Guidelines for laboratory testing and result reporting of antibody to hepatitis C virus. Centers for Disease Control and Prevention.

Testing for the presence of antibody to hepatitis C virus (anti-HCV) is recommended for initially identifying persons with hepatitis C virus (HCV) infection (CDC. Recommendations for prevention and control of hepatitis C virus [HCV] infection and HCV-related chronic disease. MMWR 1998;47[No. RR-19] :1-33). Testing for anti-HCV should include use of an antibody screening assay, and for screening test-positive results, a more specific supplemental assay. Verifying the presence of anti-HCV minimizes unnecessary medical visits and psychological harm for persons who test falsely positive by screening assays and ensures that counseling, medical referral, and evaluation are targeted for patients serologically confirmed as having been infected with HCV. However, substantial variation in reflex supplemental testing practices exists among laboratories, and an anti-HCV-positive laboratory report does not uniformly represent a confirmed positive result. These guidelines expand recommendations for anti-HCV testing to include an option for reflex supplemental testing based on screening-test-positive signal-to-cut-off (s/co) ratios. Use of s/co ratios minimizes the amount of supplemental testing that needs to be performed while improving the reliability of reported test results. These guidelines were developed on the basis of available knowledge of CDC staff in consultation with representatives from the Food and Drug Administration and public health, hospital, and independent laboratories. Adoption of these guidelines by all public and private laboratories that perform in vitro diagnostic anti-HCV testing will improve the accuracy and utility of reported anti-HCV test results for counseling and medical evaluation of patients by health-care professionals and for surveillance by public health departments.     

Genetic polymorphisms and heart failure.

Heart failure is a complex clinical syndrome. There is evidence for a genetic contribution to the pathophysiology of heart failure. Considering the fundamental role of neurohormonal factors in the pathophysiology and progression of cardiac dysfunction and hypertrophy, variants of genes involved in this system are logical candidate genes in heart failure. In this report, genetic polymorphisms of the major neurohormonal systems in heart failure will be discussed. Studies on polymorphisms of the renin-angiotensin-aldosterone system (RAAS), adrenergic receptor polymorphisms, endothelin (receptor) polymorphisms, and a group of miscellaneous polymorphisms that may be involved in the development or phenotypic expression of heart failure will be reviewed. Research on left ventricular hypertrophy is also included. The majority of genetic association studies focused on the ACE I/D polymorphism. Initial genetic associations have often been difficult to replicate, mainly due to problems in study design and lack of power. Promising results have been obtained with genetic polymorphisms of the RAAS and sympathetic system. Considering the evidence so far, a modifying role for these polymorphisms seems more likely than a role of these variants as susceptibility genes. Besides the need for larger studies to examine the effects of single nucleotide polymorphisms and haplotypes, future studies also need to focus on the complexity of these systems and study gene-gene interactions and gene-environment interactions.     

Route of lymphocyte migration through the high endothelial venule (HEV) in human palatine tonsil

Eleven palatine tonsils were collected from subjects who underwent tonsillectomy in Christian Medical College Hospital and the route of migration of lymphocytes through the high endothelial vessel was studied under EM. In the interendothelial route, migration of a lymphocyte through HEV wall began with the adhesion of a lymphocyte to the surface of endothelial cells by means of a short cytoplasmic projection in the vicinity of intercellular space. The projection extended into the cleft between adjacent endothelial cells. The lymphocyte migrated through HEV by diapedesis. After the lymphocyte had traversed the interendothelial space, it occupied the subendothelial space. In the transendothelial route, migration of a lymphocyte through HEV was initiated by adherence of the lymphocyte to the endothelial cell. The adherent lymphocyte compressed or invaginated into the cytoplasm of the endothelial cell, entered the endothelial cell, was completely enclosed within the endothelial cell cytoplasm, and emerged from the endothelial cell to occupy the subendothelial space. Evidence is presented from static transmission electron microscopic pictures for the migration of lymphocytes by both interendothelial and transendothelial routes through the high endothelial venule.     

