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Biomedical subjects

S Moriguchi

Publications and source records attributed to S Moriguchi.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effects of dietary retinyl palmitate or 13-cis-retinoic acid on the promotion of tumors in mouse skin.

The present study was designed to determine the effects of dietary 13-cis-retinoic acid and retinyl palmitate on mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Female CD-1 mice were initiated with 150 nmol of 7,12-dimethylbenz(a)anthracene and promoted twice weekly with 8 nmol of TPA. Diets supplemented with retinyl palmitate to yield 60,000 or 200,000 IU or 700,000 for 5 wk followed by 350,000 IU per kg of diet (700,000/350,000) fed to mice during tumor promotion resulted in 9%, 37%, and 65% inhibition of the papilloma yield, respectively, at 21 wk of promotion. Although topical applications of 13-cis-retinoic acid have been almost as effective as retinoic acid in preventing the appearance of mouse skin tumors, dietary 13-cis-retinoic acid at 200,000 or 700,000 IU per kg of diet resulted in no reduction in papilloma yield but did result in a dose-dependent decrease in the tumor burden (weight of tumors per mouse). Therefore, dietary retinyl palmitate yielded a dose-dependent inhibition of the number and weight of tumors promoted by TPA, whereas dietary 13-cis-retinoic acid resulted in a decrease in weight but not in number of tumors promoted by TPA.

Administration, Cutaneous↗
PubMed1987

Effects of dietary retinyl palmitate and selenium on tumoricidal capacity of macrophages in mice undergoing tumor promotion.

Dietary retinyl palmitate was administered for 22-30 weeks in CD-1 mice which had been initiated with 0.15 mumol of 7,12-dimethylbenz[a]anthracene (DMBA) and promoted with 8 nmol of 12-O-tetradecanoylphorbol-13-acetate (TPA) twice weekly thereafter. This treatment resulted in a dose response in both the tumoricidal capacity of a selected number of isolated peritoneal macrophages (PM) and in skin tumor prevention. At 350 I.U./g of diet, retinyl palmitate (RP) also resulted in a 3-fold increase in the number of DM. RP significantly increased the total capacity of macrophage host defenses by increasing the number and individual capacity for cytotoxicity. Selenium (Se), at 2 parts/million in the drinking water, did not enhance PM tumoricidal capacity, although it did result in 60% reduction of mouse tumor burden.

Animals↗
PubMed1987

[A case of double neoplasms--small cell carcinoma in the mediastinum and squamous cell carcinoma of the esophagus].

A 62-year-old Chinese man was admitted to our hospital because of dysphagia and hoarseness. Chest X-rays showed a superior mediastinal mass, and an operation for the removal of this mediastinal tumor was performed. The histological diagnosis indicated a small cell carcinoma, probably arising from the lung. He was readmitted to our clinic one year later with a complaint of dysphagia due to an esophageal cancer. Radical surgery for the esophageal cancer was performed, and the histological findings showed a well differentiated squamous cell carcinoma. The histogenesis of this carcinoma was considered to be independent of the earlier mediastinal tumor.

Adenocarcinoma↗
PubMed1987

[Brachytherapy--carcinoma of the tongue].

In a review of 193 patients with carcinoma of the tongue who underwent interstitial radiotherapy in our hospital from November 1978 to 1986, 5 year actuarial local control rate were 97%, 87%, 58% and 77% for T1, T2, T3 and T4 respectively. Mucosal ulcers with tissue defects and bone exposure of the mandible occurred in 5 years after the treatments, 6%, 22%, 44%, and 100% for T1, T2, T3 and T4, respectively. Therapeutic ratio was 1 in patients with T1 who underwent interstitial radiotherapy (70 Gy/7 days) alone while it was less than 1 in those with T2 or more. Therapeutic gain factor was less than 1 in patients with combined external radiotherapy.

Adult↗
PubMed1986

Effects of selenium in vitro on human T-lymphocyte functions and K-562 tumor cell growth.

In vitro E-rosette formation, lymphocyte mitogenesis, and natural killer (NK) cell activity of human blood lymphocytes were strongly inhibited by high concentrations (10(-4) M) of sodium selenite, sodium selenate, and selenium dioxide. Lower concentrations (10(-5) or 10(-7) M) also inhibited E-rosette formation and natural killer cell activity against K-562 tumor cells. Lymphocyte transformation induced by concanavalin A (con A) or pokeweed mitogen (PWM) was also inhibited by all selenium compounds tested, but only at the highest concentrations (10(-5) and 10(-4) M). There was depression of the total number of viable lymphocytes following incubation with selenium dioxide only at a high concentration (10(-4) M). Interferon production was enhanced at lower levels (10(-9) to 10(-6)M) of selenium dioxide while a higher concentration (10(-5) and 10(-4)M) appeared to inhibit its production. The mechanism of inhibition by selenium compounds (10(-4) M) is due, in part, to the decrease of viable lymphocytes. It is unclear how other and lower concentrations (10(-7) or 10(-9) M) of selenium compounds inhibit E-rosette formation, NK activity, or K-562 tumor cell growth.

