Biomedical subjects

Y Nio

Publications and source records attributed to Y Nio.

At least 55 records · Page 3Linked to original sources

PubMed1995

Non-insulin-dependent diabetes mellitus complicated with idiopathic hypoparathyroidism.

We report a case of non-insulin-dependent diabetes mellitus (NIDDM) complicated with idiopathic hypoparathyroidism. A 74-year-old male was hospitalized because of diplopia. He was revealed to have NIDDM. The levels of serum Ca and intact-PTH were 6.3 mg/dl and < 5 pg/ml, respectively. Brain computed tomography revealed abnormal calcification in the cerebral basal ganglia and the cerebellum. After recovery from hypocalcemia, the endogenous insulin secretion was normalized. It is suggested that the pathogenesis of NIDDM in this patient may have been related to an insulin secretory defect as a result of hypocalcemia in addition to the hereditary risk.

Aged↗

PubMed1994

Anticancer chemosensitivity profile of freshly separated human pancreatic cancer cells assessed by DNA synthesis inhibition assay.

The chemosensitivity of 49 freshly separated human pancreatic cancers to seven kinds of anticancer agents were assessed by a DNA synthesis (3H-thymidine incorporation) inhibition assay. DNA synthesis is higher in involved lymph nodes (n = 7), malignant effusion (n = 15), liver metastasis (n = 7), primary cancer (n = 15), and skin metastasis (n = 5). Chemosensitivity assay demonstrates that etoposide, 4-epirubicin, carboquone, and 5-fluorouracil are more effective than cisplatin, mitomycin-C, and Adriamycin. In general, metastatic lesions of pancreatic cancer tend to show higher chemosensitivity than primary lesions. Pathological analysis demonstrates that small primary pancreatic cancers tend to be more responsive than large primary cancers, and primary pancreatic cancers with no regional lymph node involvement also tend to be more responsive than those with nodal involvement. No significant differences are seen in terms of tumor spread, vascular involvement, sex of patient, and histological type. When chemosensitivity assay is not available, the results of the present study may be beneficial to choose the regimens.

Adult↗

PubMed1994

Enhanced antitumor effect of Bacillus Calmette-Guérin in combination with fibrinogen on urinary bladder tumor.

Although intravesical instillation of Bacillus Calmette-Guérin (BCG) is an established and effective therapy for superficial urinary bladder tumor (UBT), the current major problems are BCG-resistant UBT and recurrence after BCG therapy. The injection of BCG and fibrinogen could be expected to induce the formation of a fibrin mesh, which would trap BCG and and prolong its antitumor action. The present study has been designed to investigate whether fibrinogen has the ability to augment antitumor activity of BCG against UBT. A single injection of BCG/fibrinogen solution into the subcutaneous tissue of C3H/He mice was performed. Histopathological examination revealed prolonged accumulation of BCG and marked infiltration of inflammatory cells at the injected site, as compared with the injection of BCG or fibrinogen alone. When BCG was used in combination with gelatin sponge, prolonged BCG accumulation was also observed, but not many inflammatory cells were induced, as compared with injection of BCG/fibrinogen combination. When BCG/fibrinogen solution was injected into MBT-2 murine UBT transplanted into C3H/He mice, the formation of fibrin fibers, which trap BCG, was induced, and many inflammatory cells around the tumor were seen. A pronounced inhibitory effect on tumor growth and prolonged survival of tumor-bearing mice were achieved, as compared with the injection of BCG alone. Dead BCG/fibrinogen solution had a modest inhibitory effect on the tumor growth. This study suggests that combination treatment with BCG and exogenous fibrinogen may prolong accumulation of BCG by BCG by trapping BCG in fibrin meshwork, and may induce marked infiltration of inflammatory cells into tumor stroma, causing marked regression of the tumor. The possible clinical implications of the combined use of BCG and fibrinogen are discussed.

Administration, Intravesical↗

PubMed1994

Overcoming TNF-alpha and drug resistance of human renal cell carcinoma cells by treatment with pentoxifylline in combination with TNF-alpha or drugs: the role of TNF-alpha mRNA downregulation in tumor cell sensitization.

