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Biomedical subjects

J Han

Publications and source records attributed to J Han.

At least 181 records · Page 10Linked to original sources
PubMed2000

[Comparison of TIPS, a modified Sugiura procedure and TIPS plus a modified Sugiura procedure for portal hypertension].

OBJECTIVE: Transjugular intrahepatic portosystemic shunts (TIPS), a modified Sugiura procedure and TIPS plus a modified Sugiura procedure were compared to evaluate their clinical results in treatment of portal hypertension. METHODS: Ninety patients with portal hypertension respectively underwen TIPS (group I, n = 30), a modified Sugiura procedure (group II, n = 30) and TIPS plus a modified Sugiura procedure (group III, n = 30). The rates of rebleeding and encephalopathy, and the mortality of patients with portal hypertension were observed. RESULTS: The early postoperative complications were observed in 23.33% of the patients in group I, in 30.0% of those in group II, and in 20.0% of those in group III. The early postoperative rates of rebleeding were 6.67% in group I, 10% in group II, and 0% in group III. Hepatic encephalopathy was seen in 16.67% of the patients in group I, 0% in group II and 13.33% in group III. The early mortality was 3.33% in group I. During follow-up for 1 - 36 months, the rates of rebleeding were 34.48% in group I, 33.33% in group II, and 3.33% in group III. The rates of encephalopathy and mortality were respectively 17.20% and 20.69% in group I, 3.33% and 13.33% in group II, 3.33% and 3.33% in group III. The shunt patency in group III was higher than that in group I. CONCLUSION: Combination of TIPS and a modified Sugiura procedure can be effective to prevent and treat variceal bleeding.

Adult↗
PubMed2000

[Establishment and biological characteristics of a novel erythroleukemia cell line (HIE1)].

OBJECTIVE: To establish a novel leukemia cell line and characterize its biological characteristics. METHOD: The cell line was established by liquid cell culture. The genetic marker was analyzed by R-banding and reverse transcriptase-polymerase chain reaction (RT-PCR), cell morphology by microscopy, electron microscopy and histochemical staining, cell surface antigen by monoclonal antibody, hemoglobin by hyperomethemoglobin measurement and electrophoresis, erythroid differentiation by benzidine-staining, and monocyte-macrophage differentiation by cell morphology and phagocytosis. RESULTS: A novel erythroleukemia cell line (HIE1), with original cell genetic marker (Ph chromosome, bcr/abl fusion gene rearrangement), was established from a CML patient in blast crisis, and has been passaged for over 60 generations. Myelomonocyte marker and hemoglycoprotein A were found on the cell surface. HIE1 cells contained hemoglobin, the same HbA and HbA(2) bands as in normal individuals were displayed by Hb electrophoresis. The benzidine positive HIE1 cells were induced after exposure to 3.6 x 10(-4) mmol/L Ara-C. When HIE1 cells were treated with 100 ng/ml PMA for 3 days, one third of the cells became spindle in shape, and 6.5% of the cells exert phagocytosis. The cells were classified into two types with Wright-staining: one showing light blue cytoplasm and a few of cells with basophilic granules, the other showing dark blue cytoplasm with vacuoles and pseudopods without granules. In addition, POX, SB, CE stains were negative, and AE, PAS, ACP stains positive. Colony formation of the cells was 37%, the cell doubling time was 22 - 24 hrs, and EB virus detection was positive. CONCLUSION: A novel erythroleukemia cell line with bcr/abl fusion gene and characteristics of myelomonocytic and erythroid cells was established.

Cell Differentiation↗
PubMed2000

[Treatment of acute lymphoblastic leukemia by autologous stem cell transplantation: an analysis of 30 cases].

OBJECTIVE: To evaluate the clinical outcome of autologous stem cell transplantation (ASCT) in acute lymphoblastic leukemia (ALL) and the affected factors. METHODS: Data of 30 ALL patients received ASCT in our hospital between July 1987 and December 1997 were retrospectively analyzed. Twenty-four of them were in the first complete remission (CR(1)) and six in the second complete remission (CR(2)) or early relapse (ER). Conditioning regimens were CTX 120 mg/kg + single total body irradiation 9 - 10 Gy (sTBI) or Bu 16 mg/kg of Mel 140 - 180 mg/m(2) + Ara-c 2 - 4 g/m(2). RESULTS: All patients reconstituted hematopoiesis. The median follow-up duration was 504 (18-3043) days. Transplant-related mortality was 10%. The probabilities of 3 year disease-free survival (DFS) for ALL in CR(1) and CR(2) were 67.7% +/- 10.3% and 16.7% +/- 15.2%, respectively (P = 0.00547); the 3 year DFS was significantly better with posttransplant treatment than without it (92.3% +/- 7.4% vs 50.0% +/- 17.7%, P = 0.0130). CONCLUSION: Acute lymphoblastic leukemia patients without HLA-matched related donor are recommended for ASCT in CR(1). To reduce relapse and improve the outcome, adoptive immunotherapy or maintenance chemotherapy should be given after ASCT.

