Is inflammation related to the clinical severity of unstable angina?

The present study determined the white blood cell (WBC) count and the serum C-reactive protein (CRP) level in 27 patients with coronary spastic angina, 16 with Braunwald class IB unstable angina (UA) and 13 with Braunwald class IIIB. The relationship between the clinical presentation of UA and the requirement for emergency percutaneous transluminal coronary angioplasty (PTCA) was examined, and in patients with medically refractory angina, the determining factor among the clinical manifestations of angina was also investigated. In the acute phase, the WBC count and the serum CRP level were significantly higher in patients with Braunwald class IIIB than in those with coronary spastic angina or Braunwald class IB UA (p<0.001). In the Braunwald class IIIB group, a significantly higher rate of patients required emergency PTCA than that of the coronary spastic angina group (p<0.01). Patients with medically refractory angina had a significantly higher WBC count and higher serum CRP level on admission, and the WBC count on admission was independently associated with medically refractory angina by multivariate analysis (p<0.05). Inflammation may play a major pathological role in the rapid development of acute coronary syndrome.     

Is tremor related to celiac disease?

Neurological features in celiac disease(CD) are not rare(5%-36%), but tremor is scarcely described. Subjects with CD and healthy controls completed an online survey using WHIGET tremor rating scale. One thousand five hundred and twelve subjects completed the survey, finally 674 CD patients and 290 healthy subjects were included. A higher prevalence of tremor in CD patients was observed in comparison to controls(28% vs 14%, P 0.001). Frequency of family history of tremor in CD patients with and without tremor was 25% and 20%(P = 0.2), while in the control group it was 41% and 10%(P 0.001). Controls with tremor showed a higher frequency of family history of tremor when compared to CD patients with tremor(41.5% vs 24.6%, P = 0.03). The results suggested that tremor in CD might be more frequent and possibly related to the disease itself and not due to associated essential tremor.     

Is fledging in king penguin chicks related to changes in metabolic or endocrinal status?

This study examines the possibility that metabolic or endocrinal factors initiate fledging in the king penguin, a semi-altricial seabird species breeding a single chick on the ground. Chick fledging (departure to sea) occurred 5d after completion of the molt. It was preceded by a 16d fasting period and by a 7-fold increase in locomotor activity. From the measurement of the plasma concentration of metabolites and of glucagon and insulin, pre-fledging king penguin chicks were found to adapt to fasting in a classical way, i.e. by sparing body protein and mobilizing fat stores. At fledging, chicks were in phase II of fasting and their departure to sea was not stimulated by reaching critical energy depletion (phase III), in contrast to that which has been reported in breeding-fasting adults. The plasma level of corticosterone remained unchanged throughout the whole pre-fledging period, providing no support for a role of this stress-hormone in the facilitation of fledging. Thus, king penguin fledglings did not appear to be environmentally or nutritionally stressed. The plasma levels of thyroid hormones were elevated during the pre-fledging molt, in accordance with their key role in molt control in adult penguins. These levels declined by the time of the molt end, the plasma level of T4 thereafter being directly related to the time left before fledging. These results do not support the view that chronically elevated levels of thyroid hormones are required for the energy-demanding transition between being ashore and in cold water, but they suggest that the maintenance of high T4 levels may delay fledging.     

Is atypical sodium current related to arterial pathophysiology?

