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Fatty acids resources:

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Thromb Res. 2000 Oct 1;100(1):9-17.
Plasma level of triglyceride-rich lipoprotein remnants is closely associated with the activation of coagulation factor VII in patients with myocardial infarction.

Saigo M, Abe S, Ogawa M, Biro S, Minagoe S, Maruyama I, Toda H, Kiyonaga K, Atsuchi Y, Tahara M, Mawatari K, Tei C.

First Department of Internal Medicine, Kagoshima, 890-8520, Sakuragaoka, Japan.

Remnant-like particles, which have been recognized to be atherogenic derivatives of chylomicrons and very low density lipoproteins, can be measured using a new assay kit. The purpose of the present study was to investigate the association of remnant-like particles with the coagulation system that has an important role in the pathogenesis of myocardial infarction. We assayed blood levels of total cholesterol, triglyceride, HDL-cholesterol, apolipoproteins, remnant-like particles-cholesterol, remnant-like particles-triglyceride, fibrinogen, factor VII antigen, activated factor VII, and tissue factor in 111 patients with a history of myocardial infarction and 128 control subjects. In simple regression analysis, plasma levels of remnant-like particles-cholesterol and remnant-like particles-triglyceride showed a significant positive correlation with the levels of activated factor VII (r=0.319, p<0. 001, and r=0.286, p=0.002, respectively) and the activated factor VII/factor VII antigen ratio (r=0.241, p=0.011, and r=0.249, p=0.008, respectively) in patients with myocardial infarction. In contrast, there were no significant differences between remnant-like particles and activated factor VII in control subjects. In stepwise multivariate regression analysis, the significant determinants of activated factor VII were remnant-like particles-cholesterol (10.2%), apolipoproteins A-I (5.1%), and E (7.1%); for the activated factor VII/factor VII antigen ratio, remnant-like particles-triglyceride (6. 2%), age at blood sampling (5.1%), and apolipoprotein A-I (4.0%) in patients with myocardial infarction. However, the significant determinants of activated factor VII and the activated factor VII/factor VII antigen ratio were HDL-cholesterol (9.9% and 9.2%, respectively) in control subjects. It is concluded that remnant-like particles may be a risk factor for myocardial infarction by activating the extrinsic coagulation pathway.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053611&dopt=Abstract



Thromb Res. 2000 Oct 1;100(1):27-34.
Platelet glycoprotein expression in patients with myelodysplastic syndrome.

Seidl C, Siehl J, Ganser A, Hofmann WK, Fischer M, Kirchmaier CM, Hoelzer D, Seifried E.

Department of Haematology and Oncology, J-W Goethe University, Frankfurt/Main, Germany.

Myelodysplastic syndromes (MDS) are characterized by a haematopoetic insufficiency that can lead to acute leukemia. A multistep pathogenesis caused by a clonal stem cell defect affecting several differentiation pathways has been proposed for MDS. Contrary to the better characterized alteration of lymphoid and myeloid differentiation, defects in thrombocytopoesis in MDS remain less clear. In the present study, we analyzed the expression of platelet glycoprotein (GP) Ia/IIa, IIb/IIIa, Ib/IX, and IV in 21 MDS patients (12 RA, 2 RARS, 4 RAEB, 1 RAEB-T, 2 CMML) and healthy controls by flowcytometric analysis and quantitation of platelet GP RNA using fluorescence-based PCR. We observed a reduced cell surface expression of GPIb (p<0.01) and GPIIb/IIIa (p<0.01), while GPIa/IIa and GPIV expression was only marginally different between patients and controls. In contrast, there was a two-fold increase of platelet GPIb and GPIIb RNA and a three-fold increase of GPIV RNA among MDS patients. Increased levels of platelet GPIb and GPIIb RNA were significantly more prominent among patients with RAEB(-T)/CMML (p<0. 05) in comparison to patients with RA/RARS. In conclusion, we demonstrate alterations in the cell surface expression and RNA content of platelet GPs in MDS patients. These data are consistent with dysmegakaryocytopoiesis and a defect in thrombocytopoiesis among MDS patients resulting from the clonal stem cell defect in MDS.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053613&dopt=Abstract



Thromb Res. 2000 Oct 1;100(1):47-54.
Human anti-heparin-platelet factor 4 antibodies are capable of activating primate platelets: towards the development of a HIT model in primates.

Ahmad S, Jeske WP, Walenga JM, Aldabbagh A, Iqbal O, Fareed J.

Cardiovascular Institute and Departments of Pathology and Thoracic & Cardiovascular Surgery, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA.

