Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pons”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources

Determinants of variation in serum paraoxonase enzyme activity in baboons.

Paraoxonase (PON), an HDL-associated enzyme, is one of many circulating antioxidants thought to play a vital protective role. To better understand the determinants of quantitative variation in serum PON activity, we assayed PON in samples from 611 pedigreed baboons fed three diets. PON was measured enzymatically; the main determinant of variation was genetic and consisted of at least three components: two loci detected by linkage analyses and a residual polygenic component. Multipoint linkage analyses gave peak log of the odds (LOD) scores on the baboon homolog of human chromosome 7q21-22 (near PON1, the structural gene) of 9.1 on the low-cholesterol, high-fat diet and 4.1 on the high-cholesterol, high-fat diet (genome-wide P values were 1 x 10(-8) and 0.0018, respectively). Surprisingly, a second locus on the baboon homolog of human chromosome 12q13 gave a LOD score of 2.9 on the high-cholesterol, high-fat diet (genome-wide P value was 0.032). We identified several significant covariates, including age, sex, diet, and apolipoprotein A-I concentrations. We estimate that 53% of total trait variation in baboons is explained by genes and 17% by covariates, thus accounting for approximately 70% of total variation in baboon PON. Although the generation of free radicals is influenced primarily by environmental factors, our findings suggest strong genetic regulation of one component in the antioxidant defense system that plays a major role in susceptibility to atherosclerosis.

Aging↗

The BB-paraoxonase genotype is associated with impaired brachial reactivity after acute hypertriglyceridemia in healthy subjects.

The possible relationship between paraoxonase (PON) gene polymorphism and brachial reactivity in healthy adult subjects in the presence of acute hypertriglyceridemia (HT), as a prooxidant factor, was investigated. In 101 healthy subjects the response to flow- induced vasodilatation was measured before and after Intralipid infusion. In the same subjects the A/B PON polymorphism was detected. The frequency was 0.545 for AA genotype, 0.356 for the AB genotype, and 0.099 for the BB genotype. At baseline all genotype groups had a similar increase in brachial artery diameter and flow. After Intralipid infusion, subjects sharing the BB genotype had a significant decrease vs. baseline values in changes in brachial artery diameter (P for trend < 0.001 vs. the other genotypes), but not in flow. In a subgroup of 55 subjects distributed among the 3 PON genotypes the same study protocol was repeated by buccal nitroglycerine administration to study the endothelium-independent vasodilatation. Again, subjects with the BB genotype had the worse vasodilation (P for trend < 0.001). Furthermore, subjects sharing the BB genotype had the lowest endothelium-independent and -dependent changes in diameter (P for trend < 0.001 vs. the other genotypes) independently of gender ratio, basal plasma triglycerides concentrations, and changes in plasma triglycerides concentrations. In conclusion, our study demonstrates that transient HT decreases vascular reactivity more in subjects with the PON BB genotype than in those with the other PON genotypes.

Adult↗

LL-paraoxonase genotype is associated with a more severe degree of homeostasis model assessment IR in healthy subjects.

The LL genotype among subjects with paraoxonase (PON) polymorphism Met-Leu 54 has been shown to be associated with elevated risk of coronary heart disease. Indeed, insulin resistance (IR) is a well known cardiovascular risk factor that is likely attributable to a genetic background, lifestyle, and environmental factors such oxidative stress. Because subjects sharing the LL genotype have a more elevated degree of oxidative stress, one cannot rule out that in those subjects a more severe degree of IR can occur. Thus, the possible relationship between PON gene polymorphism and degree of IR was investigated. In 213 healthy subjects, the degree of IR was assessed by the homeostasis model assessment, and the Met-Leu 54 PON polymorphism was detected. The frequency was 0.366 for the LL genotype, 0.469 for the LM genotype, and 0.164 for the MM genotype. Comparing the three genotype groups, LL genotype had the more severe degree of IR, compared with LM (P < 0.01) and MM (P < 0.01) genotypes. No difference between LM and MM genotypes was found (P = 0.49). Subjects carrying the LL genotype were associated with the IR syndrome picture more than individuals carrying the M allele because they were more overweight and had the highest levels of triglycerides and blood pressure and the lowest values of plasma high-density lipoprotein cholesterol. In a multivariate stepwise regression analysis, LL genotype was a significant predictor of IR, independent of age, sex, body mass index, fasting plasma triglycerides, and high-density lipoprotein cholesterol (P < 0.001). In conclusion, the presence of LL PON genotype is associated with a more severe degree of IR. Thus, IR might be the possible missing link between Met-Leu 54 PON polymorphism and the increased cardiovascular risk.