Previous studies have demonstrated that one of the possible mechanisms responsible for the resistance of tumor cells to tumor necrosis factor-alpha (TNF-alpha) is the expression of TNF-alpha mRNA and/or protein. Pentoxifylline (PTX) suppressed TNF-alpha gene transcription and downregulates the expression of TNF-alpha mRNA and the secretion of TNF-alpha protein in macrophages and monocytes. This study investigates whether PTX downregulates the expression of TNF-alpha mRNA and/or protein in renal cell carcinoma (RCC) cells and whether PTX enhances the sensitivity of TNF-alpha-resistant RCC cells to TNF-alpha. Further, we explored whether PTX enhances the sensitivity of RCC cells to agents other than TNF-alpha by downregulation of the expression of TNF-alpha mRNA and protein. The R4 human RCC cell line constitutively expressed TNF-alpha mRNA and protein and was resistant to TNF-alpha. When R4 cells were incubated with PTX, the level of TNF-alpha mRNA and protein was markedly reduced. Pentoxifylline and TNF-alpha together overcame the resistance of R4 cells to TNF-alpha. The R11 human RCC cell line did not constitutively express TNF-alpha mRNA or protein, and was resistant to TNF-alpha. The expression of TNF-alpha mRNA in R11 cells, but not the production of TNF-alpha protein, was induced by TNF-alpha. When PTX was used in combination with TNF-alpha, the level of TNF-alpha mRNA induced by TNF-alpha was markedly reduced. The combination of PTX and TNF-alpha overcame the resistance of R11 cells to TNF-alpha. Pentoxifylline also enhanced the sensitivity of R4 cells to interferon-alpha. Pentoxifylline and anti-TNF-alpha monoclonal antibody augmented the sensitivity of R4 cells to cis-diamminedichloroplatinum (II) (CDDP). This study demonstrated that PTX, in combination with TNF-alpha, IFN-alpha or CDDP, overcame the drug resistance to RCC cells and that downregulation of TNF-alpha mRNA by PTX may be related to the cytotoxicity enhanced by the combination. The implications of these findings for clinical therapy are discussed.

Carcinoma, Renal Cell↗

PubMed1994

Differential gene expression and regulation of angiotensin II receptor subtypes in rat cardiac fibroblasts and cardiomyocytes in culture.

Although both rat cardiac nonmyocytes (mostly fibroblasts) and cardiomyocytes have a functional angiotensin II (AngII) receptor, the regulation mechanism of its subtype expression in the rat heart remains unknown. In this study, by using a binding assay and a competitive reverse-transcriptase polymerase chain reaction, we examined the regulation of AngII types 1a and 1b (AT1a-R and AT1b-R) and type 2 receptor (AT2-R) expression in embryonal day 19 (E19) and neonatal (1-d) rat cardiac fibroblasts and cardiomyocytes. The number of AT2-R in E19 fibroblasts was dramatically decreased (from 305 to 41 fmol/mg protein) in 1-d fibroblasts, whereas that of AT1-R and the mRNA levels remained unchanged. The ratio of AT1a-R to AT1b-R mRNA in both E19 and 1-d fibroblasts was 9:1. The number of AT2-R in E19 cardiomyocytes was also significantly decreased (from 178 to 87 fmol/mg protein) in 1-d cardiomyocytes, whereas the magnitude was less prominent compared with that in fibroblasts. AT1-R expression remained unaltered in E19 and 1-d cardiomyocytes. In E19 and 1-d cardiomyocytes, the AT1b-R mRNA level was 1.5-fold higher than that of AT1a-R mRNA. Dexamethasone induced significant increases in AT1a-R mRNA (2.1-fold) and numbers (1.8-fold) without changing the affinity, whereas neither AT1b-R mRNA nor the number of AT2-R was affected by dexamethasone. The AT1a-R gene transcription rate, determined by means of a nuclear run-off assay, was increased (2-fold) by dexamethasone. The half-life of AT1a-R mRNA (18 h) was unchanged by dexamethasone. These data indicate that AngII receptor subtype expression in the rat heart is regulated in a cell- and subtype-specific manner.