In the first step to establish an animal model of heparin-induced thrombocytopenia (HIT) that is physiologically relevant to humans, studies were undertaken to determine the similarities or differences between human and non-human primate (Macaca mulatta) platelets in HIT assay systems. The collagen-, ADP-, and TRAP-induced platelet aggregation, and flow cytometric analysis of P-selectin expression and microparticle formation were similar for both species platelets (p>0.1, n=18 each). The classical HIT assays using platelet-rich plasma (PRP) as well as a flow cytometric assay revealed the activation/aggregation and serotonin release assay (SRA) profiles for both primate and human platelets were similar in response to human HIT positive sera. All assays were heparin concentration-dependent; heparin, at 0.1 U/mL, produced maximum and similar platelet activation/aggregation and SRA responses with both primate (76+/-7%, n=18) and human (68+/-11%, n=20; p>0.1) platelets. At concentrations > or =10 U/mL, heparin suppressed the platelet aggregation and SRA responses in both systems. Primate and human platelets displayed similar behavior to low molecular weight heparin and pentasaccahride in HIT assay systems. Immunoglobulins isolated from serum of patients with HIT caused activation/aggregation of human (65+/-18%, n=10 donors) and primate (79+/-12%, n=6 monkeys, p>0.08) platelets. Unlike human platelets, the primate platelets exhibited a more consistent aggregation/release response (15 out of 18 primate platelets reactive). In contrast, human donors showed wide variations in the activation/release response (4 out of 10 reactive). These observations suggest that primate platelets are activatable by anti-H-PF4 antibodies, and support the hypothesis that primates can be used to develop an animal model to study the pathogenesis of HIT.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053616&dopt=Abstract



Thromb Res. 2000 Oct 1;100(1):61-72.
Activation of coagulation in C57BL/6 mice given verotoxin 2 (VT2) and the effect of co-administration of LPS with VT2.

Sugatani J, Igarashi T, Munakata M, Komiyama Y, Takahashi H, Komiyama N, Maeda T, Takeda T, Miwa M.

Department of Pharmaco-Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan.

To obtain better insight into the pathogenesis of verotoxin-producing Escherichia coli-associated diseases, in this study, we explored the effect of verotoxin 2 (VT2) on coagulation in an animal model. After being given VT2 (50 ng/kg, lethal dose), C57BL/6 mice showed progressively increasing expression of TF mRNA in the kidney and brain and elevated plasma levels of thrombin-antithrombin III complex (TAT), normotest, fibrinogen, and PAI-1 paralleling the disease course over 24 hours; platelet counts were decreased at 48 hours with hemorrhage in the kidney and brain. Co-administration of lipopolysaccharide (LPS, 0.5 mg/kg) with VT2 (50 ng/kg) exhibited more prominant and/or prolonged increase in not only expression of TF and PAI-1 mRNAs in the kidney and brain but also plasma levels of TAT, fibrinogen, and PAI-1 and was associated with more remarkable hemorrhage in the tissues. Although VT2 (5 ng/kg) was not a lethal dose, co-administration of LPS (0.5 mg/kg) with VT2 (5 ng/kg) enhanced the susceptibility to VT2, resulting in more prolonged elevation of TAT levels during the first 24 hours than that in the LPS group and a second elevation at 72 hours, followed by death. Plasma IL-1beta level reached a maximum at 24 hours after VT2 (50 ng/kg) injection prior to the increase in TAT levels, whereas the increase in TNFalpha level immediately after injection was associated with the increase in PAI-1 mRNA. These observations indicate that the activation of coagulation by VT2 may occur through a mechanism different from that used by LPS, since plasma TAT levels rose in the mice immediately after LPS injection and returned to normal over 36 hours.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053618&dopt=Abstract



J Cell Biochem. 2003;88(3):569-77.
Differential regulation of Notch signal transduction in leukaemia and lymphoma cells in culture.

Chiaramonte R, Calzavara E, Balordi F, Sabbadini M, Capello D, Gaidano G, Serra A, Comi P, Sherbet GV.

Department of Biomedical Sciences and Technologies, University of Milano, LITA-via Fratelli Cervi 93-20090 Segrate (MI), Italy.

The transduction of Notch signal plays an intricate role in cell differentiation and pathogenesis of haematological malignancies as well as in certain congenital conditions. We found no genomic changes in either gene in 34 leukaemic samples and 25 leukaemia and lymphoma cell lines. The functionality of Notch signalling was tested using HES1 gene activation. We show that Notch signalling is differentially regulated in T-acute lymphoblastic leukaemia (ALL) and B-lymphoma cells. The Notch pathway is intact in a majority of B-lymphoma cell lines, but EBNA2, which mimics notch function, can occasionally activate the pathway. In contrast, the Notch pathway is constitutively active in T-ALL. This is the first demonstration of a distinction between B-lymphomas and T-cell leukaemias in the functioning of the Notch-signalling pathway. This might be related to their pathogenesis. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12532332&dopt=Abstract [PubMed - in process]







The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

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