It is well established that ethnocultural groups of migrants are associated with a differential risk of communicable disease, including measles, tuberculosis and hepatitis B. Global public health agencies¹ are now focusing on improving the collection of ethnocultural data to better define communicable disease risk in migrant populations to support community-level disease prevention and control.

There is a need recognized by the National Institute of Dental & Craniofacial Research and the National Cancer Institute to advance basic, translational and clinical saliva research. The goal of the Salivaomics Knowledge Base (SKB) is to create a data management system and web resource constructed to support human salivaomics research. To maximize the utility of the SKB for retrieval,integration and analysis of data, we have developed the Saliva Ontology and SDxMart. This article reviews the informatics advances in saliva diagnostics made possible by the Saliva Ontology and SDxMart.
Biomarkers ; chemistry ; Computational Biology ; methods ; Databases, Protein ; Genomics ; methods ; Humans ; Metabolomics ; methods ; Proteomics ; methods ; Saliva ; chemistry ; Salivary Proteins and Peptides ; chemistry ; classification ; physiology

BACKGROUND: Carpal tunnel syndrome (CTS) is a common work-related peripheral neuropathy. In addition to grip force and repetitive hand exertions, wrist posture (hyperextension and hyperflexion) may be a risk factor for CTS among workers. However, findings of studies evaluating the relationship between wrist posture and CTS are inconsistent. The purpose of this paper was to conduct a meta-analysis of existing studies to evaluate the evidence of the relationship between wrist posture at work and risk of CTS. METHODS: PubMed and Google Scholar were searched to identify relevant studies published between 1980 and 2012. The following search terms were used: "work related", "carpal tunnel syndrome", "wrist posture", and "epidemiology". The studies defined wrist posture as the deviation of the wrist in extension or flexion from a neutral wrist posture. Relative risk (RR) of individual studies for postural risk was pooled to evaluate the overall risk of wrist posture on CTS. RESULTS: Nine studies met the inclusion criteria. All were cross-sectional or case-control designs and relied on self-report or observer's estimates for wrist posture assessment. The pooled RR of work-related CTS increased with increasing hours of exposure to wrist deviation or extension/flexion [RR = 2.01; 95% confidence interval (CI): 1.646-2.43; p < 0.01: Shore-adjusted 95% CI: 1.32-2.97]. CONCLUSION: We found evidence that prolonged exposure to non-neutral wrist postures is associated with a twofold increased risk for CTS compared with low hours of exposure to non-neutral wrist postures. Workplace interventions to prevent CTS should incorporate training and engineering interventions that reduce sustained non-neutral wrist postures.
Carpal Tunnel Syndrome* ; Case-Control Studies ; Hand ; Hand Strength ; Peripheral Nervous System Diseases ; Posture* ; Risk Factors ; Wrist*

