Search PubMed⌕ Search

Biomedical subjects

K Tashiro

Publications and source records attributed to K Tashiro.

At least 181 records · Page 10Linked to original sources
PubMed1998

Large quantity production with extreme convenience of human SDF-1alpha and SDF-1beta by a Sendai virus vector.

We describe a robust expression of human stromal cell-derived factor-1alpha (SDF-1alpha) and SDF-1beta, the members of CXC-chemokine family, with a novel vector system based upon Sendai virus, a non-segmented negative strand RNA virus. Recombinant SDF-1alpha and SDF-1beta were detected as a major protein species in culture supernatants, reached as high as 10 microg/ ml. This remarkable enrichment of the products allowed us to use even the crude supernatants as the source for biological and antiviral assays without further concentration nor purification and will thus greatly facilitate to screen their genetically engineered derivatives.

Anti-HIV Agents↗
PubMed1998

Localization of D-aspartic acid in elongate spermatids in rat testis.

In the current study, localization of D-aspartic acid (D-Asp) in rat testis was studied by immunohistochemical and biochemical techniques. Immunohistochemical staining of this tissue using specific polyclonal antibody to D-Asp revealed D-Asp immunoreactivity (IR) in the cytoplasm of germ cells, especially around the region rich in elongate spermatids, the most mature of the germ cells. Weak IR was also noted in cytoplasm of spermatocytes and round spermatids; however, it was negligible in interstitial cells and Sertoli cells. The intensity of immunostaining in each seminiferous tubule differed according to its distinct germ cell composition. In testis of young rats, seminiferous tubules lack elongated spermatids, and D-Asp was found to be localized in spermatocytes, the most mature population of germ cells at that age. We used various toxicants to destroy specific testicular cell populations and to confirm the localization of D-Asp in rat testis. Administration of ethane dimethane sulfonate induced a selective destruction of all Leydig cells in this tissue. This resulted in a significant decrease in the D-Asp level, which was probably due to a drop in testosterone brought about by this treatment, and this was followed by a modulation of spermatogenesis. Three days after treatment with methoxyacetic acid (MAA), many seminiferous tubules were found to lack or to have severe depletions of pachytene spermatocytes, but not of elongate spermatids. This caused reductions in protein content and in the total amount of L-Asp, but not that of D-Asp. Twenty days after treatment with MAA, the depleted population of germ cells progressed through the spermatogenic cycle from pachytene spermatocytes to elongate spermatids. At this time, the level of D-Asp decreased significantly, as did that of L-Asp and protein, consistent with D-Asp localization in elongate spermatids. This decrease in the D-Asp level was also seen with immunostaining.

Acetates↗
PubMed1998

Genetic restriction of AIDS pathogenesis by an SDF-1 chemokine gene variant. ALIVE Study, Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC)

Stromal-derived factor (SDF-1) is the principal ligand for CXCR4, a coreceptor with CD4 for T lymphocyte cell line-tropic human immunodeficiency virus-type 1 (HIV-1). A common polymorphism, SDF1-3'A, was identified in an evolutionarily conserved segment of the 3' untranslated region of the SDF-1 structural gene transcript. In the homozygous state, SDF1-3'A/3'A delays the onset of acquired immunodeficiency syndrome (AIDS), according to a genetic association analysis of 2857 patients enrolled in five AIDS cohort studies. The recessive protective effect of SDF1-3'A was increasingly pronounced in individuals infected with HIV-1 for longer periods, was twice as strong as the dominant genetic restriction of AIDS conferred by CCR5 and CCR2 chemokine receptor variants in these populations, and was complementary with these mutations in delaying the onset of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Exogastrula formation in Xenopus laevis embryos depleted with maternal XmN-cadherin mRNA by antisense S-oligo DNA.

Xenopus XmN-cadherin gene appears to have dual functions, since its mRNA is maternally provided in unfertilized eggs, once disappears almost completely during gastrula stage, then accumulates again specifically in neural tissues in later stage embryos. In the present experiment, we first followed the change in XmN-cadherin mRNA level during oogenesis by RT-PCR and showed that this mRNA exists from the earliest stage of oogenesis and at least one third of it is inherited as a maternal mRNA. We then carried out an experiment to deplete the maternal XmN-cadherin mRNA by injecting its antisense S-oligo DNA into full grown oocytes. When mRNA-depleted oocytes were matured in vitro and fertilized eggs obtained therefrom by host transfer technique were allowed to develop, embryos cleaved normally and developed until blastula stage. Such XmN-cadherin mRNA-depleted blastulae initiated invagination, but further involution did not take place, and exogastrulae were formed. These results suggest that the main function of maternally provided XmN-cadherin mRNA is to support cell movement or rearrangement required later during gastrulation, rather than to maintain adhesion of blastomeres during cleavage and blastula formation.

