Publications by authors named "Gausal A Khan"

Background: Preeclampsia (PE) is a serious inflammatory process that is unique to pregnancy, occurring at or after the 20th week of pregnancy, and leading to maternal and neonatal illness and systemic disruptions. Placental hypoxia leads to increased levels of cytokines and inflammatory syncytiotrophoblast microvillus membrane microparticles (STBM) which activates neutrophils leading to oxidative stress and endothelial dysfunction in preeclampsia. The mechanisms that cause PE in people remain unknown.

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Metformin, the primary therapy for type 2 diabetes mellitus (T2DM), showed limitations such as varying absorption, rapid system clearance, required large amount, resistance, longstanding side effects. Use of Nano formulations for pharmaceuticals is emerging as a viable technique to reduce negative consequences of drug, while simultaneously attaining precise release and targeted distribution. This study developed a Polyethylene Glycol conjugated Graphene Oxide Quantum dots (GOQD-PEG) nanocomposite for the sustained release of metformin.

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Background: Malaria has been identified as a crucial vector-borne disease around the globe. The primary aim of this study was to investigate the incidence of malaria in the district of Bannu and its relationship with climatic conditions such as temperature, rainfall, relative humidity, and topography.

Methods: Secondary data were obtained from the metrological office and government hospitals across the district for 5 years (2013-2017).

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The emergence of multidrug-resistant (MDR) bacteria has spurred the exploration of therapeutic nanomaterials such as ZnO nanoparticles. However, the inherent nonspecific toxicity of ZnO has posed a significant obstacle to their clinical utilization. In this research, we propose a novel approach to improve the selectivity of the toxicity of ZnO nanoparticles by impregnating them onto a less toxic clay mineral, Bentonite, resulting in ZB nanocomposites (ZB NCs).

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One of the most essential chemical processes that is utilized in the manufacturing of a great deal of contemporary goods is called heterogeneously catalyzed reactions, and it is also one of the most fascinating. Metallic nanostructures are heterogeneous catalysts for range reactions due to their huge surface area, large assembly of active surface sites, and quantum confinement effects. Unprotected metal nanoparticles suffer from irreversible agglomeration, catalyst poisoning, and limited life cycle.

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Medicinal plants (MPs) are natural sources of active compounds with potential therapeutic benefits in alleviating various illnesses for decades. Fijian people also are using these MPs for the management/prevention of Type 2 diabetes mellitus (T2DM) and associated complications. However, till date, none of these Fijian MP's antidiabetic potential have been explored or evaluated.

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Myocardial infarction (MI), atherosclerosis and other inflammatory and ischemic cardiovascular diseases (CVDs) have a very high mortality rate and limited therapeutic options. Although the diagnosis is based on markers such as cardiac Troponin-T (cTrop-T), the mechanism of cTrop-T upregulation and release is relatively obscure. In the present study, we have investigated the mechanism of cTrop-T release during acute hypoxia (AH) in a mice model by ELISA & immunohistochemistry.

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The outbreak of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is a global catastrophe. The elderly and people with comorbidity are facing a serious complication of the disease. The entry and infection strategy of SARS-CoV-2 in a host cell is raised by an amazing way of angiotensin-converting enzyme (ACE) 2 (ACE2) receptor recognition and imbalance of ACE/ACE2 in various organs, especially in the lungs.

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Coronavirus disease 2019 (COVID-19) has spread rapidly throughout the world. The range of the disease is broad but among hospitalized patients with COVID-19 are coagulation disorders, pneumonia, respiratory failure, and acute respiratory distress syndrome (ARDS). The excess production of early response proinflammatory cytokines results in what has been described as a cytokine storm, leading to an increased risk of thrombosis, inflammations, vascular hyperpermeability, multi-organ failure, and eventually death over time.

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Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0-24 h at standard temperature and humidity.

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Sterile inflammation (SI) is an essential process in response to snakebite and injury. The venom induced pathophysiological response to sterile inflammation results into many harmful and deleterious effects that ultimately leads to death. The available treatment for snakebite is antiserum which does not provide enough protection against venom-induced pathophysiological changes like haemorrhage, necrosis, nephrotoxicity and often develop hypersensitive reactions.

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Introduction: Garlic has been reported to stimulate nitric-oxide (NO) synthesis in various cells. The role of aqueous-extract of garlic (AEG) and a purified NO-generating protein from garlic (NGPG) was investigated to control hyperglycemia by hepatic insulin synthesis through NGPG induced synthesis of NO via glucose-activated NO-synthase and glucose transporter-4 (Glut-4) in the hepatocytes.

Methods: Type-1-diabetic mellitus mice were prepared by alloxan treatment, NO was determined by methemoglobin method, insulin synthesis was quantitated by ELISA.

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PGE plays a critical role in angiogenesis, ischemic, and neuro-inflammatory disorders of the brain, which breakdown the blood-brain barrier (BBB). However, the effects of PGE on human brain endothelial cell (HBECs) migration, a key process in the angiogenic response and BBB stability, are not well defined. In this study, we investigated the mechanism of PGE in HBECs migration in vitro.

