Advanced Criteria for Clinicopathological Diagnosis of Food Protein-induced Proctocolitis

The clinicopathological findings in previous studies concerning food protein-induced proctocolitis (FPIPC) are quite diverse in terms of results and conclusions. The aim of this study was to suggest advanced clinicopathological diagnostic criteria that facilitate the early confirmation of FPIPC. Data of 38 FPIPC patients, who had received sigmoidoscopy and biopsy, was analyzed. Microscopic findings were compared with observations of previous studies. Feeding at onset of bleeding was exclusively breast-fed (94.7%) and formula-fed or mixed-fed (5.3%). Endoscopic abnormalities were observed in all patients; nodular hyperplasias with circumscribed and/or central pit-like erosions in 94.7% and erythema in 5.3%. Histopathological findings were; lymphoid aggregates in 94.7%, eosinophils in lamina propria of ≥60 cells/10 HPF in 97.4% and of >20 cells/HPF in 63.2%, epithelial or muscularis mucosa eosinophil infiltration in 97.4%, and crypt abscess in 2.6%. The majority of FPIPC patients are exclusively breast-fed and nodular hyperplasias with erosions may be a disease specific endoscopic finding. Histologic diagnosis of FPIPC is compatible with eosinophils in the lamina propria of ≥60 cells/10 high power fields; however, >20 cells/HPF is not an appropriate diagnostic criterion

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

A Wideband Distributed Amplifier Employing an Envelope Tracking Technique

This letter presents a wideband distributed amplifier employing an envelope tracking (ET) technique for high efficiency and linearity. By applying the ET technique to the distributed amplifier after linearity optimization, the distributed amplifier's defects such as low output power and low efficiency can be overcome and high efficiency and linearity can be achieved. For verification, the distributed amplifier is designed using two Nitronex NPTB00025 GaN HEMT devices and tested with LTE signals at 2.6 GHz. From the tested results at an average output power of 37 dBm (10 dB back-off power), the proposed circuit shows an adjacent channel leakage ratio (ACLR) below -45 dBc at +/-5 MHz offset, with a gain over 14.1 dB and a power-added efficiency (PAE) over 21.9% over a 300 MHz bandwidth.X1112sciescopu

High-efficiency inverse class-E power amplifier with envelope tracking technique

This letter describes a highly efficient inverse class-E power amplifier (PA) with an envelope tracking (ET) technique.To enhance efficiency performances, the PA uses a harmonic control network with double composite right/left-handed transmission lines. The use of the ET technique also results in high efficiency for the modulated signals. For verifications, the inverse class-E PA is implemented with a 35-W GaN HEMT and tested using 3.5 GHz continuous wave (CW) and 802.16e WiMAX signals. With the CW signal, a peak drain efficiency of 79.0% with a power gain of 9.8 dB is achieved at a saturation output power of 45.6 dBm. With WiMAX signals, a drain efficiency of 37.8% with a power-added efficiency (PAE) of 33.6% is achieved at an average output power of 36 dBm, which is the 9.6 dB back-off power region, using the ET technique. After the DPD technique, the linearity significantly improved without decreasing efficiency. (c) 2012 Wiley Periodicals, Inc. Microwave Opt Technol Lett 55:866869, 2013; View this article online at wileyonlinelibrary.com. DOI: 10.1002/mop.27420X1132sciescopu

Effects of Drain Bias on Memory-Compensated Analog Predistortion Power Amplifier for WCDMA Repeater Applications

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Methylenetetrahydrofolate reductase gene A222V polymorphism and risk of ischemic stroke

The 5,10-methylenetetrahydrofolate reductase (MTHFR) gene 677C→T polymorphism causes an A222V amino acid change which affects MTHFR enzyme activity and can increase homocysteine, a vascular disease risk factor. This polymorphism was examined for association with stroke. In a case-control study of 241 ischemic stroke patients and 304 controls in Hong Kong, the V allele increased in stroke [28% vs. 20%, odds ratio (OR) 1.5, p=0.003]. A lack of significance for the increase in the VV genotype (7.5% vs. 4.6%, OR 1.7, p=0.16) may be due to its rarity in this region. V-allele carriers had more severe strokes (according to the NIH stroke scale). The association of the V allele with stroke occurred mostly in women or older subjects and was due to decreasing V allele frequency with age, as seen in other studies. This V frequency decline with age might be due to a loss of V-carrying controls from a higher risk of cancer, vascular disease, bone fracture, and kidney failure when folate is sparse. Examination of previous studies revealed that the association of VV genotype with stroke appeared stronger in Japan than elsewhere, possibly due to dietary differences. Perhaps folate supplementation for stroke prevention would particularly benefit VV individuals in such high-risk regions