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Summary Objectives To assess the efficacy and safety of tigecycline in comparison with other antimicrobial treatments for infectious diseases. Design Databases of PubMed, Embase and the Cochrane Library were searched through Feb. 2015. The reference lists of the initially identified articles and systemic review articles were manually searched. Randomized controlled trials assessing tigecycline and other antibiotics for infectious diseases in adult patients were included. Results Fifteen RCTs including 7689 cases were identified. We found that tigecycline was not as effective as the comparator agents for clinical treatment success (for the clinically evaluable population, odds ratio [OR] = 0.83, 95% confidence interval [CI] = (0.73, 0.96), P=0.01; for the clinically modified intent-to-treat (mITT) population, OR=0.81, 95% CI=(0.72, 0.92), P=0.001). There was no significant difference in microbiological treatment success with lower eradication rate in tigecycline versus comparators (for the microbiologically evaluable population, OR=0.94, 95% CI=(0.77, 1.16), P=0.56; for the microbiological mITT populations, OR=0.91, 95% CI=(0.74, 1.11), P=0.35). Adverse events and all-cause mortality were more common in the tigecycline group. Conclusions Tigecycline is not as effective as other antibiotics with relatively more frequency of adverse events and higher mortality rate.

For the axial flow fans NACA profiles have been well explored. However, the development and production of NACA profiles are also very expensive. Due to their lower cost of production circular arc blades are also applied to axial flow fans. But there is few information in the open literature focusing on flow loss and behavior of circular arc blades. Therefore, one question remains: how much is the difference of flow loss and behavior between NACA profiles and circular arc blades. In this paper NACA 65 profile and circular arc blade are examined by numerical method. The paper shows the flow loss of both blades in dependence of incidence, Reynolds number and spacing ratio. The occurrence of flow behavior, such as separation bubbles on the leading edge and flow structure on the sidewall is examined and discussed. The flow structure is given on basis of numerical flow picture. Additionally, the flow loss in the sidewall region of both investigated blades are worked out and compared.

Cerebral edema causes intracranial hypertension (ICH) which leads to severe outcome of patients in the clinical setting. Effective anti-edema therapy may significantly decrease the mortality in a variety of neurological conditions. At present drug treatment is a cornerstone in the management of cerebral edema. Osmotherapy has been the mainstay of pharmacologic therapy. Mannitol and hypertonic saline (HS) are the most commonly used osmotic agents. The relative safety and efficacy of HS and mannitol in the treatment of cerebral edema and reduction of enhanced ICP have been demonstrated in the past decades. Apart from its osmotic force, HS exerts anti-edema effects partly through inhibition of Na(+)-K(+)-2Cl(-) Cotransporter-1 (NKCC1) and aquaporin 4 (AQP4) expression in astrocytes. Melatonin may also reduce brain edema and exert neuroprotective effect on several central nervous system diseases through inhibition of inflammatory response. The inhibitors of Na/H exchanger, NKCC and AQP4 may attenuate brain edema formation through inhibition of excessive transportation of ion and water from blood into the cerebral tissue. In this review we survey some of the most recent findings in the drug treatment of brain edema focusing on the use of osmotherapy, melatonin and inhibitors of ion cotransporters and water channels. A better understanding of the molecular mechanism of these agents would help to improve in the clinical management of patients with brain edema.

