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Biomedical subjects

H Iwama

Publications and source records attributed to H Iwama.

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

Nafamostat mesilate, a kallikrein inhibitor, prevents pain on injection with propofol.

We have examined the preventative effect of nafamostat mesilate, a kallikrein inhibitor, on pain on injection with propofol in a randomized, double-blind study. A control group (n = 110) and a nafamostat (n = 103) group received 5% glucose 0.02 ml kg-1 and nafamostat 0.02 mg kg-1 diluted with 5% glucose, respectively, followed 1 min later by 1% propofol injected at a rate of 200 mg min-1. Pain scores recorded during injection of propofol were significantly less in the nafamostat than in the control group. In another 10 patients, blood concentrations of nafamostat were measured after administration of nafamostat 0.02 mg kg-1 i.v. Mean nafamostat concentration 1 min after injection was 0.1 (SD 0.05) mumol litre-1, which is sufficient to inhibit plasma kallikrein activity. We conclude that pretreatment with nafamostat 0.02 mg kg-1 significantly reduced pain on propofol injection and this effect may be caused by a reduction in kallikrein activity.

Adolescent↗
PubMed1998

Effect of an endotoxin-removing column containing immobilized polymyxin B fiber in a patient with septic shock from gram-positive infection.

A 67-yr-old patient with septic shock caused by gram-positive infection fell into circulatory collapse. Direct hemoperfusion with an endotoxin-removing column was then carried out for 120 min. As a result, blood pressure and systemic vascular resistance increased significantly during this therapy. Cardiac output changed from hyperdynamic to normodynamic, and plasma endotoxin level decreased. After this treatment, the patient recovered. From this experience, we consider that the endotoxin-removing column may be effective for septic shock patients.

Aged↗
PubMed1998

Serum soluble CD44 levels for monitoring disease states in acute leukemia and myelodysplastic syndromes.

To determine the clinical implications of soluble CD44 (sCD44) levels in hematologic neoplasias, we developed an enzyme-linked immunosorbent assay for sCD44 using two monoclonal antibodies to the standard 90 kDa form, and assessed the serum concentration of sCD44 in normal healthy volunteers, patients with acute leukemia, myelodysplastic syndromes (MDS), and those with chronic myeloid leukemia (CML). Compared to that in normal individuals (n=51; 145. 1 24.6 ng/ml), the serum sCD44 level was significantly elevated in patients with acute myeloid leukemia (AML; n=18; 331.9 99.0 ng/ml, P=0.0001), acute lymphoid leukemia (ALL; n=16; 551.3 427.8 ng/ml, P=0.0001) and CML (n=18; 262.0 97.5 ng/ml, P=0.0001). The sCD44 level was slightly elevated in patients with MDS (n=43; 173.8 54.9 ng/ml, P=0.0071). In patients with acute leukemia, serum sCD44 concentrations decreased significantly in response to treatment and reached nearly normal levels after complete remission (P=0.0005 in AML and P=0.0032 in ALL). The sCD44 levels in patients with MDS increased after they developed acute leukemia, whereas no significant difference in sCD44 levels was observed between the chronic and the blastic phases in patients with CML. Our results indicate that serum sCD44 levels may be a useful marker for monitoring response to treatment and disease progression, especially in acute leukemia.

Acute Disease↗
PubMed1998

[Induction of Ph-negative normal clone and long-term survival by combined treatment with G-CSF plus middle dose cytosine arabinoside for patients with chronic myeloid leukemia in blastic transformation].

Three patients with chronic myeloid leukemia (CML) in blastic transformation were treated with G-CSF plus middle dose cytosine arabinoside (Ara-C). G-CSF was administered (150 mg, s.c. or 300 mg, d.i.v./day) 24 hr prior to Ara-C (2-3 g/body, 6 hour d.i.v. for 2-5 days) and continued until the peripheral neutrophil count rose above 1,000/microlitre. As a supplement, VP-16 (80 mg/m2, for 2 days) was administered as warranted to control the growth of blastic cells. All 3 patients survived for more than 12 months with a favorable performance status. Normal karyotypes were detected in 2 of the patients after chemotherapy. One of those patients in paticular demonstrated normal bone marrow findings with the almost complete disappearance of the Ph-positive clone. In vitro cultures of peroxidase-negative CML blastic cells revealed that G-CSF stimulated the induction of blastic cells into the cell cycle and that blastic cell apoptosis was more pronounced in cells cultured with G-CSF plus Ara-C than with G-CSF or Ara-C alone. G-CSF plus middle dose Ara-C therapy appears to be a strong candidate for the treatment of CML in blastic transformation with a poor prognosis.

