Regulation of leukocyte transmigration: cell surface interactions and signaling events.
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Animals↗
Biomedical subjects
Lin Yang
Publications and source records attributed to Lin Yang.
Melatonin in vivo prolongs cardiac allograft survival in rats.
Melatonin, secreted by the pineal gland, is a multifunctional agent which (i) protects tissues from damage through free radical scavenging and attenuates ischemia/reperfusion injury in organ grafts; (ii) acts synergistically with cellular antioxidants; and (iii) displays complex, dose-dependent immunoenhancing and suppressing effects in vitro and in vivo. We analyzed the immunomodulatory effect of melatonin on acute allograft rejection. Cardiac grafts were transplanted from LBNF1 to LEW rats and anastomosed to the abdominal great vessels. The effect of low-dose (LD; 20 mg/kg/day) and high-dose (HD; 200 mg/kg/day) melatonin treatment in recipients compared with untreated controls was investigated. HD melatonin therapy abrogated acute rejection, significantly prolonging allograft survival (mean survival: 12.3 +/- 1 days S.D., n = 8, P < 0.0001) compared with untreated controls, which rapidly reject the transplant (6.3 +/- 1 days n = 12). LD therapy did not extend survival significantly (7.3 +/- 1.1 days, n = 12). Allospecific IgM showed a significant decrease in animals receiving HD therapy versus untreated recipients at days 10 and 14 post-transplantation (P < 0.01), whereas in the LD group at day 10, a significant increase in allospecific IgM (P < 0.01) over the HD cohort was demonstrated. HD treatment markedly reduced lymphocyte proliferative capacity compared with controls and the LD group. HD melatonin treatment abrogated acute allograft rejection and significantly prolonged graft survival. Our results suggest an involvement of melatonin in humoral and cellular immune pathways following perfused organ transplantation. These findings may indicate a novel therapeutic approach, based on modulation of the neuroendocrine/immune axis through melatonin as a possible future immunosuppressant in organ transplantation.
Animals↗
Rapid production of gene replacement constructs and generation of a green fluorescent protein-tagged centromeric marker in Aspergillus nidulans.
A method to rapidly generate gene replacement constructs by fusion PCR is described for Aspergillus nidulans. The utility of the approach is demonstrated by green fluorescent protein (GFP) tagging of A. nidulans ndc80 to visualize centromeres through the cell cycle. The methodology makes possible large-scale GFP tagging, promoter swapping, and deletion analysis of A. nidulans.
Aspergillus nidulans↗
[Transfection of human hepatic stimulator substance gene could protect BEL-7402 cells against hepatotoxins].
OBJECTIVE: To investigate protective effects of hHSS transfection against CCl4 or H2O2. METHODS: cDNA coding for hHSS was constructed into eukaryotic vector of pcDNA3.1 and transfected into BEL-7402 hepatoma cells. The expression of hHSS was analyzed with Northern blot. RESULTS: The growth of the hepatoma cells was remarkably enhanced 24 to 144h after hHSS gene transfection, which suggesting hHSS gene expression could stimulate cells activity. Meantime, incubation of both wild-type and vector-transfected as well as hHSS-transfected cells with CCl4 or H2O2 resulted in severe damage as marked by cell mortality and the rate of apoptosis. However, it appeared that the transfection of hHSS enabled the hepatoma cells to raise obvious resistance against CCl4 and H2O2 injury. Compared the vector cells to the vector-transfected cells, apoptosis ratio were (32.44+/-0.52)% and (25.60+/-0.66)% in which treated with CCl4, while (47.78+/-0.45)% and (37.40+/-0.69)% in which treated with H2O2, t value is 16.82 and 25.20, P<0.01. MAPK phosphorylation was also activated after HSS transfected. CONCLUSION: The function of hHSS gene expression could be related to proliferation of cell and protection against free radical damage.
Apoptosis↗
[A study on the effect of methanal during determination of carbon monoxide in blood].
OBJECTIVE: To confirm whether formaldehyde disturb detecting carbon monoxide in blood. To give an evidence that can be used for detecting carboxyhemoglobin more accurately in carbon monoxide posioning appraises. METHODS: Blood samples came from carbon monoxide poisoning and the health were collected. Regular methods for detecting carboxyhemoglobin were used. Observing and comparing the detection results between which were spiked with methanal and no spiked one were performed. RESULTS: Methanal will affect the result of following experiments such as heating, adding NaOH, absorbed by PdCl2 and spectrophotometry. CONCLUSION: The samples which contaminated by formaldehyde couldn't be used for detecting carboxyhemoglobin.
