A multicentre comparative study between laparoscopic and open surgery for intussusception in adults.

AIM: Intussusception in adults is rare and requires surgery in most cases. While abdominal laparoscopic surgery (LS) is becoming more popular, there are few reports on the outcomes of adult intussusception treated with LS. This study compared the feasibility of LS vs open surgery (OS) for adult intussusception. METHOD: We reviewed retrospectively the medical records of adult patients with intussusception from three tertiary hospitals between 2000 and 2016. The patients were divided into LS and OS groups, and their surgical outcomes were compared. RESULTS: Surgery was indicated in 71 patients with intussusception (41 LS and 30 OS). The median age of the patients was 49.0 and 51.5 years in the LS and OS groups, respectively (P = 0.930). Overall, nine (12.7%) patients had a negative laparotomy or laparoscopy with spontaneous reduction of the intussusception. Conversion to OS from LS was necessary in one patient (2.4%). The operative time and intra-operative and postoperative complication rates were not significantly different. However, there were more serious complications such as bowel perforation and major vessel injury in the LS group. The patients in the LS group had a shorter time to first food intake and hospital stay vs patients in the OS group (4.0 vs 6.0 days, P < 0.001, and 7.0 vs 10.5 days, P < 0.001, respectively). CONCLUSION: LS may be feasible for adult intussusception; there may be more severe intra-operative complications than in OS.

The MYTHS of De novo Crohn's Disease After Restorative Proctocolectomy with Ileal Pouch-anal Anastomosis for Ulcerative Colitis.

Background: 1.1.Inflammatory Bowel Disease (IBD) are the manifestation of overzealous dys-regulated immune response in the intestinal tract, directed primarily against the indigenous microbes combined with defective functioning of anti-inflammatory pathways. Finding a trustable lead to predicting de novo Crohn's Disease (CD) prior to performing "pouch surgery", Restorative Proctocolectomy (RPC) with Ileal Pouch-Anal Anastomosis (IPAA) for UC and/or Indeterminate Colitis (IC) is clinically important and remains debatable. De novo CD is a subsequent long-term postoperative complication in IBD patients with Ulcerative Colitis (UC) undergoing IPAA. Herewith we discuss this understanding in laboratory-based basic science research, with its molecular application as a possible corner stone tool for clinical progress and success in the IBD Clinic. Crypt Paneth cell (PCs) secreted enteroendocrine alpha-defensin 5 (DEFA5)" if developed properly is likely to solve diagnostic and prognostic difficulty in IBD Clinics. DEFA5 has shown the ability to differentiate the predominant subtypes of colonic IBD (CC vs. UC) at first endoscopy biopsy, avoiding diagnosis delay prior to colectomy. In addition, DEFA5 accurately circumvents indeterminate colitis (IC) patients into accurate IBD subtype (UC or CC). Further, DEFA5 can be used in selecting CC patients that may have positive outcomes after IPAA surgery [1]. Furthermore, likewise, DEFA5 can predict UC patients likely to have positive or poor outcome, e.g. those patients that are likely to transform/ convert and adhere to de novo Crohn's after IPAA can be picked up in endoscopy biopsy before surgery. Aim: 1.2.To assessed comprehensive state-of-the-art understanding domains on the de novo Crohn's disease subsequent to IPAA surgery for ulcerative colitis. Methods: 1.3.A literature search based on preferred reporting items for over-review and meta-analysis protocols (PRISMA-P) was performed. A comprehensive current search of PubMed, MEDLINE, CINAHL, Embase, Google® search engine and Cochrane Database of collected reviews was performed from January 1990 through December 2018. The search consists of retrospective studies and case reports of reporting postoperative de novo CD incidence and adverse events. Secondary and hand/manual searches of reference lists, other studies cross-indexed by authors, reviews, commentaries, books and meeting abstracts were also performed. Studies were included only if the diagnosis of de novo CD was established clinically and histologically based on inflammation of afferent limb(s) or perianal disease. The search excluded non-English language and non-human studies as well as editorials. Results: 1.4.Published data on de novo CD developing after RPC with IPAA are still limited. A total of three hundred and sixty-five (#365) patients in 13 publications reported de novo CD after a median follow-up of 66 (range: 3-236) months. All patients were diagnosed with clinically active pouch CD during follow-up surveillance after IPAA for UC or IC. A de novo CD diagnosis depended on either inflammation in the mucosa involving the small intestine proximal to the ileal pouch any time after IPAA surgery and/or when perianal complications developed after closure of a temporary diverting loop ileostomy. Successful management is facilitated by co-operation within a multidisciplinary team of gastroenterologists and colorectal surgeons and closely involving the patient in therapeutic decisions. Awareness of symptoms leads to timely consultation, diagnosis, treatment and restoration of intestinal continuity. Conclusion: 1.5.The nature history and risk of de novo CD after IPAA for UC remains debatable. Chronic pouchitis and/or pouch failure often precedes a diagnosis of de novo CD. A successful management is facilitated by a triad cooperation between gastroenterologists, colorectal surgeons and the patient.

