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Biomedical subjects

M Baba

Publications and source records attributed to M Baba.

At least 73 records · Page 4Linked to original sources

Development of systemic lupus erythematosus after total resection of a thymoma and the adjacent thymic gland.

We describe a woman with systemic lupus erythematosus presenting with nephropathy after the complete resection of a thymoma and the adjacent thymic gland. The woman showed no symptoms of autoimmune disorders or nephropathy at operation. One year later, however, she noticed arthralgia, and laboratory examination showed mild proteinuria, leukopenia, a high level of serum antinuclear antibody (1:1280), anti-dsDNA antibody, and a low level of complement. Renal biopsy showed focal necrotizing glomerular lesions, suggestive of lupus involvement. The pathogenesis of lupus erythematosus in our case is briefly discussed in relation to preceding thymoma and its resection.

Antibodies, Antinuclear

[A case report of patch aortoplasty for supravalvular aortic stenosis associated with Williams syndrome].

A 15-year-old girl underwent patch aortoplasty for supravalvular aortic stenosis in association with Williams syndrome. Pressure gradient of before and after stenosis of the aorta decreased from 104 mmHg to 16 mmHg at the postoperative catheterization. Angiography after the operation showed no stenosis. Postoperative course was excellent and discharged on 14th postoperative day. The problems of the operation of supravalvular aortic stenosis were discussed.

Adolescent

Prevention of asthma by ketotifen in infants with atopic dermatitis.

To evaluate the prophylactic effect of ketotifen against the onset of asthma we selected 121 infants with atopic dermatitis, without any history suggestive of asthma (cough and/or wheezing). Sixty-one children received ketotifen twice daily. Those who weighed less than 14 kg received 0.8 mg; 14 kg or more, 1.2 mg. Sixty children, a placebo syrup indistinguishable from the active syrup. Both groups were followed for 1 year, with bimonthly evaluations. The criteria for onset of asthma were two different episodes of wheezing treated with bronchodilator drugs. Both groups were comparable regarding age, sex, weight, onset, and duration of atopic dermatitis and age at the onset of asthma. During the 1 year study, asthma was observed in eight children of the ketotifen group (13.1%) and in 25 children of the placebo group (41.6%) (P less than .001). Side effects were negligible and routine laboratory tests disclosed no significant alterations. Ketotifen is a very useful drug for prevention of asthma in children with atopic dermatitis and total IgE more than 50 IU/mL.

Asthma

[Evaluation of allergen-specific IgE antibody and total IgE with a new IgE detection system named FAST: fluorescence allergosorbent test].

The measurement of IgE antibodies and total IgE was performed with FAST (fluorescene allergosrobent test) system using 171 serum samples obtained from normal donors and 789 serum samples obtained from patients with various allergic diseases. These were collected by departments of internal medicine, pediatrics, otorhinolaryngology and dermatology at 17 institutes in Japan. In addition to a comparative study with RAST, skin tests and provocation tests were also performed to establish a clinical diagnosis. Simultaneous measurements were made and an excellent correlation with RAST was observed with a concordance rate of 85.7% and correlation coefficient of 0.848. The specificity determined in the normal serum samples was 95.5% by RAST and 93.1% by FAST. The sensitivity determined in the samples, of which etiological allergens were identified clinically, was 82.3% by RAST and 85.3% by FAST. Among them, the sensitivity of skin test and provocation test were 92.4% and 94.7%, respectively. The concordance rate with clinical diagnosis was as high as 89.7% for both RAST and FAST. The normal upper limit of total IgE by cumulative 95% value was calculated to be 250 IU/ml for adult subjects. These results indicated the clinical usefulness of the FAST system in evaluating IgE antibodies and total IgE.

Allergens

Significance of lymph nodal metastases in treatment of esophagogastric adenocarcinoma.

