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K Hatake

Publications and source records attributed to K Hatake.

At least 73 records · Page 4Linked to original sources
PubMed1998

Ethanol inhibits intra- and extracellular Ca(2+)-dependent contraction of rat aorta by different mechanisms.

The mechanism of the inhibitory action of ethanol on vasoconstriction was studied by examining ethanol effects on vascular responses to different vasoconstrictive stimulants using isolated rat aorta. Ethanol pretreatment of aortic strips at 200 and 400 mM significantly inhibited contractile responses to KCl and 5-hydroxytryptamine in the standard medium. This inhibitory effect on vasoconstriction was observed whether or not the endothelium was present. Pretreatment with ethanol (400 mM) caused significant decrease of 45Ca2+ uptake induced by KCl when compared to the control. This pretreatment also significantly inhibited the contractile response to 5-hydroxytryptamine in the medium without Ca2+, decreased 5-hydroxytryptamine-stimulated inositol monophosphate accumulation, and significantly inhibited a transient contraction induced by 20 mM caffeine. Ethanol (400 mM) inhibited phorbol 12, 13-dibutyrate (PDBu)-induced contraction when Ca2+ was present in medium, but not when it was absent. These results suggest that ethanol acts on different sites of the signal transduction pathway of rat aortic smooth muscle, causing inhibition of transmembraneous Ca2+ influx through voltage-dependent Ca2+ channels, phosphoinositide hydrolysis and Ca(2+)-induced Ca2+ release. However, the cytoskeletal contractile apparatus may remain intact after ethanol treatment.

Animals↗
PubMed1997

Characterization of room temperature induced apoptosis in HL-60.

We found that exposure to room temperature (RT/21 degrees C) causes apoptosis in HL-60 cells. Here we characterized RT-induced apoptosis in HL-60. After exposure to RT, apoptosis starts within 6 h and more than 80% of the cells underwent apoptosis within 20 h. All cells, however, were committed to apoptosis after 16 h and no viable cells could be recovered. The caspase-1 inhibitor (YVAD-CHO) effectively blocked apoptosis, whereas the caspase-3 inhibitor (DEVD-CHO) did not. About 20% of newly obtained early passage HL-60 cells (passage 10) also underwent apoptosis by RT treatment. These data suggest that some population in HL-60 which responds to RT with apoptosis became dominant during passaging.

Apoptosis↗
PubMed1997

SOCS-1/JAB/SSI-1 can bind to and suppress Tec protein-tyrosine kinase.

Tec is the prototype of a recently emerging subfamily among nonreceptor type protein-tyrosine kinases and is known to become tyrosine-phosphorylated and activated by a wide range of cytokine stimulations in hematopoietic cells. Although Tec was recently shown to be involved in the cytokine-driven activation mechanism of c-fos transcription, it is yet obscure how Tec relays the signals from cell surface receptors to the nucleus. To identify signaling molecules acting downstream of Tec, we have looked for Tec-interacting proteins (TIPs) by using the yeast two-hybrid system. Here we report the identification and characterization of a novel protein, TIP3, which has been simultaneously identified by other groups as SOCS-1, JAB, or SSI-1. TIP3 carries one Src homology 2 domain with a sequence similarity to that of CIS. In 293 cells, TIP3 associates with Tec and suppresses its kinase activity. Interestingly, TIP3 can also down-regulate the activity of Jak2 but not that of Lyn. We propose that SOCS-1/JAB/SSI-1/TIP3 is a novel type of negative regulator to a subset of protein-tyrosine kinases.

Amino Acid Sequence↗
PubMed1997

Expression of Src-like adapter protein mRNA is induced by all-trans retinoic acid.

By using a differential display method, specific bands were selected from ladder PCR products derived from ATRA-dependent differentiated U937 cells, in comparison with those of untreated U937. By screening the cDNA library of ATRA-dependent differentiated U937 cells with one of the PCR products, we cloned the src-like adapter protein (SLAP). Northern blot analysis of U937 cells with or without ATRA treatment indicated that the SLAP mRNA was clearly induced by ATRA. The induction was inhibited by the addition of cycloheximide, indicating that ATRA acted indirectly through synthesis of other proteins. The SLAP mRNA was induced in HL60 and NB-4 but not in K562 or THP-1. Interestingly, these cells in which SLAP mRNA was induced by ATRA all showed ATRA-dependent cell differentiation. The relationship between SLAP and cell differentiation is unclear, but SLAP may transduce a signal for cell differentiation.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Properties of primary murine stroma induced by macrophage colony-stimulating factor.

