[A case of rectal bladder construction by Duhamel procedure for vesical extrophy].

A 4 year old boy, who underwent 2 times of unsuccessful primary closure of the extrophied bladder at 7 days and 5 months after birth, was treated with construction of a rectal bladder with sigmoid-pull through by Duhamel procedure. Vas deference, seminal vesicles and prostate were not found at the cystectomy operation. Epispadias urethral mucosa was removed and phalloplasty was performed using the ventral hooded foreskin. The results were cosmetically and functionally excellent. He could keep continence and his upper urinary tract was normal at 6 months after the operation.

Suppression of the induction of long-term depression by carbon monoxide in rat cerebellar slices.

Carbon monoxide (CO) suppresses brain functions at doses lower than that suppressing oxygen (O(2)) supply to the brain, and the cerebellum is one of the sites most susceptible to the neurotoxic effects of CO. We investigated the effects of CO on the induction of cerebellar long-term depression (LTD) in the synapses between parallel fibres (PFs) and Purkinje cells. CO, at concentrations between 8 nM and 5 microM, exhibited almost no effect on synaptic responses in Purkinje cells, O(2) consumption and NO release from PFs in rat cerebellar slices. However, the induction of LTD was significantly suppressed by CO at concentrations between 40 and 200 nM. The suppressive effect of 40 nM CO was antagonized by 10 microM NOR3, an NO donor. In contrast, CO exhibited no clear effect on the induction of LTD at concentrations between 1 and 5 microM. The induction of LTD, suppressed by 10 microM N(G)-nitro-L-arginine, an inhibitor of NO synthase, was not restored by 5 microM CO. CO is not only a neurotoxic substance but also a candidate for an intercellular messenger. delta-Aminolevulinate (30 microM), a substance facilitating endogenous CO production, suppressed the induction of LTD, and the effect of delta-aminolevulinate was antagonized by 10 microM NOR3. These findings suggest that CO may have a suppressive effect on the induction of cerebellar LTD at nanomolar concentrations, probably via its effects on NO/cGMP signalling.

Irreversible impairment of inhibitory neurons and nitric oxide release in the neocortex produced by low temperature and hypoxia in vitro.

Brain ischemia causes irreversible hyperexcitability, which may be attributed to irreversible impairment of inhibitory neurons. However, the conditions required for selective and irreversible impairment of inhibitory interneurons in vitro are unknown. In this study, we found that a combination of low temperature and hypoxia produced hyperexcitability in the neocortex. Neocortical tissue blocks isolated from rats were exposed to low temperature (1-3 degrees C) for 45 min and subsequently to room temperature (21-23 degrees C) for 60 min in the non-oxygenated medium. In experimental slices prepared from the processed blocks, hyperexcitability, similar to that elicited by an antagonist of GABA(A) receptors, was observed. Exposure of the neocortical tissue blocks to low temperature alone or room temperature alone did not elicit hyperexcitability. The excitability of pyramidal neurons, excitatory synaptic transmission and inhibitory effects of an agonist of GABA(A) receptors were normal in experimental slices. However, excitation of pyramidal neurons was inhibited after local stimulation of inhibitory neurons in control slices, but not in experimental slices. Nitric oxide (NO) release from cortical interneurons was also markedly reduced in experimental slices. These results indicate that irreversible impairment of neocortical inhibitory neurons was produced by low temperature combined with hypoxia produced in vitro.

Layer-specific NO dependence of long-term potentiation and biased NO release in layer V in the rat auditory cortex.

1. We investigated the role of nitric oxide (NO) in the induction of long-term potentiation (LTP) in slices prepared from the rat auditory cortex. 2. Tetanic stimulation of layer IV elicited LTP of field potentials in layer II-III (LTPII-III) and in layer V (LTPV). The magnitude of LTPII-III measured at 30 min after tetanic stimulation was 171 +/- 9% (n = 15, mean +/- s.e.m.) of the control measured before tetanic stimulation, while that of LTPV was 138 +/- 3% (n = 17). 3. NO synthase (NOS) inhibitors had no apparent effect on LTPII-III, but LTPV was significantly suppressed (P < 0.001). This suppression of LTPV was significantly antagonized by a NO donor (P < 0.001) or a cGMP analogue (P < 0.001). 4. Small non-pyramidal neurones in the auditory cortex were stained with an anti-neuronal NOS antibody. More neurones were stained with the antibody in the deeper cortical layers. 5. We measured neocortical NO release with electrochemical NO probes. Layer IV stimulation elicited significantly more NO release in layer V than in layer II-III (P < 0.001). The amplitude of the increase in NO concentration elicited by stimulation at 20 Hz for 5 s was 380 +/- 14 pM (n = 55) in layer V and 55 +/- 8 pM (n = 5) in layer II-III. 6. NO release in layer V was partially but significantly suppressed by non-NMDA (P < 0.002) or NMDA (P < 0.002) receptor antagonists. Simultaneous application of the antagonists of the two types blocked NO release almost completely. 7. These results clearly indicate the NO dependence of the induction of LTPV, and the greater NO release in the deeper layer of the rat auditory cortex.

