Biomedical subjects

H Ohashi

Publications and source records attributed to H Ohashi.

At least 235 records · Page 13Linked to original sources

PubMed1997

[Hemodynamic effects of amrinone in children during cardiopulmonary bypass and postoperative 12 hours].

Hemodynamic effects of amrinone in children during cardiopulmonary bypass (CPB) and postoperative 12 hours were studied. In 10 patients undergoing open heart surgery, 1 mg/kg of amrinone was infused as the initial CPB dose and 5 - 10 micrograms/kg/min of amrinone was continuously administered as the maintenance dose during CPB and postoperative 12 hours. Amrinone levels ranged from 0.9 to 1.4 micrograms/ml during CPB and postoperative 12 hours. After infusion of amrinone, mean arterial blood pressure decreased significantly, but other parameters did not show remarkable change. The administration of amrinone during CPB showed enough vasodilating effect and decreased the need of conventionally used other vasodilators (nitroglycerin or prostaglandin E1). The postoperative course of 10 patients was clinically uneventful. The administration of amrinone in 10 patients did not produce thrombocytopenia compared with the control group (5 patients) in the postoperative period. In conclusion, the administration of amrinone during CPB and postoperative 12 hours in children was useful in producing enough vasodilating effect without major side effect.

Amrinone↗

PubMed1997

[Effects of aprotinin on blood loss reduction in children undergoing repair of tetralogy of Fallot].

The effect of aprotinin on the blood loss reduction was studied in children undergoing repair of tetralogy of Fallot. We administered aprotinin to consecutive 21 patients during the repair of tetralogy of Fallot and examined the blood loss and operative time in comparison with that in a control group of 20 patients. 30,000 KIU/kg of aprotinin was infused as the initial cardiopulmonary bypass (CPB) dose and 10,000 KIU/kg/hr was continuously administered as the maintenance dose during CPB. There was no resternotomy case due to bleeding and no operative death in both groups. Blood loss after CPB during operation and total blood loss during operation were significantly lower in aprotinin group than in control group. There were no differences between two groups in the volume of chest tube drainage in the postoperative 24 hours and the duration of chest tube drainage. Time from cessation of CPB to skin closure and total operative time were significantly shorter in aprotinin group than in control group. In conclusion, aprotinin was effective on the reduction of blood loss and the shortening of operative time in children undergoing repair of tetralogy of Fallot.

Aprotinin↗

PubMed1996

Crkl is constitutively tyrosine phosphorylated in platelets from chronic myelogenous leukemia patients and inducibly phosphorylated in normal platelets stimulated by thrombopoietin.

Platelet functions such as aggregation and clot retraction are often abnormal in chronic mylogenous leukemia (CML) patients. However, the molecular mechanisms of these altered functions are unknown. As expression of the p210bcr-abl oncogene product, a constitutively active tyrosine kinase, is known to have an essential role in the pathogenesis of CML and tyrosine phosphorylation is intimately involved in various aspects of platelet activation, we examined the pattern of protein tyrosine phosphorylation in platelets from 15 CML patients by immunoblotting with a monoclonal antiphosphotyrosine antibody (4G10). Before and after stimulation with thrombin, the only consistent difference between normal and CML platelets was the presence of a tyrosine phosphorylated protein with a relative molecular weight of 39 kD. This tyrosine phosphorylated protein was identified as crid, an SH2, SH3 containing adapter protein. Thus, as previously demonstrated for neutrophils from CML patients, tyrosine phosphorylation of p39crkl persists in mature platelets. No tyrosine phosphorylation of crid was detected following stimulation with thrombin in normal platelets. However, crkl became incorporated into the Triton X-100 insoluble residue following thrombin stimulation in a manner dependent on platelet aggregation. Further, we found that crkl is an endogenous substrate for calpain, a protease that may be involved in postaggregation signaling processes. This suggests that crkl may be involved in the reorganization of the cytoskeleton during normal platelet aggregation and its tyrosine phosphorylation in CML platelets may contribute to the abnormal platelet function in CML patients. Finally, we found that thrombopoietin induces tyrosine phosphorylation of crk1 in normal platelets and FDCP cells genetically engineered to express human c-Mpl. This suggests that crk1 can be phosphorylated by a kinase other than p210bcr-abl and that crk1 may have a role in signaling by thrombopoietin.

