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Biotechnology has revolutionized the fields of rheumatology and immunology, providing innovative solutions for understanding and treating autoimmune diseases. Traditionally, these fields relied on basic immunological techniques and limited therapeutic options. However, advancements in biotechnology have introduced novel diagnostic tools, targeted therapies, and personalized medicine approaches, significantly improving patient outcomes. The aim of this overview is to provide researchers with a comprehensive understanding of the current biotechnological advancements in rheumatology and immunology, highlighting their impact on disease diagnosis, management, and treatment. The primary objective is to explore the various biotechnological innovations that have transformed rheumatology and immunology. This includes the development of biologics, biomarkers, and genetic tools that have enabled precise diagnosis and tailored treatments. Additionally, the overview seeks to examine the ongoing research and future directions in these fields, emphasizing the potential for further breakthroughs. Biotechnology has significantly advanced the fields of rheumatology and immunology, offering new hope for patients with autoimmune diseases. The introduction of biologics has been a game-changer, allowing for targeted therapies that have improved disease management and patient quality of life. Biomarker discovery has enhanced diagnostic accuracy and enabled the monitoring of disease progression. Genetic and genomic tools have paved the way for personalized medicine, tailoring treatments to individual patient profiles. As research continues to evolve, the integration of biotechnology in these fields promises to bring even more innovative solutions, ultimately transforming the landscape of autoimmune disease treatment and management. Researchers must stay abreast of these developments to continue driving progress and improving patient outcomes.

(1) Background: The current study examined the correlations between platelet count (PC), spleen diameter (SD), and their ratio to establish a non-invasive technique for predicting the presence of oesophageal varices in cirrhotic patients. (2) Methods: The current study was an observational study conducted in the Gastroenterology Department at IMS and SUM Hospital from November 2019 to November 2021. Consecutive cirrhotic patients without a history of gastrointestinal bleeding were enrolled in the study, and the esophageal varices were assessed. The patients underwent the necessary tests, including upper gastrointestinal endoscopy, liver function testing, abdominal ultrasonography, and full hemograms. All these parameters were analyzed statistically through SPSS version 23, and p ≤ 0.05 was considered statistically significant. (3) Results: There were significant differences between cases with and without esophageal varices in the following parameters: PC, SD and their ratio, hemoglobin, and ALT level. The PC/SD ratio of ≤ 1400 was associated with a sensitivity of 90.9%, specificity of 80.8%, and a positive predictive value of 82.56% in predicting the presence of oesophageal varices, as per receiver operating curve (ROC) analysis in our study. (4) Conclusions: Esophageal varices can be predicted non-invasively using the platelet count, spleen diameter, and PC/SD ratio.

Background. The present study aimed to know the association and causal relationship of neck pain with different primary and mixed-type headache disorders. Material and methods. The primary patients with headaches attending the Department of Neurology OPD throughout one-year were included in the study. The demographic features, detailed history of headaches, and the characteristics of neck pain were entered in the pre-designed proforma. With the collaboration of the Department of Neurology, All India Institute of Medical Sciences, Jodhpur, Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow and the Department of Neurology, IMS and SUM Hospital, Bhubaneswar, India. Results. A total of 601 primary headache patients were included in the study, among which a fraction of 66.4% (n=399) had the problem of neck pain either as a pre-disposing event or as a part of the headache. Females were predominately higher than males with a fraction of 67.6%. Among all the patients a fraction of 21% (n=84) had a migraine, 51% (n=203) had a tension-type headache (TTH) and 28% (n=112) had a mixed-type headache. Though several patients with migraine had neck pain as a part of migraine, neck pain was significantly associated with tension and mixed type headache than migraine headache (p

Introduction: Gastric cancer (GC) is one of the leading causes of cancer-related decimations worldwide. The gastric infection at both the stomach and duodenum with Helicobacter pylori causes inflammation by the tumor necrosis factor-alpha (TNF-α). The aim of the study was to associate and evaluate the three TNF-α gene polymorphisms at positions −308 G/A, −238 G/A, and −857 C/T with the risk of GC. Methods: A total of 156 individuals (consecutively diagnosed 95 GC patients and 61 controls) above the age of 18 years were enrolled in the study. Healthy individuals with normal upper gastrointestinal endoscopy (UGIE) irrespective of their family history of GC or peptic ulcer were included as controls. The cited three TNF-α gene polymorphisms were evaluated using polymerase chain reaction-restriction fragment length polymorphism (RFLP). Results: There was no significant difference in the distribution of gene polymorphisms as genetic factors, TNF-α−308 GA/AA (22.1% vs. 14.8%, p = 0.2), TNF-α−238 GA/AA (21% vs. 19.6%, p = 0.8), and TNF-α−857 CT/TT (8.4% vs. 11.5%, p = 0.5), between GC cases and healthy controls. A subgroup analysis of H. pylori-positive patients showed that there was no significant difference in the distribution of GA/AA polymorphisms in TNF-α−308 (15(45.5%) vs. 3(23%); p = 0.17) and −238 (12(36.3%) vs. 2(15.4%); p = 0.17), and the distribution of TT/CT −857 CT/TT (13(39.4%) vs. 2(15.4%); p = 0.13), among the GC cases and controls. Conclusion: The statistical comparisons of GA/AA vs. GG genotypes at −308 (with OR = 1.6, 95% CI: 0.6–3.8), −238 (OR = 1.09, 95% CI: 0.4–2.4) and TT/CT vs. CC genotypes at −857 (OR = 0.7, 95% CI: 0.2–2.1) did not suggest any association of TNF-α with GC in the population herein. Hence, the TNF-α (−308 G/A, −238 G/A and −857 C/T) may not be the associating factor for GC incidence determined by the PCR–RFLP method.