Adolescent↗
PubMed2000

[Factor XIIa-inhibited diluted thromboplastin time can reflect coagulation process].

OBJECTIVE: To establish a screening test that can reflect two stages of coagulation process. METHODS: With FXII a being blocked, the effects of various dilution of thromboplastin on clotting time were observed. FX a activity was determined by chromogenic assay. RESULTS: (1) At high concentration of thromboplastin, FXII a-inhibited diluted thromboplastin time (FXII ai DTT) of pooled normal plasma and FXI deficient plasma was very similar, but at low concentration, FXII ai DTT was in order of FVIII and FIX deficient plasma > FXI deficient plasma > pooled normal plasma. (2) FXI consumption by immunologic method induced FXII ai DTT of pooled normal plasma prolonged, and addition of FXI to FXI deficient plasma shortened FXII ai DTT. (3) Alpha-thrombin blocked by hirudin at different time (10 - 80 seconds) resulted in decreased FXa generation, and the earlier the block, the more the decrease. Under the same condition, the amount of FXa generation was in order of platelet-rich plasma > platelet-poor plasma > FXI deficient plasma. CONCLUSION: (1) Our data support the two-stage hypothesis and confirm the important role of FXI in the amplification stage. (2) FXII ai DTT as a screening test for coagulation process may be practicable.

Blood Coagulation↗
PubMed2000

[Altered subcellular distribution of daunorubicin in the non-P-glycoprotein-mediated multidrug-resistant cell line HL-60/ADR].

OBJECTIVE: To investigate DNR subcellular distribution in the non-P-glycoprotein-mediated multidrug-resistant cell line HL-60/ADR and its relation to multidrug resistance. METHODS: DNR subcellular disposition was studied by confocal scanning laser microscopy, fluorescent methods, MTT and RT-PCR. The effects of verapamil, brefeldin A, chloroquine were also examined. RESULTS: In the drug-sensitive cell line HL-60 DNR fluorescence distributed evenly in the nucleus and cytoplasm, while in the resistant cell line DNR distributed in a punctate pattern in the cytoplasm and was reduced in the nucleus. Verapamil, brefeldin A, but not chloroquine could recover the intracellular distribution of DNR from punctate to even in the resistant cell line. CONCLUSION: Altered subcellular disposition of DNR in resistant cell line was involved in the mechanism of multidrug resistance.

Antibiotics, Antineoplastic↗
PubMed2000

[Effects of pulsed Nd:YAG laser irradiation on shear bond strength of composite resin bonded to porcelain].

OBJECTIVE: To evaluate the shear bond strength of composite resin bonded to pretreated porcelain surfaces by use of a pulsed Nd:YAG laser irradiation and by use of 8% hydrofluoric etching. METHODS: Surfaces of porcelain were roughened with coarse diamonds until the opaque body porcelains were exposed. The samples were divided into four groups. Samples of the first group were etched with 8% hydrofluoric acid for 3 min by following the manufacter's instructions. Samples of the 2nd, 3rd and 4th groups were separately irradiated by a pulsed Nd:YAG laser of three energy parameters of 15 Hz, 40 mJ; 0.6 W; 15 Hz, 60 mJ, 0.9 W and 15 Hz, 80 mJ, 1.2 W different respectively, each specimen was irradiated for 1 min. Then, silane coupling agent was equally placed on the treated surfaces for 3 min, the activator was used on each surface. The adhesive was applied and light-cured. The composite resin material was finally bonded to the treated porcelain surface, forming a 3 mm x 3 mm x 2 mm resin mass. Samples were then tested for shear bond strength between the treated porcelain and composite resin by using a SWD-10 electric universal testing machine with a crosshead speed of 1 mm/min until fracture. At the end of testing, the data was evaluated by using a two-way analysis of variance (ANOVA) comparing the shear bond strength. On the other hand, characteristic morphology of laser irradiated surfaces of porcelain was prepared and observed by a scanning electron microscopy. RESULTS: The shear bond strength of laser groups of 0.6 W, 0.9 W, 1.2 W and etching group was respectively 8.61, 14.07, 11.22 and 13.47 MPa. There was no significantly difference among groups of laser 0.9 W, 1.2 W and the etching group. This suggested that irradiated on surfaces of porcelain by Nd:YAG laser at the above laser energy could attain the same effectiveness as hydrofluoric acid etching. But the shear bond strength of laser 0.6 W group was significantly lower than the etching group. It suggested that shear bond strength would obviously decrease when laser energy was 0.6 W or lower than this parameter, and had no use in treatment on porcelain surfaces comparing to acid etching. SEM showed that porcelain surfaces irradiated by Nd:YAG laser exhibited rough, umbilicate, lava crater-like structure. This structure helped to produce mechanical retention between resin composite and porcelain. CONCLUSION: The pulsed Nd:YAG laser could replace etching method to pretreat the fracture porcelain surfaces for bonding with composite resin at appropriate energy parameters.

