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Introduction: Baseline expression of p16INK4a characterises cellular senescence. Similarly, the measurement of 1-Gamma-H2AX (1-H2AX) foci levels in cells provides a reliable method for quantification of Deoxyribonucleic Acid (DNA) damage. Aim: To explore the role of p16INK4a and 1-H2AX as biomarkers of senescence in skin tissue. Materials and Methods: This was a cross-sectional study conducted in the Department of Anatomy, PGIMER, Chandigarh, Punjab, India from June 2022 to January 2023. Skin tissue was obtained from 30 cadavers, aged 20-90 years, from the anterior abdominal wall. The time duration of sample collection after death varied from six hours to 12 hours. Samples were divided into two groups: Group-I <30 years and Group-II >70 years, with n=15 in each group. The relative change in the expression pattern of p16INK4a and 1H2AX markers, as well as the microstructure of the skin (thickness of epidermis and dermis, distribution of collagen I/II/III fibres, architecture of sebaceous glands), were statistically analysed using an unpaired t-test. Results: Intense staining was observed with p16INK4a in Group-II, showing positivity in 60.75% of the cells, while Group-I depicted a weak staining pattern (15%). On immunostaining with 1-H2AX, only Group-II cells showed intense positivity (45%). Significant differences were observed in the epidermal and dermal thickness: Group-I (165.5267±37.73 µm; 2394.6±874.13 µm); Group-II (54.6±22.79 µm; 566.67±242.23 µm), and collagen Type-II/III fibres were found predominantly in aging skin tissue. Conclusion: The present study provides comprehensive data regarding age-associated changes between p16INK4a, 1-H2AX, and skin microstructure, which result in decreased repair and regenerative capacity of skin tissue and various age-related skin diseases. [ABSTRACT FROM AUTHOR]

Background: The auditory tube (AT), an osteocartilaginous channel, connects the nasopharynx to the middle ear cavity. At the nasopharyngeal opening of the AT, there are dense collections of submucosal glands. In a recent article, Valstar et al. proposed these nasopharyngeal tubal glands conglomerate as salivary glands, which starkly contrasts with their previously known anatomy for being a component of the respiratory tract. This study examines the contesting views regarding the taxonomical categorization of the nasopharyngeal tubal glands. Materials and Methods: The AT glands in context were examined in human cadavers grossly, and microscopically using routine and special (Hematoxylin and Eosin [H&E] and Periodic acid–Schiff [PAS] respectively), as well as immunohistochemical (for alpha‐SMA and salivary amylase) staining methods and compared with the major and minor salivary glands and the submucosal glands in the trachea. Further, a biochemical analysis was performed to detect the presence of salivary amylase in the oral and nasopharyngeal secretions of the four living human subjects, representing major salivary glands and tubal glands, respectively. Results: The submucosal seromucous glands with a surface lining of respiratory epithelium were observed at the nasopharyngeal end of AT. The cells in the tubal glands showed cytoplasmic positivity for alpha‐SMA, which indicated the presence of the myoepithelial cells; however, this expression was significantly lower than in the seromucous submucosal glands within the trachea. Salivary alpha‐amylase was undetectable in the cadaveric tissue samples. Moreover, the amylase level in the nasopharyngeal swabs was negligible compared to the oral swabs. Conclusion: The anatomical location along the respiratory tract, the presence of respiratory epithelium in the overlying mucosa, their morpho‐functional resemblance to the seromucous glands in the trachea, and the absence of salivary amylase strongly indicate that the tubal glands are taxonomically different from the salivary glands. Given the available evidence, their existing recognition as a part of the respiratory tract and an integral component of the AT seems more appropriate. [ABSTRACT FROM AUTHOR]

Young age, female sex, absence of comorbidities, and prior infection or vaccination are known epidemiological barriers for contracting the new infection and/or increased disease severity. Demographic trends from the recent coronavirus disease 2019 waves, which are believed to be driven by newer severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) variants, indicate that the aforementioned epidemiological barriers are being breached and a larger number of younger and healthy individuals are developing severe disease. The new SARS‐CoV‐2 variants have key mutations that can induce significant changes in the virus‐host interactions. Recent studies report that, some of these mutations, singly or in a group, enhance key mechanisms, such as binding of the receptor‐binding domain (RBD) of the viral spike protein with the angiotensin‐converting enzyme 2 (ACE2) receptor in the host‐cells, increase the glycosylation of spike protein at the antigenic sites, and enhance the proteolytic cleavage of the spike protein, thus leading to improved host‐cell entry and the replication of the virus. The putative changes in the virus–host interactions imparted by the mutations in the RBD sequence can potentially be the reason behind the breach of the observed epidemiological barriers. Susceptibility for contracting SARS‐CoV‐2 infection and the disease outcomes are known to be influenced by host‐cell expressions of ACE2 and other proteases. The new variants can act more efficiently, and even with the lesser availability of the viral entry‐receptor and the associated proteases, can have more efficient host‐cell entry and greater replication resulting in high viral loads and prolonged viral shedding, widespread tissue‐injury, and severe inflammation leading to increased transmissibility and lethality. Furthermore, the accumulating evidence shows that multiple new variants have reduced neutralization by both, natural and vaccine‐acquired antibodies, indicating that repeated and vaccine breakthrough infections may arise as serious health concerns in the ongoing pandemic. Highlights: Emerging SARS‐CoV‐2 variants: Harbor key mutations altering the virus‐host interactions.Show more efficient host‐cell entry and greater replication resulting in higher viral loads, prolonged viral shedding, and greater tissue injury.Show reduced neutralization by natural and vaccine acquired antibodies.Causing symptomatic illness in increasing number of young, women, and healthy individuals. [ABSTRACT FROM AUTHOR]