Biomedical subjects

S Jiang

Publications and source records attributed to S Jiang.

At least 127 records · Page 7Linked to original sources

PubMed2000

[Sodium salicylate induced intracellular Ca2+ concentration change in guinea pig outer hair cells].

OBJECTIVE: In order to explore the mechanism of sodium salicylate ototoxicity the effect of sodium salicylate on intracellular Ca2+ ([Ca2+]i) of the outer hair cells (OHCs) and the effects of calcium channel antagonist on sodium salicylate-induced [Ca2+]i changes of the OHCs were examined. METHODS: The OHCs of guinea pig cochlear were isolated using an enzyme-machine methods and loaded with 10 mumol/L Fluo-3/AM for 30 min at 37 degrees C. Individual Fluo-3 loaded OHC was examined with a confocal microscope (ACAS Ultima, USA) using a 20 x objective lens and linear scan mean. The fluorescent images, collected each 5-sec for 300 sec, were stored in a computer. The fluorescent intensity of the OHCs were analyzed by the software cooperated with the confocal microscope, and a curve of fluorescent intensity changes trend against time was obtained. RESULTS: The [Ca2+]i of OHCs were steady under normal extracellular liquid perfusion. Salicylate increased [Ca2+]i in OHCs in calcium-free medium(10/10) and standard medium (8/10). 3 mmol/L lidocaine inhibited [Ca2+]i increase in OHCs induced by salicylate(0/10). The [Ca2+]i increase in OHCs induced by salicylate could be blocked by flunarizine(3/12). Nimodipin failed to block the [Ca2+]i increase of OHCs induced by salicylate (7/7). CONCLUSION: Sodium salicylate can result in [Ca2+]i increase in OHC markedly, which may be due to the Ca2+ release from intracellular calcium stores. The effects of salicylate on [Ca2+]i in OHCs might be one of the mechanisms of salicylate ototoxicity.

Animals↗

PubMed2000

[The study on the role of telomerase activity in human nasopharyngeal carcinoma].

OBJECTIVE: To elucidate the role of telomerase activity in nasopharyngeal carcinoma (NPC). METHODS: Telomerase activity was detected using the telomere repeat amplification protocol(TRAP) combined with silver staining in 42 low-differentiated squamous carcinoma, 10 normal nasopharyngeal mucosae and 8 nasopharyngeal fibrohemangioma. RESULTS: Telomerase activity was detectable in 20% normal nasopharyngeal mucosae and 88.1% in NPC. The activity of telomerase was not detectable in 8 nasopharyngeal fibrohemangioma tissues. Telomerase activity was present more frequently in NPC biopsies with positive lymph node metastasis than in those without lymph node metastasis (P = 0.035). Furthermore, telomerase activity was observed more frequently in advanced NPC than in early stage (P = 0.048). However, there was no evidence to show the relationship between telomerase activity and other clinical features, such as age, gender and distant metastasis (P > 0.05). Serum EBV marker(VCA-IgA) was observed more frequently in NPC than in normal nasopharyngeal mucosae patients(P < 0.001). CONCLUSION: Telomerase activity may play a critical role in the tumorigenesis of NPC. Detection of telomerase activity combined with serological EBV markers may contribute to the screening and early diagnosis of NPC.

Adolescent↗

PubMed2000

[Evaluating effects of some medicine on tinnitus with animal behavioral model in rats].

