Biomedical subjects

S Hayashi

Publications and source records attributed to S Hayashi.

At least 433 records · Page 24Linked to original sources

PubMed1998

Numerical analysis for stability and self-excited oscillation in collapsible tube flow.

This paper describes numerical analysis of collapsible tube flow based on the one-dimensional distributed parameter model of Hayashi. In the present model the effect of flow separation at the collapsed part is replaced with simple viscous friction along the tube, so no ad-hoc modeling for flow separation in former studies is required. A stable semi-implicit numerical procedure based on the SIMPLE method is developed for the problem of flow and tube interaction. The numerical result for a characteristic self-excited oscillation agrees qualitatively with the experimental result. Nonlinear stability of the steady state dependent on the amplitude of the disturbance is numerically investigated and the result is compared with the linear stability analysis based on the former lumped parameter model. Finally, initiation of the self-excited oscillation is examined by applying the initial disturbance at the upstream end of the tube. The disturbance propagates in the downstream direction and is amplified to the self-excited oscillation.

Compliance↗

PubMed1998

[A case of hypoxemic acute bronchiolitis presenting with diffuse nodular shadows caused by Mycoplasma pneumoniae].

A fifty year-old female who had previously been well presented with a productive cough and a high fever. Her initial chest X-ray film showed no abnormal lung shadows. Despite partial improvement of the fever and the serum level of acute phase reactant (CRP) in response to intravenous administration of piperacillin, she complained of increasing severity of cough and dyspnea. Follow-up chest X-ray films taken five days after therapy with piperacillin showed diffuse nodular shadows in the mid-to-lower lung fields bilaterally. Chest CT scan disclosed diffuse miliary nodules at the lung periphery and thickening of bronchovascular markings. Chest auscultation revealed late inspiratory coarse crackles and expiratory wheezing, and the patient's arterial oxygen tension was 61 mmHg. Suspected of suffering from primary atypical pneumonia, she was started on therapy with intravenous minocyclin (200 mg/day), two days after treatment her symptoms began improving significantly. Anti-mycoplasma antibody was found to be x 1280, and cold hemoagglutinin x 1024, establishing the diagnosis of Mycoplasma pneumoniae infection. The patient's condition completely recovered following a one week treatment with minocyclin. We concluded that her respiratory infection was caused by piperacillin-sensitive mico-organism, and also Mycoplasma pneumoniae which brought about hypoxic acute bronchiolitis to the patient.

Acute Disease↗

PubMed1998

Effect of rebamipide, a novel antiulcer agent, on Helicobacter pylori adhesion to gastric epithelial cells.

Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H. pylori to human gastric epithelial cells is the initial step of H. pylori infection. Inhibition of H. pylori adhesion is thus a therapeutic target in the prevention of H. pylori infection. Experiments were performed to evaluate the effect of rebamipide, a novel antiulcer agent, on H. pylori adhesion to gastric epithelial cells. MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells. Ten H. pylori strains isolated from patients with chronic gastritis and gastric ulcer were used in the study. We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay. The adhesion of H. pylori to MKN-28 and MKN-45 cells was significantly inhibited by pretreatment of these cells with 100 microg of rebamipide per ml. However, the adhesion was not affected by the pretreatment of H. pylori with rebamipide. On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide. Our studies suggest that rebamipide inhibits the adhesion of H. pylori to gastric epithelial cells.

Alanine↗

PubMed1998

Analysis of immunoglobulin A antibodies to Helicobacter pylori in serum and gastric juice in relation to mucosal inflammation.

Helicobacter pylori is a major etiologic agent in gastroduodenal disorders. In this study, immunoglobulin A (IgA) antibodies to H. pylori antigens were evaluated in serum and gastric juice specimens obtained from patients with gastritis or peptic ulcers by utilizing antibody capture enzyme-linked immunosorbent assays (ACELISAs). Urease alpha subunit (UA), urease beta subunit (UB), the 66-kDa heat shock protein (HSP), and the 25-kDa protein (25K) were used as antigens for the ACELISAs. The antibody titers of the ACELISAs reflect the ratio of H. pylori-specific IgA to total IgA. The ratio is stable, although the antibody concentration fluctuates in gastric juice. By using ACELISAs it was possible to evaluate quantitatively not only serum IgA antibodies but also gastric juice secretory IgA (S-IgA) antibodies. In both serum IgA and gastric juice S-IgA ACELISAs, the titers of antibody to HSP and 25K were remarkably correlated with the histologic grade of gastritis, whereas those to UA and UB were not strongly correlated with histologic grade. Thus, it is useful for estimating the histologic grade of gastritis to quantify serum IgA and gastric juice S-IgA antibodies to HSP and 25K.

