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Biomedical subjects

W Hong

Publications and source records attributed to W Hong.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Expression of beta 2 integrins and L-selectin on CML cells after treatment with IFN-alpha and allo-bone marrow transplantation].

OBJECTIVE: To study the expression of L-selectin, Mac-1, LFA-1 on CML progenitor cells in relation to CML progression and therapeutic effect. METHODS: The expression of adhesion molecules (LFA-1, Mac-1, L-selectin) on bone marrow CD34+ cells from 34 CML patients were analyzed by three-color flow cytometry. RESULTS: The mean percentage of expression of L-selectin, and LFA-1 on CD34+ CD38-(-)+ cells from untreated CML patients was significantly lower than that from normal controls. Among 8 CML patients treated with IFN-alpha, the expression of L-selectin and LFA-1 on CD34+ CD38- cell (37.6 +/- 5.3%, 42.1 +/- 13.1%) was comparable to that from normal controls (38.2 +/- 9.4%, 48.2 +/- 12.2%). L-selectin expression in CD34+ CD38- cells from CML patients was inversely correlated with the percentage of Ph'(+) cells. In 2 CML patients treated with allo-bone marrow transplantation, the expression rate of L-selectin, IFA-1 and Mac-1 on CD38+ CD38- cells was comparable to that from normal controls. CONCLUSION: The data suggest that decreased expression of L-selectin and LFA-1 in CML CD34+ cells reflects one of the features of malignant CML progenitors. IFN-alpha and allo-BMT restore the expression of Mac-1, L-selectin and LFA-1 to normal on CML CD34+ cells.

Adult↗
PubMed2000

[Neural network based on modified simplex method and its application in studying forest self-thinning].

The mechanism of forest self-thinning is generally nonlinear and dynamic, and the artificial neural network has the characteristic of expressing arbitrary nonlinear mapping. In this paper, the feasibility and limitation of artificial neural network used to simulating forest self-thinning was expounded, and the principle and algorithms of the neural network model based on modified simplex method (BP-MSM mixed algorithms) for modeling forest self-thinning were described. Its applications in self-thinning of Populus tremula natural forest Cunninghamia lanceolata plantation were illustrated. The results of forest self-thinning examples show the BP-MSM mixed algorithms were satisfactory in simulating forest self-thinning, and its precision was higher, which develops the method and theory of artificial neural network, and enriches the simulating method of forest self-thinning.

Algorithms↗
PubMed2000

[Quantitative characteristics of rare and endangered Castanopsis kawakamii population].

In this paper, a new self-adaptive model for population growth, i.e. S = exp(alpha ln2(1 + ce-rt) + beta ln(1 + ce-rt) + gamma) was established, which combined Logistic, Smith, Gompertz, Gui-Lawson, Zhang-Logistic and Liu-Logistic models. Estimations with genetic algorithm showed that the new model was more suitable than other models to simulate the actual growth trend of Castanopsis kawakamii population.

China↗
PubMed2000

[Energy distribution of Phyllostachys pubescens ecosytem in north Fujian].

Based on the data obtrained from 40 Phyllostachys pubescens plots in Jianou City of Fujian Province, the distribution of energy was studied in this paper. The results showed that the energy contained in stems, branches and leaves, and underground parts of P. pubescens ecosystem were 4.2322 x 10(8) kJ.hm-2, 0.9230 x 10(8) kJ.hm-2 and 1.7643 x 10(8) kJ.hm-2, accounting for 61.32%, 13.11% and 25.57% of the total energy respectively.

China↗
PubMed2000

[Life table analysis of Tsuga longibracteata population].

Tsuga longibracteata is a rare and endangered tree species in China. Based on the life table of population and the theory of survival analysis, the authors worked out the life table of Tsuga longibracteata population drew the curves of mortality density function, hazard rate function and survival, and analyzed the population dynamics. The results show that the population had two peaks of mortality, and the survival curve of the population trended to the type of Deevey II.

China↗
PubMed2000

[Relationship between blast crisis of chronic myeloid leukemias and abnormality of p16 and calcitonin genes].

