Three-dimensional superlattices built from (M(4)In(16)S(33))(10-)(M = Mn, Co, Zn, Cd) supertetrahedral clusters.
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Journal Article↗
Biomedical subjects
P Feng
Publications and source records attributed to P Feng.
Antibody response to Epstein-Barr virus Rta protein in patients with nasopharyngeal carcinoma: a new serologic parameter for diagnosis.
BACKGROUND: Nasopharyngeal carcinoma (NPC) is associated closely with Epstein-Barr virus (EBV). The authors previously reported that an EBV immediate-early gene, BRLF1, was expressed frequently in NPC tumors, and a significant elevation in immunoglobulin G (IgG) antibodies directed against BRLF1 gene product Rta was detected in NPC sera by a radioactive immunoprecipitation assay. To simplify and to make the detection more quantitative, an enzyme-linked immnunosorbent assay (ELISA) was developed in this study. METHODS: Antigen domains of Rta were identified further using an immunoprecipitation assay. Two glutathione-S-transferase (GST) recombinant Rta fragments (R150-GST and R185-GST) were prepared subsequently and were used as antigens in the ELISA. Serum samples derived from 51 patients with NPC patients, 115 non-NPC ENT patients, and 47 healthy volunteers were examined for the presence of antibodies directed against Rta. RESULTS: Among the patients with NPC, 74.5% showed a positive IgG response to R150-GST, and 62.7% showed a positive IgG response to R185-GST, with 80.4% positive for either fragment. In contrast, the reactions were positive in only 8.5% of healthy volunteers and 13.0% of control patients. When using a mixture of the two recombinant Rta proteins as coating antigens, the IgG positive responses were 82.3%, 10.6%, and 14.8%, respectively, in patients with NPC, healthy volunteers, and control patients. It is noteworthy that 51.0% of the NPC sera showed a positive immunoglobulin A (IgA) response, with none of the control patients showing obvious reactivity. Both the IgG response and the IgA response to Rta protein in patients with NPC were correlated with the IgA response to EBV early antigens and virus capsid antigens, the classic serologic markers used to diagnose NPC. CONCLUSIONS: The ELISA method described for the detection of IgG antibodies directed against recombinant Rta proteins is simple and reliable and may be useful as a serologic parameter for the screening and diagnosis of patients with NPC.
Antibodies, Viral↗
Morphine inhibits mucosal antibody responses and TGF-beta mRNA in gut-associated lymphoid tissue following oral cholera toxin in mice.
In this study, we investigated the effect of morphine on the mucosal immune system using fragment cultures of ileal segments, Peyer's patches (PPs), and mesenteric lymph nodes. Mice were implanted s.c. with a morphine slow release pellet. Control groups received a naltrexone slow release pellet, a placebo pellet, or both a morphine and a naltrexone pellet. After 48 h, mice were orally immunized with cholera toxin (CT) and were boosted orally 1 wk later. Animals were sacrificed 1 wk after the booster immunization, and PPs, mesenteric lymph nodes, and ileal segments were cultured in 24-well plates for 12 days. Morphine resulted in a highly significant inhibition of CT-specific IgA and IgG production in fragment culture supernatants of all three tissues compared with placebo. Naltrexone blocked the reduction in Ab levels induced by morphine, indicating that the effect is opioid receptor mediated. Morphine did not significantly alter total IgA levels in any of the tissue culture supernatants. Morphine also inhibited CT-specific IgA and IgG levels in serum. By flow cytometry, morphine did not alter the lymphoid cell composition in PPs compared with placebo. The effect of morphine on TGF-beta, IL-5, and IL-6 mRNA expression in PPs and ileal segments was determined following oral immunization with CT. Morphine significantly decreased TGF-beta mRNA compared with that in the placebo group, and naltrexone blocked this effect. These results indicate that morphine inhibits Ag-specific IgA responses in gut-associated lymphoid tissue at least partially through the inhibition of TGF-beta, a putative IgA switch factor, in the gastrointestinal tract.
Administration, Oral↗
Ontogeny of REM rebound in postnatal rats.
