[Cardiocirculatory changes during sleep].
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Biomedical subjects
Publications and source records attributed to T Shiomi.
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DNA methylation was examined in xeroderma pigmentosum (XP) cells. The amount of 5-methylcytosine (mC) in DNA from XP cells was about 70% of that in DNA from normal controls. Southern hybridization analysis showed that the HLA-DR alpha gene in XP lymphocyte B cells was differently methylated from normals, but its expression was apparently unaffected. The methylation of dihydrofolate reductase, a housekeeping gene, was the same as in controls. The revertants to UV resistance from XP fibroblasts recovered a methylation level close to that of normal cells. Results suggested that XP DNA was undermethylated non-randomly, and that DNA methylation might be associated with DNA repair function.
From 1978 to 1985, 57 myelodysplasia patients with urinary and defecatory dysfunction underwent surgical treatment by modified seromuscular ileal flap fixation to the bladder. Followup was 1 to 88 months. Bladder capacity did not decrease, and voiding time and urine flow rate significantly improved. A urinary substitute sensation appeared in 45 of 46 patients (97.8 per cent) and urinary incontinence improved in 36 of 37 (97.3 per cent). A fecal substitute sensation appeared in 31 of 46 patients (67.4 per cent) and constipation improved in 22 (47.8 per cent). Operative complications were encountered in 5 of 57 patients (8.8 per cent), including 3 cases of prolonged paralytic ileus, 1 obstructive ileus and 1 wound herniation. Modified seromuscular ileal flap fixation to the bladder appears to be indicated for patients with the lower type of neurogenic bladder with neither a low compliance bladder nor high grade vesicoureteral reflux.
Heparin was ionically bound onto the surface of an ethylene-vinyl alcohol copolymer (EVAL) membrane which was derivatized by aminoacetalization to produce cationic surface charges. The amount of bound heparin was proportional to the ion exchange capacity of the aminoacetalized membrane and the maximal amount obtained in this experiment was 96 Unit/cm2 (0.59 mg/cm2). Plasma recalcification times were measured for the heparinized membrane thus obtained. Recalcification times increased proportionally with the amount of heparin bound on the membrane, while original EVAL membranes and the non-heparinized aminoacetalized membrane did not show increases in recalcification times. This means that the heparinized EVAL membrane has a more nonthrombogenic property due to the release of heparin. The apparent amount of heparin released from the membrane into plasma was estimated from plasma recalcification times. The release rate was 0.30-0.33 Unit/cm2/h (1.8 X 10(-3)-2.0 X 10(-3) mg/cm2/h) for the membranes whose surface was considered to be saturated with heparin. The release amount was about 0.6% compared to the adsorbed heparin in the case of the 96 Unit/cm2-heparinized membrane incubated in plasma for 60 min.
A multiple mutagen-sensitive mutant (XUM1) of mouse T-cell lymphoma line, L5178Y, is hypersensitive to ionizing radiation, ultraviolet (UV) light, and cross-linking agents (such as mitomycin C). The frequency of transfection for XUM1 cells after exposure to calcium phosphate-coprecipitated pSV2neo DNA was more than 10(4)-fold less effective than that for Ltk-aprt- (LTA) cells. Other transfection methods (DEAE-dextran and polybrene-DMSO) were not effective for L5178Y and XUM1 cells. The transfection-proficient trait of LTA cells was demonstrated to be genetically dominant by examining the the transfection frequency in hybrid clones constructed between XUM1 and LTA cells. To circumvent the problem with XUM1, the LTA genes necessary for transformation processes were introduced into XUM1 cells by constructing hybrids between XUM1 and LTA cells irradiated with X-rays which causes directional chromosome elimination for hybrid cells. Four of 194 hybrid clones tested were transfection-proficient and hypersensitive to UV (XL102, XL107, XL215, and XL216). All four clones were not hypersensitive to X-rays or mitomycin C. The frequencies of transfection for XL102 and XL216 were nearly the same level as that for LTA cells. The efficiency of transfection for XL107 and XL215 was 10 to 100-fold lower than that for LTA cells.
Two mutant lines (US31, US46) of mouse lymphoma cells that are hypersensitive to ultraviolet (UV) radiation were previously found to belong to different complementation groups. The mutants were tested for their ability to complement the six known complementation groups of UV-sensitive Chinese hamster ovary (CHO) cells, which are defective in nucleotide excision repair, as well as a seventh group represented by a V79 mutant. Hybrid cells were produced by fusion with polyethylene glycol and tested in situ for UV resistance. The mouse mutant US46 complemented all CHO mutants except UV61. Therefore, US46 is assigned to the same complementation group as UV61, and it is probably defective in the same locus. The mouse mutant US31 produced UV-resistant hybrid cells in each of the seven crosses, indicating that it forms an eighth complementation group among the rodent mutants. Thus, at least eight genes are likely required to repair UV damage in rodent cells.