Aryldialkylphosphatase↗

No association of paraoxonase gene polymorphism with atherosclerosis or Alzheimer's disease.

Both AD and paraoxonase (PON) have been reported to be related to lipids and atherosclerosis, suggesting that the PON gene (PON) is a possible genetic risk factor for AD. We found no association of PON polymorphism with severity of atherosclerosis, densities of AD-type, neuropathologic change, or development of AD in 47 AD and 90 nondemented patients. Our study suggests that PON polymorphism does not play a causal role in the development of atherosclerosis or AD.

Alzheimer Disease↗

Nerve localization techniques for interscalene brachial plexus blockade: a prospective, randomized comparison of mechanical paresthesia versus electrical stimulation.

Postoperative neurologic symptoms (PONS) are relatively common after upper extremity orthopedic surgery performed under peripheral neural blockade. In this study, we prospectively compared the incidence of PONS after shoulder surgery under interscalene (IS) block using the electrical stimulation (ES) or mechanical paresthesia (MP) techniques of nerve localization. For patients randomized to the MP group, a 1-in, 23-g long-beveled needle was placed into the IS groove to elicit a paresthesia to the shoulder, arm, elbow, wrist, or hand. For patients randomized to the ES group, a 5-cm, 22-g short-beveled insulated needle was placed into the IS groove to elicit a motor response including flexion or extension of the elbow, wrist, or fingers or deltoid muscle stimulation at a current between 0.2 and 0.5 mA. Each IS block was performed with 50-60 mL of 1.5% mepivacaine containing 1:300,000 epinephrine and 0.1meq/L sodium bicarbonate. Two-hundred-eighteen patients were randomized between the two groups. One patient was lost to follow-up. Twenty-five patients (23%) in the ES group experienced paresthesia during needle insertion. The incidence of PONS using the ES technique was 10.1% (11/109), whereas the incidence with the MP technique was 9.3% (10/108) (not significant). The PONS lasted a median duration of 2 mo, and symptoms in all patients resolved within 12 mo. The success rate, onset time, and patient satisfaction were also comparable between groups. We conclude that the choice of nerve localization technique can be made based on the patient's and anesthesiologist's comfort and preferences and not on concern for the development of PONS.

Adult↗

[Effects of nutritional status on contents of tryptophan, serotonin and 5-hydroxyindoleacetic acid in rat brain].

Effects of nutritional status on the levels of tryptophan (Trp), serotonin (5HT), and its metabolite, 5-hydroxyindoleacetic acid (5HIAA) in six brain regions of rats were investigated. 1) A low-protein high-carbohydrate diet decreased Trp, 5HT and 5HIAA levels in the cortex and hippocampus, and those of 5HT and 5HIAA in the hypothalamus. This diet did not affect the contents of Trp and 5HT in the midbrain, but decreased 5HIAA. No significant changes of Trp, 5HT and 5HIAA were observed in the pons and medulla and striatum. 2) A low-carbohydrate high-protein diet increased the levels of Trp, 5HT and 5HIAA in the striatum, and 5HT and 5HIAA in the cortex, but showed no effect on the contents of Trp, 5HT and 5HIAA in the hippocampus, midbrain, pons and medulla and hypothalamus. 3) An energy-restriction low-carbohydrate diet increased Trp, 5HT and 5HIAA contents in the striatum, and 5HT and 5HIAA in the cortex and pons and medulla. In the hypothalamus, only 5HIAA was increased by this diet. The diet did not influence Trp, 5HT and 5HIAA contents of the midbrain and hippocampus. These results suggest that i) lowered fat and carbohydrate intakes enhance 5HT synthesis and metabolism in the cortex and that lowered carbohydrate intake enhances them in the striatum, ii) energy restriction enhances the 5HT metabolism in the cortex, pons and medulla and hypothalamus, and 5HT synthesis in the cortex and pons and medulla, iii) lowered protein intake inhibits 5HT metabolism in the cortex, midbrain, hippocampus and hypothalamus, and 5HT synthesis in the cortex, hippocampus and hypothalamus.

