University of Maryland, Baltimore

Hypoglycemia can produce a spectrum of pro-inflammatory and pro-atherothrombotic changes. To date no studies appear to have investigated the effects of differing levels of hypoglycemia on the vasculature and pro-atherothrombotic balance during hypoglycemia in healthy man. The specific aim of our study will be to determine the effects of differing levels of hypoglycemia on in-vivo vascular biologic mechanisms in a healthy population.

Type: Interventional

Start Date: Jul 2015

open study

Exercise is a cornerstone of diabetes management. It helps reduce blood pressure, promote weight loss, lower insulin resistance and improve glucose and lipid (triglyceride and HDL-cholesterol) profiles. Unfortunately, the benefits of exercise are often not embraced by diabetic individuals because of the fear of low blood sugar (hypoglycemia). My laboratory has demonstrated that Autonomic nervous system (ANS) counterregulatory failure plays an important role in exercise associated hypoglycemia in Type 1 DM. ANS responses are significantly reduced in Type 1 DM and are further blunted by antecedent episodes of hypoglycemia. Furthermore, there is a large sexual dimorphism of reduced ANS responses during submaximal exercise in both Type 1 DM and healthy individuals that is unexplained. Accumulating data are demonstrating that serotonergic pathways can regulate ANS discharge. Generally, serotonergic pathways are inhibitory but both single and longer term administration of selective serotonin reuptake inhibitors (SSRI's) such as Prozac has been demonstrated to increase basal epinephrine levels and enhance baroreflex control of Sympathetic nervous system (SNS) activity. What is unknown is whether fluoxetine can also enhance SNS responses and also override the large ANS sexual dimorphism present during sub maximal exercise. Therefore, the purpose of this study is to determine if the SSRI fluoxetine (Prozac) can improve SNS responses during exercise.

Type: Interventional

Start Date: Oct 2012

open study

This clinical research study is being done to answer questions about how to treat cancer. To clear cancer cells from the body, the immune system needs the action of proteins called Type 1 interferons. The protein STING (for STimulator of INterferon Genes) stimulates the body to make Type 1 interferons. Type 1 interferons activate key molecules in cancer immunity to kill cancer cells. CRD3874 is a synthetic drug that activates STING, and STING stimulates the immune system to kill cancer cells. In experiments on blood from humans, CRD3874 makes blood cells produce molecules responsible for anti-cancer activity. CRD3874 was tested in mice with cancers including leukemia, head and neck cancer, lung cancer, pancreatic cancer and sarcoma. In these mice, CRD3874 made tumors shrink or disappear, and some mice developed long-lasting immunity against cancer. Also, when CRD3874 was given with other anti-cancer treatments, it increased their anti-cancer effects.

Type: Interventional

Start Date: Aug 2024

open study

This is a two-group randomized controlled trial conducted at five hospitals across the U.S. designed to test the effectiveness of an Integrated infectious diseases/Substance Use Disorder outpatient clinic (IC) compared to treatment as usual aimed at reducing infection related readmissions and improving health outcomes in people hospitalized with an infection related to injecting opioids or stimulants.

Type: Interventional

Start Date: Oct 2024

open study