Evaluation of the glycemic effect of methotrexate in psoriatic arthritis patients with metabolic syndrome: A pilot study

Methotrexate (MTX) is a systemic immunosuppressant drug used for the treatment of psoriasis and psoriatic arthritis. Previous studies demonstrated a potential association between psoriasis and diabetes mellitus, obesity, atherosclerosis, hypertension, eventuating into metabolic syndrome. This study aimed at exploring the glycemic effects of MTX in psoriatic arthritis (PsA) patients. In this prospective cross-sectional study, 27 patients with PsA were evaluated. The status of PsA and presence of accompanying metabolic syndrome was determined by standard criteria and indices. Blood indicators including HbA1c, erythrocyte sedimentation rate, fasting blood sugar, total cholesterol, high-density lipoprotein, triglycerides, and C-reactive protein were examined before and 12 weeks after MTX therapy. There were no significant changes between HbA1c levels before and after MTX therapy in both genders (men: P=0.131, women: P=0.803). In addition, HbA1c levels in PsA patients with metabolic syndrome were not different before and after treatment (P=0.250). Finally, HbA1c levels did not change in PsA patients without metabolic syndrome before and after therapy (P=0.506). MTX in PsA patients does not appear to have hyperglycaemic effects in the short-term and can be safely used in patients with metabolic syndrome and diabetes

The effect of the position of compression screw in plate-screws method used in fracture treatment on fatigue strength of joint

A number of combination studies on the use of plate-screws, which has become a traditional method in fracture treatment, have been conducted to obtain a more rigid joint. These studies in the literature were reviewed and it was seen that the effect of the position of the compression screw, used with the aim of making the fracture line come closer to each other during fracture fixation, on the fatigue strength of the joint hasn’t been investigated. Within the scope of this study, a screw combination study by including Limited Contact Dynamic Compression Plate (LC-DCP) plates that possess combined hole properties was carried out. Three different combinations were created during the study. In these combinations, the unlocked screw that was located on the part where the force was applied and that was used for compression was placed in different holes and fatigue strengths of the joints were investigated under dynamic bending force. As a result of the study, it was observed that as the compression screw moved away from the fracture line, fatigue strength of the joint consisting of plate, screw and bone decreased. In addition, it was found that all the joints in the 3rd combination got damaged as a result of the fracture of the bone. © Springer Nature Switzerland AG 2019

Amelioration of aluminium-induced liver damage by vitamin E

Objective: To investigate the effects of aluminium sulphate on the microscopic morphology of the liver and on vitamin E amelioration of aluminium-induced liver damage.Methods: Rats were injected intraperitoneally with aluminium sulphate alone or aluminiurn sulphate together with vitamin F, with saline injected rats used as the control group. The study took place in Pamukkale University Faculty of Medicine in 2005.Results: The rats exposed to aluminiurn showed morphological changes in addition to previously reported biochemical changes in the liver. The antioxidant vitamin E significantly diminished the liver damage seen due to aluminium.Conclusion: There is an apparent protective effect of vitamin E on parenteral aluminiurn exposure

alpha-tocopherol

The nephrotoxic actions of aluminium (Al) arise from its accumulation in the kidneys, with the resultant degeneration of the renal tubular cells. It has been suggested that Al generates reactive oxygen species that cause the oxidative deterioration of cellular lipids, proteins, and DNA. To test this hypothesis, we have here investigated the potential for a protective role of alpha-tocopherol (vitamin E) during short-term exposure of rats to Al. Al was administered intraperitoneally either alone or in combination with vitamin E at a different point of abdomen, and the alterations in the kidney tissue were analyzed histologically. The results reveal that significant light microscopical and ultrastructural damage is caused by Al, whereas with the immediate coad ministration of vitamin E, there is a protective effect against this damage to the kidney tissue. In Al-alone group, the glomeruli and proximal tubuli and the Bowman capsules had swellings, adherence, hemorrhage, increase in mesengial matrix, and marked interstitial tissue fibrosis, indicating severe damage. In the Al and vitamin E immediate coinjected group, renal tubule cells were almost of a normal appearance. A slight stenosis was seen in the capsular area in the Malpighi corpuscules. The tubular organization and the cytoplasmic basophilia were also much the same as in the control group, with the lumen clearly visible in most of the cortical tubuli. The results highlight the need to reduce exposure to Al, with particular attention being paid to the known sources of Al. At the same time, the maintenance of a diet that is rich in vitamin E should be beneficial in the alleviation of Al toxicity