Deficient cerebellar long-term depression, impaired eyeblink conditioning, and normal motor coordination in GFAP mutant mice.

Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normally and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parallel fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltered, and these synapses display normal short-term synaptic plasticity to paired stimuli in GFAP mutant mice. In contrast, long-term depression (LTD) at PF-Purkinje cell synapses is clearly deficient. Furthermore, GFAP mutant mice exhibited a significant impairment of eyeblink conditioning without any detectable deficits in motor coordination tasks. These results suggest that GFAP is required for communications between Bergmann glia and Purkinje cells during LTD induction and maintenance. The data support the notion that cerebellar LTD is a cellular mechanism closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.

Prolonged suppression of gonadotropin secretion after weight recovery in an anorectic patient with Turner's syndrome: reduced gonadal function in anorexia nervosa is independent in part on nutrition.

Two hypotheses have been postulated as to the pathogenesis of hypogonadotropinemia in anorexia nervosa; one is starvation and weight loss and the other is a psychological factor to influence gonadotropin secretion. Our patient suffered from very rare concurrence of Turner's syndrome and anorexia nervosa and a study of this experiment in nature provided important evidences concerning decreased secretion of gonadotropins in the eating disorder. The patient was diagnosed as Turner's syndrome when she was 6 years old. Her gonadotropin levels were elevated to the castrated ranges (LH 61.8 IU/l; FSH 175.8 IU/l) after 8 years of age. She was noticed to be anorectic at the age of 13 years. Serum levels of the pituitary gonadotropins were lowered (LH 2.9 IU/l; FSH 3.0 IU/l) and their responses to luteinizing hormone-releasing hormone were decreased beneath the normal prepubertal limits. After one year of the anorectic period, she recovered the weight though her gonadotropin levels remained in the very low ranges (LH 2.7 IU/l; FSH 2.5 IU/l). The results suggest that hypogonadism in anorexia nervosa is not solely caused by nutritional deficiency but rather by other factors such as psychological abnormalities.

Hypodipsic hypernatremia associated with absence of septum lucidum and olfactory dysfunction.

A case of hypodipsic hypernatremia in a 16-month-old Japanese boy is reported. Partial antidiuretic hormone deficiency was present. Computed tomography of the brain revealed absence of septum lucidum. No ophthalmological abnormality could be found. He had hyposmia, which has not been reported previously in association with hypernatremia due to hypodipsia. Forced fluid administration and nasal 1-deamino-8-d-arginine vasopressin treatment could maintain serum electrolyte levels within normal ranges. However, episodes of hypernatremia could not be completely avoided while he was treated with 1-deamino-8-d-arginine vasopressin and ad libitum oral fluid.

Spectrophotometric determination of urea in urine stains on foods and containers.

Urea is extracted from rodent urine-contaminated material with hot acetone. After the extract is evaporated to dryness, aqueous urease solution is added to produce ammonia and carbon dioxide. A blue product, indophenol, is formed by the reaction of ammonia with phenol in the presence of hypochlorite. Absorbance is maximum at 625 nm. Presence of urea is easily detected at 4 microgram. Detection of urine contamination in various materials is compared with detection by the AOAC urease-H2PtCl6 test.

Ultraviolet spectrophotometric determination of benzoic acid in soy sauce.

Proteins and other interfering substances are precipitated from soy sauce, using sodium tungstate under acidic conditions. After centrifugation, the supernate is successively extracted with ethyl ether to isolate the benzoic acid in the organic solvent. The ethyl ether extract is washed with dilute HCl. Benzoic acid is then quantitatively determined by ultraviolet spectrophotometry. Recovery of sodium benzoate added to soy sauce ranged from 94 to 104%.