Accelerated idioventricular rhythm associated to ophthalmic timolol/dorzolamide solution.
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Accelerated Idioventricular Rhythm↗
Biomedical subjects
A Attanasio
Publications and source records attributed to A Attanasio.
Increased familial risk of cluster headache.
The authors studied the occurrence of cluster headache in the families of 220 Italian patients with cluster headache. A positive family history was found in 20% (44/220) of the families. Compared with the general population, first-degree relatives had a 39-fold significantly increased risk of cluster headache. Second-degree relatives had an eightfold significantly increased risk. The increased familial risk strongly supports the hypothesis that cluster headache has a genetic component in some families.
Adult↗
The serotonergic agent m-chlorophenylpiperazine induces migraine attacks: A controlled study.
In a double-blind study versus placebo, the serotonergic agent m-chlorophenylpiperazine (mCPP) was administered to 20 healthy control subjects and 19 migraineurs to investigate the ability of mCPP (0.5 mg/kg) to induce typical migraine attacks. In the following 24 hours there were more migraines after mCPP than after placebo in both groups. These findings are consistent with involvement of 5HT2B,2C,1A receptor subtypes in the pathophysiology of migraine.
Adult↗
Verapamil in the prophylaxis of episodic cluster headache: a double-blind study versus placebo.
The authors performed a double-blind, double-dummy study to compare the efficacy of verapamil with placebo in the prophylaxis of episodic cluster headache. After 5 days' run-in, 15 patients received verapamil (120 mg tid) and 15 received placebo (tid) for 14 days. The authors found a significant reduction in attack frequency and abortive agents consumption in the verapamil group. Side effects were mild. These findings provide objective evidence for the effectiveness of verapamil in episodic cluster headache prophylaxis.
Adult↗
Asbestos body burden in decomposed human lungs.
The authors discuss the influence of postmortem tissue decomposition on the lung asbestos body (AB) burden, with the aim of evaluating the reliability of data obtained from autopsies performed for medicolegal purposes several months after deaths in possible connection with asbestos-related pathology. Eight autopsy cases were selected, each one with occupational exposure considered very probable on the basis of the history or pathologic findings. In each case the AB concentrations were assessed soon after death in one lung and after periods of 1 to 18 months in the others, which had been stored in sealed containers without fixation. AB concentrations consistently decreased with time in rotten lungs. The counts in some cases became negative a few months after death, even in cases with very high AB counts at first examination. It may be reasonably inferred that, in putrefied lungs from corpses exhumed after months of internment, the counts in digested tissues and the screening of histologic sections for AB may give false-negative results.
Air Pollutants, Occupational↗
Neuroendocrinology of cluster headache.
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Cluster Headache↗
Treatment of the Mayer-Rokitansky-Küster-Hauser syndrome in Bangladesh: results of 10 total vaginal replacements with sigmoid colon at a missionary hospital.
PURPOSE: We report our experience with treating the Mayer-Rokitansky-Kuster-Hauser syndrome in a developing country. The operations were performed by a pediatric surgical team at a missionary hospital in Khulna, Bangladesh. MATERIALS AND METHODS: From 1995 to 1998, 10 young women with the Mayer-Rokitansky-Kuster-Hauser syndrome underwent complete vaginal replacement. In 4 patients the abnormality was discovered after marriage at the initial sexual approach and, thus, the husband abandoned 3. In 4 of the 10 cases the diagnosis was suspected because of absent menstruation. A physician made the diagnosis in only 2 cases. Preoperatively abdominal ultrasound in 3 patients showed a hypoplastic uterus in all and a right solitary pelvic kidney in 1. In all 10 women a neovagina was created using a 14 cm. segment of sigmoid colon. Two weeks postoperatively patients were taught to dilate and irrigate the neovagina. RESULTS: A minimum of 1 year of followup is available in 7 of the 10 patients. The vagina had a good appearing introitus. Mucous production significantly decreased 3 to 4 months after the operation. Two patients already had an active sexual life. The remaining 3 patients underwent surgery during the last mission and they had no complications 6 months postoperatively. CONCLUSIONS: Our experience shows the feasibility of treating patients with a severe abnormality in a hospital with basic facilities in one of the poorest countries in the world.
Adolescent↗
5-HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test.
