[Progress on molecular mechanism of Staphylococcus epidermidis biofilm].
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Bacterial Adhesion↗
Biomedical subjects
Qing Zhang
Publications and source records attributed to Qing Zhang.
A new vascular prosthesis coated with polyamino-acid urethane copolymer (PAU) to enhance endothelialization.
Clinically available synthetic ePTFE vascular grafts frequently fail when used for small-diameter arterial substitution. The lower long-term patency of ePTFE grafts is due mainly to thrombogenicity and poor healing. We developed a new small-diameter (1.5-mm) ePTFE vascular prosthesis coated with polyamino-acid urethane copolymer (PAU) to enhance endothelialization. Coating with PAU made the hydrophobic ePTFE vascular graft hydrophilic. Scanning electron microscopy (SEM) observation showed that PAU was homogeneously coated on the ePTFE graft while maintaining the graft's porous structure. Fourier transform infrared attenuated total reflectance (FTIR-ATR) spectra showed PAU was present on graft inner surfaces. Noncoated and PAU-coated ePTFE vascular grafts were implanted into the rat abdominal aorta and evaluated within 1 week and at 8 weeks after implantation. We evaluated the extent of neoendothelialization by SEM, light microscopy, and immunohistochemical staining. Noncoated grafts showed partial endothelialization at proximal and distal areas of grafts but none at midsection. One-percent PAU-coated grafts showed incomplete neoendothelialization, but endothelial cells were observed in the midsection of grafts. Three-percent PAU-coated ePTFE grafts showed complete endothelialization with typical endothelial cell layers under SEM and histologic observation. Immunohistochemical staining also showed that an endothelial cell lining positively reacted with anti-von Willebrand factor (endothelial cell marker) antibody. We conclude that PAU-coated ePTFE vascular grafts enhance endothelialization.
Amino Acids↗
Biocompatibility evaluation of ePTFE membrane modified with PEG in atmospheric pressure glow discharge.
ePTFE membranes were modified by poly(ethylene glycol) having a molecular weight of 600 (PEG-600) in atmospheric pressure glow discharge (APG) plasma treatment. ePTFE membranes were immersed in 1%, 3%, or 5% (w/v) PEG-600 in dehydrated ethanol. PEG-600-penetrated ePTFE membranes were dried in a vacuum to immediately remove ethanol, then treated with APG at 20 kHz and 60-70 W for 15 min and thoroughly washed with ethanol and water. PEG-600-modified ePTFE membranes were analyzed using contact angle measurement, Fourier transform infrared attenuated total reflectance (FTIR-ATR), and scanning electron microscopy (SEM). ePTFE membrane contact angles were reduced after PEG-600 plasma treatment. FTIR-ATR spectra showed an absorption band due to a PEG hydroxyl group (-OH). SEM showed that ePTFE fiber surfaces were uniformly immobilized with PEG-600 and retained their porous structure. A general biological evaluation of the PEG-modified ePTFE membranes showed no cytotoxicity on CHO-K1 cell lines and no hemolytic action. Albumin adsorption on the PEG-modified ePTFE membranes increased with increasing PEG-600 deposited on ePTFE membranes. Fibrinogen adsorption decreased with increasing PEG-600 deposited on ePTFE membranes. gamma-Globulin adsorption did not change before or after PEG plasma modification. 1% and 3% PEG-600 plasma-treated ePTFE only slightly increased platelet adhesion, but adhering platelets evidenced no pseudopod formation. 5% PEG-600-modified ePTFE showed relatively large numbers of platelet adhesion. We concluded that 3% PEG-600-modified ePTFE membrane had the best physical properties and biological compatibility, indicating 3% PEG-600-modified ePTFE membranes exhibit the potential for blood filter application.
Adsorption↗
A comparison of whole-genome shotgun-derived mouse chromosome 16 and the human genome.
