Is there an Increase in Total Hip Arthroplasty Due to Osteonecrosis of Femoral Head After Covid-19 Pandemic?: A Retrospective Study Among Patients in Central Karnataka, India.

Introduction: Coronavirus disease 2019 (COVID-19) infection or corticosteroid usage during the COVID-19 pandemic as risk factors for avascular necrosis (AVN) of the femoral head (osteonecrosis of the femoral head/femoral head AVN [FHAVN]), as well as its link to clinical and radiological outcomes, are poorly understood. Osteonecrosis, which results from a disruption in vascular supply to the femoral head, is a prevalent cause of hip joint deterioration and one of the most common reasons for total hip arthroplasty (THA)/total hip replacement in India and other Asian countries. This study will aid in understanding the condition's epidemiology and statistically determining the risk of disease related with pandemic exposure.

Obesity Awareness and Sensitization in Schools for Improving Weight Control and Reducing Obesity Stigma in Students: A Pilot Study.

Introduction: The prevalence of obesity is increasing rapidly in the world, including India. Since obesity is a risk factor for many diseases, the prevalence of obesity-related diseases is also increasing, resulting in decreased productivity and increased disease-related expenses, causing economic loss at the individual, family, and national levels. Government funds that could be utilized for national growth are channeled into the treatment of non-communicable diseases (NCDs).

Performance of Current Diagnostic Tools in Detecting Latent Tuberculosis Among Healthcare Workers: A Systematic Review.

Testing for latent tuberculosis infection is essential for diagnosing infections in asymptomatic individuals. Preventing the transition of latent to active tuberculosis is imperative, especially in high-risk populations such as healthcare workers. Interferon-gamma release assays (IGRAs) and the Mantoux/tuberculin skin test (TST) are two examples of diagnostic instruments utilized for detection.

Diagnostic Test Precision of Modified Carbapenem Inactivation Method and Carbapenemase Nordmann-Poirel Test for Phenotypic Detection of Carbapenemase Production in Enterobacterales: A Systematic Review.

Carbapenem-resistant Enterobacterales, particularly those that produce carbapenemases, pose a significant public health concern due to very limited treatment options. The timely identification of carbapenemase-producing Enterobacterales (CPE) is essential for putting in place efficient infection control measures and selecting appropriate antimicrobial therapies, thereby improving the clinical outcome of the patient. The purpose of this systematic review is to compare the diagnostic accuracy and practicality between two phenotypic tests, namely the modified carbapenem inactivation method (mCIM) and carbapenemase Nordmann-Poirel (Carba NP) test, in detecting carbapenemase production by Enterobacterales and thereby aiding the clinician in making a decision to choose an appropriate test for their phenotypic detection.

Diastolic dysfunction in Alzheimer's disease model mice is associated with Aβ-amyloid aggregate formation and mitochondrial dysfunction.

Alzheimer's Disease (AD) is a progressive neurodegenerative disease caused by the deposition of Aβ aggregates or neurofibrillary tangles. AD patients are primarily diagnosed with the concurrent development of several cardiovascular dysfunctions. While few studies have indicated the presence of intramyocardial Aβ aggregates, none of the studies have performed detailed analyses for pathomechanism of cardiac dysfunction in AD patients.

Trends in peripheral artery disease and critical limb ischemia hospitalizations among cocaine and methamphetamine users in the United States: a nationwide study.

Background: Peripheral artery disease (PAD) is on the rise worldwide, ranking as the third leading cause of atherosclerosis-related morbidity; much less is known about its trends in hospitalizations among methamphetamine and cocaine users.

Objectives: We aim to evaluate the overall trend in the prevalence of hospital admission for PAD with or without the use of stimulant abuse (methamphetamine and cocaine) across the United States. Additionally, we evaluated the PAD-related hospitalizations trend stratified by age, race, sex, and geographic location.

Deletion of Sigmar1 leads to increased arterial stiffness and altered mitochondrial respiration resulting in vascular dysfunction.

Sigmar1 is a ubiquitously expressed, multifunctional protein known for its cardioprotective roles in cardiovascular diseases. While accumulating evidence indicate a critical role of Sigmar1 in cardiac biology, its physiological function in the vasculature remains unknown. In this study, we characterized the expression of Sigmar1 in the vascular wall and assessed its physiological function in the vascular system using global Sigmar1 knockout (Sigmar1) mice.

Pathological Sequelae Associated with Skeletal Muscle Atrophy and Histopathology in G93A*SOD1 Mice.

Amyotrophic lateral sclerosis (ALS) is a complex systemic disease that primarily involves motor neuron dysfunction and skeletal muscle atrophy. One commonly used mouse model to study ALS was generated by transgenic expression of a mutant form of human superoxide dismutase 1 (SOD1) gene harboring a single amino acid substitution of glycine to alanine at codon 93 (G93A*SOD1). Although mutant-SOD1 is ubiquitously expressed in G93A*SOD1 mice, a detailed analysis of the skeletal muscle expression pattern of the mutant protein and the resultant muscle pathology were never performed.

