Ravindra P. Veeranna

Tuberculosis (TB) continues to be the world’s deadliest infectious disease, with an estimated 10.8 million new cases reported in 2023, of which India alone accounted for 28% of the global burden. This study aims to evaluate the impact of tuberculosis on pulmonary function and exercise tolerance, and to examine how these impairments affect health-related quality of life (HRQoL). In a cross-sectional design, 96 bacteriologically confirmed TB patients and 96 age- and sex-matched community controls underwent spirometry, six-minute-walk test (6 MWT), and HRQoL evaluation. DR-TB was detected in 27 patients (28.1%): Isoniazid monoresistance 59.3%, rifampicin monoresistance 11.1%, and XDR-TB 29.6%. Dyspnoea (70.8%) and cough (37.5%) were the most commonly reported symptoms among TB patients. Mean values of FEV₁, FVC, and FEV₁/FVC were significantly lower in TB patients compared to controls (62.8%, 65.97%, and 70.08% vs. 82.55%, 80.09%, and 78.08%, respectively; p < 0.001). Recurrent or DR-TB was associated with reduced spirometric indices and 6 MWT distances (241 m vs. 358 m in drug-sensitive TB). St. George’s respiratory questionnaire (SGRQ) scores indicated significantly poorer health-related quality of life (HRQoL) in patients compared to controls across all domains—symptoms (23.7 vs. 10.7), activity (33.3 vs. 14.2), and impact (20.6 vs. 9.4; p < 0.05). SGRQ scores were inversely correlated with lung function parameters (r = −0.42 to −0.56). These findings underscore the persistent health burden TB poses post-therapy, highlighting the need for routine post-TB functional screening and robust DR-TB control to achieve End-TB goals.

Brucella melitensis is a highly infectious zoonotic pathogen responsible for brucellosis, which significantly affects both human and livestock health worldwide. This study employed whole-genome sequencing (WGS) to analyze the genetic diversity of 24 B. melitensis isolates from India. Pangenome analysis revealed a highly conserved nature with the involved strains having very limited accessory genes. Multilocus Sequence Typing (MLST) identified sequence type ST8 as predominant among Indian strains. Analysis of virulence genes revealed a total of 43 virulence-related genes in all strains, emphasizing their critical role in the pathogenicity of B. melitensis . Unique gene profiles and distinct phylogenetic clusters suggest regional adaptations and evolutionary pressures. The comprehensive genomic insights from this study help to elucidate the geographic distribution and interspecies transmission of Indian strains, highlighting the importance of targeted brucellosis control measures in India. Additionally, the identification of conserved virulence genes involved in immune evasion and intracellular survival highlights their importance in the bacterium’s pathogenicity. This research contributes to the global understanding of B. melitensis genomic diversity, providing valuable insights for broader epidemiological studies and brucellosis management strategies worldwide. IMPORTANCE: B. melitensis is a significant cause of illness in both humans and animals, particularly in India, where the disease remains a major concern. This study highlights that only a few genetic types of the bacteria are circulating in the region, which means control efforts can be better focused on these specific types. By understanding the unique characteristics of Indian strains, and how these strains spread and adapt, this research offers valuable guidance for improving brucellosis prevention strategies. These insights can help in developing more effective diagnostic tools, enhancing vaccination efforts, and strengthening disease control programs to reduce the impact of brucellosis on public health and livestock industries.

Introduction: Antimicrobial resistance (AMR) in Brucella melitensis, the causative agent of brucellosis, is of growing concern, particularly in low and middle-income countries. This study aimed to explore the genetic basis of AMR in B. melitensis strains from India.Methods: Twenty-four isolates from humans and animals were subjected to antimicrobial susceptibility testing and whole-genome sequencing.Results: Resistance to doxycycline (20.80%), ciprofloxacin (16.67%), cotrimoxazole (4.17%), and rifampicin (16.67%) was observed. Genome analysis revealed efflux-related genes like mprF, bepG, bepF, bepC, bepE, and bepD across all isolates, however, classical AMR genes were not detected. Mutations in key AMR-associated genes such as rpoB, gyrA, and folP were identified, intriguingly present in both resistant and susceptible isolates, suggesting a complex genotype–phenotype relationship in AMR among Brucella spp. Additionally, mutations in efflux genes were noted in resistant and some susceptible isolates, indicating their potential role in resistance mechanisms. However, mutations in AMR-associated genes did not consistently align with phenotypic resistance, suggesting a multifactorial basis for resistance.Discussion: The study underscores the complexity of AMR in B. melitensis and advocates for a holistic multi-omics approach to fully understand resistance mechanisms. These findings offer valuable insights into genetic markers associated with AMR, guiding future research and treatment strategies.

