Mammoplasty for symmetry of the contralateral breast and its oncologic value]

Although a broad range of neuropsychological deficits has been reported in patients with severe sleep disordered breathing (SDB), little is known about the impact of mild SDB on neuropsychological performance. In this study, we compared neuropsychological test performance in two groups of carefully screened volunteers who differed clearly according to the respiratory disturbance index (RDI). Controls (n = 20) were identified on the basis of an RDI < 5; cases (n = 32) had an RDI in the range of 10-30. Cases and controls were well matched with regard to IQ, age, and sex. Cases had significantly more self-reported snorting and apneas and a higher body mass index than controls but did not differ according to sleepiness as measured by either the multiple sleep latency test or the Epworth sleepiness scale. An extensive battery of neuropsychological and performance tests was administered after an overnight sleep study. Cases performed significantly more poorly on a visual vigilance task (perceptual sensitivity, d': 2.24 +/- 0.64 vs. 2.70 +/- 0.53, p = 0.01, for cases and controls, respectively) and a test of working memory, the Wechsler adult intelligence scale-revised digits backwards test (6.12 +/- 2.20 vs. 7.55 +/- 2.22, p = 0.02), than controls. The groups did not differ in their performance on other tests of memory, information processing, and executive functioning. In summary, subjects with mild SDB may manifest a vigilance deficit in the absence of substantial sleepiness. Subjects with a mildly elevated RDI (10-30) without sleepiness do not appear to suffer appreciable deficits in more complex neuropsychological processes (e.g. executive functions).     

Effects of basic fibroblast growth factor on anoxia/reoxygenation injury of rat neonatal cardiomyocytes

The effects of basic fibroblast growth factor (bFGF) on anoxia/reoxygenation (A/R) injury and protein kinase C (PKC) activity were studied on a model of A/R injury of neonatal rat cardiomyocytes to investigate the possibility of its using as a substrate for pharmacological preconditioning. The data indicated that bFGF improved the viability of cardiomyocytes, lowered the deplection of ATP and leakage of intracellular lactate dehydrogenase (LDH) in a concentration-dependent manner. PKC inhibitor, H7, completely abolished the protective effects. It was also found that bFGF directely activated PKC in cardiomyocytes in a time course similar to that in hypoxic preconditioning. The data suggested that the protective effect of bFGF on cardiomyocyte A/R injury might be mediated by PKC.     

Two cases of intestinal capillariasis in Korea

This study evaluates the effect of stepwise lowering of the hemoglobin (Hb) concentration on maximal walking distance (MWD) and hemodynamics in patients with intermittent claudication. The results in a study group (n = 6) were compared with those of a control group (n = 6) whose members were not subjected to venesections. An average decrease of Hb concentration from 151 +/- 4 to 121 +/- 3 g/L did not significantly influence MWD, the result being 282 +/- 62 meters before venesections and 255 +/- 54 meters after three to five (mean four) repeated venesections. Transcutaneous oxygen pressure was measured at the dorsum of the foot before and after exercise and did not change with a gradual decrease of the Hb concentration. Maximal heart rate, painfree walking distance, ankle pressure, and blood lactate concentration were also unchanged. An average venesection volume of about 1.4 liters whole blood within fourteen days, without isovolemic replacement, did not change the blood volume, which was 5.1 +/- 0.4 liters before and 5.0 +/- 0.5 liters after venesections. In conclusion, hemodilution accomplished by venesections did not have a clinically or physiologically beneficial effect in patients with severe intermittent claudication. However, hemodynamics and clinical symptoms were not affected by a considerable decrease in the arterial oxygen content within the normal Hb concentration range.     

Carbamoylation of brain glutamate receptors by a disulfiram metabolite

S-Methyl-N,N-diethylthiolcarbamate sulfoxide (DETC-MeSO), a metabolite of the drug disulfiram, is a selective carbamoylating agent for sulfhydryl groups. Treatment of glutamate receptors isolated from mouse brain with DETC-MeSO blocks glutamate binding. In vivo, carbamoylated glutathione, administered directly to mice or formed by reaction of DETC-MeSO with glutathione in the blood, also blocks brain glutamate receptors. Carbamoyl groups appear to be delivered to brain glutamate receptors or to liver aldehyde dehydrogenase in vivo by a novel glutathione-mediated mechanism. Seizures caused by the glutamate analogs N-methyl-D-aspartate and methionine sulfoximine, or by hyperbaric oxygen, are prevented by DETC-MeSO, indicating that carbamoylation of glutamate receptors gives an antagonist effect. These observations offer an explanation for some of the previously reported neurological effects of disulfiram, such as its ability to prevent O2-induced seizures. Furthermore, some of the physiology of the disulfiram-ethanol reaction, that could not be accounted for based on the known inhibition of aldehyde dehydrogenase alone, may be explained by disulfiram's effect on glutamate receptors.     