OBJECTIVE: To develop a valid behavioral animal model of tinnitus and to determine the animals whether have the perception of tinnitus and to evaluate effects of nimodipine and Chinese herbs on tinnitus using the behavioral model. METHODS: Adult male albino rats (n = 60) were fell evenly and randomly into ten groups. Animals in Group I and II were administrated sodium salicylate 350 mg/kg/d (i.p.). Instead, animals in control groups (Group III and IV) were saline injected. Pure tone (8 kHz, 65 dBSPL) was given to rats in Group V and VI instead of sodium salicylate. Nimodipine (1 mg/kg) were administrated to animals in Group VII and VIII. Gushenshuerfang, one kind of Chinese herbs were administrated to animals in Group IX and X. Medicine or pure tone were being given to all animals in Group I, III, V, VII, IX before conditioned reflex. Animals in Group II, IV, VI, VIII, X began to have medicine or pure tone after conditioned reflex. Thirsty animals (deprived of water for several days) were breeded in sound-proofed room and listened a persistent white noise (55 dB SPL) and trained daily with our instrument system, according to the procedure based on Pavlovian conditioned suppression paradigm. Subjects were permitted to lick water at an automatic dispenser during daily training sessions and the number of licks was recorded automatically. Noise offset (silence) was the conditioned stimulus and the electrical shock was the unconditioned stimulus. After two or three days training, subjects learnt rapidly to associate noise offset with shock and then established a behavioral conditioned reflex. Because of shock fear they decrease or even stop licking with the presentations of conditioned stimulus. However, subjects gradually forgot or ignored the fear without any shock present in extinction test sessions. RESULTS: Animals' licking recovered to their pre-training levels respectively at the following days: Group I--5 days, Group II--2 days, both Group III and IV--4 days, Group V--5 days, Group VI--2 days, Group VII--5 days, Group VIII--4 days, Group IX--5 days, Group X--4 days. There were much significant differences among all groups and all training days (F test, P < 0.001). Above results provided sufficient evidence for that tinnitus was induced by salicylate and tinnitus presented with noise offset. In group I, tinnitus became additional conditioned stimulus. Therefore, the fear of animals was much severe and the numbers of licking were much fewer. Extinction lasted longer. In group II, animals ignored the noise offset much easily and the extinction lasted much shorter. Moreover, results from group V and VI, pure tone instead of salicylate, indicated that sensation (tinnitus) sounded like pure tone. The groups VII, VIII, IX, X demonstrated that nimodipine and Gushenshuerfang, one kind of Chinese herbs can cure the tinnitus induced by salicylate. CONCLUSION: All behavioral evidence indicated that animals perceived tinnitus induced by salicylate and this animal model could be used in evaluating curative effects of some medicine on tinnitus.

Animals↗

PubMed2000

[Mitochondrial DNA4977 deletions associated with human presbycusis].

OBJECTIVE: To determine whether or not the mtDNA4977 deletions contribute to human aging and involve in the development of presbycusis. METHODS: 67 sides of archival temporal bone sections, 20 temporal brains, 21 cochlear nucleus, 20 hearts and 22 livers were harvested and the total DNA was extracted. The presence of mtDNA4977 deletions was examined using nest polymerase chain reaction(PCR). RESULTS: Our results showed: (1) the highly conserved mitochondrially-encoded tRNA and ND1 segments were amplified from all tissues, as well as mtDNA4977 deletions related to aging. (2) The incidence of carrying mtDNA4977 deletions in all tissues in aged group was significant higher than that of young control group (P < 0.05). (3) The incidence of carrying mtDNA4977 deletions in temporal bone sections and cochlear nucleus with presbycusis patients was significant higher than that of aged normal hearing control group (P < 0.05). However, the incidence of carrying mtDNA4977 deletions in heart and liver were no significant difference between presbycusis patients and the control group. CONCLUSION: These findings indicated that mtDNA4977 deletions in human contribute to presbycusis, as well as aging.

Adult↗

PubMed2000

[Thiol reagent thimerosal-induced Ca2+ mobilization in isolated guinea pig cochlear outer hair cells].