The high degree of similarity between the mouse and human genomes is demonstrated through analysis of the sequence of mouse chromosome 16 (Mmu 16), which was obtained as part of a whole-genome shotgun assembly of the mouse genome. The mouse genome is about 10% smaller than the human genome, owing to a lower repetitive DNA content. Comparison of the structure and protein-coding potential of Mmu 16 with that of the homologous segments of the human genome identifies regions of conserved synteny with human chromosomes (Hsa) 3, 8, 12, 16, 21, and 22. Gene content and order are highly conserved between Mmu 16 and the syntenic blocks of the human genome. Of the 731 predicted genes on Mmu 16, 509 align with orthologs on the corresponding portions of the human genome, 44 are likely paralogous to these genes, and 164 genes have homologs elsewhere in the human genome; there are 14 genes for which we could find no human counterpart.
Animals↗
Genome sequence and comparative microarray analysis of serotype M18 group A Streptococcus strains associated with acute rheumatic fever outbreaks.
Acute rheumatic fever (ARF), a sequelae of group A Streptococcus (GAS) infection, is the most common cause of preventable childhood heart disease worldwide. The molecular basis of ARF and the subsequent rheumatic heart disease are poorly understood. Serotype M18 GAS strains have been associated for decades with ARF outbreaks in the U.S. As a first step toward gaining new insight into ARF pathogenesis, we sequenced the genome of strain MGAS8232, a serotype M18 organism isolated from a patient with ARF. The genome is a circular chromosome of 1,895,017 bp, and it shares 1.7 Mb of closely related genetic material with strain SF370 (a sequenced serotype M1 strain). Strain MGAS8232 has 178 ORFs absent in SF370. Phages, phage-like elements, and insertion sequences are the major sources of variation between the genomes. The genomes of strain MGAS8232 and SF370 encode many of the same proven or putative virulence factors. Importantly, strain MGAS8232 has genes encoding many additional secreted proteins involved in human-GAS interactions, including streptococcal pyrogenic exotoxin A (scarlet fever toxin) and two uncharacterized pyrogenic exotoxin homologues, all phage-associated. DNA microarray analysis of 36 serotype M18 strains from diverse localities showed that most regions of variation were phages or phage-like elements. Two epidemics of ARF occurring 12 years apart in Salt Lake City, UT, were caused by serotype M18 strains that were genetically identical, or nearly so. Our analysis provides a critical foundation for accelerated research into ARF pathogenesis and a molecular framework to study the plasticity of GAS genomes.
Acute Disease↗
The gene for the muted (mu) mouse, a model for Hermansky-Pudlak syndrome, defines a novel protein which regulates vesicle trafficking.
The muted (mu) mouse is a model for Hermansky-Pudlak Syndrome (HPS), an inherited disorder of humans causing hypopigmentation, hemorrhaging and early death due to lung abnormalities. The mu gene regulates the synthesis of specialized mammalian organelles such as melanosomes, platelet dense granules and lysosomes. Further, balance defects indicate that it controls the synthesis of otoliths of the inner ear. The mu gene has been identified by a positional/candidate approach involving large mouse interspecific backcrosses. It encodes a novel ubiquitously expressed transcript, specifying a predicted 185 amino acid protein, whose expression is abrogated in the mu allele which contains an insertion of an early transposon (ETn) retrotransposon. Expression is likewise expected to be lost in the mu( J) allele which contains a deletion of a single base pair within the coding region. The presence of structurally aberrant melanosomes within the eyes of mutant mice together with localization of the muted protein within vesicles in both the cell body and dendrites of transfected melan-a melanocytes emphasizes the role of the mu gene in vesicle trafficking. The mu gene is present only in mice and humans among analyzed genomes. As is true for several other recently identified mouse HPS genes, the mu gene is absent in lower eukaryotes. Therefore, the mu gene is a member of the novel gene set that has evolved in higher eukaryotes to regulate the synthesis/function of highly specialized subcellular organelles such as melanosomes and platelet dense granules.
Amino Acid Sequence↗
Progression of systolic abnormalities in patients with "isolated" diastolic heart failure and diastolic dysfunction.