Angiotensin II↗

PubMed1994

cAMP responsive element-mediated regulation of the gene transcription of the alpha 1B adrenergic receptor by thyrotropin.

To elucidate the molecular mechanism of the stimulatory effect of thyrotropin on the gene regulation of alpha 1B adrenergic receptor in functioning rat thyroid (FRTL-5) cells, we established a competitive reverse-transcriptase (RT) polymerase chain reaction (PCR) and nuclear run-off assay to quantify changes in mRNA levels and transcription rates. A binding assay showed that FRTL-5 cells predominantly expressed alpha 1B adrenergic receptor and that thyrotropin increased its expression sevenfold. By means of RT-PCR, we found that thyrotropin induced an 11-fold increase in alpha 1B receptor mRNA abundance. The nuclear run-off assay demonstrated that thyrotropin caused a ninefold increase at the gene transcriptional level, which occurred in the presence of the protein synthesis inhibitor cycloheximide. The half-life of the alpha 1B receptor mRNA in cells incubated with thyrotropin for 1 h increased 1.5-fold but returned to the original value after 12 h. Dibutyryl cAMP and forskolin mimicked the stimulatory effects of thyrotropin on the gene transcriptional level. The 5'-flanking region of the rat alpha 1B receptor gene contained a putative cAMP responsive element (CRE) at nucleotide -438 relative to the translation start site. The promoter analysis using the reporter gene indicated that the CRE motif confers the cAMP sensitivity to the transcription of the rat alpha 1B receptor gene. These results demonstrated that a CRE-mediated mechanism is involved in the transcriptional regulation of the alpha 1B receptor gene by thyrotropin without requiring new protein synthesis.

Animals↗

PubMed1993

Loxiglumide (CR1505), a cholecystokinin antagonist, specifically inhibits the growth of human pancreatic cancer lines xenografted into nude mice.

BACKGROUND: Cholecystokinin is thought to be an important factor regulating the growth of human pancreatic cancers. The study was designed to evaluate the effects of the cholecystokinin antagonist loxiglumide (CR1505) on the growth of human pancreatic cancer. METHODS: Human gastrointestinal cancer xenografted tumors (one esophageal, one gastric, two colorectal, two biliary tract, and two pancreatic cancers) were transplanted into nude mice. The mice were given CR1505 at 250 mg/kg daily for 14 days, either subcutaneously or intragastrically, and the tumor volumes before and after treatment were compared. In vitro effects of CR1505 were assessed by measuring the DNA synthesis (3H-thymidine incorporation). RESULTS: CR1505 inhibited the growth of the two pancreatic cancer lines but did not inhibit the growth of the other lines. CR1505 also inhibited in vitro DNA synthesis in the two pancreatic cancer lines at lower concentrations than in the other lines. This pancreatic cancer-specific inhibitory effect of CR1505 was retarded by exogenously administered cholecystokinin in one pancreatic cancer line but was augmented in the other line. The effect of CR1505 was inhibited by oral administration of the trypsin-inhibitor camostate (FOY-305) in both pancreatic cancer lines. CONCLUSIONS: These results suggest that CR1505 may specifically inhibit the growth of human pancreatic cancers and may be suitable for clinical study. However, its antiproliferative effect may not necessarily be dependent on its cholecystokinin-antagonism but may be mediated through the proteolytic enzymes found in the lysosomes of the pancreatic cancer cells.

Animals↗

PubMed1993

Enhanced susceptibility of cis-diamminedichloroplatinum-treated K562 cells to lysis by peripheral blood lymphocytes and lymphokine activated killer cells.