Elevated body temperature can result from many agents in the natural environment, such as fever, hot weather and heavy exercise. In our modern living conditions additional sources of induced hyperthermia including hot baths, saunas, drugs, electromagnetic radiation and ultrasound have been introduced. Hyperthermia during pregnancy has been shown to cause a wide spectrun of effects in art species studied, including humans, the outcome depending on the dose of heat absorbed by the mother and embryo and the stage of enbryonic or fetal development when exposed. The dose of heat is the product of the elevation of temperature above normal and the duration of the elevation. In relatively uncontrolled natural environmental exposures, embryonic death and resorption or abortion are probably the most common outcome. In less severe exposures (smaller doses) major or minor developmental defects can result and the central nervous system appears to be a major target for its effects. Heat damage to embryos appears to be by apoptotic and other forms of cell death in organs at critical stages of development. Over many millennia all living orgaisms appear to have developed protective mechanisms against excess heat, known collectively as the heat shock response. This response has been studied intensively over the last 20 years and its mechanisms of protection are now becoming more clearly defined. Exposures to heat (and a number of other toxic agents) trigger the heat shock response which is characterized by abrupt suspension in the normal protein synthesis and the concurrent induction of heat shock genes (hsp) and the synthesis of a set of protein families known collectively as the heat shock proteins (HSP). The hsp ape known to be involved in the response in embryos, each has at least two copies, one which appears to have functions in the normal embryonic development (cognate) and another which is induced at a certain dose of heat (induced) and which can offer some protection against damage for some time after the initiating dose. Most cognate HSP can normally be found in embryos at all stages of development. At certain critical, early stages of organ formation increased activity of one or more of the hsp families can be identified at the site of the organ analogue. The inducible HSP are usually undetectable during normal development and generally become inducible at these critical inductive stages of organ development, implying a protective function for that process. Excess heat is known to cause denaturation of proteins. Each of the known HSP families appears to protect cells through their chaperone functions in which they bind to adhesive sites on newly synthesized or heat damaged and partially unfolded structural and functional proteins. This prevents the formation of function-less aggregates. The damaged proteins are then either presented for degradation or are reconstituted by orderly disengagement from the chaperone protein. The molecular mechanisms of initiating and regulating the response are now becoming more clearly defined. Trigger mechanisms include release of prostaglandin Al which can be modulated by glucocorticoids and nonsteroidal anti-inflammatory agents. A heat shock factor (HSF) binds to the heat shock element (hse) on the gene sequence and initiates the hsp response. The signal induction pathway involves mitogen activated proteins (MAP) and stress activated proteins (SAP) which are regulated by phosphorylation. Signals are amplified by kinase cascades while they are being transmitted to the nucleus. Activated MAP and SAP kinases regulate the process by phosphorylation of proteins including transcription factors, HSP, other protein kinases and phosphorylases, growth factor receptors and cytoskeletal proteins. Although this research has defined some pathways indicating how and why heat can cause some defects, a means of preventing them has not yet emerged.
Adhesives ; Anti-Inflammatory Agents, Non-Steroidal ; Apoptosis ; Baths ; Body Temperature ; Cell Cycle ; Cell Death ; Central Nervous System ; Cytoskeletal Proteins ; Electromagnetic Radiation ; Embryonic Development ; Embryonic Structures ; Environmental Exposure ; Female ; Fetal Development ; Fever ; Glucocorticoids ; Heat-Shock Proteins* ; Heat-Shock Response ; Hominidae ; Hot Temperature* ; Humans ; Hyperthermia, Induced ; Mothers ; Phosphorylases ; Phosphorylation ; Phosphotransferases ; Pregnancy ; Protein Kinases ; Receptors, Growth Factor ; Shock ; Social Conditions ; Steam Bath ; Transcription Factors ; Ultrasonography ; Weather

Purpose: Stenting is a useful treatment option for malignant colonic obstruction, but its role remains unclear. This study was designed to establish how stents have been used in Queensland, Australia, and to review outcomes. Methods: Patients diagnosed with colorectal cancer in Queensland from January 1, 2008, to December 31, 2014, who underwent colonic stent insertion were reviewed. Primary outcomes of 5-year survival, 30-day mortality, and overall length of survival were calculated. The secondary outcomes included patient and tumor factors, and stoma rates. Results: In total, 319 patients were included, and distant metastases were identified in 183 patients (57.4%). The 30-day mortality rate was 6.6% (n=21), and the 5-year survival was 11.9% (n=38). Median survival was 11 months (interquartile range, 4–27 months). A further operation (hazard ratio [HR], 0.19; P<0.001) and chemotherapy and/or radiotherapy (HR, 0.718; P=0.046) reduced the risk of 5-year mortality. The presence of distant metastases (HR, 2.052; P<0.001) and a comorbidity score of 3 or more (HR, 1.572; P=0.20) increased mortality. Surgery was associated with a reduced risk of mortality even in patients with metastatic disease (HR, 0.14; P<0.001). Twenty-two patients (6.9%) ended the study period with a stoma. Conclusion Colorectal stenting was used in Queensland in several diverse scenarios, in both localized and metastatic disease. Surgery had a survival advantage, even in patients with metastatic disease. There was no survival difference according to whether patients were socioeconomically disadvantaged, diagnosed in a major city or not, or treated at private or public hospitals. Stenting proved a valid treatment option with low stoma rates.

