BackgroundSmokers are more prone to oral infections than are non-smokers. Cigarette smoke reaches the host cells but also microorganisms present in the oral cavity. The contact between cigarette smoke and oral bacteria promotes such oral diseases as periodontitis. Cigarette smoke can also modulate C. albicans activities that promote oral candidiasis. The goal of this study was to investigate the effect of cigarette smoke condensate on C. albicans adhesion, growth, and biofilm formation as well as the activation of EAP1, HWP1 and secreted aspartic protease 2.ResultsCigarette smoke condensate (CSC) increased C. albicans adhesion and growth, as well as biofilm formation. These features may be supported by the activation of certain important genes. Using quantitative RT-PCR, we demonstrated that CSC-exposed C. albicans expressed high levels of EAP1, HWP1 and SAP2 mRNA and that this gene expression increased with increasing concentrations of CSC.ConclusionCSC induction of C. albicans adhesion, growth, and biofilm formation may explain the increased persistence of this pathogen in smokers. These findings may also be relevant to other biofilm-induced oral diseases.

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The predisposition of cigarette smokers for development of respiratory and oral bacterial infections is well documented. Cigarette smoke can also contribute to yeast infection. The aim of this study was to investigate the effect of cigarette smoke condensate (CSC) on C. albicans transition, chitin content, and response to environmental stress and to examine the interaction between CSC-pretreated C. albicans and normal human gingival fibroblasts. Following exposure to CSC, C. albicans transition from blastospore to hyphal form increased. CSC-pretreated yeast cells became significantly (P < 0.01) sensitive to oxidation but significantly (P < 0.01) resistant to both osmotic and heat stress. CSC-pretreated C. albicans expressed high levels of chitin, with 2- to 8-fold recorded under hyphal conditions. CSC-pretreated C. albicans adhered better to the gingival fibroblasts, proliferated almost three times more and adapted into hyphae, while the gingival fibroblasts recorded a significantly (P < 0.01) slow growth rate but a significantly higher level of IL-1β when in contact with CSC-pretreated C. albicans. CSC was thus able to modulate both C. albicans transition through the cell wall chitin content and the interaction between C. albicans and normal human gingival fibroblasts. These findings may be relevant to fungal infections in the oral cavity in smokers.

Electronic cigarette (e-cigarette) vapor comes in contact with the different constituents of the oral cavity, including such microorganisms as Candida albicans. We examined the impact of e-cigarettes on C. albicans growth and expression of different virulent genes, such as secreted aspartic proteases (SAPs), and the effect of e-cigarette vapor-exposed C. albicans on gingival epithelial cell morphology, growth, and lactate dehydrogenase (LDH) activity. An increase in C. albicans growth was observed with nicotine-rich e-cigarettes compared with non-exposed cultures. Following exposure to e-cigarette vapor, C. albicans produced high levels of chitin. E-cigarettes also increased C. albicans hyphal length and the expression of SAP2, SAP3, and SAP9 genes. When in contact with gingival epithelial cells, e-cigarette-exposed C. albicans adhered better to epithelial cells than the control. Indirect contact between e-cigarette-exposed C. albicans and gingival epithelial cells led to epithelial cell differentiation, reduced cell growth, and increased LDH activity. Overall, results indicate that e-cigarettes may interact with C. albicans to promote their pathogenesis, which may increase the risk of oral candidiasis in e-cigarette users.

The purpose of this study was to determine the possible deleterious effects of e-cigarette vapor on osteoblast interaction with dental implant material. Osteoblasts were cultured onto Ti6Al4V titanium implant disks and were then exposed or not to whole cigarette smoke (CS) as well as to nicotine-rich (NR) or nicotine-free (NF) e-vapor for 15 or 30 min once a day during one, two, or three days, after which time various analyses were performed. Osteoblast growth on the titanium implant disks was found to be significantly (p < 0.001) reduced following exposure to CS and to the NR and NF e-vapors. Osteoblast attachment to the dental implant material was also dysregulated by CS and the NR and NF e-vapors through a decreased production of adhesion proteins such as F-actin. The effects of CS and e-cigarette vapor on osteoblast growth and attachment were confirmed by reduced alkaline phosphatase (ALP) activity and tissue mineralization. The adverse effects of CS and the NR and NF e-vapors on osteoblast interaction with dental implant material also involved the caspase-3 pathway, as the caspase-3 protein level increased following exposure of the osteoblasts to CS or e-vapor. It should be noted that the adverse effects of CS on osteoblast growth, attachment, ALP, and mineralized degradation were greater than those of the NR and NF e-vapors, although the latter did downregulate osteoblast interaction with the dental implant material. Overall results suggest the need to consider e-cigarettes as a possible contributor to dental implant failure and/or complications.