Involvement of the cerebral serotoninergic system has been invoked to explain the origin of the pain and the vascular phenomena in migraine. To further investigate the type of cerebral serotonin receptors that may be altered in migraine, the prolactin (PRL) and cortisol responses to m-chlorophenylpiperazine (mCPP), a selective 5-HT1A,-5-HT(2A/C) receptor agonist, were monitored in 12 patients suffering from migraine without aura and in 14 matched healthy controls. Each subject underwent two challenges, one with mCPP (0.5 mg/kg) and the other with placebo (orally) using a double-blind crossover design. Anxiety level was measured by the State Trait Anxiety Inventory. Migraine patients had a greater PRL response to mCPP (p = 0.05) and greater anxiety (p < 0.01) than controls; cortisol response to mCPP did not differ suggesting that 5-HT2C receptors are normal in migraine. Augmented PRL response to mCPP could derive from 5-HT1A receptor hypersensitivity, perhaps as as a consequence of anxiety due to pain expectation. Cerebral 5-HT1A hypersensitivity could also explain the increased occurrence of migraine attacks during anxiety.
Adult↗
Cerebral hemodynamics in young hypertensive subjects and effects of atenolol treatment.
The aim of this study was to evaluate changes in cerebral hemodynamics in young patients with uncomplicated hypertension before and after effective antihypertensive treatment with a beta-blocker drug. Changes in mean flow velocity in the middle cerebral artery from normal condition to hypercapnia were evaluated by means of a transcranial Doppler in 42 hypertensive patients and 21 healthy subjects comparable for age and sex distribution. We obtained hypercapnia with breath-holding and evaluated cerebrovascular reactivity with the breath-holding index (BHI). After a baseline evaluation (time 0), patients were randomly assigned to a placebo (group 1) or atenolol (group 2) therapy. The evaluation was repeated after 30 (time 1) and 60 (time 2) days of treatment. Before treatment, hypertensive patients had significantly lower BHI values (0.96 +/- 0.1 group 1 and 0.85 +/- 0.3 group 2) than controls (1.69 +/- 0.4) (P < 0.0001). During treatment, mean blood pressure significantly decreased in group 2 patients. In the same group, BHI values significantly increased with respect to the pre-treatment evaluation: 1.39 +/- 0.2 at time 1 and 1.44 +/- 0.2 at time 2 (P < 0.0001). On the contrary, mean blood pressure and BHI values remained unchanged in the placebo group. Furthermore, BHI values were significantly higher in group 2 than in group 1 patients at times 1 (P < 0.001) and 2 (P < 0.0001). These findings suggest that hypertension causes reduced capability of cerebral vessels to adapt to functional changes. This condition, which is reversible after treatment, could be implicated in the increased susceptibility to ischemic stroke in hypertension.
Adult↗
Serum leptin levels in children and adolescents with insulin-dependent diabetes mellitus in relation to metabolic control and body mass index.
The ob protein, termed leptin, is produced by adipocytes and is thought to act as an afferent satiety signal regulating weight through suppressing appetite and stimulating energy expenditure in humans and/or rodents. Insulin has been found to be a potent stimulator of leptin expression in rodents. It is unclear at present whether this insulin action is a direct or an indirect effect. To investigate whether leptin concentrations in children and adolescents with type 1 diabetes (IDDM) were related to metabolic status, body weight, body mass index and insulin treatment, we have measured leptin concentrations in serum from 13 newly diagnosed IDDM patients before the beginning of insulin treatment (8 girls, 5 boys, aged 4.7-17.5 years) and in 134 patients with IDDM during treatment (64 girls, 70 boys, aged 2.6-20.1 years) using a specific radioimmunoassay. The data from patients with diabetes were compared with normative data that were derived from a large cohort of healthy children and adolescents. Serum from children with newly diagnosed diabetes had significantly lower levels of leptin (mean 1.28+/-1.60 ng/ml, range 0.14-6.13 ng/ml) compared with healthy children (n=710) (mean 2.2 ng/ml, range 0.26-14.4ng/ml) and compared with insulin-treated children and adolescents (mean 5.18+/-5.48 ng/ml, range 0.26-29.77 ng/ml) (P<0.0001) even after adjustment for gender and body mass index (BMI). Serum leptin levels in patients with IDDM were significantly correlated with BMI (r=0.42, P<0.0001). Multiple regression analysis showed that age and BMI were significantly correlated with leptin levels, while duration of diabetes, mean HbA1c levels, insulin dose and plasma glucose, triglyceride and cholesterol levels were not. Females had higher serum leptin concentrations than males even when adjusted for BMI (P<0.0001). Surprisingly and most importantly, leptin levels in insulin-treated young adult (Tanner stage 5) patients were significantly higher than values found in the healthy nondiabetic reference population when adjusted for sex, Tanner stage and BMI. These findings suggest that leptin levels in IDDM patients show a similar dependency on adipose tissue and age as in healthy, normal children. The data provide evidence that insulin may be of importance as a regulator of serum leptin levels in vivo not only in rodents but also in humans. It is hypothesized that the elevated BMI-adjusted leptin levels in adolescents with IDDM could indicate either that these patients may be oversubstituted by the intensified insulin therapy that they are receiving or that their body composition and body fat content may differ from that of healthy adolescents in the sense that they have a relative increase in fat mass.