Isoform specific differences in phospholipase C beta 1 expression in the prefrontal cortex in schizophrenia and suicide.

Our previous study demonstrated that phospholipase C beta 1 mRNA was down-regulated in Brodmann's area 46 from subjects with schizophrenia. However, phospholipase C beta 1 protein has also been shown to be lower in Brodmann's area 8 and 9 from teenage suicide subjects, creating a potential confound in interpreting the findings in schizophrenia due to the high suicide rate associated with this disorder. To begin to reconcile and consolidate these findings, in this study, we measured mRNA and protein levels of phospholipase C beta 1 variants a and b in Brodmann's area 46 and Brodmann's area 9 from subjects with schizophrenia, many of whom were suicide completers, and determined the diagnostic specificity of observed findings. Consistent with our previous study, levels of phospholipase C beta 1 a and b mRNA, but not protein, were lower in Brodmann's area 46 from subjects with schizophrenia. In Brodmann's area 9, phospholipase C beta 1a protein levels were lower in subjects with schizophrenia, while phospholipase C beta 1b mRNA was higher and protein was lower in those that had died of suicide. Altered protein levels in Brodmann's area 9 appeared to be diagnostically specific, as we did not detect these changes in subjects with bipolar disorder, major depressive disorder or suicide completers with no diagnosis of mental illness. We further assessed the relationship between phospholipase C beta 1 and levels of muscarinic receptors (CHRMs) that signal through this protein, in both human and Chrm knockout mouse central nervous system tissue, and found no strong relationship between the two. Understanding central nervous system differences in downstream effector pathways in schizophrenia may lead to improved treatment strategies and help to identify those at risk of suicide.

Midterm outcomes of injectable bulking agents for fecal incontinence: a systematic review and meta-analysis.

BACKGROUND: Various bulking agents have been used to treat fecal incontinence. While short-term outcomes are attractive, there is still a lack of long-term data. The aim of this systematic review and meta-analysis was to investigate the midterm outcomes of treatment with injectable bulking agents and to identify predictive factors for improvement in incontinence. METHODS: PubMed, EMBASE, Web of Science, and Cochrane Library databases were searched using the terms injection, bulking agents, and fecal incontinence. Studies with a minimum follow-up of 1 year were included. The improvement rate in incontinence was calculated by percent change in validated fecal incontinence score (FIS) following injection treatment. To explore the impact of predictive factors on improvement in incontinence, univariate meta-regressions were conducted using the random-effect model. RESULTS: A total of 889 patients in 23 articles were included. The weighted mean follow-up duration was 23.7 months (95% CI 19.3-28.2). Eleven different bulking agents were used. Four validated FISs were used. The Cleveland Clinic Fecal Incontinence score (CC-FIS) was used in 19 studies. Most studies reported a statistically significant improvement in FIS. The pooled mean preoperative CC-FIS (n = 637) was 12.4 (95% CI 11.4-13.3). The pooled mean CC-FIS at last follow-up (n = 590) was 7.7 (95% CI 6.1-9.3). The weighted mean difference in CC-FIS between preoperative visit and last follow-up was 4.9 (95% CI 4.0-5.8). Hence, the rate of improvement in incontinence was 39.5% based on CC-FIS. Meta-regression revealed that the perianal injection route and implants intact on endoanal ultrasonography were predictive of greater improvement in incontinence. The manometric data revealed that the initial increase in the mean resting pressure following injection was attenuated over time. The pooled rate of adverse events was 18.0% (95% CI 10.0-30.1). In most cases, adverse events were minor and resolved within a couple of weeks. CONCLUSIONS: Administration of injectable bulking agents results in significant midterm improvement in FIS. Perianal injection route and implants intact on EAUS were predictive of higher improvement in incontinence. However, given the paucity of randomized controlled trials in the literature, further research is needed to improve the quality of the evidence.

