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P egylated-interferon (PEG-IFN) alfa (α) in combination with ribavirin is the approved treatment for chronic hepatitis C virus (HCV) infection. Since the first report of interferon (IFN)-induced type 1 diabetes mellitus (DM) in 1992 by Fabris et al, 1 there have been numerous reports from all over the world. Interferon in combination with ribavirin induces type 1 diabetes in a much shorter period compared with plain IFN.2 Interferoninduced diabetes has not been reported from India till date. Here we report PEG-IFN-induced type 1 DM in a 16-year-old, who was on treatment for chronic HCV infection with PEG-IFN 2b and ribavirin. CASE REPORTA 16-year-old female who had undergone treatment for Ewing's sarcoma with right cleidectomy and chemotherapy turned seropositive for HCV (genotype 1 infection) at the end of the chemotherapy. She had raised HCV-RNA and was started on combination therapy with ribavirin 800 mg orally daily and plain IFN-α-2b 3MIU subcutaneously (SC) thrice weekly and completed 78 doses of the same. She did not respond to plain IFN and was switched over to PEG-IFN-α-2b 50 μg SC weekly and ribavirin 800 mg orally daily combination therapy. There was no history of diabetes or other autoimmune diseases in her family members. Her weight was 46 Kg and her body mass index (BMI) was 21.9 Kg/m 2 . Complete blood count showed a total leukocyte count of 4900/mm 3 , hemoglobin of 10.8 g/dL, and platelet count of 289,000/mm 3 . Biochemical investigations revealed random blood sugar 106 mg/dL, normal serum bilirubin, albumin 4.7, serum glutamicpyruvic transaminase (SGPT) 44 U/L, and normal thyroid functions. Ultrasound abdomen showed normal sized liver with coarse echotexture and normal portal vein. No varices were seen on endoscopy. She attained a rapid virological response. Except for mild anemia, a period of 40 weeks of the combination therapy was uneventful.She presented with features of severe ketoacidosis following the 41st dose of PEG-IFN. She gave a history of polyuria, polydipsia, and weight loss for < 2 weeks. She had a random blood sugar of 431 mg/dL, with severe metabolic acidosis and urine ketone positivity. Her ketoacidosis was managed with intravenous (i.v.) insulin infusion and fluid replacement. She was discharged on regular subcutaneous insulin. Anti-glutamic acid decarboxylase (anti-GAD) antibodies and islet cell antibodies (ICA) were negative and her fasting serum C-peptide level was <0.1 ng/ mL. Based on the clinical presentation and low C-peptide level, she was diagnosed with type 1 DM.While there have been case reports endorsing the cessation of the IFN therapy after the onset of diabetes, our patient had a low C-peptide level indicating that majority of the islet cells were destroyed by then. The risk of worsening of diabetes due to HCV-induced insulin resistance, in the absence of a sustained virological response, 3 outweighed the risks of worsening of type 1 DM due to further beta cell destruction with continuation of IFN. Hence, PEG-IFN and ribavirin were continued. Her HCV-RNA load at...

Students of our MPA program are expected to master a vast amount of information in a short 28‐ month curriculum leading up to their clinical practice. In addition, students find learning clinical pharmacology difficult as it involves memorizing hundreds if not thousands of medications, their mechanism, interactions, and adverse effects. In order to maximize learning, we delivered a Clinical Pharmacology (CP) course in a flipped classroom model using technology1.CP I and II are two 3‐credit courses taught over 4‐month each with two 2‐hour didactic lectures every week. In its place, we introduced short 15 – 20 minute videos recorded using Explain Everything or Camtasia software and posted them a couple of days prior to in‐class sessions2. In addition, a complete slide‐deck and a study guide with open‐ended questions designed to reinforce the clinically relevant facts and concepts in each class were also posted. Students listened to the recording, used the slide‐deck and study guide to master the concepts. An anonymous survey at the end of the course collected the feedback on this new model of course content delivery and their learning experience3.More than 55 students participated in the survey. An overwhelming 82% of the respondents wanted the course to be delivered based on this model in the future. About 75% agreed that the new model allowed them more time to study other subjects. Another 76% felt the new model helped them feel prepared for the exams. Although we had reduced the student‐faculty contact time by 50%, about 70% of the survey respondents felt the new model provided them adequate faculty exposure and interaction.Unlike reported by some studies that the students prefer only about half of the class sessions to be “flipped” 4; our MPA students wanted us to follow this new model for the entire course. Following our success with this new model, other Course Directors have started introducing flipped classes in their courses.Based on the favorable feedback we received from the students and performance index on their course assessments, we recommend utilizing this model of active learning in your health sciences education programs.Support or Funding InformationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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There is a lack of research on the combined effects of genetic variations (specifically CD36 SNPs—rs1761667 and rs1527483), dietary food habits (vegetarian or not), and the salivary environment on obesity and taste sensitivity, especially in the Indian population. The current study aims to better understand the relationship between impaired taste perception, fat consumption, higher BMI and obesity development by examining the combined association between CD36 SNPs, oleic acid (OA) detection threshold, and food habits among Indian participants. Furthermore, the relationship between oral fatty acid (FAs) sensitivity and taste physiology factors linked to inflammation and salivary proteins was considered. Participants with the minor allele (AA/AG) of CD36 (in both rs1527483 and rs1761667) consumed more fat, particularly saturated FAs (p = 0.0351). Salivary lipopolysaccharide, which causes inflammation, was significantly greater in non‐vegetarians with a higher BMI (p < 0.05), and it exhibited a negative correlation (r = −0.232 and p < 0.05) with Ki67 gene expression, a marker for taste progenitor cells. A positive correlation (r = 0.474, p = 0.04) between TLR4 mRNA levels and the OA detection threshold was also observed. Participants with BMI > 25 kg/m2 had substantially higher TNF‐α and IL‐6 receptor mRNA expression levels, but there were no significant differences between the vegetarian and non‐vegetarian groups. However, salivary CA‐VI, which has a buffering capability on the oral environment, was lower in non‐vegetarian adults with BMI >25. Thus, it was shown that non‐vegetarians with overweight and obesity in India were in at‐risk groups for the CD36 SNP (AA/AG at rs1761667 and rs1527483) and had higher levels of inflammatory markers, which exacerbated alterations in food behaviour and physiological changes, indicating their relevance in the development of obesity.