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Being a recognized carcinogen, hexavalent chromium is hazardous to both human and environmental health. Thus, it is imperative to regulate and oversee their levels in a variety of industries, including textiles, dyes, pigments, and metal finishing. This study strives to reduce Cr(VI) in wastewater by using capacitive deionization in conjunction with an activated carbon-based electrode and a continuous electrochemical reactor (CER). Activated carbon derived from rubberwood sawdust demonstrated excellent properties, including a high surface area of 1157 m 2  g -1 . The electrical conductivity and mechanical stability of the electrode were enhanced by the incorporation of synthesized expanded graphite (EG) into the AC. Key parameters were optimized via systematic batch electroreduction experiments with an optimal response surface design. The efficacy of the fabricated CER was proved when it successfully reduced Cr(VI) in a 5 mg L -1 solution within 15 min under optimized conditions, in contrast to the considerably longer durations anticipated by conventional methods. Validation of these findings was done by treating industrial wastewater of 30 mg L -1 in the CER. The electroreduction of Cr(VI) followed the Langmuir isotherm with a maximum capacity of 13.491 mg g -1 and pseudo-second-order kinetics. These results indicate that the combined use of the modified AC electrode and CER holds potential as a sustainable and economical approach to effectively eliminate Cr(VI) from wastewater., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: The IL-33/ST2 immune axis plays crucial roles in infection and immunity. A dysregulated IL-33/ST2 axis can induce autoimmune reaction and inflammatory responses. Guillain-Barré syndrome (GBS) is an acute peripheral neuropathy, mostly caused by post-infection autoimmunity. The role of IL-33/ST2 axis is not known in GBS. This study aimed to explore the role of IL-33/ST2 axis in GBS., Methods: Three single nucleotide polymorphisms (SNPs) of Il33 gene (rs16924159, rs7044343, rs1342336) and three SNPs of Il1rl1 gene (rs10192157, rs1041973, rs10206753) coding for suppressor of tumorigenicity 2 (ST2) were genotyped in 179 GBS patients and 186 healthy controls by TaqMan Allelic Discrimination Assay. Plasma levels of IL-33 and sST2 were measured in a subset of GBS patients (n = 80) and healthy controls (n = 80) by ELISA., Results: The frequencies of CC genotype of rs10192157 (p = 0.043) and TT genotype of rs10206753 (p = 0.036) SNPs of Il1rl1 gene differed significantly between GBS patients and healthy controls. Gene-gene interaction between Il33 and Il1rl1 genes also conferred significant risk for GBS. In addition, the plasma sST2 levels were significantly elevated in GBS patients compared to healthy subjects (24,934.31 ± 1.81 pg/ml vs. 12,518.97 ± 1.51 pg/ml, p < 0.001). Plasma sST2 levels showed a significant correlation with the disability scores at the peak of neurological deficit in GBS patients., Conclusions: The IL-33/ST2 axis is suggested to influence the immunopathogenesis of GBS. Genetic variants of Il1rl1 gene might serve as a risk determinant of GBS and plasma sST2 levels might emerge as a biomarker of severity of GBS, if replicated further by other studies., (© 2022 European Academy of Neurology.)

