Biomedical subjects

S Baba

Publications and source records attributed to S Baba.

At least 217 records · Page 12Linked to original sources

PubMed1997

Determination of [D-Ala2,D-Leu5]enkephalin and the metabolites containing C-terminal D-leucine by high-performance liquid chromatography.

A high-performance liquid chromatographic procedure has been developed for the determination of [D-Ala2,D-Leu5]enkephalin (DADLE) and the fragments containing D-leucine in rat blood. The procedure was applied to the determination of blood levels of [3H-D-Leu5]DADLE and the C-terminal fragments after intravenous administration of [3H-D-Leu5]DADLE to a rat. Unlabelled DADLE and the C-terminal fragments were spiked as carriers to rat blood samples and the blood samples were extracted with 1% trifluoroacetic acid in methanol. The recoveries from rat blood were quantitative for all compounds. DADLE and the C-terminal four fragments were well separated on a reversed-phase column with gradient elution using a mobile phase composed of 0.14% HClO4 and acetonitrile.

Animals↗

PubMed1997

Mass spectrometric gene diagnosis of one-base substitution from polymerase chain reaction amplified human DNA.

One-base substitution has been detected on the polymerase chain reaction (PCR) products amplified from human mutated DNA for the first time by using mass spectrometry. PCR fragments of 52 base pairs were produced on a collagen gene of an osteogenesis imperfecta patient's heterozygous DNAs. The products were digested with EcoRI restriction enzyme to liberate 3'-end adducts and purified by phenol + chloroform extraction, ammonium acetate addition and ethanol precipitation to remove sodium ions from the phosphoric acid backbone of the DNAs. Purified products were examined using an electrospray ionization mass spectrometer. Mass spectra showed four groups of fragment peaks with the expected molecular masses, which originate from the sense and antisense strands of the heterozygous DNAs.

Base Sequence↗

PubMed1997

Immunohistochemical studies on endothelial cell phenotype in hepatocellular carcinoma.

To examine the phenotype of the sinusoidal endothelial cells (SECs) surrounding tumor cells and the process of capillarization in hepatocellular carcinoma (HCC), 51 primary HCCs, 4 adrenal metastases, and 3 portal tumor thrombi were immunohistochemically stained with monoclonal antibodies (MAbs) for CD4, CD14 (lipopolysaccharide-binding protein complex receptors), and CD32 (Fc gamma receptor II), which are specifically found on the SECs in normal liver, but not on ordinary vascular endothelial cells (ECs). Immunostaining was also performed for CD36 (thrombospondin receptors), EN4 antigen (Ag) (a pan-vascular endothelial cell Ag), PAL-E Ag (a venous and capillary EC Ag), factor VIII-related Ag (FVIIIRAg), and laminin. MAb 25F9, which identifies macrophages, was simultaneously used with the other MAbs to distinguish macrophages from SECs in HCCs (HCC SECs). CD4, CD14, and/or CD32 were found on HCC SECs only in 12 well-differentiated primary HCCs showing a thin trabecular or pseudoglandular tumor cell arrangement. These 12 tumors were smaller than those without CD4-, CD14-, and/or CD32-positive SECs (P < .05). Among them, 7, 5, and 11 tumors were negative or only partially positive for laminin, PAL-E Ag, and FVIIIRAg, respectively. Staining for laminin and PAL-E Ag showed an inverse relationship to the expression of CD4, CD14, and CD32 on HCC SECs and the tumor differentiation. In conclusion, the phenotypes of the SECs in early and well-differentiated HCC are thought to be similar to those of the SECs in normal liver. With progressing tumor dedifferentiation the HCC SECs lose the phenotypes peculiar to liver SECs and acquire the characteristics of capillary ECs, though both types of phenotypical change occur independently of each other.

Antigens, CD↗

PubMed1997

Pancreatic damage resulting from temporary portal triad interruption during partial hepatectomy: protective effect of a prostaglandin I2 analogue.