OBJECTIVE: To understand mechanism of cochlear outer hair cells (OHCs) intracellular Ca2+ mobilization further. METHODS: Intracellular calcium of isolated guinea pig was investigated using thimerosal, a--SH group oxidizing agent, and fura-2 fluorescence ratio imaging microscopy. RESULTS: In the presence of thimerosal, intracellular Ca2+ concentrations ([Ca2+]i) of OHCs were elevated in a dose-dependent manner. Even in Ca(2+)-free medium, Ca2+ response was still induced. The effects of thimerosal on [Ca2+]i were completely blocked and reversed by (DTT). Neither 1-100 mumol/L ryanodine nor 5-20 mmol/L caffeine altered the effects of thimerosal. Pretreatment with pertussis toxin (PTX) for 30 min did not affect the thimerosal-induced increase in [Ca2+]i The increase in [Ca2+]i when Ca2+ was added during thimerosal application in Ca(2+)-free medium was almost completely blocked by 500 mol/L LaCl3, while nifedipine did not inhibit further increase in [Ca2+]i caused by thimerosal. CONCLUSION: Oxidation of the -SH group of the OHC membrane can induce a Ca2+ release from intracellular Ca2+ stores, which are ryanodine- and caffeine-insensitive, and Ca2+ influx through non-specific Ca2+ channels, but not the nifedipine-sensitive Ca2+ Channels. The possible oxidation of--SH group gated Ca2+ channels in OHCs are worthy of further study.

Animals↗

PubMed2000

[The molecular structure and the arrangement changes of stilbazoles in the phase transition process studied by temperature-variable FTIR spectroscopy].

Hydrogen bonding is one of the principal intermolecular forces to enable the construction of supramolecular structures. By choosing an appropriate proton acceptor and a proton donor, stable intermolecular hydrogen bonds can form and affect or change the phase behavior of the donor and acceptor. We have obtained two intermolecular hydrogen bonded liquid crystals using the stilbazoles as the proton acceptor. In this paper we will research the molecular structure and the arrangement changes during the phase transition process of the stilbazoles by temperature variable FTIR spectroscopy. The results show that the number of the gauche conformation is increasing as the temperature increasing. When it is coming to the isotropic phase, the alkyl chain is in disorder. The frequency shift of carbonyl stretching bands has been found to be sensitive to the change of molecular conformation, inter and intramolecular interactions.

Hydrogen Bonding↗

PubMed1999

Studies of the DXS7 polymorphism at the MAO loci in unipolar depression.

From the fact that DXS7 polymorphism is closely related to monoamine oxidase (MAO) genes and MAO inhibitors are widely used in the treatment of unipolar depression, it is of particular interest to study the relationship between the DXS7 polymorphism and unipolar depression. Thus, this study examined the possible association between DXS7 polymorphism and unipolar depression in 66 cases versus 85 controls from Shanghai. Polymerase chain reaction and amplification fragment length polymorphism techniques were used for genotyping of the DXS7 locus in this study. Four alleles at the DXS7 locus were detected with length generated by polymerase chain reaction amplification ranging from 157 to 167 bp. Comparison of allele frequency in the DXS7 locus showed no difference between unipolar depression cases and normal controls in the total population set. When subclassified by age, a significant difference of allele frequency distribution was observed between early onset (before age 40) and late onset (after age 40) patients. The frequency of the 157-bp allele was decreased, whereas the frequency of the 165 allele was increased in late onset patients (0.3810 for the 157-bp allele and 0.5238 for the 165-bp allele) compared with that of early onset patients (0.6304 for the 157-bp allele and 0. 3261 for the 165-bp allele). There was also a difference of allele frequency between patients and normal controls with age over 40 years. The frequency of 165-bp allele increased significantly in late onset patients (0.5238) compared with that of controls within the same age range (0.3454). Association studies suggested that in the population with age over 40 years, presence of the 165-bp allele of DXS7 locus was significantly associated with unipolar depression (relative risk = 2.08, P < 0.05), whereas in the total population set, this association did not exist. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:598-600, 1999.

Adolescent↗

PubMed1999

T suppressor lymphocytes inhibit NF-kappa B-mediated transcription of CD86 gene in APC.