Adolescent↗
Cardiac rhabdomyosarcoma: a clinicopathologic and electron microscopy study.
A 66-year-old woman was admitted to the hospital with a neurological syndrome characterized by ataxia and diplopia. Magnetic resonance of the brain documented an ischemic medullary lesion. Examination of the heart revealed a grade 2/6 systolic murmur at the left sternal border and apex that radiated towards the axilla. The echocardiography study showed a mild mitral regurgitation, and an abnormally enlarged posterior papillary muscle was found in the left ventricle. Two weeks after admission, the patient died suddenly due to a stroke. At autopsy, a recent vast swollen ischemic cerebral infraction was found. Furthermore, two old infarcts were observed in the spleen. A cardiac examination showed a white-gray ulcered mass in the left ventricle and histological analysis revealed a rhabdomyosarcoma.
Aged↗
Transdermal clonidine in the prophylaxis of episodic cluster headache.
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Administration, Cutaneous↗
The m-chlorophenylpiperazine test in cluster headache: a study on central serotoninergic activity.
The central serotoninergic agonist m-chlorophenylpiperazine (m-CPP) stimulates several 5HT receptor subtypes. It induces the release of both cortisol and prolactin (PRL). In this study we investigated central serotoninergic responsiveness in cluster headache by monitoring cortisol and PRL responses to m-CPP administration. Twenty-three patients with episodic cluster headache and 17 sex-matched and age-matched healthy subjects were studied. The cluster headache patients were tested during a cluster period, and none were receiving prophylaxis. A single oral dose of m-CPP, 0.5 mg/kg, was given at time 0. Blood samples were drawn at -30, 0, 30, 60, 90, 120, 150 and 180 min. PRL and cortisol levels were assayed in the samples. PRL and cortisol delta maxima (delta maximum = maximum response - baseline level at time 0/baseline level at time 0) were evaluated in each patient and mean values compared. Serum levels of m-CPP were detected by HPLC and correlated to hormonal responses. Reduced cortisol (p < 0.02) and increased PRL (p < 0.05) delta maxima were observed in cluster headache patients. Increased basal cortisol plasma levels (p < 0.05) and reduced basal PRL plasma levels (p = 0.06) also characterized cluster headache patients. This is the first study evaluating central serotoninergic responsiveness to m-CPP in cluster headache and these data suggest impaired central serotoninergic function in this pathology.
Case-Control Studies↗
Transdermal clonidine in the prophylaxis of episodic cluster headache: an open study.
Transdermal clonidine has recently been reported to be efficacious in the prophylaxis of cluster headache. A 2-week course of transdermal clonidine (5 mg the first week, 7.5 mg the second week) preceded by a 5-day run-in period, was administered to 16 patients with episodic cluster headache in an active cluster period. In 5 patients, the painful attacks disappeared after the seventh day of treatment. For the group as a whole, no significant variations in headache frequency, pain intensity, or attack duration were observed between the run-in period and the first and second weeks of treatment (ANOVA). Further studies are necessary to clarify the effectiveness of transdermal clonidine in the prophylaxis of episodic cluster headache.
Administration, Cutaneous↗
Cardiogenic syncope in temporal lobe epileptic seizures.
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Adult↗
Levels of leptin in maternal serum, amniotic fluid, and arterial and venous cord blood: relation to neonatal and placental weight.