BACKGROUND: Hyperamylasemia often occurs after hepatectomy, but the detailed mechanism of this phenomenon remains unclear. This study was designed to examine the influence on the pancreas and other organs of temporary portal triad interruption during hepatectomy and to evaluate the protective effect of a prostaglandin I2 analogue. METHODS: Sprague-Dawley rats were intravenously administered normal saline (NS group) or a prostaglandin I2 analogue (PG group) and underwent 70% hepatectomy with temporary portal triad interruption. The 7-day survival rate and the levels of plasma liver enzymes, portal pancreatic enzymes, and endotoxin were determined. Intestinal permeability was evaluated from the portal blood concentration of fluorescein isothiocyanate-labeled dextran administered into the small intestine. The liver, pancreas, small intestine, and lung were examined histologically. Apoptosis in the pancreas was observed by the terminal transferase-mediated dUTP-biotin nick end labeling method. RESULTS: The survival rate of the NS group was 50%, whereas that of the PG group was significantly higher at 100% (P < 0.05). Plasma liver enzymes increased in both groups and showed no significant difference. Portal amylase and lipase levels were significantly lower in the PG group than in the NS group at 12 and 24 h after hepatectomy. Tissue damage in the pancreas and other organs was observed histologically along with the elevation of pancreatic enzymes. Although there were no significant differences between the two groups on hematoxylin and eosin staining, apoptotic acinar cells were only seen in the NS group. The portal endotoxin level (at 3 and 6 h after hepatectomy) and small intestinal permeability (at 1 and 3 h after hepatectomy) were significantly lower in the PG group compared to the NS group. CONCLUSIONS: Temporary portal triad interruption induced hyperamylasemia, congestive damage to the pancreas, and portal endotoxemia due to increased small intestinal permeability. A prostaglandin I2 analogue was able to protect the pancreas and small intestine from such damage.

Alanine Transaminase↗

PubMed1997

Hereditary nonpolyposis colorectal cancer: an update.

UNLABELLED: Sporadic cancer develops approximately at 65 years of age. Epidemiologic data suggest that dietary factors probably are the most influential in colorectal carcinogenesis. In contrast, individuals who have relatives with colorectal neoplasia have an increased risk of these tumors themselves, which will appear earlier in life. The actual incidence of hereditary colorectal cancer is unknown. However, the incidence is much higher compared with well-known hereditary colorectal diseases, such as familial adenomatous polyposis. OBJECTIVE: An overview of the recent progress in the field of both clinical and basic research on hereditary colorectal cancer must be made. MATERIALS AND METHODS: Twenty-two family pedigrees were analyzed at Hamamatsu University School of Medicine, including the largest family pedigree in Japan, which contained 24 cases of colorectal cancer occurring over five generations. In 1995, when the International Symposium on Hereditary Cancer was held in Hamamatsu, 4,109 family pedigrees were investigated and analyzed, including 394 cases in 109 family pedigrees that met the Amsterdam Minimum Criteria. Information was collected by sending questionnaires to major hospitals in Japan. Basic updated data presented at the eighth and ninth International Collaborative Group on Hereditary Colorectal Cancer were also quoted. RESULTS AND CONCLUSIONS: Because of the discovery of mismatch repair genes as that responsible for hereditary nonpolyposis colorectal cancer, modification of the Amsterdam Criteria is necessary. Replication error, as a mutator phenotype of mismatch repair genes, is a useful predictor of second primary malignancies. Surveillance or prophylactic surgery is still a controversial issue.

Colorectal Neoplasms, Hereditary Nonpolyposis↗

PubMed1997

Adenoma of the common human bile duct in Gardner's syndrome may cause relapsing acute pancreatitis.

Familial adenomatous polyposis of the colon, or Gardner's syndrome, is often accompanied by adenomas of the stomach and duodenum. We experienced a rare case of Gardner's syndrome, with adenomas of the common bile duct, in a patient who presented with relapsing acute pancreatitis. Our findings indicate that adenoma in the common bile duct or pancreatic duct should be considered as a possible etiology when patients with familial polyposis or Gardner's syndrome present with pancreatitis, particularly relapsing acute pancreatitis.

Adenoma↗

PubMed1997

Recent advances in molecular genetics of colorectal cancer.