Animals↗
PubMed1998

Functional evaluation of inhibition of autonomic transmitter release by autoantibody from Lambert-Eaton myasthenic syndrome.

The effects of the anti-voltage-gated Ca2+ channel (VGCC) antibody obtained from patients with Lambert-Eaton myasthenic syndrome (LEMS) on autonomic neurotransmission were studied in in-vitro experiments. The releases of acetylcholine (ACh) and norepinephrine from the autonomic nerves were evaluated by changes in the contractile responses of guinea pig taenia caeci and left atria to electric field stimulation, respectively. Incubations for 6 hours with LEMS serum and IgG, both of which contain anti-VGCC antibody, markedly suppressed the parasympathetic response but did not affect the sympathetic response. Pharmacological experiments with specific blockers to the VGCC subtypes showed that the Q-type VGCC is closely linked to the genesis of the parasympathetic response. We suggest that the anti-VGCC antibody from the LEMS patients specifically reduces the ACh release from the parasympathetic nerve by binding to the Q-type VGCC.

Animals↗
PubMed1998

Mechanism of acute lung injury caused by inhalation of fabric protector and the effect of surfactant replacement.

OBJECTIVE: To evaluate the role of surfactant in the mechanism and treatment of acute lung injury caused by inhalation of fabric protector. DESIGN: Prospective, randomized study. SETTING: University laboratory. INTERVENTIONS: In vitro experiment: a porcine surfactant suspension (10 mg.ml-1) was exposed to a fabric protector aerosolized with an ultrasonic nebulizer for 1 min. Minimum surface tension (gamma min) was sequentially measured using pulsating bubble equipment. Animal experiment: 14 adult rats were anesthetized with pentobarbital and mechanically ventilated with pure oxygen. Then, all rats inhaled fabric protector aerosolized with the nebulizer for five breaths. Three hours after inhalation, the rats were randomly assigned to two groups: a surfactant group (n = 7), in which surfactant (100 mg.kg-1) was replaced, and a control group (n = 7), in which no substance was given. MEASUREMENTS AND RESULTS: In vitro experiment: exposure to fabric protector aerosol increased the mean gamma min of the surfactant from 1.7 to 19.2 mN.m-1 (n = 5, p < 0.05). Animal experiment; the mean partial pressure of oxygen in arterial blood (PaO2) in all rats decreased from 62.8 to 17.1 kPa at 3 h after inhalation. The PaO2 in the surfactant group increased to 49.8 +/- 11.1 (SD) kPa at 30 min after surfactant replacement (p < 0.05), while the PaO2 in the control group remained below 20 kPa. CONCLUSIONS: Impairment of surfactant is a factor involved in the development of acute lung injury caused by inhalation of fabric protector. Surfactant replacement may be therapeutic for such injuries.

Acetates↗
PubMed1998

Anterior temporal white matter lesions in myotonic dystrophy with intellectual impairment: an MRI and neuropathological study.

We studied 12 patients with myotonic dystrophy using MRI and the Mini-mental state examination (MMSE), to see it specific MRI findings were associated with intellectual impairment. We also compared them with the neuropathological findings in an autopsy case of MD with intellectual impairment. Mild intellectual impairment was found in 8 of the 12 patients. On T2-weighted and proton density-weighted images, high-intensity areas were seen in cerebral white matter in 10 of the 12 patients. In seven of these, anterior temporal white-matter lesions (ATWML) were found; all seven had mild intellectual impairment (MMSE 22-26), whereas none of the four patients with normal mentation had ATWML. In only one of the eight patients with intellectual impairment were white-matter lesions not found. Pathological findings were severe loss and disordered arrangement of myelin sheaths and axons in addition to heterotopic neurons within anterior temporal white matter. Bilateral ATWML might be a factor for intellectual impairment in MD. The retrospective pathological study raised the possibility that the ATWML are compatible with focal dysplasia of white matter.

Adult↗
PubMed1998

Neuropathological and molecular studies of spinocerebellar ataxia type 6 (SCA6).

SCA6 is an autosomal dominant spinocerebellar ataxia (SCA) caused by a small CAG repeat expansion of the gene encoding an alpha-1A-voltage-dependent Ca channel gene subunit on chromosome 19p13. A Japanese woman with SCA6, with a 7-year history of progressive pure cerebellar ataxia, died of malignant lymphoma. Systematic neuropathological examination showed that neuronal degeneration was confined to the cerebellar Purkinje cells and, to a lesser degree, the granular cells, without any involvement of other central nervous system structures. Such pathological selectivity correlates with the localized expression of the responsible gene, and coincides with the neurological manifestation. These findings might contribute to establishing the phenotype of the SCA6 via comparison with other dominant ataxias.