CD8+CD28- human T suppressor cells (Ts) act on APC, inhibiting their ability to elicit Th activation and proliferation. This effect is due to inhibition of the CD40 pathway which normally leads to CD80 and CD86 up-regulation. To determine whether Ts inhibit expression of B7 molecules by blocking transcription, we cloned and characterized the CD86 promoter. Mutational analysis revealed that Ts inhibit transcription driven by the CD86 promoter. The NF-kappa B binding site, at -612 of the CD86 promoter, is essential for Th-induced transcription. In cultures containing Th and Ts, Ts inhibit Th-induced NF-kappa B activation in APC. Together, these findings indicate that Ts inhibition of NF-kappa B activation in APC is a means by which they regulate the activation and proliferation of Th.

Antigen-Presenting Cells↗

PubMed1999

Characterization of human and murine PMP20 peroxisomal proteins that exhibit antioxidant activity in vitro.

We have isolated the cDNAs encoding human and mouse homologues of a yeast protein, termed peroxisomal membrane protein 20 (PMP20). Comparison of the amino acid sequences of human (HsPMP20) and mouse (MmPMP20) PMP20 proteins revealed a high degree of identity (93%), whereas resemblance to the yeast Candida boidinii PMP20A and PMP20B (CbPMP20A and CbPMP20B) was less (30% identity). Both HsPMP20 and MmPMP20 lack transmembrane regions, as do CbPMP20A and CbPMP20B. HsPMP20 mRNA expression was low in human fetal tissues, especially in the brain. In adult tissues, HsPMP20 mRNA was expressed in the majority of tissues tested. HsPMP20 and MmPMP20 contained the C-terminal tripeptide sequence Ser-Gln-Leu (SQL), which is similar to the peroxisomal targeting signal 1 utilized for protein import into peroxisomes. HsPMP20 bound directly to the human peroxisomal targeting signal 1 receptor, HsPEX5. Mutagenesis analysis showed that the C-terminal tripeptide sequence, SQL, of HsPMP20 is necessary for its binding to HsPEX5. Subcellular fractionation of HeLa cells, expressing epitope-tagged PMP20, revealed that HsPMP20 is localized in the cytoplasm and in a particulate fraction containing peroxisomes. Double-staining immunofluorescence studies showed colocalization of HsPMP20 and thiolase, a bona fide peroxisomal protein. The amino acid sequence alignment of HsPMP20, MmPMP20, CbPMP20A, and CbPMP20B displayed high similarity to thiol-specific antioxidant proteins. HsPMP20 exerted an inhibitory effect on the inactivation of glutamine synthetase in the thiol metal-catalyzed oxidation system but not in the nonthiol metal-catalyzed oxidation system, suggesting that HsPMP20 possesses thiol-specific antioxidant activity. In addition, HsPMP20 removed hydrogen peroxide by its thiol-peroxidase activity. These results indicate that HsPMP20 is imported into the peroxisomal matrix via PEX5p and may work to protect peroxisomal proteins against oxidative stress. Because some portion of PMP20 might also be present in the cytosol, HsPMP20 may also have a protective effect in the cytoplasm.

Amino Acid Sequence↗

PubMed1999

Cytochrome c-mediated apoptosis in cells lacking mitochondrial DNA. Signaling pathway involving release and caspase 3 activation is conserved.