Adolescent↗

PubMed1998

Role of tumor necrosis factor alpha in gnotobiotic mice infected with an Escherichia coli O157:H7 strain.

Gnotobiotic mice inoculated with an enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain developed a flaccid paresis, usually culminating in death. The bacteria colonized feces at 10(9) to 10(10) CFU per g (inoculum size: 2.0 x 10(9) CFU/mouse), and Shiga-like toxins (SLTs) were detected in the feces. A microscopic examination of colons showed mild inflammatory cell infiltration, thinning of the intestinal wall, or necrotic foci. Necrosis of tubular cells was noted in these symptomatic mice. Microhemorrhage, thrombosis, and edematous changes of the brain were also seen. Inflammatory cytokines, tumor necrosis factor alpha (TNF-alpha), interleukin 1alpha (IL-1alpha), and IL-6, were detected in the kidney after EHEC infection, but not in the serum. In the brain, only TNF-alpha was detected. When 2.0 x 10(2) CFU of EHEC O157:H7 was fed to germ-free mice, the number of bacteria began to rise rapidly on day 1 and was maintained at 10(8)to 10(9) CFU/g of feces. SLTs were detected in the feces of the mice. However, the mice showed no histological changes and no cytokine responses, similar to what was found for controls. Treatment with TNF-alpha modified the clinical neural signs, histopathological changes, and cytokine responses; mice treated with TNF-alpha developed severe neurotoxic symptoms and had higher frequencies of systemic symptoms and glomerular pathology. Strong cytokine responses were seen in the kidney and brain. Serum cytokines were also detected in this group. In contrast, a TNF-alpha inhibitor (protease inhibitor) inhibited these responses, especially in the brain. However, local synthesis of the cytokines was observed in the kidney. Thus, TNF-alpha and the other proinflammatory cytokines could be important in modifying the disease caused by EHEC.

Animals↗

PubMed1998

Human antibody response to Helicobacter pylori lipopolysaccharide: presence of an immunodominant epitope in the polysaccharide chain of lipopolysaccharide.

We have examined the antibody response to Helicobacter pylori lipopolysaccharides (LPS) in humans. We used sera from patients with gastroduodenal diseases and healthy adults infected or not infected with H. pylori. Data from the experiments for antibody binding to LPS suggested that the polysaccharide chains from many H. pylori strains showed high immunogenicity in humans. Sera from most (above 70%) H. pylori-infected individuals contained immunoglobulin G (IgG) antibodies against the polysaccharide region highly immunogenic H. pylori LPS. The IgG titers of individual serum samples that reacted strongly with highly immunogenic LPS were quite similar (r2 = 0.84 to 0.98). The results suggest wide distribution among H. pylori strains of a highly antigenic epitope in the polysaccharide moieties of their LPS. Also, the similarity in the titers of individual serum samples against highly immunogenic LPS points to the existence of epitopes sharing a common structural motif. However, some strains showed low antigenicity, even those with polysaccharide-carrying LPS. The dominant subclass of IgG that reacted with the highly immunogenic LPS was IgG2, which was preferentially raised against polysaccharide antigens. Recently, a structure that mimics that of the Lewis antigens was identified in the O-polysaccharide fraction of H. pylori LPS; however, no correlation between antigenicity of the polysaccharide chain in humans and the presence of Lewis antigens was found. The IgA and IgM titers against H. pylori LPS seemed to be mostly nonspecific and directed against lipid A. In a few cases, however, sera from individuals infected with H. pylori gave strong IgA and IgM titers against the highly immunogenic polysaccharide. In conclusion, the LPS of many H. pylori strains possess an antigenic epitope in their polysaccharide regions that is immunogenic in humans. However, our results show that the antigenic epitope is unlikely to be immunologically related to structures mimicking Lewis antigens.

