Severe Life Threatening Maxillofacial Infection in Pregnancy Presented as Ludwig's Angina

Background. Ludwig's angina is a rapidly spreading cellulitis that may produce upper airway obstruction often leading to death. There is very little published information regarding this condition in the pregnant patient. Case. A 24-year old black female was admitted at 26 weeks gestation with tooth pain, submandibular swelling, severe trismus, and dysphagea, consistent with Ludwig's angina. Her treatment included emergent tracheostomy, incision and drainage of associated spaces, teeth extraction, and antibiotic therapy. Conclusions. During a life threatening infectious situation such as the one described, risks of maternal and fetal morbidity include both septicemia and asphyxia. Furthermore, the healthcare provider must consider the risks that the condition and the possible treatments may cause the mother and her unborn child

Smoking, environmental tobacco smoke, and risk of renal cell cancer: a population-based case-control study

<p>Abstract</p> <p>Background</p> <p>Kidney and renal pelvis cancers account for 4% of all new cancer cases in the United States, among which 85% are renal cell carcinomas (RCC). While cigarette smoking is an established risk factor for RCC, little is known about the contribution of environmental tobacco smoke (ETS) to RCC incidence. This study assesses the role of smoking and ETS on RCC incidence using a population-based case-control design in Florida and Georgia.</p> <p>Methods</p> <p>Incident cases (n = 335) were identified from hospital records and the Florida cancer registry, and population controls (n = 337) frequency-matched by age (+/- 5 years), gender, and race were identified through random-digit dialing. In-person interviews assessed smoking history and lifetime exposure to ETS at home, work, and public spaces. Home ETS was measured in both years and hours of exposure. Odds ratios and 95% confidence intervals were calculated using logistic regression, controlled for age, gender, race, and BMI.</p> <p>Results</p> <p>Cases were more likely to have smoked 20 or more pack-years, compared with never-smokers (OR: 1.35, 95% CI: 0.93 – 1.95). A protective effect was found for smoking cessation, beginning with 11–20 years of cessation (OR: 0.39, 95% CI: 0.18–0.85) and ending with 51 or more years of cessation (OR: 0.11, 95% CI: 0.03–0.39) in comparison with those having quit for 1–10 years. Among never-smokers, cases were more likely to report home ETS exposure of greater than 20 years, compared with those never exposed to home ETS (OR: 2.18; 95% CI: 1.14–4.18). Home ETS associations were comparable when measured in lifetime hours of exposure, with cases more likely to report 30,000 or more hours of home ETS exposure (OR: 2.37; 95% CI: 1.20–4.69). Highest quartiles of combined home/work ETS exposure among never-smokers, especially with public ETS exposure, increased RCC risk by 2 to 4 times.</p> <p>Conclusion</p> <p>These findings confirm known associations between smoking and RCC and establish a potential etiologic role for ETS, particularly in the home. Differences in methods of retrospective measurement of lifetime smoking and ETS exposure may contribute to discrepancies in measures of associations across studies, and should be addressed in future research.</p

The outcome of arthroscopic treatment of temporomandibular joint arthoropathy

The document attached has been archived with permission from the Australian Dental Association. An external link to the publisher’s copy is included.Ninety patients underwent arthroscopic temporomandibular joint surgery to 124 joints for arthropathy which had failed to respond to at least six months of non-surgical treatment. They were surveyed at between 6 months and 5 years (mean 2.5 years) after surgery and 63 per cent responded to the survey. They reported an 82 per cent improvement for pain (50 to 100 per cent better), 80 per cent for clicking and 82 per cent for locking. There was no morbidity following the treatment. Arthroscopic surgery sould be considered for advanced temporomandibular joint arthropathy which is refractory to non-surgical treatment.I. Rosenburg and A. N. Gos

Impacts of global, regional, and sectoral black carbon emission reductions on surface air quality and human mortality