Adult↗
PubMed1986

Modification of cellular immune functions in humans by endurance exercise training during beta-adrenergic blockade with atenolol or propranolol.

Young, healthy, previously inactive men were trained aerobically 40 to 50 min X d-1, 5 d X wk-1 for 15 wk. They were randomly assigned to one of three medication groups: placebo, propranolol (160 mg X d-1), or atenolol (100 mg X d-1). All subjects lost weight and decreased relative body fat as a result of training. Following training, submaximal steady-state heart rates were reduced in all groups. Maximal oxygen uptake and maximal treadmill times were also increased in all groups. The VO2max of the placebo increased 18.4%. While that of the atenolol group increased 19.4%, the propranolol group went up 17.0%. After training the maximal heart rate did not change in the placebo group, while treatment with propranolol and atenolol reduced at 24.6 and 21.9%, respectively. Training caused a significant decrease in the natural killer cell activity in all three groups. The placebo group had 38.8% +/- 3.8 (SD) before and 29.3 +/- 3.2% lysis of target cells by natural killer cells after physical conditioning, which was significantly lower (P less than 0.01). The groups treated with propranolol and atenolol were also similarly decreased. The use of propranolol or atenolol had no additional significant effect on natural killer cell activity. T-cell mitogenesis stimulated with a mitogen significantly increased with conditioning. The groups given atenolol or propranolol tended to increase somewhat more than the placebo group, although this difference was not statistically significant. There was no significant change in the percentage of total lymphocytes isolated due to training or beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Effects of retinoids on human lymphocyte functions in vitro.

E-Rosette formation in vitro, lymphocyte mitogenesis and natural killer (NK) activity of human blood lymphocytes were strongly inhibited by high concentration (10(-4) M) of retinol or retinal. Other retinoids at 10(-4) M (retinoic acid and 13-cis-retinoic acid) and lower concentrations (10(-7) or 10(-9) M) of retinol, retinal and carotenes also inhibited E-rosette formation. Lymphocyte transformation responses induced by concanavalin A (Con A) or pokeweed mitogen (PWM) were also inhibited while NK activity was not affected. There was a remarkable depression of the total number of viable lymphocytes after incubation with retinol or retinal 10(-4) M. However, other retinoids, 10(-7) and 10(-9) M of retinol and retinal and carotenes did not show marked decrease of lymphocyte number or viability even after prolonged incubation (48 h). The mechanism of inhibition by retinol or retinal (10(-4) M) is due in part to the decrease of viable lymphocytes. It is unclear how other retinoids, carotenes and lower concentrations (10(-7) or 10(-9) M) of retinol or retinal inhibit E-rosette formation or lymphocyte transformation.

Adult↗
PubMed1985

High dietary vitamin A (retinyl palmitate) and cellular immune functions in mice.

High dietary intakes (4000-650,000 IU/kg diet) of vitamin A (retinyl palmitate, RP) modified the functions of peritoneal macrophages (PM). The number of peritoneal exudated cells (PEC) obtained from CD-1 mice increased significantly at both 7 and 10 weeks after initiation of the RP diets. The percentage of PM in PEC showed no significant difference between dietary groups and was at levels of 55-60%. PM from mice fed high RP diets showed higher tumoricidal activities than PM from controls without any preincubation with macrophage activators. Enhancement of in vitro tumoricidal activity of PM increased with increasing contents of RP in the diets, reaching 30% lysis by PM isolated from mice fed the highest RP (650,000 IU/kg diet) diet. However, the in vitro activation of tumoricidal ability of PM by macrophage-activating factor (MAF) was inversely correlated with the dietary RP content. The tumoricidal activities of PM from mice fed the highest RP diet were not enhanced by MAF. However, these PM showed an increased ability to phagocytose SRBC and opsonized SRBC compared to controls. Splenocytes and thymocytes were incubated with [3H]thymidine immediately after isolation and their mitogenic activities were measured. Splenocytes, but not thymocytes, isolated from mice fed the highest RP diet had increased mitogenesis. On the other hand, NK activity was not affected by dietary RP intake. There was a similar lysis of target cells by both splenocytes and thymocytes from mice fed diets with various RP levels. IL-1 was produced from PM by incubation with LPS, and its production was assessed using the proliferation of normal mice thymocytes. Production of IL-1 in vitro showed about a two-fold increase using cells from mice fed the highest RP diet compared to controls. High RP diets induced increased phagocytic ability and tumoricidal activity of PM but did not enhance NK activity. These findings suggest that high RP diet may cause activation of PM.