Objective: Epilepsy is one of the most prevalent neurological conditions and carbamazepine is a commonly used anti-seizure drug (ASD), especially in developing nations. There are reports of carbamazepine causing atrioventricular conduction defects and autonomic dysfunctions and its implication in Sudden Unexpected Death in Epilepsy (SUDEP) is controversial. We planned this study to assess the effect of carbamazepine (CBZ) on autonomic function compared to other ASDs in persons with epilepsy., Methods: In this cross-sectional study, we assessed the sympathetic and parasympathetic autonomic functions in persons with epilepsy (PWE) on CBZ versus other anti-seizure monotherapy using tests of heart rate variability including its time-, frequency- and non-linear domains, heart rate response to deep breathing, valsalva maneuver, and blood pressure response to isometric handgrip., Results: Persons with epilepsy on CBZ monotherapy did not show a significant reduction in the time domain parameter SDRR compared to other ASDs used as monotherapy (mean ± SD, 38.04 ± 18.75 ms vs 44.37 ± 20.35 ms; p = 0.125). However, PWE on CBZ had significantly lower time-domain measurements including RMSSD (mean ± SD 31.95 ± 17.29 ms vs 42.02 ± 22.29 ms; p = 0.018), SDSD (mean ± SD 31.91 ± 17.26 ms vs 41.96 ± 22.27 ms; p 0.018), and pNN50 [median (IQR) 05.45(0.69-25.37) vs 16.38(2.32-36.83); p = 0.030]. Frequency domain measures of HRV, heart rate responses to deep breathing, valsalva maneuver and tilt-testing and BP responses to valsalva and tilt-testing were not significantly different between the groups., Conclusion: The findings of our study indicate reduced parasympathetic activity in persons on CBZ monotherapy compared to other ASDs, which may pose risk of SUDEP. Carbamazepine may thus be avoided in those at risk of autonomic dysfunction and SUDEP., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Guiding and capturing photons at the nanoscale by means of metal nanoparticles and interfacial engineering for preventing back-electron transfer are well documented techniques for performance enhancement in excitonic solar cells. Drifting from the conventional route, we propose a simple one-step process to integrate both metal nanoparticles and surface passivation layer in the porous photoanode matrix of a dye-sensitized solar cell. Silver nanoparticles and Nb 2 O 5 surface passivation layer are simultaneously deposited on the surface of a highly porous nanocrystalline TiO 2 photoanode, facilitating an absorption enhancement in the 465 nm and 570 nm wavelength region and a reduction in back-electron transfer in the fabricated dye-sensitized solar cells together. The TiO 2 photoanodes were prepared by spray pyrolysis deposition method from a colloidal solution of TiO 2 nanoparticles. An impressive 43% enhancement in device performance was accomplished in photoanodes having an Ag-incorporated Nb 2 O 5 passivation layer as against a cell without Ag nanoparticles. By introducing this idea, we were able to record two benefits - the metal nanoparticles function as the absorption enhancement agent, and the Nb 2 O 5 layer as surface passivation for TiO 2 nanoparticles and as an energy barrier layer for preventing back-electron transfer - in a single step., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Following pressure overload, compensatory concentric left ventricular remodeling (CR) variably transitions to eccentric remodeling (ER) and systolic dysfunction. Mechanisms responsible for this transition are incompletely understood. Here we leverage phenotypic variability in pressure overload-induced cardiac remodeling to test the hypothesis that altered mitochondrial homeostasis and calcium handling occur early in the transition from CR to ER, before overt systolic dysfunction., Methods and Results: Sprague Dawley rats were subjected to ascending aortic banding, (n=68) or sham procedure (n=5). At 3 weeks post-ascending aortic banding, all rats showed CR (left ventricular volumes < sham). At 8 weeks post-ascending aortic banding, ejection fraction was increased or preserved but 3 geometric phenotypes were evident despite similar pressure overload severity: persistent CR, mild ER, and moderate ER with left ventricular volumes lower than, similar to, and higher than sham, respectively. Relative to sham, CR and mild ER phenotypes displayed increased phospholamban, S16 phosphorylation, reduced sodium-calcium exchanger expression, and increased mitochondrial biogenesis/content and normal oxidative capacity, whereas moderate ER phenotype displayed decreased p-phospholamban, S16, increased sodium-calcium exchanger expression, similar degree of mitochondrial biogenesis/content, and impaired oxidative capacity with unique activation of mitochondrial autophagy and apoptosis markers (BNIP3 and Bax/Bcl-2)., Conclusions: After pressure overload, mitochondrial biogenesis and function and calcium handling are enhanced in compensatory CR. The transition to mild ER is associated with decrease in mitochondrial biogenesis and content; however, the progression to moderate ER is associated with enhanced mitochondrial autophagy/apoptosis and impaired mitochondrial function and calcium handling, which precede the onset of overt systolic dysfunction., (© 2017 The Authors and Mayo Clinic. Published on behalf of the American Heart Association, Inc., by Wiley.)

