Protective effects of Scutellaria baicalensis Georgi against hydrogen peroxide-induced DNA damage and apoptosis in HaCaT human skin keratinocytes

Oxidative stress due to excessive accumulation of reactive oxygen species (ROS) is one of the risk factors for the development of several chronic diseases. In this study, we investigated the protective effects of Scutellaria bai- calensis rhizome ethanol extract (SBRE) against oxidative stress-induced cellular damage and elucidated the un- derlying mechanisms in the HaCaT human skin keratinocyte cell line. Our results revealed that treatment with SBRE prior to hydrogen peroxide (H2O2) exposure significantly increased viability of aCaT cells. SBRE also effectively attenuated H2O2-induced comet tail formation and inhibited the H2O2-induced phosphorylation levels of the histone γH2AX, as well as the number of apoptotic bodies and Annexin V-positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondrial membrane po- tential loss by H2O2. Moreover, H2O2 enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)- polymerase, a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear fac- tor-erythroid 2-related factor 2 (Nrf2). According to our data, SBRE is able to protect HaCaT cells from H2O2- induced DNA damage and apoptosis through blocking cellular damage related to oxidative stress through a mech-anism that would affect ROS elimination and activating the Nrf2/HO-1 signaling pathway

Obsessive-Compulsive Behavior Disappearing after Left Capsular Genu Infarction

This case report describes a 74-year-old woman with obsessive-compulsive behaviors that disappeared following a left capsular genu infarction. The patient's capsular genu infarction likely resulted in thalamocortical disconnection in the cortico-basal ganglia-thalamocortical loop, which may have caused the disappearance of her obsessive-compulsive symptoms. The fact that anterior capsulotomy has been demonstrated to be effective for treating refractory obsessive-compulsive disorder further supports this hypothesis

Clinical effectiveness and safety of sirolimus in pediatric patients with complex vascular anomalies: necessitating personalized and comprehensive approaches

BackgroundManaging complex vascular anomalies in pediatric care requires comprehensive approaches. Sirolimus, an mTOR inhibitor with immunosuppressive and anti-angiogenic properties, offers promise. We evaluated sirolimus's effectiveness and safety in pediatric patients with complex vascular anomalies at a tertiary children's hospital.MethodsOur study included 20 patients, aged 1 month to 19 years, with diverse vascular anomalies resistant to conventional therapies or located in high-risk areas precluding surgery. The evaluation of response encompassed measuring the reduction in the size of the targeted vascular or lymphatic lesions as observed on radiologic imaging, along with considering improvements reported by the patients.ResultsPatients used sirolimus for a median of 2.1 years, ranging from 0.6–4.3 years. Results indicated that 60% of patients achieved complete or partial response (CR/PR), whereas 40% had stable disease (SD). Notably, no disease progression occurred. Lesion size assessment was complex, yet patients' self-reported improvements were considered. Three patients reinitiated sirolimus after discontinuation due to worsening lesions. Sirolimus treatment demonstrated good tolerability, with minor complications except for one case of Pneumocystis jiroveci pneumonia. Group comparisons based on response highlighted better outcomes in patients with vascular tumors (CR/PR group 58.0% vs. SD group 0.0%, P = 0.015) or localized measurable lesions (83.3% vs. 12.5%, P = 0.005).ConclusionOur study underscores sirolimus's potential for treating complex vascular anomalies in pediatric patients. Challenges associated with optimal treatment duration and concurrent interventions necessitate a comprehensive approach and genetic testing to optimize outcomes

Observation of oxide precipitates in InN nanostructures

We observed the formation of oxide precipitates (bcc-In(2)O(3)) in InN nanostructures formed during metal-organic chemical vapor deposition (MOCVD) and/or subsequent postgrowth procedures in H(2) ambient. It was found that InN is extremely unstable in H(2) ambient and the activation energy of N(2) desorption of InN is measured to be similar to 0.28 eV, which is one order of magnitude smaller than that of reported value of InN in vacuum. Instability of InN nanostructures under H(2) ambient together with residual oxidant in the reactor facilitates the formation of indium oxide precipitates in the nanostructure matrix during MOCVD or the oxidation of residual indium at the surface, resulting in indium oxide dots.open3

Transjugular insertion of biliary stent in patients with malignant biliary obstruction complicated by ascites with/without coagulopathy: a prospective study of 12 patients

