Occupational exposure of dental staff to elemental mercury vapor released from dental amalgam is an issue of concern because of the possible immunological and neurological adverse outcomes. Recently, studies have reported that inorganic mercury induces immunosuppression by decreasing the production of thymus gland hormone (thymulin). This study aimed at investigating mercury body burden in dental staff and the relation of this burden to the potential impact of mercury on thymus gland hormone level (thymulin). Besides, the work aimed at verifying mercury effect on nitric oxide synthetase as a possible mechanism of its immunotoxicity. The study population consisted of a group of dental staff (n = 39) [21 dentists and 18 nurses] and a matched control group (n = 42). Each individual was subjected to detailed occupational and medical history taking and to estimation of urinary mercury (U-Hg) and blood mercury (B-Hg) as indicators of mercury body burden and exposure, respectively. Measurement of total thymulin hormone blood level, and plasma level of nitrite and nitrate (indicators of nitric oxide) was also done. The study showed a significantly increased U-Hg and B-Hg levels in the dental staff compared to their controls. This elevation of mercury body burden was associated with significant reduction in thymulin hormone blood level and nitric oxide parameters. These results were more evident in the group of nurses compared to the dentists. In conclusion, our results show that dentists and dental nurses have significant exposure to mercury vapor and point to the negative impact of mercury on thymus gland functions and confirm the implication that the nitric oxide pathway is a possible mechanism for this impact. Moreover, the study raises attention to the importance of hygiene measures in reduction of exposure to mercury vapor released from dental amalgam.

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Type 2 diabetes (T2DM) represents a major risk factor for atherosclerosis that is the underlying cause of most cardiovascular diseases. Identifying reliable predictive biomarkers are needed to improve the long-term outcome in diabetic patients. Autophagy plays a pivotal role in the pathogenesis of atherosclerosis. Beclin1 is a key regulatory protein of autophagy and has been localized in human atherosclerotic lesions. However, the relation of serum level of Beclin1 and atherosclerosis in patients with diabetes has not been clarified yet. To assess the relationship between serum level of Beclin1 and carotid intima-media thickness (CIMT) in patients with T2DM. In this case-control study participants were recruited from tertiary care hospitals in Egypt. The study enrolled 50 patients with T2DM and 25 healthy subjects between January, 2019 and January, 2020. Age, gender, and body mass index were recorded for all subjects. Laboratory works up including glycated hemoglobin, lipid panel, and serum Beclin1 (by enzyme-linked immunosorbent assay) were measured. CIMT was assessed by color Doppler. Comparisons between patients and the control group were done using analysis of variance and Chi-square test. Correlations between CIMT and Beclin1 level and different variables were done using the Pearson correlation coefficient. Receiver operator characteristic curve was constructed with the area under curve analysis performed to detect the best cutoff value of Beclin1 for detection of CIMT > 0.05 cm. The level of Beclin1 in the patient group was significantly lower compared with that in the control group (1.28 ± 0.51 vs 5.24 ± 1.22 ng/dL, P < .001). The level of Beclin1 apparently decreased in the higher CIMT group in T2DM patients. Serum Beclin1 levels were negatively correlated with CIMT ( r = –0.762; P < .001), low-density lipoprotein-cholesterol ( r = −0.283; P = .04), and triglycerides ( r = −0.350; P = .01) but positively correlated with high-density lipoprotein-cholesterol ( r = 0.491; P < .001) in patients with T2DM. Beclin1 level >2.2 ng/dL was an accurate predictor of CIMT >0.05 cm with an area under the curve value of 0.997, 93.9% sensitivity, and 100% specificity. Beclin1 levels were negatively correlated with atherosclerotic load in patients with T2DM and it may be considered as a promising diagnostic and therapeutic target.

The current study showed that vitamin D has significant association with LPE and correlates significantly with IELT and PEDT.

Objectives: Diabetic nephropathy is the leading cause of chronic kidney disease. The pathogenesis of DN remains incompletely understood. It has been recently demonstrated that inflammatory processes play a significant role in the development and progression of DN. Toll-like receptors play a fundamental role in the innate immune system by triggering proinflammatory signaling pathways. Our aim is to evaluate the expression of TLRs on monocytes and relate their expression with inflammation in HD patients with & without diabetic nephropathy. Method: In a case control study (60) patients from Alkasr El Aini Hospital on hemodialysis were divided into two groups: Group 1, 30 patients on heamodialysis not due to diabetic nephropathy, Group 2, 30 patients on heamodialysis due to diabetic nephropathy, compared to Group 3, including 30 healthy controls. All participants were subjected to: Full medical history, complete physical examination, Serum creatinine, uric acid, A1C, fundus examination, detection of TLR2, TLR expression by real time PCR in peripheral blood mononuclear cells. Data were statically calculated using SPSS, comparision between groups was done using student T test comparing 2 groups, correlation using spearman's correlation. Results: Diabetic had significantly increased TLR2, TLR4 mRNA in peripheral blood mononuclear cells compared to controls and non diabetics patient on heamodialysis (p < 0.001), TLR2, TLR4 significantly correlated with dialysis duration in diabetic (p < 0.001), no correlation with A1C in relation to TLR2 (p = 0.078), TLR4 (p = 0.163). Conclusion: TLR2, TLR4 were significantly elevated in diabetic on dialysis initiating event in the patho-genesis of DN, providing a link between hyperglycemia and hypoxia with inflammation and fibrosis within the kidney. Hence, therapeutic interventions aimed at targeting the inflammatory component through interruption of TLR signaling may be a novel strategy to target prevention and treatment of DN.