Animals↗

Paraoxonase as a risk marker for cardiovascular disease: facts and hypotheses.

Paraoxonase (PON1) is a Ca2+-dependent enzyme whose mechanism of action is incompletely elucidated. PON1 was originally found to be responsible for the hydrolysis of paraoxon, a catabolite of the insecticide parathion, but this enzyme is equally able to hydrolyze other substrates such as phenyl acetate. PON1 exhibits two sequence polymorphisms, Arg-->Gln 192 and Met-->Leu 55, respectively, of which the former is responsible for the distinct catalytic activity of the two corresponding allozymes against paraoxon. The PON1 gene is a member of a family of at least three related genes. Although the physiologic substrate of PON1 is unknown, a protective role against the oxidative degradation of serum lipoproteins has been attributed to this enzyme. Indeed, PON1 is a component of a spectrum of circulating high density lipoprotein particles and can hydrolyze oxidized phospholipids and cholesteryl ester hydroperoxides. Studies have been conducted to evaluate the possible "protective" role of PON, and especially the influence of the Arg-->Gln 192 polymorphism, in coronary artery disease. Results from these investigations are conflicting, and recent data suggest a complex pattern with influences from other polymorphisms in either the PON1 and/or the PON2 and PON3 genes, or even another region of the gene cluster. A number of related factors, which include the heterogeneity of the high density lipoprotein particles incorporating PON(s), the metabolism of associated apolipoproteins such as apoJ/clusterin, the respective roles of PON(s) and other high density lipoprotein-associated enzymes such as platelet-activating-factor acetyl-hydrolase and lecithin-cholesterol acyltransferase, modifications of high density lipoprotein composition and activity under acute-phase conditions, the dietary and environmental regulation of PON(s), and the actual in situ availability of PON in the atherosclerotic artery wall, must equally be taken into account.

Arteriosclerosis↗

Serum paraoxonase activity and genotype distribution in Japanese patients with diabetes mellitus.

We investigated the serum paraoxonase (PON) activity and genotype distribution in 139 patients with non-insulin-dependent diabetes mellitus and in 240 control subjects in a Japanese population. There were no significant differences in PON genotype frequencies between the diabetic and control subjects, but the PON activity was significantly less in diabetic subjects (p<0.01). PON activity was significantly related to levels of total cholesterol and high density lipoprotein (HDL) cholesterol in the control subjects, but not in the diabetic subjects. In diabetic subjects with the genotype AA, the mean maximum intimal-medial thickness (IMT) of the carotid artery was significantly greater than in subjects with genotype AB or BB. PON may play an important role in the development of atherosclerosis associated with diabetes mellitus.

Aryldialkylphosphatase↗

Mesenrhombencephalitis: MR findings in nine patients.