BACKGROUND: Previous studies have reported that cis-diamminedichloroplatinum (II) (CDDP) exhibits various immunomodulating activities. The current study investigates the effect of CDDP on the susceptibility of K562 cells to lysis by peripheral blood lymphocytes (PBL), natural killer (NK) cells, and lymphokine activated killer (LAK) cells. METHODS: Cytotoxicity was determined by the 51Cr release assay. RESULTS: Treatment of K562 cells with CDDP at 10 micrograms/ml or more for 3 hours or more enhanced their susceptibility to lysis by PBL. This CDDP-mediated enhancement of lysis was observed by PBL derived from healthy donors and from patients with urinary bladder tumor or with other malignant and nonmalignant urologic diseases. The CDDP-induced enhancement of K562 cell susceptibility to lysis by PBL also was observed when purified NK cells and LAK cells were used as effector cells. The CDDP analog, carboplatin, enhanced the susceptibility of K562 cells to lysis by PBL, but treatment with transdiamminedichloroplatinum (II) had no effect. Several experiments were done to investigate the mechanism of the enhanced susceptibility of CDDP-treated K562 cells to lysis by PBL. Treatment of K562 cells with CDDP had no effect on the expression of major histocompatibility complex (MHC) Class I, MHC Class II, neural cellular adhesion molecule, and leukocyte function antigen-1 on the tumor cells. The frequency of target cell conjugates to PBL was not changed by CDDP-treated K562 cells. Pretreatment of K562 cells with CDDP and lysosomotrophic agents (L-leucine-methyl-ester or chloroquine) abrogated their enhanced susceptibility to lysis by PBL. CDDP treatment of K562 cells did not augment their sensitivity to alpha-interferon, gamma-interferon, tumor necrosis factor alpha, or natural killer cytotoxic factor (NKCF). Treatment of effector cells with CDDP had no effect on their cytotoxic function. CONCLUSIONS: These results demonstrate that CDDP has a direct effect on the K562 target cells, rendering them more susceptible to lysis by PBL, NK cells, and LAK cells. In addition, the result suggest that CDDP-mediated enhancement of target cell lysis is not attributable to changes of surface membrane antigen expression or recruitment of precursor cells but to processing of CDDP by the cells. The possible mechanisms of the effect of CDDP on K562 cells and clinical implications are discussed.

Aged↗

PubMed1993

[Abdominal typhus and paratyphoid fever in 2 academic hospitals: 1984-1990].

A diagnosis of blood culture-positive typhoid (TF; n = 39) or paratyphoid (PTF; n = 17) fever was made in 56 patients admitted to two Dutch university hospitals in the period 1984-1990. The group of TF patients constituted 9% of the reported national total during those years. A retrospective analysis of available clinical, laboratory and epidemiological data was carried out. Without exception, infections were contracted during travel abroad, especially to India and Indonesia. The clinical features and the response to antimicrobial treatment of TF and PTF proved essentially the same. Fever, headache and anorexia were important symptoms; rose spots and splenomegaly were found in 18/38 and 10/39 with S. typhi respectively. Most patients had a normal white blood cell count; less than half of the patients had thrombocytopenia. A positive Widal-test was found in 15/24 patients with S. typhi. 18/39 patients with S. typhi had been vaccinated; 10 did not know. Amoxycillin was the preferred antimicrobial agent in 69% of cases. Median defervescence time was 5 days in TF and 4 days in PTF. Relapse occurred in 3 TF cases. The recurrence rate after amoxycillin treatment was 7.6%. Profuse intestinal bleeding (1x), septic shock (1x) and cholangitis plus ARDS (1x) were major complications, seen in TF patients only. All patients recovered fully. None of the isolated strains of S. typhi or S. paratyphi proved multiresistant. Surveillance data from the Dutch National Institute of Public Health and Environmental Protection suggest that multidrug-resistance of S. typhi is increasing, especially in strains imported from countries such as India and Pakistan.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗

PubMed1993

Inhibitory effects of a cholecystokinin antagonist, loxiglumide (CR-1505), on the growth of freshly separated and xenografted human pancreatic cancer.

