Utility of the Japanese Glomerular Filtration Rate Equation in Estimating Glomerular Filtration Rate of Donor Kidney.

BACKGROUND: An equation for the estimated glomerular filtration rate (eGFR) is generally used for evaluating renal function in Japan. OBJECTIVE: To assess the accuracy of the preoperative eGFR for estimating kidney donors' measured glomerular filtration rate (mGFR). METHODS: Between April 2009 and August 2014, 91 Japanese living kidney donors were included in this study. The eGFR was calculated as follows: eGFR = 194 × serum creatinine(-1.094) × Age(-0.287) (and × 0.739 for women), and the mGFR was evaluated using inulin clearance. The preoperative eGFR was then compared with the mGFR. RESULTS: Patients included 27 men and 64 women with a mean age of 56.8 ± 9.5 years (range, 36-79 years), mean body surface area of 1.56 ± 0.14 m(2) (range 1.27-1.92 m(2)), mean body mass index of 22.3 ± 2.3 kg/m(2) (range 14.0-27.0 kg/m(2)), and mean serum creatinine level of 0.66 ± 0.14 mg/dL (range 0.39-0.97 mg/dL). The mean eGFR was 81.3 ± 14.2 mL/min/1.73 m(2) (range 45.5-125.9 mL/min/1.73 m(2)), and the mean mGFR was 89.0 ± 15.5 mL/min/1.73 m(2) (range 45.4-130.7 mL/min/1.73 m(2)). The eGFR was significantly lower than the mGFR (P < .001). The correlation coefficient for the relationship between the eGFR and mGFR values was 0.503, and the mean difference between the 2 values was -7.8 (8.7%). CONCLUSIONS: Although the eGFR correlated with the mGFR, the eGFR values did not accurately estimate the mGFR in living kidney donors. Therefore, it is necessary to evaluate the mGFR, especially in marginal kidney donors.

Behavioural characterization and amounts of brain monoamines and their metabolites in mice lacking histamine H1 receptors.

Behavioural assessments were made of mutant mice lacking histamine H1 receptors to reveal the function of H1 receptors in the behaviour of mice. Exploratory behaviour of mice in a new environment was examined to discover whether the absence of H1 receptors in mice affects actions relating to their emotions. The H1 receptor-deficient mice showed a significant decrease in ambulation in an open field and on an activity wheel. Cognitive functions and anxiety were examined using passive avoidance response test and the elevated plus-maze test, respectively. The passive avoidance test did not show any change in latency. The elevated plus-maze test revealed that the transfer latency of the mutant mice was significantly prolonged, indicating that H1 receptors are partly associated with the control of anxiety. Aggressive behaviour was examined by a resident-intruder aggression test. When confronted with an intruder, the mutant mice attacked the intruder significantly slower and less frequently than did wild-type mice after a six-month isolation period. A formalin test and a forced swimming test were used to evaluate the nociceptive response and depressive or despairing state, respectively, of both groups. The mutant mice showed a significant decrease of nociceptive response in the late phase without affecting the early phase. There was no significant difference in the forced swimming test between the two groups. The brain content of monoamines and their metabolites was measured in the H1 receptor null and wild-type mice. The turnover rate of 5-hydroxytryptamine defined by the ratio of 5-hydroxyindoleacetic acid and 5-hydroxytryptamine was significantly increased in the cerebral cortex and hippocampus of H1 receptor null mice. These results support the previous pharmacological findings that histamine modulates various neurophysiological functions such as locomotor activity, emotion, memory and learning, nociception and aggressive behaviour through H1 receptors.

Prostaglandin E1 potentiation of the spontaneous phasic contraction of rat isolated portal vein by a cyclopiazonic acid-sensitive mechanism.