Age of Onset↗
PubMed1998

Histopathological assessment of localized proliferation in cases of Bowen's disease using immunostaining and a laser cytometer.

In order to evaluate the localized proliferative activity of intratumor cells in Bowen's disease using tissue sections, skin specimens from ten patients were compared with skin samples from seven normal individuals for their expression of proliferating cell nuclear antigen (PCNA), Ki-67 immunostaining and intranuclear DNA contents, quantitated with a laser cytometer (LCM). In normal epidermis, the largest proportion of PCNA- and Ki-67-positive cells was observed in the basal cell layer, with the amounts decreasing through the suprabasal cell layer towards the prickle cell layer. Examination by LCM also revealed the highest average fluorescence intensity of individual nuclei in the basal cell layer and, as with the immunohistological parameters, reducing towards the upper layer of the epidermis. In the Bowen's disease tissue sections, the largest proportion of PCNA- and Ki-67-positive cells was found in contact with the basement membrane (base of the tumor), with lower amounts in the center of the tumor nest and in the marginal epidermis. The average fluorescence intensities of individual nuclei were in line with these results. These results show that tumor cells distributed in Bowen's disease tumor nests have different proliferative activities depending on their location.

Bowen's Disease↗
PubMed1998

SCA6 mutation analysis in a large cohort of the Japanese patients with late-onset pure cerebellar ataxia.

Spinocerebellar ataxia type 6 (SCA6) is caused by small CAG repeat expansion in the gene encoding the alpha1A-voltage-dependent-calcium channel subunit (CACNLIA4) on chromosome 19p13, and is a subgroup of the late-onset pure cerebellar ataxia (ADCA III). To investigate the prevalence of SCA6 in the Japanese, we analyzed this mutation in 23 families and 12 probands with ADCA III. The specificity and stability of the CAG repeat were examined in additional individuals and families with other miscellaneous dominant SCAs. The CAG expansion of SCA6 gene was exclusively observed in 12 of 23 families (52%) and 12 proband cases with ADCA III, but not in others. The CAG repeat was 21-33 in the disease-associated alleles (n=56), and 4-18 in normal alleles (n=1148). Expanded alleles were stable during transmission, and a significant inverse correlation for CAG repeat number with age at onset was noted. Our results indicate that SCA6 shares approximately half of the ADCA III in the Japanese, and that gene mutations causing the remaining, have yet to be identified.

Adult↗
PubMed1998

Cloning and expression of an alpha-2,8-polysialyltransferase (STX) from Xenopus laevis.

Polysialic acid (polySia) is a carbohydrate structure found on neural cell adhesion molecules (N-CAM). Two polysialyltransferases (polySiaTs) that catalyze synthesis of polySia have been described, and designated PST-1/PST/ST8SiaIV and STX/ST8SiaII. We cloned a polySiaT (xSTX) from a nonmammalian vertebrate, Xenopus laevis . xSTX had 80% amino acid similarity to the rat STX. This clone induced polySia expression when transfected into polySia-negative COS-1 cells. Northern blot analysis of whole embryos at different stages of development revealed that xSTX mRNA was most abundantly expressed in premetamorphic stages. The relative level of xSTX and N-CAM mRNAs was also examined and found to change in parallel to the extent of polysialylation on N-CAM. In adult tissues, the expression of xSTX mRNA was restricted to brain, eye and heart, which also expressed polySia. These results suggest that xSTX is the major enzyme responsible for the synthesis of polysialylated N-CAM in embryos at certain stages of development and also in adult tissues.

Amino Acid Sequence↗
PubMed1998

Transgenic mouse expressing a full-length hepatitis C virus cDNA.

Hepatitis C virus (HCV), a major causative agent of post transfusion non-A, non-B hepatitis (NANBH), can only infect humans and chimpanzees. We produced nine transgenic mouse lines carrying a full-length HCV cDNA with the human serum amyloid P component (hSAP) promoter that can direct liver-specific expression. In one of these lines HCV mRNA and HCV core protein were detected in the liver of the transgenic mouse, although the levels of expression were very low. In addition, HCV-related antibody was detected in the serum.

Alanine Transaminase↗
PubMed1998

Exercise-induced acute renal failure in a girl with renal hypouricemia.

