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Activated hepatic stellate cells (HSCs) play a central role in the hepatic fibrosis and cirrhosis. Recently, HSCs were reported to have strong immune modulatory activities. However, the role of HSCs in hepatocellular carcinoma (HCC) remains unclear. In this study, we showed that HSCs could promote HCC growth both in vitro and in vivo. We examined the HSC-mediated inhibition of T-cell proliferation and the ability of conditioned medium from activated HSCs to promote the growth of murine HCC cell lines in vitro. We also assessed the immune suppression by HSCs during the development of HCC in immunocompetent mice. Cotransplantation of HSCs promoted HCC growth and progression by enhancing tumor angiogenesis and tumor cell proliferation and by creating an immunosuppressed microenvironment. Cotransplanted HSCs inhibited the lymphocyte infiltration in tumors and the spleens of mice bearing tumors, induced apoptosis of infiltrating mononuclear cells, and enhanced the expression of B7H1 and CD4 1 CD25 1 Treg cells. The immune modulation by HSCs seemed to be systemic. In conclusion, our data provide new information to support an integral role for HSCs in promoting HCC progression in part via their immune regulatory activities, and suggest that HSCs may serve as a therapeutic target in HCC.Hepatocellular carcinoma (HCC), a common malignant tumor worldwide, is a severe public health concern. 1 Carcinogenesis of HCC is a multifactor, multistep and complex process. Recently, many studies have demonstrated that hepatic fibrosis and liver cirrhosis, which are the ultimate results of chronic liver disease, are closely associated with HCC. 2 Liver fibrosis, cirrhosis and HCC all arise from liver parenchymal cells and mesenchymal cells. 3 Genetic and cellular biological studies on malignant tumors have shown that the interaction between parenchymal and stromal cells are important for tumor formation and development. 4 Stromal cells include myofibroblasts and endothelial cells, both of which interact with parenchymal cells via (1) the secretion of cytokines and other chemical factors, (2) extra cellular matrix (ECM)-mediated interaction and (3) direct cell-to-cell contiguity. 5 Stromal cells are closely related to angiogenesis, cancer desmoplasia and tumor immunity and are therefore important players in the progression, growth and spread of tumors. 6 Furthermore, several studies have shown that tumor cells can further induce the expression of tumorigenic factors in tumor-associated stromal cells, 7,8 indicating a mutual interaction between cancer cells and stromal cells. Thus, studies on the role of tumor stroma in the development and progression of cancer will help to clarify the mechanisms of carcinogenic lesions and lead to more effective therapeutic approaches.Hepatic stellate cells (HSCs) are the main collagen-producing cells in the injured liver. 9 Following a chronic liver injury, HSCs play important roles during the development of

BackgroundThe neutrophil to lymphocyte ratio (NLR) has been shown to predict short- and long-term outcomes in ischemic stroke patients. We sought to explore the temporal profile of the plasma NLR in stroke patients treated with intravenous thrombolysis (IVT) and its relationship with intracranial bleeding complications after thrombolysis.MethodsA total of 189 ischemic stroke patients were prospectively enrolled. Blood samples for leukocyte, neutrophil, and lymphocyte counts were obtained at admission and at 3–6, 12–18, and 36–48 h after IVT. Head CT was performed on admission and repeated after 36–48 h, and a CT scan was done immediately in case of clinical worsening. Hemorrhagic events were categorized as symptomatic intracranial hemorrhage (sICH) and parenchymal hematomas (PH) according to previously published criteria.ResultsAn increasing trend in the NLR was observed after stroke, and the NLR was higher in patients who developed PH or sICH at 3–6, 12–18, and 36–48 h after IVT (P < 0.01) than in those without PH or sICH. The optimal cutoff value for the serum NLR as an indicator for auxiliary diagnosis of PH and sICH was 10.59 at 12–18 h. Furthermore, the NLR obtained at 12–18-h post-treatment was independently associated with PH (adjusted odds ratio [OR] 1.14) and sICH (adjusted OR 1.14). In addition, patients with a NLR ≥10.59 had an 8.50-fold greater risk for PH (95 % confidence interval [CI] 2.69–26.89) and a 7.93-fold greater risk for sICH (95 % CI 2.25–27.99) than patients with a NLR <10.59.ConclusionsNLR is a dynamic variable, and its variation is associated with HT after thrombolysis in stroke patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0680-x) contains supplementary material, which is available to authorized users.

Dual-source CT can depict normal and abnormal blood perfusion distribution in a rabbit's lung. Abnormal pulmonary blood distribution, as shown at dual-source CT, improves detection of acute PE in rabbits.

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VNCT(A) may potentially replace TNCT as part of a multi-phase liver imaging protocol with consequent saving in radiation dose.

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Intracranial aneurysm is a common life-threatening disease. Computed tomography angiography is recommended as the standard diagnosis tool; yet, interpretation can be time-consuming and challenging. We present a specific deep-learning-based model trained on 1,177 digital subtraction angiography verified bone-removal computed tomography angiography cases. The model has good tolerance to image quality and is tested with different manufacturers. Simulated real-world studies are conducted in consecutive internal and external cohorts, in which it achieves an improved patient-level sensitivity and lesion-level sensitivity compared to that of radiologists and expert neurosurgeons. A specific cohort of suspected acute ischemic stroke is employed and it is found that 99.0% predicted-negative cases can be trusted with high confidence, leading to a potential reduction in human workload. A prospective study is warranted to determine whether the algorithm could improve patients’ care in comparison to clinicians’ assessment.