Proteolytic degradation and potential role of onconeural protein cdr2 in neurodegeneration.

Cerebellar degeneration-related protein 2 (cdr2) is expressed in the central nervous system, and its ectopic expression in tumor cells of patients with gynecological malignancies elicits immune responses by cdr2-specific autoantibodies and T lymphocytes, leading to neurological symptoms. However, little is known about the regulation and function of cdr2 in neurodegenerative diseases. Because we found that cdr2 is highly expressed in the midbrain, we investigated the role of cdr2 in experimental models of Parkinson's disease (PD). We found that cdr2 levels were significantly reduced after stereotaxic injection of 1-methyl-4-phenylpyridinium (MPP(+)) into the striatum. cdr2 levels were also decreased in the brains of post-mortem PD patients. Using primary cultures of mesencephalic neurons and MN9D cells, we confirmed that MPP(+) reduces cdr2 in tyrosine hydroxylase-positive dopaminergic neuronal cells. The MPP(+)-induced decrease of cdr2 was primarily caused by calpain- and ubiquitin proteasome system-mediated degradation, and cotreatment with pharmacological inhibitors of these enzymes or overexpression of calcium-binding protein rendered cells less vulnerable to MPP(+)-mediated cytotoxicity. Consequently, overexpression of cdr2 rescued cells from MPP(+)-induced cytotoxicity, whereas knockdown of cdr2 accelerated toxicity. Collectively, our findings provide insights into the novel regulatory mechanism and potentially protective role of onconeural protein during dopaminergic neurodegeneration.

Emergent Synapse Organizers: LAR-RPTPs and Their Companions.

Leukocyte common antigen-related receptor tyrosine phosphatases (LAR-RPTPs) have emerged as key players that organize various aspects of neuronal development, including axon guidance, neurite extension, and synapse formation and function. Recent research has highlighted the roles of LAR-RPTPs at neuronal synapses in mediating distinct synaptic adhesion pathways through interactions with a host of extracellular ligands and in governing a variety of intracellular signaling cascades through binding to various scaffolds and signaling proteins. In this chapter, we review and update current research progress on the extracellular ligands of LAR-RPTPs, regulation of their extracellular interactions by alternative splicing and heparan sulfates, and their intracellular signaling machineries. In particular, we review structural insights on complexes of LAR-RPTPs with their various ligands. These studies lend support to general molecular mechanisms underlying LAR-RPTP-mediated synaptic adhesion and signaling pathways.

Rubi Fructus (Rubus coreanus) activates the expression of thermogenic genes in vivo and in vitro.

OBJECTIVE: To investigate the anti-obesity effect of Rubi Fructus (RF) extract using brown adipose tissue (BAT) and primary brown preadipocytes in vivo and in vitro. METHODS: Male C57BL/6 J mice (n=5 per group) were fed a high-fat diet (HFD) for 10 weeks with or without RF. Brown preadipocytes from the interscapular BAT of mice (age, post-natal days 1-3) were cultured with differentiation media (DM) including isobutylmethylxanthine, dexamethasone, T3, indomethacin and insulin with or without RF. RESULTS: In HFD-induced obese C57BL/6 J mice, long-term RF treatment significantly reduced weight gain as well as the weights of the white adipose tissue, liver and spleen. Serum levels of total cholesterol and low-density lipoprotein cholesterol were also reduced in the HFD group which received RF treatment. Furthermore, RF induced thermogenic-, adipogenic- and mitochondria-related gene expressions in BAT. In primary brown adipocytes, RF effectively stimulated the expressions of thermogenic- and mitochondria-related genes. In addition, to examine whether LIPIN1, a regulator of adipocyte differentiation, is regulated by RF, Lipin1 small interfering RNA (siRNA) and RF were pretreated in primary brown adipocytes. Pretreatment with Lipin1 siRNA and RF downregulated the DM-induced expression levels of thermogenic- and mitochondria-related genes. Moreover, RF markedly upregulated AMP-activated protein kinase. Our study shows that RF is capable of stimulating the differentiation of brown adipocytes through the modulation of thermogenic genes. CONCLUSIONS: This study demonstrates that RF prevents the development of obesity in mice fed with a HFD and that it is also capable of stimulating the differentiation of brown adipocytes through the modulation of thermogenic genes, which suggests that RF has potential as a therapeutic application for the treatment or prevention of obesity.