OBJECTIVE: To study the relationship between homozygous deletions of p16 gene and calcitonin hypermethylation and chronic myeloid leukemia (CML) blast crisis. METHODS: Semiquantitative multiplex polymerase chain reaction (PCR) was used to detect homozygous deletions of p16 gene and semiquantitative PCR to detect calcitonin gene hypermethylation in 53 CML patients. RESULTS: In 53 CML patients, homozygous deletion of p16 gene was found in none of them in chronic phase, while in 6.3% (1/16) of them in myeloid blast crisis, 66.7% (8/12) in lymphoid blast crisis, and 2/5 (40%) in mixed cell blast crisis. Calcitonin gene hypermethylation was found in 10% (2/20), 68.8%(11/16), 16.7%(2/12), and 40% (2/5), respectively. CONCLUSION: There is intimate relationship between homozygous deletions of p16 gene and CML in lymphoid blast crisis, between calcitonin gene hypermethylation and CML in myeloid blast crisis. Moreover, abnormality of both genes may be associated with mixed cell blast crisis in CML patients. Simultaneous detection of the two genes help early pickup CML patients in blast crisis.

Adult↗
PubMed2000

[Epidemiological feature on diabetes mellitus among permanent inhabitant in the Special Economic Zone of Shenzhen].

OBJECTIVE: To investigate prevalence and relevant factors of diabetes mellitus among permanent inhabitant in Shenzhen. METHODS: The prevalence of 8 200 inhabitants aged over 20 in Shenzhen was studied. Blood glucose was determined by glucose - oxidase method. RESULTS: According to the WHO diagnostic standard, the prevalence rates of DM and IGT were 4.23% and 11.94% respectively. The prevalence increased apparently with age. The history of clan and overweight were related to the prevalence rates of DM and IGT. The people of DM and IGT were mostly accompanied with high levels of triglyceride, total cholesterol, uric acid, creatinine and low level of high dense lipoprotein (HDL). CONCLUSION: The history of clan, old age, overweight and higher fattiness were found risk factors of DM and IGT.

Adult↗
PubMed2000

[Distribution of HIV resistance CCR5-delta 32, CCR2-64 I and SDF1-3'A alleles and their polymorphisms in the Han population in China].

OBJECTIVE: To study the frequency and polymorphism of three mutations (CCR5(Delta)32, CCR2-64I and SDF1-3'A alleles) conferring resistance to determined HIV-1/AIDS in the indigenous Han population in China. METHODS: The study population included 1,267 subjects, of which consisted 98.7% (1,251/1,267) Han people. The genotypes of the three mutations were respectively, detected by polymerase chain reaction (PCR) for CCR5(Delta)32 mutation, or by PCR/RFLP (restriction fragment length polymorphism) assay with the digestion of restriction endonuclease Bsa BI and Msp I for CCR2-64I and SDF1-3'A mutations. DNA sequencing was employed to confirm the accuracy of PCR or PCR/RFLP products. RESULTS: The frequency of the mutant alleles were: 0.00119 for CCR5(Delta)32; 0.20023 for CCR2-64I, and 0.28723 for SDF1-3'A. The three heterozygous CCR5-wt/Delta32 mutants were identified and no homozygotes were detected in indigenous Han population. The frequencies of CCR2-64I and SDF1-3'A alleles in China were higher than those of Caucasians descents in the USA and Europe. CONCLUSION: Our data was the first findings on the frequency and polymorphism of CCR5(Delta)32, CCR2-64I and SDF1-3'A alleles in indigenous Han population in China which implied that the indigenous Han people might have a higher genetic susceptibility to the infection of sexually transmitted HIV-1 (R-5) strain. Further study is needed to clarify the significance of higher frequency of CCR2-64I and SDF1-3'A alleles in Han population.

Alleles↗
PubMed2000

[Polymorphisms of chemokine receptor alleles influencing genetic susceptibility to HIV-1 infection in Mongolia population in China].

