Plaque array method and proteomics-based identification of biomarkers from Alzheimer's disease serum.

Background: Progressive accumulation of amyloid plaques in the regions of brain, carotid and cerebral arteries is the leading cause of Alzheimer's disease (AD) and related dementia in affected patients. The early identification of individuals with AD remains a challenging task relying on symptomatic events and thus the development of a biomarker-based approach will significantly aid in the diagnosis of AD.

Methods: Here we describe a flow cytometer-based serum biomarker identification method using plaque particles, and applying mass spectrometry based proteomic analysis of the isolated plaque particles for the identification of serum proteins present in the plaque particles.

Functions of Varicella-zoster virus ORF23 capsid protein in viral replication and the pathogenesis of skin infection.

The assembly of herpesvirus capsids is a complex process involving interactions of multiple proteins in the cytoplasm and in the nucleus. Based on comparative genome analyses, varicella-zoster virus (VZV) open reading frame 23 (ORF23) encodes a conserved capsid protein, referred to as VP26 (UL35) in other alphaherpesviruses. Mutagenesis using a VZV bacterial artificial chromosome system showed that ORF23 was dispensable for replication in vitro.

Mechanisms of microvascular wound repair II. Injury induces transformation of endothelial cells into myofibroblasts and the synthesis of matrix proteins.

Under normal growth conditions, in vitro dermal microvascular endothelial cells (HDMEC) retain an epithelioid morphology and do not synthesize matrix proteins found increased in scar tissue. When injured by a standard scratch, cells at the wound edge and within the culture transform into spindle-shaped, myofibroblast-like cells. To determine if the transformed cells synthesize matrix proteins, expression of type I collagen and alpha smooth muscle actin (alpha-SMA) was investigated by immunohistochemistry and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).

Mechanisms of microvascular wound repair I. Role of mitosis, oxygen tension, and I-kappa B.

To better understand the mechanisms of both normal reendothelialization and neointimal hyperplasia following injury, human dermal microvascular endothelial cells (HDMEC) were isolated from neonatal foreskin and studied in an in vitro model of the microvascular endothelium. In a standard 3-mm wound of nonproliferative HDMEC cultures, reendothelialization was complete at 32 h at a 20.8% (atmospheric) O(2) level.

Regulation of skin microvasculature angiogenesis, cell migration, and permeability by a specific inhibitor of PKCalpha.

Activation of protein kinase C (PKC) induces phenotypic changes in the morphology of microvascular endothelial cells that affect major functions of the microvasculature. These functions include the first stages of sprouting in angiogenesis, cell migration following wounding, and vascular permeability. The specific isoform(s) of PKC responsible for each of these changes has not been previously identified.

Occult hepatitis B virus infection in chronic liver disease: full-length genome and analysis of mutant surface promoter.

Background And Aims: Genome sequence of hepatitis B virus (HBV) from occult chronic infection is scarce. Fifty-six (9.4%) of 591 patients seronegative for hepatitis B surface antigen (HBsAg) with chronic liver disease were positive for HBV DNA.

Evaluation of serologic screening of blood donors in India reveals a lack of correlation between anti-HBc titer and PCR-amplified HBV DNA.

Background: Transfusion associated-HBV (TAHBV) is estimated at approximately 1.5 percent in postsurgical recipients and 50 percent or more in multiple-transfusion recipients in India. Not transfusing blood with high-titer anti-HBc, which reportedly correlates with the presence of HBV DNA, helped reduce TAHBV in Japan.