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Biomedical subjects

S Kitano

Publications and source records attributed to S Kitano.

At least 235 records · Page 13Linked to original sources
PubMed1994

Hepatoprotection by a PGI2 analogue in complete warm ischemia of the pig liver. Prostanoid release from the reperfused liver.

We examined the hepatoprotective effect of a prostaglandin (PG)I2 analogue by analyzing the endogenous release of prostanoid from the pig liver. Fourteen female pigs underwent 1 hr complete hepatic vascular exclusion (HVE); the portal and vena caval circulation was actively decompressed. The animals were divided into one of two groups (n = 7, each) according to pretreatment with the prostacyclin analogue (OP 2507, OP) administered via a mesenteric vein branch for 30 min at a rate of 2 micrograms/kg/min immediately prior to HVE. The plasma levels of prostaglandin E2 (PGE2), 6-keto-prostaglandin F1-alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2), from the blood samples from the aorta, the hepatic vein, and the portal vein were serially compared for 60 min after the restoration of blood flow. Other parameters included 7-day survival rate, serum biochemistry, and endotoxin assay. A significant improvement in 7-day survival rate (6/7 vs. 1/7 for the control, P < 0.02) was observed in the OP-treated animals, associated with amelioration of serum transaminase activities but with no differences in plasma endotoxin levels. The reperfused liver progressively and substantially released PGE2 but did not generate other prostanoids (TXB2 and 6-keto-PGF1 alpha). OP pretherapy substantially suppressed hepatic generation of the PGE2 postreflow, correlating with serum transaminase levels (rs = 0.80; P < 0.01, at 60 min). We conclude that the PGI2 analogue ameliorates hepatic ischemia/reperfusion injury by down-regulating PGE2 production from the reperfused liver.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Interleukin-4 acts as a potent stimulator for expression of monocyte chemoattractant JE/MCP-1 in mouse peritoneal macrophages.

The recruitment of monocyte/macrophages to inflammatory sites is one of the important events in inflammatory reactions. We show herein that interleukin-4 (IL-4) acts as a potent stimulator for expression of monocyte chemoattractant JE/MCP-1 in mouse peritoneal macrophages. IL-4 induced the JE/MCP-1 gene expression in dose and time dependent fashion. Run-on assay suggests that IL-4 stimulates the JE/MCP-1 gene expression at transcriptional level. Monocyte chemotactic activity was detected in culture medium of the cytokine-treated cells. The chemotactic activity in the culture supernatant was completely neutralized by anti-JE/MCP-1 antiserum.

Animals↗
PubMed1994

Retinoic acid suppression of c-fos gene inhibits expression of tumor necrosis factor-alpha-induced monocyte chemoattractant JE/MCP-1 in clonal osteoblastic MC3T3-E1 cells.

Our previous study (Hanazawa, S., Takeshita, A., Amano, S., Semba, T., Nirazuka, T., Katoh, H., and Kitano, S. (1993) J. Biol. Chem. 268, 9526-9532) demonstrated that tumor necrosis factor-alpha (TNF-alpha) induces monocyte chemoattractant JE/MCP-1 expression via c-fos and c-jun genes following protein kinase C activation in osteoblastic MC3T3-E1 cells. In the present study, we examined the effect of retinoic acid (RA) on the cytokine-induced JE/MCP-1 expression in the cells. RA significantly inhibited the JE/MCP-1 gene expression by at least 6 h of pretreatment, and the inhibition was pretreatment time-dependent and occurred at the transcriptional level of the JE/MCP-1 gene expression. The RA-induced inhibition of the JE/MCP-1 gene product was also evidenced by both an assay involving immunoprecipitation with JE/MCP-1-specific antiserum and an assay for monocyte chemotaxis. Also, RA stimulated the gene expression of three different subclasses of RA receptor. RA pretreatment transcriptionally suppressed the expression of the c-fos gene but not that of the c-jun gene in TNF-alpha-treated cells. Antisense oligonucleotide to c-fos gene inhibited the cytokine-induced JE/MCP-1 gene expression in the cells. Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells.

3T3 Cells↗
PubMed1994

[MR imaging oral contrast agent mixed with milk for the small intestine].

To investigate the usefulness of MRI oral contrast media in enhancing the entire small intestine using FerriSeltz (Otsuka Pharmaceuticals, Tokyo), which contains ferric ammonium citrate, we compared the relaxation times and taste of 7 kinds of contrast media (Milk FerriSeltz A-G) that contain FerriSeltz dissolved in 7 different ratios of distilled water-milk. We also compared the homogeneity of the contrast enhancement of the entire small intestine on T1-weighted images between Milk FerriSeltz-F (a mixture of distilled water and milk at a ratio of 1:5 with FerriSeltz), which was found to be the best contrast medium based on the relaxation times and taste, and Milk FerriSeltz-A (distilled water with FerriSeltz) in 10 healthy volunteers. The T1 and T2 values decreased as the proportion of milk increased. The T1 and T2 values of Milk FerriSeltz-F were 71 msec and 28 msec, markedly shorter than those of Milk FerriSeltz-A (340 msec and 290 msec). T1-weighted images taken with Milk FerriSeltz-F showed more homogeneous enhancement of the entire small intestine than those taken with Milk FerriSeltz-A. There were no adverse effects in these 10 volunteers. Milk FerriSeltz-F seems to be an ideal oral contrast medium for enhancement of the entire small intestine.