The ability of purified human macrophage colony-stimulating factor (M-CSF) to accelerate the formation of stromal cells from murine bone marrow cells was investigated. The liquid culture of the marrow cells with M-CSF resulted in the formation of monolayers of macrophages on day 7. When the M-CSF was removed on that day and the residual adherent cells were cultured in the absence of M-CSF for an additional 7 days, many colonies appeared with cells that were morphologically distinguishable from M-CSF-derived macrophages. The appearance of the colonies was dependent on the concentration of M-CSF used at the beginning of the culture. Each colony was isolated as a single clone and analyzed. All clones were negative for esterase staining. These cells did not express M-CSF receptor mRNA and did not show a mitogenic response to M-CSF. On the contrary, these cells could be stimulated to proliferate by fibroblast growth factor and platelet-derived growth factor. The polymerase chain reaction analysis of these cells demonstrated constitutive expression of mRNA for M-CSF, stem cell factor, and interleukin (IL)-1, but not IL-3. Some clones expressed mRNA for granulocyte/M-CSF and IL-6. We also examined the ability of the cells to maintain murine bone marrow high proliferative potential colony-forming cells (HPP-CFC) in a coculture system. Most of the clones showed a significant increase in total HPP-CFC numbers after 2 weeks of coculture, although the extent of stimulation differed among clones. These results suggested that the colonies established by M-CSF were composed of functional stromal cells that were phenotypically different from macrophages.

Animals↗
PubMed1997

Rare but important adverse effects of all-trans retinoic acid in acute promyelocytic leukemia and their management.

Several adverse effects have been reported to occur after clinical application of all-trans retinoic acid (RA) in acute promyelocytic leukemia (APL). Except for severe side effects including retinoic acid syndrome, the mechanism of action of RA on adverse effects remains unclear. Here we describe some rare adverse effects and their management. We reviewed the English literature, and we added our cases of endocrine and metabolic adverse effects, such as hypercalcemia, male infertility, bone marrow necrosis, fibrosis and acute pancreatitis. We also described our cases of thromboembolic events, RA-dependent growth of pathologic cells including Sweet's syndrome, erythema nodosum, hyperhistaminemia, granulomatous proliferation, and mild cases of pulmonary complications. In addition, we reviewed the efficacy of RA administration for other types of leukemia or myelodysplastic syndrome. RA and chemotherapeutic agents might induce complete remission, but we obtained a response in only one case of M2 in the third relapse. During RA administration the patient should be monitored for these adverse effects, and early diagnosis and appropriate treatment are important.

Antineoplastic Agents↗
PubMed1997

Aberrant glycosylation based on the neo-expression of poly-N-acetyllactosamine structures in squamous cell carcinomas of the head and neck.

An immuno- and lectin-histochemical study was performed to investigate the aberrant expression of blood group-related antigens and poly-N-acetyllactosamine structures in squamous cell carcinomas of the maxillary sinus, the larynx, the apipharynx, the hypopharynx, the oral cavity, the parotid gland and the tonsil from 52 patients using monoclonal antibodies against A, B and H antigens, and six lectins, UEA-I, PNA, VVA-B4, PWM, LEA and DSA. In addition, GSA-II staining following endo-beta-galactosidase digestion procedure was also applied. A, B and H antigens were expressed in most normal epithelial cells of head and neck organs, and depended on the patient blood type. However, in squamous cell carcinoma, A antigen was not detected in eight out of 25 individuals of blood groups A and AB, although B antigen was consistently expressed in carcinoma cells from all the B and AB individuals. On the other hand, H antigen was expressed in carcinoma cells not only from all blood group O individuals, but from 32 out of 35 individuals of blood groups A, B and AB. T and Tn antigens, which are recognized by PNA and VVA-B4, were strongly expressed in carcinoma cells from 40 and 42 out of 52 individuals respectively. Reactivity with GSA-II staining following endo-beta-galactosidase digestion, which recognizes linear poly-N-acetyllactosamine structures, was found in a few malignant cells from 21 individuals. Staining with anti-A, -B and -H monoclonal antibodies and UEA-I lectin was diminished after endo-beta-galactosidase digestion in some cases. Lectins specific for poly-N-acetyllactosamine, such as PWM, LEA and DSA, exhibited reactivity in some malignant cells from 30, 22 and 32 out of 52 individuals respectively. These results suggested that the expression of the blood group-related antigens is suppressed and immature carbohydrate chains, that is H, T and Tn antigens, are accumulated in squamous cell carcinomas of the head and neck. The results further suggested that poly-N-acetyllactosamine structures are simultaneously synthesized along with the deletion of A antigen and the accumulation of precursors.