The effects of cholecystokinin (CCK) and a CCK antagonist, loxiglumide (CR-1505), on four freshly separated and six xenografted human pancreatic cancers, were investigated. The level of DNA synthesis in only one of five tested pancreatic cancers was enhanced by CCK at concentrations of 0.01-10 nM, while in the other four cancers DNA synthesis was not affected. The levels of DNA, RNA, and protein synthesis (by 3H-thymidine, 3H-uridine, and 3H-leucine incorporation tests, respectively) in all the tested cancers were dose-dependently inhibited by loxiglumide at concentrations of 20-2000 microM, and the IC50 of loxiglumide for DNA synthesis in pancreatic cancers was 156 +/- 80 microM (means +/- SD). The in vivo effect of loxiglumide was assessed using a xenografted line (PC-HN) transplanted in nude mice. The in vivo 50% lethal dose of loxiglumide for nude mice was about 500 mg/kg. Death was caused by respiratory failure due to severe congestion of the lung after the administration of a large dose of loxiglumide. The growth of a PC-HN transplanted in the nude mice was significantly inhibited by subcutaneous loxiglumide at 250 mg/kg, twice a day for 28 days, which did not cause death. It is suggested that loxiglumide inhibits the in vivo and in vitro growth of human pancreatic cancer, perhaps independently of its action as a CCK antagonist, and this study also suggests that loxiglumide may be a new type of therapeutic agent to be used for the treatment of human pancreatic cancer.

Animals↗

PubMed1993

A phase II study of 5-fluorouracil, cisplatin, and 4'-epirubicin in the treatment of advanced solid cancers.

This phase II study was designed to assess the therapeutic potential of intensive course treatment with three anticancer agents: 50 mg of cisplatin on day 1, 40 mg/m2 of epirubicin on day 2, and 250 mg of 5-fluorouracil on days 2 through 5. Drug courses were repeated every 2 weeks and most patients received between 4 and 6 courses. Thirty-five patients with measurable advanced solid cancers entered the study. They consisted of 16 gastric, 5 colorectal, 4 gallbladder, 3 pancreatic, 3 lung, 2 esophageal, 1 uterine, and 1 ovarian cancers. Of the 35 patients, 29 were evaluated for therapeutic effect of the regimen, and the overall response rate was 31.0% (5 CR + 4 PR/29). A 33.3% rate of tumor regression, consisting of 2 complete responses (CR) and 3 partial responses (PR) out of 15 patients (2 CR + 3 PR/15), was seen for gastric cancers. For the other types of tumors the responses were achieved in 2 lung cancers (1 CR + 1 PR/3). 1 uterine cancer (1 CR/1), and 1 ovarian cancer (1 CR/1). The esophageal, colorectal, pancreatic, and gallbladder cancers were unresponsive to this regimen. Toxicities of the drug treatment were clinically tolerable and consisted of general malaise, nausea, vomiting, stomatitis, alopecia, and leucopenia. However, two patients died of uncontrollable metabolic acidosis after 1 and 2 courses, respectively. This intensive course treatment appears to promote the regression of gastric, lung, and gynecologic cancers.

Adult↗

PubMed1993

Comparison of survival curves of gastric cancer patients after surgery according to the UICC stage classification and the General Rules for Gastric Cancer Study by the Japanese Research Society for gastric cancer.

OBJECTIVE: This study compared the UICC classification with the General Rules for Gastric Cancer Study (GRGCS) of the Japanese Research Society by analyzing recent results of gastric cancer surgery in Japan. SUMMARY BACKGROUND DATA: The present UICC stage classification for gastric cancer was published in 1987 and the Japanese GRGCS were published in 1985. Both are based on the results of surveys conducted in the early 1970s. METHODS: The survival curves of 926 patients, who underwent gastric cancer surgery between 1982 and 1985 at Kyoto University Hospital and its 31 associated hospitals, were analyzed according to the UICC classification and the GRGCS using SAS computer software. RESULTS: There was no difference in survival rate between UICC stages IA and IB. GRGCS stage III was found to include UICC stages II, IIIA, and IIIB, and GRGCS stage IV included UICC stages IIIA, IIIB, and IV, with significantly different survival rates. In contrast, each UICC stage included different GRGCS stages with no significant differences in survival rates. The survival rate of stage IV patients of both classifications who underwent gastrectomy was significantly higher than that of stage IV patients receiving bypass or exploratory surgeries. CONCLUSIONS: The UICC classification is better than the GRGCS for classifying gastric cancer in Japan. However, UICC stage I does not need to be subdivided into stages IA and IB, and stage IV should be further subdivided into stages IVA and IVB according to the surgery performed: IVA, gastrectomy, and IVB, bypass or exploratory surgery.