Adult↗

PubMed1998

DNA supercoiling factor localizes to puffs on polytene chromosomes in Drosophila melanogaster.

DNA supercoiling factor (SCF) was first identified in silkworm as a protein that generates negative supercoils in DNA in conjunction with eukaryotic topoisomerase II. To analyze the in vivo role of the factor, we cloned a cDNA encoding Drosophila melanogaster SCF. Northern analysis revealed 1.6- and 1.8-kb mRNAs throughout development. The longer mRNA contains an open reading frame that shares homology with mouse reticulocalbin whereas the shorter one encodes a truncated version lacking the N-terminal signal peptide-like sequence. An antibody against SCF detected a 45-kDa protein in the cytoplasmic fraction and a 30-kDa protein in the nuclear fraction of embryonic extracts. Immunoprecipitation suggests that the 30-kDa protein interacts with topoisomerase II in the nucleus, and hence that it is a functional form of SCF. Immunostaining of blastoderm embryos showed that SCF is present in nuclei during interphase but is excluded from mitotic chromosomes. In larvae, the antibody stained the nuclei of several tissues including a posterior part of the salivary gland. This latter staining was associated with natural or ecdysteroid-induced puffs on polytene chromosomes. Upon heat treatment of larvae, the staining on the endogenous puffs disappeared, and strong staining appeared on heat shock puffs. These results implicate SCF in gene expression.

Amino Acid Sequence↗

PubMed1998

Protection of xeno-hepatocytes from complement-mediated cytolysis by transduction with homologous restriction factor 20 gene using retroviral vector.

Xeno-hepatocyte transplantation has the possibility to substitute for clinical liver transplantation in certain restricted hepatic diseases such as inherited metabolic disorders. To overcome human complement-dependent cytotoxicity on xeno-hepatocytes, the effectiveness of ex vivo transfer with the homologous restriction factor 20 (HRF20, CD59) gene was examined on primary-cultured xeno-hepatocytes using a retroviral vector. Primary-cultured rat hepatocytes transduced with HRF20 cDNA expressed HRF20 antigen by flow cytometric analysis and showed the integration of HRF20 cDNA to the genomic DNA by the polymerase chain reaction. The viability of rat hepatocytes incubated with 50% human serum was decreased due to complement-dependent cytotoxicity, whereas that of the transfectant was significantly protected (77.2+/-9.4 vs. 97.8+/-5.2%, p < 0.01). It was concluded that primary-cultured xeno-hepatocytes transduced with HRF20 cDNA using a retroviral vector could escape complement-dependent cytolysis by human serum.

Animals↗

PubMed1998

Inhibition of growth of human vascular smooth muscle cells by overexpression of p21 gene through induction of apoptosis.

The senescent cell-derived inhibitor (sdi)-1 protein (p21 product) has been identified as a downstream mediator of the tumor suppressor p53 in the regulation of cell cycle progression through a G1 phase checkpoint. Given the importance of cell cycle inhibition for the treatment of restenosis, in this study we focused on the function of p21 gene in inhibiting proliferation of vascular smooth muscle cells (VSMC). To test the hypothesis, we transfected human p21 gene into human aortic VSMC using hemagglutinating virus of Japan-liposome-mediated transfer. Initially, we examined the successful transfection of human p21 gene into VSMC. p21 protein was increased in VSMC transfected with p21 vector as compared with control vector. Accompanied by increased p21 protein, transfection of p21 vector resulted in a significant decrease in number of VSMC induced by 2% serum (P<.01). Although p21 has been reported to play an important role in the regulation of apoptosis in some cells, apoptosis mediated by p21 is still controversial. Therefore, we hypothesized that overexpression of p21 mediates apoptosis in human VSMC, in addition to the blockade of cell cycle progression. First, we assessed the concordance between morphologic analysis and apoptosis as determined by nuclear staining with Hoechst 33342. Cells transfected with p21 gene exhibited the characteristic features of cell shrinkage, membrane blebbing, and rounding that are typical of apoptotic death. Of greater interest, a significant increase in apoptotic cells was observed in VSMC transfected with p21 vector as compared with control vector (P<.01). These results were confirmed by the measurement of DNA fragmentation. Consistent with nuclear staining, DNA fragmentation in VSMC transfected with human p21 gene was significantly increased as compared with that in VSMC transfected with control vector (P<.05). To study the molecular mechanisms of apoptosis mediated by overexpression of p21 gene, the protein levels of bax, a promoter of apoptosis, and bcl-2, an inhibitor of apoptosis, were also measured by Western blotting. Overexpression of p21 gene significantly increased protein of bax (P<.05), whereas transfection of p21 gene did not alter bcl-2 protein. Importantly, the ratio of bax to bcl-2 was significantly increased in VSMC transfected with human p21 vector as compared with control vector (P<.05). Overall, these results demonstrated that inhibition of VSMC growth by overexpression of human p21 gene was accompanied by induction of apoptosis through an inappropriate increase in bax protein. These results suggest that regulation of cell cycle by p21 may be closely linked to programmed cell death/apoptosis in human VSMC.