As a component of fine particulate matter (PM 2.5), black carbon (BC) is associated with premature human mor-tality. BC also affects climate by absorbing solar radiation and reducing planetary albedo. Several studies have exam-ined the climate impacts of BC emissions, but the associated health impacts have been studied less extensively. Here, we examine the surface PM 2.5 and premature mortality impacts of halving anthropogenic BC emissions globally and individ-ually from eight world regions and three major economic sec-tors. We use a global chemical transport model, MOZART-4, to simulate PM 2.5 concentrations and a health impact func-tion to calculate premature cardiopulmonary and lung can-cer deaths. We estimate that halving global anthropogenic BC emissions reduces outdoor population-weighted average PM 2.5 by 542 ng m −3 (1.8 %) and avoids 157 000 (95 % con-fidence interval, 120 000–194 000) annual premature deaths globally, with the vast majority occurring within the source region. Most of these avoided deaths can be achieved by halving emissions in East Asia (China; 54 %), followed by South Asia (India; 31 %), however South Asian emissions have 50 % greater mortality impacts per unit BC emitted than East Asian emissions. Globally, halving residential, indus-trial, and transportation emissions contributes 47 %, 35 %, and 15 % to the avoided deaths from halving all anthro-pogenic BC emissions. These contributions are 1.2, 1.2, and 0.6 times each sector's portion of global BC emissions, ow-ing to the degree of co-location with population globally. We find that reducing BC emissions increases regional SO 4 con-centrations by up to 28 % of the magnitude of the regional BC concentration reductions, due to reduced absorption of radiation that drives photochemistry. Impacts of residential BC emissions are likely underestimated since indoor PM 2.5 Correspondence to: J. J. West ([email protected]) exposure is excluded. We estimate ∼8 times more avoided deaths when BC and organic carbon (OC) emissions are halved together, suggesting that these results greatly under-estimate the full air pollution-related mortality benefits of BC mitigation strategies which generally decrease both BC and OC. The choice of concentration-response factor and health effect thresholds affects estimated global avoided deaths by as much as 56 % but does not strongly affect the regional distribution. Confidence in our results would be strength-ened by reducing uncertainties in emissions, model param-eterization of aerosol processes, grid resolution, and PM 2.5 concentration-mortality relationships globally

Dioxin-Induced Changes in Epididymal Sperm Count and Spermatogenesis

A single in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gestation day 15 decreased epididymal sperm count in adult rats and thus was used to establish a tolerable daily intake for TCDD. However, several laboratories have been unable to replicate these findings. Moreover, conflicting reports of TCDD effects on daily sperm production suggest that spermatogenesis may not be as sensitive to the adverse effects of TCDD as previously thought. We performed a PubMed search using relevant search terms linking dioxin exposure with adverse effects on reproduction and spermatogenesis. Developmental exposure to TCDD is consistently linked with decreased cauda epididymal sperm counts in animal studies, although at higher dose levels than those used in some earlier studies. However, the evidence linking in utero TCDD exposure and spermatogenesis is not convincing. Animal studies provide clear evidence of an adverse effect of in utero TCDD exposure on epididymal sperm count but do not support the conclusion that spermatogenesis is adversely affected. The mechanisms underlying decreased epididymal sperm count are unknown; however, we postulate that epididymal function is the key target for the adverse effects of TCDD.Uma única exposição in utero a 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) no 15º dia de gestação diminuiu a contagem de esperma epididimal em ratos adultos e por isso foi utilizada para estabelecer uma dosagem diária tolerável para TCDD. No entanto, diversos laboratórios não conseguiram reproduzir esses resultados. Além disso, relatórios conflitantes dos efeitos de TCDD na produção diária de esperma sugere que espermatogênese pode não ser tão sensível aos efeitos adversos do TCDD como antes se pensava. Foi feita uma pesquisa no PubMed usando termos de pesquisa relevantes, relacionados à exposição à dioxina com efeitos adversos na reprodução e na espermatogênese. Exposição em desenvolvimento ao TCDD é consistentemente relacionada à diminuição da contagem da cauda epididimal de esperma, mas não apoia a conclusão de que a espermatogênese é afetada. Os mecanismos por trás da diminuição da contagem de esperma epididimal são desconhecidos; no entanto, contestamos que a função epididimal é a chave para efeitos adversos do TCDD