Administration, Oral↗
PubMed1994

Phorbol myristate acetate stimulates osteoclast formation in 1 alpha,25-dihydroxyvitamin D3-primed mouse embryonic calvarial cells by a prostaglandin-dependent mechanism.

Our previous study provided a novel assay system utilizing devitalized bone slices for study of the differentiation of osteoclast progenitors into preosteoclasts and mature osteoclasts among calvarial cells of mouse embryos. Using this assay system, we examined the effect of phorbol myristate acetate (PMA) on osteoclast formation as assessed by the appearance of tartrate-resistant acid phosphatase (TRAP)-positive cells and bone resorption lacunae. PMA alone was directly unable to induce the appearance of TRAP-positive cells and bone resorption lacunae of calvarial bone cells of mouse embryos. However, PMA markedly stimulated increases in the number of TRAP-positive cells and area of the resorption lacunae of the calvarial cells when the bone cells were primed by 1 alpha,25-(OH)2D3. This stimulatory effect of PMA was dose dependent. H-7, having relatively high affinity for protein kinase C, strongly inhibited in a dose-dependent fashion the stimulatory effect of PMA on the bone resorption of the hormone-primed calvarial cells. We also examined the involvement of prostaglandin in this stimulatory effect of PMA. Indomethacin, a cyclooxygenase inhibitor, markedly abolished the stimulatory effect of PMA on the bone resorption of the calvarial cells. PMA stimulated prostaglandin E2 (PGE2) production by the calvarial cells primed with 1 alpha,25-(OH)2D3 in a dose-dependent fashion. However, the PMA stimulation of the PGE2 production was significantly inhibited by H-7 and also by indomethacin. Furthermore, we observed that the addition of PGE2 to the calvarial cells primed with 1 alpha,25-(OH)2D3 for 1 or 3 days resulted in an increased number of TRAP-positive cells and increased bone resorption.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Bleeding from gastric ulcer halted by laparoscopic suture ligation.

In a 48-year-old Japanese man there was an uncontrollable and recurrent bleeding from a gastric ulcer and laparoscopic surgery was done. Two cannulae were placed in the gastric cavity through the abdominal wall and suture ligation of the bleeding vessel at the posterior wall of the stomach was done under video-visual control with endoscopic guidance. The bleeding ceased, complications were nil, and he remains well. This article reports on surgery done to repair uncontrollable, recurrent bleeding from a gastric ulcer. Two cannulae were placed in the gastric cavity through the abdominal wall and suture of the vessel at the posterior wall of the stomach was done with videovisual control and endoscopic guidance. This approach is concluded to have supplied minimal-access surgery, cost effectiveness, early discharge, less pain, and doctor-patient satisfaction.

Humans↗
PubMed1994

Metoclopramide inhibits development of esophageal varices in rat model.

We examined the preventive effect of metoclopramide on the development of esophageal varices in a rat model. Thirty rats were divided into three groups: metoclopramide (7.5 mg/kg twice a day, intraperitoneally), control group I (saline 2 ml/kg twice a day, intraperitoneally), and control group II (incised lower esophageal sphincter and metoclopramide 7.5 mg/kg twice a day, intraperitoneally). On the 14th postoperative day, lower esophageal sphincter pressure in the metoclopramide group (8.6 +/- 1.4 cm H2O) increased more than in the control groups (5.4 +/- 0.5, 5.0 +/- 0.5 cm H2O, P < 0.01). Development of small collateral vessels from the spleen to the retroperitoneum was evident only in the metoclopramide group, as seen on the portography (P < 0.01). Histologically, the variceal area of the horizontal cross section of the esophagus in the metoclopramide group (0.62 +/- 0.26 mm2) was significantly smaller than in the controls (2.67 +/- 0.95, 2.78 +/- 0.82 mm2), determined using an image processor-analyzer for photographing histological specimens (P < 0.01). We also investigated the effect of metoclopramide on smooth muscle cells in the rat portal vein, using isometric-tension recording. Metoclopramide relaxed the smooth muscle precontracted with norepinephrine, in a concentration-dependent manner. Thus, metoclopramide inhibits the development of esophageal varices in this rat model due to both an increase in resistance of the lower esophagus and to development of small collaterals.