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Background: An increase in the level of cytokines like TNF-α and IL-6 causes the inflammatory surge in acute ischemic heart disease (AIHD).

Objective: A high-level dermcidin isoform-2 (DCN-2) occurrence in AIHD was subjected to determine a possible regulation of cytokines expression. The effect of estrogen to counteract the inflammatory response was determined.

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High mobility group box 1 protein (HMGB1), a sterile inflammatory molecule and damage-associated molecular pattern (DAMP) released from various cells during stress has been implicated in inflammation. Several reports show that there is a direct relationship between inflammation and cardiovascular diseases (CVDs) such as thrombosis, hypertension, insulin resistance, preeclampsia, etc. Here, we intend to summarize the concept of the emerging link between HMGB1 and CVDs.

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Increased plasma level of von Willebrand Factor (vWF) is associated with major cardiovascular diseases. We previously reported that multimeric vWF binds to NO synthase and inhibits insulin-induced production of NO, thus promoting insulin resistance during acute hypoxia (AH). However, the transcriptional regulation of vWF during AH is not clearly understood.

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A trypsin resistant oral insulin preparation was made by incubating insulin for 2 h at 23 °C with previously boiled cow milk at 100 °C that was coagulated with 0.6 M acetic acid. The precipitate was resuspended in the same volume of milk.

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Endogenous ligands released from dying cells, including extracellular RNA (eRNA), cause TLR activation, which is associated with inflammation and vascular diseases. However, the importance of this response in acute hypoxia (AH) remains unexplored. Here, we observed eRNA-mediated TLR3 activation during exposure of mice to AH in the absence of exogenous viral stimuli.

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Introduction: Glucose has been reported to have an essential role in the synthesis and secretion of insulin in hepatocytes. As the efflux of glucose is facilitated from the liver cells into the circulation, the mechanism of transportation of glucose into the hepatocytes for the synthesis of insulin was investigated.

Methods: Grated liver suspension (GLS) was prepared by grating intact liver from adult mice by using a grater.

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Hypoxic respiratory diseases or hypoxia exposures are frequently accompanied by glucose intolerance and impaired nitric oxide (NO) availability. However, the molecular mechanism responsible for impaired NO production and insulin resistance (IR) during hypoxia remains obscure. In this study, we investigated the possible mechanism of impaired NO production and IR during hypoxia in a mouse model.

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The development of mitigating agents to counter injuries induced by radiation is as important as the development of radioprotective agents. This study reports the ability of diallyl sulphide (DAS), a naturally occurring organosulfur compound, to mitigate radiation-induced mortality and injuries to the hematopoietic system in whole-body irradiated mice. Intraperitoneal administration of a single dose of DAS (160 mg/kg body weight) 2 hours after 9 Gy whole-body irradiation resulted in 37% animal survival as opposed to 100% mortality in the irradiation-only group, improved general conditions with no visual signs of sickness, and body weight loss.

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Hypoxemia in the circulation can lead to venous thrombosis (VT) through tissue factor (TF) activation, but the mechanism of TF activation in hypoxia remains obscure. Ligands released from damaged tissues or cells due to hypoxia are identified by various pattern-recognition receptors (PRR), including Toll-like receptor3 (TLR3). In the present study, we investigated the mechanism of TF activation during acute hypoxia in a rat model.

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Insulin inhibits platelet aggregation through nitric oxide synthesis by stimulating platelet insulin activated nitric oxide synthase. Impaired platelet insulin activated nitric oxide synthase in acute myocardial infarction (AMI) patients had been reported and thus our aim was to identify and isolate the factors impairing insulin activated nitric oxide in acute myocardial infarction patients' plasma and study its effect on platelets aggregation in vitro. The insulin activated nitric oxide synthase inhibitor was identified as a protein and was purified from the plasma of AMI subjects using DEAE cellulose and Sephadex G-50 column, molecular weight determined by SDS-PAGE, nitric oxide quantified by methaemoglobin method, inhibitor protein quantified in plasma by immunoblot and ELISA, platelet aggregation studies done using an aggregometer, thromboxane-A2 in the platelets determined by radioimmunoassay, (125)I-insulin radioligand binding studies done using normal subject platelets.

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Extravillous trophoblasts (EVT) of the human placenta invade the uterine decidua and its arteries to ensure successful placentation. We previously identified two decidua-derived molecules, TGF-β and a TGF-β-binding proteoglycan decorin (DCN), as negative regulators of EVT proliferation, migration, and invasiveness and reported that DCN acts via multiple tyrosine kinase receptors [epidermal growth factor-receptor (EGF-R), IGF receptor-1 (IGFR1), and vascular endothelial growth factor 2 receptor (VEGFR-2)]. Because binding of DCN to VEGFR-2 has never been reported earlier, present study explored this binding, the approximate location of VEGFR-2-binding site in DCN, and its functional role in our human first trimester EVT cell line HTR-8/SVneo.

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