270 research outputs found
Gas gangrene and osteomyelitis of the foot in a diabetic patient treated with tea tree oil
Diabetic foot wounds represent a class of chronic non-healing wounds that can lead to the development of soft tissue infections and osteomyelitis. We reviewed the case of a 44-year-old female with a diabetic foot wound who developed gas gangrene while treating her wound with tea tree oil, a naturally derived antibiotic agent. This case report includes images that represent clinical examination and x-ray findings of a patient who required broad-spectrum antibiotics and emergent surgical consultation. Emergency Department (ED) detection of these complications may prevent loss of life or limb in these patients
Hereditary prostate cancer in African American families: linkage analysis using markers that map to five candidate susceptibility loci
The rate and associated risk factors for acute carpal tunnel syndrome complicating a fracture of the distal radius
Is plasma vitamin C an appropriate biomarker of vitamin C intake? A systematic review and meta-analysis
<p>Abstract</p> <p>Background</p> <p>As the primary source of dietary vitamin C is fruit and to some extent vegetables, the plasma level of vitamin C has been considered a good surrogate or predictor of vitamin C intake by fruit and vegetable consumption. The purpose of this systematic review was to investigate the relationship between dietary vitamin C intakes measured by different dietary methods and plasma levels of vitamin C.</p> <p>Method</p> <p>We searched the literature up to May 2006 through the OVID interface: MEDLINE (from 1960) and EMBASE (from 1988). We also reviewed the reference lists in the articles, reviews, and textbooks retrieved. A total of 26 studies were selected and their results were combined using meta-analytic techniques with random-effect model approach.</p> <p>Results</p> <p>The overall result of this study showed a positive correlation coefficient between Food Frequency Questionnaire (FFQ) and biomarker (<it>r </it>= 0.35 for "both" genders, 0.39 for females, and 0.46 for males). Also the correlation between Dietary Recalls (DR)/diary and biomarker was 0.46 for "both" genders, 0.44 for females, and 0.36 for males. An overall correlation of 0.39 was found when using the weight record method. Adjusting for energy intake improved the observed correlation for FFQ from 0.31 to 0.41. In addition, we compared the correlation for smokers and non-smokers for both genders (FFQ: for non-smoker <it>r </it>= 0.45, adjusted for smoking <it>r </it>= 0.33).</p> <p>Conclusion</p> <p>Our findings show that FFQ and DR/diary have a moderate relationship with plasma vitamin C. The correlation may be affected/influenced by the presence of external factors such as vitamin bioavailability, absorption condition, stress and food processing and storage time, or by error in reporting vitamin C intake.</p
Feeder Cells Support the Culture of Induced Pluripotent Stem Cells Even after Chemical Fixation
Chemically fixed mouse embryonic fibroblasts (MEFs), instead of live feeder cells, were applied to the maintenance of mouse induced pluripotent stem (miPS) cells. Formaldehyde and glutaraldehyde were used for chemical fixation. The chemically fixed MEF feeders maintained the pluripotency of miPS cells, as well as their undifferentiated state. Furthermore, the chemically fixed MEF feeders were reused several times without affecting their functions. These results indicate that chemical fixation can be applied to modify biological feeders chemically, without losing their original functions. Chemically fixed MEF feeders will be applicable to other stem cell cultures as a reusable extracellular matrix candidate that can be preserved on a long-term basis
Regulation of expression of Na+,K+-ATPase in androgen-dependent and androgen-independent prostate cancer
The Ξ²1-subunit of Na+,K+-ATPase was isolated and identified as an androgen down-regulated gene. Expression was observed at high levels in androgen-independent as compared to androgen-dependent (responsive) human prostate cancer cell lines and xenografts when grown in the presence of androgens. Down-regulation of the Ξ²1-subunit was initiated at concentrations between 0.01 nM and 0.03 nM of the synthetic androgen R1881 after relatively long incubation times (> 24 h). Using polyclonal antibodies, the concentration of Ξ²1-subunit protein, but not of the Ξ±1-subunit protein, was markedly reduced in androgen-dependent human prostate cancer cells (LNCaP-FGC) cultured in the presence of androgens. In line with these observations it was found that the protein expression of total Na+,K+-ATPase in the membrane (measured by 3H-ouabain binding) was also markedly decreased. The main function of Na+,K+-ATPase is to maintain sodium and potassium homeostasis in animal cells. The resulting electrochemical gradient is facilitative for transport of several compounds over the cell membrane (for example cisplatin, a chemotherapeutic agent experimentally used in the treatment of hormone-refractory prostate cancer). Here we observed that a ouabain-induced decrease of Na+,K+-ATPase activity in LNCaP-FGC cells results in reduced sensitivity of these cells to cisplatin-treatment. Surprisingly, androgen-induced decrease of Na+,K+-ATPase expression, did not result in significant protection against the chemotherapeutic agent. Β© 1999 Cancer Research Campaig