Adaptor Proteins, Signal Transducing↗

PubMed1996

Functional analysis of the cytoplasmic domain of the human Mpl receptor for tyrosine-phosphorylation of the signaling molecules, proliferation and differentiation.

To investigate the functional domains for signal transduction of human Mpl, we constructed a series of human c-mpl cDNAs with various deletions in the cytoplasmic domain, and then introduced each cDNA into murine IL-3-dependent myeloid leukemia FDC/P2 cells to establish stable transformants. We examined the growth and differentiation responses and tyrosine phosphorylation of the intracellular signaling proteins including Jak2, Tyk2, Stat3, Stat5, Vav, SHPTP2, Cbl, Shc and Shc-associated p145 when receptor stimulation occurred after thrombopoietin (TPO) binding. TPO stimulated cell proliferation and induced the expression of megakaryocyte lineage-specific AP-51 and CD61 cell surface antigens and tyrosine phosphorylation of the signaling proteins in transformants expressing full length human Mpl. These results suggested that Mpl not only induced proliferation but also transduced megakaryocyte-specific differentiation signals into FDC/P2 cells. Mutational analysis of human Mpl indicated that the N-terminal region of its cytoplasmic domain is necessary and sufficient to transduce proliferation and differentiation signals into cells, while the C-terminal region may also play important roles in transducing the differentiation signals.

Animals↗

PubMed1996

Interstitial duplication 8q22-q24: report of a case proven by FISH with mapped cosmid probes.

We report on a 6-month-old malformed female infant with a de novo interstitial duplication of an 8q22-q24 segment. She had an excess dark-band on the 8q distal region by GTG-banded chromosome analysis, which was likely to be 8q23. We performed FISH analysis using cosmid probes mapped to 8q23 and proved that the patient had an 8q duplication including the 8q23 region.

Chromosome Banding↗

PubMed1996

p120c-cbl is present in human blood platelets and is differentially involved in signaling by thrombopoietin and thrombin.

To investigate the signaling processes induced by recombinant thrombopoietin, we used human platelets to recently show that thrombopoietin induces rapid tyrosine phosphorylation of Jak2, Tyk2, Shc, Stat3, Stat5, and other proteins in human platelets. Because the apparent molecular weight of a major tyrosine-phosphorylated protein in platelets stimulated by thrombopoietin is approximately 120 kD, we examined the possibility that this could be p120c-cbl, a protein known to be involved in signaling by many growth factors. Specific antisera against p120c-cbl recognized the same 120-kD protein in lysates of Jurkat cells, which are known to express p120c-cbl, and platelets, indicating that platelets have p120c-cbl. Thrombopoietin induced rapid tyrosine phosphorylation of p120c-cbl in platelets. Thrombopoietin also induced tyrosine phosphorylation of p120c-cbl in FDCP cells genetically engineered to express the thrombopoietin receptor, c-Mpl. Interestingly, FDCP cells, expressing a truncated c-Mpl devoid of the box-2 domain, proliferate in response to thrombopoietin. However, no increase in tyrosine phosphorylation of p120c-cbl was observed upon treatment of these cells with thrombopoietin, indicating that in this system tyrosine phosphorylation of p120c-cbl may not be essential for cell proliferation. This suggests that tyrosine phosphorylation of p120c-cbl may be required for nonmitogenic responses induced by thrombopoietin in postmitotic cells such as platelets. On the other hand, p120c-cbl was not significantly tyrosine-phosphorylated upon treatment of platelets with thrombin. However, it became incorporated into the Triton X-100-insoluble, 10,000g-sedimentable residue in an aggregation-dependent manner, suggesting that it may have a regulatory role in platelet cytoskeletal processes. p120c-cbl was constitutively associated with a 28-kD adapter protein, Grb2, that was also incorporated into the Triton X-100-insoluble, sedimentable residue dependent on aggregation. Further, we found that p120c-cbl is an endogenous substrate for calpain, a protease that may play a role in postaggregation signaling processes. Our data suggest that p120c-cbl may be involved in signal transduction following ligand binding to c-Mpl through its inducible tyrosine phosphorylation, and it may also be involved in signaling during platelet aggregation by its redistribution to the cytoskeleton.

Adaptor Proteins, Signal Transducing↗

PubMed1996

Diagnosis of four chromosome abnormalities of unknown origin by chromosome microdissection and subsequent reverse and forward painting.

