Variability of ovarian reserve tests

Sir, The article by Kwee et al. (2004) on the intercycle variabilityof ovarian reserve tests contains important methodological pointsthat require further explanation and clarification before validconclusions can be drawn.

1. The authors mention that cycle day2 or 3 serum FSH values weredetermined as basal values duringclomiphene citrate challengetest (CCCT). It has been reportedthat there is considerablevariation in serum FSH levels between     

Upper and lower gastrointestinal endoscopical investigation in elderly patients with iron deficiency anaemia

Iron deficiency anaemia is frequently observed in male adults and postmenopausal women due to chronic occult bleeding, usually from the gastrointestinal tract. Practically, as endoscopical investigation of the gastrointestinal system is an invasive procedure, iron replacement treatment was generally started without investigation of the underlying aetiology even in first-line health institutions. This study evaluates the role of endoscopy in the investigation of the aetiology of anaemia in 95 patients (51 males, 44 females), aged 64.9+/-12.5 years (range 50-90 years). All patients having iron deficiency anaemia were investigated by upper gastrointestinal endoscopy and colonoscopy. Upper and lower gastrointestinal pathologies were seen in 10 (10.6%) and 55 (57.8%) patients, respectively. However, no gastrointestinal lesion was found in 30 (31.6%) patients with iron deficiency anaemia. Out of the 95 patients, 16 (16.9%) had erosive gastritis, 15 (15.8%) duodenal ulcer, 8 (8.4%) gastric ulcer, 7 (7.3%) gastric tumours, 7 (7.3%) oesophagitis. 5 (5.4%) colon tumours, 3 (3.2%) haemorrhoids, 2 (2.1%) non-tropical sprue, 1 (1%) colonic polyp, and 1 (1%) colitis. In the majority of elderly patients with iron deficiency anaemia, upper gastrointestinal system disease was found. In 12 (12.7%) patients in the study group, malignancies were detected. In elderly patients with iron deficiency anaemia, the aetiology should be highlighted before giving iron supplementation.     

Apoptotic body engulfment by a human stellate cell line is profibrogenic

Hepatocyte apoptosis and stellate cell activation are both features of chronic liver diseases, but a relationship between these events has not been explored. In macrophages, engulfment of apoptotic bodies induces expression of transforming growth factor-beta (TGF-beta), a profibrogenic cytokine. We examined whether a similar response occurs in stellate cells. Fluorescently labeled hepatocyte apoptotic bodies were added to cultures of primary and immortalized human stellate cells. Stellate cells, but not hepatocytes, readily engulfed apoptotic bodies in a time-dependent manner as assessed by confocal microscopy. The activation of primary and immortalized human stellate cells after incubation with apoptotic bodies, as well as their fibrogenic activity, was indicated by an increase in alpha-smooth muscle actin (primary cells), TGF-beta1, and collagen alpha1(I) mRNA (primary and immortalized cells). The profibrogenic response was dependent upon apoptotic body engulfment, because nocodazole, a microtubule-inhibiting agent, blocked both the engulfment and the increase of TGF-beta1 and collagen alpha1(I) mRNA. As described in primary rodent stellate cells, up-regulation of collagen alpha1(I) mRNA was inhibited by a PI-3K inhibitor (LY294002) and a p38 mitogen-activated protein kinase inhibitor (SB203580) in LX-1 cells. In conclusion, these data support a model in which engulfment of hepatocyte apoptotic bodies by stellate cells leads to a fibrogenic response by eliciting a kinase-signaling pathway.     

The role of L-carnitine in treatment of a murine model of asthma

Leukotrienes, one of the mediators of inflammation in asthma, have a strong bronchoconstrictive effect. L-carnitine has been reported to influence respiratory functions. It has also been reported that L-carnitine inhibits leukotriene synthesis. To evaluate the effects of L-carnitine on oxygen saturation, urine leukotriene E4 levels and lung histopathology in a murine model of asthma, high IgE responder BALB/c mice (n = 24) were systemically sensitized to ovalbumin and chronically challenged with low particle mass concentrations of aerosolized ovalbumin, and then they were divided into 3 groups (study groups A, B, and C) each including eight mice. After methacholine-induced bronchoconstriction, the mice in groups A and B were given intraperitoneal L-carnitine (250 and 125 mg/kg, respectively), while the mice in group C were given placebo. Oxygen saturation of the mice was measured by pulse oxymeter before and after methacholine and after L-carnitine/ placebo application. In addition, urine leukotriene E4 levels were measured before asthma development, and 24-h after L-carnitine injection in asthmatic mice. Inflammation in the lung tissues of the sacrificed animals was scored histopathologically to determine the effect of L-carnitine on tissue level. A control group of non-sensitized mice (n = 8) treated with placebo only was used for comparison of urine leukotriene E4 levels and of histopathological parameters. Oxygen saturation of the mice in the study groups tended to decrease after methacholine and to improve after L-carnitine injection, although these changes were not significant at all time points. Urine leukotriene E4 levels of all 3 study groups increased significantly after asthma development. The rate of increment was smallest in the group given the highest L-carnitine dose (group A). Inflammation at the tissue level was also mildest in group A, and severest in the group that was not given carnitine (group C). All of the study groups and the control group differed significantly with respect to inflammation scores. In conclusion, L-carnitine improved oxygen saturation, and decreased urine leukotriene E4 levels and inflammation in lung tissues in the present murine model of asthma.     

A novel NPHS1 mutation associated with temporary elevation of maternal serum alfa-fetoprotein and late onset of proteinuria

International Urology and Nephrology -     

Intramural hydatid cysts of pulmonary arteries: CT and MR findings

Involvement of the pulmonary artery by echinococcosis usually occurs due to pulmonary embolization after rupture of the cyst in the right ventricle or, rarely, by dissemenation from a hepatic focus. This paper presents an adult patient with intramural hydatid cysts of the pulmonary arteries, which apparently grew slowly toward the lumina resulting in complete luminal occlusion, enabling sufficient time for development of sufficient perfusion from the bronchial arteries. The condition apparently resulted from embryos of the parasite, which entered the vasa vasorum of the pulmonary arteries, a previously unreported mechanism.     

Is a serotonergic mechanism involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced appetite suppression in the Sprague-Dawley rat?

The major cause of TCDD-induced death in rats is a progressive voluntary feed refusal which has been correlated with reduced gluconeogenesis. Since centrally administered TCDD does not cause death or decreased feed intake in rats, the ability of TCDD to suppress appetite via peripheral mechanisms acting on the central nervous system was examined in two experimental models. First, it was found that the feed intake of rats on scheduled feeding cycles was not decreased by blood transfused from rats with TCDD-induced appetite suppression (8 days after a lethal dose of TCDD, i.p.). In contrast, a similar transfusion from normal, satiated rats did reduce feed intake of recipient rats by approximately 40%, suggesting that TCDD-treated rats are not satiated but rather that they are not hungry. In the second study tryptophan (the amino acid precursor of the neurotransmitter serotonin) was measured in the plasma and tryptophan, serotonin, norepinephrine and dopamine in the hypothalamus as well as dopamine and its metabolites in the striatum 4, 8, and 16 days after TCDD dosage (125 g/kg, i.p.). Progressive time-dependent increases in tryptophan levels in plasma and brain were paralleled by increases in brain serotonin and 5-hydroxyindoleacetic acid (the primary metabolite of serotonin) in TCDD-treated rats. No changes were observed regarding the other biogenic amines. It is suggested based on these data and on substantial evidence from the published literature that a serotonergic mechanism may be involved in TCDD-induced feed intake reduction.