Mitochondria serve as a pivotal component of the apoptotic cell death machinery. However, cells that lack mitochondrial DNA (rho(0) cells) retain apparently normal apoptotic signaling. In the present study, we examined mitochondrial mechanisms of apoptosis in rho(0) osteosarcoma cells treated with staurosporine. Immunohistochemistry revealed that rho(0) cells maintained a normal cytochrome c distribution in mitochondria even though these cells were deficient in respiration. Upon staurosporine treatment, cytochrome c was released concomitantly with activation of caspase 3 and loss of mitochondrial membrane potential (Deltapsi(m)). After mitochondrial loss of cytochrome c, rho(0) cells underwent little change in glutathione (GSH) redox potential whereas a dramatic oxidation in GSH/glutathione disulfide (GSSG) pool occurred in parental rho(+) cells. These results show that mitochondrial signaling of apoptosis via cytochrome c release was preserved in cells lacking mtDNA. However, intracellular oxidation that normally accompanies apoptosis was lost, indicating that the mitochondrial respiratory chain provides the major source of redox signaling in apoptosis.

Apoptosis↗

PubMed1999

Differential expression of PSP94 in rat prostate lobes as demonstrated by an antibody against recombinant GST-PSP94.

Prostate secretory protein (PSP94, 94 amino acids) is one of the most abundant proteins secreted from the prostate. Its biological role is unknown and still controversial, although it is assumed to have the potential to be a biomarker and a suppressor of prostate cancer. In order to establish an animal model to further elucidate its biological role, we expressed the mature form of rat PSP94 in Escherichia coli, using a glutathione S-transferase (GST) fusion expression vector; we generated a polyclonal rabbit antibody against the recombinant protein. The antibody specifically recognized recombinant rat PSP94 and cross-reacted only very weakly with its human homologue. Using the characterized anti-rat PSP94 antibody, we found that PSP94 was located primarily in rat prostate. Furthermore, PSP94 is present at different levels in different lobes of rat prostate, with significant levels detectable only in the lateral lobe (LP). In addition, the most abundant PSP94 expression was found in the prostate lobe secretions, and PSP94 levels in LP secretions were at least seven times higher than in secretions from the dorsal prostate (DP). The rat ventral prostate (VP) and other regions of the male accessory glands were found to be almost completely devoid of PSP94. Since most rat prostate dysplasia induced by steroid hormone treatment occurs only in dorsolateral prostate, prostate tissue-specific expression and the expression of PSP94 in dorsolateral, but not other, lobes of the prostate suggest a potential role in prostate targeting and prostate cancer development.

Animals↗

PubMed1999

Structure-based identification of small molecule antiviral compounds targeted to the gp41 core structure of the human immunodeficiency virus type 1.

Recent X-ray crystallographic determination of the HIV-1 envelope glycoprotein gp41 core structure opened up a new avenue to discover antiviral agents for chemotherapy of HIV-1 infection and AIDS. We have undertaken a systematic study to search for anti-HIV-1 lead compounds targeted to gp41. Using molecular docking techniques to screen a database of 20 000 organic molecules, we found 16 compounds with the best fit for docking into the hydrophobic cavity within the gp41 core and with maximum possible interactions with the target site. Further testing of these compounds by an enzyme-linked immunosorbent assay and virus inhibition assays discerned two compounds (ADS-J1 and ADS-J2) having inhibitory activity at micromolar concentrations on the formation of the gp41 core structure and on HIV-1 infection. These two compounds will be used as leads to design more effective HIV-1 inhibitors targeted to the HIV-1 gp41 core structure.

Anti-HIV Agents↗

PubMed1999

Mosaic allelic insulin-like growth factor 2 expression patterns reveal a link between Wilms' tumorigenesis and epigenetic heterogeneity.

Numerous observations link the loss of imprinting of insulin-like growth factor 2 (IGF2) and an overdosage of this growth factor gene with cancer, in general, and with Wilms' tumorigenesis, in particular. It is not known, however, if loss of imprinting correlates with specific stages of neoplasia or if allelic expression patterns vary within the tumor. By applying an allele-specific in situ hybridization technique to formalin-fixed thin sections, we show that the parental IGF2 alleles can be differentially expressed, not only in Wilms' tumors, but also in nephrogenic rests (which represent premalignant lesions) of Wilms' tumor patients. Moreover, a subpopulation of mesenchymal cells, which surrounds tumor nodules, expresses IGF2 biallelically irrespective of the imprinted state of IGF2 within the tumor. These data show that Wilms' tumorigenesis involves epigenetic heterogeneity as visualized by variable allelic IGF2 expression patterns.

