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Biomedical subjects

Arjun Rao

Publications and source records attributed to Arjun Rao.

6 recordsLinked to original sources
PubMed2026

Balanced Fluid or 0.9% Saline in Children Treated for Septic Shock.

BACKGROUND: Whether treatment with balanced crystalloid fluid leads to better outcomes than 0.9% saline in children treated for septic shock is debated. METHODS: In this pragmatic clinical trial conducted at 47 emergency departments in five countries, patients (2 months to <18 years of age) with suspected septic shock and abnormal perfusion were randomly assigned to receive fluid resuscitation with either balanced fluid or 0.9% saline for up to 48 hours. The primary outcome was a major adverse kidney event (a composite of death, new renal-replacement therapy, or persistent kidney dysfunction) at 30 days after enrollment or hospital discharge, whichever occurred first. RESULTS: Of 9041 enrolled patients, 277 (6.1%) in the balanced-fluid group and 282 (6.2%) in the 0.9%-saline group withdrew from the trial, leaving 4235 and 4247 patients, respectively, for analysis. A primary-outcome event occurred in 137 patients (3.4%) in the balanced-fluid group and in 124 (3.0%) in the 0.9%-saline group (difference, 0.4 percentage points; 95% confidence interval [CI], -0.5 to 1.3; risk ratio, 1.10; 95% CI, 0.88 to 1.40; P&#x2009;=&#x2009;0.85). The median number of hospital-free days during 28 days after enrollment was 23 (interquartile range, 19 to 25) in both groups. Hyperchloremia occurred in 868 patients (31.4%) in the balanced-fluid group and in 1383 (49.0%) in the 0.9%-saline group; hypernatremia in 52 (1.8%) and 89 (3.1%), respectively; and hyperlactatemia in 260 (19.8%) and 228 (16.7%). No differences in other safety outcomes or adverse events were seen. CONCLUSIONS: Among children treated for septic shock, no significant difference was seen in the incidence of death, new renal-replacement therapy, or persistent kidney dysfunction when fluid resuscitation was administered with balanced fluid as compared with 0.9% saline. (Funded by Eunice Kennedy Shriver National Institute of Child Health and Human Development and others; PRoMPT BOLUS ClinicalTrials.gov number, NCT04102371.).

Adolescent↗
PubMed2006

OMIA (Online Mendelian Inheritance in Animals): an enhanced platform and integration into the Entrez search interface at NCBI.

Online Mendelian Inheritance in Animals (OMIA) is a comprehensive, annotated catalogue of inherited disorders and other familial traits in animals other than humans and mice. Structured as a comparative biology resource, OMIA is a comprehensive resource of phenotypic information on heritable animal traits and genes in a strongly comparative context, relating traits to genes where possible. OMIA is modelled on and is complementary to Online Mendelian Inheritance in Man (OMIM). OMIA has been moved to a MySQL database at the Australian National Genomic Information Service (ANGIS) and can be accessed at http://omia.angis.org.au/. It has also been integrated into the Entrez search interface at the National Center for Biotechnology Information (NCBI; http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=omia). Curation of OMIA data by researchers working on particular species and disorders has also been enabled.

Animals↗
PubMed2006

Analysis of laboratory critical value reporting at a large academic medical center.

Reporting of laboratory critical values has become an issue of national attention as illustrated by recent guidelines described in the National Patient Safety Goals of the Joint Commission on Accreditation of Healthcare Organizations. Herein, we report the results of an analysis of 37,503 consecutive laboratory critical values at our institution, a large urban academic medical center. We evaluated critical value reporting by test, laboratory specialty, patient type, clinical care area, time of day, and critical value limits. Factors leading to delays in critical value reporting are identified, and we describe approaches to improving this important operational and patient safety issue.

Chemistry, Clinical↗
PubMed2003

Glycogen synthesis in muscle fibers during active recovery from intense exercise.

PURPOSE: There is evidence that active recovery impairs glycogen repletion in skeletal muscles of fasted individuals. Our main goal was to examine the impact of active recovery on the glycogen stores of the different muscle fiber types. METHODS: Eight endurance-trained individuals cycled for 2.5 min at 130% [OV0312]O(2peak) followed by a 30-s all-out cycling sprint. After exercise, the participants were subjected to either a passive recovery or an active recovery protocol that consisted of pedalling for 45 min at 40% [OV0312]O(2peak). RESULTS: During active recovery, blood lactate and pH returned more rapidly toward preexercise levels than during passive recovery. In contrast, average muscle glycogen content remained at stable levels during active recovery (209 +/- 32 and 202 +/- 30 mmol.kg-1 at 0 and 45 min of recovery, respectively) but increased significantly in response to passive recovery (from 185 +/- 27 to 283 +/- 42 mmol.kg-1). The pattern of change in periodic acid-Schiff staining intensity across muscle fibers suggests that the impact of active recovery on average muscle glycogen content is different from that observed at the levels of the individual muscle fibers, with active recovery having no effect on glycogen resynthesis in Type II muscle fibers but causing glycogen breakdown in Type I muscle fibers. Although active recovery was also associated with higher plasma catecholamines and lower insulin levels, such an unfavorable hormonal environment had no effect on glycogen resynthesis in Type II muscle fibers. CONCLUSION: Active recovery in comparison to passive recovery does not affect glycogen resynthesis in Type II muscle fibers despite being associated with an unfavorable hormonal environment but results in a marked glycogen mobilization in Type I muscle fibers.

Adult↗
PubMed2002

Carbohydrate loading in human muscle: an improved 1 day protocol.

It is generally acknowledged that even without a glycogen-depleting period of exercise, trained athletes can store maximal amounts of muscle glycogen if fed a carbohydrate-rich diet for 3 days. What has never been examined is whether under these conditions this many days are necessary for the content of muscle glycogen to attain these high levels. To examine this issue, eight endurance-trained male athletes were asked to eat 10 g.day(-1).kg(-1) body mass of high-carbohydrate foods having a high glycaemic index over 3 days, while remaining physically inactive. Muscle biopsies were taken prior to carbohydrate loading and after 1 and 3 days of eating the carbohydrate-rich diet. Muscle glycogen content increased significantly ( P<0.05) from pre-loading levels of [mean (SE)] 95 (5) to 180 (15) mmol.kg(-1) wet mass after only 1 day, and remained stable afterwards despite another 2 days of carbohydrate-rich diet. Densitometric analyses of muscle sections stained with periodic acid-Schiff not only supported these findings, but also indicated that only 1 day of high carbohydrate intake was required for glycogen stores to reach maximal levels in types I, IIa, and IIb muscle fibres. In conclusion, these findings showed that combining physical inactivity with a high intake of carbohydrate enables trained athletes to attain maximal muscle glycogen contents within only 24 h.

Adolescent↗