Comparison of growth performance, carcass characteristics and meat quality of korean local chickens and silky fowl.

This study was conducted to compare growth performance, carcass characteristics and meat quality of 4 breeds of local chicken. A total of 480 1-d-old chicks were distributed to 16 pens, with 4 treatments of breed, 4 replicates and 30 chicks per pen. Three Korean local breeds of white-mini broiler, Hanhyup-3-ho, and Woorimatdag, and a breed of silky fowl were raised under identical rearing and feeding conditions for 31-d, 37-d, 36-d, and 59-d, respectively. The BW and feed consumption on a pen basis were weekly measured for all pens, and ADFI, ADG and gain:feed were calculated for each pen. The ADFI and ADG of 3 breeds of Korean local chicken were greater than those of silky fowl (p<0.05). Within the Korean local breeds, ADFI of white-mini broiler was the highest (p<0.05), and ADG of Hanhyup-3-ho and white-mini broiler was the highest (p<0.05). Gain:feed of silky fowl was less than that of the 3 breeds of Korean local chicken. The carcass and breast yield of white-mini broiler were the greater than those of other breeds (p<0.05). The breast meat color (CIE L*, a*, and b*) of 3 breeds of Korean local chicken were higher than that of silky fowl (p<0.05). The breast meat of Hanhyup-3-ho had greater cooking loss (p<0.05), whereas water holding capacity and pH were less than those of other breeds (p<0.05). The color score of 3 breeds of Korean local chicken was higher than that of silky fowl (p<0.05). Woorimatdag had a higher score on tenderness (p<0.05), whereas flavor score was less than that of other breeds (p<0.05). In conclusion, 4 local breeds of chicken have some unique features and seem to have more advantages, and this information can help consumers who prefer healthy and premium chicken meat.

Activation of TLR4 induces VEGF expression via Akt pathway in nasal polyps.

BACKGROUND: Nasal polyposis is characterized by tissue remodelling and oedematous nasal mucosa. Vascular endothelial growth factor (VEGF) plays a significant role in the regulation of remodelling in nasal polyps. TLR4 activation is associated with VEGF expression in murine macrophages and odontoblasts. OBJECTIVE: This study aimed to evaluate whether lipopolysaccharide (LPS), an inducer of TLR4, stimulates VEGF expression and to determine the mechanism underlying VEGF production in nasal polyps. METHODS: Nasal polyp-derived fibroblasts (NPDFs) were isolated from 10 patients with nasal polyps and exposed to LPS. LPS from Rhodobacter sphaeroides (LRS) was used to inhibit the expression levels of TLR4, MyD88 and VEGF. Messenger RNA (mRNA) expression levels of TLRs, MyD88 and VEGF were determined by gene expression microarray and semiquantitative reverse transcription-PCR. Protein expression levels of TLR4 and VEGF were analysed using western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Activation of MAPKs (ERK, p38, and JNK) and Akt was examined using western blot analysis. The expression level of VEGF was measured by ELISA and western blot analysis in ex vivo nasal polyp organ culture. RESULTS: The protein expression level of VEGF was increased in nasal polyp tissues compared with inferior turbinate tissues. LRS inhibited the mRNA and protein expression of TLR4, MyD88 and VEGF in LPS-stimulated NPDFs. LPS-activated MAPKs and Akt signals, whereas MAPK inhibitors did not inhibit VEGF expression, and only Akt inhibitor blocked VEGF production. LRS reduced the production of VEGF in LPS-stimulated ex vivo organ culture. CONCLUSIONS AND CLINICAL RELEVANCE: These results suggest that LPS stimulates the production of VEGF through the TLR4-Akt signalling pathway in nasal polyps. LPS may be involved in the pathogenesis of nasal polyp remodelling.

Epigenetic regulation of myofibroblast differentiation and extracellular matrix production in nasal polyp-derived fibroblasts.

