PubMed Health⌕ Search

Biomedical subjects

Y J Guo

Publications and source records attributed to Y J Guo.

At least 37 records · Page 2Linked to original sources

Population profile of stable flies (Diptera: Muscidae) caught on Alsynite traps in various feedlot habitats.

Cylindrical traps made from Alsynite fiberglass were placed in 4 habitats in a confined cattle feedlot environment from 2 May to 30 October 1996 to evaluate abundance, sex ratio, physiological age structure, and blood-fed status of trapped adult stable flies, Stomoxys calcitrans (L.). Significantly more stable flies were caught on the trap located between host cattle and trees. The abundance of stable flies decreased geometrically with increasing distance from the host cattle in the open area. The spatial distribution of adult flies in cattle feedlot habitats became less heterogeneous as the population density increased. Male stable flies clearly dominated the total collection (66.7:33.3, male:female). A higher proportion (38.9%) of female stable flies was found on the trap close to a major immature developing area (manure pile). Most of the trapped flies (64.8%) showed a positive blood-fed status, but only 331 (8.8%) of 3,767 flies had recently fed. A majority (72.6%) of the attracted females was at the early nulliparous stage. Trap positioning did not have any significant influence on specific physiological age groups of the captured flies.

Aging↗

Induction of hepatocyte proliferation and prevention of hepatocyte apoptosis by phenobarbital related to local humoral factor in mouse liver.

AIM: To study the association of phenobarbital (Phe) inducing hepatocyte proliferation and blocking hepatocyte apoptosis with local humoral factor in liver. METHODS: The ratio of liver/body weight, DNA content, regressive rate of hyperplastic liver, and DNA fragmentation were used to investigate whether the Phe-treated mouse liver extract (PMLE) and PMLE-95 (PMLE heated at 95 degrees C for 30 min) possessed Phe-like effects on mouse liver. Meantime, the effects of pretreatment with trypsin, RNAase, and DNAase on the activity of PMLE-95 were observed, and the differences of components between PMLE-95 and NMLE-95 (normal mouse liver extract, NMLE heated at 95 degrees C for 30 min) were analyzed with HPLC. RESULTS: PMLE-95 stimulated hepatocyte proliferation and prevented hepatocyte apoptosis caused by withdrawing Phe in mice, and the activity of PMLE-95 was eliminated after the pretreatment with trypsin. On the chromatograms PMLE-95 had 5 main peaks, while NMLE-95 had only 4 peaks. CONCLUSION: The effects of Phe on the liver were mediated by an intrinsic protein or peptide substance produced in response for the stimulation of Phe in mouse liver.

Animals↗

Effective tumor vaccines generated by in vitro modification of tumor cells with cytokines and bispecific monoclonal antibodies.

Antitumor immune responses are mediated primarily by T cells. Downregulation of the major histocompatibility complex (MHC) and the molecules that costimulate the immune response is associated with defective signaling by tumor cells for T-cell activation. In vitro treatment with a combination of cytokines significantly increased the expression of MHC class I and adhesion molecules on tumor cell surfaces. When tumor cells were first incubated with a bispecific monoclonal antibody that binds antigen on tumor cells to CD28 on T cells, the modified tumor cells become immunogenic and are able to stimulate naive T cells, generating tumor-specific cytotoxic T cells in vitro. Immunization with the modified tumor cells elicits an immune response mediated by CD8+ T cells. This response protected against a challenge with parental tumor cells and cured established tumors. The approach was effective in both low immunogenic and nonimmunogenic tumor model systems. Modification of tumor cells with this two-step procedure may provide a strategy for development of tumor vaccines that is effective for cancer immunotherapy.

Animals↗

[A strain of A/PR/8/34 (H1N1)-like virus isolated from men].