Diabetes mellitus (DM) is a common comorbidity in COVID-19 subjects. Hyperglycemia at hospital admission identified as a major risk factor and is responsible for poor prognosis. Hematological and inflammatory parameters have been recognized as predictive markers of severity in COVID-19. In this clinical study, we aimed to assess the impact of hyperglycemia at hospital admission on hematological and several inflammatory parameters in COVID-19 patients. A total of 550 COVID-19 subjects were primarily categorized into two major groups (normoglycemic and hyperglycemic) based on random blood sugar levels. On the first day of hospitalization, subjects’ oxygen saturation, random blood sugar, hematological variables, and inflammatory parameters were recorded. The hyperglycemic group exhibited higher levels of serum ferritin, total leukocyte count (TLC), lactate dehydrogenase (LDH), neutrophil count, and neutrophil-to-lymphocyte ratio (NLR). In contrast, oxygen saturation and lymphocyte count were lower compared to the normoglycemic group. Significantly elevated levels of hematological variables (TLC, neutrophil count, NLR) and inflammatory parameters (serum ferritin) were observed in the hyperglycemic group. Among inflammatory parameters, only serum ferritin levels showed statistical significance. This study supports the clinical association between hyperglycemia and an increased severity of COVID-19. Consequently, the identification of these parameters is a crucial and valuable prognostic indicator for assessing disease severity in hyperglycemic subjects.

Chronic diseases like cancer and diabetes are the major public health concerns of India and worldwide. Nowadays, plant-derived products are in great demand for the treatment of these diseases. Pumpkin seeds are traditionally implicated for their pharmacological properties, as exemplified by benign prostatic hyperplasia. Earlier, pumpkin seed proteins were extracted by the Osborne method, and their functional and nutritional qualities were evaluated. Here, the aim is to assess in vitro, the anticancer and antidiabetic properties of seed protein fractions. HepG2, MDA-MB-231, and MCF-7 cell lines were treated with water-soluble (WF) and alkali-soluble fractions (AF) to assess cytotoxicity, while pancreatic β-cells and insulin resistance (IR) – HepG2 cell lines were treated with WF to evaluate the antidiabetic potential. WF and AF showed cytotoxic effects towards HepG2 and MDA-MB-231 cell lines, suggesting apoptosis-mediated anticancerous activity. WF potentiates glucose-stimulated insulin secretion in pancreatic β-cells, in a dose-dependent manner. In IR-HepG2 cell line studies, control, metformin, and WF-treated groups showed uptake of glucose, when compared to the diabetic group, which is well-correlated with the upregulated expressions of GLUT2 and GLUT4 transporters in these groups. These results indicate that proteins from WF and AF may have anticancerous and antidiabetic properties and thus have the potential to utilize pumpkin proteins in the management of cancer and diabetes.

The landscape of scholarly publishing is undergoing a transformative shift through the influence of Artificial Intelligence (AI). With technology’s pervasive impact, AI is revolutionizing research creation, sharing, evaluation and accessibility. Historically labour-intensive scholarly processes are being reshaped by AI’s efficiency and accuracy. This transformation spans research inception, content production, peer review and dissemination. AI’s role in drafting, enhancing peer review, enabling personalized content recommendations and global accessibility is explored. While AI’s integration marks a significant technological leap, ethical considerations and human oversight remain essential. This article delves into AI’s recent strides in scholarly publishing, emphasizing its collaborative role alongside human expertise. APA-7 Style Dubey, M., Dubey, A.K., Veeranna, R.P. (2024). Advancing Scholarly Publishing Through Artificial Intelligence: A Paradigm Shift. Trends in Scholarly Publishing, 3(1), 1-5. https://doi.org/10.21124/tsp.2024.1.5 ACS Style Dubey, M.; Dubey, A.K.; Veeranna, R.P. Advancing Scholarly Publishing Through Artificial Intelligence: A Paradigm Shift. Trends Schol. Pub 2024, 3, 1-5. https://doi.org/10.21124/tsp.2024.1.5 AMA Style Dubey M, Dubey AK, Veeranna RP. Advancing Scholarly Publishing Through Artificial Intelligence: A Paradigm Shift. Trends in Scholarly Publishing. 2024; 3(1): 1-5. https://doi.org/10.21124/tsp.2024.1.5 Chicago/Turabian Style Dubey, Muskan, Arun Kumar Dubey, and Ravindra P Veeranna. 2024. "Advancing Scholarly Publishing Through Artificial Intelligence: A Paradigm Shift" Trends in Scholarly Publishing 3, no. 1: 1-5. https://doi.org/10.21124/tsp.2024.1.5

