A retrospective review of 400 Chinese children who had inhaled foreign bodies was undertaken. There has been a yearly increase in the total number of cases of airway foreign bodies removed in our hospital. Fifty-eight percent of the children presenting were from the countryside; 42% were townspeople. Approximately 90% of the patients were under 3 years of age, with the peak incidence of foreign body inhalation occurring between 1 and 2 years of age (57.8%). The male-female ratio was about 1.2:1. About 95% of the removed foreign bodies were organic in origin. The majority of the foreign bodies were found most often in the right bronchial tree (46%). A positive history of foreign body inhalation was obtained in 98% of the cases. Twenty-eight percent of the children presented at the hospital within 24 hours, 71% within 1 week, and 29% more than 1 week after inhaling the foreign body. The most common presenting symptoms of laryngotracheal foreign bodies were cough, wheezing, dyspnea, and hoarseness; those of bronchial foreign bodies were cough, wheezing, decreased air entry, and rhonchi. More than two-thirds of the children with larygotracheal foreign bodies had normal x-ray findings. The most common fluoroscopic findings in those children with bronchial foreign bodies were mediastinal shift (36.8%), obstructive emphysema (35.7%), and normal findings (35%). A total of 348 (87%) bronchial foreign bodies were removed by rigid bronchoscopy (81%), rod-lens bronchoscopy (5%), and spontaneous expulsion (1%); 52 (13%) laryngeal and tracheal foreign bodies were removed by direct laryngoscopy (12%) and tracheotomy (1%). A single endoscopic procedure successfully removed 92.5% of 400 foreign bodies detected in the airways. One child died during bronchoscopy, for a mortality rate of 0.25%.

Background: Patients with stable ischemic heart disease and previous myocardial infarction (MI) vary in their risk for recurrent cardiovascular events. Atherothrombotic risk assessment may be useful to identify high-risk patients who have the greatest potential to benefit from more intensive secondary preventive therapy such as treatment with vorapaxar. Methods: We identified independent clinical indicators of atherothrombotic risk among 8598 stable, placebo-treated patients with a previous MI followed up for 2.5 years (median) in TRA 2°P-TIMI 50 [Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–TIMI 50]. The efficacy and safety of vorapaxar (SCH 530348; MK-5348) were assessed by baseline risk among patients with previous MI without prior stroke or transient ischemic attack for whom there is a clinical indication for vorapaxar. End points were cardiovascular death, MI, or ischemic stroke and GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) severe bleeding. Results: The 9 independent risk predictors were age, diabetes mellitus, hypertension, smoking, peripheral arterial disease, previous stroke, previous coronary bypass grafting, heart failure, and renal dysfunction. A simple integer-based scheme using these predictors showed a strong graded relationship with the rate of cardiovascular death/MI/ischemic stroke and the individual components ( P for trend <0.001 for all). High-risk patients (≥3 risk indicators; 20% of population) had a 3.2% absolute risk reduction in cardiovascular disease/MI/ischemic stroke with vorapaxar, and intermediate-risk patients (1–2 risk indicators; 61%) had a 2.1% absolute risk reduction ( P <0.001 each), translating to a number needed to treat of 31 and 48. Bleeding increased across risk groups ( P for trend<0.01); however, net clinical outcome was increasingly favorable with vorapaxar across risk groups. Fatal bleeding or intracranial hemorrhage was 0.9% with both treatments in high-risk patients. Conclusions: Stratification of baseline atherothrombotic risk can assist with therapeutic decision making for vorapaxar use for secondary prevention after MI. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00526474.

OBJECTIVEThe glycemic management of patients with type 2 diabetes mellitus (T2DM) and renal impairment is challenging, with few treatment options. We investigated the effect of saxagliptin in the Saxagliptin Assessment of Vascular Outcomes Recorded in Patients with Diabetes Mellitus (SAVOR)-Thrombolysis in Myocardial Infarction (TIMI) 53 trial according to baseline renal function. RESEARCH DESIGN AND METHODSPatients with T2DM at risk for cardiovascular events were stratified as having normal or mildly impaired renal function (estimated glomerular filtration rate [eGFR] >50 mL/min/1.73 m 2 ; n = 13,916), moderate renal impairment (eGFR 30-50 mL/min/1.73 m 2 ; n = 2,240), or severe renal impairment (eGFR <30 mL/min/1.73 m 2 ; n = 336) and randomized to receive saxagliptin or placebo. The primary end point was cardiovascular death, myocardial infarction, or ischemic stroke. RESULTSAfter a median duration of 2 years, saxagliptin neither increased nor decreased the risk of the primary and secondary composite end points compared with placebo, irrespective of renal function (all P for interactions ‡0.19). Overall, the risk of hospitalization for heart failure among the three eGFR groups of patients was 2.2% (referent), 7.4% (adjusted hazard ratio [HR] 2.38 [95% CI 1.95-2.91], P < 0.001), and 13.0% .28], P < 0.001), respectively. The relative risk of hospitalization for heart failure with saxagliptin was similar (P for interaction = 0.43) in patients with eGFR >50 mL/min/1. CONCLUSIONSSaxagliptin did not affect the risk of ischemic cardiovascular events, increased the risk of heart failure hospitalization, and reduced progressive albuminuria, irrespective of baseline renal function.

