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Fatty acids resources:

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Zhonghua Yi Xue Za Zhi. 2003 Jan 10;83(1):24-6.
[A novel molecular mechanism of congenital FV deficiency: mutation in the intron acceptor splice site of human blood coagulation FV gene]

[Article in Chinese]

Fu WJ, Hou J, Wang DX, Yu RQ.

Department of Hematology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.

OBJECTIVE: To explore the molecular mechanism involved in patient with congenital FV deficiency. METHODS: Activity of FV was determined by biochemical method. The PCR products of FV gene was analyzed by DNA sequencing directly or cloned into T-vector prior to DNA analysis. The mutation of FV gene in proband and his family numbers was analysed by restriction enzyme analysis. Its occurrence was investigated in the control group. DNA was extracted from the peripheral blood mono1nuclear cells of the proband, male, 18 years old, and his parents. The PCR products were analyzed by direct sequencing or cloned into T-vector prior to DNA analysis. One hundred patients with different kind of hemotopathy were used as controls. RESULTS: A single point mutation, AG-->GG was found at position 3' splice site of intron 8 of the proband. This mutation was confirmed by family screening. CONCLUSION: A single point mutation, AG-->GG at position 3' splice site of intron 8 mutation of FV gene is related to the pathogenesis of congenital FV deficiency.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757640&dopt=Abstract

J Coll Physicians Surg Pak. 2003 May;13(5):297-301.
A review of rotavirus diarrhea in Pakistan: how much do we know?

Ali NK, Bhutta ZA.

Department of Paediatrics, The Aga Khan University Hospital, Karachi.

INTRODUCTION: Rotavirus diarrhea has a worldwide distribution, infecting almost all children by the age of 3-5 years. EPIDEMIOLOGY: A comparable etiological 2-year survey carried out by the W.H.O Diarrheal Disease control (CDD) Program in 1991, in a multicenter study in 5 developing countries including Pakistan revealed that Rotavirus was found to be the most frequently detected pathogen in diarrheal episodes, during the first year of life, with the highest incidence (20%) occurring among 6-11 months old. Two other studies done in Pakistan, in under five children done in Lahore (between 1985 and 1991) and Rawalpindi (between May 1983 and April 1984) showed that Rotavirus was the second most common Diarrhea causing enteric pathogen following E.Coli TRANSMISSION: Rotaviruses are shed in high concentrations 2 days before and as many as 10 days after onset of symptoms in immunocompetent hosts, thus being an important source of viral transmission. CLINICAL COURSE: A multicenter study in 5 developing countries including Pakistan conducted by WHO CDD program revealed that only 1.8 % of cases presented with severe dehydration and these were mostly due to Rotavirus, V.Cholerae and ETEC13. DIAGNOSTIC TESTS: A study conducted in local hospitals in Pakistan during the period of October 1985-April 1986 compared the different diagnostic modalities for the detection of rotavirus in the faeces of children with acute diarrhea. The study all methods detected Rotavirus to varying degrees but ELISA was found to be the most sensitive method with 72.4% stools being positive. PREVENTIVE STRATEGIES: A study was conducted in Lahore (Pakistan) among 72 infants 6 weeks old in 1991 to assess safety and efficacy of RRV vaccine. It was found that of all infants given RRV with OPV, 50% had a two to four-fold rise in neutralization titers against rotavirus. RRV was found to be safe and not associated with adverse reactions in the 6 weeks old infants. CONCLUSION: With regards to Pakistan, there is a great need for defining rotavirus associated disease burden and strain prevalence. We also need to conduct Rotavirus vaccine trials to assess its efficacy and safety in our setting.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757686&dopt=Abstract [PubMed - in process]

Cell. 2003 May 16;113(4):457-68.
Interaction of Akt-phosphorylated ataxin-1 with 14-3-3 mediates neurodegeneration in spinocerebellar ataxia type 1.

Chen HK, Fernandez-Funez P, Acevedo SF, Lam YC, Kaytor MD, Fernandez MH, Aitken A, Skoulakis EM, Orr HT, Botas J, Zoghbi HY.

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.

