The effect of 1,25-dihydroxyvitamin D3 on liver damage, oxidative stress, and advanced glycation end products in experimental nonalcoholic- and alcoholic- fatty liver disease

Background/aim: Oxidative stress and advanced glycation end products (AGEs) formation are proposed as effective mechanisms in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). 1,25(OH)(2)D-3 was proposed to have antioxidant, antiinflammatory and antiglycation properties. In this study, the effect of 1,25(OH)(2)D-3 treatment on oxidative stress parameters and AGEs levels together with hepatic histopathology was investigated in high fructose (HFr) or ethanol (EtOH)-treated rats

The effect of Nigella sativa oil on prevention of myringosclerosis in a Guinea pig model

Objectives: In this study, our aim was to identify the possible effects of Nigella sativa L. (NS) [blackcumin] seed oil on the prevention of experimentally induced myringosclerosis (MS)

Carnosine and taurine treatments diminished brain oxidative stress and apoptosis in D-galactose aging model

D-galactose (GAL) has been used as an animal model for brain aging and antiaging studies. GAL stimulates oxidative stress in several tissues including brain. Carnosine (CAR; beta-alanil-L-histidine) and taurine (TAU; 2-aminoethanesulfonic acid) exhibit antioxidant properties. CAR and TAU have anti-aging and neuroprotective effects. We investigated the effect of CAR and TAU supplementations on oxidative stress and brain damage in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days per week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days per week) or TAU (2.5 % w/w; in rat chow) for 2 months. Brain malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione transferase (GST) and acetylcholinesterase (AChE) activities were determined. Expressions of B cell lymphoma-2 (Bcl-2), Bax and caspase-3 were also evaluated in the brains by immunohistochemistry. GAL treatment increased brain MDA and PC levels and AChE activities. It decreased significantly brain GSH levels, SOD and GSH-Px but not GST activities. GAL treatment caused histopathological changes and increased apoptosis. CAR and TAU significantly reduced brain AChE activities, MDA and PC levels and elevated GSH levels in GAL-treated rats. CAR, but not TAU, significantly increased low activities of SOD and GSH-Px. Both CAR and TAU diminished apoptosis and ameliorated histopathological findings in the brain of GAL-treated rats. Our results indicate that CAR and TAU may be effective to prevent the development of oxidative stress, apoptosis and histopathological deterioration in the brain of GAL-treated rats

Sarcoidosis and Coronary Bypass Surgery: A Case Report

Sarcoidosis, a chronic granulomatous disease with unknown etiology and pathogenesis, affects the skin and many other organs and has a course characterized by remissions and relapses. We describe a patient with sarcoidosis, which we diagnosed retrospectively after we had difficulties in harvesting the left internal thoracic artery because of giant and disseminated mediastinal lymphadenopathies on the anterior thoracic wall during urgent coronary artery bypass surgery

Expression of cyclooxygenase-2, c-kit, progesterone and estrogen receptors in uterine smooth muscle tumors: differential diagnosis

We examined the expression pattern of cyclooxygenase-2 (COX-2) and c-kit in uterine smooth muscle neoplasms and tried to determine the role of these markers in differential diagnosis. Archival tissue from 64 patients with uterine smooth muscle neoplasms (20 leiomyomas (LMs), 22 atypical leiomyomas (ALMs), and 22 leiomyosarcomas (LMSs)) was immunostained with antibodies against estrogen (ER) and progesterone receptors (PR), COX-2 and c-kit. 7 of 20 LM cases and 5 of 22 ALM cases were immunopositive for COX-2, whereas none of the LMS cases stained immunopositive (p <= 0.05). 4 of 20 LM cases and 5 of 22 ALM cases were immunopositive for c-kit, whereas 15 of 22 LMS cases showed c-kit immunopositivity (p <= 0.05). In conclusion, very few LMs and ALMs show COX-2 immunopositivity. LMSs usually do not express COX-2. COX-2 expression in smooth muscle tumors is not a prominent feature. Therefore, COX-2 inhibitors may not be useful in LMS therapy. C-kit was significantly expressed in uterine LMSs

Hydrodynamic cavitation kills prostate cells and ablates benign prostatic hyperplasia tissue

Hydrodynamic cavitation is a physical phenomenon characterized by vaporization and bubble formation in liquids under low local pressures, and their implosion following release to a higher pressure environment. Collapse of the bubbles releases high energy and may cause damage to exposed surfaces. We recently designed a set-up to exploit the destructive nature of hydrodynamic cavitation for biomedical purposes. We have previously shown that hydrodynamic cavitation could kill leukemia cells and erode kidney stones. In this study, we analyzed the effects of cavitation on prostate cells and benign prostatic hyperplasia (BPH) tissue. We showed that hydrodynamic cavitation could kill prostate cells in a pressure and time dependent manner. Cavitation did not lead to programmed cell death, i.e. classical apoptosis or autophagy activation. Following the application of cavitation, we observed no prominent DNA damage and cells did not arrest in the cell cycle. Hence, we concluded that cavitation forces directly damaged the cells, leading to their pulverization. Upon application to BPH tissues from patients, cavitation could lead to a significant level of tissue destruction. Therefore similar to ultrasonic cavitation, we propose that hydrodynamic cavitation has the potential to be exploited and developed as an approach for the ablation of aberrant pathological tissues, including BPH

Tumor-derived CTF1 (cardiotrophin 1) is a critical mediator of stroma-assisted and autophagy-dependent breast cancer cell migration, invasion and metastasis

Macroautophagy/autophagy is an evolutionarily conserved cellular stress response mechanism. Autophagy induction in the tumor microenvironment (stroma) has been shown to support tumor metabolism. However, cancer cell-derived secreted factors that initiate communication with surrounding cells and stimulate autophagy in the tumor microenvironment are not fully documented. We identified CTF1/CT-1 (cardiotrophin 1) as an activator of autophagy in fibroblasts and breast cancer-derived carcinoma-associated fibroblasts (CAFs). We showed that CTF1 stimulated phosphorylation and nuclear translocation of STAT3, initiating transcriptional activation of key autophagy proteins. Additionally, following CTF1 treatment, AMPK and ULK1 activation was observed. We provided evidence that autophagy was important for CTF1-dependent ACTA2/alpha-SMA accumulation, stress fiber formation and fibroblast activation. Moreover, promotion of breast cancer cell migration and invasion by activated fibroblasts depended on CTF1 and autophagy. Analysis of the expression levels of CTF1 in patient-derived breast cancer samples led us to establish a correlation between CTF1 expression and autophagy in the tumor stroma. In line with our in vitro data on cancer migration and invasion, higher levels of CTF1 expression in breast tumors was significantly associated with lymph node metastasis in patients. Therefore, CTF1 is an important mediator of tumor-stroma interactions, fibroblast activation and cancer metastasis, and autophagy plays a key role in all these cancer-related events