Advances in molecular biology have identified two important genes responsible for the hereditary colorectal cancers familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer. They are the APC gene and mismatch repair genes. The role of these genes in colorectal carcinogenesis has been studied intensively. The adenoma-carcinoma sequence was initially proposed by Vogelstein, and the multistep carcinogenesis theory is now well accepted. The various functions of the APC gene have been elucidated. APC genes are considered to play a role in shedding of the epithelial cells into the lumen. The mechanism behind formation of a unicryptal adenoma is now better understood. Adenoma formation is a monoclonal event with two hits of the APCgene. There is no zonal extension of the proliferative zone in the background colonic mucosa of FAP patients. In addition to the adenoma-carcinoma sequence, there seem to be various carcinogenetic pathways in the development of colorectal cancer. A depressed type of early cancer was recently found by the use of magnifying endoscopy. The incidence of K-ras mutation was extremely low in this group of early cancers. Some of the minute cancers show the p53mutation before the occurrence of APC mutation. Cancers of microsatellite mutator phenotype show exaggerated genomic instability at simple repeat sequences, such as TGFbetaRII. These genes may play a suppressor role in a p53 independent pathway of colorectal carcinogenesis. We are now in an exciting era of this progressing field of science. This genetic information may be more widely applicable clinically in the near future (e.g., for presymptomatic diagnosis, selection of patients for the most appropriate treatments, and assessment of malignant potential).

Adenomatous Polyposis Coli↗

PubMed1997

Resection of liver metastases of colorectal carcinoma.

Hepatic metastasis of colorectal cancer is a life-threatening prognostic factor. The present review revealed that hepatic resection is the best treatment modality, although the overall survival rate after hepatectomy for metastatic colorectal cancer is still low (20-40%). Various prognostic factors analyzed by many authors are controversial. The number of hepatic metastases and the surgical margin were the most important prognostic factors, as seen in 10 papers previously reported including our data. A clear surgical margin is achievable, but the prognosis of patients with four or more metastatic nodules in the liver remains poor. Repeat hepatectomy is also evaluated and is believed by many surgeons to have acceptable mortality. It improved survival to a certain extent. Analysis of the biologic characteristics of primary and metastatic tumors is extremely important and is urgently indicated.

Clinical Trials as Topic↗

PubMed1997

Disordered migration and loss of virus-infected neuronal cells in developing mouse brains infected with murine cytomegalovirus.

Microcephaly is the most prominent symptom of the developmental brain abnormalities induced by congenital cytomegalovirus (CMV) infection. To investigate the effect of CMV infection on neuronal migration in developing brains, mouse embryos on one side of uteri received, on day 15.5 of gestation (E15.5), an injection of murine CMV (MCMV) into the cerebral ventricles, and the embryos on the other side of the uteri were injected with minimum essential medium (MEM). Labeling with 5-bromo-2-deoxyuridine (BrdU) was accomplished by intraperitoneal injection of BrdU 6 h later. Disturbance of the neuronal migration and loss of neurons were observed postnatally in the brains of MCMV-infected mice, which were identified by immunohistochemical staining of viral antigen. Double staining of BrdU-labeled and viral antigen-positive cells in brains on the 7th postnatal day showed that the migration of BrdU-single-labeled cells, mainly localized in cerebral layers II-III, mostly preceded that of the viral antigen-positive cells. However, about 7.5% of the cells observed were double-labeled, especially in the layers III-IV, and a few double-stained cells were markedly disturbed in migration. In the brains of offspring labeled with BrdU 72 h after infection with MCMV on E15.5, most of the double-stained cells were seen around the ventricular and subventricular zones. These findings suggest that a disturbance of neuronal migration in addition to neuronal loss may play a crucial role in the development of microcephaly in congenital CMV infection in humans.

Animals↗

PubMed1997

Direct hepatic vein anastomosis during hepatectomy for colorectal liver metastases.

