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Immunoassay interferences, including those from exogenous substances like biotin, can lead to misinterpretation of laboratory results and clinical decision-making challenges. A 28-year-old unmarried female presented to dermatologist with 4-year history of acne, hirsutism, and hair loss. Hormonal assays using chemiluminescence immunoassays (CLIA) and enzyme-linked immunosorbent assays (ELISA) revealed alarmingly high testosterone levels, suggesting neoplastic androgen excess and severe insulin resistance. This prompted referral to endocrinology for further evaluation. Patient's menarche occurred at age 11, with regular menstrual cycles. Family history indicated diabetes and hirsutism, but not infertility. Physical examination revealed body mass index (BMI) of 21.8 kg/m2 and Ferriman-Gallwey score of 11. Despite severe biochemical hyperandrogenism, her clinical presentation was mild. Differential diagnoses included polycystic ovary syndrome (PCOS) and late-onset congenital adrenal hyperplasia (CAH). Repeat hormonal testing, performed at multiple laboratories using liquid chromatography-mass spectrometry (LCMS), CLIA, and ELISA, showed normal testosterone, free testosterone, and insulin levels, suggesting that the initial results were falsely elevated. Review of her dermatology prescriptions revealed that she had taken a single 10 mg tablet of biotin 33 hours before first blood draw, leading to diagnosis of biotin interference in immunoassays. After the two-week biotin washout period, her subsequent endocrinology work-up had indicated “normalized” hormonal levels. Pelvic and abdominal ultrasound imaging revealed normal ovaries and adrenal areas. Thus, biotin associated testosterone (and insulin) immunoassay interference can confound clinical diagnosis and management. Any observed discordance between clinical symptoms, signs and hormonal levels should raise possibility of immunoassay interferences, reemphasizing need for heightened physician awareness.

A 76-year-old male was brought to the emergency room with an acute onset of breathlessness and difficulty swallowing. Examination revealed bilateral ptosis, bilateral vocal cord abductor palsy with diaphragmatic paralysis. He did not have any limb weakness. A diagnosis of acute bulbar palsy was made. Cerebrospinal fluid showed albumino-cytological dissociation. Magnetic resonance imaging of the brain (MRI) was normal, and a nerve conduction study (NCS) showed Acute Motor and Sensory Axonal Neuropathy (AMSAN). Guillain–Barré syndrome with acute bulbar palsy was considered. Here, we report a case of suspected Acute Bulbar Palsy plus (ABPp) syndrome. ABPp may be considered as a variant of GBS between the Miller–fisher and Pharyngeal-cervical-brachial variant and does not have any definite limb weakness. This patient also had ABPp with diaphragmatic palsy. However, whether this syndrome is an isolated variant of GBS or a continuum between the Miller-fisher syndrome (MFS) and Pharyngo-cervical brachial (PCB) variants remains to be elucidated. This case is relevant to primary care physicians as the disability with GBS remains high and may render a large burden to carers. The initial symptom of acute dysphagia must lead on the primary care physician to keep this disease in mind to prevent an unwarranted delay in diagnosis.

