Improved Hole-Selective Contact Enables Highly Efficient and Stable FAPbBr3 Perovskite Solar Cells and Semitransparent Modules.

Self-assembled monolayers (SAMs) as the hole-selective contact have achieved remarkable success in iodine-based perovskite solar cells (PSCs), while their impact on bromine-based PSCs is limited due to the poor perovskite crystallization behavior and mismatched energy level alignment. Here, a highly efficient SAM of (2-(3,6-diiodo-9H-carbazol-9-yl)ethyl)phosphonic acid (I-2PACz) is employed to address these challenges in FAPbBr3-based PSCs. The incorporation of I atoms into I-2PACz not only releases tensile stress within FAPbBr3 perovskite, promoting oriented crystallization and minimizing defects through halogen-halogen bond, but also optimizes the energy levels alignment at hole-selective interface for enhanced hole extraction. Ultimately, a power conversion efficiency (PCE) of 11.14% is achieved, which stands among the highest reported value for FAPbBr3 PSCs. Furthermore, the semitransparent devices/modules exhibit impressive PCEs of 8.19% and 6.23% with average visible transmittance of 41.98% and 38.99%. Remarkably, after operating at maximum power point for 1000 h, the encapsulated device maintains 93% of its initial PCE. These results demonstrate an effective strategy for achieving high-performance bromine-based PSCs toward further applications.

[Design of Remote Slit Lamp Diagnosis Platform Based on IoT Technology].

In order to realize the diagnosis of slit lamp in cross-regional patients and improve the real-time and convenience of diagnosis, a remote slit lamp diagnosis platform based on Internet of Things (IoT) technology is designed. Firstly, the feasibility of remote slit lamp is analyzed. Secondly, the IoT platform architecture of doctor/server/facility (D/S/F) is proposed and a remote slit lamp is designed. Finally, the performance of the remote slit lamp diagnostic platform is tested. The platform solves the communication problem of distributed slit lamps and realizes respectively numerical control of multi-area slit lamp by multi-eye experts. The test results show that the remote control delay of the platform is less than 20 ms, which supports multiple experts to diagnose multiple patients separately.

Pelagibacterium flavum sp. nov., Isolated from Soil Sample.

A Gram-stain-negative, yellow, moist and circular, aerobic, motile, and rod-shaped bacterium, designated YIM 151497T, was isolated from soil sample collected from Blue-Bridge, Weizhou Island, Guangxi province, China. Classification using a polyphasic approach suggested that strain YIM 151497T belonged to the genus Pelagibacterium, and was closely relevant to Pelagibacterium nitratireducens JLT2005T (98.8%), Pelagibacterium halotolerans CGMCC 1.7692T (98.7%), Pelagibacterium lixinzhangensis H64T (98.1%), and Pelagibacterium luteolum CGMCC 1.10267T (97.1%). The growth ranges of temperature, pH, and NaCl were 4-40 â„ƒ, pH 4.0-10.0, and 0-7% NaCl, respectively. It was positive for catalase and oxidase. The primary respiratory quinone was Q-10. The elemental fatty acids were Summed Feature 8 (constituting C18:1ω7c and/or C18:1ω6c), C19:0 cyclo ω8c, C16:0, and C18:1ω7c 11-methyl. The major polar lipids were phosphatidylglycerol, diphosphatidylglycerol, and three unidentified glycolipids. The DNA G+C content based on the complete genome sequence was 60.7 mol%. The average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) between strain YIM 151497T and species of Pelagibacterium were in the ranges of 73.9-86.3% and 19.7-31.3%, respectively. The Average Amino Acid Identity (AAI) between strain YIM 151497T and species of Pelagibacterium were in the ranges of 68.8-88.8%. On the basis of these data, strain YIM 151497T is considered to represent a novel species of the genus Pelagibacterium with the name of Pelagibacterium flavum sp. nov. Type strain is strain YIM 151497T (= KCTC 49826T = CGMCC 1.61521T = MCCC 1K08053T).

Marinimicrococcus flavescens gen. nov., sp. nov., a new member of the family Geminicoccaceae, isolated from a marine sediment of the South China Sea.