We determined the effect of hyperandrogenemia as observed in polycystic ovary syndrome (PCOS) on fasting and glucose-stimulated proatherogenic inflammation markers in lean healthy reproductive-age women. Sixteen lean healthy ovulatory reproductive-age women were treated with 130 mg of DHEA or placebo (n=8 each) for 5 days. Interleukin-6 (IL-6) mRNA and IL-6 release from mononuclear cells (MNC), plasma IL-6 and C-reactive protein (CRP), and MNC-derived (matrix metalloproteinase-2) MMP-2 protein were quantified in the fasting state and 2 h after glucose ingestion, before and after treatment. Before treatment, subjects receiving dehydroepinadrosterone (DHEA) or placebo exhibited no differences in androgens, or any proatherogenic inflammation markers while fasting and after glucose ingestion. Compared with placebo, DHEA administration raised levels of testosterone, androstenedione, and DHEA-sulfate (DHEA-S), and increased the percent change from baseline in fasting IL-6 mRNA, IL-6 release, plasma IL-6, and CRP and MMP-2 protein. However, there were no differences in any of the proatherogenic inflammation markers following glucose ingestion after DHEA administration. We conclude that in lean reproductive-age women, proatherogenic inflammation in the fasting state increases after raising circulating androgens to levels observed in PCOS. However, this hyperandrogenemia-induced MNC activation does not provoke a similar response to subsequent glucose ingestion., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: Measurement of physical activity in epidemiological studies requires tools which are reliable, valid and culturally relevant. We attempted to develop a physical activity questionnaire (PAQ) that would measure physical activity in various domains over a year and which would be valid for use in adults of different age groups with varying levels of activity in urban and rural settings in low and middle income countries like India. The present paper aims to assess the reliability and validity of this new PAQ- termed the Madras Diabetes Research Foundation- Physical Activity Questionnaire (MPAQ)., Methods: The MPAQ was administered by trained interviewers to 543 individuals of either gender aged 20 years and above from urban and rural areas in 10 states of India from May to August 2011, followed by a repeat administration within a month for assessing reliability. Relative validity was performed against the Global Physical Activity Questionnaire (GPAQ). Construct validity was tested by plotting time spent in sitting and moderate and vigorous physical activity (MVPA) against body-mass index (BMI) and waist circumference. Criterion validity was assessed using the triaxial accelerometer, in a separate subset of 103 individuals. Bland and Altman plots were used to assess the agreement between MPAQ and accelerometer., Results: The interclass correlation coefficients (ICC) for total energy expenditure and physical activity levels were 0.82 and 0.73 respectively, between baseline and 1st month. The ICC between GPAQ and the MPAQ was 0.40 overall. The construct validity of the MPAQ showed linear association between sitting and MVPA, and BMI and waist circumference independent of age and gender. The Spearman's correlation coefficients for sedentary activity, MVPA and overall PA for MPAQ against the accelerometer were 0.48 (95%CI-0.32-0.62), 0.44 (0.27-0.59) and 0.46 (0.29-0.60) respectively. Bland and Altman plots showed good agreement between MPAQ and accelerometer for sedentary behavior and fair agreement for MVPA., Conclusion: The MPAQ is an acceptable, reproducible and valid instrument, which captures data from multiple activity domains over the period of a year from adults of both genders and varying ages in various walks of life residing in urban and rural India.

