Tumor Necrosis Factor-alpha (TNF-α) is an immunomodulatory and proinflammatory cytokine implicated in neuro-inflammation and neuronal damage in response to cerebral ischemia. The present study tested the hypothesis that anti-TNF-α agents may be protective against cerebral infarction. Transient focal ischemia was artificially induced in anesthetized adult male Wistar rats (300-350 g) by middle cerebral artery occlusion (MCAO) with an intraluminal suture. TNF-α function was interfered with either a chimeric monoclonal antibody against TNF-α (infliximab-7 mg/kg) aiming to TNF-α soluble and membrane-attached form; or a chimeric fusion protein of TNF-α receptor-2 with a fragment crystallizable (Fc) region of IgG1 (etanercept-5 mg/kg) aiming for the TNF-α soluble form. Both agents were administered intraperitoneally 0 or 6 h after inducing ischemia. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. Cerebral infarct volume was significantly reduced in either etanercept or infliximab-treated group compared with non-treated MCAO rats 24 h after reperfusion. These results suggest that anti-TNF-α agents may reduce focal ischemic injury in rats.

Rabbits were given classical discrimination conditioning with one of two tones followed by shock. In Experiment I, 40 rabbits were trained under saline, 10, 18 or 26 mg/kg atropine sulfate or 18 mg/kg methylatropine. Six rabbits in Experiment 2 were conditioned, then given further sessions with saline, and 18, 26 and 34 mg/kg atropine sulfate and methylatropine. In Experiment 3, 18 rabbits were conditioned and then given two extinction sessions under saline or 34 mg/kg atropine sulfate or methylatropine followed by extinction under saline. Chief findings were (a) atropine sulfate but not methylatropine disrupted acquisition and maintenance of conditioned eyeblinks, (b) neither drug affected unconditioned blinks, (c) fewer blinks occurred in extinction under atropine sulfate than under methylatropine or saline, (d) rabbits extinguished under atropine sulphate showed higher percentages of eyeblinks when tested without drug. Disruptions in performance of learned eyeblink responses appeared to be due to drug interference with central cholinergic transmission.

The effect of two hydrocolloids, pectin and carboxymethyl cellulose (CMC), was evaluated in mango beverage stability (Mangifera indica L.) formulated and developed with caffeine at a concentration of 30 mg/100 mL. The physico-chemical and sensory characteristics of color, acidity, viscosity, total soluble solids, pH, flavor, aroma and texture were studied every three days over a 12-day period. The beverages were packaged in high-density polyethylene containers with a 250 mL capacity and were stored at 5 °C and 90% RH for the duration of the experimentation period. The drinks with added pectin showed greater stability and lower acidity values than the control, but higher values than those prepared with CMC. The drinks made with CMC had a significantly higher viscosity at a 95% confidence level than those made with pectin or the control beverages. The treatment that showed the lowest browning index was the one added with pectin. Concerning the sensory evaluation, the drinks showed significant differences at a 95% confidence level; the drink made with pectin was the most widely accepted. It was concluded that the most stable drinks were those made with pectin because they presented the lowest height in millimeters of precipitate solids over the storage period. No off-flavors in beverages were perceived by the judges.

Summary Introduction Candida species are the leading cause of invasive fungal infections in hospitalised patients and are the fourth most common isolates recovered from patients with bloodstream infection. Few data exist on risk factors for candidemia in non‐ICU patients. We performed a population‐based case‐control study to evaluate the main predictors for candidemia in non‐ICU patients. Methods and findings We included all non‐neutropenic, non‐critically ill and non‐surgical adult patients with candidemia between January 2010 and June 2014. Patients with positive, non‐candidal blood culture obtained at the same day (±2 days) were selected as controls. Cases and controls were matched according to hospital ward and clinical characteristics. Risk factors for candidemia were identified through a logistic regression. We included 56 candidemic and 512 bacteriemic non‐candidemic patients. Most of candidemic patients (52) had received antibiotics prior to candidemia. Among them, the 30‐day mortality rate was 34% (19/56). Multivariate analysis identified male sex, prior use of steroids, prior use of antibiotics, total parenteral nutrition and urinary catheterisation as independent predictors of candidemia. To develop the CaMed score, we rounded up weights of different risk factors as follows; total parenteral nutrition (+2), prior antibiotic therapy (+5), each of the other risk factors (+1). A score ≥ 7 identified patients at high risk of candidemia (P < 0.001; RR 29.805; CI 95% 10.652‐83.397; sensitivity 79.2, specificity 82.6%, Youden index 0,62). Conclusions Our set of easy independent predictors of candidemia in non‐neutropenic, non‐ICU, non‐surgical patients provide a rationale for early initiation of antifungals and could reduce candidemia‐related mortality.

No abstract