Magnesium deficiency as a cause of acute intractable seizures

Summary Clinical and experimental investigations have shown that magnesium depletion causes a marked irritability of the nervous system, eventually resulting in epileptic seizures. Although magnesium deficiency as a cause of epilepsy is uncommon, its recognition and correction may prove life-saving. Two case reports are presented which emphasize the importance of recognizing hypomagnesaemia in patients with acute intractable seizures.     

Protective effects of HN and F glycoprotein-specific monoclonal antibodies on experimental newcastle disease

Monoclonal antibodies directed against two different epitopes of HN protein of NDV Italien neutralised this virus in both in vitro and in vivo tests. Moreover, the combination of these two HN monoclonal antibodies neutralised the Italien virus synergistically. Five monoclonal antibodies directed against the F protein of NDV had variable neutralising activity against NDV Italien. Passive protection afforded by some anti F monoclonal antibodies was higher than that observed with the combination of the two HN monoclonal antibodies and even equivalent or better than that obtained with rabbit polyclonal antiserum. The importance of the F protein in the immune response against NDV is demonstrated.     

Enzyme-linked immunosorbent assay (ELISA) for detecting infectious laryngotracheitis viral antibodies in chicken serum

The conditions of an indirect-enzyme linked immunosorbent assay for infectious laryngotracheitis virus (ILT) antibodies have been established. The specificity of the reaction was demonstrated. The method offers a simple and specific antibody assay for the detection of antibodies to ILT virus arising from vaccination or challenge infection.     

An ELISA for the detection of antibodies to avian nephritis virus and related entero-like viruses

An ELISA for the detection of antibodies against avian nephritis virus (ANV) and related entero-like viruses was developed. Different antigenic preparations made from chicken kidney cells infected with the G-4260 strain of ANV were compared. Crude antigen obtained by fluorocarbon treatment of infected cells was found to be appropriate and to give reproducible results with antisera directed against ANV and three entero-like particles (ELPs): the Belgian entero PV2 and entero 3, and the Irish ELP-1. A cut-off value was determined using 30 specific pathogen-free (SPF) sera and the absence of antigenic relationships with nine different reference sera directed against avian viruses was demonstrated. The cross antigenic relationships between avian encephalomyelitis virus (AEV), ANV and the three ELPs was investigated by ELISA and confirms the classification of those fowl enteroviruses into two serotypes: the first including ANV and ELPs and the second including AEV. A strong correlation (94%) was demonstrated between ELISA and a seroneutralisation test. Using ELISA, antibodies against ANV and related ELPs were demonstrated in 13/14 breeding and 8/10 broiler flocks from Belgium.     

Role of NO in vagally-mediated relaxations of guinea-pig stomach

Summary Vagal stimulation of the stomach induces a relaxation mediated via non-adrenergic, non-cholinergic (NANC) nerves. The neurotransmitter which is responsible for this relaxation is still unknown. To determine whether nitric oxide (NO) or a NO related substance mediates this relaxation, an intact guinea-pig stomach was mounted in an organ bath, with electrodes surrounding the vagal nerves.Electrical stimulation of the vagal nerves, in the presence of atropine, induced frequency dependent, tetrodotoxin-(TTX) sensitive relaxations of the stomach quantified as changes in volume. These relaxations were not affected by - or -adrenoceptor antagonists or guanethidine. Thus they were evoked by non-adrenergic, non-cholinergic (NANC) inhibitory nerves. The relaxant responses could be inhibited in a concentration-dependent manner by N^G-nitro-Irarginine (IrNNA) a substance that inhibits the formation of nitric oxide (NO). Addition of L-arginine, the substrate for NO-synthase, reversed the L-NNA-induced-inhibition of the relaxation.Addition of nitroglycerin (a NO-donor) to a nonstimulated stomach mimicked the relaxations observed after vagal stimulation in a concentration dependent manner. These relaxations were insensitive to TTX. Relaxation of the stomach by vagal stimulation was prevented by an inhibitor of soluble guanylate cyclase, methylene blue, further supporting our conclusions.These data indicate that NO or a substance releasing NO plays an important role in NANC-neurotransmission after vagal stimulation of the guinea-pig stomach.Correspondence to A. L. Meulemans at the above address     

The role of nitric oxide (NO) in 5-HT-induced relaxations of the guinea-pig stomach

Summary In a previous study we showed that the relaxations induced after vagal stimulation of the guinea-pig stomach are mediated via nitric oxide (NO) or a NO-related substance. Intra-arterial injection (i.a.) of 5-hydroxytryptamine (5-HT) also induced relaxations in the guinea-pig stomach. Since it has been shown that in the guinea-pig colon 5-HT-induced relaxations are mediated via NO the aim of this study was to establish whether NO is involved in the 5-HT-induced relaxations in the guinea-pig stomach. Intra-arterial injection of 5-HT induced dose-dependent relaxations of the stomach. Since atropine and - and -adrenoceptor blocking agents did not influence the relaxation and since tetrodotoxin (TTX) blocked the relaxations, this effect is mediated via NANC-neurons. Administration of a NO-synthase-inhibitor N^G-nitro-l-arginine (L-NNA) concentration-dependently reduced the 5-HT-induced relaxations. Haemoglobin (a NO-scavanger) did not affect the relaxations to 5-HT, while addition of methylene blue, an inhibitor of soluble guanylate cyclase, reduced the relaxations by 50%. Addition of an opioid receptor agonist (loperamide), a 5-HT₁ antagonist (methiothepin or metergoline) or a 5-HT₄ receptor agonist (cisapride) or-antagonist (tropisetron in micromolar concentrations) inhibited the 5-HT-induced relaxations. Neither the 5-HT₄ receptor agonist renzapride, nor the novel 5-HT₄ receptor antagonist SDZ 205-557, affected the relaxations to 5-HT. These data indicate that 5-HT-induced relaxations of the guinea-pig stomach are mediated via NANC-inhibitory nerves on which inhibitory opioid-receptors are present. The use of selective agonists and antagonists indicates that 5-HT does not act via 5-HT₂, 5-HT₃ or 5-HT₄ receptors. 5-HT may act via 5-HT₁ receptors but the subtype involved, if any, has not yet been identified. The inhibitory neurotransmitter which is involved is NO or a NO-related substance. Correspondence to A. L. Meulemans at the above address     