Aorta↗

PubMed1998

Conditioned medium from HepG2 cells transfected with human apolipoprotein(a) gene stimulates growth of human vascular smooth muscle cells: effects of overexpression of human apolipoprotein(a) gene.

Lipoprotein(a) [Lp(a)] is well known to stimulate growth of vascular smooth muscle cells (VSMCs), resulting in atherosclerosis. Its mechanism is postulated to be decreased in active transforming growth factor (TGF)-beta. However, the exact mechanisms and cellular processing from apolipoprotein(a) [apo(a)] to Lp(a) have not yet been clarified because no cultured cells producing apo(a) are available. Therefore, it is necessary to establish apo(a)-producing cells to study the role of apo(a). We evaluated the effects of overexpression of human apo(a) gene on human aortic VSMC growth. First, we tested whether transfection of apo(a) gene into human hepatoma cells, HepG2 cells, producing human apoB resulted in the formation of Lp(a). Transfection of apo(a) gene into HepG2 cells resulted in detectable levels of Lp(a) in the medium, as assessed by ELISA and Western blot, whereas no Lp(a) was detected in the medium of HepG2 cells transfected with control vector and untransfected HepG2 cells. Expression of apo(a) mRNA was also confirmed by reverse transcription-polymerase chain reaction. In contrast, Western blotting showed a single band detected by specific anti-apo(a) antibody, but not anti-apoB antibody, in the medium of apo(a)-transfected VSMCs. These results demonstrate that Lp(a) can be formed from apo(a) on HepG2 cells, whereas transfection of apo(a) gene into VSMCs resulted in the production of apo(a) alone but not Lp(a). Next, we examined the biological effects of overexpression of apo(a) gene on growth of VSMCs and endothelial cells. Incubation of cultured medium of HepG2 cells transfected with apo(a) gene with human VSMCs or endothelial cells resulted in a significant increase in cell number compared with the conditioned medium of HepG2 cells transfected with control vector. In contrast, transfection of apo(a) gene directly into VSMCs caused no significant effect on VSMC growth. Therefore, we measured TGF-beta concentration in the conditioned medium of VSMCs. However, using ELISA, only latent but not active TGF-beta was detected in the medium of VSMCs. Moreover, addition of neutralizing anti-TGF-beta antibody did not alter VSMC growth. These results suggest that Lp(a) could stimulate growth of VSMCs via the independent mechanisms from the inhibition of TGF-beta activation. Overall, these data demonstrate that overexpression of apo(a) gene in cells producing apoB results in formation of Lp(a), resulting in a mitogenic action on human endothelial cells and VSMCs. These results provide new information to understand the mechanisms of the mitogenic action of Lp(a) and suggest the role of Lp(a) in the pathogenesis of atherosclerosis.

Apolipoproteins↗

PubMed1998

Identification of glucocorticoid- and adenovirus E1A-regulated genes in lung epithelial cells by differential display.

