Impact of tobacco habits on poor oral health status among bone-factory workers in a low literacy city in India: A cross-sectional study.

Oral health is a vital indicator of well-being that is influenced by various habits and lifestyles of individuals. Oral diseases are the bottleneck in the effective control of non-communicable diseases (NCDs) due to chronic in nature and reciprocal relationship as sharing the common risk factors and habits such as sugar, tobacco, and alcohol consumption that increase the risk of developing various inevitable diseases. However, there is a lack of literature highlighting the relationship between risk factors for oral diseases and general health among individuals. This cross-sectional study was carried out among 500 study participants aged 20 to 64 years who gave written informed consent and were recruited by Multistage Stratified Cluster Sampling technique among workers in five bone factories, working for at least one year since January 2001 to March 2022 in Sambhal city, Uttar Pradesh. WHO-Basic Oral Health Survey-1997 was used to record the data regarding sociodemographic and oral health status variables. We used the modified WHO-STEPWISE pre-structured questionnaire to record tobacco consumption habits and oral health-seeking behavior. We scheduled a clinical intra-oral examination to record the Decayed Missing Filled Teeth (DMFT) index and the interview on the premises of five bone factories. Among the 500 bone-factory workers, the total number of males was 342 (68.40%) and 158 (31.60%) were females. The mean age (Standard Deviation) was 33.18 (10), and the mean DMFT score of factory workers was 2.84 (3.12). Production workers had the highest mean DMFT score of 4.60 (3.25). More than half of the factory workers (53.2%) were tobacco users. Tobacco users were 3.52 times more likely to have a severe DMFT index. Most common pre-cancerous lesions were oral submucous fibrosis and leukoplakia. Compared to non-tobacco users, mild tobacco users have 6.80 folds higher odds of oral lesions. Tobacco consumption is not only harmful for oral health but also leads to several non-communicable and systemic diseases. NCDs and dental caries are chronic and preventable conditions with a bidirectional relationship implicated by modifiable major risk factors such as tobacco consumption. Decreasing the consumption of tobacco use may improve oral health and reduce the risk of the development of NCDs. Also, regular dental visits should be scheduled to monitor the oral health status of factory workers. Additionally, tailored intervention for tobacco cessation should be implicated to maintain the general and oral health of industrial workers.

Mechanistic Insight into the Abiotic Interactions of Selenate and Selenite with Natural Organic Matter.

Natural organic matter (NOM) decreases the selenium (Se) mobility in soil and sediment. Biotic dissimilatory reduction of selenate and selenite and assimilation of the reduced Se species into biomolecules are thought to be primarily responsible for this decreased Se mobility. However, the possibility of Se immobilization due to the abiotic interaction of Se species with NOM is still poorly understood. Equilibrating selenate and selenite with a model NOM (Pahokee peat soil), followed by X-ray absorption spectroscopic analysis, this study shows that the NOM can abiotically reduce highly mobile selenate into relatively less mobile selenite. NOM can sorb Se species, especially selenite, considerably. Preloading of the NOM with Fe(III) increases the sorption of selenite and selenate by several orders of magnitude. Modeling of the Se and Fe K-edge EXAFS data revealed that Se species are sorbed to NOM due to indirect complexation with the organically complexed Fe(O,OH)6 octahedra through the corner- (2C) and edge-sharing (1E) and direct complexation with the oxygen-containing functional groups of the NOM. This study concludes that the abiotic reduction and complexation of the Se species with NOM can be the additional or alternative route of Se immobilization in the NOM-rich soil and sediment.

Insulin-like growth factor 1 stimulation of androgen receptor activity requires ß(1A) integrins.

Despite the findings that ß1 integrins play a vital role in the regulation of cell proliferation and survival, the mechanisms through which they operate and lead to cancer progression remain elusive. Previously, our laboratory has shown that ß(1A) integrins support insulin-like growth factor 1 (IGFI)-mediated mitogenic and transforming activities. Here, we report that ß(1A) integrins regulate basal levels of IGF-IR, although they are not critical for maintaining cancer cell morphology. Upon transfection of ß(1A) siRNA and consequent downregulation of IGF-IR, we show inhibition of anchorage-independent growth of prostate cancer cells, a function which is dependent on IGF-IR expression. In addition, we demonstrate that IGFI-mediated activation of androgen receptor (AR), known to occur in prostate cancer cells, requires expression of ß(1A) integrins as evaluated by luciferase reporter assays and immunoblotting analysis. Since ß(1A) integrin levels are increased by R1881 or dihydrotestosterone (DHT), our results imply that ß(1A) integrins support an androgen-enhanced feedback loop that regulates the expression of IGF-IR. ß(1A) integrins also regulate inducible levels of IGF-IR in cells stimulated by androgen or by a combination of androgen and IGFI, as evaluated by flow cytometric analysis and immunoblotting. Furthermore, upon transfection of ß(1A) siRNA and consequent downregulation of IGF-IR, neither activation of AKT, an effector of IGF-IR, nor AR levels are affected. We conclude that ß(1A) integrin expression is critical for maintaining the regulatory crosstalk between IGF-IR and AR.

Integrin signaling aberrations in prostate cancer.

Integrins are cell surface receptors for extracellular matrix proteins and play a key role in cell survival, proliferation, migration and gene expression. Integrin signaling has been shown to be deregulated in several types of cancer, including prostate cancer. This review is focused on integrin signaling pathways known to be deregulated in prostate cancer and known to promote prostate cancer progression.

The integrin-growth factor receptor duet.

Cell adhesion receptors, referred to as integrins, are recognized as key regulators of cellular processes including growth and differentiation. Integrins communicate with growth factor receptors (GFRs) to control specific cellular responses to stimuli originating in the extracellular environment. In this article, we review the role of integrins as molecular switches that modulate GFR activation and specificity. We also examine the reciprocal modulation of integrin functions by GFRs and the mechanisms through which those actions are fine-tuned.