Antineoplastic Agents ; therapeutic use ; Antineoplastic Protocols ; standards ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; Guidelines as Topic ; Humans ; Lung Neoplasms ; drug therapy ; Neoplasm Staging ; Societies, Medical ; United States

Emerging evidence suggests that gap formation and opening of the endothelial junctions during leukocyte extravasation is actively controlled to maintain the integrity of the vascular barrier. While the role for endothelial cells to this process has been well defined, it is not clear whether leukocytes are also actively contributing to endothelial barrier function. We have recently showed that extravasating leukocytes deposit microparticles on the subendothelium during the late stages of extravasation, which is LFA-1 dependent. Using multiphotonintravital microscopy (MP-IVM) of mouse cremaster muscle vessels in the current work, we show that microparticle formation and deposition maintains the integrity of the microvascular barrier during leukocyte extravasation. Inhibition of neutrophil-derived microparticle formation resulted in dramatically increased vascular leakage. These findings suggest that deposition of microparticles during neutrophil extravasation is essential for maintaining endothelial barrier function and may result in temporal difference between neutrophil extravasation and an increase in vascular leakage.
Animals ; Endothelial Cells ; Leukocytes ; Lymphocyte Function-Associated Antigen-1 ; Mice ; Microscopy ; Monocytes ; Muscles ; Neutrophils

Hepatocytes are the primary targets of the hepatitis C virus (HCV). While immunosuppressive roles of HCV core protein have been found in several studies, it remains uncertain whether core protein expressed in hepatocytes rather than in immune cells affects the CD8+ T cell response. In order to transduce genes selectively into hepatocytes, we developed a baculoviral vector system that enabled primary hepatocytes to express a target epitope for CD8+ T cells, derived from ovalbumin (OVA), with or without HCV core protein. Culture of OVA-specific CD8+ T cells with hepatocytes infected with these baculoviral vectors revealed that core protein has no effect on proliferation or apoptosis of CD8+ T cells. Our results suggest that HCV core protein does not exert its suppressive role on the CD8+ T cell immune response through expression in hepatocytes.
Viral Core Proteins/*metabolism ; Ovalbumin/genetics/immunology ; Mice ; Hepatocytes/cytology/*virology ; Green Fluorescent Proteins/genetics ; Genetic Vectors ; Cell Proliferation ; CD8-Positive T-Lymphocytes/*immunology ; Baculoviridae/genetics ; Apoptosis ; Animals

OBJECTIVE: To determine the hepatoprotective effect of silymarin with Chang cell cultures. Specifically, to investigate the antioxidant properties of silymarin and its protective function in reducing pro-apoptotic markers. METHODS: Intracellular free radical levels were assessed with dichlorofluorescein (DCF) fluorescence after exposing cells to an oxidative stress of 400 μmol/L H2O2 for 20 min. Levels of cellular ATP and bax expression were examined to evaluate the protective effects of silymarin. RESULTS: Silymarin significantly reduced the DCF fluorescence signal. Cell viability, assessed by the MTT assay, showed that silymarin enhanced the cell growth. Drug treatment was also associated with enhanced ATP levels, and reduced Bax and protein mRNA levels. CONCLUSION Silymarin can function as a hepatoprotectant against free radical damage due to oxidative stress. The protective nature extends to reducing levels of pro-apoptotic Bax protein. Silymarin may be a useful adjuvant for the treatment of specific liver diseases.
Adenosine Triphosphate ; metabolism ; Antioxidants ; pharmacology ; Apoptosis ; drug effects ; Cell Line ; Fluoresceins ; Free Radicals ; metabolism ; Hepatocytes ; cytology ; metabolism ; Humans ; Hydrogen Peroxide ; Protective Agents ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Silymarin ; pharmacology ; bcl-2-Associated X Protein ; genetics ; metabolism