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J Neurosci Res. 2000 Nov 1;62(3):440-50.
Evidence for oxidative damage in a murine leukemia virus-induced neurodegeneration.

Wilt SG, Dugger NV, Hitt ND, Hoffman PM.

Research Service, Department of Veterans Affairs Medical Center, Baltimore, Maryland 21201, USA. swilmaryland.edu

Vacuolation in cellular organelles within the central nervous system is a common manifestation of oxidative injury. We found that the spongiform vacuolation observed in PVC-211 murine leukemia virus (PVC-MuLV) neurodegeneration was associated with oxidative damage as detected by immunoreactivity for 3-nitrotyrosine and protein carbonyl groups. This oxidative injury was present in brain before or concomitant with the appearance of activated microglia, vacuolation, and gliosis that characterize PVC-MuLV neuropathology. Treatment of infected F344 rat pups with the antioxidant vitamin E transiently protected and prolonged the latency of PVC-MuLV neurodegeneration. Taken together, these findings implicate oxidative damage and lipid peroxidation in the pathogenesis of PVC-MuLV neurodegeneration. This animal model may be useful for studies of mechanisms and potential therapies for progressive neurodegeneration following a well-defined insult.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054813&dopt=Abstract

Yeast. 2000 Nov;16(15):1397-403.
Characterization of the L41 gene in Cryptococcus neoformans: its application as a selectable transformation marker for cycloheximide resistance.

Varma A, Kwon-Chung KJ.

Molecular Microbiology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

A transformation system using resistance to the antibiotic cycloheximide as a dominant selectable marker was developed for the pathogenic yeast Cryptococcus neoformans. A 3.5 kb DNA fragment containing a gene encoding the ribosomal protein L41 was cloned from a wild-type strain of C. neoformans which is sensitive to cycloheximide. The open reading frame of the L41 gene contains five introns and encodes a protein of 107 amino acids, which is similar to those reported for other yeasts. The cycloheximide resistance gene to be used as a marker was constructed by replacing a DNA segment of the wild-type L41 gene, which contained the amino acid proline at its 56th position with a homologous DNA segment from a mutant strain resistant to cycloheximide that contained leucine in that position. Cycloheximide resistant transformants were obtained by electroporation on YEPD plates, supplemented with 10-20 microg/ml cycloheximide, at a maximum efficiency of 300 transformants/microg plasmid DNA. While with other genes, most transformants of serotype D in C. neoformans maintain the transforming DNA as episomes, the cycloheximide-resistant transformants were all the result of ectopic genomic integration events. 2000 John Wiley & Sons, Ltd.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054820&dopt=Abstract

Diabetes Metab Res Rev. 2000 Sep-Oct;16 Suppl 1:S59-65.
Management of the diabetic Charcot foot.

Frykberg RG, Mendeszoon E.

Des Moines University, College of Podiatric Medicine, 3200 Grand Ave, Des Moines, IA 50312, USA. robert.frykbersmu.edu

The diabetic Charcot foot is a major limb-threatening complication of long-term diabetes mellitus and neuropathy. Although first described over 100 years ago, we are still lacking definitive studies regarding its prevalence in this population, precise etiology, or most effective treatments. Trauma in the presence of peripheral sensory neuropathy and abundant arterial perfusion seem to be the primary causal factors leading to this severe foot deformity. Misdiagnosis or delayed diagnosis of osteoarthropathy allows the destructive phase of this disorder to continue with resultant further destruction of the foot architecture. The authors discuss the natural history of this entity as well as potential treatment options and recommendations. Through a better understanding of the underlying pathogenesis, Charcot arthropathy can be more effectively managed and thereby limit the development of severe deformity, ulceration, infection and limb loss. 2000 John Wiley & Sons, Ltd.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054891&dopt=Abstract

Hawaii Med J. 2000 Sep;59(9):362-5.
Diarrhea-associated hospitalizations among children in Hawaii.

Effler PV, Holman RC, Parashar UD, Glass RI.

Hawaii Department of Health, Honolulu 96813, USA.

OBJECTIVE: To estimate the burden of diarrhea-associated hospitalizations among children in Hawaii. DESIGN: Retrospective analysis of hospital discharge records. PATIENTS: Children from 1 month through 4 years of age with a diarrhea-associated diagnosis listed on the hospital discharge record in Hawaii. SETTING: Acute care hospitals in the state of Hawaii, 1994 through 1997. RESULTS: During 1994-1997, 2288 children (11.3% of all hospitalizations for children < 5 years of age) had a diarrhea-associated diagnosis listed at hospital discharge. The average annual incidence (per 10,000 children) of diarrhea-associated hospitalizations was 62.3; the incidence was higher for children < 1 year (101.6) than for those 1 through 4 years of age (52.7). Rates for Hawaii were lower than national rates during 1993 through 1995 (US annual rate of 89 per 10,000 children). The median length of hospital stay was 2 days for diarrhea-associated hospitalizations, and 3 days for hospitalizations specifically associated with rotavirus-related diarrhea. Diarrhea-associated hospitalizations were highest during the period December through June. CONCLUSIONS: Diarrhea is an important cause of hospitalization among children in Hawaii, where approximately 1 in 32 children may be hospitalized by 5 years of age. The age-specific and temporal trends reported here are consistent with those previously described for rotavirus-associated hospitalizations, suggesting that this pathogen is a major contributor to the overall morbidity from diarrhea.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11055116&dopt=Abstract

Gene. 2003 Mar 27;307:31-40.
Identification of opcA gene in Neisseria polysaccharea: interspecies diversity of Opc protein family.

Zhu P, Klutch MJ, Derrick JP, Prince SM, Tsang RS, Tsai CM.

Division of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, FDA, Bethesda, MD 20892, USA.

The gene encoding the outer membrane adhesin/invasin protein OpcA was previously described in the genomes of two pathogenic Neisseria species, N. meningitidis (Nm) and N. gonorrhoeae (Ng). In order to understand the presence or absence of opcA in nonpathogenic Neisseria species, 13 strains of N. polysaccharea (Np), four strains of N. lactamica, three strains of N. subflava and nine strains of other species were examined by DNA hybridization, polymerase chain reaction (PCR) and nucleotide sequencing. The opcA gene was found in two Np strains (85322 and 89357). The Np-opcA gene is a novel member of this gene family with 93% homology to Ng-opcA. Comparison of opcA-surrounding regions among eight Neisseria strains revealed five types of genetic organization at the opcA locus in Neisseria, which result from insertion or deletion of genetic elements at the upstream region of opcA. Comparison of the deduced peptide sequences from two Np strains, two representative Ng strains, two representative Nm strains and 13 Nm sequence variants demonstrates interspecies diversity of the OpcA protein family with conserved transmembrane regions and species-specific polymorphism at the surface-exposed loops and periplasmic turns. Reverse transcription-PCR analysis and Northern blotting showed that Np-opcA was transcribable. From an alignment of the Np-OpcA and Ng-OpcA sequences against the three-dimensional crystal structure of Nm-OpcA we conclude that there is no obvious structural reason why these proteins would not be able to form stable, folded, outer membrane proteins. The data presented here provide additional information for understanding the distribution, variation and expression of opcA in Neisseria.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12706886&dopt=Abstract

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