An influenza virus was isolated in May, 1991 from a child with acute respiratory disease. The identification results with serologic method have revealed that the isolate was A/PR/8/34 (H1N1)-like virus. The analyses of nucleotide sequences in HA1 domain showed that there were 12 different positions on nucleotide sequences between the isolate and the A/PR/8/34 (H1N1) virus. These differences induced substitutions of 4 amino acids in HA1 protein molecule of isolate as compared with that of A/PR/8/34 (H1N1) virus. The oligonucleotide analyses of viral genome revealed that there were 11 different points between isolate and A/PR/8/34 (H1N1) virus, e. g. 2 deleted and 9 inserted in genome of isolate as compared with A/PR/8/34 (H1N1) strain. Therefore, the isolate possibly derived from A/PR/8/34 (H1N1) virus by laboratory contamination could be ruled out. However, where did A/Guangdong/6/91 (H1N1) virus come from? This question will be settled by further study.

Amino Acid Sequence↗

Altered expression of CD44 in human prostate cancer during progression.

There is a great need for markers that distinguish slowly progressive from rapidly progressive prostate cancers in paraffin-embedded tissues. CD44, an adhesion molecule that has been useful for the prediction of prognosis in some other cancers, has not been described in prostate cancer. The expression of CD44 was investigated with the monoclonal antibody GKW.A3 in prostate cancer in formalin-fixed, paraffin-embedded tissue sections of (1) whole prostates from 50 patients with 74 prostate cancers; and (2) lymph node metastases from 14 patients. Sixty percent of primary prostate cancers expressed CD44 moderately to strongly. No metastases expressed CD44 moderately to strongly; only 14% of metastases expressed even low levels of immunohistochemically detectable CD44. There is a difference between primary and metastatic prostate cancer (P <.0006) in the expression of CD44 and an inverse correlation (P <.05) between histological differentiation (Gleason grade) and the expression of CD44. The magnitude of the differential expression of CD44 in primary and metastatic prostate cancers suggests it should be investigated as an indicator of prognosis in a large prospective study.

Disease Progression↗

Canine H(+)-K(+)-ATPase alpha-subunit gene promoter: studies with canine parietal cells in primary culture.

H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) is the principal enzyme responsible for the process of gastric acid secretion. This enzyme is expressed in a cell-type-specific manner in gastric parietal cells. To explore the mechanisms regulating its expression, we transfected differentiated canine parietal cells in primary culture with H(+)-K(+)-ATPase-luciferase reporter genes and assessed transcriptional activities. Deletional analysis of the 5'-flanking region of this gene demonstrated a remarkable increment in transcriptional activity associated with a segment between bases -54 to -45 (5' GCTCCGCCTC 3') relative to the transcriptional initiation site. Gel shift assays with competition and supershift analysis demonstrated that this segment is specifically bound by the transcription factor Sp1. A point mutation, eliminating Sp1 binding, diminished basal transcriptional activity by 80%, indicating that this Sp1 binding site is important for constitutive transcriptional activity. Although these studies indicate that Sp1 is required to maintain a high concentration of the H(+)-K(+)-ATPase gene in the parietal cell, its cell-type-specific expression must rely on other elements because Sp1 is a ubiquitously expressed transcription factor.

Animals↗

[A randomized clinical trial for the evaluation of head and neck squamous cell carcinoma treating with traditional Chinese medicine]

This paper described the research design,research process and statistical analysis of randomized clinical trial by treatment with traditional Chinese medicine in patients with squamous cell carcinoma of the head and neck.At first we found there was no significant difference between treating group and contral group(P>0.05) using log-rank test on Kaplan-Meier survival curves. With further multivariate analysis Cox model and after adjusting for sex,age,legth of taking the assigned medication,grade of tumor differentiation and using of chemotherapy,the rate of tumor-related death for control group was significantly higher than that for treating group :hazards ratio estimate was 1.939(95% confidence interval 1.008-3.729,(P<0.05).The length of taking Chinese medicine was one of the most important prognostic factors(P<0.001).The results suggest that the prescribed medication contributed to the improved survival,and it was an independent prognostic factor.

Journal Article↗

Specificity of prohormone convertase endoproteolysis of progastrin in AtT-20 cells.