1. The effect of prostaglandin E1 (PGE1) on the spontaneous phasic contraction of the rat isolated portal vein was studied. 2. The isolated portal vein exhibited spontaneous phasic contractions. Removal of Ca2+ from Krebs-Ringer solution or application of nifedipine abolished the spontaneous contraction, indicating that the contraction depends exclusively on Ca2+ influx through L-type Ca2+ channels. On the other hand, cyclopiazonic acid (CPA), a specific inhibitor of Ca(2+)-ATPase of sarcoplasmic reticulum (SR) increased the amplitude of the contractions, suggesting that the SR regulates the spontaneous contractions negatively by sequestration of Ca2+ entering through L-type Ca2+ channels and buffering the rise in cytosolic Ca2+. 3. PGE1 increased the amplitude of the spontaneous contraction in a concentration-dependent manner without affecting the resting tension. The effect was completely abolished by nifedipine. Bay K 8644 and phenylephrine (PE) also increased the amplitude of the contraction in a concentration-dependent manner. PGE1 at a concentration of 1 microM. Bay K 8644 at 100 nM and PE at 30 nM doubled the amplitude, respectively. 4. Pretreatment with 1 microM CPA abolished the effect of PGE1, but the effects of Bay K 8644 and PE were not inhibited by pretreatment with CPA. In contrast, 10 microM ryanodine attenuated the effect of PE without affecting the contractile effect of PGE1. 5. When the SR was depleted of Ca2+ by repeated applications of caffeine in a nominally Ca(2+)-free Krebs-Ringer solution, it took about 120 s to restore the spontaneous contraction after addition of Ca2+ into the solution. In CPA-treated veins, the time taken to restore the contraction was shortened significantly. Pretreatment with 1 microM PGE1 shortened the time to the same extent as pretreatment with CPA did. 6. These results suggest that PGE1 increases the amplitude of the spontaneous phasic contraction by a different mechanism from those by which PE and Bay K 8644 increase it. Inhibition of Ca(2+)-ATPase of the SR might be involved in the vasoactive effect of PGE1.

Involvement of barium-sensitive K+ channels in endothelium-dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds.

1. We examined the vasodilatory effect of hypercapnia in the rat isolated mesenteric vascular bed. The preparation was perfused constantly (5 ml min(-1) with oxygenated Krebs-Ringer solution, and the perfusion pressure was measured. In order to keep the extracellular pH (pHe) constant (around 7.35) against a change in CO2, adequate amounts of NaHCO3 were added to Krebs-Ringer solution. 2. In the endothelium intact preparations, an increase in CO2 from 2.5% to 10% in increments of 2.5% decreased the 10 microM phenylephrine (PE)-produced increase in the perfusion pressure in a concentration-dependent manner. Denudation of the endothelium by CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate) (5 mg l(-1), 90 s perfusion) abolished the vasodilatory effect of hypercapnia. 3. An increase in CO2 from 5% to 10% reduced the increases in the perfusion pressure produced by 10 microM PE and 400 nM U-46619 by 48% and 44%, respectively. NG-monomethyl-L-arginine (100 microM) and indomethacin (10 microM) did not affect the vasodilatory effect of hypercapnia, whereas the vasodilatory response of the preparation to hypercapnia disappeared when the preparation was contracted by 60 mM K+ instead of PE or U-46619. 4. The vasodilatory effect of hypercapnia observed in the PE- or U-46619-precontracted preparation was affected by neither tetraethylammonium (1 mM), apamin (500 microM), glibenclamide (10 microM), nor 4-aminopyridine (1.5 mM). On the other hand, pretreatment with Ba2+ at a concentration of 0.3 mM abolished the hypercapnia-produced vasodilation. 5. An increase in the concentration of K+ in Krebs-Ringer solution from 4.5 mM to 12.5 mM in increments of 2 mM reduced the PE-produced increase in the perfusion pressure in a concentration-dependent manner. Pretreatment of the preparations with not only Ba2+ (0.3 mM) but also CHAPS abolished the vasodilatory effect of K+. 6. The results suggest that an increase in CO2 produces vasodilation by an endothelium-dependent mechanism in the rat mesenteric vascular bed. The membrane hyperpolarization of the endothelial cell by an activation of the inward rectifier K+ channel seems to be the mechanism underlying the hypercapnia-produced vasodilation. Neither nitric oxide nor prostaglandins are involved in this response.