Humans↗

PubMed1992

The streptococcal preparation OK-432 specifically augments the susceptibility of human urinary bladder tumor cells to autologous peripheral blood lymphocytes.

The streptococcal preparation OK-432 was tested for its ability to enhance the susceptibility of fresh urinary bladder tumor (UBT) cells to autologous peripheral blood lymphocytes (PBL) in patients with UBT. PBL treated with OK-432 at 0.1 Klinishe Einheit (KE)/ml for 18 hours killed the human T24-lined UBT cells and freshly separated autologous UBT cells more efficiently than untreated PBL. Treatment of K562 erythroleukemia cells with OK-432 at 0.1 KE/ml for 18 hours had no effect on their susceptibility to lysis by fresh PBL. In contrast, treatment of T24 and fresh autologous UBT cells with OK-432 resulted in an enhancement of their susceptibility to PBL. The susceptibility of autologous UBT cells to both large granular lymphocytes (LGL) and T-lymphocytes was also enhanced by treatment of tumor cells with OK-432. Binding of PBL to T24 and fresh autologous UBT cells was also augmented by treatment of the tumor cells with OK-432. The frequency of binding of OK-432 to fresh UBT cells was positively correlated with the increased target sensitivity to autologous PBL. The inhibition of RNA synthesis in fresh UBT cells by OK-432 was also associated with the elevated susceptibility to autologous PBL. These results indicate that OK-432 activates the autologous tumor killing system through stimulation of effector cells and elevation of target susceptibility to effector cells in patients with UBT, and suggest that the OK-432-augmented target sensitivity to PBL may be oriented specifically to UBT cells and local immunotherapy with OK-432 may be remarkably beneficial in the treatment of UBT.

Adult↗

PubMed1992

Effect of short-termed pancreatico-biliary duct obstruction on lysosomal enzyme in rats: protective effect of a potent new protease inhibitor, E-3123.

To investigate the mechanism by which the pancreatic acinar cells are injured in animals with an obstructed common channel, we measured the amount of lysosomal enzymes and of amylase in the pancreatico-biliary juice in rats with pancreatico-biliary duct obstruction (PBDO). We tested the protective effect of a new potent synthetic protease inhibitor, E3123 (4-guanidinobenzoate methanesulfonate), on the exocrine pancreas in this model of PBDO and secretin infusion. Blockage of PBD for 4 hours and secretin (0.2 CU/kg.hr) infusion caused a significant rise in portal serum amylase and cathepsin B levels, pancreatic water content, and pancreatic amylase content, as well as redistribution of cathepsin B in acinar cells. These changes tended to continue for 12 hours after the removal of PBDO and disappeared at 24 hours. All the changes induced by PBDO with secretin infusion were no longer observed at 48 hours. The administration of 5 mg/kg.hr of E3123 during PBDO markedly attenuated all the parameters examined in this study. Thus, it had a significant protective effect on acinar cells in this model. E3123 in a dose of 2 mg/kg.hr had a partial, but significant, protective effect. These results indicate the possible usefulness of E3123 in the treatment of pancreatic duct obstructed pancreatitis.

Acute Disease↗

PubMed1992

Improved survival in mice with diet-induced pancreatitis treated with new potent protease inhibitor, E-3123 and a broad spectrum antibiotic, cefmetazole.