With increasing age there is a temporal relationship between the decline of mitochondrial and skeletal muscle volume, quality and function (i.e., health). Reduced mitochondrial mRNA expression, protein abundance, and protein synthesis rates appear to promote the decline of mitochondrial protein quality and function. Decreased mitochondrial function is suspected to impede energy demanding processes such as skeletal muscle protein turnover, which is critical for maintaining protein quality and thus skeletal muscle health with advancing age. The focus of this review was to discuss promising human physiological systems underpinning the decline of mitochondrial and skeletal muscle health with advancing age while highlighting therapeutic strategies such as aerobic exercise and caloric restriction for combating age-related functional impairments., (Copyright © 2013 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.)

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) enhance insulin sensitivity and glucose homeostasis in rodent models of insulin resistance. These beneficial effects have been linked with anti-inflammatory properties, but emerging data suggest that the mechanisms may also converge on mitochondria. We evaluated the influence of dietary n-3 PUFAs on mitochondrial physiology and muscle lipid metabolites in the context of high-fat diet (HFD) in mice. Mice were fed control diets (10% fat), HFD (60% fat), or HFD with fish oil (HFD+FO, 3.4% kcal from n-3 PUFAs) for 10 wk. Body mass and fat mass increased similarly in HFD and HFD+FO, but n-3 PUFAs attenuated the glucose intolerance that developed with HFD and increased expression of genes that regulate glucose metabolism in skeletal muscle. Despite similar muscle triglyceride levels in HFD and HFD+FO, long-chain acyl-CoAs and ceramides were lower in the presence of fish oil. Mitochondrial abundance and oxidative capacity were similarly increased in HFD and HFD+FO compared with controls. Hydrogen peroxide production was similarly elevated in HFD and HFD+FO in isolated mitochondria but not in permeabilized muscle fibers, likely due to increased activity and expression of catalase. These results support a hypothesis that n-3 PUFAs protect glucose tolerance, in part by preventing the accumulation of bioactive lipid mediators that interfere with insulin action. Furthermore, the respiratory function of skeletal muscle mitochondria does not appear to be a major factor in sphingolipid accumulation, glucose intolerance, or the protective effects of n-3 PUFAs.

The impact of ageing on mitochondrial function and the deterministic role of mitochondria on senescence continue to be topics of vigorous debate. Many studies report that skeletal muscle mitochondrial content and function are reduced with ageing and metabolic diseases associated with insulin resistance. However, an accumulating body of literature suggests that physical inactivity typical of ageing may be a more important determinant of mitochondrial function than chronological age, per se. Reports of age-related declines in mitochondrial function have spawned a vast body of literature devoted to understanding the underlying mechanisms. These mechanisms include decreased abundance of mtDNA, reduced mRNA levels, as well as decreased synthesis and expression of mitochondrial proteins, ultimately resulting in decreased function of the whole organelle. Effective therapies to prevent, reverse or delay the onset of the aforementioned mitochondrial changes, regardless of their inevitability or precise underlying causes, require an intimate understanding of the processes that regulate mitochondrial biogenesis, which necessitates the coordinated regulation of nuclear and mitochondrial genomes. Herein we review the current thinking on regulation of mitochondrial biogenesis by transcription factors and transcriptional co-activators and the role of hormones and exercise in initiating this process. We review how exercise may help preserve mitochondrial content and functionality across the lifespan, and how physical inactivity is emerging as a major determinant of many age-associated changes at the level of the mitochondrion. We also review evidence that some mitochondrial changes with ageing are independent of exercise or physical activity and appear to be inevitable consequences of old age.

Objective: To aid in differentiation of the two lesions, direct immunofluorescence was used to examine the fluorescence patterns in oral lichen planus and oral lichenoid reactions and to compare the degree of intensity of their fluorescence., Method and Materials: Thirty patients participated in this study. Oral mucosal biopsy specimens were obtained from the edge of fresh lesions and were hemisected. One of the sections was placed in 10% neutral buffered formalin for standard light microscopic examination and the other was washed in phosphate-buffered saline and transferred to Michel's transport media for direct immunofluorescence examination., Results: Fibrinogen was deposited in specimens from 14 of 15 patients diagnosed with oral lichen planus; lesions showed an intense positive fluorescence that outlined the basement membrane zone. Eight of 10 sections from oral lichenoid reactions exhibited fibrinogen deposition along the basement membrane zone; the specimens showed a less intense, homogeneous linear fluorescence. Specimens from five control samples showed no fluorescence., Conclusion: Fibrinogen was deposited at the basement membrane zone in both oral lichen planus and suspected oral lichenoid reactions, but the fluorescence was less intense in the oral lichenoid lesions.

