A combination of monosodium glutamate and high-fat and high-fructose diets increases the risk of kidney injury, gut dysbiosis and host-microbial co-metabolism.

Consumption of either monosodium glutamate (MSG) or high-fat and high-fructose (HFF) diets changes the gut microbiome and hence contributes to development of several diseases. In this study, with an emphasis on kidney injury, hamsters were divided into 4 groups as follows: (1) hamsters fed with standard diet (control); (2) hamsters fed with standard diet and MSG in drinking water (MSG); (3) hamsters fed with high-fat and high-fructose diets (HFF), and (4) animals fed MSG+HFF. After 8 months, the animals were used for the study. Despite showing normal kidney function, hamsters fed with MSG+HFF exhibited signs of kidney damage as demonstrated by the highest expression levels of high-mobility group box-1 and kidney injury molecule-1 in kidney tissues, while slight changes of histopathological features in H&E-stained sections and normal levels of creatinine were observed, indicating possible early stages of kidney injury. Sequencing of the microbial 16S rRNA gene revealed that animals fed with the MSG+HFF diet had a higher ratio of gut Firmicutes/Bacteroidetes along with marked changes in abundance and diversity of gut microbiome compared to hamsters fed with MSG or HFF alone. In addition, 1H Nuclear magnetic resonance spectroscopy showed an elevation of urine p-cresol sulfate levels in the MSG+HFF group. These results indicate that consumption of both MSG and HFF increases the risk of kidney injury, induces gut dysbiosis and an increase in the amount of p-cresol sulfate in hamsters

R_Table_S6 – Supplemental material for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma

<p>Supplemental material, R_Table_S6 for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma by Sudarat Onsurathum, Ornuma Haonon, Porntip Pinlaor, Chawalit Pairojkul, Narong Khuntikeo, Raynoo Thanan, Sittiruk Roytrakul and Somchai Pinlaor in Tumor Biology</p

Co-occurrence of opisthorchiasis and diabetes exacerbates morbidity of the hepatobiliary tract disease.

Complications arising from infection with the carcinogenic liver fluke Opisthorchis viverrini cause substantial morbidity and mortality in Thailand and adjacent lower Mekong countries. In parallel, the incidence rate of diabetes mellitus (DM) is increasing in this same region, and indeed worldwide. Many residents in opisthorchiasis-endemic regions also exhibit DM, but the hepatobiliary disease arising during the co-occurrence of these two conditions remains to be characterized. Here, the histopathological profile during co-occurrence of opisthorchiasis and DM was investigated in a rodent model of human opisthorchiasis in which diabetes was induced with streptozotocin. The effects of excretory/secretory products from the liver fluke, O. viverrini (OVES) on hepatocyte and cholangiocyte responses during hyperglycemic conditions also were monitored. Both the liver fluke-infected hamsters (OV group) and hamsters with DM lost weight compared to control hamsters. Weight loss was even more marked in the hamsters with both opisthorchiasis and DM (OD group). Hypertrophy of hepatocytes, altered biliary canaliculi, and biliary hyperplasia were more prominent in the OD group, compared with OV and DM groups. Profound oxidative DNA damage, evidenced by 8-oxo-2'-deoxyguanosine, proliferating cell nuclear antigen, and periductal fibrosis characterized the OD compared to OV and DM hamsters. Upregulation of expression of cytokines in response to infection and impairment of the pathway for insulin receptor substrate (IRS)/phosphatidylinositol-3-kinases (PI3K)/protein kinase B (AKT) signaling attended these changes. In vitro, OVES and glucose provoked time- and dose-dependent effects on the proliferation of both hepatocytes and cholangiocytes. In overview, the co-occurrence of opisthorchiasis and diabetes exacerbated pathophysiological damage to the hepatobiliary tract. We speculate that opisthorchiasis and diabetes together aggravate hepatobiliary pathogenesis through an IRS/PI3K/AKT-independent pathway

R_Table_S5 – Supplemental material for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma

<p>Supplemental material, R_Table_S5 for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma by Sudarat Onsurathum, Ornuma Haonon, Porntip Pinlaor, Chawalit Pairojkul, Narong Khuntikeo, Raynoo Thanan, Sittiruk Roytrakul and Somchai Pinlaor in Tumor Biology</p

Sarcopenia variables cut-points, disability and falls in older adults- a pooled analysis