OBJECTIVE: Mesenrhombencephalitis is a serious form of brainstem inflammation predominantly involving the deep and vital portions of the brain, that is, the mesencephalon (midbrain) and rhombencephalon (pons, medulla). Mesenrhombencephalitis is difficult to diagnose on the basis of clinical and laboratory findings alone, and access to this portion of the brain for surgical biopsy carries high morbidity. We describe the MR appearance of mesenrhombencephalitis and correlate the imaging findings with clinical information. MATERIALS AND METHODS: Unenhanced and contrast-enhanced MR images of nine patients with mesenrhombencephalitis were reviewed retrospectively and correlated with clinical, laboratory, and pathologic data. The patients were categorized according to the cause of the disease: three had herpes simplex, one had Listeria monocytogenes, and five had mesenrhombencephalitis of undetermined cause. The three patients with clinical and MR evidence of herpes simplex mesenrhombencephalitis (one confirmed by brain biopsy) were comatose at presentation, with cranial nerve abnormalities in two and seizures in one. One patient with L. monocytogenes (established by blood culture) had cranial nerve palsies, fever, and pain in the ear. Five additional patients had headache (three), fever (three), nausea and vomiting (four), cranial nerve palsies (three), coma (two), and hyporeflexia (one) or hyperreflexia (four). Brain biopsy performed in two patients revealed chronic inflammation of unspecified cause; in one, it was compatible with viral encephalitis. RESULTS: MR images in three patients with herpes simplex mesenrhombencephalitis showed T2 signal hyperintensity in the midbrain (two), pons (one), medulla (one), and temporal lobes (three). Parenchymal foci of hemorrhage (methemoglobin, one patient) and leptomeningeal enhancement (one patient) were identified in the temporal lobes. T2-weighted MR images in one patient with L. monocytogenes showed signal hyperintensity in the brainstem, vermis, midbrain, and internal capsules. On T1-weighted images, low signal was present in these areas, which enhanced with paramagnetic contrast agents. In the remaining five patients, T2-weighted MR images showed patchy signal hyperintensity in the pons, medulla, and thalamus in three each and in the midbrain and temporal lobes in one each. T1-weighted MR images showed normal findings (two) or signal hypointensity in the thalamus and pons in one patient each. Areas of leptomeningeal and parenchymal enhancement were identified in one patient each. Brainstem swelling was seen in three patients, one of whom had petechial hemorrhage in the pons and hydrocephalus. CONCLUSION: Mesenrhombencephalitis is a serious illness that is diagnosed by a combination of imaging, clinical, laboratory, and pathologic studies. MR imaging may be crucial to the early diagnosis of this illness, and radiologists must be familiar with this uncommon entity and its MR findings in order to make timely diagnoses and facilitate treatment.

Adult↗

Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens.

Two experiments were conducted to compare the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens. A polymeric glucomannan mycotoxin adsorbent (GM polymer) was also tested for its efficacy in preventing Fusarium mycotoxicoses. In Exp. 1, a total of 150 starter pigs (initial weight = 9.3+/-1.1 kg) were fed five diets (six pens of five pigs per diet) for 21 d. Diets (as-fed basis) included control, 17% contaminated grains, 24.5% contaminated grains, 24.5% contaminated grains + 0.2% GM polymer, and a pair-fed control for comparison with pigs receiving 24.5% contaminated grains. In Exp. 2,360 1-d-old male broiler chicks were fed for 56 d one of four diets containing the same source of contaminated grains as was fed to pigs. The diets included control, 37% contaminated grains, 58% contaminated grains, and 58% contaminated grains + 0.2% GM polymer (as fed). Neurotransmitter concentrations in the cortex, hypothalamus, and pons were analyzed by HPLC. The following brain neurotransmitter alterations (P < or = 0.05) were observed. In pigs, inclusion of contaminated grains in the diet 1) linearly increased cortex 5-hydroxytryptamine (5HT, serotonin) concentrations, while linearly decreasing hypothalamic tryptophan concentrations; 2) quadratically increased hypothalamic and pons 5-hydroxyindoleacetic acid (5HIAA):5HT ratios, whereas the ratio decreased linearly in the cortex; and 3) linearly increased the ratio of hypothalamic 3,4-dihydroxyphenylacetic acid:dopamine (DA) concentrations, whereas hypothalamic norepinephrine (NRE) and pons DA and homovanillic acid (HVA) concentrations linearly decreased. In broiler chickens, inclusion of contaminated grains in the diet 1) linearly increased concentrations of 5HT and 5HIAA in the pons and 5HT concentrations in the cortex; 2) linearly decreased 5HIAA:5HT ratio; and 3) linearly increased pons NRE, 3-methoxy-4-hydroxyphenylethylene glycol, DA, and HVA concentrations. Supplementation of GM polymer to the contaminated diet decreased (P < 0.05) 5HT and 5HIAA concentrations in the cortex of pigs. It was concluded that the differences in alterations of brain neurochemistry might explain the species differences in the severity of Fusarium mycotoxin-induced feed refusal.