BACKGROUND: When the right and middle hepatic veins (RHV and MHV) and all the short hepatic veins are removed during resection of segments (S) 7 and 8 and part of S 5 and 6 including the caudate lobe, the remainder of S 5 and 6 shows congestion, so restoration of liver function may be delayed. METHODS: In 5 patients with hepatic metastases of colorectal carcinoma, which were in the region circumscribed by the RHV, MHV, and inferior vena cava, direct hepatic vein anastomosis was performed during hepatectomy. RESULTS: Hepatic vein reconstruction took 17 to 30 minutes to complete. All 5 patients had an uneventful postoperative course, and the anastomosis was patent at 1 month after operation. One patient died of recurrent carcinoma 6 months after operation. Four have remained alive and disease free for 12, 24, 40, and 61 months. CONCLUSION: Direct hepatic vein anastomosis is an option, which should be adopted in hepatectomy, especially in patients with carcinoma invading the major hepatic veins and short hepatic veins.

Aged↗

PubMed1997

A posterior lumbar approach for retroperitoneoscopic adrenalectomy: assessment of surgical efficacy.

OBJECTIVES: To compare the efficacy of retroperitoneoscopic adrenalectomy by a posterior lumbar approach (RPA) with that obtained by a transperitoneal anterior approach (TAA) or retroperitoneal lateral flank approach (RLA). METHODS: Fifty-one patients underwent endoscopic adrenalectomy by three approaches, including laparoscopic adrenalectomy by TAA in 33, retroperitoneoscopic adrenalectomy by RLA in 5, and retroperitoneoscopic adrenalectomy by RPA in 13. RESULTS: The average adrenal tumor size was 27 mm (range 8 to 65). The average number of trocars required for RPA was 3.2 which was significantly less than that for TAA and for RLA (4.2 and 4.1, respectively). The conversion rate to open surgery was 9.1% by TAA, 0% by RLA, and 7.7% by RPA. The average operating time for TAA was 252 minutes, which was significantly shortened to 194 minutes by RLA and 142 minutes by RPA (P < 0.02). The average blood loss was 101 mL for TAA and was negligible by RLA and RPA (22 and 32 mL. respectively). CONCLUSIONS: RPA allowed direct access to the main adrenal vascular supply before the gland was greatly manipulated. Endoscopic adrenalectomy by TAA or even by RLA required extra ports for retraction of liver, spleen, vena cava, or adrenal gland, with higher chance of vein avulsion. RPA was technically feasible and most effective for retroperitoneoscopic adrenalectomy in regard to the simplicity of vascular control. The operating time, perioperative morbidity, and cost were reduced with this approach.

Adrenal Gland Neoplasms↗

PubMed1997

Beta-ray photography of lyophilized animal sections.

A new photographic method that images the density distribution of lyophilized animal sections approximately 50 microns in thickness is described. The new method involves sandwiching the animal section between a radiation sensor and a 147Pm planar radiation source. Either conventional photographic film or an imaging plate for radioluminography can be used as the sensor. The method described herein will find promising applications in whole body autoradiography as well as in the study of osteoporosis in experimental animals.

Animals↗

PubMed1997

High-intensity focused ultrasound energy for benign prostatic hyperplasia: clinical response at 6 months to treatment using Sonablate 200.

We evaluated the safety and efficacy of high-intensity focused ultrasound (HIFU) using a modified Sonablate 200 and compared the clinical response with that of the prototype Sonablate at 6 months after treatment. Since 1995, 35 patients ages 66 +/- 7 years underwent HIFU with the Sonablate 200 for symptomatic benign prostatic hyperplasia (BPH) under low spinal anesthesia. The estimated prostatic volume was 40.4 +/- 4.8 cc before treatment. A silicon-coated 16F latex catheter was indwelling during determination of the therapy zone and treatment so that critical tissue at the midline was thoroughly treated. Twenty-two patients were analyzed with complete 6-month follow-up data. Side effects were transient urinary retention in four of these patients, hematuria in five, and hematospermia in eight. Peak urinary flow rate increased from 7.4 +/- 4.0 mL/sec to 11.4 +/- 4.0 mL/sec (P < 0.001) (54% increase). During the same period, the mean International Prostatic Symptom Score decreased from 20.4 +/- 7.1 to 9.0 +/- 7.5 (P < 0.001) (56% decrease). Quality of Life score improved from 5.4 +/- 0.6 to 2.4 +/- 1.3 (P < 0.001). Magnetic resonance imaging by means of an endorectal surface coil revealed significant coagulative necrosis areas in the periurethral gland at 1 month on T2-weighted images. These data demonstrate that HIFU for BPH using the Sonablate 200 produced a better clinical response than the prototype Sonablate and is expected to provide long-term durability of the response.

