Prevalence of clonorchiasis in patients with gastrointestinal disease: A Korean nationwide multicenter survey

AIM： To investigate prevalence of C/onorchis sinensis in patients with gastrointestinal symptoms, and the relation of the infection to hepatobiliary diseases in 26 hospitals in Korea. METHODS： Consecutive patients who had been admitted to the Division of Gastroenterology with gastrointestinal symptoms were enrolled from March to April 2005. Of those who had been diagnosed with clonorchiasis, epidemiology and correlation between infection and hepatobiliary diseases were surveyed by questionnaire. RESULTS： Of 3080 patients with gastrointestinal diseases, 396 （12.9%） had clonorchiasis and 1140 patients （37.2%） had a history of eating raw freshwater fish. Of those with a history of raw freshwater fish ingestion, 238 （20.9%） patients had clonorchiasis. Cholangiocarcinoma was more prevalent in C. sinensis-infected patients than nonnfected patients [34/396 （8.6%） vs 145/2684 （5.4%）, P = 0.015]. Cholangiocarcinoma and clonorchiasis showed statistically significant positive cross-relation （P = 0.008）. Choledocholithiasis, cholecystolithiasis, cholangitis, hepatocellular carcinoma, and biliary pancreatitis did not correlate with clonorchiasis. CONCLUSION： Infection rate of clonorchiasis was still high in patients with gastrointestinal diseases in Korea, and has not decreased very much during the last two decades. Cholangiocarcinoma was related to clonorchiasis, which suggested an etiological role for the parasite.

Chronic alcohol consumption potentiates the development of diabetes through pancreatic β-cell dysfunction

Chronic ethanol consumption is well established as a major risk factor for type-2 diabetes(T2D), which is evidenced by impaired glucose metabolism and insulin resistance. However, the relationships between alcoholconsumption and the development of T2 D remain controversial. In particular, the direct effects of ethanol consumption on proliferation of pancreatic β-cell and the exact mechanisms associated with ethanolmediated β-cell dysfunction and apoptosis remain elusive. Although alcoholism and alcohol consumption are prevalent and represent crucial public health problems worldwide, many people believe that low-tomoderate ethanol consumption may protect against T2 D and cardiovascular diseases. However, the J- or U-shaped curves obtained from cross-sectional and large prospective studies have not fully explained the relationship between alcohol consumption and T2 D. This review provides evidence for the harmful effects of chronic ethanol consumption on the progressive development of T2 D, particularly with respect to pancreatic β-cell mass and function in association with insulin synthesis and secretion. This review also discusses a conceptual framework for how ethanolproduced peroxynitrite contributes to pancreatic β-cell dysfunction and metabolic syndrome.

Formation of interfacial brittle phases sigma phase and IMC in hybrid titanium-to-stainless steel joint

The microstructures of the brazed joints for commercially pure Ti and stainless steel were investigated by the applications of various filler alloys including Ag-, Ti-, Zr- and Ni-based alloys. Generally, the dissimilar joints between Ti and stainless steel were dominated by the Ti-based intermetallic compounds （IMCs）, e.g. （Ti, Zr）2（Fe, Ni）, TiFe, TiCu, and Ti2（Fe, Ni）, due to a significant dissolution of Ti from the base metal. The （Fe-Cr） cr phase was also observed near the stainless steel due to a segregation of Cr into the interface region. This research demonstrates empirically that the brittleness of the Ti and stainless steel joint can not be avoided only by applying single braze alloy or single insert metal, and thus an introduction of additional suitable interlayer between the filler alloy and the base metal is necessary to prevent the brittleness of the joint.

Cognitive Profiles and Subtypes of Patients with Mild Cognitive Impairment: Data from a Clinical Follow-Up Study

Background: Mild cognitive impairment (MCI) is a heterogeneous condition with a variety of clinical outcomes, the presence of which correlates with risk of Alzheimer’s disease as well as pre-clinical stages of other dementia subtypes. The aims of this study were to assess the specific patterns of cognitive profiles and to identify changes from baseline to 24 weeks in patients with MCI using detailed neuropsychological testing. Methods: We consecutively recruited 120 MCI patients at baseline according to the Petersen’s clinical diagnostic criteria, who were admitted to the Dementia and Memory Clinics. We analyzed patients who fulfilled both inclusion and exclusion criteria for MCI and classified them into four subtypes according to deficits in major cognitive domains;amnestic MCI single domain (aMCI-s), amnestic multiple domain MCI (aMCI-m), non-amnestic single domain MCI (naMCI-s) and non-amnestic multiple domain MCI (naMCI-m). Four groups of MCI were evaluated by a detailed neuropsychological battery test. Results: 83 patients with MCI at the 24-week follow-up were classified into four subtypes. The most frequent subtype was amnestic multi-domain MCI, with the frequency of MCI subtypes as follows: aMCI-s (n = 21, 25.3%), aMCI-m (n = 53, 63.9%), naMCI-s (n = 5, 6.0%) and naMCI-m (n = 4, 4.8%). In the major cognitive items of the SNSB-D, there were significant changes between the initial and follow-up tests in the domains of language, memory and the fron-tal/executive function (p < 0.05), except for attention, in all MCI patient subtypes. At 24-weeks follow-up, the conversion rate to Alzheimer’s disease was 2.4% (n = 2) from a subtype of amnestic multi-domain MCI. Conclusions: Our study revealed the most frequent subtype of MCI to be multiple domain amnestic MCI, with this subtype having a higher tendency of conversion to Alzheimer’s disease.

WNT5A drives interleukin-6-dependent epithelial-mesenchymal transition via the JAK/STAT pathway in keloid pathogenesis

Background:Keloid scarring is a fibroproliferative disease caused by aberrant genetic activation with an unclear underlying mechanism.Genetic predisposition,aberrant cellular responses to environmental factors,increased inflammatory cytokines and epithelial-mesenchymal transition(EMT)phenomena are known as major contributors.In this study,we aimed to identify the molecular drivers that initiate keloid pathogenesis.Methods:Bulk tissue RNA sequencing analyses of keloid and normal tissues along with ex vivo and in vitro tests were performed to identify the contributing genes to keloid pathogenesis.An animal model of inflammatory keloid scarring was reproduced by replication of a skin fibrosis model with intradermal bleomycin injection in C57BL/6 mice.Results:Gene set enrichment analysis revealed upregulation of Wnt family member 5A(WNT5A)expression and genes associated with EMT in keloid tissues.Consistently,human keloid tissues and the bleomycin-induced skin fibrosis animal model showed significantly increased expression ofWNT5A and EMT markers.Increased activation of the interleukin(IL)-6/Janus kinase(JAK)/signal transducer and activator of transcription(STAT)pathway and subsequent elevation of EMT markerswas also observed in keratinocytes co-cultured withWNT5A-activated fibroblasts or keloid fibroblasts.Furthermore,WNT5A silencing and the blockage of IL-6 secretion via neutralizing IL-6 antibody reversed hyperactivation of the STAT pathway and EMT markers in keratinocytes.Lastly,STAT3 silencing significantly reduced the EMT-like phenotypes in both keratinocytes and IL-6-stimulated keratinocytes.Conclusions:Intercellular communication via the WNT5A and STAT pathways possibly underlies a partial mechanism of EMT-like phenomena in keloid pathogenesis.IL-6 secreted from WNT5A-activated fibroblasts or keloid fibroblasts activates the JAK/STAT signaling pathway in adjacent keratinocytes which in turn express EMT markers.A better understanding of keloid development and the role of WNT5A in EMT will promote the development of next-generation targeted treatments for keloid scars.