An interesting mediastinal cyst case: Benign cystic mesothelioma.

Anterior mediastinal, well-defined, ametabolic cystic lesion was detected incidentally in a 69-year-old male patient. Uniportal videothoracoscopic surgery was performed to the lesion for diagnosis and treatment purposes. Histopathological findings were in accordance with "benign cystic mesothelioma". Benign cystic mesothelioma has been defined in the abdomen, particularly among females of reproductive age. Benign cystic mesothelioma originating from mediastinal pleura is very rare entity and was not defined in the literature. To our knowledge, we present this rare and interesting mediastinal cystic lesion for the first time in the literature.

Induction of apoptosis and down regulation of cell cycle proteins in mantle cell lymphoma by flavopiridol treatment.

Typical mantle cell lymphoma (MCL) is a distinct B-cell non-Hodgkin's lymphoma associated with over-expression of cyclin D1 related to translocation between the IgH and BCL-1 genes. Due to the important functional interaction between cyclin D1 and cyclin dependent kinases, cyclin dependent kinase inhibitors such as flavopiridol are under consideration for treatment of patients with MCL. The present study investigated the in vitro effects of flavopiridol on the MCL cell line (JeKo-1). Flavopiridol at a dose of 10nmol/L induced apoptosis by 6h of treatment as noted by flow cytometric analysis, morphologic examination and Western blotting. The cleavage of procaspase-3 and PARP and the decrease of flavopiridol-induced apoptosis by pan-caspase inhibition suggested that the caspase pathway serves an important role in the apoptotic process. Furthermore, MCL cells exposed to flavopiridol showed down regulation of key cell cycle proteins acting at the restriction point control between the G1 and S phases. The onset of flavopiridol-induced apoptosis also coincided with the down regulation of Mcl-1, anti-apoptotic protein. Collectively, our data indicates that flavopiridol may have significant therapeutic potential in the context of MCL.

Evaluation of cardiovascular risk factors in women with uterine leimyoma: is there a link with atherosclerosis?

OBJECTIVE: Both uterine leimyoma (UL) and cardiovascular disease are public health problems affecting women at different age ranges. Smoking, obesity, and hypertension have been shown to be associated with UL in different random studies. However cardiovascular risk factors have not been evaluated systematically in patients with UL. Accordingly, we aimed to evaluate the cardiovascular risk factors and their relation with the presence of UL. MATERIAL AND METHODS: One hundred and eighty nine patients with the pathological diagnosis of UL and one hundred and eighty nine age matched control subjects without UL were retrospectively included in the study from our data base of the pathology and gynecology departments. Controls were patients with intact uteri who had visited the same physicians for a routine checkup that included a pelvic examination and uterine sonogram and without mention of physical findings consistent with UL. The following clinical and demographic parameters were recorded; age, sex, hypertension, diabetes mellitus, and hypercholesterolemia. Current cigarette smoking was defined as active smoking within the past 12 months. RESULTS: Comparison of cardiovascular risk factors between with and without UL revealed that the presence of hypertension (80 (42.3%) vs 53 (28%) p=0.004) diabetes mellitus (33 (17.4%) vs. 16 (8.4%) p=0.009), smoking (31 (16.4%) vs. 11 (5.8%) p=0.001), were significantly higher in patients with UL than in control subjects. The mean-age and presence of hyperlipidemia were comparable between the two groups. Logistic regression analysis revealed an independent and positive association of UL with the presence of hypertension (odds ratio 2.02 CI: 1.25-3.27 p=0.004), diabetes mellitus (odds ratio 2.43 CI: 1.23-4.79 p=0.010), and smoking status (odds ratio 3.46 CI: 1.65-7.22 p=0.001). CONCLUSION: We have shown that major cardiovascular risk factors namely, hypertension, diabetes mellitus and smoking are significantly and independently associated with UL. Our findings highlight the possible association of UL with atherosclerosis.

Protective effect of L-carnitine versus amifostine against cisplatin-induced nephrotoxicity in rats.

