Agreements between GLIM using left calf circumference as criterion for reduced muscle mass and PG-SGA, and GLIM using ASMI for the diagnosis of malnutrition in gastric cancer patients.

OBJECTIVE: this study aimed to explore the agreements between the Global Leadership Initiative on Malnutrition (GLIM) using left calf circumference (CC) as criterion for reduced muscle mass and the Patient-Generated Subjective Global Assessment (PG-SGA), or GLIM using appendicular skeletal muscle index (ASMI) for the diagnosis of malnutrition in gastric cancer patients. METHODS: the Nutritional Risk Screening 2002 (NRS 2002) was used as nutritional risk screening. PG-SGA and GLIM were applied for malnutrition diagnosis. Agreements were evaluated by Kappa, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), accuracy, and area under the curve (AUC). RESULTS: a total of 405 gastric cancer patients were included. The values of Kappa, sensitivity, specificity, PPV, NPV, accuracy and AUC were 0.463, 67.9 %, 87.3 %, 92.9 %, 52.8 %, 73.6 % and 0.776, and 0.496, 76.7 %, 78.0 %, 89.4 %, 57.9 %, 77.0 % and 0.773, respectively, between GLIM using CC with or without NRS 2002 and PG-SGA. All values of agreement were higher than 0.800 or 80.0 % between GLIM using left CC and GLIM using ASMI. CONCLUSION: the agreements were both acceptable between GLIM using left CC and PG-SGA, and GLIM using ASMI. Left calf circumference can be one of the credible references indicating a reduced muscle mass in patients with gastric cancer.

Unveiling the biointerfaces characteristics and removal pathways of Cr(â ¥) in Bacillus cereus FNXJ1-2-3 for the Cr(â ¥)-to-Cr(0) conversion.

Although less toxic than hexavalent chromium, Cr (Ⅲ) species still pose a threat to human health. The Cr (Ⅵ) should be converted to Cr (0) instead of Cr (Ⅲ), which is still involved in biological detoxification filed. Herein, for the first time, it was found that Cr(Ⅵ) can be reduced into Cr(0) by Bacillus cereus FNXJ1-2-3, a way to completely harmless treatment of Cr(Ⅵ). The bacterial strain exhibited excellent performance in the reduction, sorption, and accumulation of Cr(Ⅵ) and Cr (Ⅲ). XPS etching characterization inferred that the transformation of Cr(Ⅵ) into Cr(0) followed a reduction pathway of Cr(Ⅵ)→Cr (Ⅲ)→metallic Cr(0), in which at least two secretory chromium reductases (ECrⅥ→Ⅲ and ECrⅢ→0) worked. Under the optimum condition, the yield ratio of Cr(0)/Cr (Ⅲ) reached 33.90%. In addition, the interfacial interactions, ion channels, chromium reductases, and external electron donors also contributed to the Cr(Ⅵ)/Cr(0) transformation. Findings of this study indicate that Bacillus cereus FNXJ1-2-3 is a promising bioremediation agent for Cr(Ⅵ) pollution control.

Schizandrin A attenuates early brain injury following subarachnoid hemorrhage through suppressing neuroinflammation.

BACKGROUND: Early brain injury (EBI) is the vital factor in determining the outcome of subarachnoid hemorrhage (SAH). Schizandrin A (Sch A), the bioactive ingredient extracted from Schisandra chinensis, has been proved to exert beneficial effects in multiple human diseases. However, the effect of Sch A on SAH remains unknown. The current study was designed to explored role and mechanism of Sch A in the pathophysiological process of EBI following SAH. METHOD: A total of 74 male C57BL/6 J mice were subjected to endovascular perforation to establish the SAH model. Different dosages of Sch A were administrated post-modeling. The post-modeling assessments included neurological test, brain water content, RT-PCR, immunofluorescence, Nissl staining. Oxygenated hemoglobin was introduced into microglia to establish a SAH model in vitro. RESULT: Sch A significantly alleviated SAH-induced brain edema and neurological impairment. Moreover, application of Sch A remarkably inhibited SAH-induced neuroinflammation, evidenced by the decreased microglial activation and downregulated TNF-α, IL-1ß and IL-6 and expression. Additionally, Sch A, both in vivo and in vitro, protected neurons against SAH-induced inflammatory injury. Mechanismly, administration of Sch A inhibited miR-155/NF-κB axis and attenuated neuroinflammation, as well as alleviating neuronal injury. CONCLUSION: Our data suggested that Sch A could attenuated EBI following SAH via modulating neuroinflammation. The anti-inflammatory effect was exerted, at least partly through the miR-155/NF-κB axis, which may shed light on a possible therapeutic target for SAH.