The mechanisms by which maternal and fetal weight are regulated during pregnancy are poorly understood. The ob protein, termed leptin, is produced by adipocytes. It is involved in the regulation of body weight by suppressing appetite and stimulating energy expenditure both in humans and rodents. In this study we examined whether leptin concentrations in the mother and the newborn correlate with birth weight, placental weight, and maternal weight at term. Leptin concentrations were measured in amniotic fluid, venous and arterial cord blood, and maternal serum at birth (n = 27) using a specific RIA employing human recombinant leptin for tracer and standard preparation. Gestational age was 38-42 weeks, maternal age was 21-42 yr, mean maternal weight at birth was 80.0 +/- 10.8 kg, and mean body mass index before pregnancy was 23.4 +/- 2.8 kg/m2. The newborns' mean weight was 3450 +/- 580 g, and mean placental weight was 616 +/- 120 g. Serum leptin levels from nonpregnant women ranged between 1.7-18.4 ng/mL, median 5.5 ng/ml (n = 30). Mean leptin concentration in maternal serum at birth was 20.0 +/- 13.2 ng/mL and was higher (P < 0.002) than in arterial cord blood (9.7 +/- 9.4 ng/mL) and venous cord blood (8.9 +/- 8.6 ng/mL). Mean amniotic fluid leptin concentration was 3.6 +/- 2.8 ng/mL. Placental weight correlated inversely with leptin levels in maternal serum at birth (r = -0.49, P < 0.01). In addition, leptin concentrations in venous cord blood correlated significantly with the levels in arterial cord blood (r = 0.98, P < 0.0001), and leptin levels in cord blood correlated positively with birth weight (r = 0.57, P = 0.03) and placental weight (r = 0.50, P < 0.01). In contrast, there was no correlation between maternal serum leptin levels and birth weight. Thus, leptin levels are high in the fetus and in the mother at term. We hypothesize that high leptin levels could represent an important feed-back modulator of substrate supply and subsequently for adipose tissue status during late gestation.
Amniotic Fluid↗
Diverse cell death pathways result from a single missense mutation in weaver mouse.
Neuronal death affects selectively granule cell precursors of the cerebellum and the dopaminergic neurons of midbrain in the weaver mutant mouse. The weaver phenotype is associated with a missense mutation in the gene coding for the GIRK2 potassium channel, which results in chronic depolarization. Using DNA gel electrophoresis, electron microscopy (EM), the in situ end-labeling (ISEL) technique at the light and EM level, and immunohistochemistry for apoptosis-related proteins c-Jun and proliferating cell nuclear antigen (PCNA), we have investigated the mechanisms of cell death in cerebellum and substantia nigra. Between postnatal day P1 and P21, in the external germinal layer of the cerebellum, most degenerating granule cell precursors were found to aggregate to form clusters. Degenerating cells exhibited strong nuclear staining for ISEL, c-Jun, and PCNA and had a typical apoptotic morphology by EM. Increased c-Jun and ISEL staining were also occasionally seen in Purkinje cells. Between P14 and P21, when dopaminergic neurons start to degenerate, staining for ISEL, c-Jun, and PCNA in weaver substantia nigra was the same as in controls. By EM, however, we found only in weaver mice numerous dopaminergic cells that showed extensive vacuolar and autophagic changes of cytoplasm, preservation of membrane and organelle integrity, and absence of chromatin condensation or DNA fragmentation by EM-ISEL. The combination of vacuolar and autophagic changes identifies a novel type of non-necrotic, nonapoptotic cell death. After biochemical analysis of DNA, a clear-cut laddering, suggestive of oligonucleosomal fragmentation, was present in samples from weaver cerebellum. Cell death diversity appears to be influenced by specific features of target cells. These findings may be relevant for understanding the mechanisms of cell death in neurodegenerative diseases.
Animals↗
High leptin concentrations in serum of very obese children are further stimulated by dexamethasone.
Serum leptin concentrations and the levels of ob mRNA in adipocytes in obese humans are elevated. Hyperphagia and obesity are characteristics of hypercortisolism. We have therefore asked whether or not leptin levels were elevated in very obese children, and whether or not dexamethasone would increase leptin levels in obese children. A single dose dexamethasone suppression test was performed in ten obese children (5 girls, 5 boys; age 6 to 16 yrs, mean 12 +/- 1, median 12 yrs) to rule out hypercortisolism. Body mass index (BMI) in the ten children was calculated to be 27-45 kg/m2. Venous blood was sampled before dexamethasone was given in the evening and at 9.00 a.m. the following morning. Endogenous cortisol production was suppressed in all patients. Leptin levels, as measured by a newly developed specific radioimmunoassay, were 31.6 +/- 12.9 microg/l, range 19.2-59.9 microg/l before dexamethasone and 39.9 +/- 16.5 microg/l, range 26.3-80.3 microg/l after dexamethasone in the obese children (ANOVA, p = 0.01). Simple regression analysis revealed that serum levels correlated significantly with body mass index (r = 0.82, p < 0.001). Non-obese children (BMI < 27 kg/m2) had leptin levels between 0.1 and 33.3 microg/l, median 2.2 microg/l (N = 713). Girls (5.5 +/- 4.6 microg/l) (N = 401) had significantly higher leptin levels than boys (1.7 +/- 2.1 microg/l (N = 312) (p < 0.0001). We conclude that 1) high serum leptin concentrations are present in obese children. 2) A single dose of dexamethasone significantly increases the high leptin serum levels in these children. We hypothesize that glucocorticosteroids up-regulate leptin levels in the human.
Adolescent↗