Interactions between integrin α9β1 and VCAM-1 promote neutrophil hyperactivation and mediate poststroke DVT.

Venous thromboembolic events are significant contributors to morbidity and mortality in patients with stroke. Neutrophils are among the first cells in the blood to respond to stroke and are known to promote deep vein thrombosis (DVT). Integrin α9 is a transmembrane glycoprotein highly expressed on neutrophils and stabilizes neutrophil adhesion to activated endothelium via vascular cell adhesion molecule 1 (VCAM-1).

Therapeutic Plasma exchange therapy in Burns.

Severe burn injury affects the body in many devastating ways, the most severe being systemic inflammatory response syndrome. This results in a myriad of effects like increasing capillary permeability, thereby fluid loss. It also causes a surge in inflammatory mediators like interleukin (IL)-6, which further increases the capillary leak and fluid loss.

Evaluating and Comparing the Effectiveness of Nano-HA and HA + β-TCP with A-PRF Clinically and Radiographically in the Treatment of Human Infrabony Defects.

Aim: To evaluate and compare the effectiveness of nanocrystalline hydroxyapatite (NcHA) with advanced platelet-rich fibrin (A-PRF) and hydroxyapatite-reinforced beta tricalcium phosphate (HA + β-TCP) with A-PRF in the treatment of human infrabony defects clinically and radiographically using cone-beam computed tomography (CBCT).

Materials And Methods: There were a total of 28 defects, with 14 defects in the test and control groups, respectively. There were total 28 patients were involved in the study.

Evaluation of PRF and PLA-PGA Membrane Along with Hydroxyapatite Crystal Collagen Fibers Bone Graft in the Treatment of Infrabony Defects.

Aim: The present study was carried out to compare the effectiveness of leukocyte platelet-rich fibrin (L-PRF) membrane and polylactic acid-polyglycolic acid (PLA-PGA) membrane along with hydroxyapatite crystal collagen fibers bone graft in the treatment of human infrabony defects using cone beam computed tomography.

Materials And Methods: A total of 28 systemically healthy patients was chosen which were found appropriate after initial therapy. Each group comprises of 14 defects, according to randomized parallel design.

Sigmar1 ablation leads to lung pathological changes associated with pulmonary fibrosis, inflammation, and altered surfactant proteins levels.

Sigma1 receptor protein (Sigmar1) is a small, multifunctional molecular chaperone protein ubiquitously expressed in almost all body tissues. This protein has previously shown its cardioprotective roles in rodent models of cardiac hypertrophy, heart failure, and ischemia-reperfusion injury. Extensive literature also suggested its protective functions in several central nervous system disorders.

Mitochondrial dysfunction and autophagy activation are associated with cardiomyopathy developed by extended methamphetamine self-administration in rats.

The recent rise in illicit use of methamphetamine (METH), a highly addictive psychostimulant, is a huge health care burden due to its central and peripheral toxic effects. Mounting clinical studies have noted that METH use in humans is associated with the development of cardiomyopathy; however, preclinical studies and animal models to dissect detailed molecular mechanisms of METH-associated cardiomyopathy development are scarce. The present study utilized a unique very long-access binge and crash procedure of METH self-administration to characterize the sequelae of pathological alterations that occur with METH-associated cardiomyopathy.

Visualizing Subcellular Localization of a Protein in the Heart using Quantum Dots-Mediated Immuno-Labeling followed by Transmission Electron Microscopy.

The subcellular localization is critical to delineating proper function and determining the molecular mechanisms of a particular protein. Several qualitative and quantitative techniques are used to determine the subcellular localization of proteins. One of the emerging techniques in determining the subcellular localization of a protein is quantum dots (QD)-mediated immunolabeling of a protein followed by imaging them with transmission electron microscopy (TEM).

Monitoring Mitochondrial Morphology and Respiration in Doxorubicin-Induced Cardiomyopathy.

Doxorubicin (DOX)-induced cardiomyopathy constitutes dose-dependent cardiac toxicity, culminating in fatal heart failure progression. Cardiac toxicity limits effective and subsequent use of DOX in chemotherapy regimens in pediatric, adult, and recurrent cancer patients. DOX-induced profound alterations in mitochondrial morphology, dynamics, and defects in mitochondrial energy metabolism in the heart comprise key stressors in DOX-induced cardiotoxicity.

To Study the Correlation of Serum Adenosine Deaminase Levels with Hba1c in Patients of Type 2 Diabetes Mellitus.

Unlabelled: Immunological dysfunction is responsible for increased morbidity and mortality due to recurrent infections and hospital admission in Type 2 DM. There are limited studies and markers for the assessment of immunological dysfunction and serum ADA is one of the marker of immunological dysfunction as proven in several studies.The present study is an attempt to correlate ADA as a marker of altered immune function in diabetes mellitus with respect to glycemic control as assessed by HbA1C.