Adsorption↗

Circadian rhythms in neurotransmitter receptors in discrete rat brain regions.

Circadian rhythms were measured in alpha 1-, alpha 2- and beta-adrenergic, acetylcholine muscarinic (ACh), and benzodiazepine (BDZ) receptor binding in small regions of rat brain. Rhythms in alpha 1-receptor binding were measured in olfactory bulb, frontal, cingulate, piriform, parietal, temporal and occipital cortex, hypothalamus, hippocampus, pons-medulla, caudate-putamen and thalamus-septum. No rhythm was found in cerebellum. Rhythms in alpha 2-receptor binding were measured in frontal, parietal and temporal cortex, and pons-medulla. No rhythm was found in cingulate, piriform or occipital cortex, or hypothalamus. Rhythms in binding to beta-receptors were measured in olfactory bulb, piriform, insular, parietal and temporal cortex, hypothalamus and cerebellum. No rhythms were found in frontal, entorhinal, cingulate, or occipital cortex, hippocampus, caudate-putamen, or pons-medulla. Rhythms in ACh receptor binding were measured in olfactory bulb, parietal cortex and caudate-putamen. No rhythms were found in frontal or occipital cortex, nucleus accumbens, hippocampus, thalamus-septum, pons-medulla or cerebellum. Rhythms in BDZ receptor binding were measured in olfactory bulb, olfactory and occipital cortex, olfactory tubercle, nucleus accumbens, amygdala, caudate-putamen, hippocampus and cerebellum. No rhythms were found in parietal cortex, pons-medulla or thalamus-septum. The 24-hr mean binding to receptors varied between 3- and 10-fold, the highest in cortex and the lowest, usually, in cerebellum. The piriform cortex was particularly high in alpha 1- and alpha 2-adrenergic receptors; the nucleus accumbens and caudate, in ACh receptors; and the amygdala, in BDZ receptors. Most adrenergic and ACh receptor rhythms peaked in subjective night (the period when lights were off under L:D conditions), whereas most BDZ receptor rhythms peaked in subjective day (the time lights were on in L:D). Perhaps in the rat, a nocturnal animal, the adrenergic and ACh receptors mediate activity and the functions that accompany it, and the BDZ receptors mediate rest, and with it, sleep.

Animals↗

[Immunohistochemical methods in the differential diagnosis of primary traumatic and subsequent secondary cerebral changes].

In a 22-year-old man, driver of a personal motor vehicle, who died within 39 hours after a traffic injury, the authors made histological and immunohistochemical examinations of the brain focused on differentiation of primary traumatic and subsequent secondary changes. In haematomas the authors revealed the presence bi- and trivalent iron by Turnbull's and Perl's reaction as well as glycophorin by immunohistochemical reactions. White matter lesions were evaluated histologically by staining according to Palmgren and immunohistochemically by detection of neuron-specific enolase, beta-amyloid protein precursor and low molecular neurofilaments. Minor contusion foci in the corpus callosum and in the peripheral portion of the pons revealed the presence of extracellular bivalent iron and exceptionally also the presence of intracellular iron. Glycophorin was present not only in erythrocyte membranes but also in the form of lumps signalizing haemolysis. In the haematoma in the median portion of the pons neither iron nor free glycophorin were detected. At all investigated sites (subcortical areas of the white matter of the hemispheres, capsula interna, corpus callosum, pons Varolii) the authors detected numerous axonal deformities (oedema or formation of retraction spheroids) which revealed on immunohistochemical examination an intense reaction with antibodies in particular against neuron-specific enolase and beta-amyloid protein precursor, and to a smaller extent against low-molecular neurofilaments. The combination of the mentioned immunohistochemical examinations seemed a suitable method for differentiating primary cerebral injury (diffuse axonal injury and minor contusion foci in the corpus callosum and the margin of the pons) from secondary changes (haemorrhages in the median portion of the pons) which developed shortly before death as a manifestation of haemodynamic disorders associated with cerebral oedema).

