Paediatric middle aortic syndrome with endovascular treatment in East Malaysia.

Middle-aortic syndrome is a surgically curable cause of childhood hypertension. Open surgery is traditionally offered but with the advance of medical technology, endovascular approached is available in many country. Failure to control BP in open surgery is as low as 4.1% compares to 13% in endovascular approaches. However, mortality is 4% in open surgery almost 2 times higher than 2.3% in endovascular approach. This article presents a case of 10 years old child treated successfully without complication with endovascular balloon dilatation, as a first case of such disease in East Malaysia.

Portacaval anastomosis induces region-selective alterations of the endogenous opioid system in the rat brain.

Portacaval anastomosis (PCA) in the rat results in a broad spectrum of neurological and neurobehavioral changes, including alterations of circadian rhythms, impaired locomotor activity, and reflexes, as well as decreased threshold to noxious stimuli. In addition, following portacaval shunting, rats drink significantly more ethanol in a free-choice drinking paradigm. Available evidence suggests that many of these behavioral changes may be modulated by the endogenous opioid system of the brain. To evaluate this possibility, the effects of PCA on circulating beta-endorphin (beta-EP), as well as beta-EP content in the pituitary and specific brain nuclei, was evaluated using a sensitive radioimmunoassay. Furthermore, the characteristics and regional densities of mu and delta opioid receptors in the brains of PCA and sham-operated control rats were studied using an in vitro technique, as well as quantitative receptor autoradiography and the specific ligands 125I [D-Ala2, MePhe4, Met(o)ol5]enkephalin (FK 33-824) and 125I [2-D-penicillamine, 5-D-penicillamine]-enkephalin (DPDPE) for micro and delta sites, respectively. PCA resulted in region-selective modifications of beta-EP in brain, but not in pituitary or blood. Autoradiographic studies revealed a generalized decrease in mu binding sites (up to 70% decreases compared with sham-operated controls) and region-selective alterations of delta receptor densities following PCA. Portacaval-shunted rats drank significantly more ethanol in a free-choice drinking paradigm, an effect that was significantly attenuated by the administration of the opiate antagonist naloxone. Increased ethanol preference thus appeared to result from modifications of the endogenous opioid system in nucleus accumbens of rats following PCA.

Quantitative autoradiography using selective radioligands for central and peripheral-type benzodiazepine receptors in experimental Wernicke's encephalopathy: implications for positron emission tomography imaging.

Wernicke's encephalopathy (WE) is difficult to diagnose during life, with up to 80% of cases being missed by routine neurological evaluation in both alcoholics and AIDS patients. Therefore, there is a need for noninvasive diagnostic procedures. Using the pyrithiamine-treated rat, an animal model of WE, we have studied, using radioligands for central (neuronal) and "peripheral-type" (glial) benzodiazepine receptors, the regional distribution of changes in the densities of these receptors in relation to the degree of reactive gliosis accompanying neuronal loss. Histological studies revealed neuronal loss in selective regions, including the thalamus, inferior colliculus, inferior olivary nucleus, and mammillary body. Autoradiographic studies demonstrated increases in densities of [3H]PK11195 binding sites that closely paralleled the topographic distribution of neuronal cell loss and reactive gliosis. In contrast, [3H]Ro15-178 showed poor spatial correlation, with the neuronal loss seen in pyrithiamine-induced thiamine deficiency. The positron emission tomography ligand [11C]PK11195 may be useful for the assessment of thiamine deficiency-induced brain damage in human alcoholics.

Neuronal cell death in Wernicke's encephalopathy: pathophysiologic mechanisms and implications for PET imaging.

Thiamine deficiency in humans is associated with Wernicke's encephalopathy (WE) which is characterized neuropathologically by neuronal loss in selective brain regions. Pyrithiamine-induced thiamine-deficiency in the rat results in lesions which are similar in nature and distribution to those seen in human WE. Several mechanisms have been implicated in the pathogenesis of neuronal loss in thiamine deficiency including, (i) impaired cerebral energy metabolism, (ii) focal lactic acidosis, (iii) NMDA-receptor mediated excitotoxicity and (iv) blood-brain barrier breakdown. WE is difficult to diagnose during life and a large number of cases are missed by routine clinical neurological evaluation. Recently, non-invasive diagnostic procedures such as CT and MRI have been used for the evaluation of acute and chronic WE. Autoradiographic studies reveal that increased densities of binding sites for the astrocytic ligand 3H-PK11195 closely parallel the topographic distribution of reactive gliosis and neuronal loss in selective brain regions of pyrithiamine-induced thiamine-deficient rats. In contrast, binding sites for the neuronal ligand 3H-Ro15-1788 show poor regional correlation with neuronal loss in thiamine deficiency. Both of these ligands are available, and have been used in PET assessment of various disorders in humans. The results of autoradiographic studies suggest that 11C-PK11195 may offer a useful PET ligand for the assessment of brain damage in WE in humans.

Densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand 3H-PK11195 are increased in brain 24 hours following portacaval anastomosis.

Quantitative receptor autoradiography was used to measure the densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand 3H-PK11195 in regions of the rat brain 1, 3, 7 and 28 days following portacaval anastomosis (PCA) and in sham-operated control animals. The results demonstrate that densities of 3H-PK11195 binding sites were significantly increased in the cerebral cortex (by 40%, p < 0.05) as early as 24 hours following PCA. In the thalamus significant increases in densities of 3H-PK11195 binding sites were seen 3 days after PCA, whereas in brain regions such as the striatum and cerebellum, significant increases in 3H-PK11195 binding sites were not evident until 7 days following PCA. By 28 days following PCA increased densities of 3H-PK11195 binding sites were well established and widespread throughout the brain. Previous studies demonstrate early increases of brain ammonia following PCA. PTBRs or their endogenous ligands could play an important role in the early astrocytic response (mitochondrial proliferation, swelling) to ammonia following PCA.

An investigation of the rheological properties of several interocclusal registration materials.

PURPOSE: To study the viscosities of eight interocclusal registration materials at 30 seconds after the start of mixing and to compare the time (Tcv) required for various interocclusal registration materials to reach a proposed critical viscosity of 5,000 poise. MATERIALS AND METHODS. One zinc-oxide eugenol, one polyether, and six vinyl-polysiloxane interocclusal registration materials were studied. The viscosities of the polymerizing materials were monitored with a cone and plate viscometer. RESULTS: One-way analysis of variance showed significant difference in the viscosity at 30 seconds and in the Tcv among the materials. A zinc oxide eugenol interocclusal registration material was found to possess the lowest viscosity at 30 seconds and the longest Tcv. CONCLUSIONS: The criteria for the selection of an interocclusal registration material should include its viscous properties because all materials behaved differently.

Increased densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand [3H]PK11195 in vulnerable regions of the rat brain in thiamine deficiency encephalopathy.

Quantitative receptor autoradiography was used to evaluate the density of high-affinity binding sites for the "peripheral-type" benzodiazepine receptor (PTBR) ligand [3H]PK11195 in brain regions of the rat at different stages of pyrithiamine-induced thiamine deficiency encephalopathy, an experimental model of the Wernicke-Korsakoff syndrome (WKS). Assessment of the density of [3H]PK11195 binding sites in thiamine-deficient animals showing no neurologic signs of thiamine deficiency encephalopathy, and revealed no significant alterations compared with pair-fed control animals in any brain region studied. Densities of [3H]PK11195 binding sites were, however, significantly increased in brain regions of the rat at the symptomatic stage, where increased densities were seen in the inferior colliculus (233% increase, p < 0.001), inferior olivary nucleus (154% increase, p < 0.001) and thalamus (up to 107% increase, p < 0.001). Histologic studies of these same brain regions revealed evidence of neuronal cell loss and concomitant gliosis. Densities of [3H]PK11195 binding sites in nonvulnerable brain regions that showed no histologic evidence of neuronal loss, such as the cerebral cortex, hippocampus, and caudate-putamen, were not significantly different from those in control animals. Increased densities of binding sites for the PTBR ligand probably reflect glial proliferation and are consistent with an excitotoxic mechanism in the pathogenesis of neuronal cell loss in thiamine deficiency encephalopathy. Positron emission tomography (PET) using [11C]PK11195 could offer a potentially useful diagnostic tool in WKS in humans.

Brain extracts containing a Huntington disease antigen inhibit [3H]kainate binding and block synaptosomal amino acid transport.