Striatum forever, despite sequence learning variability: a random effect analysis of PET data

This PET study is concerned with the what, where, and how of implicit sequence learning. In contrast with previous studies imaging the serial reaction time (SRT) task, the sequence of successive locations was determined by a probabilistic finite-state grammar. The implicit acquisition of statistical relationships between serially ordered elements (i.e., what) was studied scan by scan, aiming to evidence the brain areas (i.e., where) specifically involved in the implicit processing of this core component of sequential higher-order knowledge. As behavioural results demonstrate between- and within-subjects variability in the implicit acquisition of sequential knowledge through practice, functional PET data were modelled using a random-effect model analysis (i.e., how) to account for both sources of behavioural variability. First, two mean condition images were created per subject depending on the presence or not of implicit sequential knowledge at the time of each of the 12 scans. Next, direct comparison of these mean condition images provided the brain areas involved in sequential knowledge processing. Using this approach, we have shown that the striatum is involved in more than simple pairwise associations and that it has the capacity to process higher-order knowledge. We suggest that the striatum is not only involved in the implicit automatization of serial information through prefrontal cortex-caudate nucleus networks, but also that it plays a significant role for the selection of the most appropriate responses in the context created by both the current and previous stimuli, thus contributing to better efficiency and faster response preparation in the SRT task.     

A paradoxical increase in resting energy expenditure in malnourished patients near death: the king penguin syndrome

BACKGROUND: The metabolic expression of extreme starvation on the verge of death is unknown in humans. OBJECTIVE: The objective was to compare the resting energy expenditure (REE) of 5 extremely malnourished dying patients [body mass index (in kg/m(2)): 9.77 +/- 0.1] with that of 16 less-malnourished anorexia nervosa (AN) patients. DESIGN: REE was measured by indirect calorimetry and body composition was measured by anthropometry and dual-frequency bioelectrical impedance analysis. Fasting serum insulin, thyroid hormone, and catecholamine concentrations were also determined. RESULTS: At the start of refeeding, REE was high in each of the 5 extremely malnourished dying patients, whereas it was low in the 16 AN patients (mean +/- SD: 5174 +/- 391 kJ/d compared with 3844 +/- 619 kJ/d; P < 0.05). The high REE value in the 5 extremely malnourished dying patients was associated with almost no fat mass (FM), high urinary nitrogen loss (16.4 +/- 2.9 g/d), low serum fatty acid concentrations (0.36 +/- 0.23 mmol/L), and low or normal serum insulin, thyroid hormone, and catecholamine concentrations. During the first 2-4 wk of refeeding, REE and nitrogen loss decreased, whereas fatty acid concentrations increased in each of the 4 surviving patients; REE and urinary nitrogen output increased in the 16 AN patients. CONCLUSION: In malnourished persons near death, there is an increase in REE and in protein catabolism. The reason for this increase is unknown but could relate to consumption of the last mobilizable muscle mass and to diseased cellular membranes.     

Effects of damaging the endocardial surface on the mechanical performance of isolated cardiac muscle

The mechanical properties of mammalian ventricular cardiac muscle have been studied in the presence and in the absence of an intact endocardial surface. Isotonic and isometric twitch contractions were obtained from papillary muscles of the right ventricle of cat at 29 degrees and 37 degrees C, at different extracellular calcium concentrations ([Ca2+]o), and at different initial muscle lengths. The endocardial surface was damaged by gentle abrasion of the muscle surface with a plastic blade or by brief immersion for 1 second with 1% Triton X-100. Although there was no evidence of damage to myocardial cells, damaging the endocardial surface resulted in an immediate and irreversible abbreviation of the twitch contractions with, except at the highest ([Ca2+]o, a decrease in peak isometric twitch tension. These changes induced 1) an asymmetrical shift of the tension-[Ca2+]o relation towards increasing [Ca2+]o but with no effect at the highest [Ca2+]o, and 2) a rightward and downward shift of the length-tension relation. Both shifts were significantly more pronounced at 37 degrees C than at 29 degrees C; they were not accompanied by significant changes in Vmax. The asymmetrical shift of the tension-[Ca2+]o relation suggests that the endocardium-mediated chain of events may be mediated by changes in the sensitivity of the contractile proteins to Ca2+. This hypothesis is also supported by the similar pattern of changes (i.e., modulation of the onset of early tension decline) induced by decreasing length at each [Ca2+]o and by the removal of a functional endocardium. Accordingly, the endocardium may help to control the performance of the heart by modulating peak contractile performance and relaxation of the underlying myocardium.