Aged↗

PubMed1997

Regression of metastatic liver tumors in rats treated with angiogenesis inhibitor TNP-470: occurrence of apoptosis and necrosis.

To clarify the mechanism of the reduction of metastatic liver tumors in rats treated with angiogenesis inhibitor TNP-470, the death of tumor cells was examined pathologically and ultrastructurally. Liver metastases were developed by intravenous injection of AH-130 cells. TNP-470 was given subcutaneously after tumor cell injection. Alterations in the size and number of metastatic tumors were examined at various time points, in association with the analysis of cell death pattern. The metastatic nodules were divided into 4 groups according to the morphological patterns of cell death; no cell death, scattered apoptosis, central necrosis, and diffuse necrosis. The number and size of the metastatic tumors at 2 weeks in untreated rats were larger than those in treated rats. The number of tumors in untreated rats decreased, but the tumor size increased. All rats treated with TNP-470 were alive and free from tumors after 4 weeks, whereas all the untreated rats died of liver metastases. The percentages of the tumors with necrosis in untreated rats (61.2% at 2 weeks and 100% at 4 weeks) were significantly higher than that (31.8% at 2 weeks) in treated rats (P < 0.01). The percentage of the tumors containing apoptotic cells in treated rats was significantly higher than that in untreated rats (54.5% vs. 30.6%; P < 0.05). The growth of metastatic tumors without treatment might be faster than the growth of vessels in untreated tumors, resulting in central necrosis due to ischemia. On the other hand, the reduction of metastatic liver tumors treated with TNP-470 might be caused by inhibition of angiogenesis, providing a weak ischemic stimulus which triggers apoptosis, rather than by a direct cytotoxic effect on tumor cells, because previous in vivo experiments demonstrated that TNP-470 affected endothelial cells but not tumor cells.

Animals↗

PubMed1997

Differential diagnosis of primary benign and malignant retroperitoneal tumors.

BACKGROUND: Clinical differential diagnosis between malignant and benign tumors is important in order to select a therapeutic strategy for a primary retroperitoneal tumor. METHODS: The clinical findings and radiological features of 25 patients with primary retroperitoneal tumors were retrospectively evaluated to find those signs that might contribute to the preoperative distinction between benign and malignant tumors. RESULTS: Of 25 primary retroperitoneal tumors, 15 were benign. This may reflect the increased number of incidentally found small benign tumors. There were significant associations between the presence of symptoms and malignancy (P < 0.05), between irregular margins on imaging and malignancy (P < 0.05) and between the absence of calcification and malignancy (P < 0.05). Malignant tumors were significantly larger than benign tumors (11.45 +/- 1.90 cm vs. 5.31 +/- 0.43 cm). A retroperitoneal tumor scoring system was developed to distinguish primary retroperitoneal benign tumors from their malignant counterparts based on the: 1) maximum diameter equal to or larger than 5.5 cm, 2) presence of symptoms, 3) absence of calcification, 4) presence of irregular margins, and 5) presence of cystic degeneration or necrosis. A significant correlation was found between the incidence of malignant tumors and the total retroperitoneal tumor score (P < 0.05). CONCLUSION: This study suggests that the size of tumor, the presence of symptoms, irregular margins, and the absence of calcification may be valuable predictors of primary retroperitoneal malignant tumor.

Adolescent↗

PubMed1997

Evaluation of liver function by co-administration methodology using 13C-labelled benzoic acid and hippuric acid coupled with nuclear magnetic resonance spectroscopy.

