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Dysphagia is one of the common complications after stroke. Dysphagia significantly increases the probability of serious adverse consequences. The purpose of this study was to compare the characteristics of submental muscles electromyography and hyoid motion parameters between patients with dysphagia after stroke and healthy controls, and whether there is a synergistic effect between the function of the submental muscles and the movement of the hyoid.Fifteen patients with post-stroke dysphagia and fifteen healthy adults simultaneously underwent the videofluoroscopic and surface electromyography of the submental muscles while swallowing 5 ml of concentrated liquid barium sulphate. The electromyographic signal of the submental muscles was analysed along with parameters of hyoid movement.Stage transition duration and duration of surface electromyographic activity were extended significantly in post-stroke dysphagia patients(P 0.05). Surface electromyography amplitude and hyoid movement were significantly reduced in patients (P 0.05). There was a significant correlation between the maximum hyoid movement distance and the peak sEMG amplitude in healthy controls (r = 0.660, P = 0.014), but not in patients with dysphagia after stroke (r = 0.425, P = 0.148).Submental muscles electromyographic signal changes in patients may be the result of uncoordinated muscle contractions and decreased muscle strength. Furthermore, the reduced hyoid movement distance may be due to impaired function of the submental muscles. In addition, the submental muscles and hyoid movement or other swallowing structures functions were impaired to varying degrees, resulting in the disappearance of the correlation between the maximum movement distance of the hyoid and the peak amplitude.

Background Epithelial-mesenchymal transition (EMT) is critical for cancer cell metastasis. Recently, EMT was reported to be associated with the inflammatory tumour microenvironment and, therefore, might be a predictive biomarker for immune checkpoint blockade agents. However, the underlying mechanism is still unclear. Methods Patient survival data for our HCC cohort, TCGA and GEO datasets were determined by Kaplan-Meier analysis. The functional roles of ELMO1 in HCC were demonstrated by a series of in vitro and in vivo experiments. Gene microarray analysis was used to demonstrate potential mechanisms of ELMO1. Data retrieved from the TCGA datasets were used to determine the relationships of ELMO1, EMT and TMB. Findings Here, we report an indispensable role for ELMO1 in linking EMT with tumour mutation burden (TMB), which is a promising biomarker for the immune checkpoint blockade agent response. Upregulated ELMO1 expression is associated with a poor prognosis in hepatocellular carcinoma (HCC), as well as increased cell growth, invasion, migration, angiogenesis and EMT in vitro and in vivo. Mechanistically, we provide evidence that ELMO1 regulates SOX10 expression and induces EMT through PI3K/Akt signalling. Moreover, ELMO1 is negatively associated with TMB, indicating a negative relationship between EMT and TMB. Interpretation ELMO1 serves as a link between EMT and TMB, providing a mechanistic basis for the further development of ELMO1 as a therapeutic target against HCC and potentially a promising biomarker of the immune checkpoint blockade agent response. Fund National Natural Science Foundation of China; Natural Science Foundation of Guangdong Province; Young Teacher Training Program of Sun Yat-sen University; Science and Technology Plan of Guangdong Province; Special Support Program of Guangdong Province, Science and Technology Innovation Youth Talent Support Program; the Pearl River Science and Technology New Talent of Guangzhou City; Medical Scientific Research Foundation of Guangdong Province.

Background & Aims Shp2 is an SH2-tyrosine phosphatase acting downstream of receptor tyrosine kinases (RTKs). Most recent data demonstrated a liver tumor-suppressing role for Shp2, as ablating Shp2 in hepatocytes aggravated hepatocellular carcinoma (HCC) induced by chemical carcinogens or Pten loss. We further investigated the effect of Shp2 deficiency on liver tumorigenesis driven by classical oncoproteins c-Met (receptor for HGF), β-catenin and PIK3CA. Methods We performed hydrodynamic tail vein injection of two pairs of plasmids expressing c-Met and ΔN90-β-catenin (MET/CAT), or c-Met and PIK3CA H1047R (MET/PIK), into WT and Shp2 hep−/− mice. We compared liver tumor loads and investigated the pathogenesis and molecular mechanisms involved using multidisciplinary approaches. Results Despite the induction of oxidative and metabolic stresses, Shp2 deletion in hepatocytes suppressed hepatocarcinogenesis driven by overexpression of oncoproteins MET/CAT or MET/PIK. Shp2 loss inhibited proliferative signaling from c-Met, Wnt/β-catenin, Ras/Erk and PI3K/Akt pathways, but triggered cell senescence following exogenous expression of the oncogenes. Conclusions Shp2, acting downstream of RTKs, is positively required for hepatocyte-intrinsic tumorigenic signaling from these oncoproteins, even if Shp2 deficiency induces a tumor-promoting hepatic microenvironment. These data suggest a new and more effective therapeutic strategy for HCCs driven by oncogenic RTKs and other upstream molecules, by inhibiting Shp2 and also suppressing any tumor-enhancing stromal factors produced because of Shp2 inhibition. Lay summary Primary liver cancer is a malignant disease with poor prognosis, largely because there are limited systemic therapies available. We show here that a cytoplasmic tyrosine phosphatase Shp2 is required for liver tumorigenesis. This tumorigenesis is driven by two oncoproteins that are implicated in human liver cancer. This, together with our previous studies, uncovers the complexity of liver tumorigenesis, by elucidating the pro- and anti-tumor effects of Shp2 in mouse models. This data can be used to guide new therapies.