We report a case of spontaneous rupture of a calyceal diverticulum in a perinatal woman who was treated with percutaneous procedure. A 28-year-old woman, who delivered a full-term healthy male infant 13 days prior to hospitalization, was admitted complaining of left progressive severe flank pain. Kidney-urethra-bladder X-ray showed a space-occupying lesion in the lower pole of the left kidney. Drip intravenous pyelography revealed the left renal pelvis and calyx to be pushed up. Renal computed tomographic scan demonstrated a cystic lesion in the lower pole of the left kidney with a perirenal hematoma. After percutaneous puncture followed by indwelling of 8 Fr. balloon catheter within the cystic lesion for drainage, the patient recovered dramatically. Retrograde and antegrade pyelography showed the cystic lesion communicating with an adjacent calyx in the lower pole of the left kidney. The physiological relationship to pregnancy is discussed as a possible etiological factor in the unique occurrence of this rare rupture, and the literature is reviewed.
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Thirteen cases (20 ureters) of vesicoureteral reflux (VUR) associated with neurogenic bladder, treated with anti-reflux operation are reviewed. Twelve of the 13 cases had meningomyelocele and 1 had spina bifida occulta as an underlying disease. The type of neurogenic bladder was hypoactive detrusor-active sphincter in 11 patients and hypoactive detrusor-hypoactive sphincter in 2 patients. They were treated with an anti-reflux operation, 2 ureters by Politano-Leadbetter method and 18 ureters by Cohen method. The results were successful (success rate 85.0%). Therefore, we concluded that in neurogenic bladder patients especially with the hypoactive detrusor-active sphincter, the cause of their renal deterioration is mostly VUR. Thus we should examine such patients for VUR. On the other hand, when the renal deterioration of VUR patients cannot be improved by conservative treatment for example clean intermittent catheterization or indwelling catheter, we should perform an anti-reflux operation.
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Transurethral electroresection of external urethral sphincter (TUR-sph) was performed in sixteen male tetraplegics to obtain good voiding efficiency and to prevent autonomic dysreflexia due to detrusor sphincter dyssynergia. Ratio of residual urine as a parameter of voiding efficiency and blood pressure and plasma noradrenaline level during voiding as parameters of the significance of autonomic dysreflexia were evaluated before and after TUR-sph, and all these parameters had significantly improved after TUR-sph. After discharge from the hospital, all patients urinated comfortably with the maneuver of suprapubic percussion by themselves and/or their helpmates, and no patients complained of any inconvenience due to urinary incontinence. Moreover, no patients had the episode of autonomic dysreflexia in daily life except for one patient who had it once with urinary tract infection. TUR-sph brings not only the improvement of voiding efficiency but also the effect as a safety valve against autonomic dysreflexia by means of preventing the occurrence of autonomic dysreflexia due to detrusor sphincter dyssynergia.
In a search for cell mutants that show an increase or a decrease in the frequency of baseline sister-chromatid exchanges (SCEs) or spontaneous chromosomal aberrations (CAs), large numbers of mutagen-sensitive clones previously isolated from mouse lymphoma L5178Y cells were analyzed. In addition to two SCE mutants (ES 4 and AC 12) previously reported, three other mutants were identified as an SCE mutant. An ethyl methanesulfonate-sensitive mutant ES 2 and an alkylating agent-sensitive mutant MS 1 exhibited, respectively, 1.4-fold and 1.8-fold higher baseline SCE frequencies than did the parental L5178Y. In contrast, M10, which is sensitive to X-ray and 4-nitroquinoline 1-oxide, showed a reduced frequency of baseline SCEs (0.65-fold). These 5 mutants including ES 4 and AC 12 had 3--9-fold increases in spontaneous CA frequencies. Measurement of baseline SCE formation in inter-mutant hybrids revealed that M10 mutation is dominant, MS 1 and ES 4 mutations are semidominant, and ES 2 and AC 12 mutations are recessive. Because SCE frequencies in hybrids formed between pairs of 4 mutants (ES 2, MS 1, ES 4 and AC 12) were significantly lower than those in the tetraploid mutant cells, these 4 mutants probably belong to different complementation groups. Since M10 behaved dominantly with respect to SCE phenotype, it was not possible to determine by complementation test whether it belongs to a different group from the other mutants. However, the finding that M10 is complemented by other mutants for EMS sensitivity indicates that the M10 mutation is different from the other mutations. From these results, it is concluded that at least 4 different genes participate in the formation of high levels of baseline SCEs. The defects in ES 2, MS 1, ES 4, and AC 12 produce common lesions responsible for the formation of both SCEs and CAs. In contrast, the defect in M10 is associated with a high increase in spontaneous CA frequency, but conversely associated with a decrease in baseline SCE frequency. This suggests that M10 is defective in the process involved in the formation of baseline SCEs.