Adult↗
PubMed1998

[Telomerase activity and determination of cancer in urological neoplasias using exfoliated urinary cells: in situ TRAP assay and its application].

We determined telomerase activity semiquantitatively and in-cell telomerase activity in exfoliated urinary cells obtained from urological neoplasias. Semiquantitative determination of telomerase activity was performed using a fluorescent-based telomeric repeat amplification protocol (TRAP) and telomerase activity at the cellular level was determined by an in situ TRAP assay. Fluorescent-based TRAP assay detected urinary telomerase activity in about 80% patients with urological neoplasia before treatment, whereas urinary cells obtained from 30% patients after/during treatment with either chemotherapy or operation (class II-V) had detectable telomerase activity. In contrast, the in situ TRAP assay detected telomerase-positive cells in 85% patients before treatment and 60% patients after/during treatment. Of note is a dissociation of the results between fluorescent-based TRAP assay and that of in situ TRAP assay in some patients. Some patients without detectable telomerase activity using the fluorescent-based TRAP assay showed a low frequency of telomerase-positive cells in the urine. A combination of semiquantitative analysis and an in situ TRAP assay to detect telomerase-positive cells might be a useful tool in the detection and monitoring of patients with urological neoplasias.

Humans↗
PubMed1998

[Macrocytic anemia with anisocytosis due to alcohol abuse and vitamin B6 deficiency].

Megaloblastic anemia due to folic acid deficiency and ringed sideroblastic anemia have been reported in alcohol abusers. It has also been reported that vitamin B6 deficiency causes ringed sideroblastic anemia as well as microcytic anemia that is not associated with ringed sideroblasts. We encountered a case of macrocytic anemia with anisocytosis in a 75-year-old alcohol abuser who suffered vitamin B6 deficiency. Neither megaloblastic changes nor ringed sideroblasts were observed in specimens of the patient's bone marrow. Analyses of porphyrin content and heme biosynthetic enzyme activity suggested a decline in ALA-synthase activity (an enzyme that depends on vitamin B6) as well as decreased ferrochelatase activity or abnormal iron metabolism. Abstention from alcohol led to a reduction in mean corpuscular volume and the disappearance of Pappenheimer bodies commonly observed in the red blood cells of drinkers. Follow-up supplements of vitamin B6 resolved the patient's anisocytosis and anemia.

Aged↗
PubMed1997

Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1.

Extracellular levels of the excitatory neurotransmitter glutamate in the nervous system are maintained by transporters that actively remove glutamate from the extracellular space. Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury. These effects can be attributed to elevated levels of residual glutamate in the brains of these mice.

ATP-Binding Cassette Transporters↗
PubMed1997

The relationship between telomere length and therapy-associated cytogenetic responses in patients with chronic myeloid leukemia.

BACKGROUND: Chronic myeloid leukemia (CML) is a clonal disease with specific cytogenetic changes involving the Philadelphia (Ph) translocation. The authors examined the relationship between telomere length (terminal restriction fragment [TRF]) and therapy-associated cytogenetic responses in CML patients. METHODS: The authors examined the telomere length and telomerase activity in 44 patients with Ph-positive CML in the chronic phase. TRF was determined by Southern blot analysis using the (TTAGGG)4 probe and telomerase activity was assessed by the telomeric repeat amplification protocol and fluorescent-labeled primers. RESULTS: At the time of CML diagnosis, 19 patients had TRFs within the age-matched normal range (mean +/- 2 x standard deviation [SD]) and the remaining 25 patients had TRFs shorter than the age-matched normal range (< mean +/- 2 x SD). Hematologic findings, including leukocyte count, hemoglobin level, platelet count, and percentage of bone marrow blasts at the time of diagnosis did not significantly differ between patients with normal and shortened TRFs; however, those with shortened TRFs had high levels of telomerase activity (P = 0.045). In a group of patients treated with alpha-interferon (n = 32), those with normal TRFs had a significantly lower frequency of blast crises (P = 0.0328), a significantly higher incidence of cytogenetic responses (P = 0.0185), and a favorable prognosis (P < 0.01) compared with those with shortened TRFs. CONCLUSIONS: These findings suggest that normal TRFs in a small number of CML patients at the time of diagnosis may have a significant amount of normal stem cells remaining. The authors suggest that normal TRFs at the time of diagnosis indicate a subset of CML patients who may respond favorably to alpha-interferon therapy.

Adolescent↗
PubMed1997

Depletion of cerebral D-serine in non-ketotic hyperglycinemia: possible involvement of glycine cleavage system in control of endogenous D-serine.

