International Journal of Medical Sciences and Pharma Research

Performance Evaluation of Truenat rtPCR assay with COBAS -6800 in SARS COV-2 detection: A diagnostic accuracy study

Arindam Chakraborty , Monica Singh , Amod Kumar — Mon, 15 Sep 2025 00:00:00 -0400

Context: Diagnostic testing plays a critical role in early and accurate detection of SARS-COV-2. Real-time PCR is the Gold standard test for the diagnosis of SARS-COV-2 which requires well equipped BSL-2 Lab along with skilled manpower. There is a need for a rapid point of care test for diagnosis. TrueNat is one such testing system that is approved by Govt. of India.

Aims: To find out the performance of the TrueNat assay in comparison to cobas 6800.

Settings and Design: The Cross-sectional study was conducted in a COVID 19 Testing Laboratory in Central India.

Methods and Material: A total of 122 COVID-19 positive samples in cobas 6800 were analysed in TrueNat assay.

Results: Of the total of cobas positive122 sample TrueNat system were able to detect 116 samples with the viral load of high(n=18), medium(n=28 ), low(n=44),very low(n=26). Considering cobas 6800 as a Gold standard assay TrueNat test showed a sensitivity and specificity of 95% and 100%respectively.

Conclusions: Based on our findings we believe that TrueNat assay is equally effective for the diagnosis of SARS-COV-2 compared to a highly sophisticated instrument such as cobas 6800. Hence, it should be installed in all healthcare setups with a limited setting for rapid and reliable diagnosis of SARS-COV-2.

Keywords: cobas 6800, TrueNat, COVID-19, Point of care test.

Nitric Oxide Deficiency in Sickle Cell Anemia: Mechanisms and Interventions

Emmanuel Ifeanyi Obeagu — Mon, 15 Sep 2025 00:00:00 -0400

Nitric oxide (NO) deficiency plays a crucial role in the pathophysiology of sickle cell anemia (SCA), contributing to vascular dysfunction and related complications that significantly impact patient health. NO is vital for maintaining endothelial function, regulating vascular tone, and preventing platelet aggregation. In SCA, reduced NO bioavailability results from hemolysis, oxidative stress, and impaired nitric oxide synthase (NOS) activity. These factors lead to vascular issues such as pulmonary hypertension, vaso-occlusive crises, and stroke. This review explores the mechanisms behind NO depletion in SCA and emphasizes how NO deficiency worsens vascular dysfunction. The reduction of NO in SCA is mainly due to the release of cell-free hemoglobin from lysed red blood cells, which scavenges NO, along with increased production of reactive oxygen species (ROS) that break down NO. Additionally, endothelial dysfunction further decreases NO synthesis, creating a vicious cycle of declining NO availability. This causes elevated vascular resistance, impaired blood flow, and a higher risk of thrombotic events, all contributing to the morbidity and mortality observed in SCA patients.

Keywords: Nitric oxide, Sickle cell anemia, Vascular dysfunction, Hemolysis, Therapeutic interventions

The Role of Nitric Oxide in Enhancing Erythropoiesis in Sickle Cell Disease

Emmanuel Ifeanyi Obeagu — Mon, 15 Sep 2025 00:00:00 -0400

Sickle cell disease (SCD) is a hereditary blood disorder characterized by the production of abnormal hemoglobin, leading to the sickling of red blood cells, vaso-occlusion, hemolysis, and chronic organ damage. One of the key challenges in SCD is impaired erythropoiesis, which results from the continuous destruction of sickled red blood cells and a compensatory increase in red blood cell production. Nitric oxide (NO), a critical endothelial signaling molecule, has been identified as a key regulator of erythropoiesis. NO influences the differentiation, proliferation, and survival of erythroid progenitor cells, thereby playing a vital role in maintaining healthy red blood cell production. In SCD, NO bioavailability is often reduced due to the hemolysis of red blood cells, which releases cell-free hemoglobin that scavenges NO. This depletion of NO further exacerbates the anemia and contributes to vascular dysfunction in SCD patients. Restoring NO availability may therefore be crucial for improving erythropoiesis and reducing the anemia that is characteristic of SCD. Research has shown that NO can enhance the expression of transcription factors involved in erythropoiesis and increase the production of fetal hemoglobin (HbF), which has a protective effect against sickling.

Keywords: Nitric oxide, erythropoiesis, sickle cell disease, hemoglobinopathies, vascular health