A Gram-stain-negative, catalase-positive and oxidase-positive, nonmotile, aerobic, light yellow, spherical-shaped bacterial strain with no flagella, designated strain YIM 152171T, was isolated from sediment of the South China Sea. Colonies were smooth and convex, light yellow and circular, and 1.0-1.5×1.0-1.5 µm in cell diameter after 7 days of incubation at 28°C on YIM38 media supplemented with sea salt. Colonies could grow at 20-45°C (optimum 28-35°C) and pH 6.0-11.0 (optimum, pH 7.0-9.0), and they could proliferate in the salinity range of 0-6.0 % (w/v) NaCl. The major cellular fatty acids were summed feature 8 (C18 : 1 ω7c/C18 : 1 ω6c), C18 : 1 ω7c 11-methyl, C16 : 0, C16 : 1 ω11c, C16 : 1 ω5c, C17 : 1 ω6c and C18 : 1 ω5c. The respiratory quinone was ubiquinone 10, and the polar lipid profile included diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol mannoside, one unidentified phospholipid and one unidentified aminolipid. Phylogenetic analyses based on the 16S rRNA gene sequences placed strain YIM 152171T within the order Rhodospirillales in a distinct lineage that also included the genus Geminicoccus. The 16S rRNA gene sequence similarities of YIM 152171T to those of Arboricoccus pini, Geminicoccus roseus and Constrictibacter antarcticus were 92.17, 89.25 and 88.91 %, respectively. The assembled draft genome of strain YIM 152171T had 136 contigs with an N50 value of 134704 nt, a total length of 3 001 346 bp and a G+C content of 70.27 mol%. The phylogenetic, phenotypic and chemotaxonomic data showed that strain YIM 152171T (=MCCC 1K08488T=KCTC 92884T) represents a type of novel species and genus for which we propose the name Marinimicrococcus gen. nov., sp. nov.

Toward High-Accuracy and Low-Latency Spiking Neural Networks With Two-Stage Optimization.

Spiking neural networks (SNNs) operating with asynchronous discrete events show higher energy efficiency with sparse computation. A popular approach for implementing deep SNNs is artificial neural network (ANN)-SNN conversion combining both efficient training of ANNs and efficient inference of SNNs. However, the accuracy loss is usually nonnegligible, especially under few time steps, which restricts the applications of SNN on latency-sensitive edge devices greatly. In this article, we first identify that such performance degradation stems from the misrepresentation of the negative or overflow residual membrane potential in SNNs. Inspired by this, we decompose the conversion error into three parts: quantization error, clipping error, and residual membrane potential representation error. With such insights, we propose a two-stage conversion algorithm to minimize those errors, respectively. In addition, we show that each stage achieves significant performance gains in a complementary manner. By evaluating on challenging datasets including CIFAR-10, CIFAR-100, and ImageNet, the proposed method demonstrates the state-of-the-art performance in terms of accuracy, latency, and energy preservation. Furthermore, our method is evaluated using a more challenging object detection task, revealing notable gains in regression performance under ultralow latency, when compared with existing spike-based detection algorithms. Codes will be available at: https://github.com/Windere/snn-cvt-dual-phase.

Acinetobacter faecalis Sp. Nov., Isolated from Elephant Faeces.