BACKGROUND: Nasal polyposis is a multi-factorial disease associated with chronic inflammatory condition of the paranasal sinuses. Myofibroblast differentiation and extracellular matrix (ECM) accumulation are involved in the pathogenesis of nasal polyposis. OBJECTIVE: The aim of this study was to study the effect of trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, on transforming growth factor (TGF)-ß1-induced myofibroblast differentiation and ECM accumulation in nasal polyp-derived fibroblasts (NPDFs). METHODS: Nasal polyp-derived fibroblasts were isolated from nasal polyps of patients who have chronic rhinosinusitis with nasal polyp. TSA was treated in TGF-ß1-induced NPDFs. Expression levels of HDAC2, α-smooth muscle actin (SMA), TGF-ß1, collagen type I, acetylated Histone H3, acetylated Histone H4, phosphorylated Smad2/3 and Smad7 were determined by RT-PCR, western blot and/or immunofluorescent staining. The total collagen amount production was analysed by Sircol soluble collagen assay and contractile activity was measured by collagen gel contraction assay. HDAC2 inhibition by TSA or HDAC2 silencing was established by RT-PCR and western blot. The epigenetic effect on α-SMA gene inactivation was examined by chromatin immunoprecipitation assay. Proliferation was determined by Ki67-positive cell staining and cytotoxicity was assessed by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. RESULTS: The expression levels of HDAC2, α-SMA and TGF-ß1 were increased in nasal polyp tissues compared to normal inferior turbinate tissues. TSA and HDAC2 silencing inhibited expression levels α-SMA, collagen and HDAC2. TSA induced hyperacetylation of histone and suppressed opening of α-SMA gene promoter in TGF-ß1-induced NPDFs. TSA inhibited TGF-ß1-induced Smad 2/3 and rescued TGF-ß1-suppressed Smad7 signalling pathway. Finally, TSA blocked proliferation in TGF-ß1-induced NPDFs and has no cytotoxic effect in NPDFs. CONCLUSIONS AND CLINICAL RELEVANCE: These results suggest that HDAC inhibition is associated with myofibroblast differentiation and extracelluar matrix accumulation in nasal polyposis. TSA may be useful as an inhibitor of nasal polyp growth, and thus has potential to be used as a novel treatment option for nasal polyposis.

A small molecule inhibitor of Mitf-E-box DNA binding and its depigmenting effect in melan-a cells.

BACKGROUND: Microphthalmia associated transcription factor (Mitf) is a key regulatory transcriptional factor of pigmentation-related genes including tyrosinase. Inhibition of tyrosinase transcription by blocking the binding of Mitf with its promoter E-box DNA can control the pigmentation. However, no such chemicals were reported so far. OBJECTIVE: To discover and evaluate the small molecule inhibitors of Mitf-E-box DNA. METHODS: Candidate chemicals were screened by virtual screening from pharmacophore data followed by Mitf E-box DNA protein chip. After selecting the chemical, its inhibitory activity on binding interaction between Mitf and E-box DNA, electrophoretic mobility shift assay (EMSA) was performed. To evaluate the depigmenting activity of Compound #17, cellular melanin assa, and Western blot were performed in melan-a cells. RESULTS: Among 27 chemicals selected from a pharmacophore data by virtual screening, Compound #17 was screened, which showed the most potent inhibitory activity against Mitf-E-box DNA binding in protein chip. EMSA results confirmed the specific inhibition of Compound #17 on Mitf-E-box DNA binding. In melan-a cells, Compound #17 reduced tyrosinase expression and melanin synthesis (62.5% at 25 µM). CONCLUSIONS: The results show that Compound #17 is the first small molecule inhibitor of Mitf-E-box DNA binding with depigmenting activity.

Pouch-related dysplasia and adenocarcinoma following restorative proctocolectomy for ulcerative colitis.