Composite Resins↗
PubMed2000

[Immunocytological localization of IAA in the parenchyma cell and vascular elements in the graft union of Cucurbita pepo/Cucurbita moschata at the early developmental stage].

Immuno-gold localization of IAA in cells of the graft union in the explant internode graft of Cucurbita pepo/Cucurbita moschata were investigated with electron microscopy. In parenchyma cells near the graft union, the gold particles were mainly accumulated in nucleus, plastid and endoplasmic reticulum, while no gold particles was detected in Golgi body, mitochondrion, cell wall and vacuoles. In the differentiating xylem element, the gold particles were labeled in secondary wall and cytoplasm. In the sieve element gold particles were found in the sieve plate, sieve pore and cytoplasm. There was a dense label of the gold particles in the companion cell. The role of IAA in the differentiation of the vascular elements was discussed.

Cucurbita↗
PubMed2000

[Study on inhibitory actions of san huang yi gan capsule (SHYGC) on HBeAg with seropharmacological method].

In this paper, the inhibitory actions of SHYGC on HBeAg in vitro were studied with the seropharmacological method. By Enzyme Linked Immuno Sorbent Assay (ELISA), it was found that the rabbit sera containing SHYGC have significant inhibitory effects on HBeAg, and they become stronger with the drug concentration in sera improved and the actions time prolonged, they decrease with the HBeAg concentration improved, and the effects of the sera containing hing-dose drugs equal those of Su Xiao Jing containing 250 micrograms/g effective chloric. The direct external inhibitory effects of SHYGC in original pharmaceutics are stronger than those of the sera containing drugs. It probably indicated that the active ingredients of SHYGC could not be digested and absorbed completely from gastrointestine, or were inactived by metabolism in vivo.

Animals↗
PubMed1999

Transforming growth factor-beta induces collagenase-3 expression by human gingival fibroblasts via p38 mitogen-activated protein kinase.

Human collagenase-3 (matrix metalloproteinase 13 (MMP-13)) is characterized by exceptionally wide substrate specificity and restricted tissue specific expression. Human skin fibroblasts in culture express MMP-13 only when they are in three-dimensional collagen (Ravanti, L., Heino, J., López-Otín, C., and Kähäri. V.-M. (1999) J. Biol. Chem. 274, 2446-2455). Here we show that MMP-13 is expressed by fibroblasts during normal human gingival wound repair. Expression of MMP-13 by human gingival fibroblasts cultured in monolayer or in collagen gel was induced by transforming growth factor-beta1 (TGF-beta1). Treatment of gingival fibroblasts with TGF-beta1 activated two distinct mitogen-activated protein kinases (MAPKs): extracellular signal-regulated kinase 1/2 (ERK1/2) in 15 min and p38 MAPK in 1 and 2 h. Induction of MMP-13 expression by TGF-beta1 was blocked by SB203580, a specific inhibitor of p38 MAPK, but not by PD98059, a selective inhibitor of ERK1/2 activation. Adenovirus-mediated expression of dominant negative p38alpha and c-Jun potently inhibited induction of MMP-13 expression in gingival fibroblasts by TGF-beta1. Infection of gingival fibroblasts with adenovirus for constitutively active MEK1 resulted in activation of ERK1/2 and JNK1 and up-regulation of collagenase-1 (MMP-1) and stromelysin-1 (MMP-3) production but did not induce MMP-13 expression. In addition, activation of p38 MAPK by constitutively active MKK6b or MKK3b was not sufficient to induce MMP-13 expression. These results show that TGF-beta-elicited induction of MMP-13 expression by gingival fibroblasts is dependent on the activity of p38 MAPK and the presence of functional AP-1 dimers. These observations demonstrate a fundamental difference in the regulation of collagenolytic capacity between gingival and dermal fibroblasts and suggest a role for MMP-13 in rapid turnover of collagenous matrix during repair of gingival wounds, which heal with minimal scarring.

