Search PubMed⌕ Search

Biomedical subjects

S Shibuya

Publications and source records attributed to S Shibuya.

At least 19 recordsLinked to original sources
PubMed2002

Early scheduled laparoscopic cholecystectomy following percutaneous transhepatic gallbladder drainage for patients with acute cholecystitis.

AIM: The present study was conducted to evaluate the effectiveness of early scheduled laparoscopic cholecystectomy (LC) following percutaneous transhepatic gallbladder drainage (PTGBD) for patients with acute cholecystitis. PATIENTS AND METHODS: 31 patients with acute cholecystitis were treated by early scheduled LC following PTGBD (group 1). These patients were compared with 9 patients treated by early LC without PTGBD (group 2) and with 12 patients treated by delayed LC following conservative therapy (group 3) for the success rate of intraoperative cholangiography, the conversion rate to open cholecystectomy, operative time, and hospital stay. Early scheduled LC following PTGBD was defined as scheduled LC when the patient's condition recovered and it was performed 1-7 days (mean: 4 days) after admission. The patients' age in group 1, 2, and 3 was 66 +/- 13, 65 +/- 10, and 64 +/- 9 years, respectively, without significant difference. Most of the patients had additional diseases. RESULTS: The success rate of intraoperative cholangiography was 97% (30/31) in group 1, 67% (6/9) in group 2, and 67% (8/12) in group 3. The conversion rate to open cholecystectomy was 3% (1/31) in group 1, 33% (3/9) in group 2, and 33% (4/12) in group 3. The operative time for LC was 89 +/- 33 min in group 1, 116 +/- 24 min in group 2, and 135 +/- 30 min in group 3. The mean hospital stay after LC was 9 +/- 4 days in group 1, 9 +/- 3 days in group 2, and 17 +/- 7 days in group 3. In group 1, the success rate of intraoperative cholangiography was higher, the conversion rate to open cholecystectomy was lower, and operative time was shorter than in groups 2 and 3 with significant difference (p <0.05, p <0.05, and p <0.01, respectively). CONCLUSION: The findings of this study indicate that early scheduled LC following PTGBD is a safe and effective therapeutic option for patients with acute cholecystitis especially in elderly and complicated patients.

Acute Disease↗
PubMed2002

Embryonic intermediate filament, nestin, expression following traumatic spinal cord injury in adult rats.

Precursor cells in the ependyma of the lateral ventricles of adult mammalian brain have been reported in brain, and also in the spinal cord. The present study used antibody to the intermediate filament protein (nestin) as an immunohistochemical marker for neural stem cells and precursor cells in a rat model of spinal cord trauma. Male Sprague-Dawley rats (n=25) had a laminectomy at Thll-Thl2, and spinal cord contusion was created by compression with 30 g of force for 10 min. The rats were killed at 24 h, 1 week and 4 weeks after injury, and four levels of the spinal cord were examined: 5 mm and 10 mm, both rostral and caudal region to the injury center. Time- and region-dependent alterations of nestin immunoreactivity were analyzed. Revealed at 24 h post-injury, 5 mm rostral and caudal to the lesions, nestin expression was observed in ependymal cells and around the hemorrhagic and necrotic lesion located in dorsal spinal cord, peaking at 1 week after injury. Moreover, nestin expression was also observed in the white matter of ventral spinal cord, extending into arborizing processes centripetally from the pial surface toward the central canal. At 4 weeks after injury, nestin expression in ependyma decreased 10 mm from the injury site. But nestin expression in white matter increased dramatically with a 100-fold increase in nestin originating from the pial surface, and extension now to all the white matter. The latter was accompanied by glial fibrillary acidic protein positivity into very long arborizing processes, morphologically compatible with radial glia. The findings suggest two possible sources of precursor cells in adult mammalian spinal cord; ependyma of the central canal and subpial astrocytes. Subpial astrocytes may be associated with neural repair and regeneration after spinal cord injury.

Age Factors↗
PubMed2001

Localization of sarcoglycan, neuronal nitric oxide synthase, beta-dystroglycan, and dystrophin molecules in normal skeletal myofiber: triple immunogold labeling electron microscopy.