Adult↗

Antioxidant properties of HDL in transgenic mice overexpressing human apolipoprotein A-II.

Transgenic mice overexpressing human apolipoprotein A-II (huapoA-II) display high VLDL and low HDL levels. To evaluate the antioxidant potential of huapoA-II enriched HDL, we measured the activities of paraoxonase (PON) and platelet-activating factor acetylhydrolase (PAF-AH). Both activities decreased up to 43% in the serum of transgenic mice compared with controls, varied in parallel to HDL levels, but decreased less than HDL levels. The major part of PON and PAF-AH was associated with HDL, except in fed high huapoA-II-expressing mice, in which 20% of PAF-AH and 9% of PON activities were associated with VLDL. PON mRNA levels in the liver, its major site of synthesis, were similar in transgenic and control animals, indicating normal enzyme synthesis. In transgenic mice, the basal oxidation of lipoproteins was not increased, whereas their VLDL were more susceptible to oxidation than VLDL of controls. Interestingly, HDL of transgenic mice protected VLDL from oxidation more efficiently than HDL of controls. In conclusion, the decrease in both PON and PAF-AH activities in huapoA-II transgenic mice is best explained by their lower plasma HDL levels. However, the unchanged basal lipoprotein oxidation in transgenic mice suggests that huapoA-II-rich HDL may maintain adequate antioxidant potential.

Animals↗

[Congestive heart failure and paraoxonase].

OBJECTIVE: To determine the changes of paraoxonase activity in patients with heart failure. METHODS: The serum paraoxonase (PON) activity of the heart failure group and controls was measured with phenylacetate as the substrate. RESULTS: The serum PON activity of the heart failure patients significantly decreased as compared with the controls; after the treatment, the PON activity of heart failure was largely elevated; and the PON activity of the patients with heart failure was negatively correlated with tumor necrosis factor-alpha. CONCLUSION: The PON activity of patients with congestive heart failure significantly decreases.

Adult↗

[Effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain].

In spite of many investigations done for many years, the mechanism of general anesthesia remains still unclear. To elucidate the mechanism of general anesthesia, effects of sevoflurane anesthesia on norepinephrine metabolism in rat brain was studied. Sevoflurane 3% was administered for 20 minutes to Wistar male rats weighing 230-270g under spontaneous respiration. The rats were sacrificed by decapitation and the brains were rapidly removed. They were dissected into nine discrete regions, locus coeruleus, pons plus medulla oblongata, hypothalamus, thalamus, basal ganglia, hippocampus, amygdala and cerebral cortex. The contents of norepinephrine (NE) and one of its major metabolites, 3-methoxy-4-hydroxyphenyl-ethylene glycol (MHPG) were measured by high performance liquid chromatography with the dual-cell coulometric detector before anesthesia, 20 minutes after the start of anesthesia and at recovery from anesthesia. Significant increases in NE levels were observed in the pons, thalamus and hippocampus by sevoflurane anesthesia for 20 minutes compared with the control group and also in the pons and midbrain at recovery from anesthesia. MHPG levels were significantly decreased in the pons and cortex by sevoflurane anesthesia, while an appreciable increase in MHPG levels was observed in the thalamus by sevoflurane anesthesia. It is concluded that NE metabolism is significantly suppressed in the pons, thalamus and hippocampus during sevoflurane anesthesia and this change in NE metabolism may be associated with a mechanism of sevoflurane anesthesia.

Anesthesia, Inhalation↗

[Quantification of wallerian degeneration of the pyramidal tract in the capsular region by magnetic resonance imaging].

