Kimura's disease: effects of age on clinical presentation.

BACKGROUND: Kimura's disease (KD) is known to be dominant among young Asian men, but it can also occur in middle- and advanced-aged people. The clinical characteristics of KD, especially by age, are not well known. AIM: This study was performed to investigate the effects of age on the clinical characteristics of KD. DESIGN: We conducted a case series study. METHODS: All case studies of patients diagnosed with KD were collected via a PubMed search of studies published until August 2018. The data were analyzed by age group. RESULTS: In total, 215 studies were reviewed (238 patients; mean age of 36 years). The male:female ratio was 4:1 overall, 17:1 in patients aged <20 years, 4:1 in patients aged 20-39 years and 2:1 in patients aged ≥40 years (P = 0.01). The percentage of patients with pruritus was 15.4% overall, 3.8% in patients aged <20 years, 15.5% in patients aged 20-39 years and 21.7% in patients aged ≥40 years (P = 0.02). The time to diagnosis was 5.3 years overall, 3.2 years in patients aged <20 years, 4.7 years in patients aged 20-39 years and 7.1 years in patients aged ≥40 years (P < 0.01). CONCLUSIONS: The proportion of female patients affected the incidence of pruritus, and the time to diagnosis increased as the patients' age increased. There were no significant age-related differences in region/race, complications, multiplicity, laterality, anatomical distribution, maximum size, eosinophil count, immunoglobulin E level, initial treatment, recurrence or outcomes. This may be useful information for the diagnosis of KD.

Effects of hyperthyroidism on rat liver glutathione metabolism: related enzymes' activities, efflux, and turnover.

The effect of hyperthyroidism on liver glutathione (GSH) metabolism was studied in fed rats after the administration of 0.1 mg T3/kg body wt, for 1-3 consecutive days. T3-calorigenesis resulted in elevated rates of O2 consumption by the liver, together with higher lipid peroxidative processes and GSH depletion, compared to the euthyroid state. The study of the enzymes related to GSH metabolism revealed no significant changes in the activity of glutathione peroxidase and glutathione reductase, with decreases (27-41%) in the activity of glutathione-S-transferases and marked elevation (133%) in that of gamma-glutamyl transferase, 3 days after T3 treatment. At this experimental time, the activity of the NADPH generating enzyme glucose-6-phosphate dehydrogenase was enhanced by 84% in the liver of T3-treated rats, compared to that in the controls. In these conditions, the canalicular efflux of GSH was not altered by T3, whereas net and fractional rates of sinusoidal GSH efflux were enhanced by 86% and 288%, respectively. The latter effect of hyperthyroidism was found in parallel with an enhancement in sinusoidal lactate dehydrogenase and protein release, suggesting that loss of GSH might be related to a permeabilization of the hepatocyte plasma membrane. Liver GSH turnover assessed after a pulse of [35S]cysteine resulted in a 209% increase in the fractional turnover rate in hyperthyroid rats over controls, under steady state conditions for both hepatic GSH pools, leading to a 62% enhancement in the respective turnover flux. Data suggest that the elevation in the sinusoidal GSH efflux from the liver and in the hepatic capacity to degrade the tripeptide are major mechanisms leading to GSH depletion in the liver of T3-treated rats. As the increased GSH use is not balanced by the elevation in GSH synthesis, a lower steady state level of GSH is attained in the liver.

Prooxidant and antioxidant hepatic factors in rats chronically fed an ethanol regimen and treated with an acute dose of lindane.