Primary cultured human coronary myocytes, derived from patients with end-stage heart failure (NYHA, classes III and IV) caused by an ischemic disease and undergoing heart transplantation, express a voltage-gated tetrodotoxin-sensitive sodium current (INa). This current has atypical electrophysiological and pharmacological properties and regulates intracellular sodium ([Na+]i) and calcium ([Ca2+]i). Our work is aimed at identifying its role and regulation of expression during pathophysiology. We currently investigate whether INa is expressed in vascular smooth muscles cells (VSMCs) isolated from either healthy or diseased (atheromatous) arteries in human and, in parallel, in pig, rabbit and rat. Cells were enzymatically isolated, primary cultured and macroscopic INa were recorded using the whole cell patch clamp technique. We found that INa is expressed in VSMCs grown from human aortic (90%; n = 48) and pulmonary (44%; n = 16) arteries and in the human aortic cell line HAVSMC (94%; n = 27). INa was also detected in pig coronary (60%; n = 25) and rabbit aortic (47%; n = 15) VSMCs, but not in rat aortic myocytes (n = 30). These different INa were activated at similar range of potentials (approximately -45 mV), had similar sensitivity to tetrodotoxin (IC50 around 5 nM) and similar density (2 to 4 pA/pF). Their expression was related to cell dedifferentiation in vitro. However, INa was observed more frequently in human myocytes derived from diseased arteries (ischemic cardiopathy) than in those derived from healthy tissues (dilated cardiopathy). In conclusion, INa may contribute to increase the basal arterial contractility and play a role in pathological situations including hypertension.     

Is nonulcer dyspepsia related to Helicobacter pylori infection?

Dyspepsia, defined as pain or discomfort centered in the upper abdomen, is a common clinical problem. A variety of underlying disease states may result in dyspepsia, but commonly, diagnostic investigation will show no identifiable pathology, and the patient is diagnosed with nonulcer dyspepsia. Numerous hypothesis have been suggested as to the cause of symptoms in patients with nonulcer dyspepsia, including perturbations of gastroduodenal motility, hypersensitivity to physiologic stimuli including acid, and the effect(s) of infection within the gastric mucosa by Helicobacter pylori. Some epidemiological studies have suggested that patients with nonulcer dyspepsia may have a slightly higher prevalence of H. pylori infection. However, association does not prove causation. Causation of nonulcer dyspepsia by H. pylori could best be documented by resolution of symptoms following eradication of the infection. Early intervention studies indicated that there was a beneficial effect on symptoms of nonulcer dyspepsia with H. pylori eradication, but most of these studies had serious methodological flaws. In the last few years there have been a number of well-designed studies investigating the effect of H. pylori eradication on symptoms in patients with nonulcer dyspepsia. The results of these studies are inconsistent, but suggest that there is little, if any benefit from treatment. This case-based article on nonulcer dyspepsia discusses these studies in detail and provides a possible explanation for the differences in outcomes.     

Glycosylation,diabetes and dengue: Effect on severity?

BackgroundCo-presentation between dengue and diabetes mellitus (DM) can be expected. The author hereby assesses the effect of glycosylation process in poor glycemic control cases on the course of dengue infection.MethodsThe aim of this work is to assess the effect of glycosylation of CD61 on the pathogenesis of dengue hemorrhagic fever. The hypothetical bioinformatics approach is used in this research.ResultSignificant change of similarity between CD61 and dengue NS1 after glycosylation can be detected.ConclusionThese findings might imply that immunomimicking process should be more difficult to occur.     

Is factor XII deficiency related to recurrent miscarriage?

Factor XII (FXII) is an important protease that plays a major role in the initiation of the intrinsic pathway of blood coagulation. Although congenital FXII deficiency is not associated with a clinical bleeding tendency, it can be identified on a routine coagulation test, such as a prolonged activated partial thromboplastin time. This deficiency is a rare autosomal recessive disorder. It is still unclear whether FXII deficiency causes any disorders during pregnancy. Recurrent miscarriages and placental abruption were reported in cases with FXII deficiency. We successfully treated a woman whose pregnancy was complicated by congenital FXII deficiency. We report her clinical courses of gestation, delivery, and puerperium and discuss the role of maternal FXII associated with pregnancy. In our case, courses of gestation and delivery were normal. Postpartum uterine bleeding was, however, prolonged due to a subinvolution of the puerperal uterus. Our results indicate that, except for postpartum uterine contraction, FXII does not play a major role in gestation and delivery. We suggest that FXII deficiency is not associated with recurrent miscarriage and that normal gestation and vaginal delivery are possible even in cases with congenital FXII deficiency. We assert that the possible correlation of FXII deficiency with recurrent miscarriage merits reevaluation.     