BACKGROUND: The definition of diastolic heart failure (DHF) relies on the use of sensitive tools to exclude the presence of systolic dysfunction. The use of ejection fraction (EF) of 50% as the cutoff point may not be adequate to address such a task. We believe that systolic dysfunction is common in DHF. METHODS AND RESULTS: Echocardiography with tissue Doppler imaging was performed in 339 subjects, of whom 92 had systolic heart failure (SHF) (EF<50%), 73 had DHF (EF > or = 50% with diastolic abnormalities on Doppler echocardiography), and 68 had isolated diastolic dysfunction (DD); 106 were normal control subjects. Regional myocardial velocity curves were constructed off-line with the use of a 6-basal, 6-midsegmental model. The peak regional myocardial sustained systolic (S(M)) and early diastolic (E(M)) velocities were significantly lower in patients with SHF, DHF, and DD than in control subjects in almost all the myocardial segments. Likewise, the mean S(M) (SHF<DHF<DD<control subjects; 3.3 plus/minus 1.0 < 4.6 plus/minus 1.3 < 5.4 plus/minus 1.0 < 6.3 plus/minus 1.0 cm/s; all P less-than-or-equal 0.001) and mean E(M) (SHF=DHF<DD<control subjects; 3.6 plus/minus 1.2 =3.9 plus/minus 1.3 < 5.3 plus/minus 1.6 < 7.2 plus/minus 1.7 cm/s; all P<0.001) from the six basal segments were decreased in all the disease groups. A mean S(M) of 4.4 cm/s (-2 SD of control subjects) predicted the presence of systolic dysfunction in 92% of patients with SHF, 52% with DHF, and 14% with DD. CONCLUSIONS: Through the use of tissue Doppler imaging, systolic abnormalities were evident in patients previously labeled as DHF and to a much lesser extent, isolated DD. This indicates the common coexistence of systolic and diastolic dysfunction in a spectrum of different severity in the pathophysiological process of heart failure.
Aged↗
[Localization diagnosis of chyluria by radionuclide lymphoscintigraphy].
OBJECTIVE: To study the effect of radionuclide lymphoscintigraphy, a new method of localization diagnosis of chyluria. METHODS: Radionuclide lymphoscintigraphy was used to examine 34 patients with chyluria and the results of radionuclide lymphoscintigraphy was compared with those of cystoscopy and lymphangiography. RESULTS: Among the 34 patients 85.3% of unilateral localization diagnosis by radionuclide lymphoscintigraphy was coincident with that by cystoscopy. The positive rate of bilateral localization diagnosis was higher than that by cystoscopy. CONCLUSION: A less invasive technique, radionuclide lymphoscintigraphy can be used as a new option for the localization diagnosis of chyluria.
Adult↗
Hermansky-Pudlak syndrome is caused by mutations in HPS4, the human homolog of the mouse light-ear gene.
Hermansky-Pudlak syndrome (HPS) is a disorder of organelle biogenesis in which oculocutaneous albinism, bleeding and pulmonary fibrosis result from defects of melanosomes, platelet dense granules and lysosomes. HPS is common in Puerto Rico, where it is caused by mutations in the genes HPS1 and, less often, HPS3 (ref. 8). In contrast, only half of non-Puerto Rican individuals with HPS have mutations in HPS1 (ref. 9), and very few in HPS3 (ref. 10). In the mouse, more than 15 loci manifest mutant phenotypes similar to human HPS, including pale ear (ep), the mouse homolog of HPS1 (refs 13,14). Mouse ep has a phenotype identical to another mutant, light ear (le), which suggests that the human homolog of le is a possible human HPS locus. We have identified and found mutations of the human le homolog, HPS4, in a number of non-Puerto Rican individuals with HPS, establishing HPS4 as an important HPS locus in humans. In addition to their identical phenotypes, le and ep mutant mice have identical abnormalities of melanosomes, and in transfected melanoma cells the HPS4 and HPS1 proteins partially co-localize in vesicles of the cell body. In addition, the HPS1 protein is absent in tissues of le mutant mice. These results suggest that the HPS4 and HPS1 proteins may function in the same pathway of organelle biogenesis.
Amino Acid Sequence↗
Prediction of soil adsorption coefficients from retention parameters on three reversed-phase liquid chromatographic columns.
