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Fatty acids resources:

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Intern Med. 2003 Jul;42(7):571-5.
An association between an antibody against Chlamydia pneumoniae and ischemic stroke in elderly Japanese.

Kawamoto R, Kajiwara T, Oka Y, Takagi Y.

Department of Internal Medicine, Nomura Municipal Hospital, Ehime.

OBJECTIVE: Chlamydia pneumoniae (Cp) is an important pathogen for infections of the respiratory tract; recently, also a number of reports suggesting its relation to atherosclerosis. This study was performed to clarify the relation between Cp infection and ischemic stroke. PATIENTS: Forty elderly patients with ischemic stroke (age 75 +/- 6.6; male 57.5%) and 85 elderly control subjects without a history of ischemic stroke (age 74 +/- 8.1; male 43.5%) were investigated. METHODS: Patients were divided into four groups according to clinical diagnosis: 1) atherothrombotic infarction, 2) lacunar infarction, 3) those with cardiac embolism, and 4) non-classifiable. Cp infection was determined by measuring the anti-Cp IgG specific antibody level (Cp IgG index) using enzyme-linked immunosorbent assay (ELIZA) method. Those below the 1.10 Cp IgG index were determined as seronegative and those above 1.10 as seropositive. RESULTS: We found that 20 cases (87.0%) of atherothrombotic infarction, 6 (66.7%) of lacunar infarction, 3 (50.0%) others and 52 (61.2%) control were Cp seropositive. Cp seropositiveness, as adjusted by multiple regression analysis using various known risk factors, was a significant independent contributing factor for ischemic stroke (p = 0.017) and was associated with an increased risk for atherothrombotic infarction (odds ratio, 12.6; 95% CI, 2.0-79.3). CONCLUSION: This suggests that Cp infection is also an important risk factor for ischemic stroke, particularly atherothrombotic infarction in elderly Japanese.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12879948&dopt=Abstract [PubMed - in process]

Eat Weight Disord. 2003 Jun;8(2):130-7.
The role of leptin in the etiopathogenesis of anorexia nervosa and bulimia.

Calandra C, Musso F, Musso R.

Department of Medical and Specialist Sciences, Psychiatric Division, University of Catania, Azienda Policlinico, Catania, Italy. calandra.carmeliscalinet.it

Leptin is an adipocyte-derived signal factor (167 amino acid protein) encoded by the ob gene in chromosome 7q31 that regulates eating behaviour via central neuroendocrine mechanisms. It has been shown that serum leptin levels correlate with weight and percentage body fat in normal and obese individuals, but the exact correlation between leptin and body weight in anorexic and bulimic patients has not yet been clarified. We investigated leptin levels in the serum of 58 female subjects aged 15-36 years: 10 with bulimia nervosa (BN); 12 with anorexia nervosa (AN); 12 overweight controls (not BN); 12 weight-reduced controls (not AN); and 12 normal weight controls. The aim of the study was to evaluate the possible correlations between leptin levels and the body mass index (BMI) in all five groups. Our results showed that the serum leptin levels of the bulimic patients were similar to those of the healthy controls, with a positive correlation between leptin and BMI. Although bulimic patients have very bad nutritional behaviour, their leptin levels do not appear altered. Serum leptin was significantly (p<0.001) reduced in the anorexic patients because of the dramatic decrease in adipose mass caused by the nutritional defect, as: is further supported by the significantly (p<0.001) low level of transferrinemia. Our data suggest that, although significantly reduced, serum leptin levels in fasting anorexic patients are non-linearly related to body weight (BMI).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12880190&dopt=Abstract [PubMed - in process]

Glycobiology. 1999 May;9(5):469-79.
Sequential deglycosylation and utilization of the N-linked, complex-type glycans of human alpha1-acid glycoprotein mediates growth of Streptococcus oralis.

Byers HL, Tarelli E, Homer KA, Beighton D.

Joint Microbiology Research Unit, Faculty of Clinical Dentistry, King's College School of Medicine and Dentistry, Caldecot Road, London SE5 9RW, UK.