OBJECTIVE: Mutant frequency and polymorphism of HIV-1 resistance CCR5-Delta32, CCR2b-64I and SDF1-3'A alleles were investigated in Chinese population from Mongolian ethnic origin. METHODS: Whole blood samples from 134 Mongolian subjects were collected randomly and their genomic DNA were extracted using Qiagen Blood Kit. Allelic frequency was identified by means of PCR or PCR-RFLP analysis. Allelic polymorphism in population and between sex in the sample as well as correlation of the three genes were analyzed by chi(2) test. RESULTS: The frequencies of the three alleles were as following: CCR5-Delta32 1.1%, CCR2b-64I 24.8% and SDF1-3'A 22.0% respectively. Distribution of the three mutant alleles among the Mongolian population was in accordance with Hardy-Weinberg equilibrium. Statistical analysis showed there was a higher frequency of CCR2b-64I in female than in male subjects (29.2% vs 19.7%). No Statistical difference was found in the allelic frequencies of both CCR5-Delta32 and SDF1-3'A between male and female individuals. CONCLUSION: Compared with the Caucasian American, there were higher frequencies of CCR2b-64I and SDF1-3'A alleles and lower frequency of CCR5-Delta32 allele found in Mongolian population while the factors responsible for the variation of genetic polymorphisms in different ethnic populations need to be clarified.

Adolescent↗
PubMed1999

A family of mammalian proteins homologous to yeast Sec24p.

The Sec23p/Sec24p complex is a component of yeast coat protein II (COPII), the coat protein complex responsible for vesicle budding from the endoplasmic reticulum (ER). Database searches and molecular cloning reveal that four different mammalian Sec24p-like proteins exist, all with about 20% amino acid identity with the yeast Sec24p. Sec24A and Sec24B share about 50% amino acid identity. Sec24D is cloned by screening a human pancreas of cDNA library with an expressed sequence tag (EST) fragment that is homologous to, but distinct from, Sec24A and Sec24B. Sec24D shares about 50% amino acid identity with the gene product of KIAA0079, which we have designated as Sec24C. These mammalian Sec24s appear to form two subclasses based on homology. Sec24A/B and Sec24C/D share about 20% identity with each other and with the yeast Sec24p. The Sec24 sequences also share weak but significant homology to the mammalian Sec23A and Sec23B. Northern blot analysis revealed that Sec24C is ubiquitously expressed. Although Sec24D transcripts are detectable in all tissues examined, they are selectively enriched in certain tissues, particularly placenta and pancreas. myc-tagged Sec24C and sec24D colocalized with Sec13, another COPII component. This colocalization suggests that Sec24C and Sec24D are indeed associated with COPII structures on membranes of the ER-Golgi boundary. The existence of at least four forms of Sec24 in mammalian cells suggest that multiple forms of COPII complex may be involved in ER export.

Amino Acid Sequence↗
PubMed1999

cDNA characterization and chromosomal mapping of human golgi SNARE GS27 and GS28 to chromosome 17.

Transport of proteins along the exocytotic pathway is primarily achieved by vesicular intermediates. Two proteins, Golgi SNAREs of 27 kDa, GS27, and of 28 kDa, GS28 (HGMW-approved nomenclature GOSR2 and GOSR1, respectively), are important trafficking membrane proteins between the endoplasmic reticulum and the Golgi and between Golgi subcompartments. Here, we present the human GS27 and GS28 cDNA sequences. They encode predicted proteins of 212 and 250 amino acids, respectively. Chromosomal mapping analyses reveal that human GS27 is located on chromosome 17q21 and GS28 on approximately 17q11. The chromosomal location of GS27 near a locus implicated in familial essential hypertension and its known function in trafficking indicate that it is a potential candidate gene for this disease.

Chromosome Mapping↗
PubMed1999

GS32, a novel Golgi SNARE of 32 kDa, interacts preferentially with syntaxin 6.