Between 1973 and 1990, 104 patients with adenocarcinoma of the esophagogastric junction (EGJ) (i.e., primary tumor within 2-3cm of and including the EGJ) were operated upon. Preoperatively, all were deemed potentially resectable. In 70, the esophagogastrectomy was combined with en-bloc resection, that is, wide excision of the primary mass in conjunction with radical lymph node dissection of the posterior mediastinum and upper abdomen. Postoperative staging was done using the WNM system [i.e., wall penetration (W), lymph node involvement (N), and systemic metastases (M)]. Sixty-four patients or 62% had lymph nodes positive for metastases and these neoplastic nodes were most common in the areas between the lower mediastinum and the celiac axis. Of the 70 patients undergoing radical en-bloc resection, paracardiac lymph nodes had the highest rate of metastatic involvement (40%) while gastric lesser curvature lymph nodes had 29%, and distal splenic/pancreatic lymph nodes 11%. Overall, the frequency of intrathoracic lymph nodal metastases was 7%. Those patients who had intrathoracic lymph nodal metastasis also had intraabdominal lymph nodal secondary tumor involvement. Among postoperative survivors, the percent of 5 year survival with N0 (no positive node) and N1 (1 to 3 positive nodes) stage of disease was 38.6% and 28.9%, respectively, compared to only 11.5% in those with N2 (4 or more positive nodes) staging. Because long-term survival is dismal in patients with multiple lymph nodal metastasis, preoperative and intraoperative staging is desirable to avoid morbidity of radical resection for EGJ adenocarcinomas. With less than 3 positive nodes, en bloc resection is worthwhile.

Adenocarcinoma

[The advantages of laser assist in parenchyma-sparing pulmonary resection].

The advantages of laser irradiation were investigated retrospectively, using a total of 89 parenchyma-sparing pulmonary resection (PSPR) for localized lung lesions which included 42 conventional wedge resection (CWR), 8 PSPR using electrocoagulator (PE) and 39 PSPR using CO2 laser or Nd:YAG laser (PCYL). The major axes of the lesions in PNYL (25.4 +/- 10 mm) were significantly (p = 0.0387) longer than that in CWR (20.3 +/- 11.3 mm). The amount of bleeding during operation was similar in three groups. The mean value of the amount of postoperative exudation from the thoracic drains in PCYL (615 ml) was only 60 ml more than that in CWR. Bloody sputum was observed for 4.8 days in PCYL and 5.0 days in CWR, whereas 7.1 days in PE. Air leak was observed 33.3% in PCYL, 37.5% in PE, whereas 22.5% in CWR, that continued for 1.7 days (mean value) in PCYL, 1.6 days in PE and 2.0 days in CWR. Decrease (differences between preoperative and postoperative lung functions/volume of the lesions) in FVC and FEV1.0 in PCYL (mean values = 221, 158) and PE (174, 135) were less than that in CWR (339, 204). Laser assist in PSPR revealed advantages in hemostasis comparing with PE, and in parenchyma-sparing comparing with CWR. And no clear difference between PCYL and CWR in bleeding during operation, the amount of postoperative exudation and postoperative air leak. CO2 laser is reported that has higher potential in vaporization or cutting but lower ability in hemostasis comparing with Nd:YAG laser, so authors would express that Nd:YAG laser assist is most safe and effective in parenchyma-sparing lung resection.

Adolescent

Inhibition by the dopamine antagonist haloperidol of experimental carcinogenesis induced by azoxymethane in rat colon.

The effects of the dopamine agonist bromocriptine and antagonist haloperidol on the incidence and histology of colon tumors induced by azoxymethane and on the labeling index of colon mucosa were investigated in Wistar rats. Rats received weekly s.c. injections of 7.4 mg/kg of body weight azoxymethane for 10 weeks and s.c. injections of 2 mg/kg of body weight bromocriptine or 2 mg/kg of body weight haloperidol, in depot form, every other day until the end of the experiment in week 30. Administration of haloperidol resulted in a significant decrease in the incidence of colon tumors. It also caused a significant decrease in the incidence of adenocarcinomas, with 75% of the tumors being adenomas, and in the labeling index of the colon epithelial cells. In contrast, bromocriptine had no influence on the incidence or histology of colon tumors or the labeling index of the colon mucosa. These findings indicate that the dopamine antagonist haloperidol inhibits colon carcinogenesis and that this effect may be related to its effect in decreasing the proliferation of colon epithelial cells.

Adenocarcinoma

Inhibition by retinoic acid of hepatocarcinogenesis induced by N-nitrosomorpholine and of expression of myc oncogene protein in Sprague-Dawley rats.