[[abstract]]Sarcopenia is becoming an urgent health issue in aging population. Operational efinitions have recently been proposed to facilitate prompt recognition of sarcopenia in clinical practice. However, evidence indicated that the proper cut-off points of sarcopenia variables for Asians may be different from Westerners. The purpose of this study is to determine sarcopenia variables cut-points for identifying elevated physical disability and falls risk in a large sample of older Taiwanese adults. We pooled the primary data from three major cohort studies in Taiwan, as part of the Sarcopenia and Translational Aging Research in Taiwan (START) project. Data on 1770 adults aged ? 65 years (mean age = 74 years) were analyzed. Bioelectrical impedance analysis was used to measure appendicular skeletal muscle mass. Relative skeletal muscle was calculated as appendicular skeletal muscle mass (kg) divided by weight (kg). Gait speed was determined by measuring usual-paced walking velocity. The presence of difficulty in any ADL(eating, transfer, toilet use, bathing,mobility, dressing, bowels/bladder) or IADL (shopping, housekeeping, handling finances, food preparation, transportation, using telephone, laundry, medications), or falls in the past year was also determined. Receiver operating characteristics analysis was used to develop muscle mass cut-points (sex-specific) and gait speed cut-points (sex-and height-specific) associated with physical disability and falls. Multivariate analyses adjusted for sociodemographic variables, lifestyle factors and various medical conditions were used to compare odds for physical disability and falls for individuals whose sarcopenia variables fell above and below these cut-points. The skeletal muscle cut-points denoting high risk were 28.76 % for men and 21.76 % for women. The gait speed cut-points denoting high risk were 0.7 m/s for men with height ≦ 163 cm, 0.8m/s for men with height >163 cm, 0.6 m/s for women with height ≦ 152 cm and 0.7 m/s for women with height >152 cm. Compared with those with low-risk muscle mass values, participants with high-risk muscle mass values had higher odds for physical disability and falls (adjusted OR, 2.02 in men [95% CI, 1.17-3.49] and 1.91 in women [95 % CI, 1.09-3.35]). Compared with those with low-risk gait speed values, participants with high-risk gait speed values had higher odds for physical disability and falls (adjusted OR, 4.66 in men with height ≦ 163 cm [95% CI, 2.42-8.97], 3.87 in men with height >163 cm [95% CI, 1.52-9.89], 9.40 in women with height ≦ 152 cm [95% CI, 4.62-19.14] and 5.14 in women with height >152 cm [95% CI, 2.48-10.63]). Low muscle mass and gait speed defined using the cut-off points were independently associated with disability and falls in older adults. Further studies are needed for future applications of these cut-points in sarcopenia diagnosis and treatment

R2_Table_S2 – Supplemental material for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma

<p>Supplemental material, R2_Table_S2 for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma by Sudarat Onsurathum, Ornuma Haonon, Porntip Pinlaor, Chawalit Pairojkul, Narong Khuntikeo, Raynoo Thanan, Sittiruk Roytrakul and Somchai Pinlaor in Tumor Biology</p

R_Table_S7 – Supplemental material for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma

<p>Supplemental material, R_Table_S7 for Proteomics detection of S100A6 in tumor tissue interstitial fluid and evaluation of its potential as a biomarker of cholangiocarcinoma by Sudarat Onsurathum, Ornuma Haonon, Porntip Pinlaor, Chawalit Pairojkul, Narong Khuntikeo, Raynoo Thanan, Sittiruk Roytrakul and Somchai Pinlaor in Tumor Biology</p

Opisthorchis viverrini infection augments the severity of nonalcoholic fatty liver disease in high-fat/high-fructose diet-fed hamsters

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide, including in regions where helminth infections such as the fish-borne liver fluke Opisthorchis viverrini (Ov) also occur. We investigated the effects of a high-fat and high-fructose (HFF) diet on the development and progression of NAFLD in experimental opisthorchiasis. Two groups of hamsters were infected with Ov for 4 months before the experiment to induce chronic inflammation. One of these groups (OvHFF) was fed with a HFF diet for up to further 4 months. One uninfected group of hamsters served as the normal control group, and another received the HFF diet (HFF group) for up to 4 months. Histopathology, biochemical parameters, and ultrastructural features of liver were investigated. In a short-term treatment, the OvHFF group showed significantly better homeostatic model assessment for insulin resistance level and lower liver lipid than did the HFF group. By contrast, histopathological characteristics of severe NAFLD were prominent in the OvHFF group after 4 months on the HFF diet, findings which were supported by confirmatory ultrastructural changes. In conclusion, opisthorchiasis induced the severe NAFLD in hamsters fed high-fat/high-fructose diets

Oxidative DNA damage in hamster liver.

<p>Formation of 8-oxo-dG in the liver of <i>O</i>. <i>viverrini</i>-infected, diabetic hamsters evaluated by immunofluorescence staining. Representative micrographs showing nuclei stained bright green, to reveal 8-oxo-dG (x400 magnification). Panel A, N group; B, OV group; C and D, DM group of large and small bile ducts; E, F, OD group of large bile duct with parasite and small bile ducts. OV = <i>O</i>. <i>viverrini</i>, BD = Bile duct. Treatment groups as in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006611#pntd.0006611.g001" target="_blank">Fig 1</a>.</p

PCNA-positive pattern in biliary tract, the grade of pattern of bile canaliculi, grade of fibrosis and parentage of 8-oxo-dG-positive cells.

<p>PCNA-positive pattern in biliary tract, the grade of pattern of bile canaliculi, grade of fibrosis and parentage of 8-oxo-dG-positive cells.</p