A Gram-negative coccobacillus, YIM 103518T, isolated from wild elephant feces in Xishuangbanna, Yunnan Province, West China, was characterized and identified using a polyphasic taxonomic approach. The strain was strictly aerobic, non-motile, catalase-positive and oxidase-negative, colonies were round, convex, smooth, and pale yellow. The strain growth at 4-40 ℃ (optimum, 28 ℃), pH 6.0-10.0 (optimum, pH 7.0) and 0-4% NaCl (optimum, 0%) in culture medium YIM 38. The major fatty acids of strain YIM 103518T were summed feature 3 (C16:1 ω6c/C16:1 ω7c), C16:0, and C18:1 ω9c. The predominant ubiquinone was Q-9. The major polar lipids were diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylcholine and phospholipids. The 16S rRNA gene sequence showed moderate level of similarity with Acinetobacter portensis AC 877T (98.7%), Acinetobacter sichuanensis CCTCC AB 2018118T (97.1%), and Acinetobacter cumulans CCTCC AB 2018119T (97.1%). The G+C content of the genomic DNA was 36.5 mol%. Strain YIM 103518T showed an average nucleotide identity value of 86.6%, 77.3% and 78.5%, a digital DNA-DNA hybridizations value of 31.2%, 21.9% and 23.0% with the type strain of A. portensis, A. sichuanensis and A. cumulans based on draft genome sequences, respectively. The results of the phenotypic, chemotaxonomic and phylogenetic analyses, showed that strain YIM 103518T represents a novel species of the genus Acinetobacter, for which the name Acinetobacter faecalis sp. nov. is proposed. The type strain is YIM 103518T (=CCTCC AB 2019201T = NBRC 114057T).

Training Deep Convolutional Spiking Neural Networks With Spike Probabilistic Global Pooling.

Recent work on spiking neural networks (SNNs) has focused on achieving deep architectures. They commonly use backpropagation (BP) to train SNNs directly, which allows SNNs to go deeper and achieve higher performance. However, the BP training procedure is computing intensive and complicated by many trainable parameters. Inspired by global pooling in convolutional neural networks (CNNs), we present the spike probabilistic global pooling (SPGP) method based on a probability function for training deep convolutional SNNs. It aims to remove the difficulty of too many trainable parameters brought by multiple layers in the training process, which can reduce the risk of overfitting and get better performance for deep SNNs (DSNNs). We use the discrete leaky-integrate-fire model and the spatiotemporal BP algorithm for training DSNNs directly. As a result, our model trained with the SPGP method achieves competitive performance compared to the existing DSNNs on image and neuromorphic data sets while minimizing the number of trainable parameters. In addition, the proposed SPGP method shows its effectiveness in performance improvement, convergence, and generalization ability.

Cationic Cyclopropenium-Based Hyper-Crosslinked Polymer Enhanced Polyethylene Oxide Composite Electrolyte for All-Solid-State Li-S Battery.

The development of solid-state polymer electrolytes is an effective way to overcome the notorious shuttle effect of polysulfides in traditional liquid lithium sulfur batteries. In this paper, cationic cyclopropenium based cross-linked polymer was firstly prepared with the one pot method, and then the counter ion was replaced by TFSI- anion using simple ion replacement. Cationic cyclopropenium hyper-crosslinked polymer (HP) was introduced into a polyethylene oxide (PEO) matrix with the solution casting method to prepare a composite polymer electrolyte membrane. By adding HP@TFSI to the PEO-based electrolyte, the mechanical and electrochemical properties of the solid-state lithium-sulfur batteries were significantly improved. The PEO-20%HP@TFSI electrolyte shows the highest Li+ ionic conductivity at 60 °C (4.0 × 10-4 S·cm-1) and the highest mechanical strength. In the PEO matrix, uniform distribution of HP@TFSI inhibits crystallization and weakens the interaction between each PEO chain. Compared with pure PEO/LiTFSI electrolyte, the PEO-20%HP@TFSI electrolyte shows lower interface resistance and higher interface stability with lithium anode. The lithium sulfur battery based on the PEO-20%HP@TFSI electrolyte shows excellent electrochemical performance, high Coulombic efficiency and high cycle stability. After 500 cycles, the capacity of the lithium-sulfur battery based on PEO-20%HP@TFSI electrolytes keeps approximately 410 mAh·g-1 at 1 C, the Coulomb efficiency is close to 100%, and the cycle capacity decay rate is 0.082%.

Hydrogen-rich saline ameliorates hippocampal neuron apoptosis through up-regulating the expression of cystathionine ß-synthase (CBS) after cerebral ischemia- reperfusion in rats.