The effects of all-trans-retinoic acid (RA) on hepato-carcinogenesis induced by N-nitrosomorpholine (NNM) and on the expression of myc p110 proteins were investigated in male Sprague-Dawley rats. Rats received i.m. injections of RA twice a week and, from the beginning of the experiment, were given drinking water containing NNM for 8 weeks. Pre-neoplastic and neoplastic lesions staining positively for gamma-glutamyl transpeptidase (GGT), glutathione-S-transferase placental type (GST-P) or myc p110 protein were examined histochemically. At week 18, quantitative histological analysis showed that prolonged administration of RA resulted in a significant reduction in the number, size and volume of GGT-positive and GST-P-positive hepatic lesions. Administration of RA also caused a significant increase in the proportion of myc p110-negative lesions to the total pre-neoplastic lesions observed. Myc p110-negative lesions had a significantly lower mitotic index than myc p110-positive lesions. These findings indicate that RA inhibits hepatocarcinogenesis and suggest that this effect may be related to its influence in reducing the expression of myc gene proteins and its subsequent inhibition of cell proliferation in pre-neoplastic lesions.

Animals

Enhancement by tyrosine methyl ester of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of tyrosine methyl ester (TME) on the incidence, number, and histological types of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in male Wistar rats. Rats were subcutaneously given TME, 512 mg/kg body weight, every other day after 20 weeks of oral treatment with MNNG. Prolonged alternate-day administration of TME caused a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. However, it did not affect the histology of the cancers. TME also caused a significant increase in tissue norepinephrine concentrations in the antral portion of the gastric wall and in the labelling indices of the antral epithelial cells. However, TME had no influence on the serum gastrin level and antral pH. These findings indicate that TME enhances gastric carcinogenesis, and this may be related to its effects on increasing norepinephrine levels in the gastric wall and stimulating proliferation of the antral epithelial cells.

Adenocarcinoma

Enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats fed a low-protein diet.

The effects of ad libitum feeding of synthetic, low-protein diets on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats were fed synthetic diets of equal calorie content containing 25% casein (normal protein diet), 10% casein (low-protein diet), or 5% casein (very-low-protein diet) after treatment with N-methyl-N'-nitro-N-nitrosoguanidine p.o. for 25 weeks. Administration p.o. of a very-low-protein diet containing 5% casein resulted in a significant increase in the incidence and number of gastric cancers in experimental Week 52. However, it did not affect the histology of the cancers. The very-low-protein diet also caused a significant increase in tissue norepinephrine concentration of the antral portion of the gastric wall and in the labeling index of the antral epithelial cells. These findings indicate that a very-low-protein diet enhances gastric carcinogenesis and that this effect may be related to its effect in increasing norepinephrine in the gastric wall and stimulating proliferation of antral epithelial cells.

Animals

Attenuating effect of the monoamine oxidase inhibitor furazolidone on the anti-carcinogenetic effect of cysteamine on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of furazolidone on inhibition by cysteamine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in inbred Wistar rats. After oral treatment with MNNG for 25 weeks, rats received cysteamine, furazolidone, or both compounds. In week 52, rats treated with cysteamine had a significantly decreased incidence of gastric cancers. Concomitant treatment with furazolidone significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of furazolidone alone significantly increased the number, but not the incidence, of gastric cancers. The norepinephrine concentration of the antral portion of the gastric wall and the labelling index of the antral mucosa were significantly reduced in rats treated with cysteamine, and significantly higher in rats treated with both compounds than in those treated with cysteamine alone. These findings indicate that the cysteamine-induced inhibition of gastric carcinogenesis is mediated by catecholamines.

Adenocarcinoma

Enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in deoxycorticosterone acetate-NaCl hypertensive rats and its inhibition by potassium chloride.

The effect of s.c. administration of deoxycorticosterone acetate (DOCA) plus p.o. treatment with NaCl solution on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and the effect of p.o. potassium supplementation on the enhanced induction of gastric carcinogenesis in DOCA-NaCl rats were investigated in Wistar rats. After 25 weeks of p.o. treatment with the carcinogen, rats received s.c. injections of DOCA (50 mg/kg) twice a week and were given 1% NaCl solution with and without 1% KCl as drinking water. In Week 52, the blood pressure, the incidence of gastric cancer, and the number of cancers per rat were significantly greater in DOCA-NaCl rats than in the untreated group. Prolonged p.o. treatment of DOCA-NaCl hypertensive rats with potassium significantly reduced their blood pressure, the incidence of gastric cancers, and their number per rat. All gastric tumors were in the glandular portions of the stomach. The norepinephrine concentration in the gastric wall and the labeling indices of gastric mucosa were significantly greater in DOCA-NaCl hypertensive rats than in the untreated group, but p.o. potassium supplementation significantly reduced the norepinephrine concentration in the gastric wall and the labeling indices of the gastric mucosa in DOCA-NaCl rats. Thus, administration of DOCA and NaCl increased the norepinephrine concentration in the gastric wall and promoted gastric carcinogenesis, and p.o. potassium supplementation decreased the norepinephrine concentration in the gastric rats. Inasmuch as the norepinephrine concentration has been used as a marker of sympathetic nervous activity, these findings suggest that the sympathetic nervous system plays an important role in gastric carcinogenesis, probably associated with cell proliferation of antral epithelial cells.

