Ruptured cystic teratoma associated with mucinous cystadenoma in a pregnant woman.

Mature cystic teratoma is the most common ovarian neoplasm. However, mucinous cystadenoma with teratoma has been very rarely reported in literature. This case report, which is very rare, describes a clinical entity not previously reported in literature. A 34-year-old pregnant woman presented in the 23rd gestational week with severe right lower quadrant pain. She was diagnosed with acute abdomen and was then treated surgically. During the surgical intervention, a spontaneously ruptured mass was detected in the right ovary. This was reported histopathologically as a mature cystic teratoma in collision with mucinous cystadenoma. To the best of our knowledge, this case report is the first to have identified a ruptured mature cystic teratoma in collision with mucinous cystadenoma in a pregnant woman.

Reduced lipoapoptosis, hedgehog pathway activation and fibrosis in caspase-2 deficient mice with non-alcoholic steatohepatitis.

OBJECTIVE: Caspase-2 is an initiator caspase involved in multiple apoptotic pathways, particularly in response to specific intracellular stressors (eg, DNA damage, ER stress). We recently reported that caspase-2 was pivotal for the induction of cell death triggered by excessive intracellular accumulation of long-chain fatty acids, a response known as lipoapoptosis. The liver is particularly susceptible to lipid-induced damage, explaining the pandemic status of non-alcoholic fatty liver disease (NAFLD). Progression from NAFLD to non-alcoholic steatohepatitis (NASH) results, in part, from hepatocyte apoptosis and consequential paracrine-mediated fibrogenesis. We evaluated the hypothesis that caspase-2 promotes NASH-related cirrhosis. DESIGN: Caspase-2 was localised in liver biopsies from patients with NASH. Its expression was evaluated in different mouse models of NASH, and outcomes of diet-induced NASH were compared in wild-type (WT) and caspase-2-deficient mice. Lipotoxicity was modelled in vitro using hepatocytes derived from WT and caspase-2-deficient mice. RESULTS: We showed that caspase-2 is integral to the pathogenesis of NASH-related cirrhosis. Caspase-2 is localised in injured hepatocytes and its expression was markedly upregulated in patients and animal models of NASH. During lipotoxic stress, caspase-2 deficiency reduced apoptosis, inhibited induction of profibrogenic hedgehog target genes in mice and blocked production of hedgehog ligands in cultured hepatocytes. CONCLUSIONS: These data point to a critical role for caspase-2 in lipid-induced hepatocyte apoptosis in vivo for the production of apoptosis-associated fibrogenic factors and in the progression of lipid-induced liver fibrosis. This raises the intriguing possibility that caspase-2 may be a promising therapeutic target to prevent progression to NASH.

Myofibroblastic cells function as progenitors to regenerate murine livers after partial hepatectomy.

OBJECTIVE: Smoothened (SMO), a coreceptor of the Hedgehog (Hh) pathway, promotes fibrogenic repair of chronic liver injury. We investigated the roles of SMO+ myofibroblast (MF) in liver regeneration by conditional deletion of SMO in α smooth muscle actin (αSMA)+ cells after partial hepatectomy (PH). DESIGN: αSMA-Cre-ER(T2)×SMO/flox mice were treated with vehicle (VEH) or tamoxifen (TMX), and sacrificed 24-96 h post-PH. Regenerating livers were analysed for proliferation, progenitors and fibrosis by qRT-PCR and quantitative immunohistochemistry (IHC). Results were normalised to liver segments resected at PH. For lineage-tracing studies, αSMA-Cre-ER(T2)×ROSA-Stop-flox-yellow fluorescent protein (YFP) mice were treated with VEH or TMX; livers were stained for YFP, and hepatocytes isolated 48 and 72 h post-PH were analysed for YFP by flow cytometric analysis (FACS). RESULTS: Post-PH, VEH-αSMA-SMO mice increased expression of Hh-genes, transiently accumulated MF, fibrosis and liver progenitors, and ultimately exhibited proliferation of hepatocytes and cholangiocytes. In contrast, TMX-αSMA-SMO mice showed loss of whole liver SMO expression, repression of Hh-genes, enhanced accumulation of quiescent HSC but reduced accumulation of MF, fibrosis and progenitors, as well as inhibition of hepatocyte and cholangiocyte proliferation, and reduced recovery of liver weight. In TMX-αSMA-YFP mice, many progenitors, cholangiocytes and up to 25% of hepatocytes were YFP+ by 48-72 h after PH, indicating that liver epithelial cells were derived from αSMA-YFP+ cells. CONCLUSIONS: Hh signalling promotes transition of quiescent hepatic stellate cells to fibrogenic MF, some of which become progenitors that regenerate the liver epithelial compartment after PH. Hence, scarring is a component of successful liver regeneration.

Beneficial effects of Ankaferd Blood Stopper on caustic esophageal injuries: an experimental model.