In order to investigate the mode of existence of the sarcoglycan complex, neuronal nitric oxide synthase (nNOS), beta-dystroglycan, and dystrophin in the normal skeletal myofiber, we examined the ultrastructural localization and mutual spatial relationship of nNOS, beta-dystroglycan, dystrophin, and the individual components of the sarcoglycan complex by using triple immunogold labeling electron microscopy. Each molecule of alpha-, beta-, gamma- and delta-sarcoglycans is located intracellularly or extracellularly near the muscle plasma membrane mostly in accordance with the sarcoglycan antigenic sites against which the antibodies were generated. The association of different two and/or three sarcoglycan molecules out of alpha-, beta-, gamma- and delta-sarcoglycan molecules was frequently observed. Each molecule of nNOS, beta-dystroglycan, and dystrophin was ultrastructurally noted along the cell surface of normal skeletal myofibers. Moreover, the close relation of a sarcoglycan molecule with beta-dystroglycan and dystrophin, and the association of nNOS with dystrophin were also confirmed ultrastructurally. Thus, this study demonstrated that the constituting molecules of the sarcoglycan complex, nNOS, beta-dystroglycan, and dystrophin existed in the form of a cluster at the normal muscle plasma membrane. The association of nNOS with dystrophin and its associated glycoproteins may form a macromolecular signaling complex at the muscle plasma membrane.

Amino Acid Sequence↗
PubMed2001

Synthesis and evaluation of a difluoromethylene analogue of sphingomyelin as an inhibitor of sphingomyelinase.

A sphingomyelin analogue 2, in which the long alkenyl chain and the phosphodiester moiety of sphingomyelin were replaced by a phenyl and an isosteric difluoromethylenephosphonic acid, was prepared to evaluate its inhibitory potency to sphingomyelinase. The analogue non-competitively inhibited the neutral sphingomyelinase in bovine brain microsomes with an IC50 of 400 microM. The compound had the ability to suppress tumor necrosis factor alpha-induced apoptosis of PC-12 neurons at a low concentration of 0.1 microM.

Animals↗
PubMed2001

Laparoscopic appendectomy with the help of a wire snare.

This report describes the performance of a laparoscopic appendectomy (LA), a new technique using a "wire snare" without any specific complications. The snare consisted of an 18-gauge injection needle and folded fine wire, measuring 0.28 mm in diameter. LA was performed in 95 patients with acute appendicitis using a cheap and simple wire snare to catch the ligation thread of #0 silk. A good view of the appendix and mesoappendix was obtained in all cases by traction of the #0 silk. The operative time needed to perform LA using a wire snare for nongangrenous appendicitis in 77 cases overall, the first 10 cases, and the last 10 cases was 54+/-17, 64+/-5, and 33+/-4 min, respectively. Two of the 95 patients required conversion to an open appendectomy because of technical difficulties due to the formation of an inflammatory mass. There were no complications associated with insertion of the snare. The wire snare is an innovative technique and does not increase the costs significantly, and should help reduce the number of trocar sites and the operative time, while also making an LA easier to perform.

Adolescent↗
PubMed2001

Eight years of experience with transjugular retrograde obliteration for gastric varices with gastrorenal shunts.