Cells, Cultured↗
PubMed1999

Axin forms a complex with MEKK1 and activates c-Jun NH(2)-terminal kinase/stress-activated protein kinase through domains distinct from Wnt signaling.

Axin negatively regulates the Wnt pathway during axis formation and plays a central role in cell growth control and tumorigenesis. We found that Axin also serves as a scaffold protein for mitogen-activated protein kinase activation and further determined the structural requirement for this activation. Overexpression of Axin in 293T cells leads to differential activation of mitogen-activated protein kinases, with robust induction for c-Jun NH(2)-terminal kinase (JNK)/stress-activated protein kinase, moderate induction for p38, and negligible induction for extracellular signal-regulated kinase. Axin forms a complex with MEKK1 through a novel domain that we term MEKK1-interacting domain. MKK4 and MKK7, which act downstream of MEKK1, are also involved in Axin-mediated JNK activation. Domains essential in Wnt signaling, i. e. binding sites for adenomatous polyposis coli, glycogen synthase kinase-3beta, and beta-catenin, are not required for JNK activation, suggesting distinct domain utilization between the Wnt pathway and JNK signal transduction. Dimerization/oligomerization of Axin through its C terminus is required for JNK activation, although MEKK1 is capable of binding C terminus-deleted monomeric Axin. Furthermore, Axin without the MEKK1-interacting domain has a dominant-negative effect on JNK activation by wild-type Axin. Our results suggest that Axin, in addition to its function in the Wnt pathway, may play a dual role in cells through its activation of JNK/stress-activated protein kinase signaling cascade.

Axin Protein↗
PubMed1999

p38 mitogen-activated protein kinase is involved in Fas ligand expression.

p38 mitogen-activated protein kinase (MAPK) is activated by T cell receptor engagement. Here we showed that T cell receptor activated p38alpha but not p38delta. Inhibition of p38alpha by the specific inhibitor SB 203580 prevented activation-induced cell death in T cells. SB 203580 had no effect on Fas-initiated apoptosis. Instead, SB 203580 preferentially inhibited activation-induced Fas ligand (FasL) expression. The inhibition on FasL expression by SB 203580 was correlated with the suppression on the FasL promoter activation. Overexpression of active MAPK kinase 3b, the activator of p38 MAPK, led to activation of FasL promoter and induction of FasL transcripts in T cells. Stress stimulation of T cells by anisomycin also induced FasL expression in a p38 MAPK-dependent manner. The induction of FasL expression in nonlymphoid cells such as 293T also required activation of p38 MAPK. Our results suggest that p38 MAPK is essential for FasL expression.

Apoptosis↗
PubMed1999

Selective activation of p38alpha and p38gamma by hypoxia. Role in regulation of cyclin D1 by hypoxia in PC12 cells.

Hypoxic/ischemic trauma is a primary factor in the pathology of a multitude of disease states. The effects of hypoxia on the stress- and mitogen-activated protein kinase signaling pathways were studied in PC12 cells. Exposure to moderate hypoxia (5% O(2)) progressively stimulated phosphorylation and activation of p38gamma in particular, and also p38alpha, two stress-activated protein kinases. In contrast, hypoxia had no effect on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal kinase, another stress-activated protein kinase. Prolonged hypoxia also induced phosphorylation and activation of p42/p44 mitogen-activated protein kinase, although this activation was modest compared with nerve growth factor- and ultraviolet light-induced activation. Hypoxia also dramatically down-regulated immunoreactivity of cyclin D1, a gene that is known to be regulated negatively by p38 at the level of gene expression (Lavoie, J. N., L'Allemain, G., Brunet, A., Muller, R., and Pouyssegur, J. (1996) J. Biol. Chem. 271, 20608-20616). This effect was partially blocked by SB203580, an inhibitor of p38alpha but not p38gamma. Overexpression of a kinase-inactive form of p38gamma was also able to reverse in part the effect of hypoxia on cyclin D1 levels, suggesting that p38alpha and p38gamma converge to regulate cyclin D1 during hypoxia. These studies demonstrate that an extremely typical physiological stress (hypoxia) causes selective activation of specific p38 signaling elements; and they also identify a downstream target of these pathways.

Animals↗
PubMed1999

Cell stress and MKK6b-mediated p38 MAP kinase activation inhibit tumor necrosis factor-induced IkappaB phosphorylation and NF-kappaB activation.