Biologically active peptide hormones are synthesized from larger precursor proteins by a variety of posttranslational processing reactions. Endoproteolytic cleavage at the Lys74-Lys75 dibasic processing site of progastrin is the major determinant for the relative distribution of gastrin heptadecapeptide and tetratriacontapeptide in tissues. Thus, we explored the ability of two prohormone convertases, PC1/PC3 and PC2, to cleave this important site within progastrin. We expressed wild-type human gastrin cDNA and mutant cDNAs in which the Lys74Lys75 site was changed to Lys74Arg75, Arg74Arg75, and Arg74Lys75 residues in AtT-20 cells. Because AtT-20 cells express Pc1/PC3 but not PC2, we also coexpressed a cDNA encoding PC2 in both wild-type and mutant gastrin-producing AtT-20 cells. Wild-type Lys74Lys75 and mutant Arg74Arg75 progastrin processing sites were efficiently cleaved in AtT-20 cells only after coexpression of PC2. Mutant Lys74Arg75 progastrin was readily processed in cells in the presence or absence of PC2 coexpression, but, in contrast, mutant Arg74Lys75 progastrin was inefficiently cleaved regardless of PC2 coexpression. Northern analysis revealed the presence of PC2 but not PC1/ PC3 in canine antral gastrin-producing G cells. These data suggest that PC2 but not PC1/PC3 is responsible for the cleavage of the Lys74Lys75 site in wild-type progastrin.

Amino Acid Sequence↗

Construction of a novel bifunctional biogenic amine receptor by two point mutations of the H2-histamine receptor.

BACKGROUND: H2-histamine receptors mediate a wide range of physiological functions extending from stimulation of gastric acid secretion to induction of human promyelocyte differentiation. We have previously cloned the H2-histamine receptor gene and noted that only three amino acids on the receptor were sufficient to define its specificity and selectivity. Despite only modest overall amino acid homology (34% amino acid identity and 57.5% similarity) between the H2-histamine receptor and the receptor for another monoamine, the beta 2-adrenergic receptor, there is remarkable similarity at their critical ligand binding sites. We hypothesized that, if the specificity and selectivity of both receptors are invested in just three amino acids, it should be possible to convert one of the receptors into one that recognizes the ligand of the other by simple mutations at only one or two sites. MATERIAL AND METHODS: We explored the effect of two single mutations in the fifth transmembrane domain of the H2-histamine receptor, which encompasses the sites that determine H2 selectivity. The canine H2 receptor gene was mutated at Asp186 and Gly187 (Asp186 to Ala186 and Gly187 to Ser187) by oligonuceotide directed mutagenesis. The coding region of both the wild-type and mutated H2 receptors was subcloned into the eukaryotic expression vector, CMVneo, and stably transfected into Hepa cells and L cells. The biological activity of histamine and epinephrine on the expressed receptor was examined by measurement of cellular cAMP production and inositol trisphosphate formation. RESULTS: Hepa cells transfected with the Ala186-Ser187 mutant H2 receptor demonstrated a biphasic rise in cAMP in response to epinephrine with an early phase (ED50 approximately 10(-11) M) that could be inhibited by both propranolol and cimetidine. Epinephrine also induced IP3 generation in the same cells, a biological response that is characteristic of activation of the wild-type H2 but not of the beta-adrenergic receptor. L cells transfected with the Ala186-Ser187 mutant H2 receptor also responded to epinephrine in a cimetidine and propranolol inhibitable manner. CONCLUSIONS: We converted the H2-histamine receptor into a bifunctional one that has characteristics of both histamine and adrenergic receptors by two simple mutations. These results support the hypothesis that ligand specificity is determined by only a few key points on a receptor regardless of the structure of the remainder of the molecule. Our studies have important implications on the design of pharmacological agents targeted for action at physiological receptors.

Adrenergic beta-Antagonists↗

In vivo treatment with anti-ICAM-1 and anti-LFA-1 antibodies inhibits contact sensitization-induced migration of epidermal Langerhans cells to regional lymph nodes.