BACKGROUND AND OBJECTIVES: There is no standard treatment for gastric varices. Transjugular retrograde obliteration (TJO) is one way of obliterating gastric varices with gastrorenal shunts, in which blood flow is abundant. Our aim was to examine our experience with TJO during an 8-year period and to determine the long-term effects of this treatment. METHODS: We performed TJO procedures in 52 patients to obliterate gastric varices. All the patients had liver cirrhosis. Sixteen had hepatocellular carcinoma (HCC) without vascular invasion. We inserted an angiographic catheter with an occlusive balloon through the right internal jugular vein into the gastrorenal shunt or the gastric varices. After controlling the other blood-draining routes with a microcoil or absolute ethanol, or both, we injected 5% ethanolamine oleate with iopamidol into the gastric varices under fluoroscopy. RESULTS: The gastric varices were successfully obliterated by TJO in all cases. The complications were all minor and transient. The mortality rate for TJO was 0%. There was no recurrence and no bleeding of gastric varices at all after TJO. Patient survival differed depending on the presence or absence of HCC (P <.05). The development of HCC in the cirrhotic liver was the most common cause of late death. Gastrointestinal bleeding was not a cause of death. The occurrence rate of esophageal varices after TJO was high, but these varices could be treated easily by endoscopic injection sclerotherapy before they bled. CONCLUSIONS: Portal blood flow through the gastrorenal shunt is diverted to the porto-azygos venous system after the gastrorenal shunt is obliterated by TJO. TJO is a safe option that we recommend for treating gastric varices with gastrorenal shunts, provided that the TJO is followed by endoscopic injection sclerotherapy.

Adult↗
PubMed2001

Muscle plasma membrane changes in dystrophin gene exon 52 knockout mouse.

Changes in muscle plasma membranes in mice lacking exon 52 of the dystrophin gene (mdx52 mouse) were studied using the freeze-fracture technique. The extensor digitorum longus (EDL) muscle plasma membrane of the mdx52 mouse at 8 weeks of age showed significantly increased caveola density (p < 0.05 by two-tailed t-test) and significantly decreased densities of intramembranous particles (IMPs), orthogonal arrays (OAs) and orthogonal array subunit particles (OASPs) (p < 0.05 by two-tailed t-test, p < 0.01 by Wilcoxon rank-sum test, p < 0.05 by two-tailed t-test, respectively) on the protoplasmic face when compared with those of control EDL muscles. These changes are more similar to those seen in DMD than those in the mdx mouse at the same age as reported previously. Thus, the gene abnormality in the different exon of the mouse dystrophin gene seems to induce somewhat different changes in the muscle plasma membrane.

Animals↗
PubMed2001

Angiotensin subtype-2 receptor (AT2 ) negatively regulates subtype-1 receptor (AT1 ) in signal transduction pathways in cultured porcine adrenal medullary chromaffin cells.

BACKGROUND: Two distinct types of angiotensin II (AngII) receptors, AT1 and AT2, have been cloned. We have shown previously that stimulation of AT2 reduces intracellular cyclic guanosine monophosphate (cGMP) levels in cultured porcine chromaffin cells in which AT2 is the predominantly expressed receptor. However, it has not been determined whether AT1 or AT2 affects signal transduction pathways involving mitogen-activated protein kinases (MAPKs) and signal transducers and activators of transcription (STATs) in chromaffin cells. Also, it is unclear whether cGMP/protein kinase G (PKG) is involved in the regulation of MAPKs and STATs in these cells. DESIGN: Chromaffin cells were derived from porcine adrenal medulla. The effects of AngII alone (representing physiological conditions), AngII plus CV-11974 (an AT1 antagonist, which simulates specific AT2 stimulation), AngII plus PD 123319 (an AT2 antagonist, which simulates specific AT1 stimulation), and 8-Br-cGMP (a membrane-permeable cGMP analogue) alone on MAPKs (ERKs, JNK, p-38 MAPK) and STATs (STATs 1, 3 and 5) activity were measured. METHODS: Phosphorylated MAPKs (extracellular signal-related kinases (ERKs), c-jun N-terminal kinase (JNK) and p38 MAPK) and STATs (STATs 1, 3 and 5) were measured by immunoprecipitation-Western blot analysis (IP-Western blot). RESULTS: AT1 stimulation markedly increased expression of ERKs, JNK, p38 MAPK via Ca2+-dependent protein kinase C (PKC) isoforms (cPKC), as well as STATs 1, 3 and 5 in cultured porcine chromaffin cells. In contrast, AT2 stimulation markedly decreased the expression of these signaling molecules. Also, 8-Br-cGMP alone induced increases in ERKs, JNK, p38 MAPK, and STATs 1, 3 and 5. Because AT2 inhibits cGMP production, we speculate that AT2 may act to suppress cGMP production, which in turn reduces the activity of both MAPKs and STATs in chromaffin cells. CONCLUSION: AT2 negatively regulates AT1 in signal transduction pathways in chromaffin cells.