OBJECTIVES: This study aimed to evaluate the potential role of hydrogen in rats after cerebral ischemic/reperfusion (I/R) injury. MATERIALS AND METHODS: The experimental samples were composed of sham group, model group of rats that received middle cerebral artery occlusion (MCAO) for 2 hr followed by reperfusion for 24 hr, and the hydrogen saline group treated by hydro¬gen-rich saline (1 ml/kg) after MCAO. Hydrogen sulfide (H2S), S100-ßprotein (S100-ß), and neuron-specific enolase (NSE) levels were measured; the levels of malondialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD) were detected; the histologic structure and apoptotic cells of hippocampus were observed; the expressions of cystathionine ß-synthase (CBS), nuclear factor erythroid 2-related factor 2 (Nrf2), and hemeoxygenase-1 (HO-1) were measured. Statistical analyses were performed using one-way analysis of variance (ANOVA) followed by Fisher's least significant difference (LSD) test. RESULTS: Our results showed that hydrogen up-regulated H2S levels via promoting the expression of CBS in the hippocampus, and its treatment alleviated oxidative stress via activating the expression of Nrf2 and HO-1, and then cell apoptosis reduced, furthermore, brain function improved by down-regulating the levels of S100-ßand NSE. CONCLUSION: This study showed that hydrogen-rich saline ameliorates cell injury through up-regulating the expression of CBS in the hippocampus after cerebral ischemia reperfusion (I/R) in rats, this provides new experimental evidence for the treatment of stroke with hydrogen saline.

Endosulfan induces endothelial inflammation and dysfunction via IRE1α/NF-κB signaling pathway.

Cardiovascular diseases are related to vascular endothelial cell injury; our previous studies showed that endosulfan could cause hypercoagulation of blood by inducing endothelial cell injury. To clarify the mechanism of it, we treated human umbilical vein endothelial cells (HUVECs) with 0, 1, 5, and 10 µg/mL endosulfan, while in the inhibition groups, reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC, 3 mmol) and endoplasmic reticulum (ER) stress inhibitor (STF-083010, 10 µmol) were incubated prior to endosulfan. The results showed that endosulfan could induce inflammatory response and dysfunction by increasing the release of inflammatory cytokines such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) and endothelin-1 (ET-1), and inducing ROS production in HUVECs. We also found that endosulfan could cause ER damage, remarkably increase the expressions of inositol-requiring enzyme 1α (IRE1α), phosphorylated IRE1α (p-IRE1α), GRP78, XBP1, nuclear factor-kappa B (NF-κB), and phosphorylated NF-κB (p-NF-κB) in HUVECs. The presence of NAC antagonized the ROS production, expressions of IRE1α and p-IRE1α; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-κB, and p-NF-κB and attenuate IL-1ß, IL-6, TNF-α, VCAM-1, and ET-1 release induced by endosulfan. These results demonstrated that endosulfan-induced endothelial inflammation and dysfunction through the IRE1α/NF-κB signaling pathway may be triggered by oxidative stress. The study provided experimental basis for the correlation between environmental pollutants (endosulfan) and cardiovascular diseases.

Adiponectin alleviates blood hypercoagulability via inhibiting endothelial cell apoptosis induced by oxidative stress in septic rats.

OBJECTIVES: The purpose of this study was to detect the protective effects of adiponectin on coagulation dysfunction and its mechanism in sepsis of rats. MATERIALS AND METHODS: The experimental samples were composed of sham group, model group that was underwent cecal ligation and puncture (CLP) and three adiponectin treatment groups that treated by adiponectin with different dose (72 µg/kg, 96 µg/kg and 120 µg/kg) after CLP. The prothrombin time (PT), activated partial thromboplastin time (APTT) was measured, respectively, the level of malondialdehyde (MDA), tissue factor (TF), activated coagulation factor VIIa and Xa, p-selectin were detected, the histology structure of vascular was observed, the expressions of Caspase 9, Caspase 3, Bax, Bcl-2 and vWF in vascular were measured. RESULTS: The results demonstrated that adiponectin treatment lengthened PT and APTT, reduced the expression of MDA, TF, activated coagulation factor VIIa, Xa and p-selectin in plasma of septic rats. Additionally, adiponectin treatment alleviated endothelial cell apoptosis and oxidative stress, down-regulated the levels of Caspase 3, Caspase 9, Bax, Bcl-2 and vWF in vascular. CONCLUSION: These findings suggest that adiponectin treatment might be a promising therapeutic strategy for relieving septic endothelial cell injury and coagulation dysfunction via inhibiting endothelial cell apoptosis in septic rats.