Development of contact hypersensitivity in mice depends on the migration of Langerhans cells from the epidermis to regional lymph nodes. Since ICAM-1 and LFA-1 play important roles in leukocyte migration, we sought to determine whether in vivo administration of anti-ICAM-1 and anti-LFA-1 antibodies would inhibit contact sensitization-induced migration of epidermal Langerhans cells to regional lymph nodes. Twenty-four hours after contact sensitization of mice with FITC, a brightly FITC-stained Ia+ population of dendritic cells capable of stimulating a FITC-specific Ia-restricted T-cell hybridoma was readily detected in their draining lymph nodes. Animals treated with anti-Ia mAb, which depletes Ia+ cells in lymph nodes and spleen but not Ia+ Langerhans cells in the epidermis, had normal numbers of FITC-bearing Ia+ cells capable of stimulating the T-cell hybridoma. Dendritic lymph node cells from mice treated with anti-ICAM-1 and anti-LFA-1 mAb were devoid of brightly FITC-stained cells and cells capable of stimulating the FITC-specific T-cell hybridoma. The combination of anti-ICAM-1 and anti-LFA-1 mAb completely inhibited the induction of contact hypersensitivity to FITC. Animals treated with anti-ICAM-1 or anti-LFA-1 monoclonal antibodies alone had significantly reduced (by 79 and 36%, respectively) numbers of brightly stained cells capable of stimulating the hybridomas. These data suggest that the adhesion molecules, ICAM-1 and LFA-1, play a significant role in contact hypersensitivity-induced migration of Langerhans cells to regional lymph nodes. The immunomodulatory effects of anti-adhesion molecule antibodies in vivo may be in part due to their effects on antigen-presenting cell migration.

Animals↗

Conversion to Ca(2+)-independent form of Ca2+/calmodulin protein kinase II in rat pancreatic acini.

CCK rapidly converted Ca2+/calmodulin kinase II (CaMK II) to a Ca(2+)-independent form with peak action at 30 sec followed by decline to the basal level at 10 min. The threshold concentration of CCK for this action was 30 pM and maximum effect occurred at 1 nM, which induced a 6-10-fold increase. Bombesin and carbachol similarly induced CaMK II autonomous activity, whereas secretin and JMV 180 did not. Ionomycin induced a more stable elevation of CaMK II autonomous activity and the intracellular Ca2+ chelator, BAPTA/AM, blocked the effect of CCK. In conclusion, pancreatic CaMK II is rapidly activated by a large increase in [Ca2+]i generated by either stimulation of phosphatidylinositol pathway or by an influx of extracellular Ca2+.

Amino Acid Sequence↗

Potential use of soluble CD44 in serum as indicator of tumor burden and metastasis in patients with gastric or colon cancer.

Soluble CD44 is present in the serum of normal individuals (2.7 +/- 1.1 nM). The concentration of soluble CD44 in the serum is elevated in patients with advanced gastric (24.2 +/- 9.8 nM) or colon cancer (30.8 +/- 11 nM). Serum CD44 concentration correlated with tumor metastasis and tumor burden. Surgical resection of tumors resulted in decreases in serum CD44 levels. By Western blot analysis, monoclonal anti-CD44 antibody reacted with a major protein with molecular weight between 130,000 and 190,000. In addition, two proteins with molecular weights of 72,000 and 80,000 can also be identified. Therefore, different CD44 isoforms may be present in the serum of cancer patients. Serum CD44 concentrations may be an indicator of tumor burden and metastasis in patients with malignant diseases.

Adenocarcinoma↗

Disruption of T lymphocyte reappearance in anti-Thy-1-treated animals in vivo with soluble CD44 and L-selectin molecules.

We used polyclonal rabbit anti-Thy-1 antiserum to eliminate T lymphocytes in the peripheral blood, lymph nodes, and spleens but not in the thymus of normal mice. T lymphocytes began to reappear in the peripheral lymphoid compartments 2 weeks after termination of the treatment. By 4 weeks, the numbers of peripheral T lymphocytes had recovered to normal levels. We found that injection of recombinant soluble forms of human CD44 or L-selectin but not human CD8 molecules delayed the reappearance of peripheral T lymphocytes in anti-Thy-1-treated mice. This delay in recovery most likely reflects the ability of these soluble receptors to interfere with lymphocyte migration in vivo. Our results provide in vivo evidence that CD44 and L-selectin regulates lymphocyte trafficking and suggest that soluble forms of both molecules provide useful tools for the study of lymphocyte migration in vivo.