To determine the mutual relationships between cell survival and induction of sister-chromatid exchanges (SCEs) as well as chromosomal aberrations (CAs), mutagen-induced SCEs and CAs were analyzed in an ionizing radiation-sensitive mutant (M10) and an alkylating agent-sensitive mutant (MS 1) isolated from mouse lymphoma L5178Y cells. The levels of CA induction in both mutants strictly corresponded to the sensitivity to lethal effects of mutagens, except that caffeine-induced CAs in M10 are considerably lower than those in L5178Y. The results clearly indicate that except for caffeine-induced CAs in M10, mutagen-induced lethal lesions are responsible for CA induction. In contrast, SCE induction in mutants was complicated. In M10, hypersensitive to killing by gamma-rays, methyl methanesulfonate (MMS), and 4-nitroquinoline 1-oxide (4NQO), but not sensitive to UV or caffeine, the frequency of SCEs induced by gamma-rays was barely higher than that in L5178Y, and the frequencies of MMS- and UV-induced SCEs were similar to those in L5178Y, but 4NQO- and caffeine-induced SCEs were markedly lower than those in L5178Y. MS 1, which is hypersensitive to MMS and caffeine, but not sensitive to UV or 4NQO, responded to caffeine with an enhanced frequency of SCEs and had a normal frequency of MMS-induced SCEs, but a reduced frequency of UV- and 4NQO-induced SCEs. Thus, susceptibility to SCE induction by mutagens is not necessarily correlated with sensitivity of mutants to cell killing and/or CA induction by mutagens. Furthermore, the spontaneous levels of SCEs are lower in M10 and higher in MS 1 than that in L5178Y (Tsuji et al., 1987). Based on these results, we speculate that M10 may be partially defective in the processes for the formation of SCEs caused by mutagens. On the other hand, MS 1 may modify SCE formation-related lesions induced by UV and 4NQO to some repair intermediates that do not cause SCE formation. In addition, MMS-induced lethal lesions in MS 1 may not be responsible for SCE induction whereas caffeine-induced lethal lesions are closely correlated with SCE induction. Thus, the lesions or mechanisms involved in SCE production are in part different from those responsible for cell lethality or CA production.
A mouse-cell mutant sensitive to methyl methanesulfonate (MMS), X-rays, ultraviolet light (UV), and crosslinking agents was selected using the replica plating and cell suspension spotting methods. This mutant (XUM1) is a mitomycin C-sensitive derivative of previously reported XU1, a mutant sensitive to MMS, X-rays and UV. Since XU1 is highly susceptible to the lethal effect of 4-nitroquinoline-1-oxide (4NQO), XUM1 is also hypersensitive to 4NQO. Growth inhibition area tests showed that low concentrations of mutagens were detected with the multiple mutagen-sensitive mutant XUM1. Hence XUM1 cells will be useful in detecting with high sensitivity a wide range of mutagens and carcinogens which mimic X-rays, UV and crosslinking agents.
A pulse-generating machine which delivers exponentially decaying pulses over broad range of pulse lengths was used to determine the optimum pulse conditions for gene transfer to FM3A cells. In the transformation of tk- cells with pTK1, a single pulse of 100-2000 microseconds gave a high transformation frequency at 1.5-6 kV/cm and room temperature, the highest transformation frequency obtained being 3 X 10(-3). As the suspension buffer for cells exposed to the pulse, Saline G was better than PBS(-) for obtaining a large number of transformants because it ensured high cell viability.
Most of the literature about the urological management of spinal cord injury patients is on male patients, and the method of the urological treatment for male spinal cord injury patients is often not useful for female patients. A clinical survey was done on 28 female neurogenic bladder patients after spinal cord injury treated at our Hospital between January, 1980 and January, 1985. At discharge, 11 patients (39.3%) were catheter free, 3 (10.7%) were managed by clean intermittent self catheterization, 1 (3.6%) was managed by clean intermittent catheterization by a helper, and 13 (46.4%) were on indwelling catheters. One of the main reasons that prevents female spinal cord injury patients from becoming catheter free is that there are no effective external collecting devices or devices to prevent urinary incontinence for female neurogenic bladder patients. Another reason is that some female patients can not obtain a high enough ADL level for toilet activities by rehabilitation in spite of lower thoracic or lumbar lesions.
A case of secondary VUR in neurogenic bladder with meningomyelocele treated successfully with urethral catheterization is reported. A 4-month-old girl was introduced to our clinic for the management of incontinence following the closure of the meningomyelocele (below S1 level). Anal sphincter and bulbocavernous reflex was almost normal. Since the IVP revealed right hydronephrosis, an urethral catheter was indwelt immediately in order to decompress the vesical pressure. Three weeks later, the right hydronephrosis improved, but the cystogram revealed right vesicoureteral reflux. The urethral catheter was left for the conservative management for 20 weeks. VUR had disappeared on the cystogram and right hydronephrosis returned to normal. Thereafter, the treatment was changed from indwelling catheter to clean intermittent catheterization by her mother. No urinary tract infection has occurred. The necessity of early management, especially decompression of the vesical pressure, for patients with neurogenic bladder associated with meningomyelocele is discussed.