Carbon Monoxide↗
[Detection of pentachlorophenol in biomaterial using HPLC].
OBJECTIVE: To develop a method of detecting pentachlorophenol in biomaterial. METHODS: The samples were extracted by ether, and the characters of the high performance liquid chromatography (HPLC) method were studied. RESULTS: A method for the detection of pentachlorophenol in fish tissue samples was set up with the conditions of chromatography as follows: the compounds are separated on Hypersil ODS column(4.6 mm i.d. x 150 mm, 5 microns) and eluted with methanol which contains 2 g/L NH4Ac (20:80) using 305 nm as the detecting wavelength, the recovery of method being 76%, the linear range 0.042 microgram/g-1.344 micrograms/g, and the correlation coefficient 0.9994, the limit of quantification 0.014 microgram/g. Finally, pentachlorophenol was successfully detected in the fish tissue samples. CONCLUSION: The method has been proven useful in the forensic cases involved in the poisoning of pentachlorophenol.
Animals↗
[Adult-onset latent autoimmune diabetes and autoimmune thyroid disease].
OBJECTIVE: To investigate the relationship between latent autoimmune diabetes in adults (LADA) and thyroid autoimmunity. METHODS: The frequency of thyroid peroxidase antibody (TPO-Ab) and thyroglobulin antibody (TG-Ab) was determined with radioimmunoassay in 394 subjects, including 90 LADA, 104 classic type 1 diabetics (T1DM), 100 type 2 diabetics (T2DM) and 100 controls. Glutamic acid decarboxylase antibody (GAD-Ab) was measured with radioligand immunoassay. RESULTS: (1) TPO-Ab existed more frequently in LADA (16.7%, 15/90) than in T2DM patients (7.0%, 7/100; P < 0.05). The frequency of thyroid antibody (TPO-Ab or TG-Ab positivity) in LADA and T1DM was 18.9% (17/90) and 25.0% (26/104) respectively, being higher than that in the control group (8/100, 8.0%; P < 0.05). (2) Thyroid antibodies occurred more frequently in LADA patients with higher titer of GAD-Ab (GAD-Ab > or = 0.5) than those with lower ones (50.0% vs 12.5%, P < 0.05). (3) 47.1% (8/17) of LADA patients with thyroid autoimmunity had thyroid dysfunction as compared with 17.6% (6/34) in the group without thyroid antibodies (P < 0.05). CONCLUSIONS: (1) LADA patients, especially those with high titer of GAD-Ab, have high risk for thyroid autoimmunity. (2) The presence of thyroid antibody may predict high risk for thyroid dysfunction in LADA patients. (3) LADA may be one of the components in autoimmune polyendocrine syndrome.
Adolescent↗
[Altered expression of PTEN gene and LOH of its epigenetic microsatellite in gastric carcinoma].
OBJECTIVE: To investigate the expression of PTEN and loss of heterozygosity (LOH) of its epigenetic microsatellite in gastric carcinoma and explore their roles in progression of gastric carcinoma. METHODS: LOH of epigenetic microsatellites of PTEN (D10S541, D10S583 and D10S1687) in advanced gastric cancer was detected by PCR-SSCP. Expression of PTEN mRNA and protein in normal gastric mucosa and gastric cancer was evaluated by RT-PCR and SABC immunohistochemistry, respectively. The relationship between expression of PTEN mRNA and protein and lymph node metastasis or LOH of microsatellites was discussed. RESULTS: LOH of D10S541, D10S583 and D10S1687 was found in 37.5% (21/56) of advanced gastric cancers. The positive rates of PTEN mRNA expression were 80.4% (45/56), 45.5% (5/11) and 32.1% (18/56) in normal mucosa, early and advanced gastric carcinomas, respectively, while 78.6% (44/56), 44.5% (5/11) and 28.6% (16/56) at the protein level. PTEN mRNA and protein were less frequently expressed in early and advanced gastric carcinomas than that in normal gastric mucosa (P < 0.05). There was positive correlation between PTEN mRNA expression and LOH of microsatellites in advanced gastric carcinomas. PTEN protein expression paralleled with its mRNA expression (P < 0.05). The expression of PTEN mRNA and protein was negatively correlated with lymph node metastasis of advanced gastric carcinomas (P < 0.05). CONCLUSION: Down-regulated expression of PTEN gene is found in different stages of gastric carcinoma, and is closely correlated with LOH of its epigenetic microsatellites, which probably is its underlying molecular mechanisms. It suggests that altered PTEN gene contributes to tumorigenesis and progression of gastric carcinomas.