While acute lindane treatment and chronic ethanol feeding to rats have been associated with hepatic oxidative stress, the possible roles of these stresses in the pathogenesis of hepatic lesions reported in acute lindane intoxication and in those observed in some models of chronic alcoholism have not been established. Our previous studies in rats chronically fed ethanol regimens and then treated with a single intraperitoneal (i.p.) dose of lindane (20 mg/kg) showed that while lindane per se was invariably associated with hepatic oxidative stress, chronic ethanol feeding only produced this stress when the dietary level of vitamin E was relatively low. Chronic ethanol pretreatment did not significantly affect the lindane-associated oxidative stress, and neither chronic ethanol feeding nor acute lindane, single or in combination, produced any histologic and biochemical evidence of liver damage. In the present experiment, the acute dose of lindane was increased to 40 mg/kg, and we have studied a larger number of prooxidant and antioxidant hepatic factors. Male Wistar rats (115.5 +/- 5.4 g) were fed ad lib for 11 weeks a calorically well-balanced and nutritionally adequate basal diet, or the same basal diet plus a 32% ethanol/25% sucrose solution, also ad lib, and were then injected i.p. with a single dose of lindane or with equivalent amounts of corn oil. The results indicated that acute lindane treatment to naive rats increased practically all the prooxidant hepatic factors examined (cytochromes P450 and b5, NADPH cytochrome c reductase, NADPH oxidase), as well as the generation of microsomal superoxide radical and thiobarbituric acid reactive substances of liver homogenates, but did not modify any of the antioxidant hepatic factors studied. Conversely, the chronic administration of ethanol alone did not significantly affect the prooxidant hepatic factors but reduced some of the antioxidants (i.e., the activities of GSH-Px and the contents of alpha-tocopherol and ubiquinols 9 and 10). Although chronic ethanol pretreatment further increased the superoxide generation induced by lindane per se, it did not increase but generally reduced the effects of lindane per se on the other prooxidant factors studied. Furthermore, although acute lindane administration to ethanol-pretreated rats was associated with decreases in GSH and catalase (not affected by ethanol or lindane treatment alone), it did not substantially modify the reducing effects of ethanol feeding per se on GSH-Px, alpha-tocopherol, and ubiquinols. Once again, neither chronic ethanol feeding nor lindane treatment, single or in combination, was associated with any evidence of liver damage.

Localization of post-traumatic trochlear nerve palsy associated with hemorrhage at the subarachnoid space by magnetic resonance imaging.

PURPOSE: To report evaluation of traumatic trochlear nerve palsy using head magnetic resonance imaging. DESIGN: Observational case reports. METHODS: We examined two cases involving trochlear nerve palsy after closed head injury. RESULTS: Using a fluid attenuated inversion recovery pulse sequence, MRI showed a high-intensity lesion consistent with subarachnoid hemorrhage at the trochlear nerve area in the ambient cisterns. CONCLUSION: An impact force directed toward the tentorium can be a mechanism of injury in some post-traumatic trochlear nerve palsies. Fluid attenuated inversion recovery pulse sequence is a sensitive method for detection of abnormalities in cases associated with head injury.

Dose-dependent study of the effects of acute lindane administration on rat liver superoxide anion production, antioxidant enzyme activities and lipid peroxidation.

The administration of single i.p. doses of lindane (20, 40, 60 and 80 mg/kg) to rats produced a progressive increase in the liver microsomal content of cytochrome P-450 and in the rate of superoxide anion generation, as measured by adrenochrome formation. A dose-dependent increase in lipid peroxidation of liver homogenates, assessed by measuring thiobarbituric acid reactants, was also found. Lindane treatment did not alter the activity of liver glucose-6-phosphate dehydrogenase, glutathione reductase or glutathione peroxidase, while that of superoxide dismutase and catalase was significantly reduced. These changes were accompanied by a progressive liver steatosis. The collected metabolic data were interpreted in terms of a causal relationship between an increase in superoxide radical generation, secondary to cytochrome P-450 induction and a resulting increase in lipid peroxidation. The decrease in superoxide dismutase and catalase activities is likely to contribute to the increased levels of lipid peroxidation in view of their antioxidant properties.

Liver lipid peroxidation-related parameters after short-term administration of hexachlorocyclohexane isomers to rats.

Rats treated with diets containing 20 ppm of alpha- or gamma-hexachlorocyclohexane (HCH) for 15 or 30 days showed increased levels of liver cytochrome P-450 followed by increased production of both thiobarbituric acid reactants by liver homogenates and microsomes and superoxide anion production by liver microsomes. In these animals superoxide dismutase (SOD) activity was also increased. In consequence, the ratio between SOD activity and microsomal superoxide radical (O2-.) production showed a slight increase after 15 days of treatment. However, after 30 days, there was a tendency for this ratio to decrease. Other parameters studied were liver glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase and catalase (CAT) activities. Among them, only CAT activity showed a 26% and 38% increase after 15 or 30 days of treatment with the alpha-isomer. It is suggested that when lipid peroxidation is involved in the mechanism of toxicity of a xenobiotic, this parameter can be used to determine the no-observed-effect level.

Dose-dependent study of liver lipid peroxidation related parameters in rats treated with pp'-DDT.

