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Fatty acids resources:

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J Orthop Res. 2002 Nov;20(6):1185-9.
Tenofovir treatment at 30 mg/kg/day can inhibit cortical bone mineralization in growing rhesus monkeys (Macaca mulatta).

Castillo AB, Tarantal AF, Watnik MR, Martin RB.

Orthopedic Research Laboratories, School of Medicine, University of California at Davis Medical Center, 4635 Second Avenue Suite 2000, Sacramento, CA 95817, USA. abcastillcdavis.edu

The acyclic nucleoside phosphonate analog, 9-[2-(R)-(phosphonomethoxy)propyl]adenine (PMPA; Tenofovir: Gilead Sciences, Inc., Foster City, CA), has been shown to effectively inhibit simian immunodeficiency virus (SIV) replication in rhesus macaques by blocking reverse transcription. However, chronic long-term tenofovir treatment at 30 mg/kg/day, intended to reduce viral replication and illness, has been shown to result in bone deformities and spontaneous fractures in rhesus monkeys. Based on these findings, we studied the effects of tenofovir treatment and pathogenic SIV infection on cortical bone remodeling in rhesus monkeys. Tibiae from tenofovir-treated or untreated, SIV-infected or uninfected, rhesus macaques were evaluated for bone microdamage and remodeling. We found that tenofovir treatment had a significant effect on osteoid (unmineralized bone) seam width in tibial cross-sections. Regardless of SIV infection status, half of the tenofovir-treated animals had significantly increased osteoid seam widths in tibial cortical bone resulting in an osteomalacia-like condition. Pathogenic SIV infection significantly increased tibial resorption cavity density. and this increase was normalized by tenofovir treatment. These results suggest that tenofovir treatment at 30 mg/kg/day inhibits mineralization of newly formed bone. SIV infection results in increased tibial resorption cavity density, while tenofovir treatment tends to minimize this increase. Both defective mineralization of newly formed bone and increased resorption cavity density may result in greater bone fragility.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12472227&dopt=Abstract

Plant Physiol. 2002 Sep;130(1):487-93.
Nitric oxide negatively modulates wound signaling in tomato plants.

Orozco-Cardenas ML, Ryan CA.

Institute of Biological Chemistry, Washington State University, Pullman, Washington 99164-6340, USA.

Synthesis of proteinase inhibitor I protein in response to wounding in leaves of excised tomato (Lycopersicon esculentum) plants was inhibited by NO donors sodium nitroprusside and S-nitroso-N-acetyl-penicillamine. The inhibition was reversed by supplying the plants with the NO scavenger 2-(4-carboxiphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. NO also blocked the hydrogen peroxide (H(2)O(2)) production and proteinase inhibitor synthesis that was induced by systemin, oligouronides, and jasmonic acid (JA). However, H(2)O(2) generated by glucose oxidase and glucose was not blocked by NO, nor was H(2)O(2)-induced proteinase inhibitor synthesis. Although the expression of proteinase inhibitor genes in response to JA was inhibited by NO, the expression of wound signaling-associated genes was not. The inhibition of wound-inducible H(2)O(2) generation and proteinase inhibitor gene expression by NO was not due to an increase in salicylic acid, which is known to inhibit the octadecanoid pathway. Instead, NO appears to be interacting directly with the signaling pathway downstream from JA synthesis, upstream of H(2)O(2) synthesis. The results suggest that NO may have a role in down-regulating the expression of wound-inducible defense genes during pathogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226527&dopt=Abstract

Plant Physiol. 2002 Sep;130(1):494-503.
Resistance of cultivated tomato to cell content-feeding herbivores is regulated by the octadecanoid-signaling pathway.

Li C, Williams MM, Loh YT, Lee GI, Howe GA.

Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824, USA.