Fractions isolated from mammalian brain which had previously been shown to inhibit the rate of migration of peripheral blood leukocytes taken from Huntington disease cases, and also to inhibit [3H]kainic acid binding, were characterized further. By use of repeated ultrafiltration onto a 1000D MW cutoff filter, and by the isolation and extensive washing of an enriched ammonium sulfate fraction, their activity was shown not to be due to the presence of endogenous glutamate, and to be relatively selective for brain glutamate receptor binding sites. Inhibitory activity at [3H]GABA, 5-[3H]hydroxytryptamine 5HT1 and dopamine D1 or D2 binding sites was much weaker or absent. Factor extracts were also shown to act as non-competitive inhibitors of synaptosomal amino acid transport: increasing concentrations of the factor had no significant effect on the KM for the uptake of either [3H]glutamate or [3H]GABA, but at a final concentration of 66 micrograms protein x ml-1 had reduced the VMAX for [3H]glutamate uptake to approximately 20% of control, and the VMAX for [3H]GABA uptake to approximately 40% of control. This may enhance the factor's potential excitotoxicity.

Plasma GABA-like activity in rats with hepatic encephalopathy is due to GABA and taurine.

Significant discrepancy exists between radioreceptor and high-performance liquid chromatographic estimates of plasma GABA concentrations in animal models of hepatic encephalopathy. A possible explanation for this discrepancy is the presence in plasma of a substance that can inhibit [3H]-GABA binding but is not GABA itself. The aim of this study was to determine whether any of the amino acids that are increased in the plasma of animal models of acute and chronic hepatic encephalopathy (glutamine, glutamate, phenylalanine, tyrosine, citrulline and taurine) can significantly inhibit [3H]-GABA binding and contribute to the GABA-like activity of plasma aliquots. At final assay concentrations equivalent to plasma concentrations found in hepatic encephalopathy, only taurine was found to significantly inhibit [3H]-GABA binding to whole rat brain synaptosomal membranes (36% inhibition at 30 mumol/L final assay concentration). The concentration of taurine that resulted in 50% inhibition (final assay concentration) was 158 mumol/L, corresponding to a plasma concentration of 1.58 mmol/L. Taurine inhibition of [3H]-GABA binding was competitive because the receptor density was unaltered, but the receptor affinity decreased with increasing concentration of taurine. Plasma GABA-like activity (determined by radioreceptor assay) and plasma GABA and taurine concentrations (determined by high-performance liquid chromatography) were measured in 18 rats with acute or chronic hepatic encephalopathy and 9 control rats. Plasma GABA-like activity and plasma GABA and taurine concentrations were significantly increased in rats with hepatic encephalopathy compared with control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Whole-body vibration in underground load-haul-dump vehicles.

Whole-body vibrations (WBV) were measured at the seatpan of load-haul-dump (LHD) vehicles of 3.5-, 5-, 6- and 8-yard capacity at two underground mines. Twenty-two sets of measurements were made involving 11 vehicles, 8 operators and 4 work locations. In each set frequency-weighted rms and peak accelerations were measured in the x, y and z directions, as defined by the ISO (1982), during mucking, driving full, dumping and driving empty. Significant differences in rms accelerations were found between vehicle sizes and between operational tasks (less than or equal to 0.05). The smallest (3.5 yd) vehicle produced the greatest accelerations in the x and z directions. Accelerations in the x and z directions were also greater when driving full and empty than when mucking and dumping. The highest frequency-weighted rms accelerations of 2.0 to 2.8 m/s-2 were recorded in the z (longitudinal) direction. Peak accelerations ranged from 1.2 to greater than or equal to 20 m/s2, resulting in crest-factor ratios in excess of six. The exposure periods for each task were used to calculate mean daily acceleration exposures (m/s2). Of the 22 sets of measurements, 20 exceeded the International Standards Organization (ISO) six-hour daily exposure limit in the z direction of acceleration, and 9 exceeded the six-hour daily exposure limits in all three directions. Acceleration exposure ratios calculated using resultant acceleration vectors as described in ISO (1982), were found to exceed the ISO exposure limit for health or safety in all 22 cases. One-third octave band frequency analysis of the weighted signals indicated that the dominant frequencies were usually 1.6 to 3.15 Hz, except when the vehicles were idling and higher frequencies predominated.