Animals↗
PubMed1984

Phagocytosis of alveolar macrophages of pyridoxine-deficient rats.

We measured phagocytosis of opsonized sheep red blood cells by alveolar macrophages (AM) of rats fed a diet with or without pyridoxine for 4 weeks. In pyridoxine-deficient (DEF) and pair-fed control (PF) groups AM showed a higher degree of phagocytosis than those of rats in the ad libitum-fed control (AL) group. After in vitro treatment with a macrophage-activating factor (MAF), such as lymphokines, for 4 hours at 37 degrees C, AM from the PF and AL groups showed a greater enhancement of phagocytic activity than AM from the DEF group, which was slightly enhanced. When the effect of MAF prepared from splenic cells of rats of the PF or DEF groups on the phagocytosis of AM was observed, MAF from the PF group showed an approximate 35% increase of phagocytic ability compared to the supernatant of splenic cells cultured with medium only. However, MAF from the DEF group had no effect on phagocytosis. These results suggest that pyridoxine deficiency affects not only phagocytic function of AM responsible for host defense in the lung but also MAF production by splenic cells.

Animals↗
PubMed1983

Changes of alveolar macrophages in protein-deficient rats.

Protein malnutrition was achieved by feeding female F344 rats a 5% casein diet for 7 weeks. At appropriate times, animals were killed and their alveolar macrophages (AM) were obtained by broncho-pulmonary lavage of the lung. Functional changes of AM were determined by measuring phagocytosis of latex beads, yeast cells or opsonized sheep red blood cells (SRBC) and the ability to respond to a macrophage-activating factor (MAF) such as lymphokines. After 3 weeks on a low casein diet, the number of AM was much lower than in rats on control diet, but the abilities of the AM to phagocytose latex and yeast cells were the same as those of controls. Phagocytosis of opsonized SRBC was higher than in control rats but could not be enhanced by in vitro treatment with MAF. The most striking ultrastructural feature of these AM was the abundance of finger-like microvilli on the cell surface before phagocytosis; after ingestion of SRBC into phagocytic vacuoles there were only a few short microvilli on the surface. These data suggest that dietary protein malnutrition affects the number and phagocytic functions of AM responsible for host defense in the lung.

Animals↗
PubMed1983

Ultrastructural changes of alveolar macrophages of protein-deficient rats.

Enhancement of phagocytosis of alveolar macrophages (AM) was examined by cytochemical and electron microscopic studies on macrophages from protein-deficient rats. The macrophages from rats fed on 5% casein diet had longer microvilli, more phagocytic vacuoles and more lysosomes with acid phosphatase activity than those from control rats. Many phagocytic vacuoles were seen close to the site of attachment of opsonized sheep red blood cells (SRBC) and were mainly located in the subplasmalemmal layer which was rich in microfilaments but contained few cytoplasmic organelles. After attachment, opsonized SRBC were engulfed through a hemispherical crater into the phagocytic vacuoles. The phagocytic vacuoles seemed to be formed by invagination of the cell surface because they had membrane ATPase activity continuous with that of the outer surface of the plasma membrane. In the cell, the vacuoles fused with the numerous preexisting lysosomes in the interior of the cell receiving the contents of the latter. The mechanism of enhancement of phagocytosis in protein-deficiency is discussed.

Animals↗
PubMed1982

In vitro generation of tumoricidal properties in human alveolar macrophages following interaction with endotoxin.

Human alveolar macrophages (AM) obtained by bronchoalveolar lavage from healthy nonsmoking donors exhibited primarily low levels of cytolytic activity against allogeneic tumor target cells. These AM acquired enhanced capacity to kill tumor cells following a 24-hr incubation in vitro with endotoxin [lipopolysaccharide (LPS)]. Maximal tumoricidal activity of LPS-activated AM as measured by lysis of tumor target cells was obtained after incubation with tumor cells for 72 hr. LPS-activated AM lysed allogeneic tumor cell lines of different origins but did not affect normal, nonneoplastic cells. We conclude that LPS induces human AM to become tumoricidal. This method should be useful in studies on therapeutic agents enhancing AM-mediated cytotoxicity in situ.

Carcinoma, Squamous Cell↗