Spinocerebellar ataxia type 1 (SCA1) is one of several neurological disorders caused by a CAG repeat expansion. In SCA1, this expansion produces an abnormally long polyglutamine tract in the protein ataxin-1. Mutant polyglutamine proteins accumulate in neurons, inducing neurodegeneration, but the mechanism underlying this accumulation has been unclear. We have discovered that the 14-3-3 protein, a multifunctional regulatory molecule, mediates the neurotoxicity of ataxin-1 by binding to and stabilizing ataxin-1, thereby slowing its normal degradation. The association of ataxin-1 with 14-3-3 is regulated by Akt phosphorylation, and in a Drosophila model of SCA1, both 14-3-3 and Akt modulate neurodegeneration. Our finding that phosphatidylinositol 3-kinase/Akt signaling and 14-3-3 cooperate to modulate the neurotoxicity of ataxin-1 provides insight into SCA1 pathogenesis and identifies potential targets for therapeutic intervention.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757707&dopt=Abstract

Cell. 2003 May 16;113(4):469-82.
The pathogen-inducible nitric oxide synthase (iNOS) in plants is a variant of the P protein of the glycine decarboxylase complex.

Chandok MR, Ytterberg AJ, van Wijk KJ, Klessig DF.

Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, NY 14853, USA.

A growing body of evidence indicates that nitric oxide (NO) plays important signaling roles in plants. However, the enzyme(s) responsible for its synthesis after infection was unknown. Here, we demonstrate that the pathogen-induced, NO-synthesizing enzyme is a variant form of the P protein of glycine decarboxylase (GDC). Inhibitors of the P protein of GDC block its NO synthase (NOS)-like activity, and variant P produced in E. coli or insect cells displays NOS activity. The plant enzyme shares many biochemical and kinetic properties with animal NOSs. However, only a few of the critical motifs associated with NO production in animals can be recognized in the variant P sequence, suggesting that it uses very different chemistry for NO synthesis. Since nitrate reductase is likely responsible for NO production in uninfected or nonelicited plants, our results suggest that plants, like animals, use multiple enzymes for the synthesis of this critical hormone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757708&dopt=Abstract

Int Immunopharmacol. 2003 May;3(5):693-706.
The use of selective pharmacological inhibitors to delineate signal transduction pathways activated during complement receptor-mediated degranulation in chicken heterophils.

Kogut MH, Lowry VK, Farnell M.

USDA-ARS, Southern Plains Agricultural Research Center, 2881 F&B Road, College Station, TX 77845, USA. kogufsru.tamu.edu

Complement receptors (CRs), along with Fc receptors, play a primary role in the removal of bacterial pathogens in poultry. The binding of serum-opsonized bacteria to CR results in the secretion of both toxic oxygen metabolites and antibacterial granules. We have previously shown that the stimulation of chicken heterophils with serum-opsonized Salmonella enteritidis induced tyrosine kinase-dependent phosphorylation regulated degranulation. In the present studies, we used selective pharmacological inhibitors to investigate the roles of protein tyrosine kinases, phospholipases C and D (PLC and PLD), phosphatidylinositol 3'-kinase (PI3-K), and the super family of mitogen-activated protein kinases (MAPKs) on CR-mediated heterophil degranulation. Inhibitors of receptor-linked tyrosine kinases (the tryphostins AG1478 and AG1296) had no attenuating effects on CR-mediated degranulation. However, PP2, a selective inhibitor of the src family of protein tyrosine kinases, and piceatannol, an inhibitor of Syk tyrosine kinases, both significantly attenuated the CR-mediated degranulation. Additionally, the specific inhibitors of PLC, U73122, and PI3-K, LY294002, significantly decreased CR-mediated heterophil degranulation. Two inhibitors of PLD-mediated signaling, 2,3-diphosphoglycerate (2,3-DPG) and 1-butanol, hindered degranulation. Addition of purified PLD restored control levels of degranulation in heterophils in which PLD was inhibited. Lastly, SP600125, a selective inhibitor of c-Jun N-terminal kinase (JNK), inhibited degranulation; whereas neither PD98059, the inhibitor of p38 MAPK, nor SB203580, the inhibitor of extracellular signal-regulated kinase, had any effect on CR-mediated heterophil degranulation. These studies demonstrate that CRs on chicken heterophils lack intrinsic tyrosine kinase activity, but that binding of serum-opsonized bacteria activates both proximal tyrosine kinases (src and Syk kinases), but differentially activates downstream tyrosine kinases (JNK, but not p38 nor ERK). Activation of src and Syk kinases plays a significant role in signal transduction of heterophil degranulation probably by stimulating downstream phosphorylation of PLC, PLD, and PI3-K. PI3-K has also been recently shown to be an upstream mediator of JNK activation, suggesting that this enzyme can induce signaling as both a lipid kinase and protein kinase. Engaging CRs on chicken heterophils activates a proximal tyrosine kinase (src and Syk kinases)-->PLC (PLD)-->PI3-K-->JNK signal transduction pathway that induces degranulation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757738&dopt=Abstract [PubMed - in process]

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