Publications by authors named "Vishal J Patel"

Chronic diseases associated with inflammation cause early destruction of RBCs. Complement system, part of innate immunity, is involved in such RBC destruction. Persistent inflammation causes kidney injury, leading to reduced erythropoietin release and functional iron deficiency, causing anaemia.

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Article Synopsis
  • - Autoimmune hemolytic anemia (AIHA) is a disease caused by the body's immune system attacking red blood cells, leading to rapid hemolysis and anemia, with varying onset based on triggers.
  • - Desidustat, a medication primarily used for anemia related to chronic kidney disease, was tested in a study on mice with AIHA and showed positive results, improving levels of hemoglobin and red blood cells while reducing white blood cells and oxidative stress.
  • - The treatment with desidustat enhanced erythropoiesis (the production of red blood cells) and prevented antibody-mediated damage to red blood cells, suggesting that desidustat could be an effective option for treating AIHA.
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Complement cascade is a defence mechanism useful for eliminating pathogenic microorganisms and damaged cells. However, activation of alternative complement system can also cause inflammation and promote kidney and retinal disease progression. Inflammation causes tissue hypoxia, which induces hypoxia-inducible factor (HIF) and HIF helps the body to adapt to inflammation.

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Hypoxia-inducible factors (HIFs) are transcription factors that are responsible for adapting to the changes in oxygen levels in the cellular environment. HIF activity determines the expression of cellular proteins that control the development and physiology of the cells and pathophysiology of a disease. Understanding the role of specific HIF (HIF-1-3) in cellular function is essential for development of the HIF-targeted therapies.

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Iron deficiency anemia is caused by many pathological conditions like chronic kidney disease (CKD), inflammation, malnutrition and gastrointestinal abnormality. Current treatments that are erythropoiesis stimulating agents (ESAs) and iron supplementation are inadequate and often lead to tolerance and/or toxicity. Desidustat, a prolyl hydroxylase (PHD) inhibitor, is clinically used for the treatment of anemia with CKD.

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Article Synopsis
  • Many patients with chronic kidney disease experience anemia that is resistant to erythropoietin (EPO) due to factors like inflammation and improper iron usage.
  • The study tested desidustat, a drug that inhibits certain enzymes, in rats to see if it could help manage anemia in cases where EPO was ineffective.
  • Results showed that desidustat reduced resistance to EPO, lowered inflammation markers, and maintained healthy hemoglobin levels, suggesting it could be a new treatment option for EPO-resistant renal anemia.
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Objective: Ventriculoperitoneal shunts (VPSs) for hydrocephalus in patients with achondroplasia are known to have a higher failure rate than in other hydrocephalus populations. However, the etiology of hydrocephalus in this group is considered "communicating," and, therefore, potentially not amenable to endoscopic third ventriculostomy (ETV). ETV has, nonetheless, been reported to be successful in a small number of patients with achondroplasia.

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Article Synopsis
  • Chronic kidney disease (CKD) leads to inflammation in the body, and desidustat is a medicine that might help treat anemia related to CKD.
  • In experiments with rats and mice that had kidney problems, desidustat showed positive effects by lowering harmful substances in the blood and helping with anemia.
  • The treatment also reduced inflammation and damage in the kidneys, suggesting it could be beneficial for people with CKD.
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Dental injection needle migration is a rare complication of orthodontal procedures. When these needles fracture, they typically dislodge into the cervical space or the facial musculature. Migration into the cranial vault is difficult because of the obstacle created by the skull base.

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Background: Balanced coagonists of glucagon-like peptide-1 (GLP-1) and glucagon receptors are emerging therapies for the treatment of obesity and diabetes. Such coagonists also regulate lipid metabolism, independent of their body weight lowering effects. Many actions of the coagonists are partly mediated by fibroblast growth factor 21 (FGF21) signaling, with the major exception of bile homeostasis.

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  • The study aimed to evaluate the effects of a coagonist targeting GLP-1 and glucagon receptors on kidney problems caused by diabetes and obesity in mouse models.
  • Researchers used different groups of mice fed a high-fat diet or treated with a diabetes-inducing agent to assess changes in kidney function and overall health after 12 to 40 weeks of coagonist treatment.
  • Results showed significant improvements in kidney health, weight loss, and reduced inflammation and fibrosis, indicating that this treatment could mitigate kidney dysfunction linked to diabetes and obesity.
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  • * Hypoxia triggers the production of hypoxia-inducible factor (HIF), which increases erythropoietin (EPO) levels and helps stimulate red blood cell formation.
  • * Prolyl hydroxylase domain (PHD) inhibitors, which stabilize HIF and lower hepcidin levels (regulating iron), are being tested in clinical trials as a new oral treatment for anemia linked to chronic diseases, with several compounds such as roxadustat and vadadustat in advanced trial phases.
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Background And Purpose: Dipeptidyl peptidase (DPP)-4 inhibitors increase levels of glucagon-like peptide-1 (GLP-1) and provide clinical benefit in the treatment of type 2 diabetes mellitus. As longer acting inhibitors have therapeutic advantages, we developed a novel DPP-4 inhibitor, ZY15557, that has a sustained action and long half-life.