Tumor necrosis factor (TNF) exerts many actions through activation of the transcription factor NF-kappaB. NF-kappaB is sequestered in the cytosol by an inhibitory subunit IkappaB, which is inducibly phosphorylated by an IkappaB kinase complex and subsequently degraded. Sodium salicylate (NaSal) can block NF-kappaB activation by inhibiting IkappaBalpha phosphorylation. Recently, we used the specific p38 mitogen-activated protein (MAP) kinase inhibitor SB203580 to demonstrate that inhibition of TNF-induced IkappaBalpha phosphorylation requires NaSal-induced p38 activation. We demonstrate that NaSal similarly inhibits TNF-induced IkappaBbeta degradation in a p38-dependent manner. To further examine the role of p38, we determined whether other agents that activate p38 can block TNF-induced IkappaB phosphorylation and degradation. Sorbitol, H(2)O(2), and arsenite each blocked IkappaBalpha phosphorylation induced by TNF, and SB203580 reversed the inhibitory effects of sorbitol and H(2)O(2), but not arsenite. In addition, sorbitol and H(2)O(2) blocked TNF-induced but not interleukin-1-induced IkappaBalpha phosphorylation, whereas arsenite inhibited IkappaBalpha phosphorylation induced by TNF and interleukin-1. Transient expression of MAP kinase kinase (MKK) 6b(E), a constitutive activator of p38, reduced both TNF-induced phosphorylation of IkappaBalpha and NF-kappaB-dependent reporter activity. However, MKK7(D), a constitutive activator of c-Jun N-terminal kinases, failed to inhibit these TNF actions. Thus, sustained p38 activation by various stimuli inhibits TNF-induced IkappaB phosphorylation and NF-kappaB activation.

Animals↗
PubMed1999

RGS16 attenuates galphaq-dependent p38 mitogen-activated protein kinase activation by platelet-activating factor.

The large gene family encoding the regulators of G protein signaling (RGS) proteins has been implicated in the fine tuning of a variety of cellular events in response to G protein-coupled receptor activation. Several studies have shown that the RGS proteins can attenuate G protein-activated extracellular signal-regulated kinase (ERK) group of mitogen-activated protein kinases. We demonstrate herein that the production of inositol trisphosphate and the activation of the p38 group of mitogen-activated protein kinases by the G protein-coupled platelet-activating factor (PAF) receptor was attenuated by RGS16 in both CHO cells transiently and stably expressing RGS16. The inhibition was not observed with RGS2, RGS5, and a functionally defective form of RGS16, RGS16(R169S/F170C). The PAF-induced p38 and ERK pathways appeared to be preferentially regulated by RGS16 and RGS1, respectively. Overexpression of a constitutively active form of Galpha11 (Galpha11Q209L) prevented the RGS16-mediated attenuation of p38 activity, suggesting that Galphaq/11 is involved in PAF activation of p38. The Galphaq/11 involvement is further supported by the observation that p38 activation by PAF was pertussis toxin-insensitive. These results demonstrate for the first time that apart from ERK, p38 activation by a G protein-coupled receptor can be attenuated by an RGS protein and provide further evidence for the specificity of RGS function in G protein signaling pathways.

Animals↗
PubMed1999

Cloning and characterization of RLPK, a novel RSK-related protein kinase.

A novel protein kinase whose activity can be stimulated by mitogen in vivo was cloned and characterized. The cDNA of this gene encodes an 802-amino acid protein (termed RLPK) with the highest homology (37% identity) to the two protein kinase families, p90(RSK) and p70(RSK). Like p90(RSR), but not p70(RSK), RLPK also contains two complete nonidentical protein kinase domains. RLPK mRNA is widely expressed in all human tissues examined and is enriched in the brain, heart, and placenta. In HeLa cells, transiently expressed epitope-tagged RLPK can be strongly induced by epidermal growth factor, serum, and phorbol 12-myristate 13-acetate, but only moderately up-regulated by tumor necrosis factor-alpha and other stress-related stimuli. The activity of RLPK stimulated by epidermal growth factor was not inhibited by several known protein kinase C inhibitors nor by rapamycin, a known specific inhibitor for p70(RSK), but could be inhibited by herbimycin A, a tyrosine kinase inhibitor, and partially inhibited by PD98059 or SB203580, inhibitors for the mitogen-activated protein kinase pathways. Recombinant RLPK possesses high phosphorylation activity toward histone 2B and the S6 peptide, RRRLSSLRA. Although purified recombinant RLPK can be phosphorylated by ERK2 and p38alpha in vitro, its activity is not affected by this phosphorylation. Moreover, the treatment of RLPK with acid phosphatase did not reduce its in vitro kinase activity. These data suggest that RLPK is structurally similar to previously isolated RSKs, but its regulatory mechanism may be distinct from either p70(RSK) or p90(RSK)s.

Amino Acid Sequence↗