BACKGROUND: Restorative proctocolectomy (RPC) is the criterion standard surgical treatment for ulcerative colitis (UC). Restorative proctocolectomy is indicated for UC that is refractory to medical treatment, for emergency conditions, and in case of neoplastic transformation. The procedure substantially reduces the risk of UC-associated dysplasia/neoplasia. However, after RPC surgery, even with mucosectomy, cancers of the pouch and/or the anal-transitional zone (ATZ) have been reported with increasing frequency since the first report in 1984. This review highlights pouch-related dysplastic and neoplastic transformation, prevalence and adverse events, risk factors and surveillance following surgery for UC. METHODS: Reports in the literature about patients undergoing pouch surgery from different institutions reported through May 2010 were reviewed to identify patients who developed these complications, and an attempt was made to develop a rational follow-up policy based on the data available. RESULTS: To date, there are 43 reported cancers of the pouch or inlet after RPC for UC: 16 from retrospective series, 1 from a prospective study, and 26 in case reports. Thirty patients underwent mucosectomy and 13 had stapled anastomoses. To date, the number of 28 patients has been diagnosed with dysplasia after RPC for UC. Mucosectomy was performed in 27 of them and in 1 a stapled anastomosis was constructed without mucosectomy. In all cases reviewed, the time interval from the onset of UC to dysplasia/neoplasia was over 10 years. CONCLUSION: Neoplastic lesions occurring in UC patients after RPC have been shown to be absolutely inevitable. Even mucosectomy does not completely eliminate the risk. There is little evidence to support routine biopsy of the ileal mucosa or the anal-transition zone except in patients with histological type C changes, sclerosing cholangitis, and unremitting pouchitis in the ileal mucosa. Such patients should be selected for endoscopic surveillance to detect dysplasia preceding pouch adenocarcinoma.

Giant magnetoresistance of coiling polymers.

We examine the magnetoresistance (MR) of conducting polymers with interest paid on the role of structural flexibility. Through Monte Carlo simulation and Green function method, we evaluate the electric transmission for a variety of polymer configurations. It is found that for a single polymer the transmission displays a complex oscillation and also a parity-dependent periodicity. For an ensemble of polymers the averaged transmission yields the nonlinear behavior of MR under varying magnetic fields. Interestingly, more flexible polymers are shown to achieve higher MR, depending on the population and the size of the loops.

Activation of hypoxia-inducible factor-1 regulates human histidine decarboxylase expression.

Histidine decarboxylase (HDC) catalyzes the formation of histamine from histidine. Histamine has various effects in physiological and pathological reactions, such as inflammation, cell growth, and neuro-transmission. We investigated the role of hypoxia-inducible factor (HIF)-1 on hypoxia-induced HDC expression in human mast cell line, HMC-1 cells and mouse bone marrow-derived mast cells (BMMCs). Hypoxia significantly increased histamine production. HDC expression and activity were induced by hypoxia. Additionally, when cells were transfected with a native form of HIF-1alpha, hypoxia could induce higher HDC expression than in the nontransfected cell. HIF-1 binding activity for HDC 5' flanking region (HFR) was similar to that for the hypoxia-responsive element. Using HDC promoter deletion analysis, we also demonstrated that HFR was regulated by HIF-1 activation. In addition, depletion of HIF-1alpha prevents hypoxic induction of HDC in BMMCs. In conclusion, these results demonstrate that hypoxia induces HDC expression by transcriptional mechanisms dependent upon HIF-1.

Complete eversion and prolapse of bladder concurrent with primary adenocarcinoma.

Complete eversion and prolapse of the urinary bladder is extremely rare. To the best of our knowledge, the imaging findings of complete bladder eversion have not been documented in the literature. Here, we report a case of complete eversion and prolapse of the urinary bladder demonstrated on MRI. Concurrent primary adenocarcinoma was found in the thickened wall of the everted urinary bladder.

Inhibitory effects of Rumex japonicus Houtt. on the development of atopic dermatitis-like skin lesions in NC/Nga mice.

BACKGROUND: Rumex japonicus Houtt. (RJH) is one of the herbs used in Eastern countries for the treatment of atopic dermatitis (AD). It has been shown to have an antioxidative effect in human skin disease. OBJECTIVES: To examine whether RJH extract (RJH-E) suppresses the development of AD-like skin lesions in NC/Nga mice, which are induced by the repeated application of picryl chloride (PC). METHODS: The efficacy of RJH-E in NC/Nga mice was assessed by measuring symptom severity, scratching behaviour, Staphylococcus aureus numbers on an ear, and serum levels of IgE, interleukin (IL)-4 and interferon (IFN)-gamma. RESULTS: Oral administration of RJH-E to NC/Nga mice treated with PC inhibited the development of AD-like skin lesions as exemplified by a significant decrease in total skin symptom severity scores, and a decrease in hypertrophy, hyperkeratosis and infiltration of inflammatory cells in the skin. The scratching behaviour and numbers of S. aureus, which are known to be exacerbated in AD, were also significantly reduced by RJH-E. No significant change was observed in the serum levels of IFN-gamma, whereas IgE and IL-4 levels were significantly reduced by RJH-E. CONCLUSIONS: These results suggest that RJH-E inhibits the development of AD-like skin lesions in NC/Nga mice by suppressing the T-helper 2 cell response. Our results indicate that RJH treatment could provide an effective alternative therapy for the management of AD.

