ABSTRACT
Diabetes mellitus and its complications are major international health problems in which there are many limitations to the orthodox approaches in the treatment. Sodium glucose cotransporter 2 (SGLT2) inhibitors are a new class of diabetic medications, with a different mechanism of action that may reduce risk of cardiovascular complications. To evaluate the effect of SGLT2 inhibitor monotherapy on cardiovascular complications in patients with type-2 diabetes and to compare its effect with the first-line therapy, metformin. Eighty rats divided into four groups were used: nondiabetic, diabetic nontreated, diabetic ? met and diabetic ? dapa. At the end, the arterial blood pressure and cardiac performance were assessed. Glycemic index, lipid profile, total antioxidant capacity, malondialdehyde, tumour necrosis factor a were measured. DNA changes were assessed from the hearts and aortae. Aortic tissue changes recorded using haematoxylin and eosin, Masson trichrome and iNOS immune stain. Glycemic index, lipid profile, oxidative stress and inflammatory parameters were significantly improved in both metformin and dapagliflozin treated groups with significant improvement in blood pressure and cardiac performance. Also, there were noticeable significant reduction in DNA fragmentation in aortic and cardiac tissues and reduction in collagen deposition and iNOS expression in aortic tissue. Dapagliflozin treatment results’ significantly surpassed improvement of metformin treatment nearly in all parameters. Total genomic DNA extraction proved that SGL2 inhibitor (dapagliflozin) has superior glycemic control and cardiovascular protective effect over metformin especially in type-2 diabetes with high fat intake.
ABSTRACT
Burned patients are at increased risk for hospital-acquired infections. Pseudomonas aeruginosa is the most common bacterial pathogen involved in these infections. Epidemiologic typing is needed to discover the source of infection. Phenotypic characteristics of Pseudomonas aeruginosa could be used for this purpose. However, the genomic fingerprinting methods are now regarded as more accurate typing methods. Random amplified polymorphic DNA is thought to be an efficient genetic typing method. In the Burn Unit of Menoufyia University Hospital this study was carried out in order to overview the problem of hospital acquired infections in this unit, to identify the most common pathogen and to find out probable sources of infections. Fifty-three cases of nosocomial burn wound infections, ten medical personnels and thirty-one environmental samples were screened, bacterial isolates were identified. Epidemiologic study for the most common isolate [Pseudomonas aeruginosa] was done using antibiogram and pyocin production in addition to some genetic studies as plasmid profile and random amplification polymorphic DNA [RAPD] typing. Total number of Pseudomonas aeurginosa strains isolated from burn wound infections, medical staff and Burn Unit environment and equipments was 36. These P. aeurginosa strains were mostly sensitive to imipinem [69.5%] followed by amikin [61.2%]. Antibiogram typing classified these isolates into 9 groups. beta lactamase prduction was proved in 58% of strains. Pyocin typing revealed 5 types. Sixteen strains had plasmids with 7 different profiles. According to RAPD 24 different patterns were distinguished. Identical clones of Pseudomonas aeurginosa were identified: two clones were related to environmental sources [Hydrotherapy tub and stretcher of hydrotherapy]. Horizontal acquisition through health care worker [finger tips] was proved.Endogenous colonization was also found in two cases. The RAPD method is simple, fast and has high discriminatory power suitable for application in epidemiologic studies. Stringent infection control policies and education campaign are urgently needed
ABSTRACT
The use of Psoralen combined with exposure to ultraviolet - A radiation [PUVA] is a long-term major treatment for a number of skin diseases as well as for controlling graft versus host reaction. Although PUVA treatment is highly effective, careful follow-up cohort studies have shown that it greatly increases the risk for the development of hepatotoxicity, immunotoxicity and cutaneous squamous cell carcinoma. Strategies to reduce the risk of these toxic effects particularly cancer development in PUVA treated population is highly desirable. Because of the complexity of the processes involved in photocarcinogenesis, it is clear that more information particularly regarding its genotoxic effects is needed at cellular and molecular levels in order to develop optimal protection against photocarcinogenic risks related to UVA exposure. In the present study we used single cell gel electrophoresis assay [comet assay] to determine DNA damage, mainly strand breaks and alkali labile sites in the DNA molecule of lymphocytes of 3 groups of persons. Group [1] consisted of 30 patients treated with oral Psoralen while group [2] consisted of 30 patients treated with bath PUVA therapy, each group was then subdivided according to the number of sessions into less than and more than 30 PUVA sessions treated subgroups. Group [3] consisted of 15 healthy individuals served as control. The results indicated that patients treated by oral PUVA for more than 30 sessions have shown significant increase in the percentage of damaged and strongly damaged DNA spots of lymphocytes measured by comet assay as compared to their corresponding values in bath PUVA treated group, while there was insignificant increase in the percentage of damaged DNA spots of lymphocytes from patients treated by less than 30 sessions of oral PUVA therapy as compared to its corresponding percentages in the group of patients treated by bath PUVA therapy. P53 started to accumulate after at least 18 sessions of oral PUVA therapy while in patients under bath PUVA therapy it was not detected until they reached 25 sessions. The intensity of P53 bands increased as the number of sessions increased. The present study documented that, oral PUVA therapy is more genotoxic than bath PUVA therapy especially with cumulative doses. In conclusion, early detection of the genotoxic effects of PUVA therapy could be achieved by detection of DNA damage using comet assay together with the analysis of P53 expression status