI biomarkers of renal function judiciously merging separate formalisms capturing microscopic flow and structural anisotropy. The resulting analysis
in healthy kidney and diabetic nephropathy
workflow is expected to dramatically enhance diagnostic specificity in complex pathologies like diabetic nephropathy,
where separating microstructure, perfusion, tubular flow changes, and water exchange is crucial.
Sigurdsson, Einar
[email protected]
The lab is developing a vaccine to clear aggregates of islet amyloid polypeptide in a mouse model of type-2 diabetes.
Immunotherapy targeting pathological islet amyloid polypeptide
The project entails evaluating the immune response to the vaccine as well as its efficacy using biochemical and
in type-2 diabetes
histological assays.
Skolnik, Edward
[email protected]
Role of the histidine phosphatase, PHPT1 in pancreatic beta
cell function
Sun, Tung-Tien
[email protected]
Identification and characterization of urothelial stem cells
To use a wide range of approaches that we previously used to identify corneal epithelial and hair follicular epithelial
stem cells, to identify and localize urothelial stem cells in the lower urinary tract.
Regulated trafficking of urothelial membrane proteins
Uroplakins are major urothelial differentiation products that form 2D crystals covering the apical surface of bladder
epithelium, and they play key roles in forming urothelial barrier. Studies will be done to better understand how
uroplakins are synthesized, assembled, and targetted to the apical surface of bladder urothelium.
Weiser, Jeffrey
[email protected]
Pathogens subvert metabolism of their host
Wu, Xue-Ru
[email protected]
Role of Tamm-Horsfall protein in urinary tract defense
Uroplakins in bacterial infection
Updated 12.2.14
We have developed a “high throughput" assay to screen for small molecules that block the interaction of the RAGE
cytoplasmic domain with mDia1. In this project, further in vitro and in vivo analysis of lead hit molecules in the assay
will be tested.
To assess the mechanism whereby PHPT1 knockout beta cells have impaired glucose-induced insulin release
One aspect of this project examines how pathogens take advantage of the metabolism of their host to proliferate and
cause infection. Current models of this process use the bacterium, Streptococcus pneumoniae, and influenza virus.
The project is focused on understanding the role of Tamm-Horsfall protein, the most abundant urinary protein, in
kidney stone formation.
The project aims to understand the involvement of uroplakins in bladder infections by uropathogenic E. coli.
NIDDK T35 Medical Student Training Program
June – August 2015
Core Competencies and Expectations
Core competencies in a Research Lab Environment
1. Professionalism (behavior that promotes a scholarly, intellectual, cooperative, respectful,
productive, safe and ethical lab environment)
2. Ability to read and understand the literature
3. Hypothesis formulation and experimental design
4. Technical lab skills
After the T35 summer project, trainees should be able to:
a) Critically review basic science research papers.
b) Design a research proposal that is realistic and specific.
c) Follow methods, procedures, and techniques. Be familiar with lab equipment.
d) Demonstrate professionalism in a research lab by participating in the intellectual life of the
lab, being respectful of and helpful to others, and ethical in decision-making.
e) Demonstrate strong written and oral communication skills by writing clear, concise abstracts,
proposal, and papers, and speaking clearly and precisely during talks, group meetings,
presentations, and poster sessions.
Program Requirements
Date
May 2015
June 2015
Activity
Attend Orientation #1, Human Resources
Payroll Paperwork
Attend Orientation #2, Meet the Program
Directors
June 2015
Finalize your research plan
June 15-August 14, 2015
Participate in up to 8 weeks of NIDDKrelated research
June 15-August 14, 2015
Attend weekly seminars and Journal Club
September 2015
May 2016
January 2016, April 2018, April 2019
Submit Progress Report, including project
summary, abstract, and survey
Participate in the Department of Medicine
Research Day
Complete trainee surveys
Program Activities
Seminars will be held throughout the summer, and trainees are expected to attend them.
Seminars include the following:
• Translational Research in Progress (TRIP) Seminar
• How to Read Papers and Generate Ideas
• How to Get Lab Techniques to Work
• Scientific Integrity and Responsible Conduct of Research
Journal Club will be held weekly. Trainees will be assigned a date and partner(s). Trainees
must submit their article to Dr. Blaser and Dr. Munger for approval two weeks before the
presentation. They must then circulate their article to the group one week before they present. If
trainees cannot present on the day they are assigned, they are responsible for swapping among
themselves.