Animals↗

Palmitoylation of CD44 interferes with CD3-mediated signaling in human T lymphocytes.

We studied the interactions between CD44 and four different monoclonal anti-CD44 antibodies. All four monoclonal anti-CD44 antibodies studied (P3H9, Bu52, IM.7, and GKW.A3) act in synergy with human anti-CD2 antibodies in stimulating normal human peripheral blood lymphocytes to proliferate. GKW.A3 and IM.7 but not P3H9 or Bu52 inhibited the proliferation of normal human peripheral blood lymphocytes stimulated by anti-CD3. Interestingly, only GKW.A3 and IM.7 stimulated the incorporation of [3H]palmitic acid and palmitoylation of CD44 molecules by normal human peripheral blood lymphocytes. The two monoclonal anti-CD44 antibodies (P3H9 and Bu52) that failed to inhibit anti-CD3 induced proliferation also failed to induce the incorporation of [3H]palmitic acid. More importantly, the inhibitory effects of GKW.A3 were reversed in the presence of cerulenin, an inhibitor of protein palmitoylation. Therefore, palmitoylation of CD44 may interfere with anti-CD3 mediated signaling pathways. These data support the hypothesis that palmitoylation of cell surface receptors may play an active role in receptor and receptor interactions and signal transduction in normal human T lymphocytes.

Antibodies, Monoclonal↗

Trinitrophenol reactive T-cell hybridomas recognize antigens that require antigen processing.

Protein antigens must be taken up, processed, and displayed on the surface of antigen-presenting cells in association with major histocompatibility complex molecules before they can be recognized by T cells. Whether recognition of the haptens used to study allergic contact hypersensitivity in murine models similarly requires processing has not been determined. We analyzed whether presentation of trinitrophenol to trinitrophenol reactive T-cell hybridomas requires antigen processing by studying the effects of inhibitors of antigen processing and presentation on the ability of a syngeneic B-cell tumor (A20) to present trinitrophenol to a series of interleukin-2 producing, trinitrophenol specific, major histocompatibility complex class II-restricted T-cell hybridomas. The ability of trinitrophenol modified A20 cells to stimulate the hybridomas was completely inhibited by monoclonal, anti-trinitrophenol, or anti-Ia antibodies and was significantly reduced by paraformaldehyde fixation immediately after trinitrophenol modification. Trinitrophenol-modified A20 cultured at 37 degrees C for 2 h prior to fixation was significantly more effective at stimulating the hybridomas than trinitrophenol-modified A20 fixed immediately. The ability of A20 to present trinitrophenol was inhibited by chloroquine. Paraformaldehyde fixation and chloroquine treatment had similar effects on the ability of trinitrophenol modified lymph node dendritic cells to stimulate the trinitrophenol specific hybridomas. Paraformaldehyde fixation and chloroquine treatment had similar effects on the ability of A20 cells to present ovalbumin to ovalbumin-specific hybridomas as they had on the ability of trinitrophenol modified A20 cells to present trinitrophenol to the trinitrophenol specific hybridomas. One of seven T-cell hybridomas responded to trinitrophenol modified ovalbumin but not other trinitrophenol modified proteins. These results suggest that, at least in part, T cells in the contact hypersensitivity response to trinitrophenol recognize antigens that require processing and that trinitrophenol modified proteins can be recognized.

Albumins↗

[Alterations of oncogenes in human fetal esophageal epithelium induced by N-methylbenzylnitrosamine (NMBzA)].