This review summarizes the recent studies to understand the mechanisms of sarcopenia of aging. A decrease in mitochondrial and nuclear gene transcriptions in skeletal muscle is likely to be responsible for reduced synthesis rates of muscle mitochondrial protein, myosin heavy chain (MHC) and actin. A decrease in muscle mitochondrial protein synthesis could contribute to reduced mitochondrial function. A decrease in synthesis rate of MHC and actin, the key contractile proteins could be responsible for reduced muscle strength. The MHC synthesis rate seems to result from a selective decrease in transcription of MHC isoforms (MHCIIa and IIx) responsible for fast-twitch fibers. Resistance training increases MHC-I isoform mRNA levels with an overall increase in MHC synthesis rate. Aerobic training increases muscle oxidative enzymes equally in young and old but its impact on overall mitochondrial function remains to be clearly defined. Long-term studies are needed to determine the potential benefits and undesirable effects of replacements of various hormones that decline with aging. An individualized exercise prescription involving both aerobic and resistance training is definitely helpful to overcome many aging-related muscle dysfunctions.

The intactness of DNA is an important part of the normal cellular structure. Any change to the DNA in the form of breaks leads to a change in the integrity, which in turn leads to abnormality in the cellular activity. Many discrepancies have been reported among the various methods of detecting DNA damage. Here, a simple, sensitive and reproducible method has been developed for the detection of DNA breaks by radioactive labelling of 5' broken ends. The method was evaluated by studying chemically induced DNA damage by using both organochloride (2,4-dichlorophenoxyacetic acid and lindane) and organophosphorus (sevin and phosphamidon) compounds at different concentrations. Phosphamidon, one of the organophosphorus compounds studied, showed complete degradation of the DNA after treatment. Radioactive analysis of phosphamidon showed higher counts at the lowest concentration (20 microg) of the chemical when compared with the control (2752 scintillation counts per minute, scm). Studies on the chemically induced DNA breaks by radiolabelling revealed that the cumulative effect of the organophosphorus and organochloride compounds showed maximum counts in all the samples (the highest being 2904 scm) when compared with the organophosphorus and organochloride compounds studied separately (the highest being 1881 and 2260 scm, respectively). Radiolabelling studies on the blood samples of 23 pesticide workers by the newly developed assay showed a significant positive correlation (0.893) between the number of years of exposure and the scintillation counts. A maximum of 11,702 scm (for 18 years of exposure) and a minimum of 1682 scm (for 4 years of exposure) were recorded compared with 1253 scm for the negative control. This method can be used effectively for estimation of the DNA breaks, irrespective of its nature., (Copyright 2002 John Wiley & Sons, Ltd.)

Studies on site specific risks for oral cancers are few. Present investigation explores the possible role of human sociodemographic factors in causing oral cancer. Majority of patients had poor oral hygiene (85.5%) and belonged to 51-60 years age group (35.7%). Most of the subjects were agriculture workers (30.3%). Tongue and floor of mouth included majority of the affected sites (77.2%). Male to female ratio was highest for tonsil (32.3%) but differed marginally for other subsites. Majority of females used tobacco (81%) while males users of tobacco, alcohol and smoking reported in nearly equal proportions. Tobacco and smoking were found as primary risk factors for several intraoral subsites. However, for tongue, palate and lip no risk factor could be identified from given patients' characteristics. In general, tobacco posed high risk for buccal mucosa and alveolus in comparison to other subsites. Smoking affected tonsil and floor of mouth more than other sites. Alcohol posed more risk for buccal mucosa and floor of mouth than tongue.