We aimed to compare the protective effect of L-carnitine (CAR) and amifostine (AMF) against cisplatin (CDDP)-induced nephrotoxicity through biochemical markers and histopathological evaluation. Fifty-seven Wistar albino male rats were randomly classified into six groups, which were AMF+CDDP (n = 11; 200 mg/kg AMF 30 min prior to 7 mg/kg CDDP), CAR+CDDP (n = 11; 300 mg/kg CAR 30 min prior to 7 mg/kg CDDP), CDDP (n = 11; 1 mL/kg isotonic saline 30 min prior to 7 mg/kg CDDP), AMF (n = 8; 200 mg/kg AMF alone), CAR (n = 8; 300 mg/kg CAR alone), and control (n = 8; 1 mL/kg isotonic saline alone). All drugs were given intraperitoneally. Five days after medication, animals were killed, and samples of blood and kidney tissues were collected for biochemical and histopathological evaluation. The serum urea level was highest in AMF+CDDP group among CDDP-applied groups without statistical significance (median, range: 88, 56-21 mg/dL; P > 0.05). There was no statistical significance among CDDP-applied groups in terms of creatinine level (P > 0.05). In the AMF+CDDP group, the median glomerular, tubular, and tubulointerstitial inflammatory damage scores were significantly higher than the other CDDP-applied groups (P < 0.001). The difference between CAR+CDDP and CDDP groups was not statistically significant in terms of renal damage scores. AMF+CDDP group had significantly higher median total nephrotoxicity score than all the other groups (P < 0.001). To conclude, AMF or CAR has no protective effect on CDDP-induced nephrotoxicity. Furthermore, our findings suggest that application of AMF before CDDP may enhance CDDP-induced nephrotoxicity histopathologically.

Influence of N-acetylcysteine on renal toxicity of cadmium in rats.

The aim of this study was to investigate the ability of N-acetylcysteine (NAC) to prevent cadmium (Cd)-induced renal damage and whether NAC would reverse cadmium damage to the kidney. Fifty adult male rats were divided into five experimental groups: group 1 received tap water for 3 months and 7 days, group 2 received cadmium chloride (CdCl(2)) for 3 months, group 3 (NAC cotreatment group) received CdCl(2) and 0.5% NAC in tap water for 3 months, group 4 received CdCl(2) in tap water for 3 months and 3 months later received only tap water for 7 days, and group 5 (NAC posttreatment group) received CdCl(2) in tap water for 3 months and 3 months later received 2% NAC in tap water for 7 days. NAC significantly decreased the elevated kidney malondialdehyde levels, as a marker of lipid peroxidation, in both cotreatment and posttreatment modalities. Cotreatment and posttreatment with NAC significantly increased kidney superoxide dismutase enzyme activity and glutathione level but did not change kidney catalase enzyme activity. NAC decreased fractional excretion of sodium in posttreatment group. Neither Cd nor NAC affected the glomerular filtration rate (GFR). Cotreatment and posttreatment with NAC reduced the effects of Cd on proximal tubules. It was found that NAC showed these effects without changing kidney accumulation of cadmium. Exogenously administrated NAC might reduce toxic effects of Cd on the kidney without any reduction in tissue Cd level.

Survival role of protein kinase C (PKC) in chronic lymphocytic leukemia and determination of isoform expression pattern and genes altered by PKC inhibition.

Recent studies have suggested that protein kinase C (PKC) activation plays an important role in survival of chronic lymphocytic leukemia (CLL). In order to characterize the role of PKC in CLL, we investigated the expression pattern of PKC isoforms in CLL cells (7 cases) and evaluated the effect of PKC inhibition on the survival of CLL cells (20 cases). Expression of the classical PKC isoforms beta and gamma, the novel isoform delta and the atypical isoform zeta was seen in all analyzed patient samples by Western blot analysis. Expression of the PKC isoforms alpha, epsilon, and iota was variable. Following incubation with the PKC inhibitor, safingol, CLL cells underwent marked apoptosis in all cases. In order to characterize the molecular events associated with the apoptotic effect of PKC inhibition, gene expression patterns in CLL cells were evaluated by cDNA-microarray analysis. Following safingol treatment, several genes showed marked downregulation and PKC-related proteins demonstrated decreased hybridization signals. Among these proteins, CREB and Daxx were further studied by using Western blotting, nuclear binding assay and confocal immunofluorescent microscopy. These studies showed significant inhibition of these proteins, consistent with the results of microarray gene analysis. Overall, these findings suggest that PKC activation is important for CLL cell survival and that inhibitors of PKC may have a role in the treatment of patients with CLL.