BackgroundObesity is a medical problem with an increased risk for other metabolic disorders like diabetes, heart problem, arthritis, etc. Leptin is an adipose tissue-derived hormone responsible for food intake, energy expenditure, etc., and leptin resistance is one of the significant causes of obesity. Excess leptin secretion by poor diet habits and impaired hypothalamic leptin signaling leads to LR. Melatonin a sleep hormone; also possess antioxidant and anti-inflammatory properties. The melatonin can attenuate the complications of obesity by regulating its targets towards LR induced obesity.AimThe aim of this study includes molecular pathway and network analysis by using a systems pharmacology approach to identify a potential therapeutic mechanism of melatonin on leptin resistance-induced obesity.MethodsThe bioinformatic methods are used to find therapeutic targets of melatonin in the treatment of leptin resistance-induced obesity. It includes target gene identification using public databases, Gene ontology, and KEGG pathway enrichment by ‘ClusterProfiler’ using the R language, network analysis by Cytoscape, and molecular Docking by Autodock.ResultsWe obtained the common top 33 potential therapeutic targets of melatonin and LR-induced obesity from the total melatonin targets 254 and common LR obesity targets 212 using the data screening method. They are involved in biological processes related to sleep and obesity, including the cellular response to external stimulus, chemical stress, and autophagy. From a total of 180 enriched pathways, we took the top ten pathways for further analysis, including lipid and atherosclerosis, endocrine, and AGE-RAGE signaling pathway in diabetic complications. The top 10 pathways interacted with the common 33 genes and created two functional modules. Using Cytoscape network analysis, the top ten hub genes (TP53, AKT1, MAPK3, PTGS2, TNF, IL6, MAPK1, ERBB2, IL1B, MTOR) were identified by the MCC algorithm of the CytoHubba plugin. From a wide range of pathway classes, melatonin can reduce LR-induced obesity risks by regulating the major six classes. It includes signal transduction, endocrine system, endocrine and metabolic disease, environmental adaptation, drug resistance antineoplastic, and cardiovascular disease.ConclusionThe pharmacological mechanism of action in this study shows the ten therapeutic targets of melatonin in LR-induced obesity.

In this modern industrialized era of large-scale production of agrochemicals, various emerging contaminants form the main components of waste water and sludge in most of the developing countries of the world. In this concern, phenol- an inevitable and alarming chemical pollutant in aquatic ecosystem, gains a speedy access into the water bodies as an industrial by-product. Though the detrimental effects of phenol have been studied in various aspects of aquatic life, current study is an initiative to unravel the toxic effects of phenol at molecular level in Cirrhinus mrigala. Plasma cortisol level and acetylcholine esterase activity in fish was estimated by Chemiluminescent immunoassay technique and Ellman assay respectively. Scanning electron microscopic studies were carried out to unravel the gill histopathological alterations in exposed fish. It was observed that phenol (22.32 mg/l) inhibits 50 % of acetylcholine esterase activity in brain thereby affecting the locomotion of the targeted carp. Cortisol elevated during the 7th day in exposed fish, but declined progressively on the forthcoming 21st and 28th days. Manifestations in gill encompass curling, fusion, aberrations, sloughing of gill epithelium, wider inter filamentary space and mucus coating in the primary gill filament. It concludes that the discernable deviations produced in both biochemical parameters and key organ gill can be used as a biomarker and bio-indicator respectively for assessing the existence of emerging toxicants in aquatic ecosystem., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Phenol, an aromatic chemical commonly found in domestic and industrial effluents, upon its introduction into aquatic ecosystems adversely affects the indigenous biota, the invertebrates and the vertebrates. With the increased demand for agrochemicals, a large amount of phenol is released directly into the environment as a byproduct. Phenol and its derivatives tend to persist in the environment for longer periods which in turn poses a threat to both humans and the aquatic ecosystem. In our current study, the response of Labeo rohita to sublethal concentrations of phenol was observed and the results did show a regular decrease in biochemical constituents of the targeted organs. Exposure of Labeo rohita to sublethal concentration of phenol (22.32 mg/L) for an epoch of 7, 21 and 28 days shows a decline in lipid, protein, carbohydrate content and phosphatase activity in target organs such as the gills, muscle, intestine, liver and kidney of the fish. The present study also aims to investigate the toxic effects of phenol with special reference to the haematological parameters of Labeo rohita. At the end of the exposure period, the blood of the fish was collected by cutting the caudal peduncle with a surgical scalpel. And it was observed that the red blood corpuscle count (RBC), white blood corpuscle (WBC), haemoglobin count (Hb), packed cell volume (PCV), mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH) and mean corpuscular haemoglobin concentration (MCHC) values showed a decline after exposure to phenol for 7 days, while white blood corpuscle (WBC) shows an increased count. At 21 days and 28 days, all the haematological parameters showed a significant decrease., (© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)