Volume control associated with better cardiac function in long-term peritoneal dialysis patients.

BACKGROUND: This study was undertaken to investigate the effect of long-term blood pressure (BP) reduction, achieved with salt restriction and strict volume control, on frequency and regression of left ventricular hypertrophy (LVH) in long-term peritoneal dialysis (PD) patients. METHODS: 56 patients who had been treated for more than 2 years under our care were enrolled. After echocardiographic (Echo) evaluation, 46 patients were included in the follow-up study. In our unit, we aim to keep patients' BP below 130/85 mmHg and cardiothoracic index below 0.50. To reach these targets, moderate salt restriction is advised, and if necessary, hypertonic PD solutions are used. Echo was performed at the beginning of the study (after a mean period of 36 months on PD) and at the end of the prospective follow-up period (24 months later). RESULTS: At the time of the first Echo, LVH was detected in only 8 (21%) patients. Residual urine volume was significantly decreased compared to data taken when they first started PD (658 +/- 795 vs 236 +/- 307 mL/day). Mean left ventricular mass index (LVMI) was 107 +/- 26.5 g/m2. LVMI was significantly decreased at the end of the follow-up in patients who had LVH at baseline. No LVH developed in patients who had normal LVMI at baseline. CONCLUSION: Our results indicate that control of hypertension is possible when extracellular fluid volume is kept under control using hypertonic PD solutions in case of recruitment in addition to salt restriction in long-term PD patients. Sustained normovolemia is associated with low incidence and regression of LVH.     

Electrocardiographic criteria of left ventricular hypertrophy in the presence of left bundle branch block

When left bundle branch block (LBBB) is present on the electrocardiogram, the diagnosis of left ventricular hypertrophy (LVH) may be difficult. The left ventricular mass in 70 patients with LBBB was estimated by echocardiography, and was compared to the QRS configuration on the electrocardiogram. We found that there was agreement between a monophasic R pattern in lead 1 or V6 (sensitivity 79.3%, 70.7%) and left ventricular hypertrophy. We suggest that a monophasic R pattern in L1 and V6 may provide a useful simple index of left ventricular hypertrophy in the presence of left bundle branch block.     

CT and MRI of the middle ear

Summary High-resolution computed tomography (HRCT) provides excellent contrast between osseous structures, air and soft tissue in conjunction with high spatial resolution. Therefore, thin-section HRCT with bone window setting is the method of choice for the examination of the middle ear structures. The indications are acute and chronic inflammatory changes, cholesteatoma and tumor, the “postoperative middle ear”, and malformations. In most cases, HRCT enables differentiation between inflammatory changes, cholesteatoma, and tumor. The excellent depiction of subtle osseous details enables the identification of erosions of the ossicles or of the bony walls of the mastoid cells, of osseous defects of the tegmen, of the bony labyrinth, and of the tympanic course of the facial canal. In addition, HRCT enables excellent depiction of reconstructions of the ossicles or prosthesis of the ossicles. Although HRCT is the first method of choice, magnetic resonance imaging (MRI) may provide additional information and lead to a more accurate diagnosis in some cases. This is explained by the excellent soft tissue contrast provided by MRI. In addition, MRI offers the possibility of using various pulse sequences and the administration of IV contrast material. Therefore, MRI may allow the differentiation between inflammatory changes, cholesteatoma, and tumor in those cases in which accurate diagnosis cannot be made by HRCT. The differentiation between a meningocele or meningoencephalocele and other entities such as tumors or cholesteatoma can be established by MRI. Furthermore, MRI can accurately depict cases of labyrinthitis or of neuritis of the facial nerve or of intracranial disease caused by middle ear processes, while this is not always possible by HRCT. In summary, HRCT of the middle ear is the method of choice, but MRI may provide supplementary information in those cases in which accurate diagnosis cannot be established by HRCT.      

A neurotrophic model for stress-related mood disorders.

There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.     

