PubMed Health⌕ Search

Biomedical subjects

Masaru Nakano

Publications and source records attributed to Masaru Nakano.

10 recordsLinked to original sources
PubMed2006

Hormone profiles after intramuscular injection of testosterone enanthate in patients with hypogonadism.

To examine hormone levels after androgen replacement therapy (ART) in Japanese male patients with hypogonadism, nine Japanese male patients with hypogonadism (serum total testosterone (tT) or free testosterone (fT) levels of < or = 2.7 ng/mL or < or = 10 pg/mL, respectively; average age, 59 years) were enrolled. They were treated with 125 mg of testosterone enanthate by single intramuscular injection. Blood samples were collected on the morning of the day of treatment, pre-ART, as well as on days 1 to 7 and day 14 after administration. Serum levels of tT, fT, estradiol (E2), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and sex hormone-binding globulin (SHBG) were determined. On day 1 after administration, the mean serum levels of tT and fT were 7.62 ng/mL and 23.22 pg/mL, respectively. Serum levels of tT and fT on day 14 after administration were lower than their pre-ART values. One patient exhibited abnormally high serum tT and fT levels of 19.6 ng/mL and 44.4 pg/mL, respectively. Serum levels of LH and FSH began to decrease gradually on day 5 after administration. Serum levels of SHBG did not change throughout the observation period. Serum levels of E2 increased 1.7 times on day 1 after administration but returned to its pre-ART value by day 14 after administration. The dose of testosterone enanthate for male patients with hypogonadism requiring ART should be determined carefully because some patients exhibited high serum levels of androgen beyond the physiological range and gonadotropin was suppressed in all treated patients.

Aged↗
PubMed2005

Intraperitoneal injection of adenovirus expressing antisense K-ras RNA suppresses peritoneal dissemination of hamster syngeneic pancreatic cancer without systemic toxicity.

We examined the antitumor effect and safety of the adenovirus-mediated expression of antisense K-ras RNA in two peritoneal dissemination models of pancreatic cancer. First, we found that the infection of an adenovirus vector expressing antisense human K-ras RNA (AxCA-AS) induced significant apoptosis in vitro in human pancreatic cancer cells with K-ras mutation. Second, the intraperitoneal (ip) injection of AxCA-AS effectively suppressed the growth of human pancreatic cancer cells in the peritoneal cavity of nude mice. Third, in the hamster syngeneic peritoneal dissemination model, the ip injection of an adenovirus expressing antisense hamster K-ras RNA significantly suppressed the peritoneal growth of hamster pancreatic cancer cells, and no significant systemic toxicity was observed in the treated hamsters. This study suggests a feasibility of the development of a therapeutic strategy against pancreatic cancer based on the adenovirus-mediated transduction of an antisense K-ras construct.

Adenoviridae↗
PubMed2005

The modified ABC model explains the development of the petaloid perianth of Agapanthus praecox ssp. orientalis (Agapanthaceae) flowers.

The class B genes, which belong to the MADS-box gene family, play important roles in regulating the development of petals and stamens in flowering plants. To understand the molecular mechanisms of floral development in Agapanthus praecox ssp. orientalis (Agapanthaceae), we isolated and characterized the homologs of the Antirrhinum majus genes GLOBOSA and DEFICIENS in this plant. These were designated as ApGLO and ApDEF, respectively. ApGLO and ApDEF contain open reading frames that encode deduced protein with 210 and 214 amino acid residues, respectively. Phylogenetic analysis indicated that ApGLO and ApDEF belong to the monocot class B gene family. In situ hybridization experiments revealed that hybridization signals of ApGLO and ApDEF were observed in whorl 1 as well as in whorls 2 and 3. Moreover, the flowers of transgenic Arabidopsis plants that ectopically expressed ApGLO formed petal-like organs in whorl 1. These observations indicate that the flower developmental mechanism of Agapanthus follows the modified ABC model.

Amino Acid Sequence↗
PubMed2005

Ethanol-induced CXC-chemokine synthesis and barrier dysfunction in intestinal epithelial cells.

BACKGROUND: Ethanol exposure contributes to infectious complications in burn and trauma patients through a process known as "bacterial translocation." Two major factors, 1) physical disruption of the intestinal mucosal barrier and 2) suppression of immune defense, explain this phenomenon. However, little information is available concerning the immune mechanisms of ethanol-induced bacterial translocation. In this study we investigated the effect of physiological concentrations of ethanol on immune function, especially on CXC-chemokine secretion, neutrophil migration, and barrier function in the small intestine METHODS: A rat small intestinal intestinal cell line (IEC-18 cells) was exposed to 50-500 mM ethanol for 24 hr with or without IL-1 beta. Secretion of CXC chemokines (GRO/CINC-1 and MIP-2) was measured by ELISA assay, and barrier dysfunction was assessed by the apical-to-basolateral flux of HRP-dextran. Neutrophil transmigration was assessed by enzyme histochemistry (AS-D chloroesterase staining) RESULTS: Exposure to ethanol concentrations of 200 mM and over increased GRO/CINC-1 secretion, and MIP-2 secretion increased at 500 mM. Administration of ethanol in combination with IL-1 beta had no additive effect on the release of GRO/CINC-1 and MIP-2. Exposure of IEC-18 monolayers to ethanol resulted in a dose-dependent increase in permeability but IL-1 beta had no effect on barrier function. Ethanol had no effect on neutrophil migration in enzyme histochemistry analysis CONCLUSIONS: The above observations suggest that ethanol induced physical disruption of the intestine but not neutrophil transmigration is the main cause of the bacterial translocation that leads to bacteremia and endotoxemia in alcoholics.

Alcoholic Intoxication↗
PubMed2003

Oxidative DNA damage (8-hydroxydeoxyguanosine) and body iron status: a study on 2507 healthy people.

To clarify the relationship of oxidative stress and body iron status, we detected urinary 8-hydroxydeoxyguanosine (8-OHdG) as a biomarker of oxidative DNA damage, and measured serum ferritin and total iron-binding capacity (TIBC), both reflecting body iron store, on 2507 healthy people aged between 22 and 89 years (males, 1253; females, 1254). The urinary 8-OHdG excretion of males showed almost no change with age, but the excretion of premenopausal females was lower than that of males, whereas postmenopausal females excreted significantly more than males. The values of serum ferritin showed no remarkable change with age in males, but increased gradually in postmenopausal females without iron loss due to bleeding, although the males' values remained higher than those of females at all ages (p<.05). On the other hand, the values of TIBC remained within the narrow limits in males, regardless of age, whereas those of females always stayed at a higher level than the males (p<.05). Conclusively, urinary 8-OHdG correlated with serum ferritin positively and with TIBC inversely, which suggested that body iron status would control the generation of 8-OHdG in vivo. After all, the increase of urinary 8-OHdG excretion in postmenopausal females may be caused by the decrease of body iron loss.

8-Hydroxy-2'-Deoxyguanosine↗