Syntaxin 1, synaptobrevins or vesicle-associated membrane proteins, and the synaptosome-associated protein of 25 kDa (SNAP-25) are key molecules involved in the docking and fusion of synaptic vesicles with the presynaptic membrane. We report here the molecular, cell biological, and biochemical characterization of a 32-kDa protein homologous to both SNAP-25 (20% amino acid sequence identity) and the recently identified SNAP-23 (19% amino acid sequence identity). Northern blot analysis shows that the mRNA for this protein is widely expressed. Polyclonal antibodies against this protein detect a 32-kDa protein present in both cytosol and membrane fractions. The membrane-bound form of this protein is revealed to be primarily localized to the Golgi apparatus by indirect immunofluorescence microscopy, a finding that is further established by electron microscopy immunogold labeling showing that this protein is present in tubular-vesicular structures of the Golgi apparatus. Biochemical characterizations establish that this protein behaves like a SNAP receptor and is thus named Golgi SNARE of 32 kDa (GS32). GS32 in the Golgi extract is preferentially retained by the immobilized GST-syntaxin 6 fusion protein. The coimmunoprecipitation of syntaxin 6 but not syntaxin 5 or GS28 from the Golgi extract by antibodies against GS32 further sustains the preferential interaction of GS32 with Golgi syntaxin 6.

Amino Acid Sequence↗
PubMed1999

Morphological and functional association of Sec22b/ERS-24 with the pre-Golgi intermediate compartment.

Yeast Sec22p participates in both anterograde and retrograde vesicular transport between the endoplasmic reticulum (ER) and the Golgi apparatus by functioning as a v-SNARE (soluble N-ethylmaleimide-sensitive factor [NSF] attachment protein receptor) of transport vesicles. Three mammalian proteins homologous to Sec22p have been identified and are referred to as Sec22a, Sec22b/ERS-24, and Sec22c, respectively. The existence of three homologous proteins in mammalian cells calls for detailed cell biological and functional examinations of each individual protein. The epitope-tagged forms of all three proteins have been shown to be primarily associated with the ER, although functional examination has not been carefully performed for any one of them. In this study, using antibodies specific for Sec22b/ERS-24, it is revealed that endogenous Sec22b/ERS-24 is associated with vesicular structures in both the perinuclear Golgi and peripheral regions. Colabeling experiments for Sec22b/ERS-24 with Golgi mannosidase II, the KDEL receptor, and the envelope glycoprotein G (VSVG) of vesicular stomatitis virus (VSV) en route from the ER to the Golgi under normal, brefeldin A, or nocodazole-treated cells suggest that Sec22b/ERS-24 is enriched in the pre-Golgi intermediate compartment (IC). In a well-established semi-intact cell system that reconstitutes transport from the ER to the Golgi, transport of VSVG is inhibited by antibodies against Sec22b/ERS-24. EGTA is known to inhibit ER-Golgi transport at a stage after vesicle/transport intermediate docking but before the actual fusion event. Antibodies against Sec22b/ERS-24 inhibit ER-Golgi transport only when they are added before the EGTA-sensitive stage. Transport of VSVG accumulated in pre-Golgi IC by incubation at 15 degreesC is also inhibited by Sec22b/ERS-24 antibodies. Morphologically, VSVG is transported from the ER to the Golgi apparatus via vesicular intermediates that scatter in the peripheral as well as the Golgi regions. In the presence of antibodies against Sec22b/ERS-24, VSVG is seen to accumulate in these intermediates, suggesting that Sec22b/ERS-24 functions at the level of the IC in ER-Golgi transport.

Animals↗
PubMed1999

Localization and recycling of gp27 (hp24gamma3): complex formation with other p24 family members.