Adenocarcinoma

Potent and selective inhibition of human immunodeficiency virus type 1 (HIV-1) by 5-ethyl-6-phenylthiouracil derivatives through their interaction with the HIV-1 reverse transcriptase.

In the search for 1-[(2-hydroxyethoxy)-methyl]-6-(phenylthio)thymine (HEPT) derivatives, we have found several 5-ethyl-6-(phenylthio)uracil analogues to be highly potent and selective inhibitors of human immunodeficiency virus (HIV) type 1. 1-Benzyloxymethyl-5-ethyl-6-phenylthiouracil, the most potent congener of the series, inhibits HIV-1 replication in a variety of cell systems, including peripheral blood lymphocytes, at a concentration of 1.5-7.0 nM, which is lower by a factor of 10(3) than the 50% antivirally effective concentration of the parent compound HEPT. The 5-ethyl-6-(phenylthio)uracil analogues, like HEPT itself, do not inhibit HIV-2 replication but do inhibit replication of 3'-azido-3'-deoxythymidine-resistant mutants of HIV-1. 1-Benzyloxy-methyl-5-ethyl-6-phenylthiouracil and its congeners are targeted at the HIV-1 reverse transcriptase (RT). They do not inhibit HIV-2 RT. They do not need to be metabolized to exert their inhibitory effect on HIV-1 RT. Yet this inhibitory effect is competitive with the natural substrate dTTP. The HEPT derivatives represent a group of RT inhibitors with a unique mode of interaction with HIV-1 RT.

Antiviral Agents

Inhibition by putrescine of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.

Adenocarcinoma

Inhibition by neurotensin of azaserine-induced carcinogenesis in rat pancreas.

The effect of neurotensin on pancreatic carcinogenesis induced by azaserine was investigated in Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 200 micrograms/kg body weight of neurotensin in depot form every other day for 62 weeks. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of neurotensin significantly reduced the volume (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the ultimate development of pancreatic cancer. Histologically, pancreatic adenocarcinomas occurred at a significantly lower rate in rats treated with neurotensin than in untreated rats. Administration of neurotensin also significantly decreased the labelling indices of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. These findings indicate that neurotensin inhibits pancreatic carcinogenesis, and that this may be related to the reduction of ATPase-positive lesions and to the inhibition of cell proliferation in neoplastic lesions of the pancreas.

Animals

Enhancement by methionine enkephalin of colon carcinogenesis induced by azoxymethane.

The effect of the opioid receptor agonist methionine enkephalin (Met-enkephalin) and the opioid receptor antagonist naloxone on colonic carcinogenesis induced by azoxymethane was investigated in Wistar rats. Rats received ten weekly injections of 7.4 mg/kg of body weight of azoxymethane and injections of Met-enkephalin (50 micrograms/kg of body weight), naloxone (2 mg/kg of body weight), or Met-enkephalin (50 micrograms/kg of body weight) plus naloxone (2 mg/kg of body weight) once every 2 days. In wk 40, the group treated with Met-enkephalin had a significantly increased incidence of colonic tumors. A combination of Met-enkephalin and naloxone attenuated the enhancing effect by Met-enkephalin on the development of colonic tumors. Administration of naloxone alone had no influence on colonic tumorigenesis. During and after administration of the carcinogen, the bromodeoxyuridine-labeling indices of the colon mucosa and/or cancers were significantly increased in rats treated with Met-enkephalin. However, a combination of Met-enkephalin and naloxone significantly decreased the labeling indices of the colon mucosa and/or cancers. These findings indicate that Met-enkephalin enhanced colon carcinogenesis and that naloxone attenuated this enhancement. Because naloxone is an opioid receptor antagonist, these findings also indicate that the enhancing effect of Met-enkephalin on colon carcinogenesis may be mediated through opioid receptors.

Adenocarcinoma