The octadecanoid signaling pathway has been shown to play an important role in plant defense against various chewing insects and some pathogenic fungi. Here, we examined the interaction of a cell-content feeding arachnid herbivore, the two-spotted spider mite (Tetranychus urticae Koch), with cultivated tomato (Lycopersicon esculentum) and an isogenic mutant line (defenseless-1 [def-1]) that is deficient in the biosynthesis of the octadecanoid pathway-derived signal, jasmonic acid (JA). Spider mite feeding and fecundity on def-1 plants was significantly greater than on wild-type plants. Decreased resistance of def-1 plants was correlated with reduced JA accumulation and expression of defensive proteinase inhibitor (PI) genes, which were induced in mite-damaged wild-type leaves. Treatment of def-1 plants with methyl-JA restored resistance to spider mite feeding and reduced the fecundity of female mites. Plants expressing a 35S::prosystemin transgene that constitutively activates the octadecanoid pathway in a Def-1-dependent manner were highly resistant to attack by spider mites and western flower thrips (Frankliniella occidentalis), another cell-content feeder of economic importance. These findings indicate that activation of the octadecanoid signaling pathway promotes resistance of tomato to a broad spectrum of herbivores. The techniques of amplified fragment length polymorphism (AFLP) and bulk segregant analysis were used to map the Def-1 gene to a region on the long arm of chromosome 3 that is genetically separable from the map position of known JA biosynthetic genes. Tight linkage of Def-1 to a T-DNA insertion harboring the maize (Zea mays) Dissociation transposable element suggests a strategy for directed transposon tagging of the gene.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226528&dopt=Abstract

J Atheroscler Thromb. 2002;9(3):139-44.
Oxidized LDL antibodies (OLAB) in patients with beta-thalassemia major.

Brizzi P, Isaja T, D'Agata A, Malaguarnera L, Malaguarnera M, Musumeci S.

Department of Internal Medicine, University of Sassari, Sassari, Italy.

Thalassemic (TM) patients are subjected to peroxidative tissue injury because of continuous blood transfusions. It has been documented that circulating LDL from TM patients show marked oxidative modification, that could represent an event leading to atherogenesis. We investigated in 75 beta-TM patients the levels of oxidized LDL antibody (OLAB) to asses their correlation with total cholesterol, LDL and HDL cholesterol, triglycerides Apo A-1 and Apo B. OLAB/mg chol-LDL is greater in TM patients than healthy controls (p<0.001). No correlation was found between OLAB and age, sex of patients, mean blood consumption, mean serum ferritin, mean transaminases, PT, PTT, and fibrinogen. A significant positive correlation was found between OLAB and triglycerides in TM patients (p<0.001). Also a significant correlation was found between OLAB/mg chol-LDL and level of triglycerides in TM patients, but not with total cholesterol, LDL and HDL chols, Apo A-1 and Apo B. On the contrary in the healthy controls this correlation between OLAB and OLAB/mg chol-LDL versus triglycerides was negative and not significant. High levels of OLAB/mg chol-LDL in patients with beta-thalassemia, in absence of evident signs of atherosclerosis, suggest some regulatory mechanisms on the lipid peroxidation which modulate the deposition of ox-LDL in the macrophages and support the hypothesis that both serum iron and triglycerides are involved in the pathogenesis of LDL oxidation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226555&dopt=Abstract

IM4520.spb.edu

A molecular epidemiologic study of 35 Mycobacterium tuberculosis isolates from 19 patients was conducted to define a nosocomial outbreak of multidrug-resistant tuberculosis in St. Petersburg, Russia. IS 6110-restriction fragment length polymorphism (RFLP) fingerprinting, together with investigations to detect mutations conferring drug resistance, revealed relationships between the isolates and links between the cases. Three patients and a nurse exposed to active tuberculosis were proved to be involved in the outbreak; the source case was identified. The outbreak strain possessed a 17-band RFLP pattern and a spoligoprofile (signals 35-43) characteristic of the W-Beijing family as well as distinctive mutations in katG315, rpoB531, embB306 and rpsL43. This specific RFLP pattern has previously been identified among Mycobacterium tuberculosis W-Beijing strains isolated across the former Soviet Union and in the St. Petersburg area of Russia. The spread of multidrug-resistant strains of W-Beijing genotype in the general population and in hospital settings presents a serious threat for public health in Russia. Specific pathogenic properties of W-Beijing genotype strains, such as enhanced transmissibility and the ability to cause reinfection and to readily acquire drug resistance to major antituberculosis drugs, along with special features of host response, have yet to be investigated.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226690&dopt=Abstract

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