STUDY OBJECTIVES: The aim of this study was to determine developmental changes (ontogeny) of REM rebound in postnatal rats. DESIGN: Different groups of 2, 3, and 4-week-old experimental rats were instrumentally REM sleep deprived (RSD rats) for 33-48 hours and their sleep was monitored polysomnographically for 48 hours after the REM sleep deprivation (RSD). Age-matched control (RSC) rats also had polysomnographic recordings. SETTINGS: N/A. PARTICIPANTS: Subjects were 18 male Long-Evans RSD rats (5 age 2 weeks, 5 age 3 weeks, and 8 age 4 weeks); and 17 age-matched male Long Evans RSC rats (5 age 2 weeks, 5 age 3 weeks, and 7 age 4 weeks). INTERVENTIONS: Implants for the polysomnographic recordings of the RSD and RSC rats were made by the soft head plug method which permitted continuous, 24 hour/day records during the REM deprivation and post deprivation periods. RSD rats had instrumental RSD by the shaking platform method. RSC rats remained in stationary cages. MEASUREMENTS AND RESULTS: At age 2 weeks, compared with age-matched RSC rats, RSD rats had no REM rebound. At age 3 weeks, compared with age-matched RSC rats, RSD rats had a small but significant REM rebound limited to the first 6 hours after RSD. At age 4 weeks, compared with RSC rats, RSD rats had a larger REM rebound that extended for 18 hours after RSD. The size and duration of REM rebound at the different ages was significantly different. Total sleep lost during the RSD process at each age was made up. CONCLUSIONS: The findings possibly indicate that in rats a REM sleep homeostatic process develops between ages 2 and 4 weeks and that a total sleep homeostatic process is already developed by age 2 weeks.
Animals↗
Arsenate zeolite analogues with 11 topological types.
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Journal Article↗
Total internal reflected resonance light scattering determination of chlortetracycline in body fluid with the complex cation of chlortetracycline-europium-trioctyl phosphine oxide at the water/tetrachloromethane interface.
A highly selective method of chlortetracycline (CTC) is proposed on the basis of the measurements of total internal reflected resonance light scattering (TMR-RLS) at water/tetrachloromethane (H20/CCl4) interfaces. In the pH range of 7.54-8.14, the interaction of the binary complex of Eu(III)/CTC in the presence of trioctyl phosphine oxide (TOPO) occurs at the H20/CCl4 interface, resulting in greatly enhanced TIR-RLS signals with the maximum peak located at 340 nm. The enhanced TIR-RLS intensity is in proportion to the CTC concentration in the range 0.98 to approximately 20.0 x 10(-7) mol/L. The limit of detection is 9.8 x 10(-9) mol/L. Synthetic samples and body fluid samples including human urine, human serum, and fresh milk were determined with the recovery of 95.4-106.4% and RSD of 2.9-3.9%.
Animals↗
Interferon-kappa, a novel type I interferon expressed in human keratinocytes.
High throughput cDNA sequencing has led to the identification of interferon-kappa, a novel subclass of type I interferon that displays approximately 30% homology to other family members. Interferon-kappa consists of 207 amino acids, including a 27-amino acid signal peptide and a series of cysteines conserved in type I interferons. The gene encoding interferon-kappa is located on the short arm of chromosome 9 adjacent to the type I interferon gene cluster and is selectively expressed in epidermal keratinocytes. Expression of interferon-kappa is significantly enhanced in keratinocytes upon viral infection, upon exposure to double-stranded RNA, or upon treatment with either interferon-gamma or interferon-beta. Administration of interferon-kappa recombinant protein imparts cellular protection against viral infection in a species-specific manner. Interferon-kappa activates the interferon-stimulated response element signaling pathway and a panel of genes similar to those regulated by other type I interferons including anti-viral mediators and transcriptional regulators. An antibody that neutralizes the type I interferon receptor completely blocks interferon-kappa signaling, demonstrating that interferon-kappa utilizes the same receptor as other type I interferons. Interferon-kappa therefore defines a novel subclass of type I interferon that is expressed in keratinocytes and expands the repertoire of known proteins mediating host defense.
Amino Acid Sequence↗
The critical window of brain development from susceptive to insusceptive. Effects of clomipramine neonatal treatment on sexual behavior.
The immature brain is much more sensitive to abnormal experience, particularly sleep deprivation, drug exposure, and maternal separation. The critical time period during which features in the brain's susceptibility to such experience change, however, has not yet been determined. In previous studies on rats, we found that neonatal treatment with clomipramine (CLI) during postnatal days 8--21 (P8-21) produced behavioral and physiological abnormalities in adult rats that resembled the abnormalities found in human endogenous depression. The objective of the present study is to determine (1) the critical (more specifically, the latest) time frame in which CLI treatment will produce adult depression and (2) the shortest treatment window during which CLI can induce adult depression. Male rats were neonatally treated with CLI (20 mg/kg, sc) twice daily or with an equivolume of saline. The treatment windows were P12--17, P14--20, P16--22, and P12--15. Six variables, including number of mounts, intromission, ejaculation, mount latency, ejaculation latency, and post-ejaculation interval, were measured visually between the ages of 4 and 5 months. Rats treated with CLI showed significant sexual impairment in treatment windows P12--17 and P14--20 and slight sexual deficiency in the short window P12--15. No significant sexual impairment was found in window P16--22. We concluded that P14--20 was the latest window during which CLI treatment produces adult sexual deficiency and that 6 days might be the shortest treatment window to produce significant behavior abnormalities.