Brain and kidney of progressive multifocal leukoencephalopathy patients contain identical rearrangements of the JC virus promoter/enhancer

The kidneys of six progressive multifocal leukoencephalopathy (PML) patients were examined by PCR amplification for the presence of JC virus. Amplification of three different areas of the viral genome from multiple samples of each kidney revealed three that were positive for the virus. The use of a PCR-based typing assay on all tissue samples, and cloned sequences from the viral coding region from each positive kidney showed that the same viral genome was present in the kidney as in the brain of the patient. Regulatory region clones all had the archetypal promoter/enhancer structure. However, when PCR fragments from the regulatory region were digested with a restriction enzyme which cuts in region D, the region most often deleted in PML-type promoters, a low level of undigested DNA remained. This DNA refractory to digestion had a rearranged sequence identical to that of the unique rearranged promoter in the brain of each patient. © 1994 Wiley-Liss, Inc.     

Effects of Ethanol on Arachidonic Acid Incorporation Into Lipids of a Plasma Membrane Fraction Isolated from Brain Cerebral Cortex

In the presence of ATP, MgCl2, and CoASH, somal plasma membranes isolated from rat cerebral cortex were active in transferring arachidonic acid to phosphatidylinositols, phosphatidylcholines, and triacylglycerols. Ethanol (350-525 mM) added to the incubation mixture inhibited arachidonic acid incorporation into phospholipids, while it enhanced the incorporation into triacylglycerols. Under these conditions, ethanol was found to react with arachidonic acid to form arachidonoyl ethyl ester. The incorporation of labeled arachidonic acid into glycerolipids as well as the synthesis of ethyl esters required the presence of ATP and CoASH for maximal activity. Nevertheless, each uptake process exhibited a unique pH profile. The esterification of arachidonic acid was not specific for ethanol as other aliphatic alcohols (e.g., propanol and butanol) were also able to react with labeled arachidonic acid to form the respective esters. Somal plasma membranes isolated from mice after chronic ethanol administration showed an increase in arachidonoyl transfer to both phospholipids and triacylglycerols. When these membranes were challenged with ethanol (325 mM), those isolated from the chronic ethanol group showed a greater increase in the labeling of triacylglycerols and ethyl esters than those from controls. Thus, different acyltransferases exhibite different responses to the effects of ethanol in vitro and in vivo.     

Actinobacillus actinomycetemcomitans prosthetic valve endocarditis

Actinobacillus actinomycetemcomitans, a fastidious gram-negative bacillus, has been reported as the cause of prosthetic valve endocarditis in 11 patients. Two additional patients are reported and the literature is reviewed. All cases occurred greater than 1 year after implantation of the prosthesis. Six of the 13 patients had had recent dental work or had poor dentition. Three patients had received endocarditis prophylaxis. Ten of 13 were cured with antibiotics alone. Only one patient suffered from congestive heart failure, and only one had documented evidence of major systemic emboli during antimicrobial therapy. Valve replacement was necessary in only two during antimicrobial therapy. A actinomycetemcomitans should be considered as a possible etiologic agent in late prosthetic valve endocarditis, particularly when blood cultures are initially negative. A regimen of a beta-lactam antibiotic in combination with an aminoglycoside is recommended for 4-6 weeks. The excellent in vitro activity of the third-generation cephalosporins and rifampin promise new therapeutic options.     

Patellar instability after total knee arthroplasty

Twenty-five knees with symptomatic lateral patellar instability after total knee arthroplasty (TKA) were treated by operative realignment. Causes of instability include errors in surgical technique, quadriceps imbalance, and trauma. Fourteen knees had proximal realignment, nine had combined proximal and distal realignment, and two had component revision. At an average follow-up period of 50 months, 20 knees had normal patellar tracking and five had recurrent instability. Two patellar tendon ruptures occurred after combined realignment. Proximal realignment alone, in the absence of component malposition, is recommended for the management of patellar instability. Component malposition should be corrected by component revision. Combined proximal and distal realignment procedures are recommended only with great caution because of the predisposition to serious complications such as patellar tendon rupture.