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Biomedical subjects

K Hatake

Publications and source records attributed to K Hatake.

At least 127 records · Page 7Linked to original sources
PubMed1994

Induction of tumor necrosis factor in mice by recombinant human macrophage colony-stimulating factor.

The effect of recombinant human macrophage colony-stimulating factor (rhM-CSF) on endogenous production of tumor necrosis factor (TNF) was investigated in mice. The intravenous injection of lipopolysaccharide (LPS) after the administration of rhM-CSF via the same route induced the production of endogenous cytotoxic activity in serum as assessed by using TNF-sensitive murine L929 cells. The intravenous injection of LPS alone or rhM-CSF alone did not induce cytotoxic activity. The priming effect of rhM-CSF was transient and the optimal duration between injections of primer and trigger was 3 h, while the optimal duration between trigger injection and serum sampling was 1 h after LPS injection. Moreover, preinjection of rhM-CSF enhanced the priming effect of recombinant mouse interferon-gamma. No triggering effect of rhM-CSF was observed. The cytotoxic activity in the serum was completely neutralized by anti-mouse TNF-alpha polyclonal antibody. These results indicate that rhM-CSF can be used as a priming agent for endogenous production of TNF in vivo, and raise the possibility of using rhM-CSF in cancer immunotherapy.

Animals↗
PubMed1994

Development of acute myeloblastic leukaemia in a case of aplastic anaemia treated with granulocyte colony-stimulating factor.

We report a case of aplastic anaemia (AA) treated with granulocyte colony-stimulating factor (G-CSF) terminating as acute myeloblastic leukaemia (AML). Because of severe pneumonia, 250 micrograms of G-CSF was administered for 30 d to promote neutrophil recovery. Following G-CSF therapy, myeoblasts appeared, and the diagnosis of AML was then made. The myeloblasts proliferated in response to G-CSF in vitro and in vivo. In AA, development of AML after treatment with G-CSF is rare. Therefore a careful observation for leukaemic transformation is necessary in long-term administration of G-CSF for AA.

Aged↗
PubMed1994

Increased endothelium-dependent vascular relaxation in ethanol-fed rats.

We investigated the mechanism underlying increased relaxation of aortic strips to acetylcholine in rats chronically treated with ethanol. Rats were divided into three groups and maintained on liquid diets containing ethanol (35% of total calories) as the ethanol-fed group or an equicaloric volume of sucrose instead of ethanol as the sucrose-fed group for 10 weeks. The control group was also maintained on modified American Institute of Nutrition diet for the same period. Vascular strips of isolated rat aortas were mounted in organ chambers to record isometric tension. The endothelium-dependent relaxation responses to acetylcholine and calcium ionophore A23187 were greater in ethanol-fed rats than in control and sucrose-fed rats. However, the relaxation response to sodium nitroprusside or nifedipine did not differ among the three groups. Acetylcholine, calcium ionophore A23187, and sodium nitroprusside caused an increase in the cGMP contents of rat aortic strips that was similar among the three groups. These results suggest that a cGMP-independent relaxation mechanism is involved in the increased relaxation response to acetylcholine after chronic treatment with ethanol.

Acetylcholine↗
PubMed1994

Inhibitory effects of daunorubicin on endothelium-dependent vasorelaxing response to acetylcholine of rat aorta.

The effect of daunorubicin on the endothelium-dependent vasorelaxing response to acetylcholine was investigated using rat isolated aorta and compared with the effect of aclarubicin. Treatment of aortic strips with daunorubicin (20 microM) significantly attenuated the relaxing response to acetylcholine in the absence of tetraethylammonium, but not in its presence. Pretreatment with daunorubicin at a higher concentration (50 microM) or with aclarubicin (20 microM) strongly attenuated the relaxing response to acetylcholine; this attenuation was unaffected by the presence of tetraethylammonium. The increase in aortic cGMP in response to acetylcholine was also significantly suppressed by pretreatment with 50 microM daunorubicin or 20 microM aclarubicin, but not by treatment with 20 microM daunorubicin. The inhibitory effect of 20 microM aclarubicin on the acetylcholine-induced responses was stronger than that of 50 microM daunorubicin. Even in strips pretreated with both 50 microM daunorubicin and 20 microM aclarubicin, relaxation induced by 0.1 microM sodium nitroprusside was retained. These results suggest that daunorubicin at 20 microM inhibits the endothelium-dependent vasorelaxing response to acetylcholine via a mechanism other than the nitric oxide-mediated pathway, whilst at 50 microM, it inhibits the nitric oxide-mediated vasorelaxation.

Acetylcholine↗
PubMed1994

Vasorelaxant effects of oxpentifylline and theophylline on rat isolated aorta.