Angiotensin II↗
PubMed2001

Correlation between endoscopic and angiographic findings in patients with esophageal and isolated gastric varices.

BACKGROUND/AIM: The correlation between angiographic vascular patterns and endoscopic findings in portal hypertension is not sufficiently known, and knowledge of the vascular anatomy may contribute to an improvement in endoscopic embolization and transjugular retrograde obliteration procedures. We propose a new vascular map that should prove useful for this purpose. METHODS: Between April 1985 and December 1997 we performed percutaneous transhepatic portography in a selected group of 75 patients (16 women and 59 men), aged 43-71 years, from whom informed consent was obtained. All patients had been diagnosed endoscopically as having either esophageal or isolated gastric varices. According to the Child-Pugh classification, class A, B, and C cirrhosis was seen in 19, 40, and 16 patients, respectively. We created a vascular map of esophageal and isolated gastric varices, based on the opacification of the portal venous collaterals on percutaneous transhepatic portography. We compared the patients in both variceal groups in terms of portal venous pressure, main blood supply, and drainage routes. RESULTS: We found that the portal collateral system was divided into two systems: the portoazygos venous system and the portophrenic venous system. The former contributed to the formation of esophageal and cardiac varices and the latter to the formation of isolated gastric varices located at the fundus or at both the cardia and fundus. The left gastric vein participated as blood supply in 70% of the isolated gastric varices and in 100% of the esophageal varices (p < 0.01). The posterior gastric vein participated as blood supply in 70% of the isolated gastric varices and in 24% of the esophageal varices (p < 0.01). We classified the main blood drainage routes of isolated gastric varices functionally into three types: gastrorenal shunt (85%), gastrophrenic shunt (10%), and gastropericardiac shunt (5%). The portal venous pressure in patients with esophageal varices was 358 +/- 66 mm H(2)O, whereas in patients with isolated gastric varices it was 262 +/- 44 mm H(2)O (p < 0.01). CONCLUSION: We suggest that this new vascular map will be useful in endoscopic embolization and transjugular retrograde obliteration procedures for esophageal and isolated gastric varices.

Adult↗
PubMed2001

Leptin stimulates catecholamine synthesis in a PKC-dependent manner in cultured porcine adrenal medullary chromaffin cells.

We have previously shown that murine recombinant leptin directly stimulates catecholamine synthesis through the long form of the leptin receptor (Ob-Rb) expressed in cultured porcine chromaffin cells. Additionally, we found that leptin activates IP3 production after PLC activation. It is well established that activation of PLC elicits IP3 production as well as an increase in diacylglycerol, a compound that stimulates PKC. Therefore, we investigated the involvement of PKC in leptin-induced catecholamine synthesis. Leptin was found to induce significant increases in PKC activity in a dose-dependent manner (1, 10, and 100 nM); chelation of extracellular Ca(2+) by EDTA abolished this PKC stimulatory activity. We also confirmed by Western blot analysis that leptin (at 100 nM) induced significant increases in Ca(2+)-dependent PKC alpha, -beta(I), and -gamma expression. The activity of the rate-limiting enzyme tyrosine hydroxylase (TH) in the biosynthesis of catecholamine is regulated at the transcriptional and posttranscriptional levels. TH enzyme activity and TH mRNA levels induced by 100 nM leptin were significantly inhibited by the PKC inhibitor Ro 32-0432 as well as by EDTA. In addition, increases in TH protein and intracellular catecholamine content stimulated by leptin were completely inhibited by Ro 32-0432. Leptin markedly activated ERKs and, to a lesser extent, JNK; these stimulatory effects on ERKs and JNK were completely inhibited by Ro 32-0432 as well as EDTA. In contrast, leptin did not activate P38 MAPK. Similar to leptin, PMA activated ERK and JNK. Nicardipine and omega-conotoxin GVIA, each at 1 microM, were effective at inhibiting leptin-induced TH enzyme activity, TH mRNA accumulation, PKC activity, and ERK activity. Leptin increased activating protein-1 DNA-binding activity, and this was diminished by Ro 32-0432 as well as EDTA, similar to the reduction of TH mRNA levels. In addition, using supershift analysis, we documented the involvement of c-Fos and, to a lesser extent, c-Jun in leptin-induced activating protein-1 activity. These results indicate that leptin stimulates Ca(2+)-dependent PKC isoform-dependent catecholamine synthesis in porcine chromaffin cells. Previously, we had shown that leptin stimulated cAMP. The present study also showed that H89 (a PKA inhibitor) moderately, but significantly, inhibited leptin-induced ERK and TH mRNA. Consistent with this finding, leptin is shown here to activate novel PKC epsilon, which is assumed to stimulate Raf, upstream of ERKs, via cAMP, supporting the suggestion that Ca(2+)-independent novel PKC may also play some physiological role in regulating catecholamine synthesis.