ABO Blood-Group System↗
PubMed1997

Human urinary macrophage colony-stimulating factor reduces the incidence and duration of febrile neutropenia and shortens the period required to finish three courses of intensive consolidation therapy in acute myeloid leukemia: a double-blind controlled study.

PURPOSE: To determine whether macrophage colony-stimulating factor (M-CSF) reduces the incidence and duration of febrile neutropenia during three courses of intensive consolidation therapy and whether it shortens time to complete consolidation therapy. PATIENTS AND METHODS: In 198 adult patients with acute myeloid leukemia (AML) in complete remission (CR), M-CSF (8 x 10(6) U/d) or placebo was administered from 1 day after the end of each consolidation chemotherapy for 14 days. RESULTS: The duration and incidence of febrile neutropenia was significantly reduced by 34% (P = .00285) and 17% (P = .02065), respectively, in 88 assessable patients in the M-CSF group compared with those in 94 assessable patients in the placebo group. Patients in the M-CSF group had 565 days and 133 episodes of febrile neutropenia during 7,901 days at risk, while patients in the placebo group had 977 days and 185 episodes during 9,077 days at risk. The median period required to finish the three courses of consolidation therapy was 93 days in the M-CSF group, which was significantly shorter than 110 days in placebo group (P = .0050). In the M-CSF group, the recovery of neutrophils and platelets was significantly faster (P = .0348 and P = 0.0364, respectively), the administration of systemic antimicrobial agents tended to be less (P = .0839), and the frequency of platelet transfusion (P = .0259) and the total volume of transfused platelets (P = .0292) were significantly less. However, there was no significant difference in the disease-free survival. CONCLUSION: M-CSF significantly reduced the incidence and duration of febrile neutropenia during the intensive consolidation therapy, and shortened the time to complete consolidation chemotherapy in AML.

Acute Disease↗
PubMed1997

[Acute myeloid leukemia with monosomy 7 accompanied by central diabetes insipidus].

A 27-year-old female was diagnosed as having atypical aplastic anemia in 1979 because of hypercellular bone marrow with abnormal erythroblasts and megakaryocytes. Afterward the diagnosis was corrected to myelodysplastic syndrome (RA) due to the reevaluation of the bone marrow smears. In March, 1995, thirst and polyurea occurred. In April, 1995, bone marrow aspiration biopsy showed the proliferation of atypical blasts (28%), and two months later, the number of the blasts increased (30%) and leukemic progression was noticed. Only 0.5 percent of the blasts showed weak peroxidase activity, and most of the blasts had CD13, CD33 and several adhesion molecules as CD11a, CD11b, CD44, CD54 and CD56. Karyotype of the bone marrow cells was 45, XX, -7. Her polyurea was caused by central diabetes insipidus. She was also complicated by pleuritis, colon ulcer, sinusitis and hypothalamic dysfunction. The etiology of these signs was due to the leukemic cell infiltration. She died despite of receiving multi-drug chemotherapy.

Adult↗
PubMed1997

[Potentiating effect of ethanol on alpha 1 adrenergic receptor mediated contraction of thoracic aorta from guinea pig].

Using aortic strips isolated from guinea pigs, effects of ethanol on vascular smooth muscle tonus were studied. 50mM of ethanol significantly potentiated the contractions induced by norepinephrine and phenylephrine, but did not influence those induced by KCl and clonidine. Furthermore, ethanol significantly augmented the contraction induced by phenylephrine in the presence of verapamil, and did not have any effects on the contractions induced by A23187, Ba2+, PDBu and BAY K 8644. These results indicate that ethanol potentiates the alpha 1 adrenergic receptor-mediated contraction, depending on the extracellular calcium influx via the receptor-operated calcium channel.

Adrenergic alpha-Agonists↗
PubMed1997

[Cerebral infarction due to bacterial emboli associated with methamphetamine abuse].