Epidemiological investigation showed that N-methylbenzylnitrosamine (NMBzA) has been associated with increased incidence of esophageal cancer (EC) in Linxian county, a high incidence area. In present study, our results indicate that NMBzA can induce amplification and over-expression of EGFr gene in human fetal esophageal epithelium (HFE) treated with NMBzA for 24 hours as shown by southern blot assay and immunohistochemistry. The papillary hyperplasia was induced in HFEs that cultured with NMBzA for 1 to 3 weeks. Amplification of c-myc and int-2 gene in HFEs treated by NMBzA for 1 week and 3 weeks was found, respectively. Deletions of p53 and Rb gene were found in human fetal esophageal carcinomas induced by NMBzA. Overexpression of p53 protein in human fetal esophageal carcinomas detected by immunohistochemical methods indicates that p53 gene mutation(s) may be occured. The HFE explants treated in vitro with NMBzA for 3 weeks were inoculated subcutanously into balb/c nude mice. No tumor was found in 5 months after inoculation, suggesting that only changes of oncogene(s) are insufficient to induce full transformation. Other genetic alterations (such as functional inactivation of Rb or/and p53 tumor suppressor genes) may be necessary in the further progression of malignant lesions.

Carcinogens↗

[Changes in glucocorticoid receptor and phospholipase A2 in guinea pig asthma models].

In this study we determined the glucocorticoid receptor (GR) level (using 3H-dexamethasone as a ligand) and phospholipase A2 (PLA2) activity of lung tissue in guinea pig asthma models at 1st, 3rd, 7th and 14th day of asthma attacks. The results showed that the GR maximal binding capacity (Bmax, fmol/mg pro.) were 54.36 +/- 26.57, 30.99 +/- 10.01, 19.40 +/- 10.06, and 29.16 +/- 11.35; GR dissociation constant (Kd, nmol/L) were 12.73 +/- 4.06, 8.28 +/- 3.23, 5.70 +/- 2.91, and 6.40 +/- 2.64 respectively; and PLA2 actisis (U) were 181.58 +/- 41.50, 239.80 +/- 61.15, 243.08 +/- 31.35, and 235.71 +/- 86.13 respectively. The GR Bmax, Kd and PLA2 of actisis control group were 61.48 +/- 27.60 (fmol/mg pro.), 13.11 +/- 2.88 (nmol/L), 81.06 +/- 15.97 (U). The GR Bmax and Kd of asthmatic animals decreased significantly since the 3rd day, but the PLA2 activity increased significantly since the 1st day as compared to the control group (P < 0.01). The changes of GR Bmax had significant negative correlation with those of the PLA2 activity (r = -0.9023, P < 0.05). The mechanism of the GR and PLA2 actisis changes of asthma animal models were discussed.

Animals↗

Ecology and control of dengue vector mosquitoes in Taiwan.

Due to rapid urbanization, industrialization and social changes in recent years, the use of packing materials and tires has dramatically increased in the Taiwan area. What is more is that some parts of southern Taiwan are short of water resources and water preservation with huge containers becomes part of custom in those areas. Storage water containers, waste vessels and tires are good habitats for Aedes. Meanwhile, some persons traveling to dengue endemic countries bring the dengue disease back to Taiwan. Surveys taken since 1988 show that dengue occurs mainly in the urban and coastal areas where Aedes aegypti is prevalent. This species is the most important, if not the only, vector of dengue in Taiwan. It appears that the types of Aedes breeding have changed quickly. In dengue fever epidemic areas, the most popular breeding sites are ornamental containers (38.8%), storage water containers (30.1%), discarded containers (25.4%), receptacles (3.3%) and water collection in the basement (2.2%). In dengue fever epidemic areas, those building basements, huge water containers, waste vessels and waste tires in open fields are most difficult to clean up and manage and become the most popular Aedes habitats. We established a waste recycling system and promoted a breeding site reduction campaign for waste management, including the application of Temephos in containers to kill larvae. For the drinking water management, fish were released in water containers to prevent larval breeding. It should be mentioned that with the integrated pest control and regular inspections of Aedes larvae in Taiwan the density figures 1, 2-5, and 6 or above for Aedes aegypti were 38.7%, 42.9%, and 18.4%, respectively, in 1988, and in 1993 were 90.8%, 9.2% and 0%. The incidence of dengue fever cases has 98% decreased since 1988. In 1990 and 1993, there was no indigenous cases. We have concluded that integrated pest control is the best and most effective method for dengue fever control, including solid waste and drinking water management.

Aedes↗