A molecular cytogenetic method consisting of chromosome microdissection and subsequent reverse/forward chromosome painting is a powerful tool to identify chromosome abnormalities of unknown origin. We present 4 cases of chromosome structural abnormalities whose origins were ascertained by this method. In one MCA/MR patient with an add(5q)chromosome, fluorescence in situ hybridization (FISH), using probes generated from a microdissected additional segment of the add(5q) chromosome and then from a distal region of normal chromosome 5, confirmed that the patient had a tandem duplication for a 5q35-qter segment. Similarly, we ascertained that an additional segment of an add(3p) chromosome in another MCA/MR patient had been derived from a 7q32-qter segment. In a woman with a history of successive spontaneous abortions and with a minute marker chromosome, painting using microdissected probes from the whole marker chromosome revealed that it was i(15)(p10) or psu dic(15;15)(q11;q11). Likewise, a marker observed in a fetus was a ring chromosome derived from the paracentromeric region of chromosome 19. We emphasize the value of the microdissection-based chromosome painting method in the identification of unknown chromosomes, especially for marker chromosomes. The method may contribute to a collection of data among patients with similar or identical chromosome abnormalities, which may lead to a better clinical syndrome delineation.

Abnormalities, Multiple↗

PubMed1996

Modulation of peristalsis by neurotensin in isolated guinea-pig intestinal segments.

Neurotensin (1-100 nM) produced an inhibitory effect and an excitatory effect on the peristaltic activity elicited by intraluminal distension using the Trendelenburg method or the intraluminal perfusion method in isolated segments of guinea-pig small intestine. The relative contribution of these effects to the overall effect varied from one region to another of the small intestine. In the Trendelenburg preparation, the excitatory effect was found to be accompanied by a decrease in the threshold intraluminal pressure required to trigger a peristaltic reflex. A substantial difference between the jejunum and the ileum was noted in that neurotensin-induced stimulation of peristaltic activity was observed in a smaller number of the segments in the jejunum than in the ileum. A nonpeptide neurotensin receptor antagonist, SR 48692, 2-[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxyphenyl) pyrazol-3-yl)carbonylamino]tricyclo(3.3.1.1.(3.7))decan++ +-2-carboxylic acid (90 nM), abolished both the inhibitory and excitatory effects. Apamin (10 nM) abolished the inhibitory effect. From these results, neurotensin appears to exert both excitatory and inhibitory actions, via its receptors sensitive to SR 48692, on peristaltic activity in guinea-pig small intestine. The excitatory action varies with an increasing gradient toward the terminal end of the small intestine, and the inhibitory action involves apamin-sensitive mechanism.

Animals↗

PubMed1996

Carbachol-induced [Ca2+]i oscillations in single smooth muscle cells of guinea-pig ileum.

1. Changes in cytosolic Ca2+ concentration ([Ca2+]i) produced by carbachol (CCh) were measured in single smooth muscle cells of guinea-pig ileum using a Ca(2+)-sensitive fluorescent dye, fura-2, to clarify the underlying mechanisms of muscarinic [Ca2+]i oscillations. 2. Half of the cells, when exposed to 0.2 microM CCh, exhibited repeated changes in [Ca2+]i giving a serrated appearance. The oscillatory changes in [Ca2+]i were very similar to those evoked by increasing extracellular K(+) concentration ([K+]o) to 30 mM, which were abolished by removal of extracellular Ca2+, nifedipine and La3+, but remained unchanged after depletion of internal Ca2+ stores with cyclopiazonic acid, thapsigargin and ryanodine. 3. Every individual [Ca2+]i oscillation was just like a [Ca2+]i increase generated spontaneously in about 8% of cells or triggered by an action potential evoked by a current pulse in current-clamped cells. 4. In the remaining half of the cells exposed to 0.2 microM CCh, slower [Ca2+]i oscillations were elicited and every individual [Ca2+]i oscillation was always preceded by the fast brief increase in [Ca2+]i. 5. [Ca2+]i oscillations elicited by 2 microM CCh were temporally and functionally distinct from those induced by high [K+]o. They were more or less regular in the periodicity and pattern, comprised pacemaker potential-like [Ca2+]i increases or sinusoidal types of [Ca2+]i increases, and could be elicited even in 100 mM K+(o). 6. Removal of extracellular Ca2+ or application of nifedipine, methoxyverapamil (D600), diltiazem or La3+ during CCh (2 micro M)-induced [Ca2+]i oscillations caused them to disappear. In cells i which internal Ca2+ stores were depleted, 2 microM CCh did not evoke [Ca2+]i oscillations but occasionally induced single or repeated generation of the increase in [Ca2+]i with a serrated appearance. 7. The results indicate that CCh can induce two types of [Ca2+]i oscillation in guinea-pig ileal smooth muscle cells; one arises from Ca2+ influx associated with action potential discharges and the other from periodic release of Ca2+ from internal stores. The latter [Ca2+]i oscillation requires extracellular Ca2+ to sustain it.