The number of stimulant-drug addicts has recently been on the rise again, and they are being increasingly encountered in the emergency room. There are also frequent reports of cerebrovascular disorders complicating drug toxicity. These cerebrovascular disorders have included subarachnoid hemorrhage, intracranial hematoma, and a few cases of cerebral infarction. Here, we report the case of a 37-year-old male with drug toxicity, consciousness disorder, and hyperthermia. He was in a coma with a temperature of 43.1 degrees C and blood pressure of 58/35 mmHg when brought to our hospital. His condition worse rapidly deteriorated, and he died the same day. Cerebral infarction caused by gram-positive bacillus embolism, not necrotizing angiitis, was found at autopsy. Because drug addicts, especially stimulant-drug addicts, tend to inject themselves drug under unsanitary conditions, the possibility of this type of complication is always present. This is the first such case ever reported, and is therefore regarded as a rare complication of stimulant-drug intoxication.

Adult↗
PubMed1997

Liver cytosolic aldehyde dehydrogenase (ALDH1) polymorphism and its inheritance in Wistar rats.

Rats are very important experimental animal to study alcohol related problems. Liver aldehyde dehydrogenases (ALDHs) which metabolize aldehydes are reported to have several isozymes which are distributed in mitochondrial, microsomal and cytosolic fractions. However, there is discrepancy on reports concerning properties of cytosolic ALDH from normal liver. We report here the liver cytosolic ALDH (ALDH1) polymorphism and its inheritance in Wistar rats. Isoelectrophoretic focusing technique reveals the three ALDH1 phenotypes (termed AA, AC and CC) which are inherited in accordance with Mendelian fashion, indicating the existence of two alleles, ALDH1A and ALDH1C. In the range of pI 5.3 to 5.8, the AA phenotype possesses a major anodic band with pI 5.3 and CC phenotype also has a cathodic pI 5.8 band. In contrast, AC phenotype exhibits five bands with pIs of 5.3, 5.4, 5.5, 5.7 and 5.8. Intensity of these bands gradually diminishes from the main band with pI 5.5 to the both opposite ends. These findings suggest that AC phenotype as well as AA and CC types has a structure of tetramer which consist of the combination of subunit of the A and C gene products.

Aldehyde Dehydrogenase↗
PubMed1997

[Clinicopathological features in HLA-DR-negative acute myeloid leukemia].

From a series of 176 patients with acute myeloid leukemia (AML), we have identified 11 patients with HLA-DR-negative AML excluding acute promyelocytic leukemia. All patients showed not (15; 17) or consistent chromosomal abnormalities. According to the French-British-American criteria, seven, three, and one patients were classified into M1, M2, and M4, respectively. Blasts from these patients were CD33+, HLA-DR-, and lymphoid-antigen-. All patients entered complete remission after induction therapy. Of these, blasts from four patients had strikingly invaginated nuclear membrane and finely granular peroxidase activity. The phenotype of the blasts was CD33+, CD34-, CD2-, and HLA-DR-. All four patients showed hyperleukocytosis on initial presentation. One patient received all-trans retinoic acid at relapse, however, the drug did not induce the differentiation of the blasts. These four patients were suspected to have acute myeloid/natural killer (NK) leukemia because of the prominent morphological feature of the blasts and the initial hyperleukocytosis, although NK cell activity of the blasts was not examined. Since HLA-DR-negative AML is heterogeneous, it is necessary for identifying acute myeloid/ NK leukemia within the disorder.

Adult↗
PubMed1997

[Double autologous peripheral blood stem cell transplantation (double APBSCT) for lymphoblastic lymphoma].

A 24-year-old male was admitted to our hospital, complaining of right back pain, in May 1995. Chest X-ray films showed an abnormal mass in the mediastinum. Computed tomography revealed massive effusion in the pleural and pericardial space. A biopsy specimen of the pleural lesion demonstrated lymphoblastic lymphoma of T cell type. After the completion of intensive chemotherapy by our original protocol, he entered into partial remission. Peripheral blood stem cells (PBSC) were harvested using a high-dose cytarabine (Ara-C) followed by granulocyte-colony stimulating factor (G-CSF) mobilization regimen. The total number of collected PBSC was enough to perform two courses of PBSCT. In January 1996, following the conditioning regimen of nimustine hydrochloride, etoposide (VP-16), Ara-C, thiotepa, he received PBSCT. Complete remission was achieved after the 1st PBSCT. In March 1996, he received the 2nd PBSCT following the conditioning regimen of carboplatin, VP-16, ifosfamide. No regimen-related toxity or delayed engrafment was observed. Subsequently, he received irradiation to his neck and mediastinum, the primary site of the disease. As of February 1997, he has no evidence of the disease.

Adult↗