Accurate Nonlinearity and Temperature Compensation Method for Piezoresistive Pressure Sensors Based on Data Generation.

Piezoresistive pressure sensors exhibit inherent nonlinearity and sensitivity to ambient temperature, requiring multidimensional compensation to achieve accurate measurements. However, recent studies on software compensation mainly focused on developing advanced and intricate algorithms while neglecting the importance of calibration data and the limitation of computing resources. This paper aims to present a novel compensation method which generates more data by learning the calibration process of pressure sensors and uses a larger dataset instead of more complex models to improve the compensation effect. This method is performed by the proposed aquila optimizer optimized mixed polynomial kernel extreme learning machine (AO-MPKELM) algorithm. We conducted a detailed calibration experiment to assess the quality of the generated data and evaluate the performance of the proposed method through ablation analysis. The results demonstrate a high level of consistency between the generated and real data, with a maximum voltage deviation of only 0.71 millivolts. When using a bilinear interpolation algorithm for compensation, extra generated data can help reduce measurement errors by 78.95%, ultimately achieving 0.03% full-scale (FS) accuracy. These findings prove the proposed method is valid for high-accuracy measurements and has superior engineering applicability.

Electrocatalytic Oxidation and Determination of Nitrite at Multi-Walled Carbon Nanotubes Modified Electrode.

Electrocatalytic oxidation of nitrite at multi-walled carbon nanotubes (MWCNTs) modified electrode was investigated by using voltammetric techniques. The kinetic parameters such as diffusion coefficient (D), standard heterogeneous rate constant (ks) and catalytic constant (kh) were studied by chronocoulometry and chronoamperometry. The corresponding parameters for D, ks, and kh were caculated to be 3.56×10-5 cm² s-1, 6.29×10-3 cm s-1 and 7.02×10² M-1 s-1, respectively. The modified electrode was used for the determination of nitrite with a concentration range of 0.5 to 36 µM and a detection limit of 0.08 µM. The proposed method was successfully applied for the determination of nitrite in real samples of tap water and juice of pickled garlic.

Rolipram Attenuates Early Brain Injury Following Experimental Subarachnoid Hemorrhage in Rats: Possibly via Regulating the SIRT1/NF-κB Pathway.

Early brain injury (EBI) is the primary cause of poor outcome in subarachnoid hemorrhage (SAH) patients. Rolipram, a specific phosphodiesterase-4 inhibitor which is traditionally used as an anti-depressant drug, has been recently proven to exert neuroprotective effects in several central nervous system insults. However, the role of rolipram in SAH remains uncertain. The current study was aimed to investigate the role of rolipram in EBI after SAH and explore the potential mechanism. Adult male Sprague-Dawley rats were subjected to an endovascular perforation process to produce an SAH model. Rolipram was injected intraperitoneally at 2 h after SAH with a dose of 10 mg/kg. We found that rolipram significantly ameliorated brain edema and alleviated neurological dysfunction after SAH. Rolipram treatment remarkably promoted the expression of Sirtuin 1 (SIRT1) while inhibited NF-κB activation. Moreover, rolipram significantly inhibited the activation of microglia as well as down-regulated the expression of pro-inflammatory cytokines TNF-α, IL-1ß, and IL-6. In addition, rolipram increased the expression of protective cytokine IL-10. Furthermore, rolipram significantly alleviated neuronal death after SAH. In conclusion, these data suggested that rolipram exerts neuroprotective effects against EBI after SAH via suppressing neuroinflammation and reducing neuronal loss. The neuroprotective effects of rolipram were associated with regulating the SIRT1/NF-κB pathway. Rolipram could be a novel and promising therapeutic agent for SAH treatment.

SIRT1 activation by resveratrol reduces brain edema and neuronal apoptosis in an experimental rat subarachnoid hemorrhage model.

