Publications by authors named "Naveen Bhatraju"

Background: Sarcoidosis and tuberculosis (TB) are the two most common causes of granulomatous mediastinal lymphadenopathy. These often exhibit overlapping clinical and radiological characteristics, rendering accurate diagnosis difficult. MicroRNA (miRNA) analysis is increasingly utilised as a potential biomarker for various diseases.

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INPP4A has been shown to be involved in the regulation of cell proliferation and apoptosis of multiple cell types including fibroblasts. Previous reports from our group have demonstrated the role of inositol polyphosphate 4-phosphatase Type I A (INPP4A) in these functions. Though existing evidences suggest a critical role for INPP4A in the maintenance of lung homeostasis, its role in chronic lung diseases is relatively under explored.

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Article Synopsis
  • * The study involved profiling EBC samples from 20 lung cancer patients and 20 healthy subjects, leading to the identification of 78 miRNAs that were significantly upregulated in lung cancer patients.
  • * Three specific miRNAs (miR-31-3p, let7i, and miR-449c) showed strong potential for distinguishing lung cancer patients from healthy individuals, suggesting that miRNA profiling in EBC could aid in early lung cancer detection.
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Despite the progress made in the development of new antiepileptic drugs (AEDs), poor response to them is a rising concern in epilepsy treatment. Of several hypotheses explaining AED treatment failure, the most promising theory is the overexpression of multidrug transporters belonging to ATP-binding cassette (ABC) transporter family at blood-brain barrier. Previous data show that AEDs themselves can induce these transporters, in turn affecting their own brain bioavailability.

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Essential hypertension (EH) is a significant health issue around the globe. The indifferent therapy regimen suggests varied physiological functions due to the lifestyle and genetic presentations of an individual. The endothelial nitric oxide synthase (NOS3) gene is a crucial vascular system marker in EH that contributes significantly to the phenotype.

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Early detection of asymptomatic cases through mass screening is essential to constrain the coronavirus disease 2019 (COVID-19) transmission. However, the existing diagnostic strategies are either resource-intensive, time-consuming, or less sensitive, which limits their use in the development of rapid mass screening strategies. There is a clear pressing need for simple, fast, sensitive, and economical diagnostic strategy for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) screening even in resource-limited settings.

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Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, we elucidate the therapeutic effects and mechanistic basis of (AV) aqueous extract on mouse models of acute allergic as well as severe asthma subtypes at physiological, histopathological, and molecular levels.

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The bidirectional epidemiological association between asthma and obesity is well known. Recent evidence suggests that there is an intersection of the pathophysiological molecular pathways leading to either obesity or asthma, at the level of mitochondria. This is not surprising, because mitochondria, beyond their roles as the metabolic powerhouses of the cell, serve as sensors of threats, regulators of stress signaling, and effectors of cytotoxicity.

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Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (ρ cells) is linked to the acquisition of the host mtDNA. However, the mechanism of mtDNA movement between cells remains unresolved. To determine whether the transfer of mtDNA involves whole mitochondria, we injected B16ρ mouse melanoma cells into syngeneic C57BL/6N mice that express red fluorescent protein in their mitochondria.

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There is limited knowledge regarding the consequences of hyperinsulinemia on the lung. Given the increasing prevalence of obesity, insulin resistance, and epidemiological associations with asthma, this is a critical lacuna, more so with inhaled insulin on the horizon. Here, we demonstrate that insulin can adversely affect respiratory health.

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Background: Obesity is known to increase asthma risk and severity. Increased levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, are associated with mitochondrial toxicity, asthma, and metabolic syndrome. IL-4 upregulates the expression of protein arginine methyltransferases, which are essential for ADMA formation.

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