Adrenal Medulla↗
PubMed2001

[A case of polyneuropathy associated with increased levels of vascular endotherial growth factor (VEGF) insera].

A 54-year-old woman began to notice numbness and motor weakness in the lower extremities in July 1999. These symptoms rapidly progressed and she could not walk any more. When she admitted to our hospital, she showed peripherally dominant, moderate motor weakness, drop foot and loss of superficial and deep sensation in the lower extremities, but only slight weakness in the hands. Cranial nerves were intact. Deep tendon reflexes were all absent. Nerve conduction velocities were reduced and cerebrospinal fluid protein was elevated. VEGF was greatly increased in serum (1,850 pg/ml), which has been found to be increased exclusively in patients with Crow-Fukase syndrome. Many characteristic manifestations of the syndrome except polyneuropathy are well explained to be resulted from the abnormal production of VEGF. She did not, however, exhibit any constellation of Crow-Fukase syndrome such as edema, skin change, organomegaly, bone lesions or M-proteinemia. Steroid therapy improved her symptoms and lessened the levels of serum VEGF and cerebrospinal fluid protein. This case indicated that overproduction of VEGF could induce polyneuropathy rather than the other symptoms of Crow-Fukase syndrome, and that a polyneuropathy associated with increased VEGF might exist.

Endothelial Growth Factors↗
PubMed2000

Aquaporin 4: lack of mRNA expression in the rat regenerating muscle fiber under denervation.

The recently identified water channel aquaporin 4 is a major component of the orthogonal arrays observed with freeze-fracture electron microscopy. We examined the expression of aquaporin 4 mRNA and protein in rat regenerating muscle under innervated and denervated conditions. We found decreased sarcolemmal immunostaining of aquaporin 4 in denervated regenerating muscle as opposed to innervated muscle. Quantitative reverse transcription-polymerase chain reaction revealed that aquaporin 4 mRNA was expressed in the innervated regenerating muscle; whereas it was not expressed in denervated muscle. Thus, lack of aquaporin 4 protein may be due to lack of aquaporin 4 mRNA in the denervated regenerating muscle. We conclude that the nerve supply influences expression of aquaporin 4 at the mRNA level in regenerating muscle.

Animals↗
PubMed2000

Aciculin and its relation to dystrophin: immunocytochemical studies in human normal and Duchenne dystrophy quadriceps muscles.