Animals↗
Biomarker risk assessment and bladder cancer detection in a cohort exposed to benzidine.
BACKGROUND: Cancer screening with highly sensitive, specific biomarkers that reflect molecular phenotypic alterations is an attractive strategy for cancer control. We examined whether biomarker profiles could be used for risk assessment and cancer detection in a cohort of Chinese workers occupationally exposed to benzidine and at risk for bladder cancer. METHODS: The cohort consisted of 1788 exposed and 373 nonexposed workers, followed from 1991 through 1997. We assayed urothelial cells from voided urine samples for DNA ploidy (expressed as the 5C-exceeding rate [DNA 5CER]), the bladder tumor-associated antigen p300, and a cytoskeletal protein (G-actin). Workers were stratified into different risk groups (high, moderate, and low risk) at each examination based on a predefined biomarker profile. For workers who developed bladder cancer, tumor risk assessment was analyzed from samples collected 6-12 months before the cancer diagnosis. The associations between risk group and subsequent development of bladder cancer were analyzed by Cox proportional hazards regression analysis and logistic analysis, after adjustment. All statistical tests were two-sided. RESULTS: Twenty-eight bladder cancers were diagnosed in exposed workers and two in nonexposed workers. For risk assessment, DNA 5CER had 87.5% sensitivity, 86.5% specificity, an odds ratio (OR) of 46.2 (95% confidence interval [CI] = 8.1 to 867.0), and a risk ratio (RR) of 16.2 (95% CI = 7.1 to 37.0); p300 had 50.0% sensitivity, 97.9% specificity, an OR of 40.0 (95% CI = 9.0 to 177.8), and an RR of 37.9 (95% CI = 16.8 to 85.3). The risk of developing bladder cancer was 19.6 (95% CI = 8.0 to 47.9) times higher in workers positive for either the DNA 5CER or p300 biomarkers than in workers negative for both biomarkers and 81.4 (95% CI = 33.3 to 199.3) times higher in workers positive for both biomarkers. G-actin was a poor marker of individual risk. CONCLUSIONS: Occupationally exposed workers at risk for bladder cancer can be individually stratified, screened, monitored, and diagnosed based on predefined molecular biomarker profiles.
Actins↗
Macroscopic shear alignment of bulk transparent mesostructured silica.
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Journal Article↗
Synthesis and release of B-lymphocyte stimulator from myeloid cells.
B-lymphocyte stimulator (BLyS) is a recently identified novel member of the tumor necrosis factor ligand superfamily shown to exist in a membrane-bound and soluble form. BLyS was found to be specifically expressed on cells of myeloid lineage and to selectively stimulate B-lymphocyte proliferation and immunoglobulin production. The expression of a cytokine involved in potentiation of humoral immune responses, such as BLyS, is expected to be strictly controlled. The goal of the present study was to examine regulation of BLyS levels in monocytic cells in response to cytokines and during their differentiation to macrophages and dendritic cells. The presence of BLyS on the cell surface and in the culture medium of both normal blood monocytes and on tumor cells of myelomonocytic origin was demonstrated. BLyS gene expression and levels of membrane-associated and soluble BLyS were found to be regulated by cytokines, in particular interferon (IFN)-gamma and to a lesser extent interleukin-10 (IL-10). The expression of BLyS on monocyte membranes was retained following differentiation into macrophages, but detection on the surface of monocyte-derived dendritic cells required stimulation with IFN-gamma. Both IFN-gamma and IL-10 enhanced the release of soluble BLyS that was active in B-cell proliferation assays. Cells transfected with BLyS complementary DNA mutated in a predicted cleavage site failed to release BLyS into the culture medium, thereby suggesting that soluble BLyS was derived from the membrane form. These results provide further support for an important role for BLyS expressed in myeloid cells in B-cell expansion and antibody responses.
Antibodies↗
Determination of proteins by their enhancement of resonance light scattering by fuchsine acid.