PURPOSEIn patients with malignant biliary obstruction complicated by massive ascites, when endoscopy fails, safe routes for biliary decompression are needed as an alternative to percutaneous approach. We aimed to evaluate the safety and effectiveness of transjugular insertion of biliary stent (TIBS) in patients with malignant biliary obstruction complicated by massive ascites with or without coagulopathy.METHODSFrom March 2012 to December 2017, a total of 12 consecutive patients with malignant biliary obstructions treated with TIBS were enrolled in this study. Five patients had jaundice and cholangitis, while seven had jaundice only. Clinical parameters including technical and clinical success rates and complications following TIBS were evaluated. Overall survival and stent occlusion-free survival were assessed using Kaplan-Meier analysis.RESULTSThe indications for transjugular approach were massive ascites with (n=2) or without (n=10) coagulopathy. TIBS was technically successful in 11 of 12 patients. Clinical success was defined as successful internal drainage and was achieved in eight patients. The mean serum bilirubin level was initially 13.9±6.3 mg/dL and decreased to 4.9±5.3 mg/dL within 1 month after stent placement (P = 0.037). Two patients had procedure-related complications (hemobilia). During the follow-up period (mean, 30 days; range, 1–146 days), all 12 patients died of disease progression. The median overall survival and stent occlusion-free survival times were 19 days (95% confidence interval [CI], 16–22 days) and 19 days (95% CI, 12–26 days), respectively. There was no stent dysfunction in the eight patients that had successful internal drainage.CONCLUSIONTIBS appears to be safe, technically feasible, and clinically effective for patients with malignant biliary obstruction complicated by massive ascites with or without coagulopathy

Detection of ureaplasmas by the polymerase chain reaction in the amniotic fluid of patients with cervical insufficiency