Is hypertension related to the number of nephrons?

The kidney has a key role in blood pressure control, and an abnormal regulation of sodium balance is involved in essential hypertension. It has been suggested that a reduced nephron number at birth could be one possible mechanism. Indeed various strains of hypertensive animals exhibit a reduced nephron number. In human beings, two autopsy studies have clearly shown a lower (about 50%) nephron number in hypertensive subjects. The glomeruli are also enlarged, indicating hyperfiltration. This could be the cause of both high blood pressure and later nephrosclerosis. A low number of nephrons is part of the perinatal programming which occurs together with fetal growth retardation, and this has been reproduced experimentally. There is a negative correlation between birth weight and glomerular number. Such a situation is associated with a largely increased risk of cardiovascular complications in adulthood.     

Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?

Several recent publications have drawn attention to the role of the thyroid hormone status of the mother on the future neuropsychological development of the child. The screening of pregnant women for clinical or subclinical hypothyroidism based on second trimester elevated maternal TSH values has been proposed. Here, we have summarized present epidemiological and experimental evidence strongly suggesting that conditions resulting in first trimester hypothyroxinemia (a low for gestational age circulating maternal free T4, whether or not TSH is increased) pose an increased risk for poor neuropsychological development of the fetus. This would be a consequence of decreased availability of maternal T4 to the developing brain, its only source of thyroid hormone during the first trimester; T4 is the required substrate for the ontogenically regulated generation of T3 in the amounts needed for optimal development in different brain structures, both temporally and spatially. Normal maternal T3 concentrations do not seem to prevent the potential damage of a low supply of T4, although they might prevent an increase in circulating TSH and detection of the hypothyroxinemia if only TSH is measured. Hypothyroxinemia seems to be much more frequent in pregnant women than either clinical or subclinical hypothyroidism and autoimmune thyroid disease, especially in regions where the iodine intake of the pregnant woman is inadequate to meet her increased needs for T4. It is proposed that the screening of pregnant women for thyroid disorders should include the determination of free T4 as soon as possible during the first trimester as a major test, because hypothyroxinemia has been related to poor developmental outcome, irrespective of the presence of high titers of thyroid autoantibodies or elevated serum TSH. The frequency with which this may occur is probably 150 times or more that of congenital hypothyroidism, for which successful screening programs have been instituted in many countries.     

Is placental iodine content related to dietary iodine intake?

Objective Delivery of iodine to the foetus depends not only on maternal dietary iodine intake but also on the presence of a functioning placental transport system. A role for the placenta as an iodine storage organ has been suggested, and this study compares the iodine content of placentas from women giving birth at term in Ireland and Iran, areas with median urinary iodine of 79 and 206 μg/l respectively. Design Placental cotyledon iodine was measured using an alkaline ashing technique with Sandell–Kolthoff kinetic colorimetry. Samples were taken from six sites from the centre and periphery of each cotyledon. Placentas (Ireland n = 58; Iran n = 45) were obtained from consecutive euthyroid women delivering at term. Results The median placental iodine (μg/g wet weight) was significantly higher in Iranian than in Irish women (187·2 μg/g vs 34·3 μg/g; P < 0·001). The distribution of individual placental iodine values showed that values >50 μg/g were found in 71·0% of Iranian and in only 21·0% of Irish samples. In Irish subjects, the relationship of placental iodine to pregnant population urinary iodine (UI) (ng/g:μg/l) was 1:2 (40:79), while in Iranians this ratio is closer to 1:1 (211:206). Conclusions These findings, by demonstrating an apparent ability of the placenta to store iodine in a concentration‐dependent manner, suggest a hitherto undetected role for the placenta. Whether placental iodine has a role in protecting the foetus from inadequacies in maternal dietary iodine intake is as yet unknown.