Based on the measurement of the enhancement of resonance light scattering (RLS) of fuchsine acid (FSA) by proteins, a novel sensitive assay of proteins in body fluid samples has been developed. Proteins, including bovine serum albumin (BSA), human serum albumin (HSA), pepsin (Pep), alpha-chymotrypsin (Chy), lysozyme (Lys), and cellulase (Cel), can bind to fuchsine acid (FSA), resulting in enhanced RLS signals at 277.0 nm. Linear relationships between the enhanced RLS intensity and the protein concentration were measured at different concentration of FSA, and the limits of detection for BSA, HSA, and Lys were found to lie in the nanogram range.
Animals↗
Recombinant human extracellular matrix protein 1 inhibits alkaline phosphatase activity and mineralization of mouse embryonic metatarsals in vitro.
Two mRNAs are transcribed from the extracellular matrix protein 1 gene (Ecm1): Ecm1a and an alternatively spliced Ecm1b. We studied Ecm1 mRNA expression and localization during endochondral bone formation and investigated the effect of recombinant human (rh) Ecm1a protein on organ cultures of embryonic mouse metatarsals. Of the two transcripts, Ecm1a mRNA was predominantly expressed in fetal metacarpals from day 16 to 19 after gestation. Ecm1 expression was not found in 16- and 17-day-old metatarsals of which the perichondrium was removed. In situ hybridization and immunohistochemistry demonstrated Ecm1 expression in the connective tissues surrounding the developing bones, but not in the cartilage. Biological effects of rhEcm1a protein on fetal metatarsal cultures were biphasic: at low concentrations, Ecm1a stimulated alkaline phosphatase activity and had no effect on mineralization, whereas at higher concentrations, Ecm1a dose dependently inhibited alkaline phosphatase activity and mineralization. These results suggest that Ecm1a acts as a novel negative regulator of endochondral bone formation.
Alkaline Phosphatase↗
Extracellular matrix protein 1 (ECM1) has angiogenic properties and is expressed by breast tumor cells.
Tumor growth and metastasis are critically dependent on the formation of new blood vessels. The present study found that extracellular matrix protein 1 (ECM1), a newly described secretory glycoprotein, promotes angiogenesis. This was initially suggested by in situ hybridization studies of mouse embryos indicating that the ECM1 message was associated with blood vessels and its expression pattern was similar to that of flk-1, a recognized marker for endothelium. More direct evidence for the role of ECM1 in angiogenesis was provided by the fact that highly purified recombinant ECM1 stimulated the proliferation of cultured endothelial cells and promoted blood vessel formation in the chorioallantoic membrane of chicken embryos. Immunohistochemical staining with specific antibodies indicated that ECM1 was expressed by the human breast cancer cell lines MDA-435 and LCC15, both of which are highly tumorigenic. In addition, staining of tissue sections from patients with breast cancer revealed that ECM1 was present in a significant proportion of primary and secondary tumors. Collectively, the results of this study suggest that ECM1 possesses angiogenic properties that may promote tumor progression.
Angiogenesis Inducing Agents↗
Glutamate decarboxylase genes as a prescreening marker for detection of pathogenic Escherichia coli groups.
The enzyme glutamate decarboxylase (GAD) is prevalent in Escherichia coli but few strains in the various pathogenic E. coli groups have been tested for GAD. Using PCR primers that amplify a 670-bp segment from the gadA and gadB genes encoding GAD, we examined the distribution of the gadAB genes among enteric bacteria. Analysis of 173 pathogenic E. coli strains, including 125 enterohemorrhagic E. coli isolates of the O157:H7 serotype and its phenotypic variants and 48 isolates of enteropathogenic E. coli, enterotoxigenic E. coli, enteroinvasive E. coli, and other Shiga toxin-producing E. coli (STEC) serotypes, showed that gadAB genes were present in all these strains. Among the 22 non-E. coli isolates tested, only the 6 Shigella spp. carried gadAB. Analysis of naturally contaminated water and food samples using a gadAB-specific DNA probe that was labeled with digoxigenin showed that a gadAB-based assay is as reliable as standard methods that enumerate E. coli organisms on the basis of lactose fermentation. The presence of few E. coli cells initially seeded into produce rinsates could be detected by PCR to gadA/B genes after overnight enrichment. A multiplex PCR assay using the gadAB primers in combination with primers to Shiga toxin (Stx) genes stx(1) and stx(2) was effective in detecting STEC from the enrichment medium after seeding produce rinsate samples with as few as 2 CFU. The gadAB primers may be multiplexed with primers to other trait virulence markers to specifically identify other pathogenic E. coli groups.
Biomarkers↗
Isogenic strain of Escherichia coli O157:H7 that has lost both Shiga toxin 1 and 2 genes.