Rats treated with increasing doses of pp'-DDT (60, 100 and 180 mg/kg body wt.) i.p., for 24 h, showed a dose-independent increase in liver cytochrome P450 levels, together with an increase in lipid peroxidation, measured as production of thiobarbituric acid reactants. This oxidant condition elicited in the liver by DDT was not accompanied by any change in the activity of NADPH-cytochrome c reductase or in the rate of superoxide anion generation by liver microsomal fraction. The activities of superoxide dismutase and glutathione peroxidase were found to be increased in the higher dose DDT-treated rats, without any change in those from catalase and glutathione reductase. The results presented showed an oxidant condition in the liver elicited by DDT treatment of rats, without any adequate hypothesis proposed to explain these data.

Brain and liver lipid peroxidation levels following acute and short-term lindane administration in the rat.

Oxidative stress-related parameters in rat brain and liver were evaluated following acute (60 mg/kg i.p., 2 and 24 h after dosing) or short-term (1000 ppm in the diet for 90 days) lindane administration. Both treatments elicited a significant accumulation of lindane in brain and liver, with convulsions observed in short-term and 24-h lindane-treated rats. In these conditions, lindane exposure did not alter brain lipid peroxidation, assessed as thiobarbituric acid reactants formation and spontaneous chemiluminescence, parameters that were enhanced in the liver. The activities of antioxidant enzymes in the brain (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) were not modified by acute lindane treatment, while brain glutathione content was significantly reduced by 13%. It is concluded that lindane does not alter the oxidative stress status of the brain as occurs in liver, regardless of the time of exposure of rats to either acute or short-term administration of the insecticide.

Turnover of hepatic glutathione after acute lindane intoxication.

The administration of lindane (60 mg/kg) to fed rats diminished the content of hepatic glutathione (GSH) 4 h after treatment, which was recovered at 24 h. At these experimental times, the activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferases and gamma-glutamyltransferase in the liver of lindane-treated rats and control animals were comparable. Liver GSH turnover, measured after a pulse of [35S]cysteine, was enhanced by 69% (P < 0.05) in lindane-treated rats 24 h after intoxication compared to controls, with a 63% (P < 0.05) increase in the estimated rate of GSH synthesis. It is concluded that lindane enhances GSH synthesis in rat liver 24 h after treatment as a consequence of the decrement in its content observed at early times of intoxication (4 h), thus allowing the recovery of the normal level of hepatic GSH.

[Investigation of etiologies for acute renal failure due to rhabdomyolysis in 5 patients].

We experienced 5 cases of acute renal failure due to rhabdomyolysis during the last two years and investigated those etiologies. Diagnosis of rhabdomyolysis was established by the detection of elevated serum creatine phosphokinase, myoglobin, aldolase, myoglobinuria as well as by the clinical course. The respective underlying illness of the 5 cases were grand mal seizures, infection (high fever), heat stroke, diabetes mellitus with hyperosmolar nonketotic coma and cerebral infarction treated by barbiturate. In this investigation, however, any single cause was not enough as the etiologies of rhabdomyolysis. There were multiple factors responsible to rhabdomyolysis in each case, such as hypokalemia, hypophosphatemia, shock, arteriosclerosis, etc. Some cases could not be classified as traumatic or non-traumatic rhabdomyolysis. Thus, in one case, acute renal failure due to rhabdomyolysis induced by the combination of grand mal seizures and serum potassium/phosphate depletion. 2 cases recovered without hemodialysis. 3 cases died in multiple organ failure, included a case treated by hemodialysis. We conclude that acute renal failure due to rhabdomyolysis induced easily by numerous diseases and early diagnosis is recommended.

[Novel transforming genes detected in human stomach cancer cells].

The DNAs of six human stomach cancer cell lines were analysed, and specific gene amplification was observed; namely, an 8-fold amplified c-Ki-ras-2 gene (1 case) and a 20-fold amplified c-myc gene (1 case). In addition, it was found that a single 11-kbp-Eco-R1 fragment, having weak homology to the Ki-ras gene, was amplified 5-10 fold in three out of the six cell lines. The DNAs of two of these three cell lines gave rise to foci upon transfection into NIH3T3 cells and the primary and secondary transformants seemed to carry a similar 11-kbp-Eco-R1 fragment. It was also found that one of the DNAs from human stomach cancers gave rise to NIH3T3 cell foci upon DNA transfection. DNAs of secondary transformants commonly retained six Eco-R1 fragments that contained human Alu repeats. The size of this gene was estimated to be about 50 kbp. The Southern blot hybridization profile of this gene revealed it to be clearly different from known active human oncogenes. Furthermore, about 70% of this gene has been isolated and portions of it used as probes to test for homologies to known viral oncogenes. The gene appears to be unrelated to 14 viral oncogenes so far tested.

Genomic prediction in Japanese Black cattle: application of a single-step approach to beef cattle.

