Rapid dark aging of biomass burning as an overlooked source of oxidized organic aerosol

Oxidized organic aerosol (OOA) is a major component of ambient particulate matter, substantially impacting climate, human health, and ecosystems. OOA is readily produced in the presence of sunlight, and requires days of photooxidation to reach the levels observed in the atmosphere. High concentrations of OOA are thus expected in the summer; however, our current mechanistic understanding fails to explain elevated OOA during wintertime periods of low photochemical activity that coincide with periods of intense biomass burning. As a result, atmospheric models underpredict OOA concentrations by a factor of 3 to 5. Here we show that fresh emissions from biomass burning exposed to NO₂ and O₃ (precursors to the NO₃ radical) rapidly form OOA in the laboratory over a few hours and without any sunlight. The extent of oxidation is sensitive to relative humidity. The resulting OOA chemical composition is consistent with the observed OOA in field studies in major urban areas. Additionally, this dark chemical processing leads to significant enhancements in secondary nitrate aerosol, of which 50 to 60% is estimated to be organic. Simulations that include this understanding of dark chemical processing show that over 70% of organic aerosol from biomass burning is substantially influenced by dark oxidation. This rapid and extensive dark oxidation elevates the importance of nocturnal chemistry and biomass burning as a global source of OOA.

Highly oxidized organic aerosol (OOA) is a dominant component of particulate matter air pollution globally (1–3); however, sources of OOA remain uncertain, limiting the ability of models to accurately represent OOA and thus predict the associated climate, ecosystem, and health implications (4, 5). The current conceptual model of OOA formation suggests that anthropogenic OOA predominantly originates from the oxidation of volatile (VOCs), intermediate volatility (IVOCs), and semivolatile (SVOCs) organic compounds by the OH radical, resulting in lower-volatility products that condense to the particle phase (6). As the OH radical is formed through photolysis and has a very short atmospheric lifetime [less than a second (7)], this oxidation mechanism only occurs in the presence of sunlight. Further, the time scale for OOA formation through oxidation with OH in models is on the order of a few days (8). While this understanding is sufficient in explaining OOA concentrations in summer or periods with high solar radiation, atmospheric models fail to reproduce the observed concentration of OOA in the ambient atmosphere during winter and low-light conditions (9, 10). Fountoukis et al. (9) found simulated OOA concentrations significantly underestimated in wintertime Paris. Tsimpidi et al. (10) also reported an underprediction of simulated OOA globally in winter, suggesting missing sources of both primary OA (POA) and secondary formation pathways. This underproduction suggests a possible overlooked conversion pathway of organic vapors or particles to OOA that is not accounted for in current chemical transport and climate models.As stricter controls on fossil fuel combustion are implemented, residential biomass burning (BB) as a source of heating or cooking is becoming an increasingly important source of OA in urban environments (1, 11, 12). Further, increasing rates of wildfires from climate change are increasing the frequency of smoke-impacted days in urban areas (12–14). BB emissions include high concentrations of POA, SVOCs, IVOCs, and VOCs (15, 16), thus making BB a key source of OOA. Previous research has focused on quantifying the concentration of OOA formed through photochemical oxidation reactions (i.e., OH) with BB emissions (17, 18). However, oxidation of BB emissions in low or no sunlight is less well understood and is not included in chemical transport models. As opposed to OH, the NO₃ radical is formed through reactions with NO₂ and O₃ and is rapidly lost in the presence of sunlight (19). Thus, the NO₃ radical is only available in significant concentrations at night or other low-light conditions (20, 21). Previous research has established that biogenic VOCs may undergo oxidation at night when mixed with anthropogenic emissions containing NO₂ and O₃ (19, 22–27). There have been only a few studies that consider that nighttime oxidation of residential wood combustion may proceed through similar pathways (28–31); however, the magnitude and relevance to observed OOA in the ambient atmosphere has not yet been established. By combining laboratory experiments and ambient observations to inform a chemical transport model, we present strong evidence that nighttime oxidation of BB plumes (proceeding through reactions with O₃ and the NO₃ radical) is an important source of OOA.     

Prophylactic total gastrectomy in the management of hereditary tumor syndromes

Purpose

Germline mutations in several genes confer a relevant lifetime risk of gastric cancer. In this context, an increasing involvement of a surgeon can be seen, mainly with the question of performing a prophylactic operation.

Methods

Patients with hereditary tumor syndromes predisposing for gastric cancer who received care leading to prophylactic total gastrectomy in our Center for Hereditary Tumor Syndromes were analyzed. For each patient, the multidisciplinary decision-making process, the perioperative course, and the histopathologic findings were assessed. Short-term morbidity was evaluated based on the medical reports.

Results

The analysis includes nine patients (six female, three male) with a median age of 41.6 (range 23–60) years. Indication for prophylactic total gastrectomy was based on family history and genetic analysis (eight patients with a germline mutation of the CDH1 gene and one patient with a SMAD4 mutation). Removal of the entire gastric mucosa was documented intraoperatively by fresh frozen section examination. Extended (DII) lymphadenectomy was performed in four patients. Histopathologic examination of gastrectomy specimens revealed six patients (6/9, 67 %) with multifocal signet ring cell carcinomas. In our series, prophylactic total gastrectomy was a safe procedure without mortality and low morbidity.

Conclusions

Patients with hereditary syndromes predisposing for gastric cancer should be evaluated for this curative procedure in a specialized center. Further research is necessary, and the implementation of nationwide registers including patients with prophylactic gastrointestinal operations due to hereditary tumor syndrome is advisable.