Aims: The purpose of this study was to determine the clinical significance of detecting microbial footprints of ureaplasmas in amniotic fluid (AF) using specific primers for the polymerase chain reaction (PCR) in patients presenting with cervical insufficiency. Methods: Amniocentesis was performed in 58 patients with acute cervical insufficiency (cervical dilatation, >= 1.5 cm) and intact membranes, and without regular contractions (gestational age, 16-29 weeks). AF was cultured for aerobic and anaerobic bacteria as well as genital mycoplasmas. Ureaplasmas (Ureaplasma urealyticum and Ureaplasma parvum) were detected by PCR using specific primers. Patients were divided into three groups according to the results of AF culture and PCR for ureaplasmas: those with a negative AF culture and a negative PCR (n = 44), those with a negative AF culture and a positive PCR (n = 10), and those with a positive AF culture regardless of PCR result (n = 4). Results: 1) Ureaplasmas were detected by PCR in 19.0% (11/58) of patients, by culture in 5.2% (3/58), and by culture and/or PCR in 22.4% (13/58); 2) Among the 11 patients with a positive PCR for ureaplasmas, the AF culture was negative in 91% (10/11); 3) Patients with a negative AF culture and a positive PCR for ureaplasmas had a significantly higher median AF matrix metalloproteinase-8 (MMP-8) concentration and white blood cell (WBC) count than those with a negative AF culture and a negative PCR (P < 0.001 and P < 0.05, respectively); 4) Patients with a positive PCR for ureaplasmas but a negative AF culture had a higher rate of spontaneous preterm birth within two weeks of amniocentesis than those with a negative AF culture and a negative PCR (P < 0.05 after adjusting for gestational age at amniocentesis); 5) Of the patients who delivered within two weeks of amniocentesis, those with a positive PCR for ureaplasmas and a negative AF culture had higher rates of histologic amnionitis and funisitis than those with a negative AF culture and a negative PCR (P < 0.05 after adjusting for gestational age at amniocentesis, for each); 6) However, no significant differences in the intensity of the intra-amniotic inflammatory response and perinatal outcome were found between patients with a positive AF culture and those with a negative AF culture and a positive PCR. Conclusions: 1) Cultivation techniques for ureaplasmas did not detect most cases of intra-amniotic infection caused by these microorganisms (91% of cases with cervical insufficiency and microbial footprints for ureaplasmas in the amniotic cavity had a negative AF culture); 2) Patients with a negative AF culture and a positive PCR assay were at risk for intra-amniotic and fetal inflammation as well as spontaneous preterm birth.Park CW, 2009, PLACENTA, V30, P56, DOI 10.1016/j.placenta.2008.09.017KIEFER DG, 2009, AM J OBSTET GYNECOL, V200Mazaki-Tovi S, 2008, J PERINAT MED, V36, P485, DOI 10.1515/JPM.2008.084Park CW, 2008, J PERINAT MED, V36, P497, DOI 10.1515/JPM.2008.079Viscardi RM, 2008, J PERINATOL, V28, P759, DOI 10.1038/jp.2008.98Lee SE, 2008, J PERINAT MED, V36, P316, DOI 10.1515/JPM.2008.067Gotsch F, 2008, J MATERN-FETAL NEO M, V21, P529, DOI 10.1080/14767050802127349Hamill N, 2008, J PERINAT MED, V36, P217, DOI 10.1515/JPM.2008.034Gotsch F, 2008, J MATERN-FETAL NEO M, V21, P605, DOI 10.1080/14767050802212109Nhan-Chang CL, 2008, J MATERN-FETAL NEO M, V21, P763, DOI 10.1080/14767050802244946Kusanovic JP, 2008, J MATERN-FETAL NEO M, V21, P902, DOI 10.1080/14767050802320357BUJOLD E, 2008, J OBSTET GYNAECOL CA, V30, P882ONDERDONK AB, 2008, AM J OBSTET GYNECOL, V199, pNI114Erez O, 2008, J PERINAT MED, V36, P377, DOI 10.1515/JPM.2008.082LEE SE, 2008, AM J OBSTET GYNECOL, V198Holst RM, 2007, J MATERN-FETAL NEO M, V20, P885, DOI 10.1080/14767050701752601Aaltonen R, 2007, BJOG-INT J OBSTET GY, V114, P1432, DOI 10.1111/j.1471-0528.2007.01410.xFriel LA, 2007, J PERINAT MED, V35, P385, DOI 10.1515/JPM.2007.101LEE SE, 2007, AM J OBSTET GYNECOL, V197Hassan S, 2006, J PERINAT MED, V34, P13, DOI 10.1515/JPM.2006.002Waites KB, 2005, CLIN MICROBIOL REV, V18, P757, DOI 10.1128/CMR.18.4.757-789.2005Biggio JR, 2005, AM J OBSTET GYNECOL, V192, P109, DOI 10.1016/j.ajog.2004.06.103Shim SS, 2004, AM J OBSTET GYNECOL, V191, P1339, DOI 10.1016/j.ajog.2004.06.085Perni SC, 2004, AM J OBSTET GYNECOL, V191, P1382, DOI 10.1016/j.ajog.2004.05.070Yoon BH, 2003, AM J OBSTET GYNECOL, V189, P919, DOI 10.1067/S0002-9378(03)00839-1Jacobsson B, 2003, ACTA OBSTET GYN SCAN, V82, P423Gerber S, 2003, J INFECT DIS, V187, P518Fortunato SJ, 2002, J ASSIST REPROD GEN, V19, P483Viscardi RM, 2002, PEDIATR DEVEL PATHOL, V5, P141, DOI 10.1007/s10021-001-0134-yYoon BH, 2001, AM J OBSTET GYNECOL, V185, P1130Park JS, 2001, AM J OBSTET GYNECOL, V185, P1156Yoon BH, 2000, AM J OBSTET GYNECOL, V183, P1130, DOI 10.1067/mob.2000.109036Maymon E, 2000, AM J OBSTET GYNECOL, V183, P94, DOI 10.1067/mob.2000.105344Li YH, 2000, PEDIATR RES, V48, P114Mays JK, 2000, OBSTET GYNECOL, V95, P652Yoon BH, 2000, AM J OBSTET GYNECOL, V182, P675BASHIRI N, 1999, PRIMARY CARE UPDATE, V6, P82Luki N, 1998, EUR J CLIN MICROBIOL, V17, P255Yoon BH, 1997, AM J OBSTET GYNECOL, V177, P19Cunliffe NA, 1996, J MED MICROBIOL, V45, P27AbeleHorn M, 1996, EUR J CLIN MICROBIOL, V15, P595YOON BH, 1995, AM J OBSTET GYNECOL, V172, P960TENG K, 1994, J CLIN MICROBIOL, V32, P2232BLANCHARD A, 1993, CLIN INFECT DIS S1, V17, P148ROMERO R, 1992, AM J OBSTET GYNECOL, V167, P1086GRAY DJ, 1992, PRENATAL DIAG, V12, P111TREADWELL MC, 1991, AM J OBSTET GYNECOL, V165, P555ROMERO R, 1989, AM J OBSTET GYNECOL, V161, P817CHARLES D, 1981, AM J OBSTET GYNECOL, V141, P1065

