The frequency of herbal medications and supplements in a series of medical examiner scene investigations

Complementary and alternative medicine use has been increasing worldwide. Although many studies have attempted to elucidate the levels of herbal medicine use in certain communities, many factors have led to limitations on the data collected. Self-report surveys are currently the only studies that have been done to quantify the actual use of herbal medications to date. This project uses a more comprehensive and objective means of examining the use of herbal medications in the state of New Mexico. Data from deaths investigated by the New Mexico Office of the Medical Investigator were examined to determine a more accurate picture of herbal use in New Mexico. Examining 1,112 deaths investigated during the first six months of 2006, we found that 5% of deaths had herbal medications or supplements present within the residence, with 4.6% having 3 or more supplements. Decedents with three or more prescription/OTC drugs found at the death scene were 3.03 times more likely to have three or more supplements as well, compared to those with two or fewer prescription/OTC drugs found on scene. The most commonly identified health complaints of patients in this study were hypertension, cardiac conditions and diabetes. Although the study was possibly limited by variations in the collection of data at scene investigations, the potential adverse interactions of herbal supplements with other medications warrants additional investigation

Shiga Toxin–producing Escherichia coli, New Mexico, USA, 2004–2007

Sporadic infection with Shiga toxin–producing Escherichia coli (STEC) in New Mexico increased from 0.9 cases per 100,000 population (95% confidence interval [CI] 0.5–1.36) in 2004 to 1.7 (95% CI 1.14–2.26) in 2007. Non-O157 STEC was more common in nonwhite residents, children <5 years of age, and urban residents

The Sad State of Healthcare in New Mexico: Healthcare Worker Suicide in New Mexico 2004-2005

THE SAD STATE OF HEALTH CARE IN NEW MEXICO: HEATHCARE WORKER SUICIDE IN NEW MEXICO 2004-2005. KL Bradley*, KD Martinez*, MB Barry**, S Lathrop**, K Fraser***, and K Peters**** * University of New Mexico School of Medicine, Albuquerque, NM, ** New Mexico Office of the Medical Investigator, Albuquerque, NM, *** University of New Mexico School of Medicine, Department of Psychiatry, Albuquerque, NM, **** New Mexico Bureau of Vital Records and Health Statistics, Santa Fe, NM PURPOSE. To determine if there is a statistically significant relationship between suicide and the healthcare occupations in New Mexico for the years 2004-2005. METHODS. We collected suicide and occupational data from the New Mexico Office of the Medical Investigator and the N.M. Bureau of Vital Records and Health Statistics for the years 2004-2005. Other data collected included race, age, veteran status, county of occurrence and residence, location, method, presence of suicide note, toxicology, and psychiatric, medical and other risk factors. Statistical analysis was performed on the data collected. RESULTS. Our database included 658 suicides, including 34 healthcare worker suicides during this two-year period. The suicide rate for healthcare workers (HCWs) in 2004 was higher than the suicide rate of the New Mexico adult population. The suicide rate for HCWs in 2005 was lower than that of the New Mexico adult population. There were significantly more women among the healthcare workers who committed suicide than among the non-healthcare workers. The most commonly represented healthcare professionals among the HCWs who committed suicide were: Nurses, Home Health Aides, Obstetrician/Gynecologists, Laboratory Technicians, Social Workers, and Medical Assistants. Healthcare workers who committed suicide in New Mexico in 2004 and 2005 were 3.7 times more likely to commit suicide by ingesting or injecting medication than the non-healthcare workers who committed suicide during this time frame. CONCLUSION. This study demonstrates that healthcare workers, particularly females, had a higher rate of suicide that the NM adult population in 2004, but not it 2005. Thus, we cannot comment on a trend at this time. Further investigation would be useful in determining the presence of a trend and guiding prevention efforts

Lymphotoxin-α Gene and Risk of Myocardial Infarction in 6,928 Cases and 2,712 Controls in the ISIS Case-Control Study

Lymphotoxin-α (LTA) is a pro-inflammatory cytokine that plays an important role in the immune system and local inflammatory response. LTA is expressed in atherosclerotic plaques and has been implicated in the pathogenesis of atherosclerosis and coronary heart disease (CHD). Polymorphisms in the gene encoding lymphotoxin-α (LTA) on Chromosome 6p21 have been associated with susceptibility to CHD, but results in different studies appear to be conflicting. We examined the association of seven single nucleotide polymorphisms (SNPs) across the LTA gene, and their related haplotypes, with risk of myocardial infarction (MI) in the International Study of Infarct Survival (ISIS) case-control study involving 6,928 non-fatal MI cases and 2,712 unrelated controls. The seven SNPs (including the rs909253 and rs1041981 SNPs previously implicated in the risk of CHD) were in strong linkage disequilibrium with each other and contributed to six common haplotypes. Some of the haplotypes for LTA were associated with higher plasma concentrations of C-reactive protein (p = 0.004) and lower concentrations of albumin (p = 0.023). However, none of the SNPs or related haplotypes were significantly associated with risk of MI. The results of the ISIS study were considered in the context of six previously published studies that had assessed this association, and this meta-analysis found no significant association with CHD risk using a recessive model and only a modest association using a dominant model (with narrow confidence intervals around these risk estimates). Overall, these studies provide reliable evidence that these common polymorphisms for the LTA gene are not strongly associated with susceptibility to coronary disease