Alginic acid has anti-anaphylactic effects and inhibits inflammatory cytokine expression via suppression of nuclear factor-kappaB activation.

BACKGROUND: Alginic acid is comprised of complex polymerized polysaccharides, and can be chemically extracted from seaweed. Alginic acid has an inhibitory effect on histamine release, but its molecular mechanisms are not well understood. OBJECTIVE: To investigate the effect of alginic acid on the mast cell-mediated anaphylactic and inflammatory reaction using in vivo and in vitro models and elucidate its molecular mechanisms. MATERIALS AND METHOD: The effect of alginic acid on an allergy model was analysed by anaphylaxis, a histidine decarboxylase (HDC) assay, and a histamine assay. Cytokine production was analysed by means of ELISA. Cytokine expression was analysed by means of RT-PCR, and Western blotting. Transcription factor activity was analysed by a luciferase assay and a transcription factor-enzyme linked immunoassay. RESULTS: Alginic acid dose dependently inhibited compound 48/80-induced systemic anaphylaxis with doses of 0.25-1 g/kg 1 h (P<0.01, n=6) and significantly inhibited passive cutaneous anaphylaxis by 54.8%. Alginic acid (0.01-1 microg/mL) inhibited histamine release from serum and peritoneal mast cells (P<0.01). All these effects were stronger than those of disodium cromoglycate (DSCG), the reference drug tested. Alginic acid also inhibited HDC expression and activity on the phorbol myristate acetate (PMA)+A23187-stimulated human mast cell line, HMC-1 cells. Moreover, alginic acid significantly inhibited the production of PMA+A23187-induced inflammatory cytokines, IL-1beta and TNF-alpha, but not that of IL-6 or IL-8. In activated HMC-1 cells, the expression level of nuclear factor (NF)-kappaB/Rel A protein increased in the nucleus, whereas the level of NF-kappaB/Rel A in the nucleus was decreased by alginic acid treatment. In addition, alginic acid (0.01 microg/mL) decreased the PMA+A23187-induced luciferase activity and DNA-binding activity. CONCLUSION: The present results indicate that alginic acid has potent anti-anaphylactic and anti-inflammatory properties.

Anti-inflammatory effect of jeongshintang through suppression of p38 activation in human astrocytoma, U373MG cells.

Jeongshintang (JST) is a Korean herbal prescription, which has been successfully used for cerebral diseases. However, the anti-inflammatory effect of JST on Alzheimer's disease (AD) is still not fully understood. In this study, we investigated the effects of JST in attenuating the inflammatory response induced by interleukin (IL)-1beta plus beta-amyloid [1-42] fragment (A beta) in the human astrocyte cell line, U373MG. The production of IL-6, IL-8, and prostaglandin (PG)E2 was significantly increased by IL-1beta plus A beta (1-42) in a time-dependent manner (P < 0.05). JST significantly inhibited the IL-1beta plus A beta (1-42)-induced IL-6, IL-8, and PGE2 production at 24 h (P < 0.05). Maximal inhibition rate of IL-6, IL-8, and PGE2 production by JST was about 54.40%, 56.01%, and 44.06% respectively. JST (0.01-1 mg/ml) also attenuated the expression of cyclooxygenase (COX)-2 and activation of p38 MAPK induced by IL-1beta and A beta (1-42). These results demonstrated that JST has an anti-inflammatory effect, which might explain its beneficial effect in the treatment of various neurodegenerative diseases such as AD.

Deep tracheal laceration after balloon dilation for benign tracheobronchial stenosis: case reports of two patients.

We report two cases of deep tracheal laceration in female patients after balloon dilation for benign tracheobronchial stenosis. Immediate post-procedure bronchoscopy and CT including 3D reconstructions showed deep lacerations in the posterior tracheal wall. Clinically, the patients' dyspnoea subsided and there has been no recurrence during follow-up after balloon dilation. On the follow-up 3D-reconstructed CT scans obtained 2 months and 8 months following balloon dilation, respectively, the lacerations had healed completely and there was considerable improvement in lumen size.