Atherothrombotic risk stratification using the TRS 2°P identifies high-risk patients who derive greatest benefit from the addition of ezetimibe to statin therapy for secondary prevention after ACS. (Improved Reduction of Outcomes: Vytorin Efficacy International Trial [IMPROVE-IT]; NCT00202878).

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We conducted a series of in vivo experiments to clarify the hepatoprotective activity of green tea against lipopolysaccharide (LPS) + D-galactosamine (GalN)-induced liver injury and to elucidate the mechanism by which green tea exerts its effect in 7-wk-old male Wistar rats. Liver injury was assessed by plasma alanine aminotransferase and aspartate aminotransferase activities. Green tea extract significantly suppressed LPS + GalN-induced liver injury when added to the diet (30 or 35 g/kg) and fed to rats for 14 d or when force-fed alone (0.4-1.2 g/kg body) 1.5 h before the injection of drugs. Although all five of the fractions extracted from green tea extract with different organic solvents had significant suppressive effects, the caffeine-containing fraction exhibited the strongest effect, suggesting that the protective effect of green tea against LPS + GalN-induced liver injury is attributable mainly to caffeine. Authentic caffeine also significantly suppressed LPS + GalN-induced liver injury when added to the diet (2 g/kg) and fed to rats for 14 d. Dietary green tea suppressed LPS + GalN-induced apoptosis of liver cells, as assessed by DNA fragmentation. However, dietary green tea did not suppress LPS-induced enhancement of plasma concentration of tumor necrosis factor (TNF)-alpha, the cytokine that is thought to play a pivotal role in the pathogenesis of LPS-induced liver injury, although it significantly suppressed plasma concentrations of interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-10 and interferon (IFN)-gamma. TNF-alpha + GalN-induced liver injury and apoptosis were also suppressed by dietary green tea. In contrast, dietary caffeine significantly suppressed LPS-induced enhancement not only of plasma IL-1beta, IL-6, IL-10 and IFN-gamma concentrations, but also of TNF-alpha concentration. The results suggest that green tea might suppress LPS + GalN-induced liver injury mainly through the inhibition of TNF-alpha-induced apoptosis of hepatocytes, rather than through the suppression of TNF-alpha production, although the suppressed production of TNF-alpha may be associated with the hepatoprotective effect of caffeine.

The utilization of photochemical reaction channel based on radical process is rarely reported, which might be a very efficient and feasible strategy for improving generation of Type I reactive oxygen species (ROS). In this work, a double ionic-type aggregation-induced emission luminogen (AIEgen) of TIdBO was developed as a photosensitizer, of which the potential photocyclization characteristic involving an electron-transfer process had a positive effect on Type I ROS generation in aggregates under continuous light irradiation. Its noticeable photodynamic therapy (PDT) performance and self-monitoring of PDT process by the relationship between cellular morphology change and fluorescence intensity enhancement were achieved. In addition, it showed a good killing ability to microbes and specific interactions with microbes but not cells by regulating the incubation time. These intriguing results reveal a feasible design principle for the implementation of efficient PS preparation in clinical treatment under hypoxic conditions.

To evaluate the protective activity of fruits against liver injury, 22 different fruits were fed to rats with liver damage caused by D-galactosamine, a powerful liver toxin. As measured by changes in the levels of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), avocado showed extraordinarily potent liver injury suppressing activity. Five active compounds were isolated and their structures determined. These were all fatty acid derivatives, of which three, namely, (2E,5E,12Z,15Z)-1-hydroxyheneicosa-2,5,12,15-tetraen-4-one, (2E,12Z,15Z)-1-hydroxyheneicosa-2,12,15-trien-4-one, and (5E,12Z)-2-hydroxy-4-oxoheneicosa-5,12-dien-1-yl acetate, were novel.