A5064848473- Pancreatic function and diabetes
- Diabetes and associated disorders
- Endoplasmic Reticulum Stress and Disease
- Diabetes Management and Research
- Adipose Tissue and Metabolism
- Diet, Metabolism, and Disease
- Metabolism, Diabetes, and Cancer
- Hyperglycemia and glycemic control in critically ill and hospitalized patients
- COVID-19 Clinical Research Studies
- Diet and metabolism studies
- Diabetes Treatment and Management
- Adipokines, Inflammation, and Metabolic Diseases
- Organ Transplantation Techniques and Outcomes
- Genetics and Neurodevelopmental Disorders
- Liver Disease and Transplantation
- Virus-based gene therapy research
- Long-Term Effects of COVID-19
- Birth, Development, and Health
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Pancreatitis Pathology and Treatment
- Wnt/β-catenin signaling in development and cancer
- Liver Disease Diagnosis and Treatment
- Hair Growth and Disorders
- Circular RNAs in diseases
Cornell University
2020-2025
Weill Cornell Medicine
2020-2025
Administración Nacional de Laboratorios e Institutos de Salud
2025
Cornell College
2025
New York Proton Center
2024
Ministerio de Salud - Provincia de Buenos Aires
2023
Hospital Universitario Puerta de Hierro Majadahonda
2020-2021
Hospital Universitario De Cabueñes
2021
University of Massachusetts Chan Medical School
2013-2019
Massachusetts Academy of Math and Science
2018-2019
Rationale and Objectives: Although many clinical physiology epidemiology studies show an association between obstructive sleep apnea (OSA) markers of insulin resistance, no causal pathway has been established. The purpose the current study was to determine if intermittent hypoxia (IH) stimulus that characterizes OSA causes resistance in absence obesity. Furthermore, we assessed impact IH on specific metabolic function liver muscle. Finally, examined potential mechanistic role autonomic...
Although stem cell populations mediate regeneration of rapid turnover tissues, such as skin, blood, and gut, a reservoir has not been identified for some slower the pancreatic islet. Despite lacking identifiable cells, murine β number expands in response to an increase insulin demand. Lineage tracing shows that new cells are generated from proliferation mature, differentiated cells; however, mechanism by which these mature sense systemic demand initiate proliferative remains unknown. Here,...
Developing new techniques to induce β-cells replicate is a major goal in diabetes research. Endogenous response metabolic changes, such as obesity and pregnancy, which increase insulin requirement. Mouse genetic models promise reveal the pathways responsible for compensatory β-cell replication. However, no simple, short-term, physiological replication stimulus exists test mouse Here, we present tool living mice. Four-day glucose infusion well tolerated by mice measured hemodynamics, body...
Using conditional gene targeting in mice, we show that BMP receptor IA is essential for the differentiation of progenitor cells inner root sheath and hair shaft. Without BMPRIA activation, GATA-3 down-regulated its regulated control IRS compromised. In contrast, Lef1 up-regulated, but still blocked, BMPRIA-null follicles fail to activate Lef1/β-catenin–regulated genes, including keratin genes. Wnt-mediated transcriptional activation can be restored by transfecting keratinocytes with a...
Type 2 diabetes (T2D) is caused by relative insulin deficiency, due in part to reduced β-cell mass (11, 62). Therapies aimed at expanding may be useful treat T2D (14). Although feeding rodents a high-fat diet (HFD) for an extended period (3-6 mo) increases inducing proliferation (16, 20, 53, 54), evidence suggests that adult human β-cells not meaningfully proliferate response obesity. The timing and identity of the earliest initiators rodent compensatory growth response, possible therapeutic...
Glucose stimulates rodent and human β-cell replication, but the intracellular signaling mechanisms are poorly understood. Carbohydrate response element-binding protein (ChREBP) is a lipogenic glucose-sensing transcription factor with unknown functions in pancreatic β-cells. We tested hypothesis that ChREBP required for glucose-stimulated proliferation. The relative expression of was determined liver β-cells using quantitative RT-PCR (qRT-PCR), immunoblotting, immunohistochemistry. Loss-...