Gastric Mucosa↗
[Predicting human tumor-specific promoter using transcription factor binding sites].
To predict human tumor-specific promoters using computer technology, three data sets of tumor-specific promoter sequences, transcription factor binding site sequences and non-tumor promoter sequences were collected, and the tumor-specific promoter sequences and non-tumor promoter sequences were analyzed for the comparative density of each unique transcription factor binding site. The density of each transcription factor binding site in the corresponding data set was used to derive the density ratio, from which the eigenvector was constructed to identify human tumor-specific promoters. This method proved to be highly accurate in predicting the tumor-specific promoters, with recognition rates of over 90% of the training sequences and over 80% of the testing sequences.
Algorithms↗
[Phase II study of paclitaxel and cisplatin for advanced squamous-cell carcinoma of esophagus].
OBJECTIVE: Paclitaxel was used in a phase II trial in combination with cisplatin for esophageal cancer. The anti-tumor response, toxicity and survival of the treated patients were evaluated. METHODS: Thirty patients with advanced, unresectable, or complicated with metastasis were allotted, twenty-seven patients had no prior chemotherapy while 3 patients had received adjuvant chemotherapy. Patients were given paclitaxel 175 mg/m(2) by 3-hour infusion on D1, and cisplatin 40 mg/m(2) daily on D2 and D3. Granulocyte colony-stimulating factor (G-CSF) was not routinely administered unless the patient had neutropenia. Treatment was recycled every 21 days. RESULTS: Thirty patients (male/female, 28/2; median age 58) completed a median of 3 cycles and 27 patients were evaluable for response. Major objective responses were observed in 16 patients (59.3%; 95% confidence interval, 38.9% to 75.5%), including 5 complete responses (18.5%) and 11 partial responses (40.7%). The median time to tumor progression was 5.0 months (range, 1 to 23 months). The median actuarial survival was 9.7 months (range, 1 to 23 months). Twenty-eight patients were assessable for toxicity. The most common nonhematologic toxicity was alopecia. Grade 3 to 4 neutropenia was observed in 17.9% of the patients. Toxicity was manageable with dose attenuation and G-CSF support. CONCLUSION: The combination of paclitaxel and cisplatin can be considered as a main regimen in the treatment of advanced esophageal cancer.
Adult↗
[Spectrophotometric study on the color reaction of multicomponent complex of tungsten-3,5-dibromosalicyl fluorone-CTMAB-Tween80].
In the presence of mixed surfactant cetyl trimethyl ammonium bromide(CTMAB) and Tween80, the photometric analysis properties of color reaction of 3,5-dibronosalicyl fluorone (DBSAF) with tungsten(VI) were studied. The experimental result showed that tungsten(VI) reacted with DBSAF to form a micelle complex with a maximum absorption at 527 nm in a 0.60 mol x L(-1) hydrochloric acid medium. The mixed surfactant remarkably improved the sensitivity of the method and the dissolubility of the complex. The apparent molar absorptivity of the complex is 2.64 x 10(5) L x mol(-1) x cm(-1) at 527 nm. Tungsten (VI) reacted with DBSAF to form a complex with a stoichiometric ratio of 1:2, which was determined by mole ratio method and continual method of transformation, respectively. Beer's law was obeyed in the range of 0-400 microg tungsten (VI) per L. The proposed method has been applied to the determination of trace amount of tungsten in alloy steel samples.
English Abstract↗
[Improved radioligand assay of insulin autoantibody].
OBJECTIVE: To establish an improved radioligand assay of insulin autoantibody (IAA) and to investigate the diagnostic role of IAA in type 1 diabetes (T1DM). METHODS: 125I-insulin antigens were mixed with sera samples in the Eppendorf tubes. The immunocomplexes were precipitated with protein A-agarose, then washed with TBST buffer and counted the cpm value using liquid scintillation counter. The assay results were expressed by IAA index and compared with those of an international standardized laboratory and a domestic anti-insulin antibody kit. Sera of 32 recent-onset type 1 diabetic patients and 120 healthy controls were screened for IAA and the consistency, sensitivity, specificity and the diagnostic value of IAA were evaluated. RESULTS: (1) The intra-assay coefficient of variation (CV) was 5.8% - 8.3%, and the inter-assay CV 7.0% - 11.0%. The IAA indices of 41 samples tested in our laboratory and in an international standardized laboratory were strongly positively related (r = 0. 783, P < 0. 01) (100.0% concordance). Arrayed according to their antibody titers, the IAA indices of 82 samples measured in our laboratory and in a domestic anti-insulin antibody kit were also strongly positively related (r = 0.982, P < 0.0001) (89.0% concordance, Kappa value 0.813), but 9 samples were positive with low titer (index 0.05 - 1.00) by the radioligand assay or negative by the kit. 2) The IAA index cut-off point was determined according to the upper limit of 99.5% percentile of 120 healthy controls. The index of 0.051 or higher was defined as positive. The IAA positivity prevalence was 18.8% (6/32) in type I diabetes and 0.8% (1/120) in the healthy controls (P < 0.001). The positivity frequency of IAA was 28.6% (4/14) in patients younger than 15 years of age and the duration less than half a year, while 11.1% (2/ 18) in those older than 15. CONCLUSION: The improved radioligand assay for IAA has a high sensitivity and specificity and can be used in clinical practice, especially for the low-titer positive subjects.
