Air quality–related health damages of food

Agriculture is a major contributor to air pollution, the largest environmental risk factor for mortality in the United States and worldwide. It is largely unknown, however, how individual foods or entire diets affect human health via poor air quality. We show how food production negatively impacts human health by increasing atmospheric fine particulate matter (PM_2.5), and we identify ways to reduce these negative impacts of agriculture. We quantify the air quality–related health damages attributable to 95 agricultural commodities and 67 final food products, which encompass >99% of agricultural production in the United States. Agricultural production in the United States results in 17,900 annual air quality–related deaths, 15,900 of which are from food production. Of those, 80% are attributable to animal-based foods, both directly from animal production and indirectly from growing animal feed. On-farm interventions can reduce PM_2.5-related mortality by 50%, including improved livestock waste management and fertilizer application practices that reduce emissions of ammonia, a secondary PM_2.5 precursor, and improved crop and animal production practices that reduce primary PM_2.5 emissions from tillage, field burning, livestock dust, and machinery. Dietary shifts toward more plant-based foods that maintain protein intake and other nutritional needs could reduce agricultural air quality–related mortality by 68 to 83%. In sum, improved livestock and fertilization practices, and dietary shifts could greatly decrease the health impacts of agriculture caused by its contribution to reduced air quality.

The health and environmental consequences of feeding the increasingly large and affluent global population are becoming increasingly apparent. These consequences have spurred interest in identifying food production practices and diets that improve human health and reduce environmental harm. Recent work has demonstrated that many of the opportunities for food producers and consumers to improve nutritional outcomes also have environmental benefits, such as reducing greenhouse gas emissions, land and water use, and eutrophication (1–6). It is largely unknown, however, how individual foods and diets affect air quality, even though air pollution is the largest environmental mortality risk factor in the United States and globally (7, 8), and agriculture is itself known to be a major contributor to reduced air quality (8, 9). In the United States alone, atmospheric fine particulate matter (PM_2.5) from anthropogenic sources is responsible for about 100,000 premature deaths each year, one-fifth of which are linked to agriculture (10, 11).Here, we show how different foods affect human health by reducing air quality. We consider the emission of pollutants that contribute to atmospheric PM_2.5, the chronic exposure to which increases the incidence of premature mortality from cardiovascular disease, cancer, and stroke (12, 13). These pollutants include directly emitted PM_2.5 (primary PM_2.5) and PM_2.5 formed in the atmosphere (secondary PM_2.5) from the precursors ammonia (NH₃), nitrogen oxides (NO_x), sulfur dioxide (SO₂), and nonmethane volatile organic compounds (NMVOCs). From a spatially explicit inventory of emissions of primary PM_2.5 and secondary PM_2.5 precursors from agricultural supply chain activities for commodities in the contiguous United States (SI Appendix, Figs. S1 and S2) (14, 15) (Materials and Methods), we estimate increases in atmospheric concentrations of total (primary + secondary) PM_2.5 attributable to agricultural emissions; total PM_2.5 transport, chemistry, and removal; and exposure of populations to total PM_2.5 using an ensemble of three independent air quality models (16–19). We describe damages attributable to 95 agricultural commodities and 67 final food products (full list in SI Appendix, Table S1), which cover >99% of US agricultural production (20).     

Effect of alcohol on viral hepatitis and other forms of liver dysfunction

Alcohol is a known hepatotoxic agent, which may exacerbate liver injury caused by other agents. The wide prevalence of alcohol use and abuse in society makes it an important cofactor in many other liver diseases. Examples of liver diseases that are significantly influenced by ingestion of alcohol include chronic viral hepatitis, disorders of iron overload, and obesity-related liver disease.     