A comparison of vaginal versus buccal misoprostol for cervical ripening in women for labor induction at term (the IMPROVE trial): a triple-masked randomized controlled trial

Background Cervical ripening is commonly needed for labor induction. Finding an optimal route of misoprostol dosing for efficacy, safety, and patient satisfaction is important and not well studied for the buccal route. Objective To compare the efficacy and safety of vaginal and buccal misoprostol for women undergoing labor induction at term. Study Design The IMPROVE trial was an institutional review board–approved, triple-masked, placebo-controlled randomized noninferiority trial for women undergoing labor induction at term with a Bishop score ≤6. Enrolled women received 25 mcg (first dose), then 50 mcg (subsequent doses) of misoprostol by assigned route (vaginal or buccal) and a matching placebo tablet by the opposite route. The primary outcomes were time to delivery and the rate of cesarean delivery performed urgently for fetal nonreassurance. A sample size of 300 was planned to test the noninferiority hypothesis. Results The trial enrolled 319 women, with 300 available for analysis, 152 in the vaginal misoprostol group and 148 in the buccal. Groups had similar baseline characteristics. We were unable to demonstrate noninferiority. The time to vaginal delivery was lower for the vaginal misoprostol group (median [95% confidence interval] in hours: vaginal: 20.1 [18.2, 22.8] vs buccal: 28.1 [24.1, 31.4], log-rank test P = .006, Pnoninferiority = .663). The rate of cesarean deliveries for nonreassuring fetal status was 3.3% for the vaginal misoprostol group and 9.5% for the buccal misoprostol group (P = .033). The rate of vaginal delivery in <24 hours was higher in the vaginal group (58.6% vs 39.2%, P = .001). Conclusion We were unable to demonstrate noninferiority. In leading to a higher rate of vaginal deliveries, more rapid vaginal delivery, and fewer cesareans for fetal issues, vaginal misoprostol may be superior to buccal misoprostol for cervical ripening at term

Associations of vitamin D pathway genes with circulating 25-hydroxyvitamin-D, 1,25-dihydroxyvitamin-D, and prostate cancer:a nested case-control study

Vitamin D pathway single nucleotide polymorphisms (SNPs) are potentially useful proxies for investigating whether circulating vitamin D metabolites [total 25-hydroxyvitamin-D, 25(OH)D; 1,25-dihydroxyvitamin, 1,25(OH)2D] are causally related to prostate cancer. We investigated associations of sixteen SNPs across seven genes with prostate-specific antigen-detected prostate cancer

Novel Crohn Disease Locus Identified by Genome-Wide Association Maps to a Gene Desert on 5p13.1 and Modulates Expression of PTGER4

To identify novel susceptibility loci for Crohn disease (CD), we undertook a genome-wide association study with more than 300,000 SNPs characterized in 547 patients and 928 controls. We found three chromosome regions that provided evidence of disease association with p-values between 10(−6) and 10(−9). Two of these (IL23R on Chromosome 1 and CARD15 on Chromosome 16) correspond to genes previously reported to be associated with CD. In addition, a 250-kb region of Chromosome 5p13.1 was found to contain multiple markers with strongly suggestive evidence of disease association (including four markers with p < 10(−7)). We replicated the results for 5p13.1 by studying 1,266 additional CD patients, 559 additional controls, and 428 trios. Significant evidence of association (p < 4 × 10(−4)) was found in case/control comparisons with the replication data, while associated alleles were over-transmitted to affected offspring (p < 0.05), thus confirming that the 5p13.1 locus contributes to CD susceptibility. The CD-associated 250-kb region was saturated with 111 SNP markers. Haplotype analysis supports a complex locus architecture with multiple variants contributing to disease susceptibility. The novel 5p13.1 CD locus is contained within a 1.25-Mb gene desert. We present evidence that disease-associated alleles correlate with quantitative expression levels of the prostaglandin receptor EP4, PTGER4, the gene that resides closest to the associated region. Our results identify a major new susceptibility locus for CD, and suggest that genetic variants associated with disease risk at this locus could modulate cis-acting regulatory elements of PTGER4

Texas Lifestyle Limits Transmission of Dengue Virus

Urban dengue is common in most countries of the Americas, but has been rare in the United States for more than half a century. In 1999 we investigated an outbreak of the disease that affected Nuevo Laredo, Tamaulipas, Mexico, and Laredo, Texas, United States, contiguous cities that straddle the international border. The incidence of recent cases, indicated by immunoglobulin M antibody serosurvey, was higher in Nuevo Laredo, although the vector, Aedes aegypti, was more abundant in Laredo. Environmental factors that affect contact with mosquitoes, such as air-conditioning and human behavior, appear to account for this paradox. We conclude that the low prevalence of dengue in the United States is primarily due to economic, rather than climatic, factors

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis