High wall shear stress beyond a certain range in the parent artery could predict the risk of anterior communicating artery aneurysm rupture at follow-up.

Objective: Among clinical and morphological criteria, hemodynamics is the main predictor of aneurysm growth and rupture. This study aimed to identify which hemodynamic parameter in the parent artery could independently predict the rupture of anterior communicating artery (ACoA) aneurysms by using multivariate logistic regression and two-piecewise linear regression models. An additional objective was to look for a more simplified and convenient alternative to the widely used computational fluid dynamics (CFD) techniques to detect wall shear stress (WSS) as a screening tool for predicting the risk of aneurysm rupture during the follow-up of patients who did not undergo embolization or surgery.

The role of wall shear stress in the parent artery as an independent variable in the formation status of anterior communicating artery aneurysms.

Objectives: The study aimed to determine which hemodynamic parameters independently characterize anterior communicating artery (AcomA) aneurysm formation and explore the threshold of wall shear stress (WSS) of the parent artery to better illustrate the correlation between the magnitude of WSS and AcomA aneurysm formation.

Methods: Eighty-one patients with AcomA aneurysms and 118 patients without intracranial aneurysms (control population), as confirmed by digital subtraction angiography (DSA) from January 2014 to May 2017, were included in this cross-sectional study. Three-dimensional-DSA was performed to evaluate the morphologic characteristics of AcomA aneurysms.

A novel small-molecule activator of Sirtuin-1 induces autophagic cell death/mitophagy as a potential therapeutic strategy in glioblastoma.

Sirtuin-1 (SIRT1), the mammalian ortholog of yeast Sir2p, is well known to be a highly conserved NAD-dependent protein deacetylase that has been emerging as a key cancer target. Autophagy, an evolutionarily conserved, multi-step lysosomal degradation process, has been implicated in cancer. Accumulating evidence has recently revealed that SIRT1 may act as a tumor suppressor in several types of cancer, and thus activating SIRT1 would represent a possible therapeutic strategy.

Cerebral Microbleeds Could Be Independently Associated with Intracranial Aneurysm Rupture: A Cross-Sectional Population-Based Study.

Objective: To determine whether the presence of cerebral microbleeds (CMBs) is independently associated with intracranial aneurysm rupture and to identify the time interval of CMB-related intracranial aneurysm rupture.

Methods: This cross-sectional study included 1847 patients with unruptured and ruptured intracranial aneurysms from January 2010 to November 2017. Clinical records and imaging, including T2-weighted gradient-recalled echo sequence magnetic resonance imaging that identified the presence of CMBs preoperatively, were evaluated.

Swimming attenuates inflammation, oxidative stress, and apoptosis in a rat model of dextran sulfate sodium-induced chronic colitis.

Increasing evidence suggests that regular physical exercise suppresses chronic inflammation. However, the potential inhibitory effects of swimming on dextran sulfate sodium (DSS)-induced chronic colitis, and its underlying mechanisms, remain unclear. In this study, rats were orally administered DSS to induce chronic colitis, and subsequently treated with or without swimming exercise.

Sequence analysis of the human fucosyltransferase 1 and 2 genes in Tibetan blood donors: identification of three novel alleles.

Background: The α(1,2)-fucosyltransferase gene 1 (FUT1) and 2 (FUT2), respectively, regulate H antigen synthesis in red blood cells and body fluids. Genetic polymorphisms of FUT1 and FUT2 are ethnically and geographically specific.

Study Design And Methods: Healthy unrelated Tibetan blood donors (n = 200) from the Tibet Autonomous Region of China were recruited for this study.

A family study of the Chinese Rhnull individual of the regulator type: a novel single missense mutation identified in RHAG gene.

Background: Rh(null) is a rare autosomal recessive disorder, and Rh(null) of the regulator type may result from mutation of the RHAG gene, which encodes RhAG glycoprotein and modulates Rh antigen expression. This study described the molecular genetic analysis of a Chinese Rh(null) family and identified a novel mutation in the RHAG gene.

Study Design And Methods: RBCs from the Rh(null) family members were analyzed for Rh phenotype by standard methods.