Adenovirus infection has been implicated in the pathogenesis of lung inflammatory diseases for which glucocorticoids provide effective antiinflammatory treatment. In this study, the differential display assay was used to identify messenger RNAs (mRNAs) differentially expressed in dexamethasone (1 microM for 24 h)-treated A549 lung epithelial cells compared to A549 cells transfected with the adenoviral E1A gene. Thirty-seven complimentary DNAs (cDNAs) (15 glucocorticoid-regulated, 22 adenovirus E1A-regulated) were isolated. DNA sequence analysis showed that 35 of these were unique, 2 were identical with each other, and 3 were common to the glucocorticoid- and E1A-regulated groups. Genes identified included those involved in transcription/translation, cytoskeletal/contractile element genes, metabolic enzyme genes, and genes associated with cell regulation/signal transduction. After further analysis of the isolated clones by Northern blotting, ribonuclease protection, and semiquantitative RT-PCR (reverse transcriptase-polymerase chain reaction), 10 of the 14 glucocorticoid-regulated and one of the three common to both the adenovirus E1A- and glucocorticoid-regulated cDNAs were confirmed for this control of their expression. We conclude that the strategy of identifying cDNAs regulated by both adenovirus E1A and glucocorticoids provides a promising approach for identifying genes that may be important in the pathogenesis of lung inflammation and therefore targets for glucocorticoid treatment.

Adenovirus E1A Proteins↗

PubMed1998

Transgene expression of steel factor in the basal layer of epidermis promotes survival, proliferation, differentiation and migration of melanocyte precursors.

Mutations at the murine dominant white spotting (KitW) and steel (MgfSl) loci, encoding c-Kit receptor kinase and its ligand respectively, exert developmental defects on hematopoietic cells, melanocytes, germ cells and interstitial cells of Cajal. The expression patterns of steel factor (SLF) observed in the skin and gonads suggest that SLF mediates a migratory or a chemotactic signal for c-Kit-expressing stem cells (melanocyte precursors and primordial germ cells). By targeting expression of SLF to epidermal keratinocytes in mice, we observed extended distribution of melanocytes in a number of sites including oral epithelium and footpads where neither melanocytes nor their precursors are normally detected. In addition, enlarged pigmented spots of KitW and other spotting mutant mice were observed in the presence of the SLF transgene. These results provide direct evidence that SLF stimulates migration of melanocytes in vivo. We also present data suggesting that SLF does not simply support survival and proliferation of melanocytes but also promotes differentiation of these cells. Unexpectedly, melanocyte stem cells independent of the c-Kit signal were maintained in the skin of the SLF transgenic mice. After the elimination of c-Kit-dependent melanoblasts by function-blocking anti-c-Kit antibody, these stem cells continued to proliferate and differentiate into mature melanocytes. These melanoblasts are able to migrate to cover most of the epidermis after several months. The SLF transgenic mice described in this report will be useful in the study of melanocyte biology.

Animals↗

PubMed1998

Interaction between Drosophila EGF receptor and vnd determines three dorsoventral domains of the neuroectoderm.

Neurogenesis in Drosophila melanogaster starts by an ordered appearance of neuroblasts arranged in three columns (medial, intermediate and lateral) in each side of the neuroectoderm. Here we show that, in the intermediate column, the receptor tyrosine kinase DER represses expression of proneural genes, achaete and scute, and is required for the formation of neuroblasts. Most of the early function of DER is likely to be mediated by the Ras-MAP kinase signaling pathway, which is activated in the intermediate column, since a loss of a component of this pathway leads to a phenotype identical to that in DER mutants. MAP-kinase activation was also observed in the medial column where esg and proneural gene expression is unaffected by DER. We found that the homeobox gene vnd is required for the expression of esg and scute in the medial column, and show that vnd acts through the negative regulatory region of the esg enhancer that mediates the DER signal, suggesting the role of vnd is to counteract DER-dependent repression. Thus nested expression of vnd and the DER activator rhomboid is crucial to subdivide the neuroectoderm into the three dorsoventral domains.

Animals↗

PubMed1998

Molecular cloning, sequencing and characterization of the genes for adenosylcobalamin-dependent diol dehydratase of Klebsiella pneumoniae.