Adiponectin is protective against endoplasmic reticulum stress-induced apoptosis of endothelial cells in sepsis.

Endoplasmic reticulum (ER) stress is a critical molecular mechanism involved in the pathogenesis of sepsis. Hence, strategies for alleviating this stress may be essential for preventing cardiovascular injuries under sepsis. Adiponectin is secreted by adipocytes and its levels are decreased in sepsis. The purpose of this study was to investigate the protective effects of adiponectin treatment on endothelial cells and its mechanism. Male Wistar rats underwent cecal ligation and puncture (CLP) before being treated with adiponectin (72 and 120 µg/kg). The levels of malondialdehyde (MDA) in plasma, histological structure, and apoptosis of endothelial cells were evaluated. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with adiponectin at 10 and 20 µg/mL for 24 h after stimulation by lipopolysaccharide (LPS). The levels of reactive oxygen species (ROS), ultrastructure, rate of apoptosis, the expression of inositol-requiring enzyme 1α (IRE1α) protein, and its downstream molecules (78 kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP), and caspase-12) were detected. The results showed that the levels of MDA and ROS induced by CLP or LPS stimulation were increased. Furthermore, endothelial cell apoptosis was increased under sepsis. The IRE1α pathway was initiated, as evidenced by activated IRE1α, increased GRP78, and up-regulated CHOP and caspase-12 in HUVECs. Following treatment with adiponectin, the number of apoptotic endothelial cells was markedly decreased. These findings demonstrated that treatment with adiponectin decreased apoptosis of endothelial cells caused by sepsis by attenuating the ER stress IRE1α pathway activated by oxidative stress.

Tetramethylpyrazine ameliorates experimental autoimmune encephalomyelitis by modulating the inflammatory response.

Multiple sclerosis (MS) is a disabling inflammatory and demyelinating disorder of the central nervous system. Tetramethylpyrazine (TMP) has been demonstrated to ameliorate cerebral ischemic injury and spinal cord injury by inhibiting inflammatory cell activation and pro-inflammatory cytokine production. However, the effects of TMP on MS have not been studied. In this study, we evaluated the effects of TMP on the inflammatory response in experimental autoimmune encephalomyelitis (EAE), which is an animal model of MS. TMP (30 mg/kg) treatment significantly reduced the expression levels of NLR Family, Pyrin Domain-Containing 3 Protein inflammasome and caspase-1and decreased inflammatory infiltration and glial activation. Moreover, TMP (30 mg/kg) suppressed the expression of pro-inflammatory cytokines (interleukin-18 [IL-18] and IL-17) and promoted the expression of an anti-inflammatory cytokine (IL-10). The reduced inflammatory response resulted in improvement in clinical scores and decreased demyelination in EAE mice. Therefore, our results demonstrate that TMP (30 mg/kg) improved functional recovery in part by reducing inflammation in EAE mice. TMP may be a potential therapeutic agent for MS therapy.

Adiponectin is protective against endoplasmic reticulum stress-induced apoptosis of endothelial cells in sepsis

Endoplasmic reticulum (ER) stress is a critical molecular mechanism involved in the pathogenesis of sepsis. Hence, strategies for alleviating this stress may be essential for preventing cardiovascular injuries under sepsis. Adiponectin is secreted by adipocytes and its levels are decreased in sepsis. The purpose of this study was to investigate the protective effects of adiponectin treatment on endothelial cells and its mechanism. Male Wistar rats underwent cecal ligation and puncture (CLP) before being treated with adiponectin (72 and 120 μg/kg). The levels of malondialdehyde (MDA) in plasma, histological structure, and apoptosis of endothelial cells were evaluated. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with adiponectin at 10 and 20 μg/mL for 24 h after stimulation by lipopolysaccharide (LPS). The levels of reactive oxygen species (ROS), ultrastructure, rate of apoptosis, the expression of inositol-requiring enzyme 1α (IRE1α) protein, and its downstream molecules (78 kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP), and caspase-12) were detected. The results showed that the levels of MDA and ROS induced by CLP or LPS stimulation were increased. Furthermore, endothelial cell apoptosis was increased under sepsis. The IRE1α pathway was initiated, as evidenced by activated IRE1α, increased GRP78, and up-regulated CHOP and caspase-12 in HUVECs. Following treatment with adiponectin, the number of apoptotic endothelial cells was markedly decreased. These findings demonstrated that treatment with adiponectin decreased apoptosis of endothelial cells caused by sepsis by attenuating the ER stress IRE1α pathway activated by oxidative stress.