Treatment of gastrointestinal bleeding in left ventricular assist devices: A comprehensive review

Left ventricular assist devices(LVAD) are increasingly become common as life prolonging therapy in patients with advanced heart failure. Current devices are now used as definitive treatment in some patients given the improved durability of continuous flow pumps. Unfortunately, continuous flow LVADs are fraught with complications such as gastrointestinal(GI) bleeding that are primarily attributed to the formation of arteriovenous malformations. With frequent GI bleeding, antiplatelet and anticoagulation therapies are usually discontinued increasing the risk of life-threatening events. Small bowel bleeds account for 15%as the source and patients often undergo multiple endoscopic procedures.Treatment strategies include resuscitative measures and endoscopic therapies.Medical treatment is with octreotide. Novel treatment options include thalidomide, angiotensin converting enzyme inhibitors/angiotensin Ⅱ receptor blockers, estrogen-based hormonal therapies, doxycycline, desmopressin and bevacizumab. Current research has explored the mechanism of frequent GI bleeds in this population, including destruction of von Willebrand factor,upregulation of tissue factor, vascular endothelial growth factor, tumor necrosis factor-α, tumor growth factor-β, and angiopoetin-2, and downregulation of angiopoetin-1. In addition, healthcare resource utilization is only increasing in this patient population with higher admissions, readmissions, blood product utilization, and endoscopy. While some of the novel endoscopic and medical therapies for LVAD bleeds are still in their development stages, these tools will yet be crucial as the number of LVAD placements will likely only increase in the coming years.     

We Built This House; It’s Time to Move in: Leveraging Existing DICOM Structure to More Completely Utilize Readily Available Detailed Contrast Administration Information

The Digital Imaging and Communications in Medicine (DICOM) standard is the universal format for interoperability in medical imaging. In addition to imaging data, DICOM has evolved to support a wide range of imaging metadata including contrast administration data that is readily available from many modern contrast injectors. Contrast agent, route of administration, start and stop time, volume, flow rate, and duration can be recorded using DICOM attributes [1]. While this information is sparsely and inconsistently recorded in routine clinical practice, it could potentially be of significant diagnostic value. This work will describe parameters recorded by automatic contrast injectors, summarize the DICOM mechanisms available for tracking contrast injection data, and discuss the role of such data in clinical radiology.     

Study of human papillomavirus infection in patients with anal squamous carcinoma

PURPOSE: The purpose of this study was to determine the incidence of human papillomavirus deoxyribonucleic acid (HPV DNA) in anal squamous carcinoma. METHODS: HPV DNA in situ hybridization for HPV Types 6, 11, 16, 18, 31, 33, and 35 was performed on the formalin-fixed, paraffinembedded tissue from 53 perianal and anal squamous carcinomas and 10 controls. RESULTS: HPV DNA sequences were identified in 18 of 53 anal squamous carcinomas (34 percent). All 10 controls were negative for HPV DNA. Of the 18 positive patients, 10 were perianal squamous carcinomas, and 8 were anal canal squamous carcinomas. Six of the perianal carcinomas were positive for HPV Types 6 and 11. The remaining four perianal carcinomas and all eight of the anal canal carcinomas were positive for HPV Types 16 and 18. CONCLUSION: HPV DNA sequences can be identified in anal squamous carcinomas. Anal squamous epithelium is another site where HPV infection may carry a risk for malignant transformation. One-third of anal squamous carcinomas may be associated with prior HPV infection. Patients with anogenital HPV infection should be routinely screened for anal squamous lesions.     

Thalidomide teratogenesis: evidence for a toxic arene oxide metabolite.

It was postulated that thalidomide causes birth defects by being metabolized to a toxic electrophilic intermediate. This hypothesis was tested by using an in vitro assay in which drug toxicity to human lymphocytes was assessed in the presence of a hepatic microsomal drug metabolizing system. Maternal hepatic microsomes from pregnant rabbits mediated the production of a metabolite that was toxic to lymphocytes. Toxicity was enhanced by inhibitors of epoxide hydrolase (EC 3.3.2.3) and abolished by adding the purified enzyme to the incubation medium. The metabolite thus appears to be in arene oxide, consistent with the previously reported isolation of phenolic metabolites of thalidomide from the urine of treated animals. Two teratogenic analogs of thalidomide (phthalimidophthalimide and phthalimidinoglutarimide) were also toxic in the system; two nonteratogenic analogs (phthalimide and hexahydrothalidomide) were not toxic, even in the presence of epoxide hydrolase inhibitors. The toxic metabolite of thalidomide was not produced by rat liver microsomes (the rat is not sensitive to thalidomide teratogenesis) but was produced by hepatic preparations from maternal rabbits, and rabbit, monkey, and human (all sensitive species) fetuses. A toxic arene oxide therefore may be involved in the teratogenicity of thalidomide.     