Amyotrophic lateral sclerosis (ALS) is a multi-systemic, incurable, amyloid disease affecting the motor neurons, resulting in the death of patients. The disease is either sporadic or familial with SOD1, C9orf72, FUS, and TDP-43 constituting the majority of familial ALS. Multi-omics studies on patients and model systems like mice and yeast have helped in understanding the association of various signaling and metabolic pathways with the disease. The yeast model system has played a pivotal role in elucidating the gene amyloid interactions. We carried out an integrated transcriptomic and metabolomic analysis of the TDP-43 expressing yeast model to elucidate deregulated pathways associated with the disease. The analysis shows the deregulation of the TCA cycle, single carbon metabolism, glutathione metabolism, and fatty acid metabolism. Transcriptomic analysis of GEO datasets of TDP-43 expressing motor neurons from mice models of ALS and ALS patients shows considerable overlap with experimental results. Furthermore, a yeast model was used to validate the obtained results using metabolite addition and gene knock-out experiments. Taken together, our result shows a potential role for the TCA cycle, cellular redox pathway, NAD metabolism, and fatty acid metabolism in disease. Supplementation of reduced glutathione, nicotinate, and the keto diet might help to manage the disease.

Recent evidence relating to the impact of COVID-19 on people with diabetes is limited but continues to emerge. COVID-19 pneumonia is a newly identified illness spreading rapidly throughout the world and causes many disabilities and fatal deaths. Over the ensuing 2 years, the indirect effects of the pandemic on healthcare delivery have become prominent, along with the lingering effects of the virus on those directly infected. Diabetes is a commonly identified risk factor that contributes not only to the severity and mortality of COVID-19 patients, but also to the associated complications, including acute respiratory distress syndrome (ARDS) and multi-organ failure. Diabetic patients are highly affected due to increased viral entry into the cells and decreased immunity. Several hypotheses to explain the increased incidence and severity of COVID-19 infection in people with diabetes have been proposed and explained in detail recently. On the other hand, 20–50% of COVID-19 patients reported new-onset hyperglycemia without diabetes and new-onset diabetes, suggesting the two-way interactions between COVID-19 and diabetes. A systematic review is required to confirm diabetes as a complication in those patients diagnosed with COVID-19. Diabetes and diabetes-related complications in COVID-19 patients are primarily due to the acute illness caused during the SARS-CoV-2 infection followed by the release of glucocorticoids, catecholamines, and pro-inflammatory cytokines, which have been shown to drive hyperglycemia positively. This review provides brief insights into the potential mechanisms linking COVID-19 and diabetes, and presents clinical management recommendations for better handling of the disease.

The incidence and death toll due to SARS-CoV-2 infection varied time-to-time; and depended on several factors, including severity (viral load), immune status, age, gender, vaccination status, and presence of comorbidities. The RNA genome of SARS-CoV-2 has mutated and produced several variants, which were classified by the SARS-CoV-2 Interagency Group (SIG) into four major categories. The first category; “Variant Being Monitored (VBM)”, consists of Alpha (B.1.1.7), Beta (B.1.351), Gamma (P.1), Delta (B.1.617.2), Epsilon (B.1.427, B.1.429), Eta (B.1.525), Iota (B.1.526), Kappa (B.1.617.1), Mu (B.1.621), and Zeta (P.2); the second category; “Variants of Concern” consists of Omicron (B.1.1.529). The third and fourth categories include “Variants of Interest (VOI)”, and “Variants of High Consequence (VOHC)”, respectively, and contain no variants classified currently under these categories. The surge in VBM and VOC poses a significant threat to public health globally as they exhibit altered virulence, transmissibility, diagnostic or therapeutic escape, and the ability to evade the host immune response. Studies have shown that certain mutations increase the infectivity and pathogenicity of the virus as demonstrated in the case of SARS-CoV-2, the Omicron variant. It is reported that the Omicron variant has >60 mutations with at least 30 mutations in the Spike protein (“S” protein) and 15 mutations in the receptor-binding domain (RBD), resulting in rapid attachment to target cells and immune evasion. The spread of VBM and VOCs has affected the actual protective efficacy of the first-generation vaccines (ChAdOx1, Ad26.COV2.S, NVX-CoV2373, BNT162b2). Currently, the data on the effectiveness of existing vaccines against newer variants of SARS-CoV-2 are very scanty; hence additional studies are immediately warranted. To this end, recent studies have initiated investigations to elucidate the structural features of crucial proteins of SARS-CoV-2 variants and their involvement in pathogenesis. In addition, intense research is in progress to develop better preventive and therapeutic strategies to halt the spread of COVID-19 caused by variants. This review summarizes the structure and life cycle of SARS-CoV-2, provides background information on several variants of SARS-CoV-2 and mutations associated with these variants, and reviews recent studies on the safety and efficacy of major vaccines/vaccine candidates approved against SARS-CoV-2, and its variants.