Search

Due to the low production cost, circular arc blades are often applied to axial fans as outlet guide vane. At present, there is less available information focusing on the flow loss and flow structure of circular arc blades in the open literature. In particular, the influence of leading edge and trailing geometries on the aerodynamic performance of circular arc blades remains unknown. In this study, the circular arc blades edge with different leading edge and trailing edge are investigated and compared with numerical and experimental methods to detect the aerodynamic performance of the circular arc blades and the influence of their leading edge and trailing edge on the flow loss and flow structure. The flow loss and turning angle of both investigated blades are shown to dependent on the incidence angle. The flow structures of both blades are built on the basis of numerical and experimental oil-flow pictures. Additionally, the separation bubbles at the leading edge of the blade and the distribution of the flow loss on the measuring plane are shown and discussed.

To explore whether the cholinergic anti-inflammatory pathway is involved in the neuroprotective effect of acetylcholinesterase inhibitor huperzine A (HupA) on sepsis-associated encephalopathy (SAE) by observing the effect of HupA on the expressions of choline acetyltransferase (CHAT) and cholinergic muscarinic receptor M1 (CHRM1) of sepsis rats.Fifty-four male Wistar rats, 8 weeks old, were divided into three experimental groups according to random number table:control group,sepsis group, and HupA group, with 18 rats in each group. The rat model of sepsis was reproduced by intraperitoneal injection of 10 mg/kg lipopolysaccharide (LPS,1 mL),and the rats in control group were given the same volume of normal saline. The rats in HupA group were intraperitoneally administered with HupA 0.04 mg/kg (1 mL) at 30 minutes before model reproduction, while the rats in control group and sepsis group were treated with the same volume of saline instead. At 3,12,and 24 hours after model reproduction,6 rats in each group were sacrificed after clinical manifestation observation, and cerebral cortex tissue was collected. Pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1 β) in cerebral cortex were determined with enzyme linked immunosorbent assay (ELISA),along with the measurement of neuronal apoptosis by caspase-3 and neuronal nuclear antigen (NeuN) immune double standard staining. The mRNA expressions and positive expressions of ChAT and CHRM1 were detected by real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and immunofluorescence methods.Clinical manifestations of sepsis rats were present at 3 hours and reached a peak at 12 hours, including lethargy,vertical hair and lazy to move. Over-expression of pro-inflammatory cytokines TNF-α and IL-1β was found in sepsis group, and apoptotic neurons marked by two fluorescences were significantly increased in sepsis rats ,in comparison with deficient ChAT and CHRM1 proteins marked by red fluorescence, and low-expressed ChAT and CHRM1 mRNA as well. The differences between sepsis group and control group were statistically significant [12-hour TNF-α (ng/L):84.97±31.84 vs.40.31 ± 10.37,12-hour IL-1 β (ng/L):1 095.98± 127.09 vs.622.62± 117.25,12-hour ChAT mRNA (2-△△Ct):1.34 (0.67,1.86) vs.1.92 (1.12,2.87),12-hour CHRM1 mRNA (2-△△Ct):0.65±0.12 vs.1.16±0.42,all P ＜ 0.05].The septic symptoms were relieved after HupA administration,as well as the reduction of pro-inflammatory cytokines and the neuronal apoptosis, which might attribute to the increased expressions of ChAT and CHRM1.The differences between HupA group and sepsis group were statistically significant [12-hour TNF-α (ng/L):48.38 ± 12.62 vs.84.97 ± 31.84,12-hour IL-1 β (ng/L):718.13 ± 163.33 vs.1 095.98 ± 127.09,12-hour ChAT mRNA (2-△△Ct):18.04 (17.22,19.23) vs.1.34 (0.67,1.86),12-hour CHRM1 mRNA (2-△ △Ct):1.46 ± 0.69 vs 0.65 ± 0.12,all P ＜ 0.05].The clinical manifestations and neuroinflammation mainly recovered at 24 hours.The cortical cholinergic neurons dysfunction and the abnormal inflammatory response are involved in the onset of SAE process. HupA plays a protective role in SAE through recovering the function of cholinergic neurons and cholinergic anti-inflammatory pathway.

Neuroinflammation elicited by microglia plays a key role in periventricular white matter (PWM) damage (PWMD) induced by infectious exposure. This study aimed to determine if microglia-derived interleukin-1β (IL-1β) would induce hypomyelination through suppression of maturation of oligodendrocyte progenitor cells (OPCs) in the developing PWM. Sprague-Dawley rats (1-day old) were injected with lipopolysaccharide (LPS) (1 mg/kg) intraperitoneally, following which upregulated expression of IL-1β and IL-1 receptor 1 (IL-1R1 ) was observed. This was coupled with enhanced apoptosis and suppressed proliferation of OPCs in the PWM. The number of PDGFR-α and NG2-positive OPCs was significantly decreased in the PWM at 24 h and 3 days after injection of LPS, whereas it was increased at 14 days and 28 days. The protein expression of Olig1, Olig2, and Nkx2.2 was significantly reduced, and mRNA expression of Tcf4 and Axin2 was upregulated in the developing PWM after LPS injection. The expression of myelin basic protein (MBP) and 2',3'-cyclic-nucleotide 3"-phosphodiesterase (CNPase) was downregulated in the PWM at 14 days and 28 days after LPS injection; this was linked to reduction of the proportion of myelinated axons and thinner myelin sheath as revealed by electron microscopy. Primary cultured OPCs treated with IL-1β showed the failure of maturation and proliferation. Furthermore, FYN/MEK/ERK signaling pathway was involved in suppression of maturation of primary OPCs induced by IL-1β administration. Our results suggest that following LPS injection, microglia are activated and produce IL-1β in the PWM in the neonatal rats. Excess IL-1β inhibits the maturation of OPCs via suppression of FYN/MEK/ERK phosphorylation thereby leading to axonal hypomyelination.