The potential effects of climate change on air quality across the conterminous US at 2030 under three Representative Concentration Pathways

The potential impacts of climate change on regional ozone (O3) and fine particulate (PM2.5) air quality in the United States (US) are investigated by linking global climate simulations with regional-scale meteorological and chemical transport models. Regional climate at 2000 and at 2030 under three Representative Concentration Pathways (RCPs) is simulated by using the Weather Research and Forecasting (WRF) model to downscale 11-year time slices from the Community Earth System Model (CESM). The downscaled meteorology is then used with the Community Multiscale Air Quality (CMAQ) model to simulate air quality during each of these 11-year periods. The analysis isolates the future air quality differences arising from climate-driven changes in meteorological parameters and specific natural emissions sources that are strongly influenced by meteorology. Other factors that will affect future air quality, such as anthropogenic air pollutant emissions and chemical boundary conditions, are unchanged across the simulations. The regional climate fields represent historical daily maximum and daily minimum temperatures well, with mean biases of less than 2&thinsp;K for most regions of the US and most seasons of the year and good representation of variability. Precipitation in the central and eastern US is well simulated for the historical period, with seasonal and annual biases generally less than 25&thinsp;%, with positive biases exceeding 25&thinsp;% in the western US throughout the year and in part of the eastern US during summer. Maximum daily 8&thinsp;h ozone (MDA8 O3) is projected to increase during summer and autumn in the central and eastern US. The increase in summer mean MDA8 O3 is largest under RCP8.5, exceeding 4&thinsp;ppb in some locations, with smaller seasonal mean increases of up to 2&thinsp;ppb simulated during autumn and changes during spring generally less than 1&thinsp;ppb. Increases are magnified at the upper end of the O3 distribution, particularly where projected increases in temperature are greater. Annual average PM2.5 concentration changes range from −1.0 to 1.0&thinsp;µg&thinsp;m−3. Organic PM2.5 concentrations increase during summer and autumn due to increased biogenic emissions. Aerosol nitrate decreases during winter, accompanied by lesser decreases in ammonium and sulfate, due to warmer temperatures causing increased partitioning to the gas phase. Among meteorological factors examined to account for modeled changes in pollution, temperature and isoprene emissions are found to have the largest changes and the greatest impact on O3 concentrations.</p

Interaction Networks in Yeast Define and Enumerate the Signaling Steps of the Vertebrate Aryl Hydrocarbon Receptor

The aryl hydrocarbon receptor (AHR) is a vertebrate protein that mediates the toxic and adaptive responses to dioxins and related environmental pollutants. In an effort to better understand the details of this signal transduction pathway, we employed the yeast S. cerevisiae as a model system. Through the use of arrayed yeast strains harboring ordered deletions of open reading frames, we determined that 54 out of the 4,507 yeast genes examined significantly influence AHR signal transduction. In an effort to describe the relationship between these modifying genes, we constructed a network map based upon their known protein and genetic interactions. Monte Carlo simulations demonstrated that this network represented a description of AHR signaling that was distinct from those generated by random chance. The network map was then explored with a number of computational and experimental annotations. These analyses revealed that the AHR signaling pathway is defined by at least five distinct signaling steps that are regulated by functional modules of interacting modifiers. These modules can be described as mediating receptor folding, nuclear translocation, transcriptional activation, receptor level, and a previously undescribed nuclear step related to the receptor's Per–Arnt–Sim domain

The role of endogenous aryl hydrocarbon receptor signaling in cardiovascular physiology

The aryl hydrocarbon receptor (AHR) is an orphan nuclear receptor with a primary function of mediating xenobiotic metabolism through transcriptional activation of Phase I and Phase II drug-metabolizing enzymes. Although no high-affinity physiological activators of AHR have been discovered, the endogenous signaling of the AHR pathway is believed to play an important role in the development and function of the cardiovascular system, based on the observations on ahr gene-deficient mice. The AHR knockout mice develop cardiac hypertrophy, abnormal vascular structure in multiple organs and altered blood pressure depending on their host environment. In this review, the endogenous role of AHR in cardiovascular physiology, including heart function, vascular development and blood pressure regulation has been summarized and discussed