Adolescent↗
[Islet beta cell function in latent autoimmune diabetes in adults with islet cell antibodies].
OBJECTIVE: To explore the predictive value and influence of islet cell antibody (ICA) and glutamic acid decarboxylase antibody (GAD-Ab) for beta cell function in latent autoimmune diabetes in adults (LADA) patients. METHODS: Fifty-six patients with initially diagnosed type 2 diabetes (including 10 cases of GAD-Ab-positive alone, 14 ICA-positive alone, 7 GAD-Ab and ICA-positive and 25 GAD-Ab and ICA negative) were followed up every 6 months (except the 2nd year) until the 5th year. Their fasting and postprandial C-peptide and glycemic control were measured. GAD-Ab was determined by radioimmunoprecipitation assay and ICA by ELISA kit. RESULTS: Decreased fasting C-peptide was found in patients with GAD-Ab alone and patients with GAD-Ab and ICA in the 2.5th year and to the end of the follow-up. The percentage of patients whose C-peptide decreased 50% or more compared with the baseline in the above 2 groups reached 60.0% in the 3nd year and 71.4% in the 3.5th year, respectively. No changes of the above parameters were found in ICA-positive alone group and GAD-Ab and ICA negative group. Complete beta-cell failure was found in 4 of the 10 patients in GAD-Ab alone group and in 1 of the 10 patients in ICA and GAD-Ab positive group. The number of failure patients in GAD-Ab alone group was more than that of the other 2 groups (P < 0.05 in both groups). There was no significant correlation between ICA index and FCP. Multiple stepwise regression analysis demonstrated that GAD-Ab contributed much more to FCP than ICA did. CONCLUSION: The islet beta cell function decreases more quickly in GAD-Ab positive LADA patients than in ICA positive ones. The titer of GAD-Ab is an important prognostic factor in islet beta cell function, and the presentation of ICA-positive alone can not predict beta cell function in LADA patients.
Adolescent↗
Interfacial molecular recognition between polysaccharides and calcium carbonate during crystallization.
Based on the basic principles of biomineralization, using beta-cyclodextrin, hepatin and soluble starch as organic matrices, employing the biomimetic method, the crystallization of CaCO(3) was studied by Fourier transform infrared spectroscopy (FT-IR), X-ray powder diffraction analysis (XRD), scanning electronic microscopy (SEM), thermal gravity-differential thermal analysis and conductivity analysis. The results show that polysaccharides have an effect on the crystallization of CaCO(3). CaCO(3) crystals also have an effect on polysaccharides. The possible mechanism of this interaction is discussed.
Biomimetics↗
Interruption of nuclear factor kappaB signaling by the androgen receptor facilitates 12-O-tetradecanoylphorbolacetate-induced apoptosis in androgen-sensitive prostate cancer LNCaP cells.
