Severe Hypokalemia Secondary to Distal Renal Tubular Acidosis in a Hispanic Man

Introduction: Renal tubular acidosis is a rare renal disorder that can cause severe electrolyte imbalances which can be life threatening. Case: A 21-year-old man presented to the ED on account of generalized weakness and body aches of one day duration. He reported no past medical history other than a previous episode of similar symptoms with improvement after IV hydration and electrolytes replacements about 2 months prior. He was not taking any medications and denied vomiting, diarrhea nor any significant family history. He admitted to alcohol and marijuana use. Physical examination was significant for reduced muscle power, tone, and reflexes in all extremities. He was unable to move his limbs against gravity. Admission laboratory findings revealed severe hypokalemia 1.1 mEq/L, metabolic acidosis with bicarbonate of 10.1 and EKG showed QT prolongation. Patient received a total of about 200 mEq of potassium through a central line in 24 hours with serum level of 3.7mmol/l in addition to intravenous bicarbonates with a resolution of the presenting symptoms. Discussion: The causes of hypokalemia are broad however a methodical approach can be helpful to rule out the many causes and narrow down the differential diagnosis. Distal RTA is caused by the inability of the distal renal tubule to secrete hydrogen ions due to the selective failure of activity or expression of the H+-ATPase. Conclusion: This case underscores the importance of systematic approach to the evaluation of patients with hypokalemia to uncover the cause of the underlying disease before life threatening complications occur. Our patient remains under close follow up

Improving fairness in machine learning systems: What do industry practitioners need?

The potential for machine learning (ML) systems to amplify social inequities and unfairness is receiving increasing popular and academic attention. A surge of recent work has focused on the development of algorithmic tools to assess and mitigate such unfairness. If these tools are to have a positive impact on industry practice, however, it is crucial that their design be informed by an understanding of real-world needs. Through 35 semi-structured interviews and an anonymous survey of 267 ML practitioners, we conduct the first systematic investigation of commercial product teams' challenges and needs for support in developing fairer ML systems. We identify areas of alignment and disconnect between the challenges faced by industry practitioners and solutions proposed in the fair ML research literature. Based on these findings, we highlight directions for future ML and HCI research that will better address industry practitioners' needs.Comment: To appear in the 2019 ACM CHI Conference on Human Factors in Computing Systems (CHI 2019

Deficits in a Radial-Arm Maze Spatial Pattern Separation Task and Cell Proliferation in a Mouse Model for Down Syndrome

poster abstractDown syndrome (DS) is caused by three copies of human chromosome 21 (Hsa21) and results in an array of phenotypes including intellectual disability. Ts65Dn mice have three copies of ~50% of the genes on Hsa21 and display many phenotypes associated with DS, including cognitive deficits. DYRK1A is found in three copies in humans with Trisomy 21 and in Ts65Dn mice, and is involved in a number of critical pathways including CNS development. Epigallocatechin-3-gallate (EGCG), the main polyphenol in green tea, inhibits Dyrk1a activity. We have shown that a three-week EGCG treatment normalizes skeletal abnormalities in Ts65Dn mice, yet did not rescue deficits in the Morris water maze spatial learning task or novel object recognition. The current study investigated deficits in a radial arm maze pattern separation task in Ts65Dn mice. Pattern separation requires differentiation between similar memories acquired during learning; distinguishing between these similar memories is thought to depend on distinctive encoding in the hippocampus. Pattern separation has been linked to functional activity of newly generated granule cells in the dentate gyrus. Recent studies in Ts65Dn mice have reported significant reductions in adult hippocampal neurogenesis, and after EGCG treatment, enhanced hippocampal neurogenesis. Thus, it was hypothesized that Ts65Dn mice would be impaired in the pattern separation task, and that EGCG would alleviate the pattern separation deficits seen in trisomic mice, in association with increased adult hippocampal neurogenesis. Beginning on postnatal day 75, mice were trained on a radial arm maze-delayed non-matching-to-place pattern separation task. Euploid mice performed significantly better over training than Ts65Dn mice, including better performance at each of the three separations. EGCG did not significantly alleviate the pattern separation deficits in Ts65Dn mice. The euploid controls had significantly more BrdU labeled cells than Ts65Dn mice, however, EGCG does not appear to increase proliferation of the hippocampal neuroprogenitor cells

A Case for Humans-in-the-Loop: Decisions in the Presence of Erroneous Algorithmic Scores