Identification and characterization of histamine H1- and H2-receptors in guinea-pig left atrial membranes by [3H]-mepyramine and [3H]-tiotidine binding.

1. Histamine receptors in the membranes prepared from guinea-pig left atria were characterized with [3H]-mepyramine and [3H]-tiotidine binding. 2. The binding of the H1-antagonist, [3H]-mepyramine, was saturable and of high affinity with a maximum binding capacity of 307 +/- 27 fmol mg-1 protein (n = 14) and with an equilibrium dissociation constant (KD) of 1.5 +/- 0.2 nM (n = 14). The binding was rapid and readily reversible. 3. The competition curve for [3H]-mepyramine binding by histamine was biphasic and revealed high and low affinity states of binding. The addition of 5'-guanylylimidodiphosphate (GppNHp) (100 microM) converted this heterogeneous binding into homogeneous binding of low affinity. 4. The competition curves of H1-antagonists with [3H]-mepyramine had Hill coefficients not significantly different from unity, consistent with competition with [3H]-mepyramine at a single site. GppNHp did not shift the competition curves. 5. Dissociation constants for H1-antagonists determined from inhibition of [3H]-mepyramine binding correlated well with the constants derived from inhibition of the positive inotropic response of guinea-pig left atria to histamine. 6. The H2-antagonist, [3H]-tiotidine, labelled an apparently homogeneous population of recognition sites with a maximum binding capacity of 41 +/- 8 fmol mg-1 protein (n = 6) and a KD of 10.8 +/- 1.2 nM (n = 6). 7. Although histamine competed for [3H]-tiotidine binding in a concentration-dependent manner, the curve was monophasic and was not shifted by GppNHp. 8. It is concluded that both H1- and H2-receptors exist in guinea-pig left atria. H1-receptors probably couple to intracellular effector(s) through a guanine nucleotide-dependent transducing mechanism. On the other hand, H2-receptors seem unlikely to be linked to guanine nucleotide regulatory proteins in guineapig left atria, which may explain the failure of histamine to cause an increase in cyclic AMP in spite of the presence of H2-receptors.

Inability of endothelin to increase Ca2+ current in guinea-pig heart cells.

Effects of endothelin, a novel vasoconstrictor peptide derived from vascular endothelial cells, on cardiac contractility and membrane currents, were examined in guinea-pig cardiac preparations. Endothelin (3-1000 nM) produced a positive inotropic effect in papillary muscles in a concentration-dependent manner. In whole-cell voltage clamp recording, endothelin (250 nM) decreased the amplitude of Ca2+ current (ICa, 25.0 +/- 6.6%) in ventricular myocytes. The endothelin-induced decrease in ICa was abolished by pretreatment with ryanodine (1 microM). These results suggest that endothelin does not activate cardiac sarcolemmal Ca2+ channels. The enhancement of the sarcoplasmic reticulum function may play an important role in the positive inotropic effect of endothelin.

Microangiopathy without hemolysis in a patient following allogeneic bone marrow transplantation.

Thrombotic microangiopathy (TMA) is one of the complications of bone marrow transplantation (BMT) which includes hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Red cell fragmentation is the most consistent laboratory finding. We present a case of TMA with endothelial damage but without the signs of hemolysis. The patient was not receiving cyclosporine. Partial activation of platelets was also observed. This case represents a new form of TMA in transplant recipients.

Food-deprived activity stress decreased the activity of the histaminergic neuron system in rats.

