The obesity pandemic has brought forth a scientific interest in food intake and sensory perception interactions. Olfactory perception and gustatory perception are very complex and under the influence of many factors, including the menstrual cycle. This study aims to clarify conflicting findings on the influence of the menstrual cycle on olfactory and gustatory perception. Women were assessed during four consecutive phases of one complete cycle (mid-follicular, ovulatory, mid-luteal, and late luteal phases (N = 21)), in contrast to women measured across the same phases belonging to two menstrual cycles (N = 29). Additional control groups were men (N = 17), postmenopausal women (N = 14), oral contraceptive users (N = 10), and women with an anovulatory cycle (N = 8). Olfactory threshold, odor discrimination, and identification were tested using the “Sniffin Sticks“ test kit. Suprathreshold intensity and hedonic ratings for sweet, salty, sour, and bitter solutions were assessed. One-way ANOVA and ANOVA for repeated measurements was applied in the analysis, along with linear and trigonometric data fitting and linear mixed models. Linear increases in olfactory discrimination, identification, and overall olfactory performance were observed only in women followed across a complete menstrual cycle. Compared to other groups, these women displayed a cyclic pattern characterized by a predilection for sweet solution; reduced distaste for salty and sour solutions; and increased intensity perception of salty, sour, and bitter solutions towards the end of the cycle. These results suggest that a distinct hormonal milieu of a complete menstrual cycle may be affecting both olfactory and gustatory perception.

DNA-protein cross-links (DPCs) are highly toxic DNA lesions that block replication and transcription, but their impact on organismal physiology is unclear. We identified a role for the metalloprotease SPRTN in preventing DPC-driven immunity and its pathological consequences. Loss of SPRTN activity during replication and mitosis lead to unresolved DNA damage, chromosome segregation errors, micronuclei formation, and cytosolic DNA release that activates the cyclic GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway. In a Sprtn knock-in mouse model of Ruijs-Aalfs progeria syndrome, chronic cGas-Sting signaling caused embryonic lethality through inflammation and innate immune responses. Surviving mice displayed aging phenotypes beginning in embryogenesis, which persisted into adulthood. Genetic or pharmacological inhibition of cGas-Sting rescued embryonic lethality and alleviated progeroid phenotypes.

Bladder cancer (BC) is the ninth leading cause of cancer death with one of the highest recurrence rates among all cancers. One of the main risks for BC development is exposure to nitrosamines present in tobacco smoke or in other products. Aberrant epigenetic (DNA methylation) changes accompanied by deregulated gene expression are an important element of cancer pathogenesis. Therefore, we aimed to determine DNA methylation signatures and their impacts on gene expression in mice treated with N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), a carcinogen similar to compounds found in tobacco smoke. Following BBN administration mice developed non-invasive or invasive bladder cancers. Surprisingly, muscle- and neuronal-related pathways emerged as the most affected in those tumors. Hypo- and hypermethylation changes were present within non-invasive BC, across CpGs mapping to the genes involved in muscle- and neuronal-related pathways, however, methylation differences were not sufficient to affect the expression of the majority of associated genes. Conversely, invasive tumors displayed hypermethylation changes that were linked with alterations in gene expression profiles. Together, these findings indicate that bladder cancer progression could be revealed through methylation profiling at the pre-invasive cancer stage that could assist monitoring of cancer patients and guide novel therapeutic approaches.

Chronic stress has various effects on organisms and is sex-specific. The aim of the study was to describe the expression of synapse strengthening protein, dendrin, in the spinal cord (SC) and the dependence of its expression on chronic stress and sex hormones. Thirteen-month-old female and male rats were castrated (ovariectomy [F-OVX] or orchidectomy [M-ORX]) or sham-operated (F-SH or M-SH), respectively. At age 15 months, three 10-day-sessions of sham stress (control, C) or chronic stress (S) were conducted. Dendrin expression was present in the thoracic SC segments and the dorsal root ganglia (DRG). In the SC, dendrin expression was prominent in superficial laminae of the dorsal horn and lamina X (central canal). The M-ORX-S group had the highest dendrin expression in the dorsal horn, being significantly higher than the M-ORX-C or M-SH-S groups (P < 0.05). Dendrin expression was significantly higher in the F-SH-S group than the F-SH-C group (P < 0.05), as well as in the F-SH-S than the M-SH-S (P < 0.05). Co-localization with the α-d-galactosyl-specific isolectin B4 (IB4) in central projections of the DRG neurons in the dorsal horn of the SC was 7.43 ± 3.36%, while with the calcitonin gene-related peptide (CGRP) was 8.47 ± 4.45%. Localization of dendrin was observed in soma and nuclei of neurons in the dorsal horn. Dendrin expression in pain-processing areas of the SC, the DRG neurons and their peripheral projections suggest possible roles in pain perception and modulation. Stress-induced increase in dendrin expression and its dependence on sex hormones may partially explain sex-specific pain hypersensitivity induced by stress.