The amount of hippuric acid synthesized and excreted in the urine after benzoic acid loading (hippuric acid test) is a useful index of liver function. However, the hippuric acid test gives erroneous results in the event of failure of renal excretory function. A new stable isotope co-administration methodology using nuclear magnetic resonance (NMR) spectroscopy has been developed to overcome this defect. [7-(13)C]Benzoic acid and [glycine carbonyl-13C]hippuric acid ([gly-13C]hippuric acid), each 0.4-0.6 mmol kg(-1) were simultaneously administered intravenously as probes to normal or liver-injured rats and the urine was analysed by 100 MHz 13C NMR spectroscopy. Consequently, urinary excretion of [7-(13)C]hippuric acid formed from [7-(13)C]benzoic acid and [gly-13C]hippuric acid was successfully traced with very simple and convenient procedures. The urinary excretion of [7-(13)C]hippuric acid indicated the combined functions of hippuric acid synthesis and renal excretion, whereas that of [gly-13C]hippuric acid was indicative of renal excretion of hippuric acid only. The heights of resonances for C7 of [7-(13)C]hippuric acid and the glycine carbonyl carbon of [gly-13C]hippuric acid were used to calculate the concentrations of labelled hippuric acids. [7-(13)C]Hippuric acid was excreted more slowly than [gly-13C]hippuric acid by both normal and liver-injured rats. The liver-injured rats excreted the labelled hippuric acids more slowly than the normal rats. The kinetic parameters were computed for the individual rats on the basis of Michaelis-Menten elimination for benzoic acid and first-order elimination for hippuric acid. The maximum rates of metabolism (Vmax) (4.8-5.8 micromol min(-1) kg(-1)) and the renal elimination rate constants of hippuric acid (Kre) (0.010-0.021 min(-1)) in the liver-injured rats were lower than those (Vmax 6.7-11.8 micromol min(-1) kg(-1); Kre 0.026-0.045 min(-1)) in the normal rats. These results have demonstrated that liver function can be evaluated from the Vmax value even though the renal function of hippuric acid excretion (Kre) is impaired. Thus the co-administration methodology is feasible and can remove the defect of the previous hippuric acid test. These results could form the basis for a more convenient and reliable hippuric acid test in man.

Animals↗

PubMed1997

Differential effects of tumor necrosis factor-alpha and -beta on rat ventromedial hypothalamic neurons in vitro.

The effects of tumor necrosis factor (TNF)-alpha and -beta on the spontaneous firing rate of ventromedial hypothalamic (VMH) neurons were examined in rat brain slice preparations. Of 89 neurons, 36 (40%) showed a decrease in the firing rate to -78.2 +/- 4.0% (n = 36, mean +/- SE) of the preapplication level after a bath application of 20 ng/ml (approximately 1.2 nM) of TNF-alpha. This response to TNF-alpha still persisted in a low-Ca2+, high-Mg2+ medium. Six (7%) of the 89 neurons were excited and 47 (53%) were unaffected by TNF-alpha. The inhibitory responses induced by TNF-alpha were abolished in a solution that contained sodium salicylate (1.9 x 10(-8)M). In contrast, TNF-beta at a dose of 20 ng/ml (approximately 1.1 nM) increased the firing rate to +39.2 +/- 6.5% (n = 11) of the preapplication level in 11 (24.5%) of 45 VMH neurons. Two of the 45 neurons (4.5%) were inhibited and 32 (71%) were unaffected by TNF-beta. The threshold concentration of TNF-alpha to alter the VMH neuron activity was lower than that of TNF-beta. Heat-inactivated TNFs were without effect. These findings suggest that TNF-alpha and -beta act as neuromodulators in the VMH, at least partly through prostaglandin synthesis, and differentially modulate the VMH neuron activity.

Animals↗

PubMed1997

p53 overexpression and proliferative activity do not correlate with lymph node metastasis in early gastric cancer.

We investigated p53 overexpression and the proliferative activity of the primary lesion as well as the clinicopathological features of 75 patients with gastric cancer invading the submucosa (sm cancer), of whom 14 (18.7%) had lymph node metastasis. Among the clinicopathologic features studied, only lymphatic invasion by the primary tumor was related to lymph node metastasis. There was no relationship between immunohistochemical staining for p53 protein or Ki-67 and lymph node metastasis. The p53-positive rate was 35.7 and 57.1% in patients with and without metastasis, respectively, while the mean Ki-67 labeling index was 38.9 and 38.1%, respectively. Our results suggest that p53 mutation or the proliferative activity of sm cancer do not influence lymph node metastasis, even though p53 mutation may enhance the proliferative activity and metastatic potential of advanced gastric cancer.

Adenocarcinoma↗