Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression.

Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion.

Ucf-101 protects against cerebral oxidative injury and cognitive impairment in septic rat.

Background: Omi/HtrA2 is a proapoptotic mitochondrial serine protease involved in caspase-dependent and caspase-independent cell apoptosis. It has been verified that Omi/HtrA2 is related to apoptosis due to oxidative stress, which may play an important role in the integrity of mitochondria. Ucf-101 is a specific inhibitor of Omi/HtrA2 and it has been demonstrated that Ucf-101 has organ protective effects in a variety of in vitro and in vivo studies.

The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain.

Ethnopharmacological Relevance: Oxymatrine is extracted from the traditional Chinese herb Sophora flavescens Ait, possesses anti-inflammatory, anti-oxidative and anti-apoptotic properties, and has been used for the treatment of chronic viral hepatitis and many other diseases.

Aims Of The Study: This study aimed to investigate the effects of oxymatrine on inflammatory response mediated by Toll-like receptor4 (TLR4) and nuclear factor kappa-B (NF-κB), oxidative injury induced by 12/15 lipoxygenase (12/15-LOX), phosphorylated p38 mitogen activated protein kinase (phosphor-p38 MAPK) and cytosolic phospholipase A2 (cPLA2), and neuronal cell apoptosis in rat brain with intracerebral hemorrhage (ICH).

Materials And Methods: Wistar rats were treated intraperitoneally with 60 or 120mg/kg of oxymatrine daily for 5 days following ICH.

Ginkgolide B reduces neuronal cell apoptosis in the traumatic rat brain: possible involvement of toll-like receptor 4 and nuclear factor kappa B pathway.

Ginkgolide B (GB) has been demonstrated to have a variety of pharmacological actions. Accumulating evidence indicates that GB may exert a protective effect on brain injury. The study was designed to investigate the influence of GB on toll-like receptor 4 (TLR-4) and nuclear factor κB (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI).

Ginkgolide B reduces neuronal cell apoptosis in the hemorrhagic rat brain: possible involvement of Toll-like receptor 4/nuclear factor-kappa B pathway.

Ethnopharmacological Relevance: Ginkgolide B (GB) is one of the ginkgolides that have been isolated from leaves and root bark of the Chinese tree Ginkgo biloba L. (Ginkgoaceae), and is a specific and potent antagonist of platelet activating factor. There is a large body of data showing that GB possesses a markedly neuroprotective property against ischemia-induced impairment in vivo and in vitro.

Time course of plasma leptin concentrations after acute spontaneous basal ganglia hemorrhage.

Background: Brain cortex leptin messenger ribonucleic acid (mRNA) expression and serum leptin level are up-regulated in ischemic mouse brain, as well as in rat brain with traumatic brain injury. Elevated leptin plasma levels predict cerebral hemorrhagic stroke independently of traditional risk factors. The goal of this study was to investigate change in plasma leptin level after intracerebral hemorrhage (ICH) and to evaluate its relation with disease outcome.

Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury.

Objective: To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI).

Materials And Methods: Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg OMT after TBI once a day till day 5. Rats were killed by decapitation at hours 2, 6 and 12, and days 1, 2, 3 and 5 after TBI.

[Change in plasma microparticle procoagulant activity after traumatic brain injury].

Objective: To observe the serial changes of plasma microparticle procoagulant activity in patients with traumatic brain injury (TBI) and evaluate its correlations with outcome and pathophysiology of TBI.

Methods: A total of 139 consecutive patients with isolated moderate or severe head trauma and 40 age- and sex-matched healthy controls were enrolled. Plasma samples were obtained on entry in healthy controls, as well as on admission and at day 1, day 2, day 3, day 5, and day 7 after TBI in the patients.

High S100B levels in cerebrospinal fluid and peripheral blood of patients with acute basal ganglial hemorrhage are associated with poor outcome.

Background: S100B is involved in brain injury. This study aimed to determine plasma and cerebral spinal fluid (CSF) levels of S100B in patients with spontaneous intracerebral hemorrhage (ICH), and to correlate S100B levels with Glasgow Coma Scale (GCS) scores, ICH volumes, presence of intraventricular hemorrhage (IVH), and survival rate, and to correlate CSF S100B levels with plasma S100B levels as well as CSF interleukin-1beta (IL-1β) levels.

Methods: Ten patients with suspicion of subarachnoid hemorrhage and 38 patients with spontaneous basal ganglia hemorrhage were included in the study.

High concentrations of resistin in the peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

Purpose: Resistin increases in peripheral blood of patients with intracerebral hemorrhage (ICH). We sought to evaluate its relation with disease outcome.

Materials And Methods: Thirty healthy controls and 86 patients with acute ICH were included.

Change in plasma S100B level after acute spontaneous basal ganglia hemorrhage.

S100B has been described as a marker of brain injury. However, not much is known regarding change in plasma S100B and its relation with mortality after spontaneous intracerebral hemorrhage (ICH).Thus, we sought to investigate change in plasma S100B level after ICH and to evaluate its relation with disease outcome.

High concentrations of procoagulant microparticles in the cerebrospinal fluid and peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

Background: Apoptosis plays an important role in further brain injury after intracerebral hemorrhage (ICH). Procoagulant microparticles (MPs) are shed from the plasma membrane of apoptotic cells. The objective of this study was to determine plasma and cerebrospinal fluid (CSF) levels of MPs in patients with spontaneous ICH and to correlate MP levels with Glasgow Coma Scale (GCS) scores, ICH volumes, presence of intraventricular hemorrhage (IVH), and survival rate.

[Electrophysiological study of 16 patients with severe N-hexane neuropathy].

Objective: To observe electrophysiological changes of severe N-hexane neuropathy getting active therapies and discuss its prognosis.

Methods: A follow-up study involved 16 adult severe N-hexane neuropathy patients who got active therapies was performed. EMG in right muscle of thenar, tibial muscle, and vastus medialis, NCV in right median nerve, common peroneal nerve, and sural nerve were determined and analyzed before treatment and in the first, the third, the ninth, and the twenty-fourth month after treatment.