Experimental Approach: We studied the potency, selectivity, efficacy and duration of action of ZY15557, in vitro, with assays of DPP-4 activity.

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ZYDPLA1 is a long acting enzyme dipeptidyl peptidase-4 (DPP-4) inhibitor. The comparative effect of DPP-4 inhibition after intravenous (IV) and oral administration of ZYDPLA1 in a rat model was evaluated to answer the question of route dependency and/or the need of high plasma levels of ZYDPLA1. The study was conducted using parallel design in male Wistar rats for IV/oral route (n=9 and 6, for IV and oral respectively).

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  • ZYAN1, a prolyl hydroxylase inhibitor, is being researched for treating anemia caused by chronic kidney disease (CKD), with studies conducted on its pharmacokinetics in rat models experiencing kidney impairment.
  • In the experiment, acute kidney injury was induced using cisplatin, while chronic kidney injury was induced through nephrectomy, and the effects on ZYAN1 were evaluated by measuring its levels in blood and urine after a single oral dose.
  • Results showed that peak concentration and overall exposure of ZYAN1 were largely unaffected in mild kidney injury cases, but a significant increase in drug exposure occurred in severely impaired rats, suggesting that CKD patients might experience minimal changes in ZYAN1 processing.
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Objective To determine whether patient race and ethnicity affect nasopharyngeal cancer survival. Study Design Retrospective database analysis. Setting National Cancer Institute's SEER database (Surveillance, Epidemiology, and End Results), 1988-2010.

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Introduction: The use of intraoperative CT-guidance during the percutaneous treatment of trigeminal neuralgia has become increasingly popular due to the greater ease of foramen ovale cannulation and decreased procedure times. Concerns regarding radiation dose to the patient, however, remain unaddressed. We sought to compare the emitted radiation dose from fluoroscopy with intraoperative CT for these procedures.

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Developmental venous anomalies (DVA) are among the most common congenital malformations of the cerebral angioarchitecture. Spontaneous thrombosis of this entity is rare, and our review of the literature found only 31 reported cases of symptomatic spontaneous thrombosis of developmental venous anomalies. Here, we report a unique case describing the spontaneous thrombosis of a DVA leading to venous infarction and subsequent recanalization.

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Dual agonism of glucagon and glucagon-like peptide-1 (GLP-1) receptors reduces body weight without inducing hyperglycemia. In addition, coagonists have demonstrated lipid lowering property, which was independent of their anorectic effect. Similarly, GLP-1 modulates cardiovascular function which is favorable for treatment of myocardial injury, cardiac dysfunction, cardiac arrhythmias, endothelial dysfunction, and blood pressure, while glucagon has a positive impact on heart rate, cardiac output, ventricular contraction and enhances cardiac performance in animals and humans.

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Objective: Dipeptidyl peptidase-4 (DPP-4) is responsible for degradation of glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP), the endogenous incretins that stimulate glucose-dependent insulin secretion. The objective was to evaluate preclinical profile of a novel DPP-4 inhibitor ZYDPLA1.

Methods: In vitro inhibition potency and selectivity were assessed using recombinant enzymes and/or plasma.

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Glucagon-like peptide-1 (GLP-1), is a hormone secreted by small intestine. Consumption of food or glucose stimulates synthesis and secretion of GLP-1 in the bloodstream, which in turn stimulates insulin secretion from pancreas and delays gastric emptying. Owing to the favorable spectrum of effects on reduction of hyperglycemia and body weight, GLP-1 mimetics are intensely pursued as therapies for the treatment of type 2 diabetes (T2DM).

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Aim: To develop a simple, accurate, sensitive, rapid and precise method for the determination of galantamine hydrobromide in bulk drug and pharmaceutical dosage form.

Material And Methods: The method employs wavelength detection and determination of galantamine hydrobromide at excitation wavelength 282 nm and emission wavelength 607 nm in a solution of simple distilled water.

Result And Conclusion: The method was found to be linear in the range of 2-14 μg/ml having r (2) = 0.

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The method we describe in this chapter describes the synthesis and use of cDNA macroarrays for determining changes in gene expression due to environmental toxicants as well as the methods and materials that are required to do this work. While the details are for investigators working with nontraditional species for which commercial arrays are unavailable, anyone can design and use their own custom arrays using these protocols. We have intentionally left out details for statistical analysis for the arrays as the methods for doing this are still being developed and would need to be specific to the experiment being done.

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