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Orthopade. 2002 Sep;31(9):900-7.
[Indication for and results of intertrochanteric osteotomy in slipped capital femoral epiphysis]

[Article in German]

Schai PA, Exner GU.

Orthopadische Universitatsklinik, Klinik Balgrist, Zurich, Switzerland. paschaplanet.ch

The progression of degenerative changes of the hip after slipped capital femoral epiphysis (SCFE) largely correlates with the patient's age at the time the deformity occurs and with the degree of the epiphyseal gliding. From the pathogenetic point of view, the altered biomechanical conditions of the hip joint with deformation of the proximal femur may result in an impingement of the femoral neck metaphysis against the anterior acetabular rim. Observations of the "natural course" or after "in situ fixation" of the epiphysis show the development of secondary hip arthritis at an average of 20 years after SCFE, specifically in slips with more than 30 degrees of epiphyseal gliding.The intertrochanteric osteotomy as introduced by G. Imhauser aims at restoring joint congruity to reduce the prearthrotic deformity and thus to decrease the incidence of later hip arthritis. The reorientation of the predominantly posteriorly slipped femoral epiphysis is achieved by an intertrochanteric flexion osteotomy, which reduces the potential for femoroacetabular impingement. On the basis of a long-term evaluation, the indication for and results of an intertrochanteric osteotomy for chronic unilateral SCFE were presented. Of the 51 patients operated on between 1962 and 1972 and examined clinically and radiographically at an average follow-up time of 24 years (20-29 years) after osteotomy, 55% showed a hip free of degenerative changes, 28% had developed moderate degenerative changes, and 17% had advanced arthritis. Aside from a few technical errors, the correction at the intertrochanteric level for moderate slips proved to be a safe procedure regarding risk for femoral head necrosis.The long-term development after SCFE is most important for patients with SCFE. More than half of the patients have hip joints free of degenerative changes more than 20 years after intertrochanteric osteotomy according to G. Imhauser, which compares favorably to the "natural course" or to "in situ fixation" and which supports the indication for this corrective procedure in SCFE.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232709&dopt=Abstract

Mol Psychiatry. 2002;7(8):867-73.
A transcript map encompassing a susceptibility locus for bipolar affective disorder on chromosome 4q35.

Blair IP, Adams LJ, Badenhop RF, Moses MJ, Scimone A, Morris JA, Ma L, Austin CP, Donald JA, Mitchell PB, Schofield PR.

Garvan Institute of Medical Research, 384 Victoria Street, Sydney 2010, Australia.

Bipolar affective disorder is one of the most common mental illnesses with a population prevalence of approximately 1%. The disorder is genetically complex, with an increasing number of loci being implicated through genetic linkage studies. However, the specific genetic variations and molecules involved in bipolar susceptibility and pathogenesis are yet to be identified. Genetic linkage analysis has identified a bipolar disorder susceptibility locus on chromosome 4q35, and the interval harbouring this susceptibility gene has been narrowed to a size that is amenable to positional cloning. We have used the resources of the Human Genome Project (HGP) and Celera Genomics to identify overlapping sequenced BAC clones and sequence contigs that represent the region implicated by linkage analysis. A combination of bioinformatic tools and laboratory techniques have been applied to annotate this DNA sequence data and establish a comprehensive transcript map that spans approximately 5.5 Mb. This map encompasses the chromosome 4q35 bipolar susceptibility locus, which localises to a "most probable" candidate interval of approximately 2.3 Mb, within a more conservative candidate interval of approximately 5 Mb. Localised within this map are 11 characterised genes and eight novel genes of unknown function, which together provide a collection of candidate transcripts that may be investigated for association with bipolar disorder. Overall, this region was shown to be very gene-poor, with a high incidence of pseudogenes, and redundant and novel repetitive elements. Our analysis of the interval has demonstrated a significant difference in the extent to which the current HGP and Celera sequence data sets represent this region.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232780&dopt=Abstract

Mol Psychiatry. 2002;7(8):899-902.
Polymorphism in the cholesterol 24S-hydroxylase gene is associated with Alzheimer's disease.

Kolsch H, Lutjohann D, Ludwig M, Schulte A, Ptok U, Jessen F, von Bergmann K, Rao ML, Maier W, Heun R.