N'-(2-Furylmethyl-ene)nicotinohydrazide.

The asymmetric unit of the title compound, C(11)H(9)N(3)O(2), contains two independent mol-ecules: the dihedral angles between the pyridine ring and the furyl ring are 17.00 (16) and 34.12 (15)°.

1-[4-(2-Fur-yl)but-3-en-2-yl-idene]-2-(2-nitro-phen-yl)hydrazine.

In the title Schiff base compound, C(14)H(13)N(3)O(3), the furan and benzene rings are oriented at a dihedral angle of 10.24 (13)°. Intra-molecular N-H⋯O hydrogen bonding is observed between the imino and nitro groups.

1-(Butan-2-yl-idene)-2-(2-nitro-phen-yl)hydrazine.

Crystals of the title compound, C(10)H(13)N(3)O(2), were obtained from a condensation reaction of butan-2-one and 1-(2-nitro-phen-yl)hydrazine. The mol-ecule exhibits a nearly coplanar structure, except for the methyl and methyl-ene H atoms, the largest deviations from the mean plane defined by all non-H atoms, except for the nitro group, being 0.120 (2) Å for one of the nitro O atoms.

Differential regulation of SOCS-1 signalling in B and T lymphocytes by hepatitis C virus core protein.

Hepatitis C virus (HCV) infection is characterized by a strong propensity toward chronicity, autoimmune phenomena and lymphomagenesis, supporting a role for lymphocyte dysregulation during persistent viral infection. We have shown that HCV core protein inhibits T-cell functions through interaction with a complement receptor, gC1qR. Here, we further report that B cells also express gC1qR that can be bound by HCV core protein.

gC1qR expression in chimpanzees with resolved and chronic infection: potential role of HCV core/gC1qR-mediated T cell suppression in the outcome of HCV infection.

Chimpanzee is a unique animal model for HCV infection, in which about 50% of infections resolve spontaneously. It has been reported that the magnitude of T cell responses to HCV core in recovered chimpanzees is greater than that in chronically infected ones. However, the mechanism(s) by which the chimpanzees with resolved infection overcome core-mediated immunosuppression remains unknown.

SOCS1 and SOCS3 are targeted by hepatitis C virus core/gC1qR ligation to inhibit T-cell function.

T cells play an important role in the control of hepatitis C virus (HCV) infection. We have previously demonstrated that the HCV core inhibits T-cell responses through interaction with gC1qR. We show here that core proteins from chronic and resolved HCV patients differ in sequence, gC1qR-binding ability, and T-cell inhibition.

Hepatitis C virus core selectively suppresses interleukin-12 synthesis in human macrophages by interfering with AP-1 activation.

Hepatitis C virus (HCV) is remarkably efficient at establishing persistent infection, suggesting that it has evolved one or more strategies aimed at evading the host immune response. T cell responses, including interferon-gamma production, are severely suppressed in chronic HCV patients. The HCV core protein has been previously shown to circulate in the bloodstream of HCV-infected patients and inhibit host immunity through an interaction with gC1qR.

The molecular basis of HCV-mediated immune dysregulation.

Chronic hepatitis C virus (HCV) infection, which occurs in over 85% of patients and causes mild to severe liver disease, is a growing burden to health systems worldwide. The propensity of HCV to establish persistent infection suggests that the virus, which is non-cytopathic, has evolved one or more mechanisms aimed at evading host immunity. In addition to the appearance of quasispecies, which may arise under selective pressure during B and T cell responses, HCV gene products interact with host proteins in order to subvert immune surveillance.

HCV core/gC1qR interaction arrests T cell cycle progression through stabilization of the cell cycle inhibitor p27Kip1.

Hepatitis C virus (HCV) is efficient in the establishment of persistent infection. We have previously shown that HCV core protein inhibits T cell proliferation through its interaction with the complement receptor, gC1qR. Here we show that HCV core-induced inhibition of T cell proliferation involves a G(0)/G(1) cell cycle arrest, which is reversible upon addition of anti-gC1qR antibody.