Transcriptional profiling of rat hypothalamus response to 2,3,7,8-tetrachlorodibenzo-p-dioxin

In some mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as significant weight loss associated with lethal outcomes. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR). Since TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, it was hypothesized that wasting syndrome is a result of to TCDD-induced dysregulation of genes involved in regulation of food-intake. As the hypothalamus is the central nervous systems' regulatory center for food-intake and energy balance. Therefore, mRNA abundances in hypothalamic tissue from two rat strains with widely differing sensitivities to TCDD-induced wasting syndrome: TCDD-sensitive Long-Evans rats and TCDD-resistant Han/Wistar rats, 23 h after exposure to TCDD (100 mu g/kg) or corn oil vehicle. TCDD exposure caused minimal transcriptional dysregulation in the hypothalamus, with only 6 genes significantly altered in Long-Evans rats and 15 genes in Han/Wistar rats. Two of the most dysregulated genes were Cyp1a1 and Nqo1, which are induced by TCDD across a wide range of tissues and are considered sensitive markers of TCDD exposure. The minimal response of the hypothalamic transcriptome to a lethal dose of TCDD at an early time-point suggests that the hypothalamus is not the predominant site of initial events leading to hypophagia and associated wasting. TCDD may affect feeding behaviour via events upstream or downstream of the hypothalamus, and further work is required to evaluate this at the level of individual hypothalamic nuclei and subregions. (C) 2014 The Authors. Published by Elsevier Ireland Ltd.Peer reviewe

The methodological quality of systematic reviews comparing temporomandibular joint disorder surgical and non-surgical treatment

<p>Abstract</p> <p>Background</p> <p>Temporomandibular joint disorders (TMJD) are multifactor, complex clinical problems affecting approximately 60–70% of the general population, with considerable controversy about the most effective treatment. For example, reports claim success rates of 70% and 83% for non-surgical and surgical treatment, whereas other reports claim success rates of 40% to 70% for self-improvement without treatment. Therefore, the purpose of this study was to (1) identify systematic reviews comparing temporomandibular joint disorder surgical and non-surgical treatment, (2) evaluate their methodological quality, and (3) evaluate the evidence grade within the systematic reviews.</p> <p>Methods</p> <p>A search strategy was developed and implemented for MEDLINE, Cochrane Library, LILACS, and Brazilian Dentistry Bibliography databases. Inclusion criteria were: systematic reviews (± meta-analysis) comparing surgical and non-surgical TMJD treatment, published in English, Spanish, Portuguese, Italian, or German between the years 1966 and 2007(up to July). Exclusion criteria were: <it>in vitro </it>or animal studies; narrative reviews or editorials or editorial letters; and articles published in other languages. Two investigators independently selected and evaluated systematic reviews. Three different instruments (AMSTAR, OQAQ and CASP) were used to evaluate methodological quality, and the results averaged. The GRADE instrument was used to evaluate the evidence grade within the reviews.</p> <p>Results</p> <p>The search strategy identified 211 reports; of which 2 were systematic reviews meeting inclusion criteria. The first review met 23.5 ± 6.0% and the second met 77.5 ± 12.8% of the methodological quality criteria (mean ± sd). In these systematic reviews between 9 and 15% of the trials were graded as high quality, and 2 and 8% of the total number of patients were involved in these studies.</p> <p>Conclusion</p> <p>The results indicate that in spite of the widespread impact of TMJD, and the multitude of potential interventions, clinicians have expended sparse attention to systematically implementing clinical trial methodology that would improve validity and reliability of outcome measures. With some 20 years of knowledge of evidence-based healthcare, the meager attention to these issues begins to raise ethical issues about TMJD trial conduct and clinical care.</p