Reversed-phase high-performance liquid chromatographic (RP-HPLC) retention parameters, which are determined by the intermolecular interactions in retention process, can be considered as the chemical molecular descriptors in linear free energy relationships (LFERs). On the basis of the characterization and comparison of octadecyl-bonded silica gel (ODS), cyano-bonded silica gel (CN), and phenyl-bonded silica gel (Ph) columns with linear solvation energy relationships (LSERs), a new multiple linear regression model using RP-HPLC retention parameters on ODS and CN columns as variables for estimation of soil adsorption coefficients was developed. It was tested on a set of reference substances from various chemical classes. The results showed that the multicolumn method was more promising than a single-column methpd was for the estimation of soil adsorption coefficients. The accuracy of the suggested model is identical with that of LSERs.
Adsorption↗
Egg ovomucin attenuates hypercholesterolemia in rats and inhibits cholesterol absorption in Caco-2 cells.
This experiment was designed to evaluate the effect of casein or ovomucin (OV) on the micellar solubility of cholesterol and the taurocholate binding capacity in vitro. We also evaluated the effects of casein or OV on cholesterol metabolism in rats and Caco-2 cells. OV had a significantly greater bile acid-binding capacity than that of casein in vitro. Micellar cholesterol solubility in vitro was significantly lower in the presence of OV compared to casein. The cholesterol micelles containing OV significantly suppressed cholesterol uptake by Caco-2 cells compared to the cholesterol micelles containing casein. Consistent with these in vitro findings, OV-feeding significantly increased the fecal excretion of bile acids or cholesterol compared with casein-feeding. Serum total cholesterol was significantly lower in rats fed OV than in those fed casein. The concentrations of total lipids in liver were significantly lower in the OV-fed group compared with the casein group. These results suggest that the suppression of cholesterol absorption by direct interaction between cholesterol mixed micelles and OV in the jejunal epithelia is part of the mechanism underlying the hypocholesterolemic action of OV. OV may also inhibit the reabsorption of bile acids in the ileum, thus lowering the serum cholesterol level.
Animals↗
Interleukin-1 receptor antagonist allele 2 and familial alopecia areata.
Alopecia areata affects 1%-2% of the population and is hypothesized to be an autoimmune, organ specific T-cell mediated reaction directed against the human hair follicle. It is characterized by loss of hair in patches (alopecia areata) with progression in some individuals to total loss of scalp hair (alopecia totalis) or to loss of all scalp and body hair (alopecia universalis). The interleukin-1 receptor antagonist (IL-1RN) gene was found to be associated with more severe clinical outcome in several chronic inflammatory diseases, including alopecia areata. The IL-1RN*2 allele was found to be associated with alopecia areata severity in a British case-control study. In this paper, we analyzed alopecia areata probands in a family-based sample (n = 131 parent-offspring trios) to study the association between alleles of the IL-1RN and various phenotypes of alopecia areata. In considering all patients with any form of alopecia areata, no association was found with IL-1RN. IL-1RN*2 allele was not associated with alopecia totalis and alopecia universalis. A borderline association was observed between IL-1RN and patchy alopecia areata but it was not statistically significant (p =0.06). We also observed an association between IL1-RN*1 allele and patchy alopecia areata (p =0.045).
Alleles↗
Cell-specific abnormal prenylation of Rab proteins in platelets and melanocytes of the gunmetal mouse.
The mutant gunmetal mouse exhibits reduced rates of platelet synthesis, abnormalities of platelet alpha and dense granules and hypopigmentation. Several of these features resemble those of human alpha/delta platelet storage pool disease, grey platelet syndrome and Hermansky-Pudlak syndrome. Gunmetal mice have reduced levels of Rab geranylgeranyltransferase (RabGGTase), which adds lipophilic prenyl groups to the carboxyl terminus of Rab proteins. The degree of prenylation and the subcellular distribution of several Rab proteins were evaluated in mutant platelets, melanocytes and other tissues. Significant deficits in prenylation and membrane binding of most Rabs were observed in platelets and melanocytes. In contrast, minimal alterations in Rab prenylation were apparent in several other gunmetal tissues despite the fact that RabGGTase activity was equally diminished in these tissues. The mutant tissue-specific effects are probably due to increased concentrations of Rab proteins in platelets and melanocytes. These experiments show that Rab proteins are differentially sensitive to levels of RabGGTase activity and that normal platelet synthesis, platelet organelle function and normal pigmentation are highly sensitive to the degree of prenylation and membrane association of Rab proteins. Further, the tissue-specific effects of the gunmetal mutation suggest that RabGGTase is a potential target for therapy of thrombocytosis.
