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Background: Vitamin B12 deficiency can cause peripheral neuropathy. Metformin use is associated with vitamin B12 deficiency. Objective: To define the prevalence of vitamin B12 deficiency in patients with type 2 diabetes mellitus (T2DM) and its possible relation to metformin therapy. Patients and Methods: A crosssectional study of T2DM patients on chronic metformin therapy was conducted at Benghazi Diabetic Center during 2011. Demographic data, type, and duration of treatment reported adherence, and vitamin B treatment were all documented. History and examination for evidence of peripheral neuropathy were recorded. Serum vitamin B12 levels were measured (reference value 159-1000 pg/ml). Results: 500 patients were included of whom 175 were males (35%). Mean (SD) age was 58.6 ± 9.9 years and duration of diabetes 13.6 ± 8.4 years. Of these 358 (71.8%) were on insulin and metformin' 93 (18.6%) on sulphonylureas and metformin, 26 (5.2%) were on insulin and sulphonylurea and metformin triple monotherapy. Mean serum B12 level for all patients was 439 ± 212 pg/ml with males having significantly higher levels than females (512 ± 226 vs. 399± 193; p=0.001). Vitamin B12 levels were <159 pg/ml in 2%, <200 p g/ml in 7.4%, and <300 pg/ml in 30.8% of the patients. There was no significant difference in the B12 levels among patients who were adherent to metformin therapy and those who were not (432 ± 206 vs. 448 ± 219 pg/ml; p=0.4). Serum B12 levels were not different in the patient with history and/or examination suggestive of neuropathy and patients who have any (443 ± 216 vs. 423 ± 204; p=0.5. Conclusions: The prevalence of vitamin B12 deficiency in diabetic patients attending Benghazi diabetic center was dependent on the cut off points used. This is comparable with previous studies. No clear relationship was evident with metformin therapy nor with neuropathy.

Introduction Ulcerative colitis (UC) is a chronic non-specific inflammatory bowel disease, and until now therapeutic agents for UC still cannot exert satisfied effects. Therefore, this study aimed to investigate the ameliorative effect of boswellic acid coated zinc nanoparticles (BAs-ZnNPs) on dextran sodium sulphate (DSS) induced-UC in rats. Methods Rats were divided into five groups; control, BAs-ZnNPs, DSS, DSS+BAs, and DSS + BAs-ZnNPs. The activity of alkaline phosphatase (ALP) was determined colorimetrically, while the concentration of IgM, IgG, TNF-α, IL-1β, and IL-8 were measured by ELISA. Levels of gene expression of NF-κB and COX-2 genes were evaluated by RT-qPCR, while the expression of protein levels of PI3K and STAT-3 were done by western blotting. Finally, histopathological examination of colon tissues of different groups of rats was done. Results The depicted ball-like structure of the BAs-ZnNPs in the TEM images ranging in size from 50 to 100 nm in diameter while their formation was confirmed by UV–visible spectroscopy with a sharp peak of maximum absorbance at 266 nm. Our results revealed that BAs-ZnNPs exerted an anti-inflammatory effect in the experimental model of colitis, demonstrated histologically and biochemically as shown by the improvement of ALP, IgM, IgG, and the gene expression levels of NF-κB and COX-2. Also, this beneficial effect was associated with the reduction in the expression of TNF-α, IL-1β, IL-8, PI3K, and STAT-3. Thus, this effect improves the altered immune response associated with the colonic inflammation. Conclusion BAs-ZnNPs can be proposed as a therapeutic candidate to attenuate UC. The potential underlying mechanism includes suppression of ALP, IgM, IgG, IL-1β, and IL-8 levels via regulation of NF-κB and COX-2 gene expression and STAT-3 and PI3K protein expression in a UC rat model.

Objective: Hepatocellular carcinoma (HCC) is one of the most leading causes of death worldwide. Previous studies reported that gallium alone and cetyltrimethylammonium bromide (CTAB) have antineoplastic activities; therefore, this study aimed to evaluate the activity of copper‐cetyl tri‐methyl ammonium bromide with gallium oxide nanoparticles (Cu‐CTAB+GaO‐NPs) against HCC by using in vitro and in vivo studies. Methods: In vitro study was performed to evaluate the cytotoxic effects of Cu‐CTAB+GaO‐NPs and GaO‐NPs on HepG‐2 cell line using crystal violet dye assay. In vivo study was done on diethyl nitrosamine (DEN) induced HCC Wister rats. Rats were randomly divided into eight groups; control, Cu‐CTAB, GaO‐NPs, Cu‐CTAB+GaONPs, DEN, DEN+Cu‐CTAB, DEN+GaO‐NPs and DEN+Cu‐CTAB+GaO‐NPs. Histopathological examination of liver and biochemical parameters such as liver function markers, oxidative stress-antioxidants markers, tumor makers, apoptosis makers were studied. Results: Results obtained from in vitro study revealed that Cu‐CTAB+GaO‐NPs and GaO‐NPs affect the cell viability of HepG‐2 cancer cell with IC50 0.2 μg/ml and 360 μg/ml, respectively. Cu‐CTAB+GaO‐NPs exerted an antiproliferative effect in experimental rat models of HCC, as demonstrated both histologically, since it facilitated the tissue recovery of the damaged liver, and biochemically as showed by the reduction of liver function markers (ALT & AST), oxidative stress markers (MDA) and tumor makers (AFP,TGF‐β1,α‐L–Fucosidase); while antioxidants markers (SOD), apoptosis markers (caspase‐3 mRNA) and araginase activity were elevated in DEN+Cu‐CTAB, DEN+GaO‐NPs and DEN+Cu‐CTAB+GaO‐NPs groups when compared to DEN group. Conclusion: The present study demonstrated that both Cu‐CTAB alone and/or combined with GaO‐NPs exerted cytotoxic effects against DEN-induced HCC, which would in turn, speculate a possible therapeutic role of the novel Cu‐CTAB+GaO‐NPs compound.