Ankaferd Blood Stopper (ABS) is an herbal extract that enhances mucosal healing. The aim of this study was to investigate the efficacy of ABS on the healing of the esophagus and prevention of stricture development after esophageal caustic injuries in rats. The study included 50 rats. Rats were divided into five groups: group 1 (no injury, sham surgery), group 2 (injury + no ABS + study after 2 weeks of injury), group 3 (injury + ABS + study after 2 weeks of injury), group 4 (injury + no ABS + study after 4 weeks of injury), and group 5 (injury + ABS + study after 4 weeks of injury). Standard esophageal burn injury was created by applying 50% NaOH solution to distal esophagus of about 1.5 cm. To rats in the sham group, isotonic solution was given instead of NaOH. ABS (2 mL/day) was given via oral route to group 3 and 5 rats. Fourteen days (group 2 and 3) and 28 days (group 4 and 5) later, all the live rats were killed. The distal esophageal segments of all rats were removed and divided into two equal parts for biochemical and histopathological examination. Mortality rate, weight changes, inflammation, stenosis index (SI), and biochemical measurements were evaluated. The SI was found as 0.31 ± 0.03 in group 1, 0.533 ± 0.240 in group 2, 0.568 ± 0.371 in group 3, 0.523 ± 0.164 in group 4, and 0.28 ± 0.03 in group 5. The SI and inflammation in ABS-treatment group 5 was significantly lower than that in non-treatment group 4 (P= 0.005). There were no significant differences between inflammation and SI among other groups. The mortality rate was 14.2% in group 1, 37.5% in untreated group 2, 14.2% in ABS-treated group 3, 80% in untreated group 4, and 33.3% in ABS-treated group 5. The mortality rate in group 4 was significantly higher than other groups (P= 0.025). Decrease rates in mean body weights of the groups were as follows: group 1, 1%; group 2, 15%; group 3, 14%; group 4, 46%; and group 5, 15%. Biochemical tests other than albumin and creatinine were comparable among the groups. Treatment with ABS prevents inflammation, scar formation, weight loss, and mortality in esophageal caustic injuries. Additional studies to evaluate the clinical benefits of ABS in esophageal caustic injury are recommended.

Survey of Turkish practice evaluating the management of postdural puncture headache in the obstetric population (1).

Many surveys and meta-analysis concerning the management of postdural puncture headache (PDPH) in the obstetric population were published in the literature. Therefore, we aimed to determine the current practice and ideas in the management of PDPH in the Turkish obstetric population and to provide awareness of the responders about new solutions with a survey. The response rate was 70%. The management strategies against accidental dural puncture during epidural insertion were to leave the catheter in situ as a spinal catheter (36%, n = 28) or to re-site it at a different level (64%, n = 50). Although these results might reflect the current practice of this small sample, in order to follow the changes in these strategies and to catch almost a standard approach for the prevention and management of PDPH which is a serious complication affecting morbidity in this particular population, further surveys including most of the centers are required.

Stage is a prognostic factor for surgically treated patients with early-stage lip cancer for whom a 'wait and see' policy in terms of neck status has been implemented.

OBJECTIVES: To determine the locoregional control and survival rates (in terms of risk factors) of patients who underwent surgical resection of early-stage lip cancer and for whom a 'wait and see' policy in terms of neck status had been implemented. METHODS: The sociodemographic data, tumour stage, tumour characteristics and histopathological features of 41 patients with early-stage lip cancer were evaluated. Factors predictive of survival and locoregional recurrence were analysed. The five-year overall survival and disease-free survival rates were determined, and the prognostic risk factors were compared. RESULTS: The mean follow-up period was 60.5 months (range, 4-92 months). Age, sex, tumour stage, tumour thickness and volume, and perineural involvement were not predictive of locoregional recurrence or survival. Pathological tumour stage (T1 vs T2) was a prognostic factor for both five-year overall survival (87.3 vs 65.6 per cent, p = 0.042) and disease-free survival (88.6 vs 65.6 per cent, p = 0.037). CONCLUSION: Tumour stage was clearly a major factor affecting the prognosis of surgically treated patients with early-stage lip cancer for whom a 'wait and see' policy in terms of neck status had been implemented.

Prevention strategy for post dural puncture headache.

We report the anesthetic management of a parturient after an unintentional dural puncture while performing epidural anaesthesia for caesarean section and the strategy to prevent postdural puncture headache (PDPH). We injected the cerebrospinal fluid (CSF) back into the subarachnoid space and then administered intrathecal 1.5 mL 0.5% hyperbaric bupivacaine and fentanyl 20 microg to maintain CSF volume via epidural needle. The epidural catheter was inserted following re-identification of the epidural space for possible epidural top-up requirement and postoperative pain relief. After adding 3 mL of 0.5% isobaric bupivacaine via epidural catheter, sensory block level reached at T4 bilaterally. No PDPH was observed.

Evaluation of matrix metalloproteinase, myeloperoxidase, and oxidative damage in mesenteric ischemia-reperfusion injury.