The mechanism of the relaxation response of rat aorta to the phosphodiesterase inhibitors oxpentifylline and theophylline was studied. Oxpentifylline induced a greater vasorelaxation response in the intact strips than in those without endothelium. The endothelium-dependent relaxation response to oxpentifylline was inhibited by nitro-L-arginine but not by indomethacin, and the endothelium-independent relaxation response was potentiated by the combination with isoprenaline but not sodium nitroprusside. Theophylline induced a similar relaxation response in vascular strips with and without endothelium. The relaxation response to theophylline was not inhibited by indomethacin or nitro-L-arginine in intact strips, but was potentiated by combination with isoprenaline or sodium nitroprusside in the denuded strips. These results suggest that the two phosphodiesterase inhibitors oxpentifylline and theophylline induce vasorelaxation by different mechanisms. Oxpentifylline can induce both endothelium-dependent relaxation, which is probably mediated by an endothelium-derived relaxing factor, and endothelium-independent relaxation, which may be due to an inhibitory action on phosphodiesterase of vascular smooth muscle. In contrast, theophylline can induce endothelium-independent relaxation alone, without modulation by the endothelium.

Animals↗
PubMed1994

[A case of sudden death of a patient with hypopituitarism].

We report a 29-year-old woman who died due to pituitary insufficiency. After a normal delivery 2 years previously, she had suffered from amenorrhea and displayed decreased libido. She was discovered in convulsions by her husband when he returned home, and was admitted to an emergency hospital. Despite various treatments, she died. Her blood glucose level on admission was low, 32 mg/dl. Autopsy findings showed thin public hair and almost no axillary hair. The right and left adrenal glands weighed 1.7 g and 1.2 g, respectively. Histologically, the anterior pituitary gland showed severe bleeding and necrosis, and the middle lobe showed lymphocytic infiltration; the posterior lobe was almost normal. The adrenal glands showed marked atrophy of the cortex and deposition of calcium in the medulla. The thyroid gland, which weighted 15 g, showed diffuse interstitial lymphocytic infiltration, indicative of chronic lymphocytic thyroiditis. Atrophy of the ovaries and uterine endometrium was also observed. These findings indicated that death had been due to pituitary insufficiency. The histopathology of the pituitary, which showed lymphoid hypophysitis, and its association with lymphoid thyroiditis suggested that the pituitary insufficiency was not due to ischemic injury after delivery, a condition which can result from massive hemorrhage, but rather had arisen as a result of an autoimmune process.

Death, Sudden↗
PubMed1994

[A case of acute promyelocytic leukemia (APL) with myeloblastoma in the oral cavity developing after receiving all-trans retinoic acid (ATRA)].

A 44-year-old woman was diagnosed as having acute promyelocytic leukemia (APL) in April 1988. On her first admission, chromosomal translocation (15; 17), +8, and +12 was detected. When she was readmitted to our hospital with the second relapse in May 1990, t(3; 13) and +8 was detected, instead of t(15;17). Complete remission was re-achieved with VP-16, MIT, and BHAC, but the third relapse occurred in September 1990. After obtaining informed consent, she was given etretinate 40 mg per day orally for 17 days, without any effect on leukemia. She was then given all-trans retinoic acid (ATRA) 60 mg per day orally for 29 days. Although a mild granulocytic recovery was observed, no sufficient hematological recovery was obtained (minor response). Besides common side effects of ATRA, such as dry skin and hypertriglycedemia, she had a myeloblastoma in the oral cavity, but it is unknown whether the symptom was a complication of ATRA therapy or not.

Administration, Oral↗
PubMed1994

[Co-operative study of all-trans retinoic acid as a differentiation induction therapy of acute promyelocytic leukemia].

Efficacy and safety of tretinoin (all-trans retinoic acid, ATRA, Ro01-5488) for refractory and relapsed acute promyelocytic leukemia were studied by multi-institutional study in Japan. 22 out of 27 (81.5%) patients with previously untreated who were intolerable to chemotherapy, relapsed and refractory were achieved CR. And 4 out of 11 (36.4%) in relapsed patients who received ATRA remission induction therapy previously responded. Side effects, such as dryness of the lip and skin, headache, increase of triglyceride, beta-lipoprotein and lactate dehydrogenase, were observed in 36 of 41 eligible patients (87.8%) but these were well tolerated. In addition to these, hyperleukocytosis in 4 cases and retinoic acid syndrome in 3 cases were observed. However, all patients were prescribed tretinoin again by adequate management.

Administration, Oral↗
PubMed1994

Alteration of the proteoglycan form of macrophage colony-stimulating factor produced by a human stromal line stimulated by tumor necrosis factor-alpha.

Immunoblot analysis of macrophage colony-stimulating factor (M-CSF) in KM 102 cell-conditioned medium showed the presence of two M-CSF molecular types, one being 85-kd M-CSF, the other a proteoglycan form (PG-M-CSF) carrying a chondroitin sulfate chain of variable length. When KM 102 cells were stimulated by TNF-alpha, they produced more M-CSF than that produced in unstimulated condition, in which PG-M-CSF had a shorter chondroitin sulfate chain. Although PG-M-CSF has binding affinity for type V collagen, the PG-M-CSF with the shorter chondroitin sulfate chain shows lower affinity. This spreads in type V collagen-containing agarose gel more easily than does PG-M-CSF with a longer chondroitin sulfate chain.