Department of Psychiatry, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. heike.kolsckb.uni-bonn.de

Cholesterol and 24S-hydroxycholesterol are involved in the pathogenesis of Alzheimer's disease (AD). Increased serum cholesterol concentrations have been detected in patients with AD. 24S-Hydroxycholesterol is the primary cholesterol elimination product of the brain and possesses neurotoxic properties in vitro. The enzyme catalyzing the conversion of cholesterol to 24S-hydroxycholesterol, cholesterol 24S-hydroxylase (CYP46), is mainly expressed in neurons. Concentrations of 24S-hydroxycholesterol in cerebrospinal fluid (CSF) and serum differ significantly between AD patients and non-demented subjects. To test the hypothesis if polymorphisms in the CYP46 gene might influence the function of the respective enzyme and thus cholesterol metabolism in the human brain, we screened for polymorphisms in 114 AD patients and 144 healthy controls. Two intronic single nucleotide polymorphisms were observed and their allelic distribution was investigated. In our study sample, carriers of the C allele of the IVS3+43C --> T polymorphism were more prevalent in the group of AD patients than in healthy controls, while another IVS2-150A --> G polymorphism did not show a significant association with AD. The CC genotype of the IVS3+43C --> T polymorphism was associated with an increased 24S-hydroxycholesterol/cholesterol ratio in the CSF of AD patients. Our results indicate that the CYP46 gene locus may predispose to AD by increasing the 24S-hydroxycholesterol/cholesterol ratio in the brain.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232784&dopt=Abstract

J Infect Dis. 2002 Oct 1;186(7):976-82. Epub 2002 Sep 13.
Molecular basis for up-regulation by inflammatory cytokines of Shiga toxin 1 cytotoxicity and globotriaosylceramide expression.

Stricklett PK, Hughes AK, Ergonul Z, Kohan DE.

Division of Nephrology, University of Utah School of Medicine, and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah 84132, USA.

Mortality in postdiarrheal hemolytic-uremic syndrome (HUS) is associated with brain injury. Normally, brain cells are resistant to Shiga toxin (Stx), the putative pathogenic toxin in HUS. However, exposure of human brain endothelial cells (HBECs) to tumor necrosis factor (TNF) and/or interleukin (IL)-1 markedly up-regulates Stx receptor (globotriaosylceramide; Gb3) expression and cytotoxicity. To investigate how Gb3 is augmented, ceramide glucosyltransferase (CGT), lactosylceramide synthase (GalT2), Gb3 synthase (GalT6), and alpha-galactosidase were studied in HBECs exposed to TNF and IL-1. TNF, both alone and in combination with IL-1, increased Stx-1 toxicity, Gb3 content, and Stx-1 binding. TNF in combination with IL-1 increased CGT, GalT2, and GalT6 but did not change alpha-galactosidase activities or mRNA levels. Cytokine treatment did not change CGT, GalT2, or GalT6 mRNA half-lives. Thus, inflammatory cytokine up-regulation of the sensitivity of HBECs to Stx-1 is the result of up-regulation, most likely via transcription, of the activities of 3 enzymes involved in Gb3 synthesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232838&dopt=Abstract

J Infect Dis. 2002 Oct 1;186(7):1034-8. Epub 2002 Sep 13.
Correlation of phylogenetic lineages of group B Streptococci, identified by analysis of restriction-digestion patterns of genomic DNA, with infB alleles and mobile genetic elements.

Takahashi S, Detrick S, Whiting AA, Blaschke-Bonkowksy AJ, Aoyagi Y, Adderson EE, Bohnsack JF.

Division of Microbiology, Joshi-Eiyoh University, Chiyoda, Sakado, Saitama, Japan.

Phylogenetic lineages of pathogenic Streptococcus agalactiae (group B streptococci [GBS]) can be identified by analysis of restriction-digestion patterns (RDPs) of chromosomal DNA. The purpose of the present study was to correlate GBS RDP types and (1) alleles of the highly conserved gene encoding translation-initiation factor IF2, infB, and/or (2) the inserted elements IS1548 and GBSi1. Only 1 combination of serotype and infB allele was found within each RDP type. Strains within a particular RDP type also tend to have the same inserted elements in each of 3 loci examined. A novel insertion sequence, designated "IS1563," was found within all RDP type II-2 strains. Most RDP types could be identified by a combination of serotype, infB allele, and inserted elements at each of the loci. These molecular markers can be used to identify GBS populations and to correlate RDP types and phylogenetic lineages identified by different methods.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232847&dopt=Abstract

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