This study was designed to evaluate the infectious factor in the pathogenesis of acute pancreatitis and the effects of a combination therapy with a new potent protease inhibitor, E-3123, and a broad spectrum antibiotic cefmetazole (CMZ) in mice with CDE diet-induced severe acute pancreatitis. Combination therapy with E-3123 and CMZ showed significant protective effects against the high mortality rate, increased serum amylase and ascitic fluid amylase levels, pancreatic amylase and lysosomal enzyme content, plasma endotoxin levels, redistribution of lysosomal enzyme from the lysosomal to the zymogen fraction, lysosomal and mitochondrial fragility, and also improved the histological findings when compared with the E-3123 alone. These results suggest that infections factors play an important role in the development of severe acute pancreatitis and that protease inhibitors in combination with antibiotics may be clinically beneficial.

Acute Disease↗

PubMed1992

Protective effects of combined therapy with a protease inhibitor, ONO 3307, and a xanthine oxidase inhibitor, allopurinol on temporary ischaemic model of pancreatitis in rats.

The protective effect of a new potent protease inhibitor, ONO 3307, in combination with a xanthine oxidase inhibitor, allopurinol, was tested in pancreatico-biliary duct obstruction (PBDO) with temporary pancreatic ischemia in rats. After PBDO with ischemia, we observed hyperamylasemia, pancreatic edema, congestion of amylase and lysosomal enzyme cathepsin B as well as impaired output of amylase and cathepsin B into the pancreatic juice and a redistribution of lysosomal enzyme from the lysosomal fraction to the zymogen fraction. The administration of ONO 3307 plus allopurinol almost completely prevented the pancreatic injuries induced by PBDO with ischemia. These results indicate the important roles of temporary pancreatic ischemia in the pathogenesis of pancreatic damage and the usefulness of combination therapy with a new potent protease inhibitor and xanthine oxidase inhibitor in the protection against clinical acute pancreatitis.

Acute Disease↗

PubMed1992

Effects of bacillus Calmette-Guerin on cytotoxic activities of peripheral blood lymphocytes against human T24 lined and freshly isolated autologous urinary bladder transitional carcinoma cells in patients with urinary bladder cancer.

The effects of bacillus Calmette-Guerin (BCG) on the cytotoxic activities of peripheral blood lymphocytes against human T24 lined and freshly separated autologous urinary bladder transitional carcinoma cells in patients with urinary bladder cancer were analyzed in a 12-hour chromium 51 (51Cr) release assay. The results of this study indicate that BCG activates the tumor killing system through stimulation of effector cells and elevation of target cell susceptibility in patients with urinary bladder cancer, suggesting that BCG-augmented cytotoxicity may be oriented specifically to urinary bladder cancer cells. This could explain the remarkable clinical benefits of intravesical instillation of BCG against urinary bladder cancer.

Aged↗

PubMed1992

Metabolic bone disease following gastrectomy: assessment by dual energy X-ray absorptiometry.

Although disorders in bone metabolism have long been recognized as typical sequelae of gastrectomy, there has until now been no reliable method of providing precise assessment of bone mass, resulting in a variation of reported incidence. In this study, metabolic bone disease was evaluated in a well characterized population: 34 men 2-5 years after gastrectomy; 11 men 6-10 years after gastrectomy; eight men 2-5 years after colonic resection; and 115 healthy men. The age range was 50-69 years. An innovative reliable method of dual energy X-ray absorptiometry was used which allows quantitative assessment of bone mineral content. Measurement of lumbar spine bone mineral density revealed that the mean(s.e.m.) bone mineral density in patients who had had a gastrectomy (2-5 years 0.84(0.03) g/cm2, 6-10 years 0.85(0.05) g/cm2) was significantly lower than that of patients who had undergone colonic resection (0.96(0.04) g/cm2) or healthy men (0.96(0.03) g/cm2). This study demonstrates that a high incidence of bone atrophy is induced at the relatively early period of 2-5 years after gastrectomy.

Absorptiometry, Photon↗