Animals↗
PubMed1994

Laparoscopic splenectomy.

A technique for laparoscopic splenectomy is described. The patient is placed in the right semidecubitus position and pneumoperitoneum is prepared. The splenic artery and vein are exposed near the hilum, using a laparoscopic ultrasonic dissector. The larger vessels are doubly ligated, and the spleen is resected and maneuvered into a nylon surgical sack; the sack is removed through a 2-cm incision along the midaxillary line. This procedure has been used for four patients requiring splenectomy for benign disease, and the outcome has been entirely satisfactory for all concerned.

Adult↗
PubMed1994

Laparoscopy-assisted surgery: a new technique for transhiatal esophageal dissection.

Esophageal dissection under laparoscopic monitoring is performed during total esophagectomy to treat patients with cervical esophageal carcinoma. Using this technique, a safe esophageal dissection can be made from the surrounding mediastinal tissues. Some of the disadvantageous consequences of a blunt dissection, including the blind maneuver, may thus be prevented and various intraoperative and postoperative complications may be avoided.

Esophageal Neoplasms↗
PubMed1994

Clinical significance of esophageal variceal pressure in patients with esophageal varices.

In 40 patients with esophageal varices, esophageal variceal pressure was assessed endoscopically using a pneumatic pressure sensor. The effects of vasopressin or nitroglycerin on variceal pressure and endoscopic findings were also assessed in two groups of seven patients. The results were as follows: (1) Variceal pressure was increased above 250 mmH2O in all patients who had bled, and the mean variceal pressure was significantly higher in patients who had bled than in those who had not (301 +/- 47 vs. 230 +/- 58 mmH2O respectively, p < 0.001). (2) Variceal pressure correlated with endoscopic findings, determined using the criteria of the Japanese Research Society for Portal Hypertension. It was significantly higher when varices with a feature of F2-F3 or RC(+2)-RC(+3) were compared to those with a feature of F1 or RC(-)-RC(+), respectively. (3) Both groups given vasopressin or nitroglycerin had significant reductions in variceal pressure; however, there was little improvement in endoscopic findings in those given nitroglycerin, compared to the improvement in those given vasopressin. Thus, use of a pneumatic pressure sensor proved to be a pertinent tool for assessing esophageal varices, along with endoscopic signs.

Aged↗
PubMed1994

Laparoscopy-assisted devascularization of the lower esophagus and upper stomach in the management of gastric varices.

Devascularization of the lower esophagus and the upper stomach is one method of treating patients with clinically significant gastric varices. We describe a new method of laparoscopically-assisted devascularization which has been applied in seven patients with esophagogastric varices. Three of the seven patients had an episode of gastric variceal bleeding, and the remaining four had moderate to large gastric varices with red color signs. The operative procedure was carried out without pneumoperitoneum by using an ordinary forceps and laparoscopic instruments through a small skin incision (3-5 cm); the abdominal wall was elevated with a U-shaped retractor. The operative field was obtained by laparoscopic and direct vision illuminated by laparoscopic light. The procedure time ranged from 100 to 180 minutes with minimal blood loss (70-320 g). No complications were encountered. All patients could be discharged within one week; postoperative pain was minimal and all patients returned to work early. Follow-up (mean 11.4 months) showed no recurrence of gastric varices although, due to an incomplete procedure in two cases, two patients were treated additionally by endoscopic injection of histoacryl.

Esophageal and Gastric Varices↗
PubMed1994

Porphyromonas gingivalis fimbriae induce a 68-kilodalton phosphorylated protein in macrophages.

The present study was performed to examine whether Porphyromonas gingivalis fimbriae induce specifically a protein kinase-mediated phosphorylated protein that is involved in the mechanism of signal transduction. The fimbriae induced a 68-kDa phosphorylated protein (pp68) in a dose-dependent manner in mouse peritoneal macrophages. A marked appearance of pp68 was observed 20 min after the initiation of fimbrial treatment. The fimbria-induced pp68 was inhibited dramatically by staurosporine, a potent inhibitor of protein kinase C. pp68 induction was also inhibited by H-7, a potent inhibitor of several types of protein kinase. However, the induction was not inhibited by HA-1004 and H-8, relatively high-affinity inhibitors of protein kinase A. Phorbol myristate acetate and 1-oleoyl-2-acetyl-sn-glycerol, activators of protein kinase C, were able to induce pp68 in mouse peritoneal macrophages. This protein was localized in the cytosolic fraction of fimbria-treated macrophages. pp68 also was induced in fimbria-treated human monocyte-like cells. Finally, we observed that gene expression of the fimbria-induced neutrophil chemoattractant KC was inhibited markedly by staurosporine.

Alkaloids↗
PubMed1994

Porphyromonas gingivalis fimbriae stimulate bone resorption in vitro.