12-O-tetradecanoylphorbolacetate (TPA) influences proliferation, differentiation, and apoptosis in a variety of cells including prostate cancer cells. Here, we show that androgen treatment potentiates TPA-induced apoptosis in androgen-sensitive prostate cancer LNCaP cells but not in androgen-independent prostate cancer cell lines DU145 and PC-3. The use of the antiandrogen bicalutamide (Casodex) rescued LNCaP cells from 5-alpha-dihydrotestosterone (DHT)/TPA-induced apoptosis, suggesting that DHT/TPA-induced apoptosis is mediated by androgen/androgen receptor (AR). In addition, a caspase-3 inhibitor (Ac-DEVD-CHO) reduced the level of apoptosis, suggesting that DHT/TPA-mediated apoptosis occurs through a caspase-3-dependent pathway. A functional reporter assay using nuclear factor (NF) kappaB-luciferase and an electromobility gel shift assay showed that DHT suppressed NFkappaB activity. In addition, apoptosis mediated by combined DHT/TPA treatment was abrogated by overexpression of the NFkappaB subunit p65 in LNCaP-p65 cells, suggesting that NFkappaB may play an important role in regulating the effects of androgen/AR and TPA on apoptosis. Furthermore, use of the c-Jun N-terminal kinase (JNK) inhibitor SB202190 showed that the combination of DHT/TPA increased JNK activation in LNCaP cells but not in LNCaP-p65 cells, demonstrating that NFkappaB may be able to suppress JNK activity. These results indicate that androgen/AR facilitates TPA-induced apoptosis by interruption of the NFkappaB signaling pathway, leading to activation of JNK in LNCaP cells. These data describe a signaling pathway that could potentially be useful in proposed therapeutic treatment strategies exploiting combinations of different agents that control apoptosis in prostate tumors.
Androgens↗
Interaction of antimicrobial peptides with lipopolysaccharides.
We study the interaction of antimicrobial peptides with lipopolysaccharide (LPS) bilayers to understand how antimicrobial peptides interact with the LPS monolayer on the outer membrane of Gram-negative bacteria. LPS in water spontaneously forms a multilamellar structure composed of symmetric bilayers. We performed X-ray lamellar diffraction and wide-angle in-plane scattering to study the physical characteristics of LPS multilayers. The multilayer alignment of LPS is comparable to phospholipids. Thus, it is suitable for the application of oriented circular dichroism (OCD) to study the state of peptides in LPS bilayers. At high hydration levels, the chain melting temperature in multilamella detected by X-ray diffraction is the same as that of LPS aqueous dispersions, as measured by calorimetry. LPS has a strong CD, but with a careful subtraction of the lipid background, the OCD of peptides in LPS is measurable. The method was tested successfully with melittin. It was then applied to two representative antimicrobial peptides, magainin and protegrin. At peptide concentrations comparable to the physiological conditions, both peptides penetrate transmembrane in LPS bilayers. The results imply that antimicrobial peptides readily penetrate the LPS monolayer of the outer membrane.
Antimicrobial Cationic Peptides↗
Suppression versus induction of androgen receptor functions by the phosphatidylinositol 3-kinase/Akt pathway in prostate cancer LNCaP cells with different passage numbers.
The phosphatidylinositol 3-kinase (PI3K)/Akt pathway controls several important biological functions, such as cell growth regulation, apoptosis, and migration. However, the way in which PI3K/Akt controls androgen receptor (AR)-mediated prostate cancer cell growth remains unclear and controversial. Here, we demonstrate that the PI3K/Akt pathway regulates AR activity in a cell passage number-dependent manner. Specifically, PI3K/Akt pathway can suppress AR activity in androgen-dependent LNCaP cells with low passage numbers. In contrast, it can also enhance AR activity in LNCaP cells with high passage numbers. Furthermore, we also demonstrate that insulin-like growth factor-1 can activate the PI3K/Akt pathway that results in the phosphorylation of AR at Ser210 and Ser790. The consequence of these events may then change the stability of AR protein. Together, our results demonstrate that the PI3K/Akt pathway may have distinct mechanisms to modulate AR functions in various stages of prostate cancer cells and that a combined therapy of antiandrogens and anti-PI3K/Akt inhibitors may be worth considering as a future therapeutic approach to battle prostate cancer.
Binding Sites↗
A JNK-dependent pathway is required for TNFalpha-induced apoptosis.
Tumor necrosis factor (TNFalpha) receptor signaling can simultaneously activate caspase 8, the transcription factor, NF-kappaB and the kinase, JNK. While activation of caspase 8 is required for TNFalpha-induced apoptosis, and induction of NF-kappaB inhibits cell death, the precise function of JNK activation in TNFalpha signaling is not clearly understood. Here, we report that TNFalpha-mediated caspase 8 cleavage and apoptosis require a sequential pathway involving JNK, Bid, and Smac/DIABLO. Activation of JNK induces caspase 8-independent cleavage of Bid at a distinct site to generate the Bid cleavage product jBid. Translocation of jBid to mitochondria leads to preferential release of Smac/DIABLO, but not cytochrome c. The released Smac/DIABLO then disrupts the TRAF2-cIAP1 complex. We propose that the JNK pathway described here is required to relieve the inhibition imposed by TRAF2-cIAP1 on caspase 8 activation and induction of apoptosis. Further, our findings define a mechanism for crosstalk between intrinsic and extrinsic cell death pathways.
Animals↗