These results suggest that α-tocopherol may play an active role in countering the damaging effect of LPS by reducing inflammatory cytokines, increasing β-defensins and promoting fibroblast growth, migration and wound healing.

Introduction: Female sexual dysfunction (FSD) is a common health problem that is inadequately investigated in Saudi Arabia. Aim: To assess the prevalence and predictors of FSD in a sample of Saudi women attending the primary care and gynecology clinics. Methods: A cross-sectional clinic-based survey involved Saudi women attending primary care and gynecology clinics in a teaching hospital in Riyadh during the period from January to June 2019. Data were collected using a structured interview questionnaire. Female sexual function has been evaluated by the Arabic version of the Female Sexual Function Index. Main outcome measures: The main outcome measure of this study was female sexual function using the Arabic version of the Female Sexual Function Index. Results: 200 Saudi women were included in this study. Their age ranged from 18 to 50 years. Most of the participants (88.5%) were fairly satisfied or satisfied with their spouse's sexual ability and 120 (60%) had a risk of FSD. Participants with FSD reported the lowest scores for arousal and desire domains (3.03 ± 1.3 and 3.12 ± 1.1, respectively) followed by orgasm domain (3.48 ± 1.4). Predictive factors for risk of FSD in our participants were age greater than 40 years (P ¼ .012), unemployment (P ¼ .035), low/moderate family income (P ¼ .014), dissatisfaction with the spouse's sexual ability (P ¼ .005), and higher weight (P ¼ .010) and height (P ¼ .043). Only age greater than 40 years (P ¼ .041), low family income (P ¼ .007), and dissatisfaction with spouse's sexual ability (P ¼ .011) sustained independent significance in a multivariate logistic regression analysis. Conclusion: A high prevalence of FSD was encountered in our sample of Saudi women. Desire and arousal were the most significantly affected domains followed by orgasmic problems. Age greater than 40 years, low socioeconomic level, and dissatisfaction with the spouse's sexual ability are the most significant predictors. Madbouly K, Al-Anazi M, Al-Anazi H, et al. Prevalence and Predictive Factors of Female Sexual Dysfunction in a Sample of Saudi Women. Sex Med 2020;XX:XXXeXXX.

Urease is an amidohydrolase enzyme that is responsible for fatal morbidities in the human body, such as catheter encrustation, encephalopathy, peptic ulcers, hepatic coma, kidney stone formation, and many others. In recent years, scientists have devoted considerable efforts to the quest for efficient urease inhibitors. In the pharmaceutical chemistry, the thiourea skeleton plays a vital role. Thus, the present work focused on the development and discovery of novel urease inhibitors and reported the synthesis of a set of 1-aroyl-3-[3-chloro-2-methylphenyl] thiourea hybrids with aliphatic and aromatic side chains 4a–j. The compounds were characterized by different analytical techniques including FT-IR, 1H-NMR, and 13C-NMR, and were evaluated for in-vitro enzyme inhibitory activity against jack bean urease (JBU), where they were found to be potent anti-urease inhibitors and the inhibitory activity IC50 was found in the range of 0.0019 ± 0.0011 to 0.0532 ± 0.9951 μM as compared to the standard thiourea (IC50 = 4.7455 ± 0.0545 μM). Other studies included density functional theory (DFT), antioxidant radical scavenging assay, physicochemical properties (ADMET properties), molecular docking and molecular dynamics simulations. All compounds were found to be more active than the standard, with compound 4i exhibiting the greatest JBU enzyme inhibition (IC50 value of 0.0019 ± 0.0011 µM). The kinetics of enzyme inhibition revealed that compound 4i exhibited non-competitive inhibition with a Ki value of 0.0003 µM. The correlation between DFT experiments with a modest HOMO-LUMO energy gap and biological data was optimal. These recently identified urease enzyme inhibitors may serve as a starting point for future research and development.