Early brain injury is considered to be a major risk that is related to the prognosis of subarachnoid hemorrhage (SAH). In SAH model rats, brain edema and apoptosis have been closely related with death rate and neurological function. Sirtuin 1 (SIRT1) was reported to be involved in apoptosis in cerebral ischemia and brain tumor formation through p53 deacetylation. The present study aimed to evaluate the role of SIRT1 in a rat endovascular perforation model of SAH. The SIRT1 activator resveratrol (RES) was administered 48 h prior to SAH induction and the SIRT1 inhibitor Sirtinol (SIR) was used to reverse the effects of RES on SIRT1 expression. Mortality rate, neurological function and brain water content were measured 24 h post­SAH induction. Proteins associated with the blood brain barrier (BBB), apoptosis and SIRT1 in the cortex, such as zona occludens 1 (ZO­1), occludin, claudin­5, SIRT1, p53 and cleaved caspase3 were investigated. mRNA expression of the p53 downstream molecules including Bcl­associated X protein, P53 upregulated modulator of apoptosis, Noxa and BH3 interacting­domain death agonist were also investigated. Neuronal apoptosis was also investigated by immunofluorescence. RES pretreatment reduced the mortality rate and improved neurological function, which was consistent with reduced brain water content and neuronal apoptosis; these effects were partially reversed by co­treatment with SIR. SIRT1 may reduce the brain water content by improvement of dysfunctional BBB permeability, and protein analysis revealed that both ZO­1, occludin and claudin­5 may be involved, and these effects were reversed by SIRT1 inhibition. SIRT1 may also affect apoptosis post­SAH through p53 deacetylation, and the analysis of p53 related downstream pro­apoptotic molecules supported this hypothesis. Localization of neuron specific apoptosis revealed that SIRT1 may regulate neuronal apoptosis following SAH. SIRT1 may also ease brain edema and neuronal protection through BBB improvement and p53 deacetylation. SIRT1 activators such as RES may have the potential to improve the prognosis of patients with SAH and clinical research should be investigated further.

Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis.

Aberrant modulation of mitochondrial dynamic network, which shifts the balance of fusion and fission towards fission, is involved in brain damage of various neurodegenerative diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. A recent research has shown that the inhibition of mitochondrial fission alleviates early brain injury after experimental subarachnoid hemorrhage, however, the underlying molecular mechanisms have remained to be elucidated. This study was undertaken to characterize the effects of the inhibition of dynamin-related protein-1 (Drp1, a dominator of mitochondrial fission) on blood-brain barrier (BBB) disruption and neuronal apoptosis following SAH and the potential mechanisms. The endovascular perforation model of SAH was performed in adult male Sprague Dawley rats. The results indicated Mdivi-1(a selective Drp1 inhibitor) reversed the morphologic changes of mitochondria and Drp1 translocation, reduced ROS levels, ameliorated the BBB disruption and brain edema remarkably, decreased the expression of MMP-9 and prevented degradation of tight junction proteins-occludin, claudin-5 and ZO-1. Mdivi-1 administration also inhibited the nuclear translocation of nuclear factor-kappa B (NF-κB), leading to decreased expressions of TNF-ɑ, IL-6 and IL-1ß. Moreover, Mdivi-1 treatment attenuated neuronal cell death and improved neurological outcome. To investigate the underlying mechanisms further, we determined that Mdivi-1 reduced p-PERK, p-eIF2α, CHOP, cleaved caspase-3 and Bax expression as well as increased Bcl-2 expression. Rotenone (a selective inhibitor of mitochondrial complexes I) abolished both the anti-BBB disruption and anti-apoptosis effects of Mdivi-1. In conclusion, these data implied that excessive mitochondrial fission might inhibit mitochondrial complex I to become a cause of oxidative stress in SAH, and the inhibition of Drp1 by Mdivi-1 attenuated early brain injury after SAH probably via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis.

Molecularly Imprinted Polymers Based Electrochemical Sensor for 2,4-Dichlorophenol Determination.

A molecularly imprinted polymers based electrochemical sensor was fabricated by electropolymerizing pyrrole on a Fe3O4 nanoparticle modified glassy carbon electrode. The sensor showed highly catalytic ability for the oxidation of 2,4-dichlorophenol (2,4-DCP). Square wave voltammetry was used for the determination of 2,4-DCP. The oxidation peak currents were proportional to the concentrations of 2,4-DCP in the range of 0.04 to 2.0 µM, with a detection limit of 0.01 µM. The proposed sensor was successfully applied for the determination of 2,4-DCP in water samples giving satisfactory recoveries.

The operating performance of a biotrickling filter with Lysinibacillus fusiformis for the removal of high-loading gaseous chlorobenzene.

Removal of gaseous chlorobenzene (CB) by a biotrickling filter (BTF) filled with modified ceramics and multi-surface hollow balls during gas-liquid mass transfer at the steady state was by microbial degradation rather than dissolution in the spray liquid or emission into the atmosphere. The BTF was flexible and resistant to the acid environment of the spray liquid, with the caveat that the spray liquid should be replaced once every 6-7 days. The BTF, loaded with Lysinibacillus fusiformis, performed well for purification of high-loading CB gas. The maximum CB gas inlet loading rate, 103 g m(-3) h(-1), CB elimination capacity, 97 g m(-3) h(-1), and CB removal efficiency, 97.7 %, were reached at a spray liquid flow rate of 27.6 ml min(-1), an initial CB concentration of up to 1,300 mg m(-3), and an empty bed retention time of more than 45 s.