Absence of truncating BRIP1 mutations in chromosome 17q-linked hereditary prostate cancer families
Background:In a genome-wide scan (GWS) of 175 multiplex prostate cancer (PCa) families from the University of Michigan Prostate Cancer Genetics Project (PCGP), linkage was observed to markers on chromosome 17q21β24, a region that includes two breast cancer susceptibility genes, BRCA1 and BRIP1. BRIP1 is a Fanconi anaemia gene (FANCJ) that interacts with the BRCT domain of BRCA1 and has a role in DNA damage repair. Protein truncating mutations in BRIP1 have been identified in hereditary breast and ovarian cancer families, and a recent report suggested that a recurrent truncating mutation (R798X) may have a role in PCa susceptibility.Methods:We examined the role of BRIP1 mutations in hereditary PCa through sequence analysis of 94 individuals from PCGP families showing linkage to 17q.Results:A total of 24 single-nucleotide polymorphisms, including 7 missense variants but no protein truncating mutations, were observed.Conclusion:The data presented here suggest that BRIP1 truncating mutations are uncommon in PCa cases and do not account for the linkage to chromosome 17q observed in our GWS. Additional investigation is needed to determine the significance, if any, of the observed BRIP1 missense variants in hereditary PCa
RNAi-Mediated Knock-Down of Arylamine N-acetyltransferase-1 Expression Induces E-cadherin Up-Regulation and Cell-Cell Contact Growth Inhibition
Arylamine N-acetyltransferase-1 (NAT1) is an enzyme that catalyzes the biotransformation of arylamine and hydrazine substrates. It also has a role in the catabolism of the folate metabolite p-aminobenzoyl glutamate. Recent bioinformatics studies have correlated NAT1 expression with various cancer subtypes. However, a direct role for NAT1 in cell biology has not been established. In this study, we have knocked down NAT1 in the colon adenocarcinoma cell-line HT-29 and found a marked change in cell morphology that was accompanied by an increase in cell-cell contact growth inhibition and a loss of cell viability at confluence. NAT1 knock-down also led to attenuation in anchorage independent growth in soft agar. Loss of NAT1 led to the up-regulation of E-cadherin mRNA and protein levels. This change in E-cadherin was not attributed to RNAi off-target effects and was also observed in the prostate cancer cell-line 22Rv1. In vivo, NAT1 knock-down cells grew with a longer doubling time compared to cells stably transfected with a scrambled RNAi or to parental HT-29 cells. This study has shown that NAT1 affects cell growth and morphology. In addition, it suggests that NAT1 may be a novel drug target for cancer therapeutics
Super-resolution imaging as a method to study GPCR dimers and higher-order oligomers
The study of G protein-coupled receptor (GPCR) dimers and higher-order oligomers has unveiled mechanisms for receptors to diversify signaling and potentially uncover novel therapeutic targets. The functional and clinical significance of these receptorβreceptor associations has been facilitated by the development of techniques and protocols, enabling researchers to unpick their function from the molecular interfaces, to demonstrating functional significance in vivo, in both health and disease. Here we describe our methodology to study GPCR oligomerization at the single-molecule level via super-resolution imaging. Specifically, we have employed photoactivated localization microscopy, with photoactivatable dyes (PD-PALM) to visualize the spatial organization of these complexes to <10 nm resolution, and the quantitation of GPCR monomer, dimer, and oligomer in both homomeric and heteromeric forms. We provide guidelines on optimal sample preparation, imaging parameters, and necessary controls for resolving and quantifying single-molecule data. Finally, we discuss advantages and limitations of this imaging technique and its potential future applications to the study of GPCR function
Ptenb Mediates Gastrulation Cell Movements via Cdc42/AKT1 in Zebrafish
Phosphatidylinositol 3-kinase (PI3 kinase) mediates gastrulation cell migration in zebrafish via its regulation of PIP2/PIP3 balance. Although PI3 kinase counter enzyme PTEN has also been reported to be essential for gastrulation, its role in zebrafish gastrulation has been controversial due to the lack of gastrulation defects in pten-null mutants. To clarify this issue, we knocked down a pten isoform, ptenb by using anti-sense morpholino oligos (MOs) in zebrafish embryos and found that ptenb MOs inhibit convergent extension by affecting cell motility and protrusion during gastrulation. The ptenb MO-induced convergence defect could be rescued by a PI3-kinase inhibitor, LY294002 and by overexpressing dominant negative Cdc42. Overexpression of human constitutively active akt1 showed similar convergent extension defects in zebrafish embryos. We also observed a clear enhancement of actin polymerization in ptenb morphants under cofocal microscopy and in actin polymerization assay. These results suggest that Ptenb by antagonizing PI3 kinase and its downstream Akt1 and Cdc42 to regulate actin polymerization that is critical for proper cell motility and migration control during gastrulation in zebrafish
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