Using magnetic resonance imaging, we studied 23 patients with motor deficit associated with cerebrovascular disease of the internal capsule. According to the severity of the motor deficits, 23 patients were divided into three groups (severe group...9, moderately severe group...8, mild group...6). A coronal T2-weighted image was obtained along a straight line between the front edge of the medulla and the deepest point of the interpeduncular cistern in a midsagittal T1-weighted image. It was revealed that wallerian degeneration extended continuously from part of the internal capsule down to the pons or medulla or the decussation in all patients. The area of wallerian degeneration in the pons and the area of half the pons were calculated from the coronal T2-weighted image. Moreover, the wallerian index was calculated as: (area of wallerian degeneration in pons divided by area of half the pons) X 100. Values of the wallerian index +/- SD were 26.4 +/- 5.1 in the severe group, 19.2 +/- 5.6 in the moderately severe group, and 10.0 +/- 5.4 in the mild group. There were significant differences among the three groups. We concluded that the area of wallerian degeneration was related to the severity of motor deficits.

Adult↗

[An MRI study of hereditary spinocerebellar degenerations].

We evaluated magnetic resonance image (MRI) in 21 cases of hereditary spinocerebellar degenerations (SCD) of autosomal dominant trait. By the discriminant formula based on size of the cerebellar vermis and ventral pons, which was reported in our previous study, the patients were classified into three types. Group 1 included the cases with atrophies in the vermis and pons; OPCA type. Group 2 showed vermian atrophy and less significant atrophy in pons; LCCA type. And Group 3 was no significant atrophies both in vermis and pons. Cases in Group 1 were furthermore divided into two groups according to width of the midbrain tegmentum. Group 1A, with normal midbrain tegmentum, was consisted of five cases. Four cases were diagnosed as Menzel type OPCA. Another case showed various clinical symptoms and relatively mild atrophies for his duration of illness. His family members were classified to Group 3. Seven cases in Group 1B showed reduced midbrain tegmentum. Four cases showed ataxia, spasticity, ocular symptoms, bladder dysfunction and amyotrophy with or without fasciculation, and they seemed to be a special type of SCD mimicking Joseph disease. One case showed bulging eyes, ocular movement palsy and dystonia. However, his sister manifested only ataxia with very mild ocular movement disorder. Their MRI demonstrated severe atrophies in the cerebellum, pons and afferent cerebellar peduncli, and this pedigree was thought to be Menzel type OPCA with various associated disorders. Another case was clinically diagnosed as dentate-rubro-pallido-luysian atrophy. Group 2 was consisted of 6 cases who were clinically diagnosed as Holmes type LCCA. MRI demonstrated medial dominant cerebellar atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of electroacupuncture on brain enkephalins content at different times in rats.

The basic level of methionin-enkephalin (MEK) in rat medulla oblongata plus pons was the highest at 05:00 o'clock and the lowest at 23:00. In both hypothalamus and striatum at 05:00 it was higher than at 11:00, 17:00 and 23:00. In both hippocampus and midbrain at 05:00 and 23:00 it was higher than those at 11:00 and 17:00. In the cortex it was higher at 05:00 than at 11:00 and 17:00. The basic level of leucine enkephalin (LEK) in the medulla oblongata plus pons was the highest at 11:00 and the lowest at 17:00 and 23:00. Electroacupuncture (EA) at 05:00 increased the MEK content in the medulla oblongata plus pons and the LEK level in the hypothalamus. It decreased the MEK content in the hypothalamus and the LEK level in the cortex; EA at 11:00 produced decreases of MEK concentrations in the medulla oblongata plus pons and the midbrain and increases of MEK content in the cortex, hypothalamus and striatum. At 17:00 it increased the MEK level in the hypothalamus and the LEK content in the hippocampus. At 23:00 it reduced the levels of MEK and LEK in the hippocampus. The results suggest that there are very marked circadian rhythms in the MEK basic levels of the six discrete brain regions observed and the LEK of the medulla oblongata plus pons; EA at different times produces different effects on brain MEK and LEK levels.

Acupuncture Therapy↗