Summary. Fibrocalculous pancreatic diabetes (previously known as tropical pancreatic diabetes) is a rare cause of diabetes confined to countries within the tropical belt. The aetiology of fibrocalculous pancreatic diabetes is thought to be environmental although the agent(s) is unknown. We have investigated a possible genetic basis of this disease by looking for restriction fragment length polymorphisms of genes implicated in the aetiology of diabetes rnellitus. Seventy-six Dravidian patients with fibrocalculous pancreatic diabetes were studied, and the restriction fragment length polymorphisms obtained compared to racially matched control subjects (n=94), patients with Type2 (non-insulin-dependent) diabetes (n=87) and Type 1 (insulin-dependent) diabetes (n = 58). No association of fibrocalculous pancreatic diabetes was found with restriction fragment length polymorphisms of the insulin receptor gene. Although no association of fibrocalculous pancreatic diabetes was found with polymorphism of the HLA DRc~/DQc~/DXct genes, an association was found with the Taq 1 restriction fragment length polymorphisms of the DQ[~ gene (DQ[~ T2/T6 present in 39% of patients with fibrocalculous pancreatic diabetes compared to 19% in control subjects; p = 0.01 ; corrected p value = 0.04) which is similar to that found in Type 1 but not Type 2 diabetes. An association of fibrocalculous pancreatic diabetes was also found with the hypervariable region in the 5-prime flanking region of the insulin gene; 40% of patients possessed the class 3 allele compared to 9.5% of control subjects p = 0.0001 ; corrected p value = 0.0008). In Type 2 diabetes, similar results were obtained with 33% subjects possessing the class 3 allele (t7 value compared to control subjects = 0.0005; corrected p value = 0.004). This study suggests that fibrocalculous pancreatic diabetes has a genetic component in its aetiology. Furthermore, its origin might be related to an individual with part of the genetic predisposition to diabetes (Type 1 or Type 2) who additionally has evidence of chronic calcific pancreatitis.

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Considering our depleting resources, efficient energy production and transmission is the need of the hour. This paper focuses on the concept of using Reinforcement Learning (RL) to control the power systems unit commitment and economic dispatch problem. The idea of reinforcement learning strives to present an ever optimal system even when there are load fluctuations. This is done by training the agent (system), thereby enriching its knowledge base which ensures that even without manual intervention all the available resources are used judiciously. Also the agent learns to reach long term objective of minimizing cost by autonomous optimization. A model free reinforcement learning method called, Q learning is used to find the cost at various loadings and is compared with the conventional priority list method and the performance improvement due to Q learning is proved.

Using the data obtained in this case series an official protocol could be created to wean P-LTEC residents from PMV, with reasonable expectations of the process.

Neurologic complications are not uncommon following bariatric surgery. Hyperammonemic encephalopathy (HAE) due to an acquired or unmasked urea cycle deficit is among the rarest of these. Pediatric nutrition support specialists are familiar with recognizing urea cycle deficits, but adult specialists may not be. Here we present a case of a patient initially misdiagnosed with cirrhosis who presented with recurrent HAE 4 years after Roux-en-Y gastric bypass. She was diagnosed with a proximal urea cycle deficit and severe protein calorie malnutrition. The patient recovered with specialized nutrition and medical support targeting this condition. A literature review indicates multiple fatalities from this condition, indicating the importance of early diagnosis and appropriate nutrition support.