A 10-year-old Japanese girl developed acute renal failure following a 100-meter dash during physical training at school. After the run, she experienced intense pain in the loins with nausea and vomiting lasting more than 12 h. On the following morning, she was found to have mild proteinuria and acute renal failure (ARF). Serum creatinine and blood urea nitrogen were elevated, but the serum uric acid level was normal (3.1 mg/dL). With recovery of renal function over the ensuing days, hypouricemia (0.6 mg/dL) became evident in the patient. Although the pathophysiological association between renal hypouricemia and ARF is not known, oxygen free radicals have been implicated in the pathogenesis for ischemic-reperfusion ARF. Superoxide production by neutrophils stimulated by N-formyl methionine leucyl-phenylalanine was normal in the patient both before and following exercise. Pyrazinamide and probenecid tests were undertaken on both the patient and her parents, who had borderline hypouricemia, to determine their renal tubular handling of uric acid. Results showed that the patient and her mother had a subtotal reabsorption defect, while the father had defective postsecretory uric acid reabsorption.

Acute Kidney Injury↗
PubMed1998

Detection of apoptotic cells in glomeruli of patients with IgA nephropathy.

The purpose of the present study was to determine the relationship between the existence of apoptotic cells in glomeruli, clinical or histopathological findings and response to treatment in patients with IgA nephropathy. Renal biopsy specimens were obtained from 23 patients with IgA nephropathy. These patients were divided into two groups: mild glomerular damage (12 patients), and severe glomerular damage (11 patients). The nick end-labelling method (TUNEL) and fluorescent staining (Hoechst 33258) were used for the detection of apoptotic cells. Five of 6 patients with apoptotic cells in the glomeruli detected by TUNEL were in the severe glomerular damage group, and only 1 patient was in the mild glomerular damage group. Apoptotic cells in glomeruli were also detected by fluorescent staining in 3 of 5 patients in the severe glomerular damage group who showed apoptotic cells in TUNEL. However, no apoptotic cells were detected in patients in the mild glomerular damage group in fluorescent staining. Mean levels of urinary protein excretion at the time of renal biopsy in the patients with apoptotic cells were significantly higher than those in patients without apoptotic cells (p < 0.01). The mean levels of creatinine clearance (Ccr) in the patients with apoptotic cells were slightly lower than those in patients without such cells. There were no significant differences in the levels of serum creatinine (s-Cr) and BUN in patients with or without apoptotic cells. In the severe glomerular damage group, urinary protein excretion after treatment in the patients with apoptotic cells was significantly improved compared with that in the patients without such cells (p < 0.01). It appears that the levels of proteinuria and renal function tests might be influenced by apoptosis in patients with IgA nephropathy. It is postulated that apoptosis may induce reduction of excess proliferative mesangial cells and/or infiltrated cells, and tissue repair. Thereafter, these histological alterations may improve proteinuria and renal function.

Adult↗
PubMed1998

Role of umbilical vein endothelial cells in hematopoiesis.

Effective hematopoiesis is usually induced by interactions between hematopoietic progenitor cells (HPC) and stromal cells. In cord blood (CB), umbilical vein endothelial cells (HUVEC) can support HPC as a stromal microenvironment. EC activated mainly by IL-1 and TNFalpha produce a variety of cytokines and growth factors such as IL-1, IL-4, IL-6, GM-CSF and G-CSF. Since HPC express c-kit on their surface, the SCF produced by HUVEC plays an important role in the hematopoiesis of CB. We examined the expression of cytokines and growth factors on HUVEC by PCR. Resting HUVEC expressed high level of SCF, and low levels of IL-6, IL-7, and IL-8. Thus, a variety of cytokines and growth factors are produced by EC, and this cytokine network is thought to play an important role in regulating hematopoiesis. Activated EC can also express various adhesion molecules including E-selectin, VCAM-1 and ICAM-1, and facilitate the adhesion of hematopoietic cells to the endothelium. Furthermore, the interaction of CB cells with HUVEC has recently been shown in vitro. We previously showed that the culture media of HUVEC induced high numbers of colony formation. Suitable cytokine productions are thus provided to HPC by the interaction of HUVEC and cord MNC. On the basis of these findings, several mechanisms to support hematopoiesis in CB can be considered. Specific growth factors produced by EC bind to HPC to induce proliferation. While cell-cell interactions involve adhesion of HPC to HUVEC via adhesion molecules, and the adhesion of HPC to EC will facilitate interaction with cytokines and growth factors. Thus HPC in CB proliferate and are maintained by growth factors, and adhesion molecules produced by HUVEC, and HPC themselves.

Cell Adhesion Molecules↗