Alkyl and Aryl Transferases↗
The expression of secretory leukocyte protease inhibitor (SLPI) in the fallopian tube: SLPI protects the acrosome reaction of sperm from inhibitory effects of elastase.
BACKGROUND: Secretory leukocyte protease inhibitor (SLPI) is a protein found in various fluids, including parotid secretions, cervical mucus, seminal plasma and ascites, and is a potent inhibitor of human leukocyte elastase activity. The objective of the study was 2-fold, to evaluate (i) the presence of SLPI in the Fallopian tube, and (ii) the effect of SLPI on the acrosome reaction of sperm. METHODS AND RESULTS: Western blot analysis revealed that SLPI protein was detected as a 12 kDa band in the isthmus, ampulla and infundibulum of the Fallopian tube. Immunohistochemistry using an anti-SLPI polyclonal antibody revealed positive staining of epithelial cells in the Fallopian tube. RT-PCR demonstrated that SLPI transcripts were expressed in the Fallopian tube. To determine the function of SLPI in the Fallopian tube, the effects of SLPI and elastase on the sperm acrosome reaction were examined. SLPI prevented the reduction of the acrosome reaction by elastase in a dose-dependent manner. CONCLUSION: The present findings suggest that SLPI in the Fallopian tube contributes to sperm-oocyte interaction.
Acrosome Reaction↗
Detection of fractalkine in human seminal plasma and its role in infertile patients.
BACKGROUND: Fractalkine is a relatively newly discovered CX(3)C chemokine, which is a chemoattractant for T cells, monocytes and natural killer cells. Several reports have demonstrated the association between chemokine levels in seminal plasma and semen quality. The fractalkine levels in ejaculates from normal donors and infertile male patients with or without asthenozoospermia, were examined and correlated with sperm motility and morphology. METHODS AND RESULTS: Western blot analysis showed fractalkine protein to be present in the seminal plasma. Fractalkine titres in the seminal plasma of infertile men with asthenozoospermia (0.64 +/- 0.04 microg/ml; n = 58) were lower than those in patients without asthenozoospermia (0.94 +/- 0.10 microg/ml; n = 22, P < 0.01) and fertile donors (1.04 +/- 0.07 microg/ml; n = 10, P < 0.001). There was no significant difference between fractalkine levels in patients with and without leukospermia. No significant correlation was found between fractalkine and interleukin-8 levels in seminal plasma. Sperm motility was positively correlated (R(2) = 0.14, P < 0.001) with fractalkine concentration. The existence of CX(3)CR-positive leukocytes in semen was confirmed using specific primers for CX(3)CR. CONCLUSIONS: These results suggest that fractalkine is a chemokine associated with sperm motility and the migration of CX(3)CR-positive leukocytes into semen.
Base Sequence↗
Association between the A/A genotype at the lymphotoxin-alpha+250 site and increased mortality in children with positive blood cultures.
INTRODUCTION: Tumor necrosis factor-alpha has been implicated in the hemodynamic manifestations of sepsis. Genetic polymorphisms located in the first intron of the lymphotoxin-alpha gene have been associated with increased secretion of tumor necrosis factor-alpha. We hypothesized that bacteremic children with the high secretor genotype, AA, have higher levels of tumor necrosis factor-alpha and a worse outcome. METHODS: Genotypic analysis was performed in children with bacteremia using polymerase chain reaction amplification and restriction enzyme digestion. The serum tumor necrosis factor-alpha levels were measured by enzyme-linked immunosorbent assay technique. RESULTS: Genotypic frequencies at the lymphotoxin-alpha+250 site were 11 of 34 (0.32) AA, 16 of 34 (0.47) GA, and 7 of 34 (0.21) GG. Serum tumor necrosis factor-alpha levels were 324 +/- 124 pg/mL in bacteremic children with the AA genotype at the lymphotoxin-alpha+250 site compared with 92 +/- 59 pg/mL in bacteremic children with the AG genotype (p < .001) and 92 +/- 21 pg/mL in bacteremic children with the GG genotype (p < .001). Eight of 11 bacteremic children with the AA genotype died compared with 3 of 16 bacteremic children with the GA genotype (p < .001) and zero of seven bacteremic children with the GG genotype (p < .001). CONCLUSION: The AA genotype at the lymphotoxin-alpha+250 site is associated with higher serum tumor necrosis factor-alpha levels and a higher mortality in children with bacteremia.