     

Hyperlipidemia prevents the expected reduction of myocardial ischemia on repeated balloon inflations during angioplasty

BACKGROUND: Controversy exists regarding inhibition of ischemic preconditioning in hyperlipidemic animals. In this study, we tested the hypothesis that hyperlipidemia inhibits the normal reduction of myocardial ischemia on repeated balloon inflations (BIs) during angioplasty. METHODS: We studied 33 patients undergoing coronary angioplasty. All underwent a minimum of three BIs. Patients were grouped according to the following plasma cholesterol levels: 13 patients had total cholesterol levels < 200 mg/dL (the normal cholesterol group); and 20 patients had total cholesterol levels > or = 200 mg/dL (the elevated cholesterol group). Surface ST-segment elevations were recorded at the end of each BI. RESULTS: In the normal cholesterol group, the mean (+/- SD) ST-segment elevation decreased from 0.21 +/- 0.15 mV during the first BI to 0.11 +/- 0.11 mV during the third BI (p < 0.05). In the elevated cholesterol group, the respective decrease was from 0.18 +/- 0.16 to 0.14 +/- 0.15 mV (p = not significant) [between-group comparisons: F = 3.97; p = 0.02]. The decrease in ST-segment elevation was correlated with the total cholesterol levels (r = -0.48; p = 0.005), the low-density lipoprotein (LDL) cholesterol levels (r = -0.50; p = 0.003), and the high-density lipoprotein/LDL levels (r = 0.44; p = 0.01). CONCLUSION: Hyperlipidemia prevents the normal reduction of myocardial ischemia on repeated BIs during angioplasty. This leads to the clinical implication that reduction of cholesterol plasma levels, apart from its other known benefits, could also have a beneficial effect on cardioprotection.     

Helicobacter pylori infection upregulates endothelial nitric oxide synthase expression and induces angiogenesis in gastric mucosa of dyspeptic patients

BACKGROUND: Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated. The aim of this study was to evaluate the effect of H. pylori infection in the expression of eNOS in gastric mucosa. PATIENTS AND METHODS: We prospectively studied 30 nonsmoking dyspeptic patients (12 men, 18 women, mean age 54.26+/-12.89 years). The diagnosis of H. pylori infection was based mainly on histology. The histological grading of H. pylori infection was evaluated according to the modified Sydney classification. Histological grading of eNOS expression and microvessel density as estimated by CD34 expression were determined by immunohistochemistry (degree 0-3) and correlated with H. pylori infection and histological degree of gastritis. RESULTS: Twelve patients were H. pylori-positive and 18 patients were H. pylori-negative. The two groups were matched for age (P=0.139), sex (P=0.342) and similar degree of gastritis. Intensity of eNOS and CD34 expression in the corpus and antrum were significantly correlated (P<0.001). eNOS expression was correlated with H. pylori infection in the mucosa of the body and antrum (P=0.013 and 0.037, respectively) but not with gastric inflammation and activity (P=0.848 and 0.871, respectively, for the corpus and P=0.565 and 0.793, respectively, for the antrum). H. pylori-positive patients showed higher expression of CD34-positive blood vessels in the mucosa of the antrum (P=0.048). CD34 expression was correlated with gastric inflammation and activity (P=0.03 and 0.044, respectively) in the mucosa of the antrum of H. pylori-positive patients. CONCLUSION: H. pylori infection upregulates eNOS, and induces angiogenesis, contributing to H. pylori-associated pathophysiology in gastric mucosa.     

Big Events in Greece and HIV Infection Among People Who Inject Drugs

Big Events are processes like macroeconomic transitions that have lowered social well-being in various settings in the past. Greece has been hit by the global crisis and experienced an HIV outbreak among people who inject drugs. Since the crisis began (2008), Greece has seen population displacement, inter-communal violence, cuts in governmental expenditures, and social movements. These may have affected normative regulation, networks, and behaviors. However, most pathways to risk remain unknown or unmeasured. We use what is known and unknown about the Greek HIV outbreak to suggest modifications in Big Events models and the need for additional research.     

Pattern of sensitization to honeybee venom in beekeepers: a 5-year prospective study.

Beekeepers are at increased risk for honeybee (Hb) venom allergy and they represent a unique population for Hymenoptera venom studies. The aim of this was to prospectively examine the pattern of Hb venom sensitization over a 5-year period in new beekeepers and define possible predisposing factors. Thirty-five beekeepers were tested every 6 months for 5 years with in vivo and in vitro methods to detect the possible development of sensitization to Hb and common wasp (Cw) venom. Inclusion criteria included the lack of previous beekeeping activity and absence of sensitization or reported reaction to Hymenoptera stings. Subjects with both in vivo and in vitro tests that were definitely positive or with one definitely positive and the other doubtful were considered sensitized. Ten of 35 new beekeepers (28.6%) and 3 of 36 controls (8.3%) developed sensitivity to Hb venom during the 5-year period. The risk ratio in incidence studies was calculated at 3.43 (SE of log risk ratio = 0.61; 95% CI of risk ratio = 1.03-11.42). All sensitized beekeepers were detected within the first 18 months of occupational exposure; 8 of 10 (80%) beekeepers were detected during the initial 12 months and the 2 remaining beekeepers were detected between 12 and 18 months. One of 35 (2.9%) beekeepers and 1 of 36 controls (2.8%) were sensitized to Cw venom. The number of stings per year and atopy had no effect on sensitization rate. Although predisposing factors to sensitization or anaphylaxis could not be identified, beekeepers developed sensitization to bee venom in <18 months.