Background aims Assessing mesenchymal stromal cells (MSCs) after grafting is essential for understanding their migration and differentiation processes. The present study sought to evaluate via cellular magnetic resonance imaging (MRI) if transplantation route may have an effect on MSCs engrafting to fibrotic liver of rats. Methods Rat MSCs were prepared, labeled with superparamagnetic iron oxide and scanned with MRI. Labeled MSCs were transplanted via the portal vein or vena caudalis to rats with hepatic fibrosis. MRI was performed in vitro before and after transplantation. Histologic examination was performed. MRI scan and imaging parameter optimization in vitro and migration under in vivo conditions were demonstrated. Results Strong MRI susceptibility effects could be found on gradient echo-weighted, or T2∗-weighted, imaging sequences from 24 h after labeling to passage 4 of labeled MSCs in vitro . In vivo , MRI findings of the portal vein group indicated lower signal in liver on single shot fast spin echo-weighted, or T2-weighted, imaging and T2∗-weighted imaging sequences. The low liver MRI signal increased gradually from 0–3 h and decreased gradually from 3 h to 14 days post-transplantation. The distribution pattern of labeled MSCs in liver histologic sections was identical to that of MRI signal. It was difficult to find MSCs in tissues near the portal area on day 14 after transplantation; labeled MSCs appeared in fibrous tuberculum at the edge of the liver. No MRI signal change and a positive histologic examination were observed in the vena caudalis group. Conclusions The portal vein route seemed to be more beneficial than the vena caudalis on MSC migration to fibrotic liver of rats via MRI.

Community structures of soil Sarcodina in 7 different habitats within Baiyun Mountain in Guangzhou. China were investigated with qualitative and quantitative analyses. The abundance, dominance, species diversity and community similarity index of soil sarcodina with different physicochemical parameters were comparatively analyzed. A total 67 species of sarcodina belonging to 4 Super-groups, 6 First ranks and 14 Second ranks were identified. The first dominant group was Tubulinea, followed by Flabellinea, with dominance of 59.7% and 13.4%, respectively. The highest abundance of sarcodina appeared in autumn of Site 5, reaching 1.20 x 10(5) ind g(-1); the lowest in spring of Site 2 with 1.73 x 10(3) ind g(-1). Margalers biodiversity index ranged from 1.26 (winter of Site 6) to 2.51 (summer of Site 1). Statistical analyses showed the sarcodina abundance was positively correlated with organic matter, soil moisture, soil pH, ammonia nitrogen and total nitrogen, but the correlation coefficient of total potassium was negative. Total phosphorus, nitrate nitrogen and sulphate showed no significant effect on sarcodina abundance in the present study. (C) 2009 Elsevier Masson SAS. All rights reserved.

During liver injury, bone marrow-derived mesenchymal stem cells (MSCs) can migrate and differentiate into hepatocytes. Hepatic stellate cell (SC) activation is a pivotal event in the development of liver fibrosis. Therefore, we hypothesized that SCs may play an important role in regulating MSC proliferation and differentiation through the paracrine signaling pathway. We demonstrate that MSCs and SCs both express hedgehog (Hh) pathway components, including its ligands, receptors, and target genes. Transwell co-cultures of SCs and MSCs showed that the SCs produced sonic hedgehog (Shh), which enhanced the proliferation and differentiation of MSCs. These findings demonstrate that SCs indirectly modulate the activity of MSCs in vitro via the Hh pathway, and provide a plausible explanation for the mechanisms of transplanted MSCs in the treatment of liver fibrosis.