Our previous study demonstrated that Porphyromonas gingivalis fimbriae induce the expression of interleukin-1, a potent bone-resorbing cytokine, in macrophages. This demonstration suggested to use the possibility that the fimbriae may stimulate bone resorption via the generation of an inflammatory cytokine(s). The present study was performed to test this suggestion. The bone-resorbing activity was evaluated by measuring the area of resorption lacunae on bone slices incubated with calvarial bone cells taken from 14-day-old mouse embryos. Fimbriae at 0.5 micrograms of protein per ml stimulated the bone-resorbing activity significantly, and the effect was dose and treatment time dependent. Since it is well known that interleukin-1 and granulocyte macrophage colony-stimulating factor induce differentiation of osteoclast lineage cells, we examined the involvement of these cytokines in fimbria-stimulated bone resorption. Fimbria-stimulated bone resorption was abolished significantly by antisera against both cytokines. We observed by Northern (RNA) blot assay that both cytokine genes were markedly expressed in the fimbria-treated calvarial bone cells. Our present data demonstrate that P. gingivalis fimbriae stimulate bone resorption in vitro.

Animals↗
PubMed1994

Endothelin-1 in cerebrospinal fluid in elderly patients with hypertension and dementia.

Endothelin-1, a potent endothelium-derived vasoconstrictive peptide, is also known to exist in the central nervous system. We determined endothelin-1-like immunoreactivity in cerebrospinal fluid by a radioimmunoassay in 32 normotensive or hypertensive elderly subjects (79 +/- 8 years old) with or without multi-infarction dementia. The mean value of endothelin-1-like immunoreactivity in cerebrospinal fluid was significantly (P < .05) elevated in subjects with essential hypertension (> or = 160/95 mm Hg, n = 5, 79 +/- 9 years old) compared with those with borderline hypertension (140-159/90-94 mm Hg, n = 4, 78 +/- 5 years old) and normotensive subjects (< 140/90 mm Hg, n = 23, 79 +/- 8 years old). The value of endothelin-1-like immunoreactivity in cerebrospinal fluid was significantly (P < .05) positively correlated with both systolic (r = .38) and diastolic (r = .42) blood pressures in all subjects. On the other hand, mean values of endothelin-1-like immunoreactivity in cerebrospinal fluid were also significantly (P < .05) elevated in the groups of patients with multi-infarction dementia that had profoundly decreased Mini-Mental State scores (< or = 10, n = 6) and moderately decreased Mini-Mental State scores (11 to 20, n = 14) compared with those values in subjects with normal cognitive function (score for Mini-Mental State > or = 21, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Cerebrospinal fluid edema associated with shunt obstruction.

The authors report four hydrocephalic children with cerebrospinal fluid (CSF) edema extending along the ventricular catheter of an obstructed CSF shunt. Three of the patients exhibited massive CSF edema along the ventricular catheter, yet they manifested neither ventricular enlargement nor apparent periventricular CSF edema despite increased intraventricular pressure. These findings suggested ventricular tautness. The remaining patient, who had dilated ventricles with periventricular CSF edema, displayed CSF edema in a limited area along the ventricular catheter. Replacement of the obstructed peritoneal catheter of the shunt resulted in rapid improvement of the edema in all patients. In the three patients with massive CSF edema, however, a small lesion remained in the subcortical white matter along the ventricular catheter as demonstrated by computerized tomography and/or magnetic resonance imaging 3 to 5 years after shunt revision. It is concluded that shunt obstruction may result in massive CSF edema along the ventricular catheter in hydrocephalic children who have ventricular tautness after installation of the shunt causing irreversible although usually asymptomatic damage to the affected area of the brain.

Adult↗
PubMed1994

[Induction of anti-cancer cells and systemic immune response in hepatocellular carcinoma by OK-432].

We examined whether anti-cancer cells are induced in vivo in hepatocellular carcinoma (HCC) by OK-432. Ten patients with HCC were randomly divided into two groups. The group I patient (n = 5) served as the control. In group II (n = 5), OK-432 was preoperatively administered via the hepatic artery. Tumor infiltrating lymphocytes (TILs) were collected from resected tumors. Cytotoxicity of TILs against K562 cells and Raji cells was studied with phenotypic analysis by flow cytometry. Freshly isolated TILs, whether or not treated with OK-432, showed low cytotoxicity. When TILs were co-cultured with recombinant interleukin-2 (rIL-2), the cytotoxicity was significantly activated in the OK-432 treated group, whereas untreated TILs showed no activation. The natural killer (NK) activity and the lymphokine-activated killer (LAK) activity were depressed in group I after hepatic resection, but patients in group II had no depression. Our data indicate that LAK precursor cells are induced in TILs and the prevention of post-operative immune suppression is made possible by OK-432.

Carcinoma, Hepatocellular↗