The implementation of genomic selection for Japanese Black cattle, known for rich marbling of their meat, is now being explored. Although multiple-step methods are often adopted for dairy cattle, they present shortcomings such as bias and loss of information in addition to operational complexity. These can be avoided using single-step genomic BLUP (ssGBLUP) based on the relationship matrix H, which is constructed from the numerator relationship matrix (A) augmented by the genomic relationship matrix (G). This study assessed the use of ssGBLUP for 3 economically important traits in Japanese Black cattle. Three aspects of ssGBLUP that are important for practical use were examined specifically: the mixing proportions of blending G with A, selection of subsets of genotyped animals used for constructing H, and prediction ability for ungenotyped animals. Different mixing proportions were tested to assess the influence of these proportions on variance component estimation and prediction accuracy. For all traits, the highest or nearly highest accuracy was obtained when the adopted mixing proportion provided heritability closest to that inferred based on A. However, the accuracy did not increase greatly under adjustment of the mixing proportion, thereby suggesting that the influence of the mixing proportion on the accuracy was limited. Genotype data of influential bulls showed a greater contribution to accuracy than that of bulls that were less influential. Genotyping animals with phenotypic records increased the accuracy. It can be prioritized over genotyping bulls that are not influential on the population. These results are expected to present good guides to the future expansion of genotyped populations. Even for animals without genotype data but with genotyped sires, ssGBLUP provided more accurate prediction than BLUP did. For both phenotype and breeding value prediction, ssGBLUP provides more accurate prediction than BLUP, suggesting its usefulness in genomic selection in Japanese Black cattle.

Ability of young children to button and unbutton clothes.

From 2 years of age, children enjoy trying to button and unbutton their jacket. The clothing of the children at this stage should have the form which fits their motor skills so as to develop their interest in buttons and to help their study in manipulating buttons. We observed processes of dressing and actions of buttoning and unbuttoning at the nursery school, for children in the 3.3-5.9 year range. Also, we experimented about dressing mainly for children in 2 year range to observe the process of manipulating buttons. As factors of experiment, we took two buttonhole directions (vertical and across) and three sizes of buttons (1, 2, 3 cm). The direction of buttonholes was significant at the 5% level. We recognized that buttonholes in the vertical direction were easier for children to button. We came to the following conclusion: for an open front of children's clothing, buttons having a 2 cm diameter and buttonholes in the vertical direction were the best.

The effect of beta-bromopyruvic acid on fructose-1, 6-diphosphate aldolase from rabbit muscle.

Rabbit muscle aldolase (RMA) is 96 per cent inhibited in the presence of beta-bromopyruvic acid (BPA) in a molar ratio of 1/250, during 60 minutes incubation. The chemical reaction of higher significance in this phenomenon is the alkylation of -SHgroups of both apparent and buried types, with formation of S-pyruvil-cystein. The previous treatment of the enzyme with FDP protects aldolase, decreasing the rate of inhinition by BPA to about 56 per cent. FDP protection of the enzyme protects nearly 5-SH groups against the alkylating effect of BPA. Cyanogen bromide hydrolysis of the carboxymethylated protein results in the classical formation of 4 fragments, peptides F1, the NH-2terminal; F2, the COOH-terminal; F3, the active site containing peptide; and F4, a small peptide located between F2 F3. The protection bestowed upon the enzyme by FDP, against the alkylating effect of BPA, is located in the F1, F2, and F3 either in BPA treated aldolases or in the BPA treated FDP-aldolase. Part of the inhibiting effect of BPA is then attributed to the possible interaction between this compound and the basic aminoacids in the aldolase molecule.

Mechanisms of lindane-induced hepatotoxicity: alterations of respiratory activity and sinusoidal glutathione efflux in the isolated perfused rat liver.

1. Lindane (25-60 mg/kg) at 24 h after dosage induced a dose-dependent increase in oxygen consumption by perfused rat livers, an effect not observed at early times (2-6 h) after administration. About 60% of the increase in liver oxygen uptake is suppressed by the antioxidant, desferrioxamine, indicating enhanced free radical activity induced by the insecticide. 2. The hepatic content of total GSH equivalents (GSH + 2GSSG) decreased 4 h after lindane treatment (60 mg/kg), together with significant diminution in net and fractional rates of sinusoidal GSH efflux, that returned to control values 24 h after treatment. 3. These data indicate that lindane resulted in marked changes in hepatic oxidative capacity and glutathione metabolism, which condition the production of oxidative stress in the liver at different times of intoxication.