Animals↗

PubMed1996

[A family of hereditary motor and sensory neuropathy type I with a mutation (Arg98-->His) in myelin Po--report on a second Japanese family].

A 46-year-old housewife had complaints of insidiously progressive muscle weakness and paresthesia in the distal lower limbs. On neurological examination, a slight to moderate degree of muscle weakness with slight atrophy was observed in the bilateral intrinsic hand muscles. A severe degree of muscle weakness with moderate atrophy was observed in tibialis anterior, gastrocnemius and soleus muscles. Muscle stretch reflexes were decreased in the upper limbs and absent in the lower limbs, without pathologic reflexes. She had a steppage gait. Vibratory sensation was slightly decreased in the hands and moderately decreased in the feet. Touch, pain and temperature sensations were also moderately decreased only in the feet. On laboratory examination, glycosuria (5.6g/dl) was noted. Fasting blood sugar was 226mg/dl with an elevated hemoglobin A1C level (12.7%). The right median motor and sensory nerve conduction velocities were 14.8 and 20.3 m/sec, respectively, with a markedly prolonged distal latency. No muscle action potential was obtained from stimulation of the right tibial nerve. Also, no nerve action potential was elicited from stimulation of the right sural nerve. A fascicular biopsy of the right sural nerve revealed the presence of both demyelinated and remyelinated axons, and an onion-bulb formation with a marked decrease in the density of the myelinated fibers. Based on the neurological examination and nerve conduction studies of the family members, a younger sister, younger brother and an elder daughter of the proband were found to be affected by demyelinating polyneuropathy. Diabetes mellitus was not found among the family members with laboratory evidences of demyelinating polyneuropathy. Based on the family history, an uncle on the mother's side of the proband, the proband's grandmother and a younger daughter of a proband's brother were considered to be affected. The uncle and grandmother had diabetes mellitus. Therefore, we concluded that this family had HMSN type I with autosomal dominant inheritance. In the studies on fluorescence in situ hybridization, and restriction fragment length polymorphism of the genomic DNA of the proband, a DNA duplication in the 17p11.2-12 region was not observed. However, the direct sequencing analysis of DNA fragments from genomic DNA encoding the Po gene of the proband revealed a substitution of histidine for arginine at the codon 98 in the extramembranous domain of Po. She was heterozygous for the mutant allele and normal allele. Alterations in the tertiary structure of the extramembranous domain of Po may result in an impairment of the peripheral myelin compaction. This is the second Japanese family with the same mutation (Arg98-->His) of myelin Po as reported previously by us, and this type of case is rare in the literature. Therefore, the mutation at the codon 98 may play a critical role in the development of the myelin abnormality in HMSN type IB.

Arginine↗

PubMed1996

Thrombopoietin induces tyrosine phosphorylation of Stat3 and Stat5 in human blood platelets.

Thrombopoietin is known to be essential for megakaryocytopoiesis and thrombopoiesis. Recently, we and others have shown that thrombopoietin induces rapid tyrosine phosphorylation of Jak2 and other proteins in human platelets and BaF3 cells, genetically engineered to express c-Mpl, a receptor for thrombopoietin. The Jak family of tyrosine kinases are known to mediate some of the effects of cytokines or hematopoietic growth factors by recruitment and tyrosine phosphorylation of a variety of Stat (signal transducers and activators of transcription) proteins. Hence, we have investigated whether Stat proteins are present in platelets and, if so, whether they become tyrosine phosphorylated in response to thrombopoietin. We immunologically identified Stat1, Stat2, Stat3, and Stat5 in human platelet lysates. Thrombopoietin induced tyrosine phosphorylation of Stat3 and Stat5 in these cells. Thrombopoietin also induced tyrosine phosphorylation of Stat3 and Stat5 in FDCP-2 cells genetically engineered to constitutively express human c-Mpl. Thus, our data indicate that Stat3 and Stat5 may be involved in signal transduction after ligand binding to c-Mpl and that this event may have a role in megakaryopoiesis/thrombopoiesis or possibly a mature platelet function such as aggregation.

