Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Cinchona bark contains alkaloids like quinine, quinidine, cinchonine and cinchonidine. These agents are effective antimalarial drugs and have been used clinically in malaria caused by Plasmodium falciparum. Previous studies show that quinine and quinidine exert effects on cardiovascular system. This study was conducted to examine the effect of cinchonine on human platelet aggregation. The results show that cinchonine inhibited platelet aggregation mediated by platelet agonists, epinephrine (200 microM), ADP (4.3 microM), platelet activating factor (PAF; 800 nM) and collagen (638 nM) but had no effect on arachidonic acid (AA; 0.75 mM). Cinchonine was most effective in inhibiting aggregation induced by platelet activating factor and epinephrine with IC50 values of 125 and 180 microM respectively, however, higher concentrations of cinchonine were required to inhibit aggregation mediated by ADP or collagen (IC50; 300 microM). Pretreatment of platelets with cinchonine inhibited aggregation caused by Ca2+ ionophore, A-23187 (6 microM), in a dose-dependent manner (IC50; 300 microM) indicating an inhibitory effect on Ca2+-signaling cascade. This was supported by measuring [Ca2+]i in platelets loaded with Fura-2AM where cinchonine inhibited the rise in cytosolic Ca2+ mediated by A-23187 (6 microM) or collagen (638 nM). Results show that cinchonine (20 microM) also inhibited aggregation when platelets were pretreated with protein kinase C (PKC) activator, phorbol myristate acetate (PMA; 0.1 microM) in combination with low doses of platelet activating factor (80 nM). Cinchonine, however, had no effect on AA-induced platelet aggregation and thromboxane A2 (TXA2) synthesis in platelets. These results suggest that antiplatelet effects of cinchonine are mediated mainly through inhibition of Ca2+-influx and protein kinase C pathways in platelets.
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PMID:The inhibitory effect of cinchonine on human platelet aggregation due to blockade of calcium influx. 977 5

According to the World Health Organization low birth weight (LBW) babies are those born with less than 2500g. A descriptive retrospective cross - sectional study using existing data from a one-year (2001) block of birth registers of 3464 pregnant women was done at Kilimanjaro Christian Medical Centre in Moshi, Tanzania. The objective was to determine factors associated with LBW and their contribution to the problem. Out of 648 pregnant women who were tested for HIV infection 59 (9.1%) were positive for the infection. Twelve (20.3%) of HIV positive women gave birth to LBW neonates. HIV positive women were twice more likely to give birth to LBW infants than HIV negative ones (chi2 = 6.7; P < 0.01; OR = 2.4; 1.1, 5.1). Mothers without formal education were 4 times more likely to give birth to LBW neonates than those who had attained higher education (OR = 3.6; 2.2, 5.9). There was a linear decrease in low birth weights of newborns as fraternal educational level increased (chi2 for linear trend = 42.7; P < 0.01). There was no statistically significant difference among parents' occupations regarding LBW of their newborns. Unmarried mothers were more likely to give birth to LBW neonates as compared to their married counterparts (OR = 1.65; 1.2, 2.2) and the difference was statistically significant (chi2 = 13.0, P < 0.01). Hypertension, pre-eclampsia and eclampsia disease complex had the highest prevalence (46.67%) and population attributable fraction of low birth weight (PAF = 25.2%; CI = 22.0-27.6). Bleeding and schistosomiasis had the same prevalence (33.33%) of LBW babies. Other complications and diseases which contributed to high prevalence of LBW included anaemia (25%), thromboembolic diseases (20%), tuberculosis (17%) and malaria (14.8%). Prevalence of LBW was high in women with premature rupture of membrane (38%), placenta previa (17%) and abruption of placenta (15.5%). LBW was strongly associated with gestational age below 37 weeks (OR = 2; CI = 1.5, 2.8) contributing to 42% of LBW deliveries in the study population (PAF = 42.4%: 25, 55). Pregnant women with malnutrition (BMI < 18) gave the highest proportions 17% of LBW children followed by underweight (BMI; 18-22) who gave 15.5% of LBW neonates. There was a statistical significant difference between the proportions of LBW infants from mothers who did not receive antenatal care (28.6%) and those who attended for the services (13.8%) (chi2 = 8.8; P = 0.01). There is need of increasing promotion of reproductive health services in relation to safe motherhood at community level in order to reduce risk factors of LBW.
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PMID:Risk factors associated with low birth weight of neonates among pregnant women attending a referral hospital in northern Tanzania. 1868 Sep 58

The suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling resulting in phosphatidylserine exposure at the cell surface. Eryptosis is stimulated in a wide variety of diseases including sepsis, haemolytic uremic syndrome, malaria, sickle-cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency and Wilson's disease. Moreover, eryptosis is elicited by osmotic shock, oxidative stress, energy depletion as well as a wide variety of endogenous mediators and xenobiotics. Excessive eryptosis is observed in erythrocytes lacking the cGMP-dependent protein kinase type I (cGKI) or the AMP-activated protein kinase AMPK. Inhibitors of eryptosis include erythropoietin, nitric oxide NO, catecholamines and high concentrations of urea. Eryptosis-triggering diseases and chemicals are partially effective by stimulating the formation of ceramide, which in turn fosters cell membrane scrambling. Accordingly, ceramide-induced eryptosis participates in the pathophysiology of several diseases and contributes to the effects of a large number of xenobiotics. The mechanisms underlying ceramide formation in erythrocytes are, however, still ill defined. In case of osmotic cell shrinkage, ceramide formation is apparently due to activation of phospholipase 2, leading to formation of platelet activating factor PAF and PAF-dependent stimulation of ceramide formation, which possibly involves acid sphingomyelinase. Additional experiments are needed to conclusively define the ceramide-generating enzyme and the ceramide-dependent cellular events eventually leading to suicidal erythrocyte death.
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PMID:Ceramide in suicidal death of erythrocytes. 2050 1