Preliminary Experience of Amnioinfusion

Oligohydramnios is considered as one of the major obstetrical dilemmas for the multiple serious complications associated with the condition. The condition hampers an appropriate ultrasonographic evaluation of the fetal anatomy and frequently causes variable fetal heart rate decelerations by compressing the fetal cord, often to incur irreversible damage to the fetus. Based on precedent reports regarding the effect of amnioinfusion in managing oligohydramnios-complicated pregnancies, we report here our experience of amnioinfusion in 8 cases complicated by oligohydramnios which we have experienced from November of 1990 to May of 1993 at Seoul National University Hospital(SNUH). The procedure was applied largely for three purposes, viz., diagnostic(3cases), therapeutic (4cases), and prophylactic(lcase) with favorable results. We concluded that amnioinfusion can be of important use in the detection of fetal anomalies, relief of abnormal fetal heart rate pattern, and prevention of intrapartum fetal complications

Duodenal Mucosa-Associated Lymphoid Tissue Lymphoma: A Case Report

Primary duodenal mucosa associated lymphoid tissue (MALT) lymphoma is very rare, and little is known about its clinical course or effective treatment. We describe a case of primary duodenal MALT lymphoma that was resistant to Helicobacter pylori (H. pylori) eradication and regressed after chemotherapy with cyclophosphamide, vincristine, and prednisolone (CVP). A 71-year-old woman was referred to our department because of epigastric pain and dyspepsia. Gastroduodenoscopy revealed an irregular mucosal nodular lesion with ulceration extending from the bulb to the second portion of the duodenum. Histopathological examination of a biopsy specimen disclosed low-grade MALT lymphoma composed of atypical lymphoid cells with lymphoepithelial lesion. Abdominal CT scans revealed 0.5 to 1.5 cm lymph nodes in the peritoneal cavity, suggestive of lymph node metastasis. We successfully eradicated H. pylori but did not see signs of remission. We administered systemic CVP chemotherapy every 3 weeks. After 6 courses of CVP, the patient achieved complete remission and was followed up without recurrence for about a year

Recessive C10orf2 mutations in a family with infantile-onset spinocerebellar ataxia, sensorimotor polyneuropathy, and myopathy

Recessive mutations in chromosome 10 open reading frame 2 (C10orf2) are relevant in infantile-onset spinocerebellar ataxia (IOSCA). In this study, we investigated the causative mutation in a Korean family with combined phenotypes of IOSCA, sensorimotor polyneuropathy, and myopathy. We investigated recessive mutations in a Korean family with two individuals affected by IOSCA. Causative mutations were investigated using whole exome sequencing. Electrophysiological analyses and muscle and nerve biopsies were performed, along with magnetic resonance imaging (MRI) of the brain and lower extremities. Compound heterozygous mutations c.1460C>T and c.1485-1G>A in C10orf2 were identified as causative of IOSCA. Skeletal muscle showed mitochondrial DNA (mtDNA) deletions. Both patients showed a period of normal development until 12–15 months, followed by ataxia, athetosis, hearing loss, and intellectual disability. Electrophysiological findings indicated motor and sensory polyneuropathies. Muscle biopsy revealed variations in the size and shape of myofibers with scattered, small, and angulated degenerating myofibers containing abnormal mitochondria; these observations are consistent with myopathy and may be the result of mtDNA deletions. Sural nerve biopsy revealed an axonal neuropathy. High-signal-intensity lesions in the middle cerebellar peduncles were correlated with clinical severity, and MRI of the lower legs was compatible with the hypothesis of length-dependent axonal degeneration. We identified novel compound heterozygous mutations of the C10orf2 gene as the cause of IOSCA with sensorimotor polyneuropathy and myopathy. Signs of motor neuropathy and myopathy were discovered for the first time in IOSCA patients with C10orf2 mutations. These results suggest that the clinical spectrum of IOSCA caused by C10orf2 mutations may be more variable than previously reported. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10048-014-0405-1) contains supplementary material, which is available to authorized users