aluminium

Different forms of Aluminium (Al) are environmental xenobiofics that induce free radical-mediated cytotoxicity and reproductive toxicity. Vitamin E (alpha -tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyaed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lu-men. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation

copper on fetal rat liver tissue

During the entire period of their pregnancies, three groups of adult pregnant Wistar albino rats were provided with tap water (control; group I) or with tap water containing 10 mg/kg CdCl2 (group II) or 10 mg/kg CdCl2 Plus 10 mg/kg CuSO4 (group III). At term, the animals were sacrificed and the fetal livers were removed and examined under electron microscopy. The liver tissue of the fetuses in maternal groups II and III showed degenerative changes to their hepatocytes. In group II, the smooth endoplasmic reticulum tubules showed dilatation, and the mitochondria showed a dense matrix. In group III, some mitochondrial degeneration was also seen, with a diluted matrix and mitochondrial dilatation. There were also more heterochromatic nuclei and an increased number of ribosomes. None of these histopathological changes were present in the fetal liver samples from the maternal group I control animals

Vitamin E protection from testicular damage caused by intraperitoneal aluminium.

Different forms of Aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Vitamin E (alpha -tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyzed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lumen. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation

Histological and ultrastructural evidence for protective effects on aluminium-induced kidney damage by intraperitoneal administration of alpha-tocopherol.

The nephrotoxic actions of aluminium (Al) arise from its accumulation in the kidneys, with the resultant degeneration of the renal tubular cells. It has been suggested that Al generates reactive oxygen species that cause the oxidative deterioration of cellular lipids, proteins, and DNA. To test this hypothesis, we have here investigated the potential for a protective role of alpha-tocopherol (vitamin E) during short-term exposure of rats to Al. Al was administered intraperitoneally either alone or in combination with vitamin E at a different point of abdomen, and the alterations in the kidney tissue were analyzed histologically. The results reveal that significant light microscopical and ultrastructural damage is caused by Al, whereas with the immediate coadministration of vitamin E, there is a protective effect against this damage to the kidney tissue. In Al-alone group, the glomeruli and proximal tubuli and the Bowman capsules had swellings, adherence, hemorrhage, increase in mesangial matrix, and marked interstitial tissue fibrosis, indicating severe damage. In the Al and vitamin E immediate coinjected group, renal tubule cells were almost of a normal appearance. A slight stenosis was seen in the capsular area in the Malpighi corpuscules. The tubular organization and the cytoplasmic basophilia were also much the same as in the control group, with the lumen clearly visible in most of the cortical tubuli. The results highlight the need to reduce exposure to Al, with particular attention being paid to the known sources of Al. At the same time, the maintenance of a diet that is rich in vitamin E should be beneficial in the alleviation of Al toxicity

Transmission electron microscopy study of the effects of cadmium and copper on fetal rat liver tissue.

During the entire period of their pregnancies, three groups of adult pregnant Wistar albino rats were provided with tap water (control; group I) or with tap water containing 10 mg/kg CdCl2 (group II) or 10 mg/kg CdCl2 plus 10 mg/kg CuSO4 (group III). At term, the animals were sacrificed and the fetal livers were removed and examined under electron microscopy. The liver tissue of the fetuses in maternal groups II and III showed degenerative changes to their hepatocytes. In group II, the smooth endoplasmic reticulum tubules showed dilatation, and the mitochondria showed a dense matrix. In group III, some mitochondrial degeneration was also seen, with a diluted matrix and mitochondrial dilatation. There were also more heterochromatic nuclei and an increased number of ribosomes. None of these histopathological changes were present in the fetal liver samples from the maternal group I control animals