The hypothalamus, which is rich in histaminergic neurons, is highly sensitive to aversive stimuli such as stress. Histamine H3 receptors, which regulate histamine release from the presynaptic site, are associated with stress-induced brain activity. In this study, we investigated the changes of histamine content and histamine H1 and H3 receptors in the brains of rats subjected to stress induced through food deprivation and physical activity on a running wheel (food-deprived activity stress). For purposes of comparison, we also examined the stressful effects of forced swimming on the histaminergic neuron system of rats. The H3 receptor density rapidly declined in the acute phase of stress but gradually returned to the control level in the chronic phase. On the other hand, the H1 receptor slowly decreased and remained at a low level during the chronic phase. These results reveal that there is a discrepancy between the levels of H1 and H3 receptors in the acute and chronic phases of stress. Brain histamine content gradually increased during the late phase of both food-deprived activity stress and forced swimming stress. These changes presumably resulted in the inhibition of histaminergic neuronal activity in the chronic stress condition. In accordance with this hypothesis, the intraventricular administration of histamine significantly reduced the hyperactivity caused by food-deprived activity stress. Since extensive exercise and restricted feeding are thought to be associated with anorexia nervosa, the abnormalities in the histaminergic neuron system might contribute to trait status in anorexia nervosa.

Characterization of histamine receptors modulating inotropic and biochemical activities in rabbit left atria.

The experiments were performed to identify histamine H1- and H2-receptors in rabbit left atrium and to characterize the pharmacological properties mediated by the respective subtypes of histamine receptors. High-affinity saturable binding to the left atrial membranes was obtained for [3H]mepyramine, yielding a maximum binding capacity (Bmax) of 96 fmol/mg of protein and an equilibrium dissociation constant (KD) of 3.8 nM and also for [3H]tiotidine, yielding a Bmax of 126 fmol/mg of protein and a KD of 14.7 nM. In isolated left atrium, histamine produced a concentration-dependent positive inotropic effect, an effect which was competitively antagonized by cimetidine but not altered by chlorpheniramine. Schild analysis showed that the pA2 value for cimetidine was 6.55 and the slope was not significantly different from unity. An excellent correlation was found between the increase in force of contraction and cyclic AMP in the presence of histamine, suggesting that the positive inotropic effect of histamine in rabbit left atrium is dependent on an increased level of intracellular cyclic AMP through stimulation of histamine H2-receptors. Histamine also produced concentration-dependent stimulation of phosphoinositide hydrolysis as measured by [3H]inositol monophosphate accumulation. The phosphoinositide response to histamine was blocked by chlorpheniramine and mepyramine but not by cimetidine. The data indicate that histamine H1-receptors, in addition to histamine H2-receptors, are present in the rabbit left atrium. Although this tissue lacks an inotropic response to histamine H1-receptor stimulation, the histamine H1-receptors interact with histamine to mediate the stimulation of phosphoinositide hydrolysis.

Giant epiphrenic diverticulum with achalasia occurring 20 years after Heller's operation.

We report a case of giant epiphrenic diverticulum in a 43-year-old woman who underwent Heller's myotomy because of achalasia 20 years earlier. She complained of heartburn and dysphagia from March of 1991 and was hospitalized in our institution. An upper gastrointestinal X-ray examination with contrast medium revealed a large hemispheric lesion (7.8 x 4.8 cm) occupying the right posterior wall of the lower thoracic and abdominal esophagus. Manometry revealed a motility disorder and high pressure of the lower esophageal sphincter due to achalasia. Therefore she was diagnosed as having a giant diverticulum with achalasia after Heller's operation. She underwent transhiatal esophagectomy and reconstruction with placement of a gastric tube on June 4, 1992. Pathology results on the resected specimen revealed a false diverticulum. She has been doing well for 4 years since the operation. It has been said that a complication of incomplete long myotomy causes pulsion diverticulum, but we could not find a case of epiphrenic diverticulum after myotomy for achalasia reported in the literature in the last 10 years.

Dissociation of phosphoinositide hydrolysis and positive inotropic effect of histamine mediated by H1-receptors in guinea-pig left atria.