Adeno-associated viral (AAV) vectors have shown promise as a platform for gene therapy of neurological disorders. Achieving global delivery to the central nervous system (CNS) is key development effective therapies many these diseases. Here we report isolation novel CNS tropic AAV capsid, AAV-B1, after single round in vivo selection from an capsid library. Systemic injection AAV-B1 vector adult mice and cat resulted widespread transfer throughout with transduction multiple neuronal...
Hepatocyte growth factor (HGF) is a mitogen and insulinotropic agent for the β-cell. However, whether HGF/c-Met has role in maternal β-cell adaptation during pregnancy unknown. To address this issue, we characterized glucose homeostasis pregnant mice lacking c-Met pancreas (PancMet KO mice). Circulating HGF islet expression were increased mice. Importantly, PancMet displayed decreased replication apoptosis at gestational day (GD)15. The was associated with reductions prolactin receptor...
An important goal in diabetes research is to understand the processes that trigger endogenous β-cell proliferation. Hyperglycemia induces replication, but mechanism remains debated. A prime candidate insulin, which acts locally through insulin receptor. Having previously developed an vivo mouse hyperglycemia model, we tested whether glucose proliferation signaling. By using mice lacking signaling intermediate receptor substrate 2 (IRS2), confirmed hyperglycemia-induced requires IRS2 both and...
Obstructive sleep apnoea (OSA) and type 2 diabetes frequently co-exist potentially interact haemodynamically metabolically. However, the confounding effects of obesity have obscured examination any independent or interactive hypoxic stress OSA hyperglycaemia on haemodynamic metabolic outcomes. We developed a chronically catheterized, unhandled, lean murine model to examine intermittent (IH) exposure exogenous glucose infusion diurnal pattern arterial blood pressure glucose, as well...
To determine the role of hepatocyte growth factor (HGF)/c-Met on β-cell survival in diabetogenic conditions vivo and response to cytokines vitro.We generated pancreas-specific c-Met-null (PancMet KO) mice characterized their diabetes induced by multiple low-dose streptozotocin (MLDS) administration. We also analyzed effect HGF/c-Met signaling vitro cytokine-induced death mouse human islets, specifically examining nuclear (NF)-κB.Islets exposed or from MLDS-treated displayed significantly...
Pancreatic β-cell proliferation is infrequent in adult humans and not increased type 2 diabetes despite obesity insulin resistance, suggesting the existence of inhibitory factors. Free fatty acids (FFAs) may influence proliferation. In order to test whether FFAs restrict vivo, mice were intravenously infused with saline, Liposyn II, glucose, or both, continuously for 4 days. Lipid infusion did alter basal proliferation, but blocked glucose-stimulated without inducing excess death. vitro...
Insulin receptor (Insr) protein is present at higher levels in pancreatic β-cells than most other tissues, but the consequences of β-cell insulin resistance remain enigmatic. Here, we use an Ins1
Background Telemedicine is now common practice for many fields of medicine, but questions remain as to whether telemedicine will continue an important patient care modality once COVID-19 becomes endemic. We explored provider and patients’ perspectives on implementation. Methods Physicians from three specialties within the Department Medicine a single institution were electronically surveyed regarding their perceptions satisfaction, benefits, challenges video visits, well quality interactions...
β-catenin regulates the establishment of hepatic metabolic zonation. To elucidate functional significance liver zonation in chronically overfed state vivo, we fed a high-fat diet (HFD) to hepatocyte-specific transgenic (TG) and knockout (KO) mice. Chow-fed TG KO mice had normal histologic findings body weight. However, HFD-fed developed prominent perivenous steatosis with periportal sparing. In contrast, increased lobular inflammation hepatocyte apoptosis. rapidly diet-induced obesity...