Animals↗

PubMed1996

Increased production of B cell growth factor (BCGF) in Sjögren's syndrome.

The objective of this investigation to clarify possible roles of B cell growth factor (BCGF) in the abnormal activation of B cells in Sjögren's syndrome (SS). Lymphocyte subsets of peripheral blood from 20 patients with SS (14 with primary SS and six with secondary SS) and 11 healthy donors were analysed by flow cytometry. Supernatants of peripheral blood T cells obtained from patients with SS and from donors, cultured with or without PHA, were studied using bioassay with a B cell line, KS-3.F10. The number of CD20+ cells and CD4+DR+ cells was significantly increased in SS patients compared with healthy donors. T cells from SS patients showed increased production of BCGF, whether or not they were stimulated with PHA. The enhancement of BCGF production by PHA had a positive correlation with the percentage of CD4+CD45RA+ cells, and a negative correlation with the focus score of lip biopsy. Our experiments showed that BCGF production by T cells was spontaneously increased in SS patients. The accelerated BCGF production with PHA stimulation may be related to the increase of CD4+CD45RA+ cells and the decrease of the inflammation determined by the grade of cell infiltration into salivary glands, but not by the increase of CD20+ cells.

Adult↗

PubMed1996

Precise chromosomal locations of the genes for dentatorubral-pallidoluysian atrophy (DRPLA), von Willebrand factor (F8vWF) and parathyroid hormone-like hormone (PTHLH) in human chromosome 12p by deletion mapping.

The precise chromosomal localization of the gene for dentatorubral-pallidoluysian atrophy (DRPLA) was detected by deletion mapping. Segregation patterns of genotypes of polymerase chain reaction products of DRPLA, von Willebrand factor (F8vWF), antigen CD4(p55) (CD4) and parathyroid hormone-like hormone (PTHLH) loci were studied in patients with del(12)(p13.3p13.3), del(12)(p12.3-p11.2), del(12)(p12.1-p11.2), del(12) (p11.2p11.2) and their parents. The gene for DRPLA was assigned to p13.1-p12.3 of chromosome 12. In addition, genes for F8vWF and PTHLH were mapped to p13.2 and p11.2 of chromosome 12, respectively.

Alleles↗

PubMed1996

Staged repair of tetralogy of Fallot and pulmonary atresia without central pulmonary arteries.

A 15-year-old boy with tetralogy of Fallot and pulmonary atresia without central pulmonary arteries who was successfully treated using a staged approach is presented. The first stage consisted of the creation of central pulmonary arteries. In the second stage, the continuity between the right ventricle and the pulmonary arteries was established with closure of the ventricular septal defect. Some patients previously considered to be unsuitable candidates for correction may be successfully repaired using this approach.

Adolescent↗

PubMed1996

PRL-1, a protein tyrosine phosphatase, is expressed in neurons and oligodendrocytes in the brain and induced in the cerebral cortex following transient forebrain ischemia.

Protein tyrosine phosphorylation is thought to play an important role in the regulation of neural function. We reported previously that CL100, a cytoplasmic type protein tyrosine phosphatase (PTP), was induced after transient forebrain ischemia. In the present study, changes in the mRNA levels after ischemia of PRL-1, a cytoplasmic type PTP and immediate-early gene similar to CL100, was examined. In situ hybridization histochemistry showed that PRL-1 mRNA was expressed in normal adult rats in neurons and oligodendrocytes in widespread regions including the cerebral cortex, hippocampus and cerebellum. PRL-1 mRNA was expressed in the developing brains on embryonic days 15 and 19 and postnatal day 1. Northern blot analysis showed that PRL-1 mRNA was induced from 6 h to 9 h after reperfusion in the cerebral cortex of postischemic rats. These findings suggest that PRL-1 plays a role in neurons and oliogodendrocytes, and that expression of PRL-1 mRNA is regulated by a mechanism different from those of other immediate-early genes such as c-fos and c-jun.