The present study was undertaken to determine whether the phosphoinositide hydrolysis is responsible for the positive inotropic effect of histamine in guinea-pig left atria. Histamine induced hydrolysis of phosphoinositides and a positive inotropic effect in a concentration-dependent manner. These effects were antagonized by chlorpheniramine (0.1 mumol/l) but not by cimetidine (10 mumol/l). At a concentration of 1 mumol/l histamine produced a dual-component positive inotropic response composed of an initial increasing phase and a second and late developing, greater positive inotropic phase. Histamine (10 mumol/l) caused a gradual increase in the formation of [3H]inositol trisphosphate (IP3) and a significant increase in the [3H]IP3 level was detected 10 min after the stimulation. Thus, the increase in IP3 did not precede the increase in force of contraction. The phospholipase C inhibitors 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (100 mumol/l) and neomycin (100 mumol/l) significantly reduced the histamine-induced [3H]inositol monophosphate accumulation. However, pretreatment with the phospholipase C inhibitors did not affect the positive inotropic effect of histamine, either in its extent or in its pattern. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (100 nmol/l) and phorbol-12,13-dibutyrate (PDBu) (100 nmol/l) also significantly inhibited the phosphoinositide hydrolysis induced by histamine. The inhibitory effect of the phorbol esters on the phosphoinositide response was completely abolished in the presence of 10 mumol/l 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a protein kinase C inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic and anticholinergic effects of pirmenol enantiomers in guinea-pig myocardium.

Since it has been reported that several class I drugs stereoselectively block sodium channels, potassium channels and muscarinic receptors in cardiac tissues, electrophysiologic and anticholinergic effects of enantiomers of pirmenol, a class I antiarrhythmic drug, were examined. Both (+) and (-) pirmenol depressed the maximum upstroke velocity (Vmax) of the action potential in a concentration-dependent manner in guinea-pig papillary muscles driven at 1.0 Hz, and there was no significant difference in the potency of the class I effect between the enantiomers. The onset rates of use-dependent block (UDB) of Vmax at 2.0 Hz for 10 mumol/l (+) and (-) pirmenol were 0.30 +/- 0.03 and 0.29 +/- 0.01 per action potential, and the recovery time constants from UDB for (+) and (-) pirmenol were 27.0 +/- 2.7 and 27.7 +/- 1.9 s, respectively, indicating no difference in the binding and unbinding kinetics to the sodium channel between the enantiomers. Both (+) pirmenol and (-) pirmenol prolonged action potential duration (APD) at low concentrations (1-10 mumol/l) and shortened it at high concentrations (30-100 mumol/l). Again, there was little difference with respect to the effects on APD between the enantiomers. However, in the isolated guinea-pig left atria (-) pirmenol more potently antagonized the negative inotropic effect of carbachol than (+) pirmenol, and the pA2 values for (+) and (-) pirmenol were 6.41 and 6.71, respectively. The functional study was supported by the radioligand binding experiments using [3H]N-methylscopolamine ([3H]NMS) in guinea-pig left atrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of class III antiarrhythmic drugs with muscarinic M2 and M3 receptors: radioligand binding and functional studies.