We report here the characterization of gp27 (hp24gamma3), a glycoprotein of the p24 family of small and abundant transmembrane proteins of the secretory pathway. Immunoelectron and confocal scanning microscopy show that at steady state, gp27 localizes to the cis side of the Golgi apparatus. In addition, some gp27 was detected in COPI- and COPII-coated structures throughout the cytoplasm. This indicated cycling that was confirmed in three ways. First, 15 degrees C temperature treatment resulted in accumulation of gp27 in pre-Golgi structures colocalizing with anterograde cargo. Second, treatment with brefeldin A caused gp27 to relocate into peripheral structures positive for both KDEL receptor and COPII. Third, microinjection of a dominant negative mutant of Sar1p trapped gp27 in the endoplasmic reticulum (ER) by blocking ER export. Together, this shows that gp27 cycles extensively in the early secretory pathway. Immunoprecipitation and coexpression studies further revealed that a significant fraction of gp27 existed in a hetero-oligomeric complex. Three members of the p24 family, GMP25 (hp24alpha2), p24 (hp24beta1), and p23 (hp24delta1), coprecipitated in what appeared to be stochiometric amounts. This heterocomplex was specific. Immunoprecipitation of p26 (hp24gamma4) failed to coprecipitate GMP25, p24, or p23. Also, very little p26 was found coprecipitating with gp27. A functional requirement for complex formation was suggested at the level of ER export. Transiently expressed gp27 failed to leave the ER unless other p24 family proteins were coexpressed. Comparison of attached oligosaccharides showed that gp27 and GMP25 recycled differentially. Only a very minor portion of GMP25 displayed complex oligosaccharides. In contrast, all of gp27 showed modifications by medial and trans enzymes at steady state. We conclude from these data that a portion of gp27 exists as hetero-oligomeric complexes with GMP25, p24, and p23 and that these complexes are in dynamic equilibrium with individual p24 proteins to allow for differential recycling and distributions.

Amino Acid Sequence↗
PubMed1999

A role for Tlg1p in the transport of proteins within the Golgi apparatus of Saccharomyces cerevisiae.

Members of the syntaxin protein family participate in the docking-fusion step of several intracellular vesicular transport events. Tlg1p has been identified as a nonessential protein required for efficient endocytosis as well as the maintenance of normal levels of trans-Golgi network proteins. In this study we independently describe Tlg1p as an essential protein required for cell viability. Depletion of Tlg1p in vivo causes a defect in the transport of the vacuolar protein carboxypeptidase Y through the early Golgi. Temperature-sensitive (ts) mutants of Tlg1p also accumulate the endoplasmic reticulum/cis-Golgi form of carboxypeptidase Y at the nonpermissive temperature (38 degrees C) and exhibit underglycosylation of secreted invertase. Overexpression of Tlg1p complements the growth defect of vti1-11 at the nonpermissive temperature, whereas incomplete complementation was observed with vti1-1, further suggesting a role for Tlg1p in the Golgi apparatus. Overexpression of Sed5p decreases the viability of tlg1 ts mutants compared with wild-type cells, suggesting that tlg1 ts mutants are more susceptible to elevated levels of Sed5p. Tlg1p is able to bind His6-tagged Sec17p (yeast alpha-SNAP) in a dose-dependent manner and enters into a SNARE complex with Vti1p, Tlg2p, and Vps45p. Morphological analyses by electron microscopy reveal that cells depleted of Tlg1p or tlg1 ts mutants incubated at the restrictive temperature accumulate 40- to 50-nm vesicles and experience fragmentation of the vacuole.

Adenosine Triphosphatases↗
PubMed1999

Forward and retrograde trafficking in mitotic animal cells. ER-Golgi transport arrest restricts protein export from the ER into COPII-coated structures.

Protein transport arrest occurs between the ER and Golgi stack of mitotic animal cells, but the location of this block is unknown. In this report we use the recycling intermediate compartment protein ERGIC 53/p58 and the plasma membrane protein CD8 to establish the site of transport arrest. Recycled ERGIC 53/p58 and newly synthesised CD8 accumulate in ER cisternae but not in COPII-coated export structures or more distal sites. During mitosis the tubulovesicular ER-related export sites were depleted of the COPII component Sec13p, as shown by immunoelectron microscopy, indicating that COPII budding structures are the target for mitotic inhibition. The extent of recycling of Golgi stack residents was also investigated. In this study we used oligosaccharide modifications on CD8 trapped in the ER of mitotic cells as a sensitive assay for recycling of Golgi stack enzymes. We find that modifications conferred by the Golgi stack-resident GalNac transferase do occur on newly synthesised CD8, but these modifications are entirely due to newly synthesised transferase rather than to enzyme recycled from the Golgi stack. Taken together our findings establish for the first time that the site of ER-Golgi transport arrest of mitotic cells is COPII budding structures, and they clearly speak against a role for recycling in partitioning of Golgi stack proteins via translocation to the ER.

Animals↗