The increased use of algorithmic predictions in sensitive domains has been accompanied by both enthusiasm and concern. To understand the opportunities and risks of these technologies, it is key to study how experts alter their decisions when using such tools. In this paper, we study the adoption of an algorithmic tool used to assist child maltreatment hotline screening decisions. We focus on the question: Are humans capable of identifying cases in which the machine is wrong, and of overriding those recommendations? We first show that humans do alter their behavior when the tool is deployed. Then, we show that humans are less likely to adhere to the machine's recommendation when the score displayed is an incorrect estimate of risk, even when overriding the recommendation requires supervisory approval. These results highlight the risks of full automation and the importance of designing decision pipelines that provide humans with autonomy.Comment: Accepted at ACM Conference on Human Factors in Computing Systems (ACM CHI), 202

INTERNATIONAL JOURNAL OF PHARMACY & LIFE SCIENCES Screening of potential efficacy of dietary ginger on ethanol induced oxidative stress in rat cardiac tissue: A study on changes in basic metabolic profiles

Abstract The present study was premeditated to examine the possible mechanisms where by ginger (Zingiber officinale) could protect cardiac tissue from alcohol toxicity in rats. The carbohydrate metabolic profiles like total carbohydrates, pyruvate, total proteins, free amino acids and lactate levels were measured in heart tissue. The total carbohydrates, pyruvate, and total proteins were significant declined while free amino acids, lactate levels were significant increased in alcohol intoxicated rats. Whereas with ginger (200 mg/kg body weight) treatment shown significant increase in the total carbohydrates, total proteins and pyruvate levels, whereas free amino acids, lactate levels were significant drop in the cardiac tissues. From the present study, we conclude that ginger protects the heart tissue from alcohol toxicity in rats, this may be due to the presence of many bioactive compounds in ginger

VEGF and Angiopoietin-1 Exert Opposing Effects on Cell Junctions by Regulating the Rho GEF Syx

Vascular endothelial growth factor (VEGF) and Ang1 (Angiopoietin-1) have opposing effects on vascular permeability, but the molecular basis of these effects is not fully known. We report in this paper that VEGF and Ang1 regulate endothelial cell (EC) junctions by determining the localization of the RhoA-specific guanine nucleotide exchange factor Syx. Syx was recruited to junctions by members of the Crumbs polarity complex and promoted junction integrity by activating Diaphanous. VEGF caused translocation of Syx from cell junctions, promoting junction disassembly, whereas Ang1 maintained Syx at the junctions, inducing junction stabilization. The VEGF-induced translocation of Syx from EC junctions was caused by PKD1 (protein kinase D1)-mediated phosphorylation of Syx at Ser806, which reduced Syx association to its junctional anchors. In support of the pivotal role of Syx in regulating EC junctions, syx−/− mice had defective junctions, resulting in vascular leakiness, edema, and impaired heart function

Towards interpreting recurrent neural networks through probabilistic abstraction

National Research Foundation (NRF) Singapore under its AI Singapore Programm

Chick Embryo Partial Ischemia Model: A New Approach to Study Ischemia Ex Vivo

Background: Ischemia is a pathophysiological condition due to blockade in blood supply to a specific tissue thus damaging the physiological activity of the tissue. Different in vivo models are presently available to study ischemia in heart and other tissues. However, no ex vivo ischemia model has been available to date for routine ischemia research and for faster screening of anti-ischemia drugs. In the present study, we took the opportunity to develop an ex vivo model of partial ischemia using the vascular bed of 4th day incubated chick embryo. Methodology/Principal Findings: Ischemia was created in chick embryo by ligating the right vitelline artery using sterile surgical suture. Hypoxia inducible factor- 1 alpha (HIF-1a), creatine phospho kinase-MB and reactive oxygen species in animal tissues and cells were measured to confirm ischemia in chick embryo. Additionally, ranolazine, N-acetyl cysteine and trimetazidine were administered as an anti-ischemic drug to validate the present model. Results from the present study depicted that blocking blood flow elevates HIF-1a, lipid peroxidation, peroxynitrite level in ischemic vessels while ranolazine administration partially attenuates ischemia driven HIF-1a expression. Endothelial cell incubated on ischemic blood vessels elucidated a higher level of HIF-1a expression with time while ranolazine treatment reduced HIF-1a in ischemic cells. Incubation of caprine heart strip on chick embryo ischemia model depicted an elevated creatine phospho kinase-MB activity under ischemic condition while histology of the treated heart sections evoked edema and disruption of myofibril structures. Conclusions/Significance: The present study concluded that chick embryo partial ischemia model can be used as a novel ex vivo model of ischemia. Therefore, the present model can be used parallel with the known in vivo ischemia models in understanding the mechanistic insight of ischemia development and in evaluating the activity of anti-ischemic drug.status: publishe