Estimating residence times and their associated errors in patient absorbed-dose calculation

OBJECTIVES: Apolipoprotein (apo) A-IV genetic polymorphism and its effect on serum lipids, apoA-I and apoA-IV were investigated in order to clarify the role of apoA-IV gene during the development of hyperlipidemia. METHODS: Four polymorphic sites (codon 127, 167, 347 and 360) of apoA-IV gene (exon 3) were determined in two groups of inhabitants in Beijing (Group I: 145 healthy individuals; Group II: 41 cases of hyperlipidemic patients and controls) by PCR-RFLP technique. Serum concentrations of HDL-cholesterol (HDL-C), HDL3-C, HDL2-C, triglyceride (TG), total cholesterol (TC), apoA-I and apoA-IV were studied among the individuals with different genotypes of apoA-IV. RESULTS: In Group I, frequencies of the alleles were 0.648 and 0.352 in codon 127; 0.972 and 0.028 in codon 167; 0.817 and 0.183 in codon 347. Two common alleles were 0.941 and 0.059 in codon 360. The results indicated that cases of codon 127 heterozygotes had a significantly higher serum TC level and cases of apoA-IV Ser127 homozygotes kept a markedly low TG level. Both homozygotes and heterozygotes which carried apoA-IV His 360 exhibited a significantly higher concentration of TC in comparing with that of apoA-IV Gln 360 homozygotes. The data from Group II showed that the allele frequency of His 360 had a significant difference between patients and controls. CONCLUSIONS: Certain polymorphic sites of apoA-IV gene might influence the serum lipid levels in both healthy persons and hyperlipidemic patients. His 360 polymorphic position might have a relationship with the development of hyperlipidemia.     

PD98059 is an equipotent antagonist of the aryl hydrocarbon receptor and inhibitor of mitogen-activated protein kinase kinase

Striatal dopamine transporter function and dopamine D2 receptor status were evaluated in 15 patients with early untreated Parkinson's disease using single photon emission tomography (SPECT) with 123I-Iodo-2beta-carboxymethoxy-3beta-(4-idiophenyl)tropane (beta-CIT) and 123I-Iodobenzamide (IBZM) as pre- and postsynaptic ligands. Symptoms were unilateral in five patients and bilateral but asymmetric in 10 patients. Patients with bilateral symptoms had significantly lower 18-hour striatal/cerebellar beta-CIT binding ratios (3.59 +/- 0.79) than hemiparkinsonian patients (5.76 +/- 1.48, p < 0.05) reflecting more advanced disease in this subgroup. Patients with bilateral parkinsonism were also found to have a significant side-to-side difference in striatal beta-CIT binding with more marked reduction contralateral to the presenting limb (18-hour striatal/cerebellar ratio: 4.13 +/- 0.78 [ipsilateral] versus 3.59 +/- 0.79 [contralateral], p < 0.05). Dopamine D2 receptor binding as measured by IBZM was significantly elevated contralateral to the affected side in hemiparkinsonian patients (striatal/cerebellar ratio: 2.42 +/- 0.90 [contralateral] versus 2.19 +/- 0.80 [ipsilateral], p < 0.05). This asymmetric upregulation was absent in the patients with bilateral parkinsonism (striatal/cerebellar ratio: 1.85 +/- 0.43 [contralateral to more severely affected side] versus 1.83 +/- 0.34 [ipsilateral], p > 0.05). Our data suggest that postsynaptic dopamine receptor upregulation contralateral to the presenting side occurs in untreated unilateral PD and disappears in untreated bilateral (asymmetric) PD despite a greater loss of dopamine transporter function. Combined beta-CIT and IBZM SPECT studies may be helpful to monitor the progression of nigrostriatal dysfunction in early PD.     

Neurobehavioral development of neonatal mice following blockade of VIP during the early embryonic period

Previous work has shown that blockade of VIP function in the early postimplantation embryo results in growth retardation and microcephaly. In the present work, the neurobehavioral development of neonatal mice was examined following treatment of dams with a VIP antagonist during this period. Inhibition of VIP functions during early embryogenesis impaired the performance of 5 of 10 developmental behaviors. These behaviors included developmental milestones (first appearance of ear twitch and eye opening) and complex motor behaviors (negative geotaxis, surface righting, and air righting). The retardation of neurobehavioral development produced by inhibition of VIP action indicates that this peptide is important to the progression of embryonic development.