Journal Article↗
Colorectal cancer incidence and mortality in Texas 1990-1992: a comparison of rural classifications.
Although cancer incidence and mortality rates are known to be higher in urban populations, more unstaged tumors and later staged cancer are diagnosed in rural populations. Most investigators have used a dichotomous definition of urban and rural in studying these populations, and they have not considered whether a more detailed categorization of rural areas could influence their findings. The objective of this study was to evaluate colorectal cancer incidence and mortality rates in Texas from 1990 to 1992 by using a dichotomous definition (Metropolitan Area vs. Nonmetropolitan Area [MA/non-MA]) and two more detailed rural classifications (the Rural-Urban Continuum Code [RUCC] and the Urban Influence Code [UIC]). Cancer data were obtained from the Texas Cancer Registry for 1990 to 1992 and supplemented with data from the Texas State Department of Vital Statistics (mortality), the US Census Bureau (age, gender, race) and the Area Resource File (rural and urban definitions). Incidence and mortality rates, age-adjusted to the 1970 US standard population, were calculated for non-Hispanic White, African American, and Hispanic males and females. Results revealed a nonlinear relationship between rural category and colorectal cancer incidence or mortality for all races. Applying the MA definition yielded rates in the middle of the ranges obtained with using RUCC or UIC classifications and most closely reflected the result for non-Hispanic Whites using the more detailed scales. Our results suggest that a dichotomous definition of rural and urban may mask important variation in colorectal cancer incidence and mortality rates within rural areas.
Adolescent↗
Pseudoepidemic due to a unique strain of Mycobacterium szulgai: genotypic, phenotypic, and epidemiological analysis.
In mid-1999, we noted multiple isolations at the Veterans Affairs Medical Center (VAMC) Houston Tex. of an unusual nonpigmented Mycobacterium species. Since, on the basis of 16S rRNA gene sequence analysis, the strains were identical to the Mycobacterium szulgai type strain and since M. szulgai has been reported only rarely as a commensal or environmental isolate, we were concerned about laboratory contamination, nosocomial spread, or even the possibility that this could be a novel organism associated with disease. Our investigation found that from 1999 to 2000, 37 strains of M. szulgai were isolated from patients at the VAMC (the base rate for the previous 10 years had been <1 isolation per year). We compared the phenotypic properties and genetic relatedness of these 37 strains (31 of which were nonpigmented) as well as eight stock strains and the M. szulgai type strain. All strains were similar in cellular fatty acid patterns, growth rates, and biochemical characteristics. However, we found three genogroups by gene sequence analysis. Genogroup I comprised the M. szulgai type strain, all the tested nonpigmented strains (27 of the 31 strains were tested), two pigmented strains isolated in 1999 and 2000, and five pigmented stock strains. Genogroup II comprised five pigmented strains: three were isolated from 1999 to 2000 and two were stock strains. The single strain (isolated in 1996) in genogroup III was pigmented and was the only strain associated with disease. Whereas the randomly amplified polymorphic DNA (RAPD) patterns of all nonpigmented strains were identical, indicating that they came from a common source (the pseudoepidemic strain), the RAPD patterns of the other strains were varied. In our investigation for a possible source, we found that there were no common reagents, specimen-processing or patient locations, or procedures linking the 31 pseudoepidemic strains. However, a nonpigmented M. szulgai strain with a gene sequence and RAPD pattern identical to those of the pseudoepidemic strain was recovered from a water storage tank serving the hospital. We concluded that the strains most likely originated from hospital water, which transiently inoculated our patients. Although no disease was associated with this cluster of isolates, the event was costly because identification was problematic and we could not easily discount the isolations, since most of the patients were immunocompromised and were candidates for opportunistic infection.
Bacterial Typing Techniques↗