The aim of the study is to validate of the use of plasma B-type natriuretic peptide (BNP) point-of-care test platform in preliminary recognition of cardioembolic stroke patients in the emergency department (ED).In our ED, emergency physicians prospectively assessed consecutive adult patients with acute phase of ischemic stroke and measured plasma BNP by point-of-care test platform on admission. The included patients with plasma BNP concentration more than 66.50 pg/mL were presumed to be classified as the cardioembolism (CE) subtype and were then followed up. Stroke neurologists evaluated patients' functional outcome at hospital discharge and also made discharge diagnosis and stroke etiologic subtypes according to Trial of ORG 10172 in Acute Stroke Treatment criteria: large artery atherosclerosis, CE, small artery occlusion, stroke of other determined etiology, and stroke of other undetermined etiology.In this study, 172 of 262 acute ischemic stroke patients met the study criteria (mean age, 71.18 ± 11.65 years; 53.49% female). Of the 172 patients, 38.95% were diagnosed with large artery atherosclerosis at discharge; 26.16%, with CE; 24.42%, with small artery occlusion; and 10.47%, with stroke of other determined etiology or stroke of other undetermined etiology. Age, previous cardiac disease, atrial fibrillation, length of hospital stays, Scandinavian Stroke Scale score on admission less than or equal to 25, and modified Rankin Scale greater than or equal to 3 or death at discharge were all significantly higher in the CE patients compared to other subtypes (P.01). The mean BNP concentration was significantly higher in the CE group than in other 3 subtypes (P.01). The plasma BNP level greater than 66.50 pg/mL had good corresponding diagnostic performance in preliminary recognition of cardioembolic stroke patients (sensitivity, 75.56%; specificity, 87.40%).In this study, we found that the plasma BNP level greater than 66.50 pg/mL as a reference index had good corresponding diagnostic performance in preliminary recognition of cardioembolic stroke patients. However, the single BNP biomarker panel cannot be used to confidently identify CE subtype as a diagnosis and must be taken in context with clinical assessment and judgment before making management decisions.

Many studies have indicated that hypernatremia is associated with increased mortality. In this study, we aimed to explore the relationship between intensive care unit (ICU)-acquired hypernatremia and the prognosis of critically neurological patients. Based on serum sodium level in the ICU, 450 patients were divided into 3 groups: 222 had normal serum sodium, 142 had mild hypernatremia, and 86 had severe hypernatremia. Kaplan–Meier and multivariable binary logistic regression analyses were performed to evaluate the prognostic value of hypernatremia in critically neurological patients. Receiver operating characteristic (ROC) curve was constructed for serum sodium levels to determine their roles in predicting ICU mortality. Hypernatremia was significantly related with age, Glasgow Coma Scale (GCS) score, serum sodium, APACHE II score, and serum creatinine. Moreover, the different treatment outcome including mechanical ventilation, the days of stayed in ICU, and Glasgow Outcome Scale score had correlation with serum sodium levels. Old ages, GCS score, therapeutic intervention scoring system (TISS) score, APACHE II score, serum sodium peak, and so on were all associated with the mortality. In addition, hypernatremia was an independent prognostic factor for critically neurological patients by logistic regression analysis (odds ratio = 1.192, 95% confidence interval = 1.135–1.252, P = 0.000). Moreover, we got the sensitivity of 79.4% and specificity of 74.5% in the ROC analysis between peak serum sodium and the mortality. The area under the ROC curve was 0.844, and the optimal cutoff value was 147.55. Our results showed that ICU-acquired hypernatremia may be a potential prognosis marker for critically neurological patients.

Background Ischemic stroke is a major disease that threatens human health in ageing population. Increasing evidence has shown that neuroinflammatory mediators play crucial roles in the pathophysiology of cerebral ischemia injury. Notch signaling is recognized as the cell fate signaling but recent evidence indicates that it may be involved in the inflammatory response in activated microglia in cerebral ischemia. Previous report in our group demonstrated hypertonic saline (HS) could reduce the release of interleukin-1 beta and tumor necrosis factor-alpha in activated microglia, but the underlying molecular and cellular mechanisms have remained uncertain. This study was aimed to explore whether HS would partake in regulating production of proinflammatory mediators through Notch signaling. Results HS markedly attenuated the expression of Notch-1, NICD, RBP-JK and Hes-1 in activated microglia both in vivo and in vitro. Remarkably, HS also reduced the expression of iNOS in vivo, while the in vitro levels of inflammatory mediators Phos-NF-κB, iNOS and ROS were reduced by HS as well. Conclusion Our results suggest that HS may suppress of inflammatory mediators following ischemia/hypoxic through the Notch signaling which operates synergistically with NF-κB pathway in activated microglia. Our study has provided the morphological and biochemical evidence that HS can attenuate inflammation reaction and can be neuroprotective in cerebral ischemia, thus supporting the use of hypertonic saline by clinicians in patients with an ischemia stroke. Electronic supplementary material The online version of this article (doi:10.1186/s12868-017-0351-6) contains supplementary material, which is available to authorized users.