Animals↗

PubMed1996

An imprinted gene p57KIP2 is mutated in Beckwith-Wiedemann syndrome.

p57KIP2 is a potent tight-binding inhibitor of several G1 cyclin/Cdk complexes, and is a negative regulator of cell proliferation. The gene encoding p57KIP2 is located at 11p15.5 (ref. 2), a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome, a cancer-predisposing syndrome, making it a tumour-suppressor candidate. Several types of childhood tumours including Wilms' tumour, adrenocortical carcinoma and rhabdomyosarcoma exhibit a specific loss of maternal 11p15 alleles, suggesting that genomic imprinting is involved. Genetic analysis of the Beckwith-Wiedemann syndrome indicated maternal carriers, as well as suggesting a role of genomic imprinting. Previously, we and others demonstrated that p57KIP2 is imprinted and that only the maternal allele is expressed in both mice and humans. Here we describe p57KIP2 mutations in patients with Beckwith-Wiedemann syndrome. Among nine patients we examined, two were heterozygous for different mutations in this gene-a missense mutation in the Cdk inhibitory domain resulting in loss of most of the protein, and a frameshift resulting in disruption of the QT domain. The missense mutation was transmitted from the patient's carrier mother, indicating that the expressed maternal allele was mutant and that the repressed paternal allele was normal. Consequently, little or no active p57KIP2 should exist and this probably causes the overgrowth in this BWS patient.

Beckwith-Wiedemann Syndrome↗

PubMed1996

A sensitive sandwich ELISA for measuring thrombopoietin in human serum: serum thrombopoietin levels in healthy volunteers and in patients with haemopoietic disorders.

A sensitive sandwich enzyme-linked immunosorbent assay (ELISA) has been established to estimate serum thrombopoietin (TPO) concentrations in healthy volunteers and patients with haemopoietic disorders. The ELISA uses a mouse monoclonal antibody (Ab) as the capture Ab and a biotinylated rabbit polyclonal Ab as the detector. The ELISA was reproducible, highly sensitive and specific for human TPO. The coefficients of intra-and inter assay variation were from 3.0% to 4.9% and from 5.9% to 6.1%, respectively. The quantitative limit of the ELISA was 0.09 fmol/ml in serum. The quantitative limit was lower than the normal level. The dose-response curves of serum samples from healthy volunteers and patients with haemopoietic disorders were parallel to the standard curves. The ELISA did not cross-react with a variety of blood components and cytokines to produce false-positive results. The serum TPO concentrations from 29 normal males and 21 females were 0.79 +/- 0.35 and 0.70 +/- 0.26 fmol/ml, respectively. Serum TPO levels in patients with aplastic anaemia (AA), acute lymphocytic leukemia (ALL) and essential thrombocythaemia (ET) were measured using the ELISA. The serum TPO levels in the patients with ET (n = 6, 2.80 +/- 1.55 fmol/ml) were higher than the normal level. The patients with AA (n = 7, 18.53 +/- 12.37 fmol/ml) and ALL (n = 5, 10.36 +/- 5.57 fmol/ml) had significantly higher serum TPO levels than normal individuals. These results indicate that the ELISA specific to TPO should prove useful in measuring the TPO concentration in serum samples.

Adult↗

PubMed1996

Effect of recombinant human thrombopoietin in nonhuman primates with chemotherapy-induced thrombocytopenia.

We examined the effects of recombinant human thrombopoietin (rhTPO) on myelosuppressive chemotherapy-induced thrombocytopenia in cynomolgus monkeys. After treatment with nimustine (ACNU) on day 0, the monkeys intravenously received rhTPO at a dose of 0.04, 0.2 or 1 microgram/kg/d or monkey's serum once each day from day 1 to day 28. Administration of rhTPO reduced the severity of thrombocytopenia and accelerated the rate of platelet recovery in a dose-dependent fashion. Treatment with the highest rhTPO dose completely prevented thrombocytopenia and stimulated a marked increase in platelet counts over the normal values. Animals treated with ACNU also became neutropenic and slightly anaemic. Administration of rhTPO following ACNU treatment significantly improved neutropenia with increasing doses of rhTPO, but had no effect on anaemia. Compared to the control animals, rhTPO-treated animals exhibited no significant changes in several serum parameters. C-reactive protein concentration and some blood coagulation profiles within the study period. These results suggest a therapeutic efficacy of rhTPO in improving chemotherapy-induced thrombocytopenia.

Animals↗