Protective effect of interferon-α on the DNA- and RNA-degrading pathway in anti-Fas-antibody induced apoptosis

Aim: Fas membrane-associated polypeptide antigen is a receptor molecule responsible for apoptosis-mediated signals. In animal models of acute viral hepatitis, apoptosis of hepatocytes is mediated by Fas-death receptors; therefore, the aim of this study was to evaluate the effect of interferon (IFN)-alpha on apoptotic markers and nuclease activity against different coding and non-coding single and double stranded RNAs during Fas-induced liver apoptosis. Methods: An in vivo experiment was performed with simultaneous administration of anti-Fas (CD95) antibodies and IFN-alpha, and an in vitro experiment was performed in hepatocyte cultures treated with anti-Fas antibodies and IFN-alpha. Results: Detection of apoptosis using Annexin V-FITC/propidium iodide, Bcl-2 and Bax expression in hepatocyte cultures confirmed the appearance of early apoptotic events and progression toward late apoptosis after anti-Fas antibody treatment. IFN-alpha had a tendency to retard the apoptosis process in Fas-induced apoptosis by increasing the number of viable cells and decreasing the number of cells in late apoptosis, by increasing the percentage of Bcl-2 positive cells, by decreasing the percentage of Bax positive cells, and by decreasing the nuclease activity compared to the anti-Fas antibody treated group. Total DNA and RNA concentration was much reduced in the Fas group and DNA fragmentation assay provided evidence for increased DNA degradation. Enhanced nuclease activity against DNA, rRNA, poly(A), poly(C), poly(U), poly(I:C), and poly(A:U) was manifested in the anti-Fas antibody treated group, except for the inhibitory-bound alkaline RNase. Conclusions: The results demonstrate that the RNA-degrading pathway in Fas-induced apoptosis can accelerate the liberation of the latent enzyme from the inhibitor complex. IFN-alpha prevented enormous, Fas-ligand induced degradation of all the substrates used in this experimental study, most probably due to similarities in the signal transduction pathways. Investigations of death receptor-induced apoptosis may lead to novel treatment combinations for patients with acute or chronic liver diseases.     

Relations of the pterygoid hamulus and hard palate in children and adults: anatomical implications for the function of the soft palate.

We investigated spatial relations of the pterygoid hamuli to the hard palate on 65 skull bases: 31 disarticulated sphenoidal bones from the newborn up to 9 years of age, 19 skulls of adult skeletons (21-59 age group), and 15 skulls aged 60-100 years. We measured: (a) width of the hard palate in the choanal region, (b) length of the hamulus, (c) inclination of the hamulus from the perpendicular line, and (d) distance between the tips of the contralateral hamuli. The width of the hard palate in the choanal region was smallest in children (mean +/- standard deviation, 21.5 +/- 2.6 mm) compared with adult skulls (26.8 +/- 2.3 mm in the 21-59 age group and 25.4 +/- 1.9 mm in the 60-100 age group; P<0.05, one-way analysis of variance (ANOVA) and Student-Newman-Keuls post hoc test). Children had the shortest hamulus (3.6 +/- 1.5mm), and its length increased in the adult age group to 6.9+1.7mm (P<0.05), and then again decreased to 5.0 +/- 1.9 mm in the 60-100 age group (P<0.05 vs. adults and children). The distance between the tips of the contralateral hamuli and their lateral inclination from the perpendicular plane were also greater in the adult age group (38.0 +/- 2.7mm and 35.9 +/- 13.7 degrees, respectively) than either in children (31.0 +/- 3.7mm and 19.6 +/- 12.1 degrees) or the elderly (32.7 +/- 3.9mm and 19.7 +/- 10.3 degrees) (P<0.05). Our study showed that the anatomical measures of the pterygoid hamulus and its relation to the surrounding structures change with age, and occur with the changes in the function of pharyngeal and palatal muscles in deglutition. These changes may have clinical relevance for sleep apnoea and snoring.     

Mucous Gland Adenoma Simulating Bronchial Asthma: Case Report and Literature Review

We report a case of mucous gland adenoma arising in the left main bronchus which was initially misdiagnosed as asthma and review the previous reported cases of this rare tumor published in the available literature.     