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.

To observe the axonal development in the corpus callosum of septic neonatal rats, and its effect on the neurological function after birth.Forty-eight 1-day-old Sprague-Dawley (SD) rats were randomly divided into two groups: control group and sepsis group, with 24 rats in each group. The rat model of sepsis was reproduced by intraperitoneal injection of 1 mg/kg lipopolysaccharide (LPS), and the rats in control group were injected with an equal volume of phosphate buffered saline (PBS). The corpus callosum in brain was harvested at 7, 14, and 28 days after model reproduction, and double immunofluorescence staining and Western Blot were used to observe the expression of neurofilament heavy chain (NFH), neurofilament medium chain (NFM) and neurofilament light chain (NFL) in the corpus callosum. The morphology and number of axon were observed in the corpus callosum of rats at 28 days using electron microscopy. The number of myelin basic protein (MBP) positive cells in the corpus callosum of rats was determined by in situ hybridization.The immunofluorescence intensities of NFH, NFM, and NFL in the corpus callosum of rats at 7, 14, and 28 days after model reproduction in sepsis group were significantly lower than those of control group. In addition, it was revealed by Western Blot results that the protein expression levels of NFH, NFM, and NFL in sepsis group were significantly lower than those of control group [NFH (gray value): 0.16±0.03 vs. 0.34±0.04 at 7 days, 1.75±0.11 vs. 2.42±0.17 at 14 days, 3.39±0.25 vs. 5.11±0.23 at 28 days; NFM (gray value): 0.34±0.04 vs. 0.53±0.04 at 7 days, 0.74±0.04 vs. 1.12±0.07 at 14 days, 0.92±0.06 vs. 1.52±0.07 at 28 days; NFL (gray value): 0.12±0.02 vs. 0.26±0.14 at 7 days, 0.32±0.03 vs. 0.81±0.04 at 14 days, 0.85±0.08 vs. 1.81±0.05 at 28 days; P0.05 or P0.01]. In the control group, an obvious myelination was found in the corpus callosum of rats on the 28th day after the birth, and the nodes of Ranvier were clearly distinguishable, with intact structure and smooth edges. The number of myelinated axons was reduced and the nodes of Ranvier were impaired in the corpus callosum of rats at 28 days after LPS injection. The expression of MBP in the corpus callosum of rats at 28 days after LPS injection was obviously decreased compared with control group (cells/LP: 23.67±3.21 vs. 35.00±3.61, P0.01).The axonal development in the corpus callosum of septic neonatal rats on the 28th day after the birth was impaired, and lead to reduced myelination and further deterioration of neurological function.

Neuroinflammation elicited by microglia plays a key role in periventricular white matter (PWM) damage (PWMD) induced by infectious exposure. This study aimed to determine if microglia-derived interleukin-1β (IL-1β) would induce hypomyelination through suppression of maturation of oligodendrocyte progenitor cells (OPCs) in the developing PWM. Sprague-Dawley rats (1-day old) were injected with lipopolysaccharide (LPS) (1 mg/kg) intraperitoneally, following which upregulated expression of IL-1β and IL-1 receptor 1 (IL-1R1 ) was observed. This was coupled with enhanced apoptosis and suppressed proliferation of OPCs in the PWM. The number of PDGFR-α and NG2-positive OPCs was significantly decreased in the PWM at 24 h and 3 days after injection of LPS, whereas it was increased at 14 days and 28 days. The protein expression of Olig1, Olig2, and Nkx2.2 was significantly reduced, and mRNA expression of Tcf4 and Axin2 was upregulated in the developing PWM after LPS injection. The expression of myelin basic protein (MBP) and 2',3'-cyclic-nucleotide 3"-phosphodiesterase (CNPase) was downregulated in the PWM at 14 days and 28 days after LPS injection; this was linked to reduction of the proportion of myelinated axons and thinner myelin sheath as revealed by electron microscopy. Primary cultured OPCs treated with IL-1β showed the failure of maturation and proliferation. Furthermore, FYN/MEK/ERK signaling pathway was involved in suppression of maturation of primary OPCs induced by IL-1β administration. Our results suggest that following LPS injection, microglia are activated and produce IL-1β in the PWM in the neonatal rats. Excess IL-1β inhibits the maturation of OPCs via suppression of FYN/MEK/ERK phosphorylation thereby leading to axonal hypomyelination.

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.