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Injury Leading (injury + leading)

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Medical Sciences100%

Selected Abstracts

Human herpes virus 6B: A possible role in epilepsy?

EPILEPSIA, Issue 11 2008
William H. Theodore
Summary Human herpes virus 6 (HHV6) infection is nearly ubiquitous in childhood and may include central nervous system invasion. There are two variants, HHV6A and HHV6B. Usually asymptomatic, it is associated with the common, self-limited childhood illness roseola infantum and rarely with more severe syndromes. In patients with immune compromise, subsequent reactivation of viral activity may lead to severe limbic encephalitis. HHV6 has been identified as a possible etiologic agent in multiple sclerosis, myocarditis, and encephalitis. A preponderance of evidence supports an association between HHV6 and febrile seizures. An ongoing multicenter study is investigating possible links between HHV6 infection, febrile status epilepticus, and development of mesial temporal sclerosis (MTS). Investigation of temporal lobectomy specimens showed evidence of active HHV6B but not HHV6A replication in hippocampal astrocytes in about two-thirds of patients with MTS but not other causes of epilepsy. It has been suggested that HHV6B may cause "excitotoxicity" by interfering with astrocyte excitatory amino acid transport. Although conventional inflammatory changes are not found in most MTS specimens, inflammatory modulators may play a role in neuronal injury leading to MTS as well. If the link between early viral infection, complex or prolonged febrile seizures, and later development of intractable temporal lobe epilepsy is confirmed, new therapeutic approaches to a common intractable epilepsy syndrome may be possible. [source]

Involvement of reactive oxygen species and nitric oxide radicals in activation and proliferation of rat hepatic stellate cells

LIVER INTERNATIONAL, Issue 1 2001
Gianluca Svegliati-Baroni
Abstract:Background /Aims: Reactive oxygen species (ROS) induce HSCs activation, proliferation and collagen gene expression in vitro. Nitric oxide (NO) represents a reactive molecule that reacts with ROS, yielding peroxynitrite. We thus verified the effect of NO on ROS-induced HSCs proliferation in vitro and correlated iNOS expression and ROS formation to HSCs activation in the early phase of liver injury leading to hepatic fibrosis in vivo. Methods/Results: HSCs were incubated with iron ascorbate (FeAsc) in vitro, which induced ROS production, ERK1/2 phosphorylation and increased cell proliferation. This effect was significantly reduced by the presence of the NO donor S-nitroso-N-acetylpenicillamine. Liver injury was induced in vivo in rats by dimethylnitrosamine administration. HSCs activation started 6 h after DMN administration and peaked at 1 week. ROS generation and neutrophil infiltration were evident for at least 48 h after DMN treatment, showing an identical distribution pattern. Only a few inflammatory cells expressed iNOS 6 h after DMN administration. Conclusions: we have shown that NO acts as a ROS scavenger in vitro, thus inhibiting HSCs proliferation. ROS production by infiltrating neutrophils occurs in the early phase of liver fibrosis and can represent a stimulus to HSCs activation in vivo. The reduced iNOS expression may account for the low NO levels and the inability to prevent the ROS-induced HSC activation in vivo. [source]

Radiation-induced conduction block: Resolution following anticoagulant therapy

MUSCLE AND NERVE, Issue 5 2005
Oscar Soto MD
Abstract Neurophysiologic studies documented proximal conduction blocks in a patient harboring a delayed radiation-induced brachial plexopathy. Since anticoagulants have been reported to be beneficial in radiation-induced neuropathies, the patient was started on acenocumarol. After 3 months of treatment there was significant improvement of clinical deficits, which correlated with resolution of conduction blocks. This observation suggests that ischemic nerve injury leading to disruption of the conduction properties of motor axons contributes to the pathogenesis of delayed radiation-induced peripheral nerve injuries. Muscle Nerve, 2005 [source]

Central bisectionectomy for centrally located hepatocellular carcinoma

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2008
J. G. Lee
Background: Central bisectionectomy, which involves the removal of the central hepatic segments (IVA, IVB, V, VIII) for hepatocellular carcinoma (HCC), is performed to reduce the volume of resected liver and to overcome the problem of insufficient future residual volume. Methods: Twenty-seven patients with HCC underwent central bisectionectomy from January 1998 to April 2007 in one hospital. The surgical techniques, clinicopathological characteristics and outcomes were reviewed. Results: The median operating time was 330 min. Twelve patients developed postoperative complications and two died. The most common complication, occurring in five patients, was bile duct injury leading to biloma or bile leakage. Median follow-up was 19·1 (range 1·4,102·2) months and eight patients developed a recurrence. Twenty-four patients were alive at the time of writing. Conclusion: Although biliary complications occur somewhat frequently, central bisectionectomy in centrally located HCC can be performed safely to preserve liver volume. Copyright © 2008 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]