Tissue concentrations of D-serine and other chiral and non-chiral amino acids were measured post-mortem in the cerebral cortex of the neonatal or infantile individuals with (three cases) or without (seven cases) non-ketotic hyperglycinemia (NKH) using high performance liquid chromatography with fluorometric detection. In the cortical tissues of the NKH patients lacking activity of glycine cleavage system, there was a marked reduction and elevation of the contents of D-serine and glycine, respectively, compared to non-NKH controls. Systemic administration of an inhibitor of glycine cleavage system (GCS), cysteamine, mimicked the changes in the cortical concentrations of these amino acids in the 8-day-old rats. Augmentation of brain glycine levels by means of intraperitoneal injection of glycine itself resulted in an increase in cortical D-serine contents in the neonatal rats with normal activity of GCS. These findings provide the first evidence that GCS might be implicated in the biosynthesis or content regulation of endogenous D-serine in the mammalian brain.

Amino Acid Oxidoreductases↗
PubMed1997

Telomerase activity and cytogenetic changes in chronic myeloid leukemia with disease progression.

Progressive telomere shortening is thought to be important in the regulation of cellular senescence and that the upregulation or reactivation of telomerase activity may be a critical if not rate limiting step in the development of neoplastic cells. To obtain information about telomeres and telomerase activity in hematopoietic neoplasia at various disease stages, we evaluated 54 samples obtained from 41 patients with chronic myeloid leukemia (CML) using a combination of fluorescent-telomeric repeat amplification protocol and an internal telomerase assay standard. The terminal restriction fragment (TRF) lengths in the blast phase was reduced compared to that in the chronic phase (4.53 +/- 0.72 kb vs 6.13 +/- 1.68 kb; P = 0.0005). All samples obtained from CML in the chronic phase (n = 33) had detectable telomerase activity above background, regardless of age. In the blast phase (n = 21), a significant increase of telomerase activity was detected compared to that in the chronic phase (33.84 +/- 37.86% vs 6.08 +/- 3.21; P = 0.016). Among patients in the blastic phase, 50% of patients had moderate to high telomerase activity (>10 relative value), and the remaining patients had telomerase activity higher than that in the normal peripheral blood cells. No significant differences in hematologic findings, duration of chronic phase or blast phase, and telomere length in the blastic phase were noted between these two groups separated by telomerase activity. CML patients with moderate to high telomerase activity had a high frequency of additional cytogenetic changes (P = 0.01).

Adolescent↗
PubMed1997

[The effect of nicardipine hydrochloride upon the pulmonary arterial pressure].

This study examines the effects of induced hypotension with intravenous administration of nicardipine hydrochloride (NIC) upon pulmonary arterial pressure (PAP) undergoing modified radical mastectomy with neuroleptanesthesia (NLA-group; 3 cases) and inhalation anesthesia (N2O+ isoflurane; GOI-group; 3 cases). Systolic arterial pressure was reduced and maintained at 80 mmHg. During and after induced hypotension in NLA-group, heart rate (HR), cardiac index, pulmonary arterial pressure (PAP) increased remarkably. On the other hand, systemic vascular resistance index was reduced. In GOI group, no significant changes were seen in PAP. The acceleration of the autonomic baro-reflex induced by decreased blood pressure produced by NIC may be depressed under anesthesia to initiate this difference in response of HR to NIC. The data indicate that this depressive effect of NLA on this reflex is weak, and NIC is a potent systemic vasodilator with hyperdynamic hemodynamic effects in addition to an increase in right ventricular function, and PAP was increased.

Adult↗
PubMed1997

[Essential thrombocythemia in transformation to acute leukemia (FAB-M0) as a natural history from myelofibrosis with t(1;7)].

A 34-year-old man was found to have leukocytosis and thrombocytosis in 1983. In 1988, his leukocyte count was 10,400/microliter, Hb 16.5g and a platelet was 73 x 10(4)/microliter. A bone marrow examination showed megakaryocyte hyperplasia. Essential thrombocythemia (ET) was diagnosed but no treatment was given. In February 1993, anemia and hepatosplenomegaly developed and cytogenetic study of the peripheral blood demonstrated t(1;7) (q10;p10). Myelofibrosis was diagnosed as by bone marrow biopsy. The patient was treated with blood transfusion, oxymetholone and prednisolone, but without effect. In 1995, acute myeloid leukemia developed, and he died in December 1995 due to septicemia. We report here a case of the ET developed myelofibrosis with t(1;7) (q10;p10) anomaly and acute leukemia.

Acute Disease↗