Alleles↗

PubMed1999

The receptor protein tyrosine phosphatase, PTP-RO, is upregulated during megakaryocyte differentiation and Is associated with the c-Kit receptor.

We have recently isolated a cDNA encoding a novel human receptor-type tyrosine phosphatase, termed PTP-RO (for a protein tyrosine phosphatase receptor omicron), from 5-fluorouracil-treated murine bone marrow cells. PTP-RO is a human homologue of murine PTPlambda and is related to the homotypically adhering kappa and mu receptor-type tyrosine phosphatases. PTP-RO is expressed in human megakaryocytic cell lines, primary bone marrow megakaryocytes, and stem cells. PTP-RO mRNA and protein expression are upregulated upon phorbol 12-myristate 13-acetate (PMA) treatment of the megakaryocytic cell lines CMS, CMK, and Dami. To elucidate the function of PTP-RO in megakaryocytic cells and its potential involvement in the stem cell factor (SCF)/c-Kit receptor pathway, COS-7 and 293 cells were cotransfected with the cDNAs of both the c-Kit tyrosine kinase receptor and PTP-RO. PTP-RO was found to be associated with the c-Kit receptor in these transfected cells and the SCF/Kit ligand induced a rapid tyrosine phosphorylation of PTP-RO. Interestingly, these transfected cells demonstrated a decrease in their proliferative response to the SCF/Kit ligand. In addition, we assessed the association of PTP-RO with c-Kit in vivo. The results demonstrated that PTP-RO associates with c-Kit but not with the tyrosine kinase receptor FGF-R and that PTP-RO is tyrosine-phosphorylated after SCF stimulation of Mo7e and CMK cells. Antisense oligonucleotides directed against PTP-RO mRNA sequences significantly inhibited megakaryocyte progenitor proliferation. Therefore, these data show that the novel tyrosine kinase phosphatase PTP-RO is involved in megakaryocytopoiesis and that its function is mediated by the SCF/c-Kit pathway.

Adolescent↗

PubMed1999

Abnormal expression and subcellular distribution of subunit proteins of the AP-3 adaptor complex lead to platelet storage pool deficiency in the pearl mouse.

The pearl mouse is a model for Hermansky Pudlak Syndrome (HPS), whose symptoms include hypopigmentation, lysosomal abnormalities, and prolonged bleeding due to platelet storage pool deficiency (SPD). The gene for pearl has recently been identified as the beta3A subunit of the AP-3 adaptor complex. The objective of these experiments was to determine if the expression and subcellular distribution of the AP-3 complex were altered in pearl platelets and other tissues. The beta3A subunit was undetectable in all pearl cells and tissues. Also, expression of other subunit proteins of the AP-3 complex was decreased. The subcellular distribution of the remaining AP-3 subunits in platelets, macrophages, and a melanocyte-derived cell line of pearl mice was changed from the normal punctate, probably endosomal, pattern to a diffuse cytoplasmic pattern. Ultrastructural abnormalities in mutant lysosomes were likewise apparent in mutant kidney and a cultured mutant cell line. Genetically distinct mouse HPS models had normal expression of AP-3 subunits. These and related experiments strongly suggest that the AP-3 complex regulates the biogenesis/function of organelles of platelets and other cells and that abrogation of expression of the AP-3 complex leads to platelet SPD.

Adaptor Protein Complex alpha Subunits↗

PubMed1999

Selective activation of the versican promoter by epithelial- mesenchymal interactions during hair follicle development.