BACKGROUND: In this study, we investigated the alterations of matrix metalloproteinase (MMP) and tissue inhibitors of metalloproteinases (TIMPs), acute inflammation, and oxidative damage in the circulatory system and the intestine in response to mesenteric ischemia/reperfusion (I/R). METHODS: Twenty-one rats were divided randomly into the following three groups (n = 7 in each group): a sham group (CG), an ischemic group (IG), and an I/R group (I/RG). MMP-9, TIMP-1, and myeloperoxidase (MPO) were measured using the enzyme-linked immunosorbent assay method, and lipid peroxidation (quantified as thiobarbituric acid reactive substances (TBARS) content), ischemia-modified albumin, the prooxidant-antioxidant balance (PAB), and ferric-reducing antioxidant power (FRAP) were measured spectrophotometrically. The degree of intestinal injury was evaluated according to the Chiu scoring system. RESULTS: A significant difference between the mean serum TIMP-1 and MMP-9 levels and the alanine transaminase activity was found among the groups. Compared with the I/RG group a significant difference in the mean tissue MMP-9, MPO, and TBARS levels in addition to the PAB and FRAP was found between the CG and IG groups. The level of MMP-9 also demonstrated a strong, positive, and valid correlation with the TBA-RS levels. A significant morphological change was observed in both the IG and the I/RG groups. The degree of intestinal injury was more severe in the I/R group and was characterized by either villous denudation or villous loss. CONCLUSIONS: These results suggest that MMP-9, TIMP-1, MPO, and oxidative stress may be important in the intestinal injury development that is induced by acute mesenteric I/R in a rat model. MMP-9 overexpression may increase the extent of intestinal villous loss, particularly when MMP-9 is upregulated by the TBARS present in the intestinal injury.

First Report of Root Rot of Bean and Soybean Caused by Rhizoctonia zeae in Turkey.

To determine the species of Rhizoctonia on bean and soybean plants grown in Samsun (Turkey), field surveys were performed at 104 locations during 2001 and 2002. Rhizoctonia spp. were obtained from isolations from the necrotic lesions on the hypocotyl and rhizosphere soils. Species were identified according to Ogoshi (3) on the basis of hyphal and colony morphology and anastomosis reaction with known tester isolates (provided by M. Hyakumachi, Gifu University, Japan). Fifty Rhizoctonia spp. isolates obtained from these locations were identified as Rhizoctonia zeae (teleomorph Waitea circinata var. zeae). Nine of the 27 bean isolates and 8 of the 23 soybean isolates were recovered from plant tissues. These isolates had optimum temperature (32°C) for growth. Colonies were orange when young, becoming salmon colored with age. Sclerotia formed both on the agar surface or submerged in the medium. Superficial sclerotia were more uniform and nearly spherical, mostly 0.2 to 0.5 mm in diameter, and they were first orange and then turned brown. Pathogenicity was tested with three R. zeae isolates grown on sterile oat seeds at 25°C for 10 days. Bean and soybean seedlings grown in 1-liter plastic pots containing sterile potting mix (field soil/composted manure/sand 2:2:1 [v/v]) at true-leaf stage were inoculated by placing five infested oat seeds adjacent to the roots. Sterile oat seeds were used for controls. After 3 to 4 weeks of incubation at 17 to 25°C in a glasshouse, roots of the plants were cleaned with tap water and evaluated for disease severity. Four replicate pots were used for each isolate/plant combination. All isolates produced superficial brown lesions on roots and hypocotyls similar to those observed on plants used for isolations and root growth declined. R. zeae was reisolated from the lesions on all bean and soybean plants used for the pathogenicity test. While R. zeae was previously reported from Johnsongrass roots (1) and corn kernels (2), to our knowledge, this is the first report of R. zeae isolated from bean and soybean plants and rhizosphere soils in Turkey. References: (1) E. Demirci, and C. Eken. Plant Dis. 83:200, 1999. (2) E. Demirci and S. Kordali. Plant Dis. 83:879, 1999. (3) A. Ogoshi. Rev. Plant. Prot. Res. 8:93, 1975.

Topoisomerase IIalpha maintains genomic stability through decatenation G(2) checkpoint signaling.

Topoisomerase IIalpha (topoIIalpha) is an essential mammalian enzyme that topologically modifies DNA and is required for chromosome segregation during mitosis. Previous research suggests that inhibition of topoII decatenatory activity triggers a G(2) checkpoint response, which delays mitotic entry because of insufficient decatenation of daughter chromatids. Here we examine the effects of both topoIIalpha and topoIIbeta on decatenatory activity in cell extracts, DNA damage and decatenation G(2) checkpoint function, and the frequencies of p16(INK4A) allele loss and gain. In diploid human fibroblast lines, depletion of topoIIalpha by small-interfering RNA was associated with severely reduced decatenatory activity, delayed progression from G(2) into mitosis and insensitivity to G(2) arrest induced by the topoII catalytic inhibitor ICRF-193. Furthermore, interphase nuclei of topoIIalpha-depleted cells showed increased frequencies of losses and gains of the tumor suppressor genetic locus p16(INK4A). This study shows that the topoIIalpha protein is required for decatenation G(2) checkpoint function, and inactivation of decatenation and the decatenation G(2) checkpoint leads to abnormal chromosome segregation and genomic instability.