We have recently reported that class III antiarrhythmic drugs inhibit the muscarinic acetylcholine (ACh) receptor-operated K+ current (IK,ACh) in guinea-pig atrial cells by different molecular mechanisms. The data obtained from the patch-clamp study suggest that D,L-sotalol inhibits IK,ACh by blocking the muscarinic receptors, whereas MS-551 inhibits the K+ current by blocking the muscarinic receptors and depressing the function of the K+ channel itself and/or the guanine nucleotide-binding protein (G protein). This study was undertaken to determine whether the class III antiarrhythmic drugs D,L-sotalol and MS-551 interact with the muscarinic receptors of cardiac and peripheral tissues. Both drugs inhibited concentration dependently the specific [3H]N-methylscopolamine ([3H]-NMS) binding to membrane preparations obtained from guinea-pig atria and submandibular glands. The competition curves of these drugs for [3H]-NMS binding to glandular membranes were monophasic, suggesting competition with [3H]-NMS at a single site. Although the competition curve of D,L-sotalol for [3H]-NMS binding to atrial membranes was monophasic, that of MS-551 was biphasic and showed high- and low-affinity states of binding. D,L-Sotalol showed slightly, but significantly, higher affinity for cardiac-type muscarinic receptors (M2) than for glandular-type muscarinic receptors (M3). The inhibition constant (Ki) for MS-551 in glandular membranes was also slightly greater than the high-affinity Ki value for the drug in atrial membranes. In guinea-pig left atria and ilea, D,L-sotalol shifted the concentration-response curves for the negative inotropic effect and the contracting effect of carbachol in a parallel manner. The slopes of Schild plot were not significantly different from unity, suggesting competitive antagonism, and the pA2 for D,L-sotalol in left atria was slightly greater than that in ilea. MS-551 also shifted the concentration response curve for the negative inotropic effect of carbachol in atrial preparations to a greater extent than that for the contracting effect in ileal preparations, although MS-551 failed to show a pure competitive antagonism. These results suggest that both D,L-sotalol and MS-551 interact with cardiac M2 and peripheral M3 receptors, and that at high concentrations they exert anticholinergic activity in cardiac and peripheral tissues.

Targeting disruption of histamine H1 receptors in mice: behavioral and neurochemical characterization.

With gene targeting, one can practically knock out a gene in vivo and create a mutant organism that completely lacks the gene product. The mutant mice lacking histamine H1 receptors was generated by the method of gene targeting. In brains of homozygous mutant mice, no specific binding of [3H]pyrilamine was seen. The mutant mice showed impaired locomotor activity and exploratory behavior in an open field and activity wheel. Behaviors of the mutant mice were examined with several other tasks such as passive avoidance test, resident-intruder aggression test and formalin test to clarify the role for the H1 receptors in behaviors. Behavioral changes observed in the mutant mice are almost compatible with those obtained by the classical pharmacological tools. In correlation to the behavioral changes in the mutant mice, 5-hydroxytryptamine release was significantly increased in the brains of mutant mice.

Generalized peritonitis caused by spontaneous intraperitoneal rupture of the urinary bladder.

We report a case of generalized peritonitis caused by spontaneous intraperitoneal rupture of the urinary bladder. A 74-year-old female was admitted with abdominal pain and biochemical findings of acute renal failure (ARF). She had recently complained of macrohematuria. She had a past history of radiotherapy for uterine cervical cancer and Parkinson's disease treated with levodopa and amantadine. We diagnosed this case as intraperitoneal rupture of the bladder by cystogram. Biochemical findings of ARF might have resulted from urine reabsorption. Intraperitoneal rupture of the bladder should be considered in all cases of peritonitis, especially in patients with urological symptoms and features of ARF.

Production of exfoliative toxin A by Staphylococcus aureus isolated from mastitic cow's milk and farm bulk milk.

The production of exfoliative toxins A and B (ETA and ETB) by Staphylococcus aureus isolated from mastitic cow's milk and farm bulk milk was examined by the reverse passive latex agglutination method (RPLA). ETA was detected in 2 (1.2%) of 162 isolates from mastitic cow's milk and in 1 (0.6%) of 166 isolates from farm bulk milk. RPLA titers of these isolates were much lower than in human isolates. No ETB was detected in any of the isolates tested. These ETA-positive isolates belonged to bovine ecovar. They were non-typable using the international phage set for human strains. When these ETA-positive isolates were subcutaneously inoculated into neonatal mice, general exfoliation of the epidermis accompanied by the so-called Nikolsky sign was not recognized. By the immunoblotting and PCR methods, however, ETA and eta gene were recognized in the ETA-positive isolates from mastitic cow's milk and farm bulk milk. These data suggest that ETA is also produced by bovine isolates of S. aureus, but in smaller quantities.

[A comprehensive fact finding study of home care elderly for planning of the community based rehabilitation system in Koga City, Ibaraki Prefecture].