Aciculin is a novel adherens junction antigen extracted from human uterine smooth muscle that is reported to associate biochemically with dystrophin. We attempted to determine (i) the immunostainability of anti-aciculin antibody for the 6 histochemically normal human muscles and seven muscles from boys with Duchenne muscular dystrophy (DMD) and 11 disease control muscles, (ii) the ultrastructural localization of aciculin in normal skeletal myofibers, (iii) aciculin's spacial relationship with dystrophin and beta-spectrin, and (iv) if the aciculin is ultrastructurally colocalized with dystrophin, the distance from the aciculin epitope to the epitope of the dystrophin N- or C-terminal domain. For this, rabbit anti-aciculin antibody was generated against the synthetic peptide of aciculin fragment D [4]. Immunohistochemical staining showed that the immunostainability of DMD muscles for anti-aciculin antibody was markedly decreased as compared with normal and disease control muscles. Single and double immunogold labeling electron microscopy of 6 histochemically normal human quadriceps femoris muscles revealed that aciculin was present along the inner surface of muscle plasma membrane and that aciculin formed doublets more frequently with dystrophin (23.5 +/- 1.8%; group mean +/- SE) than with beta-spectrin (12.8 +/- 1.1%; P < 0.01 two tailed t test). Rabbit anti-aciculin antibody frequently formed doublets with monoclonal antibodies against the N- or C-terminal domain of dystrophin at the muscle cell surface. These results suggest that aciculin is associated with dystrophin and may interact with both the N- and C-terminal domains of dystrophin.

Child↗
PubMed2000

Synthesis and evaluation of multisubstrate analogue inhibitors of purine nucleoside phosphorylases.

1,1-Difluoro-2-(tetrahydro-3-furanyl)ethylphosphonic acids (+/-)-cis-4a and (+/-)-trans-4a possessing a (purine-9-yl)methyl functionality at the ring as well as their homologues (+/-)-cis-4b and (+/-)-trans-4b were synthesized and tested as 'multi-substrate analogue' inhibitors for purine nucleoside phosphorylases. Radical cyclization of allylic alpha,alpha-difluorophosphonates 8a,b was applied to construct the alpha,alpha-difluorophosphonate-functionalized oxacycles 9a,b. The IC50 values of the nucleotide analogues (+/-)-cis-4a and (+/-)-cis-4b were 88 and 38 nM, respectively, for human erythrocyte PNP-catalyzed phosphorylation of inosine in the presence of 100mM orthophosphate. The stereochemistry of the inhibitors was found to affect significantly the inhibitory potency. The transisomers (+/-)-trans-4a and (+/-)-trans-4b were ca. 4-fold less potent than the corresponding cis-isomers. At an intracellular concentration of orthophosphate (1 mM), (+/-)-cis-4b, the most potent compound of this series, was shown to have IC50 and Ki values of 8.7 and 3.5 nM, respectively.

Enzyme Inhibitors↗
PubMed2000

Blood supply routes of recurrent esophageal varices following endoscopic embolization.

BACKGROUND/AIM: The blood supply routes of recurrent esophageal varices following complete endoscopic embolization (EE) are not yet known. The purpose of this study is to identify these blood supply routes by comparing endoscopic varicography and percutaneous transhepatic portography (PTP). METHODS: Eleven cases of recurrent esophageal varices following EE are included in this study. The blood supply routes of primary and recurrent varices were analyzed by comparing the varicography obtained at the initial and repeat EE with PTPs before and after the initial EE. RESULTS: Endoscopic varicography at the time of initial EE could show the vessels of the left gastric vein (LGV) system, such as the cardiac branch of the LGV, and the cardiac venous plexus (CP) in 100% of cases, and the trunk of the LGV in 73% (8/11) of cases, whereas the posterior gastric vein was seen in only 18% (2/11) of cases. PTP performed 2 weeks after the initial EE confirmed that the routes visualized by endoscopic varicography could be obliterated in 10 of 11 cases. The blood supply routes of recurrent varices, demonstrated by varicography, were the vessels of the short gastric vein (SGV) system, such as the fundic branch of the SGV or the posterior gastric vein in 82% (9/11) of cases, and the partially reformed fine CP in 27% (3/11) of cases. Varicography revealed the remnant vessels of the LGV in only 1 case. CONCLUSIONS: The primary esophageal varices are supplied with blood mainly from the cardiac branch of the LGV through the CP. However, the blood supplies of recurrent varices following EE come from the fundic branch of the SGV or the posterior gastric vein. We conclude that three-dimensional obliteration of esophageal varices and their feeders, the LGV and SGV systems, is completed by initial and repeat EEs.

Adult↗