An Escherichia coli O157:H7 strain isolated from a patient with hemorrhagic colitis was found to exhibit two slightly different colony morphology types on differential medium. Each morphological type, designated TT12A and TT12B, was isolated, and serological testing using various assays confirmed that both strains carried the O157 and the H7 antigens. Biochemical testing showed that the strains had identical profiles on AP120E analysis and, like typical O157:H7 strains, did not ferment sorbitol or exhibit beta-glucuronidase activity. Analysis with a multiplex PCR assay showed that TT12B did not carry the gene for either Shiga toxin 1 (Stx1) or Stx2, whereas these genes were present in TT12A and the toxins were produced. Apart from that, both strains carried the +93 gusA mutation, the cluster I ehxA gene for enterohemolysin, and the eae gene for gamma-intimin, which are all characteristics of the O157:H7 serotype. Phenotypic assays confirmed that both strains exhibited enterohemolysin activity and the attachment and effacing lesion on HeLa cells. Multilocus enzyme electrophoresis analysis showed that the strains are closely related genetically and belong in the same clonal group. Pulsed-field gel electrophoresis (PFGE) typing of XbaI-digested genomic DNA revealed that the two strains differed by two bands but shared 90% similarity and clustered in the same clade. All other non-Stx-producing O157:H7 strains examined clustered in a major clade that was distinct from that of Stx-producing O157:H7 strains. The findings that TT12B was identical to TT12A, except for Stx production, and its PFGE profile is also more closely related to that of Stx-producing O157:H7 strains suggest that TT12B was derived from TT12A by the loss of both stx genes.
Blotting, Southern↗
Genetic analysis for virulence factors in Escherichia coli O104:H21 that was implicated in an outbreak of hemorrhagic colitis.
Isolates of enterohemorrhagic Escherichia coli (EHEC) of serotype O104:H21 implicated in a 1994 outbreak of hemorrhagic colitis in Montana were analyzed for the presence of trait EHEC virulence markers. By using a multiplex PCR that specifically amplifies several genes, the O104:H21 strains were found to carry only the Shiga toxin 2 gene (stx2) and to express Stx2. They did not have the eaeA gene for gamma-intimin, which is typically found in O157:H7, or the alpha- or beta-intimin derivatives, which are common in other EHEC and enteropathogenic E. coli serotypes. Results of the multiplex PCR also indicated that the ehxA gene for enterohemolysin was absent from O104:H21. This, however, was not consistent with the results of a phenotypic assay that showed them to be hemolytic or a PCR analysis with another set of ehxA-specific primers, which indicated the presence of ehxA. To resolve this discrepancy, the ehxA region in O104:H21 and O157:H7 strains, to which the multiplex PCR primers anneal, was cloned and sequenced. Comparison of the sequences showed that the upstream primer binding site in the ehxA gene of O104:H21 was not identical to that of O157:H7. Specifically, there were several base mutations, including an A-to-G substitution at the 3' end of the primer binding site. These base mutations are presumably not unique to O104:H21, since other enterohemolytic serotypes were also not detected with the ehxA primers used in the multiplex PCR. Comparison of the ehxA sequences of O104:H21 strains with those of other Stx-producing E. coli strains showed that they more closely resembled those of O8:H19 strains, which have cluster II ehxA genes, than those of O157:H7 strains, which have cluster I ehxA sequences. By modifying the upstream ehxA primer, the multiplex PCR was able to detect ehxA genes in both O157:H7 and O104:H21 strains.
Adhesins, Bacterial↗
mRNA decay during herpesvirus infections: interaction between a putative viral nuclease and a cellular translation factor.
During lytic infections, the virion host shutoff (Vhs) protein (UL41) of herpes simplex virus destabilizes both host and viral mRNAs. By accelerating mRNA decay, it helps determine the levels and kinetics of viral and cellular gene expression. In vivo, Vhs shows a strong preference for mRNAs, as opposed to non-mRNAs, and degrades the 5' end of mRNAs prior to the 3' end. In contrast, partially purified Vhs is not restricted to mRNAs and causes cleavage of target RNAs at various sites throughout the molecule. To explain this discrepancy, we searched for cellular proteins that interact with Vhs using the Saccharomyces cerevisiae two-hybrid system. Vhs was found to interact with the human translation initiation factor, eIF4H. This interaction was verified by glutathione S-transferase pull-down experiments and by coimmunoprecipitation of Vhs and epitope-tagged eIF4H from extracts of mammalian cells. The interaction was abolished by several point mutations in Vhs that abrogate its ability to degrade mRNAs in vivo. The results suggest that Vhs is a viral mRNA degradation factor that is targeted to mRNAs, and to regions of translation initiation, through an interaction with eIF4H.
Amino Acid Sequence↗