Spirometric prediction equations and the relationship between metabolic syndrome and spirometric parameters from an island in Fujian, China.

BACKGROUND: We investigated risk factors for decreased lung function among Chinese island residents (≥30 years) to determine the relationship between metabolic syndrome (MS) and decreased lung function. METHODS: From October 17, 2011 to November 1, 2011, 2607 residents aged ≥30 years who lived on the Huangqi Peninsula of Fujian were enlisted by random cluster sampling. They completed a questionnaire designed according to the Burden of Obstructive Lung Disease (BOLD) questionnaire, and underwent physical examination, blood test, and lung function evaluation. We constructed spirometric prediction equations for forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), determined the lower limits of normal for FVC, FEV1 and FEV1/FVC, and examined the relationship between lung function and MS. RESULTS: Prediction equations for normal island residents were as follows: FVC (L) = -0.023 × age (years) + 0.042 × height (cm) + 0.641 × weight (kg) - 3.607 (males); FVC (L) = -0.017 × age (years) + 0.030 × height (cm) + 0.009 × weight (kg) - 1.741 (females); FEV1 (L) = -0.023 × age (years) + 0.040 × height (cm) + 0.010 × weight (kg) - 2.999 (males); FEV1 (L) = -0.017 × age (years) + 0.026 × height (cm) + 0.007 × weight (kg) -1.135 (females). The odds ratio for MS for increased risk of decreased FVC was 4.623 (95%CI =3.626-5.894, P<0.001), and for increased risk of decreased FEV1 was 3.043 (95%CI =2.447-3.785, P<0.001). CONCLUSIONS: MS is a risk factor for decreased lung function in island residents ≥30 years old.

Endosulfan inhibiting the meiosis process via depressing expressions of regulatory factors and causing cell cycle arrest in spermatogenic cells.

Endosulfan is a persistent organic pollutant and widely used in agriculture as a pesticide. It is present in air, water, and soil worldwide; therefore, it is a health risk affecting especially the reproductive system. The aim of this study was to evaluate the toxicity of endosulfan in the reproductive system. To investigate the effect of endosulfan on meiosis process, 32 rats were divided into four groups, treated with 0, 1, 5, and 10 mg/kg/day endosulfan, respectively, and sacrificed after the 21 days of treatments. Results show that endosulfan caused the reductions in sperm concentration and motility rate, which resulted into an increased in sperm abnormality rate; further, endosulfan induced downregulation of spermatogenesis- and oogenesis-specific basic helix-loop-helix transcription factor (Sohlh1) which controls the switch on meiosis in mammals, as well cyclin A1, cyclin-dependent kinases 1 (CDK1), and cyclin-dependent kinases 2 (CDK2). In vitro, endosulfan induced G2/M phase arrest in the spermatogenic cell cycle and caused proliferation inhibition. Moreover, endosulfan induced oxidative stress and DNA damage in vivo and vitro. The results suggested that endosulfan could inhibit the start of meiosis by downregulating the expression of Sohlh1 and induce G2/M phase arrest of cell cycle by decreasing the expression of cyclin A1, CDK1, and CDK2 via oxidative damage, which inhibits the meiosis process, and therefore decrease the amount of sperm.

Retinoic acid amide inhibits JAK/STAT pathway in lung cancer which leads to apoptosis.