A Novel Approach to Justify Dissolution Differences in an Extended Release Drug Product using Physiologically Based Biopharmaceutics Modeling and Simulation.

Dr Reddy's Laboratories Ltd. developed generic version of XYZ extended release tablets (ER) and achieved bioequivalence as per criteria mentioned by USFDA in both fasting and fed conditions for higher strength formulation (1200 mg). However, on comparison of multimedia dissolution profiles in pH 4.

The molecular role of Sigmar1 in regulating mitochondrial function through mitochondrial localization in cardiomyocytes.

Sigmar1 is a widely expressed molecular chaperone protein in mammalian cell systems. Accumulating research demonstrated the cardioprotective roles of pharmacologic Sigmar1 activation by ligands in preclinical rodent models of cardiac injury. Extensive biochemical and immuno-electron microscopic research demonstrated Sigmar1's sub-cellular localization largely depends on cell and organ types.

Molecular Characterization of Skeletal Muscle Dysfunction in Sigma 1 Receptor (Sigmar1) Knockout Mice.

Sigma 1 receptor (Sigmar1) is a widely expressed, multitasking molecular chaperone protein that plays functional roles in several cellular processes. Mutations in the Sigmar1 gene are associated with several distal neuropathies with strong manifestation in skeletal muscle dysfunction with phenotypes like muscle wasting and atrophy. However, the physiological function of Sigmar1 in skeletal muscle remains unknown.

Sigmar1's Molecular, Cellular, and Biological Functions in Regulating Cellular Pathophysiology.

The Sigma 1 receptor (Sigmar1) is a ubiquitously expressed multifunctional inter-organelle signaling chaperone protein playing a diverse role in cellular survival. Recessive mutation in Sigmar1 have been identified as a causative gene for neuronal and neuromuscular disorder. Since the discovery over 40 years ago, Sigmar1 has been shown to contribute to numerous cellular functions, including ion channel regulation, protein quality control, endoplasmic reticulum-mitochondrial communication, lipid metabolism, mitochondrial function, autophagy activation, and involved in cellular survival.

Augmenting Transfer Learning with Feature Extraction Techniques for Limited Breast Imaging Datasets.

Computer aided detection (CADe) and computer aided diagnostic (CADx) systems are ongoing research areas for identifying lesions among complex inner structures with different pixel intensities, and for medical image classification. There are several techniques available for breast cancer detection and diagnosis using CADe and CADx systems. However, some of these systems are not accurate enough or suffer from lack of sufficient data.

Dysfunctional Mitochondrial Dynamic and Oxidative Phosphorylation Precedes Cardiac Dysfunction in R120G-αB-Crystallin-Induced Desmin-Related Cardiomyopathy.

Background The mutated α-B-Crystallin (CryAB) mouse model of desmin-related myopathy (DRM) shows an age-dependent onset of pathologic cardiac remodeling and progression of heart failure. CryAB expression in cardiomyocytes affects the mitochondrial spatial organization within the myofibrils, but the molecular perturbation within the mitochondria in the relation of the overall course of the proteotoxic disease remains unclear. Methods and Results CryAB mice show an accumulation of electron-dense aggregates and myofibrillar degeneration associated with the development of cardiac dysfunction.

Methamphetamine induces cardiomyopathy by Sigmar1 inhibition-dependent impairment of mitochondrial dynamics and function.

Methamphetamine-associated cardiomyopathy is the leading cause of death linked with illicit drug use. Here we show that Sigmar1 is a therapeutic target for methamphetamine-associated cardiomyopathy and defined the molecular mechanisms using autopsy samples of human hearts, and a mouse model of "binge and crash" methamphetamine administration. Sigmar1 expression is significantly decreased in the hearts of human methamphetamine users and those of "binge and crash" methamphetamine-treated mice.

Chemical Architecture of Block Copolymers Differentially Abrogate Cardiotoxicity and Maintain the Anticancer Efficacy of Doxorubicin.

The molecular architecture of pH-responsive amphiphilic block copolymers, their self-assembly behavior to form nanoparticles (NPs), and doxorubicin (DOX)-loading technique govern the extent of DOX-induced cardiotoxicity. We observed that the choice of pH-sensitive tertiary amines, surface charge, and DOX-loading techniques within the self-assembled NPs strongly influence the release and stimulation of DOX-induced cardiotoxicity in primary cardiomyocytes. However, covalent conjugation of DOX to a pH-sensitive nanocarrier through a "conditionally unstable amide" linkage (PCPY-cDOX; PC = polycarbonate and PY = 2-pyrrolidine-1-yl-ethyl-amine) significantly reduced the cardiotoxicity of DOX in cardiomyocytes as compared to noncovalently encapsulated DOX NPs (PCPY-eDOX).