Interaction between the epithelium and the mesenchyme is an essential feature of organogenesis, including hair follicle formation. The dermal papilla (DP), a dense aggregate of specialized dermis-derived stromal cells located at the bottom of the follicle, is a major component of hair that signals the follicular epithelial cells to prolong the hair growth process. However, little is known about DP-specific gene activation with regard to hair induction. In this study we demonstrate that a short fragment (839 bp) of the human versican (a core protein of one of the matrix chondroitin sulfate proteoglycans) promoter is sufficient to activate lacZ reporter gene expression in the DP of postnatal transgenic mice and also in the condensed mesenchyme (the origin of the DP) beneath the hair placode during hair follicle embryogenesis. Using the same versican promoter with green fluorescent protein (GFP), large numbers of fresh pelage DP cells were isolated from newborn transgenic skin by high-speed cell sorting. These GFP-positive DP cells showed abundant versican mRNA, confirming that the reporter molecules reflected endogenous versican gene expression. These sorted GFP-positive cells showed DP-like morphology in culture, but both GFP and versican expression was lost during primary culture. In vivo hair growth assays showed that GFP-positive cells could induce hair when grafted with epithelial cells, whereas GFP-negative cells grafted with epithelium or GFP-positive cells alone did not. These results suggest that versican may play an essential role both in mesenchymal condensation and in hair induction.

Animals↗

PubMed1999

The Csk homologous kinase associates with TrkA receptors and is involved in neurite outgrowth of PC12 cells.

Csk homologous kinase (CHK), a member of the Csk regulatory tyrosine kinase family, is expressed primarily in brain and hematopoietic cells. The role of CHK in the nervous system is as yet unknown. Using PC12 cells as a model system of neuronal cells, we show that CHK participates in signaling mediated by TrkA receptors. CHK was found to be associated with tyrosine-phosphorylated TrkA receptors in PC12 cells upon stimulation with NGF. Binding assays and far Western blotting analysis, using glutathione S-transferase fusion proteins containing the Src homology 2 (SH2) and SH3 domains of CHK, demonstrate that the SH2 domain of CHK binds directly to the tyrosine-phosphorylated TrkA receptors. Site-directed mutagenesis of TrkA cDNA, as well as phosphopeptide inhibition of the in vitro interaction of the CHK-SH2 domain or native CHK with TrkA receptors, indicated that the residue Tyr-785 on TrkA is required for its binding to the CHK-SH2 domain upon NGF stimulation. In addition, overexpression of CHK resulted in enhanced activation of the mitogen-activated protein kinase pathway upon NGF stimulation, and microinjection of anti-CHK antibodies, but not anti-Csk antibodies, inhibited neurite outgrowth of PC12 cells in response to NGF. Thus, CHK is a novel signaling molecule that participates in TrkA signaling, associates directly with TrkA receptors upon NGF stimulation, and is involved in neurite outgrowth of PC12 cells in response to NGF.

Animals↗

PubMed1999

[The relation between alpha1-antichymotrypsin gene polymorphism and epsilon4 allele of apolipoprotein E gene in Alzheimer disease in Chinese]

OBJECTIVE: To detect the relation between alpha1-antichymotrpsin(AACT)gene polymorphism and epsilon4 allele of apolipoprotein E (ApoE) gene in Alzheimer disease (AD) in Chinese. METHODS: The gene polymorphisms of ApoE and AACT were genotyped in 125 AD cases and 140 controls with PCR methods and RFLP typing. Then the association between AACT polymorphism and ApoE epsilon4 was analysed. RESULTS: There was no association between AD and any allele or genotype of AACT polymorphism; AACT polymorphism was not associated with AD ApoE epsilon4 or without ApoE epsilon4. In AACT* AT and AACT* TT genotypes, ApoE epsilon4 allele was associated with AD, but no association was observed in AACT* AA genotype. CONCLUSION: AACT may not be associated with AD in Chinese, and this effect can not be influenced by ApoE epsilon4, but AACT gene polymorphism may affect the association between ApoE epsilon4 allele and AD.

Journal Article↗