Bone Marrow Cells↗
PubMed1994

[Inhibitory effect of fentanyl citrate on endothelium-dependent relaxation in rat aorta].

We studied the effect of fentanyl on the endothelium-dependent vascular responses in isolated rat aortic strips. Fentanyl depressed the endothelium-dependent relaxation induced by acetylcholine but not that induced by the calcium ionophore, A23187. Endothelium-independent relaxation in response to sodium nitroprusside (SNP), a soluble guanylate cyclase activator, was not depressed by fentanyl. On the other hand, fentanyl depressed the increase in cyclic GMP level stimulated by acetylcholine but not that stimulated by A23187 or SNP. Furthermore, fentanyl depressed the vasocontraction by acetylcholine but not that by histamine or KCl in isolated pig coronary artery strips without endothelium, suggesting that fentanyl can inhibit endothelium-independent contraction via muscarinic receptor on smooth muscle cells. These results suggest that fentanyl can inhibit endothelium-dependent vasorelaxation via endothelium-derived relaxing factor (EDRF) by acting on endothelial cells but not on smooth muscle cells. The inhibitory effect of fentanyl on the relaxation probably occurs at the level of muscarinic receptor on endothelial cells or at a site before biochemical pathways converting L-arginine to EDRF.

Acetylcholine↗
PubMed1993

Effects of ethanol on contractile response of gall bladder isolated from guinea pig.

The effects of ethanol treatment in vitro and in vivo on gall bladder contraction were investigated using gall bladder strips isolated from guinea pigs. In vitro pretreatment of the strips with ethanol at a concentration of over 50 mM significantly attenuated the reactivity and sensitivity of contractile responses to KCl, acetylcholine and histamine in a concentration-dependent manner. Indomethacin treatment or removal of extracellular calcium remarkably reduced gall bladder contractile response to acetylcholine. The depressive effect of ethanol in vitro on gall bladder contraction was also noted in the presence of indomethacin or absence of calcium in the medium. The concentration-response curve of calcium-induced contraction in 40 mM KCl-depolarized gall bladder strip shifted to the right on pretreatment with ethanol. In the case of strips following the chronic administration of 3% ethanol solution ad libitum for 4 weeks, contractile responses to KCl, acetylcholine and histamine did not differ, compared to those in the pair-fed group. This chronic ethanol administration induced tolerance to the acute inhibitory effect of ethanol on gall bladder contractile responses to the agonists. Ethanol is thus shown to exert direct inhibitory action on gall bladder contraction by lowering the calcium sensitivity of the contractile apparatus of smooth muscle; it is unlikely that ethanol consumption would affect gall bladder motility in vivo, owing to the tolerance produced toward the acute inhibitory action of ethanol.

Acetylcholine↗
PubMed1993

Mechanism of inhibitory action of ethanol on endothelium-dependent relaxation in rat aorta.

Using isolated rat aortic strips, we investigated the inhibitory effect of ethanol on endothelium-dependent relaxation induced by acetylcholine, especially on that mediated by endothelium-derived relaxing factor. Ethanol depressed the relaxation induced by acetylcholine and inhibited the increase in the content of intravascular cyclic GMP induced by acetylcholine, but not that induced by sodium nitroprusside or calcimycin. Ethanol also inhibited the acetylcholine-induced relaxation resistant to nitro-L-arginine. These results suggest that ethanol can inhibit the cyclic GMP-dependent relaxation mediated by endothelium-derived relaxing factor. Furthermore, ethanol seems to depress the cyclic GMP-independent relaxation mechanism.

Acetylcholine↗
PubMed1993

Establishment and characterization of an erythropoietin-dependent subline, UT-7/Epo, derived from human leukemia cell line, UT-7.

UT-7 is a human leukemic cell line capable of growing in interleukin-3 (IL-3), granulocyte/macrophage colony-stimulating factor (GM-CSF), or erythropoietin (Epo) (Komatsu et al, Cancer Res 51:341, 1991). To study the effect of Epo on proliferation and differentiation of UT-7, we maintained the UT-7 cell culture for more than 6 months in the presence of Epo. As a result, a subline, UT-7/Epo, was established. The growth of UT-7/Epo could be supported by Epo but not by GM-CSF or IL-3. UT-7/Epo showed a greater level of heme content and ratio of benzidine-positive staining cells than did UT-7. Butyric acid promoted the synthesis of hemoglobin in UT-7/Epo, but not UT-7. Further, the mRNA concentrations of the c-myb oncogene and GM-CSF receptor beta-subunit were decreased substantially in UT-7/Epo cells. These findings showed that UT-7/Epo cells had progressed further in erythroid development than UT-7 cells, and suggested that long-term culture in Epo had promoted this differentiation. Whereas availability of the Epo receptor (Epo-R) for binding of Epo was reduced in UT-7/Epo cells compared with UT-7 cells, the Epo-R showed a similar affinity for Epo. This observation suggested that change(s) in postreceptor signaling step might be involved in the establishment and maintenance of the UT-7/Epo phenotype.

Butyrates↗