Lupus vulgaris in a patient with systemic lupus erythematosus and persistent IgG deficiency

We present the case of a patient with juvenile onset systemic lupus erythematosus (SLE) who developed a persistent, acquired hypogammaglobulinaemia with IgG deficiency. The hypogammaglobulinaemia was probably a complication of high dose corticosteroid treatment. The serum IgG level remained subnormal despite intravenous immunoglobulin therapy. Lupus vulgaris, which developed on the nasal cartilage in this patient with SLE, is not an expected finding. This patient is probably the first reported case of SLE associated with lupus vulgaris.     

Cell proliferation in adult hippocampus is decreased by inescapable stress: reversal by fluoxetine treatment.

Adult hippocampal neurogenesis has been demonstrated in several species and is regulated by both environmental and pharmacological stimuli. The present study seeks to determine whether hippocampal proliferation and neurogenesis are altered in adult animals exposed to inescapable shock (IS) in the learned helplessness model of depression. We report that exposure to avoidance testing, regardless of pre-exposure to IS, decreases cell proliferation in the hippocampus, extending previous studies demonstrating downregulation of neurogenesis by exposure to acute stressors. In addition, when the analysis was conducted 9 days after exposure to IS we observed a significant decrease in cell proliferation compared to nonshocked animals. Administration of fluoxetine, a serotonin selective reuptake inhibitor, from days 2-8 blocked the downregulation of cell proliferation resulting from IS. Fluoxetine treatment also reversed the deficit in escape latency observed in animals exposed to IS. Finally, at the 9 day time point, there was no significant difference in blood levels of corticosterone between nonshocked and IS exposed animals, indicating that the decreased cell proliferation that is observed is not due to increased levels of this adrenal steroid. These findings demonstrate that exposure to IS, which results in a state of behavioral despair, decreases hippocampal cell proliferation and that this effect can be reversed by fluoxetine treatment.     

Biochemical actions of chronic ethanol exposure in the mesolimbic dopamine system

In previous studies, we have demonstrated that chronic administration of morphine or cocaine produces some common biochemical adaptations in the ventral tegmental area (VTA) and nucleus accumbens (NAc), components of the mesolimbic dopamine system implicated in the reinforcing actions of these and other drugs of abuse. Since this neural pathway is also implicated in the reinforcing actions of ethanol, it was of interest to determine whether chronic ethanol exposure results in similar biochemical adaptations. Indeed, as seen for chronic morphine and cocaine treatments, we show here that chronic ethanol treatment increased levels of tyrosine hydroxylase and glial fibrillary acidic protein immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA. Also like morphine and cocaine, ethanol increases levels of cyclic AMP-dependent protein kinase activity in the NAc. These actions of ethanol required long-term exposure to the drug, and were in most cases not seen in the substantia nigra or caudate-putamen, components of the nigrostriatal dopamine system studied for comparison. Altered levels of tyrosine hydroxylase in catecholaminergic cells frequently reflect altered states of activation of the cells. Moreover, increasing evidence indicates that ethanol produces many of its acute effects on the brain by regulating NMDA glutamate and GAB_A receptors. We therefore examined the influence of chronic ethanol treatment on levels of expression of specific glutamate and GABA receptor subunits in the VTA. It was found that long-term, but not short-term, ethanol exposure increased levels of immunoreactivity of the NMDARl subunit, an obligatory component of NMDA glutamate receptors, and of the Glu Rl subunit, a component of many AMPA glutamate receptors; but at the same time, long-term ethanol exposure decreased immunoreactivity levels of the α1 subunit of the GABA_A receptor complex. These changes are consistent with an increased state of activation of VTA neurons inferred from the observed increase intyrosine hydroxylase (TH) expression. These results demonstrate that chronic ethanol exposure results in several biochemical adaptations in the mesolimbic dopamine system, which may underlie prominent changes in the structural and functional properties of this neural pathway related to alcohol abuse and alcoholism. © 1995 Wiley-Liss, Inc.