Klebsiella pneumoniae and some of the other Enterobacteriaceae form both diol dehydratase and glycerol dehydratase in response to growth substrates. To compare these enzymes produced by the same bacterium, the pdd genes of K. pneumoniae encoding adenosylcobalamin-dependent diol dehydratase were cloned and sequenced. The sequential three open reading frames (pddA, pddB, and pddC genes) encoded polypeptides of 554, 228, and 174 amino acid residues with predicted molecular weights of 60,379(alpha), 24,401(beta), and 19,489(gamma), respectively. The deduced amino acid sequences of the subunits were 84-100% and 54-71% identical with those reported for diol dehydratases and glycerol dehydratases, respectively.

Amino Acid Sequence↗

PubMed1998

Intramedullary hemangioblastoma of the medulla oblongata--two case reports and review of the literature.

We determined the treatment modality of hemangioblastoma of the brain stem on the bases of our two cases and 31 cases searching from the literature since 1960 which were treated surgically. Hemangioblastomas of the brain stem were categorized according to one of three locations: hemangioblastoma of the fourth ventricle attached to the floor of the ventricle (Type A), hemangioblastoma of the fourth ventricle partially embedded in the floor of the ventricle (Type E), and intramedullary hemangioblastoma of the medulla oblongata (Type I); and were evaluated their clinical features including the operative mortality and morbidity of each location. In our two cases of Type I hemangioblastoma, Case 1, removed partially, died due to sleep apnea and Case 2 lead to normal school life after hemangioblastomas were removed radically. In our review of the 33 surgically-treated cases, radical excision was carried out in 29 cases (87.9%). The mortality was 24.2% overall; that of Type A was 25%, Type E was 28.6%, and Type I was 14.3%. In terms of postoperative mortality, the location of the hemangioblastoma was irrelevant and radical excision was much better than partial removal. Hemangioblastomas of the brain stem could be removed radically by meticulous dissection of the tumor on distinct cleavage, even in cases of intramedullary location. Microsurgical dissection of medullary hemangioblastomas with low morbidity is feasible and prudent postoperative care is mandatory to reduce the operative mortality and morbidity.

Adolescent↗

PubMed1998

Assessment of aortic invasion by esophageal carcinoma using intraaortic endovascular sonography.

OBJECTIVE: Accurate preoperative assessment of aortic invasion by esophageal carcinoma is of great importance for planning surgery. We compared the accuracy of intraaortic endovascular sonography with that of CT in the diagnosis of aortic invasion by esophageal carcinoma. CONCLUSION: In this study, intraaortic endovascular sonography was sensitive in detecting aortic invasion; both sensitivity and specificity were 100%. Intraaortic endovascular sonography proved useful in detecting aortic invasion by esophageal carcinoma.

Aorta, Thoracic↗

PubMed1998

A heterozygous frameshift mutation of the PTEN/MMAC1 gene in a patient with Lhermitte-Duclos disease - only the mutated allele was expressed in the cerebellar tumor.

Lhermitte-Duclos disease is a rare disorder of the cerebellum which exhibits a focally indolent growth of the cerebellar cortex. The disease is sometimes associated with multiple hamartoma syndrome, or Cowden disease, an autosomal, dominantly inherited cancer syndrome. Germline mutations of the PTEN/MMAC1 gene, a gene recently discovered to be a tumor suppressor, have been documented in four families with Cowden disease. A family member in one of these families have had Lhermitte-Duclos disease, indicating that mutations of the gene are responsible for the development of Lhermitte-Duclos disease. However, the occurrence of Lhermitte-Duclos disease is mostly sporadic. It is unknown whether the PTEN/MMAC1 gene is involved in these cases. We performed a genetic analysis on a patient with Lhermitte-Duclos disease, as well as analyses on his family members, and found a germline mutation of the PTEN/MMAC1 gene. An insertion of A at nucleotide 83 in codon 28 was apparent in both the patient and members of his family. This mutation caused a frame shift that generated a premature stop codon in codon 43. The mutation was heterozygous, although only the mutated allele was expressed in the cerebellar tumor of the patient. A monoallelic expression of the mutated PTEN/MMAC1 gene may have been responsible for the development of a cerebellar tumor in the patient.

Adolescent↗

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↗