An interview survey was held with the purpose of grasping the problems faced by the home care elderly living in Koga city in Ibaraki prefecture. The subjects of the study were 100 cases who had been registered as elderly requiring home care in the municipality. The main results were as follows: (1) The most frequent underlying disorders that were considered as causes of disabilities in the home care elderly were cerebrovascular diseases, senile dementia and external injuries. In 67 percent of the subjects, one of these three disorders had caused the disabilities. (2) Disabilities in self care activities and in mobility were closely related to each other and the order of the difficulty in performing these activities was similar in many cases. A large number of the subjects sustaining severe disabilities expressed discontent with their daily life. (3) Forty two percent of the subjects were so-called bedridden elderly who got out of bed for less than 3 hours a day. The Barthel index score was 60 or less in all of the bedridden subjects. (4) For most of the bedridden elderly, bed rest was not required and probably exacerbated the disuse syndrome. In order to ameliorate their condition, adequate rehabilitation programs and assistance in their daily activities need to be offered. (5) Seventy eight percent of the care givers complained about the burden of care. Those who had no assistant care giver complained more frequently. Many of the care givers complaining about their burden had their own health problems. (6) The utilization of social welfare services were not always without any problems. The number of the experts who can deal with the psychosocial aspects in the elderly should be increased in order to improve the situation.

[Observation of the posterior urethra by transrectal linear ultrasonography].

Transrectal linear ultrasonography was performed on 59 male patients with dysuria, and voiding movement of the posterior urethra was observed with a videomonitor. Uroflowmetry was performed simultaneously, and the results were compared with those obtained in a previous study. On the image synchronized with maximum flow rate, the diameter of the bladder neck, and the center of the prostatic urethra were measured as parameters and the correlation with maximum flow rate, average flow rate, and residual urine rate, was examined. The forward movement of the ventral side of the posterior urethra was found to play a more important role in the opening of the posterior urethra, than the opening of the bladder neck, and the width of the prostatic urethra to play a more important role in the efficiency of urination than the width of the bladder neck.

[Type and screen system for efficient use of blood on elective surgery].

For the efficient use of blood resources, we have adopted the Type and Screen system (T & S) and Maximum Surgical Blood Order Schedule (MSBOS) for elective operations. To evaluate the usefulness of these systems, we analyzed the crossmatched to transfused blood ratio (C/T ratio) for the period of one year before and after the adoption of the systems. C/T ratio were 4.65 and 2.38 respectively and crossmatched blood units decreased from 3799 to 2511 units. These results show the usefulness of these systems in perioperative blood transfusion system. It is possible to make use of blood more efficiently by further detailed re-evaluation of both T & S and MSBOS systems.

[Focal segmental glomerulosclerosis associated with type C virus hepatitis and decrement of proteinuria by interferon-alpha therapy].

Focal segmental glomerulosclerosis (FSGS) associated with type C virus (HCV) hepatitis has not been described in the literature to date. However, we experienced a 30-year-old man, who had had HCV hepatitis, developed nephrotic syndrome and was admitted to our hospital. The first renal biopsy showed FSGS which was diagnosed by light, immunofluorescent, and electron microscopic study. FSGS diagnosis was based upon the findings of focal segmental glomerular sclerosis associated with hyalinosis and foam cells, segmental deposition of IgM and C3 on glomeruli, and epithelial cell vacuolization in the Bowman's space. HCV hepatitis was treated with interferon-alpha (INF-alpha) over 6 months. The treatment brought the disappearance of not only HCV-RNA from the blood, but also the manifestation of nephrotic syndrome. Therefore, the second renal biopsy was performed, but did not reveal any great pathological improvement. Five months later after the remission, he again had an elevated HCV-RNA level and a relapse of nephrotic syndrome. He was retreated with the same therapy and achieved a second remission of nephrotic syndrome. FSGS associated with HCV hepatitis is described first and the implication of INF-therapy in the improvement of proteinuria is discussed.