Drug resistant Haemophilus influenzae from respiratory tract infection in a tertiary care hospital in north India

Haemophilus influenzae is an important respiratory pathogen. Emergence of resistance to various antibiotics is a major problem in patient management. A total of 90 strains of H. influenzae were characterized from specimens obtained from patients of acute respiratory tract infection; 13 (14.4%) belonged to type beta. On biotyping, 90% strains belonged to biotype II. The frequency of resistance to various antibiotics was as follows: cotrimoxazole 33.3% ampicillin 21.1%, cephalexin 7.8%, chloramphenicol 7.8%, ciprofloxacin 2.5% erythromycin and tetracycline 5% each. All the ampicillin-resistant strains produced beta-lactamase as detected by nitrocefin disc method. None of the strains exhibited resistance to cefaclor and third generation cephalosporins. The present study showed emergence of variable resistance to ampicillin, cotrimoxazole and other antibiotics. It is important for the clinical microbiology laboratory to monitor drug resistant strains for instituting appropriate antibiotic therapy of respiratory infections due to H. influenzae.     

Characterization of rat100, a 300-kilodalton ubiquitin-protein ligase induced in germ cells of the rat testis and similar to the Drosophila hyperplastic discs gene

Conjugation of ubiquitin to proteins is activated during spermatogenesis. Ubiquitination is mediated by ubiquitin-activating enzyme (E1), ubiquitin-conjugating enzymes (UBCs or E2s), and ubiquitin protein ligases (E3s). Since we previously showed that the activated ubiquitination is UBC4 dependent, we characterized Rat100, a UBC4-dependent E3 expressed in the testis. Analysis of expressed sequence tag sequences and immunoblotting showed that Rat100 is actually a 300-kDa protein expressed mainly in the brain and testis and is similar to the human E3 identified by differential display (EDD) protein and the Drosophila hyperplastic discs gene, mutants of which cause a defect in spermatogenesis. Rat100 is induced during postnatal development of the rat testis, peaking at d 25. It is localized only in germ cells and is highly expressed in spermatocytes, moderately in round and slightly in elongating spermatids. In contrast to UBC4 whose removal from a testis extract abrogates much of the conjugation activity, immmunodepletion of Rat100 from the extracts had little effect. Rat100 therefore has a limited subset of substrates, some of which appear associated with the E3 as the immunoprecipitate containing Rat100 supported incorporation of (125)I-ubiquitin into high molecular weight proteins. Thus, Rat100 is the homolog of human EDD and likely of Drosophila hyperplastic discs. This homology, together with our results, suggests that induction of this E3 results in ubiquitination of specific substrates, some of which are important in male germ cell development.     

Progestins and cortisol delay while estradiol-17 beta induces early parturition in the guppy, Poecilia reticulata

Fertilization and gestation are intrafollicular in the guppy (Poecilia reticulata), and ovulation occurs at the end of gestation prior to parturition. In this study, the effects in vivo of the ovarian steroids, progesterone, 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-P), cortisol and estradiol-17 beta, the antiprogestin RU 486, and aromatase inhibitor, 4-hydroxyandrost-4-ene-3,17-dione (4-HAD), on gestation and parturition were studied in the guppy. Progesterone (0.05 and 0.10 micrograms/ml of water), 17 alpha,20 beta-P (0.01 micrograms/ml and greater), cortisol (0.10 micrograms/ml) and 4-HAD (0.10 micrograms/ml) all prolonged gestation presumably by inhibiting ovulation. 17 alpha,20 beta-P was most effective in inhibiting ovulation and parturition for up to 36 days postpartum. This inhibition was reversed when fish were transferred to steroid-free water. Besides extending gestation, 17 alpha,20 beta-P and 4-HAD also inhibited development of vitellogenic oocytes. Estradiol-17 beta (0.05 and 0.10 micrograms/ml) and RU 486 (10 micrograms/g body weight) both induced premature parturition presumably by accelerating onset of ovulation. These results, together with our previous observations on the steroid profile in the guppy, strongly suggest roles for estradiol-17 beta and cortisol in regulating ovulation and parturition.