Streptococcus oralis is the agent of a large number of infections in immunocompromised patients, but little is known regarding the mechanisms by which this fermentative organism proliferates in vivo. Glycoproteins are widespread within the circulation and host tissues, and could provide a source of fermentable carbohydrate for the growth of those pathogenic organisms with the capacity to release monosaccharides from glycans via the production of specific glycosidases. The ability of acute phase serum alpha1-acid glycoprotein to support growth of S.oralis in vitro has been examined as a model for growth of this organism on N-linked glycoproteins. Growth was accompanied by the production of a range of glycosidases (sialidase, N-acetyl-beta-D-glucosaminidase, and beta-D-galactosidase) as measured using the 4-methylumbelliferone-linked substrates. The residual glycoprotein glycans remaining during growth of this organism were released by treatment with hydrazine and their analysis by HPAEC-PAD and MALDI demonstrated extensive degradation of all glycan chains with only terminal N-acetylglucosamine residues attached to asparagines of the protein backbone remaining when growth was complete. Monosaccharides were released sequentially from the glycans by S.oralis glycosidases in the order sialic acid, galactose, fucose, nonterminal N-acetylglucosamine, and mannose due to the actions of exo-glycosidic activities, including mannosidases which have not previously been reported for S.oralis. All released monosaccharides were metabolized during growth with the exception of fucose which remained free in culture supernatants. Direct release of oligosaccharides was not observed, indicating the absence of endo-glycosidases in S.oralis. We propose that this mechanism of deglycosylation of host glycoproteins and the subsequent utilization of released monosaccharides is important in the survival and persistence of this and other pathogenic bacteria in vivo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10207179&dopt=Abstract

IUBMB Life. 2003 Apr-May;55(4-5):267-71.
The role of c-Jun N-terminal kinase (JNK) in Parkinson's disease.

Peng J, Andersen JK.

Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA.

Given the critical role that the c-Jun N-terminal kinase (JNK) pathway plays in regulating many of the cellular processes which are affected in Parkinson's disease (PD), the possible importance of JNK in disease pathogenesis is being increasingly recognized. Here we review recent findings implicating the JNK signaling pathway in animal models of Parkinson's disease and discuss the relationship between this pathway and the prominent pathological processes observed in the disease state. We suggest that regulation of the JNK signaling pathway may be a central facet in potential treatments for the disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12880208&dopt=Abstract [PubMed - in process]

J Parasitol. 2003 Jun;89(3):620-2.
Development of patent infection in immunosuppressed C57Bl/6 mice with a single Cryptosporidium meleagridis oocyst.

Huang K, Akiyoshi DE, Feng X, Tzipori S.

College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, Jiangsu Province, People's Republic of China.

The ability of Cryptosporidium meleagridis to produce patent infection was studied in adult C57BL/6 mice that were immunosuppressed with dexamethasone phosphate provided in the drinking water at a dosage of 16 microg/ml. Four days after the onset of immunosuppression, mice were orally challenged with 1, 3, 10, or 1,000 C. meleagridis TU1867 oocysts per mouse. The mice were monitored daily for 18 days postinoculation for oocyst shedding. Five of 10 mice given a single oocyst, 4 of 5 mice given 3 oocysts, and all 9 mice given either 10 or 1,000 oocysts became infected and began shedding oocysts 5-7 days after challenge and continued to shed oocysts until the end of the experiment on day 18 postchallenge. Approximately 10(7) oocysts per mouse per day were excreted, regardless of the challenge dose. Neither the noninfected, immunosuppressed nor the inoculated, nonimmunosuppressed control mice shed oocysts. The excreted oocysts were confirmed to be those of C. meleagridis by polymerase chain reaction-restriction fragment length polymorphism analysis. We show that C. meleagridis, originally classified as an avian pathogen but recently found in humans with cryptosporidiosis, can produce patent infection in mice infected with a single oocyst. Moreover, we demonstrate that the immunosuppressed C57BL/6 adult mouse is an ideal host for the propagation of clonal populations of C. meleagridis isolates for laboratory studies.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12880270&dopt=Abstract

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