Small cell lung cancer (SCLC) accounts for 12 to 16% of lung neoplasms and has a high rate of metastasis. The present study demonstrates the antiproliferative effect of retinoic acid amide in vitro and in vivo against human lung cancer cells. The results from MTT assay showed a significant growth inhibition of six tested lung cancer cell lines and inhibition of clonogenic growth at 30 µM. Retinoic acid amide also leads to G2/M-phase cell cycle arrest and apoptosis of lung cancer cells. It caused inhibition of JAK2, STAT3, and STAT5, increased the level of p21WAF1, and decreased cyclin A, cyclin B1, and Bcl-XL expression. Retinoic acid amide exhibited a synergistic effect on antiproliferative effects of methotrexate in lung cancer cells. In lung tumor xenografts, the tumor volume was decreased by 82.4% compared to controls. The retinoic acid amide-treated tumors showed inhibition of JAK2/STAT3 activation and Bcl-XL expression. There was also increase in expression of caspase-3 and caspase-9 in tumors on treatment with retinoic acid amide. Thus, retinoic acid amide exhibits promising antiproliferative effects against human lung cancer cells in vitro and in vivo and enhances the antiproliferative effect of methotrexate.

Risk factors for small airway obstruction among Chinese island residents: a case-control study.

BACKGROUND: We investigated the prevalence of and risk factors for small airway obstruction (SAO) among Chinese island residents to establish means to prevent and treat SAO. METHODS: From October 17, 2011 to November 1, 2011, a total of 2,873 residents aged >20 years who lived on the Huangqi Peninsula of Fujian were recruited by random cluster sampling. They were asked to complete a Burden of Obstructive Lung Disease (BOLD) questionnaire and underwent physical examinations and lung function evaluations. SAO was defined as a forced expiratory flow at 50% of vital capacity, Vmax50%, of less than 70% of predicted. Risk factors for SAO were assessed from among demographic and anthropometric variables, blood chemistry results, and questionnaire response items. RESULTS: A total of 216 (7.52%) Chinese island residents were identified as having SAO (95 males; 121 females). Their survey and test results were compared with 432 age and sex-matched healthy controls (192 males; 240 females) for SAO risk factors. Among numerous factors investigated, only diabetes mellitus (p = 0.039), smoking index (SI, p<0.001 for SI>600), second hand smoke (p = 0.002), and lack of regular exercise (p<0.001) were significant risk factors for SAO. CONCLUSIONS: The risk factors for SAO among Chinese island residents appeared to be similar to those among people who live in high-density urban environments and impoverished rural areas. Public health policies and medical practices directed toward improving respiratory health for island residents should be comparable to those used for urban and rural dwellers.

[A case-control study on the risk factors for lower respiratory tract infection by Stenotrophomonas maltophilia in a medical intensive care unit].

OBJECTIVE: To explore the risk factors for lower respiratory tract infection by Stenotrophomonas maltophilia in the medical intensive care unit (MICU) in Fujian Provincial Hospital. METHODS: A 1:4 matched case-control study was carried out in the MICU in Fujian Provincial Hospital. Thirty-five patients with hospital-acquired lower respiratory tract infection by Stenotrophomonas maltophilia from 2007 to 2010 were included as cases, and 140 patients without lower respiratory tract infection served as controls. The case group included 22 cases with respiratory diseases, 4 with cerebrovascular diseases, 4 with cardiovascular diseases, 1 with hemorrhage of the digestive tract, 1 with acute pancreatitis, 1 with chronic kidney disease, 1 with cervical cancer and 1 with Alzheimer's disease. While the control group included 30 cases with respiratory diseases, 44 with cerebrovascular diseases, 14 with cardiovascular diseases, 2 with malignant tumors and 50 with others. Patients' information, general situation before being admitted to MICU, drug therapy, invasive procedures and hospital-acquired infection were analyzed. Conditional logistic regression was performed to identify independent risk factors. RESULTS: Univariate analysis showed that factors such as more than 4 underlying diseases (OR = 4.63), APACHE-II score ≥ 20(OR = 10.29), stay in the general ward more than 1 week before being admitted to MICU, treatment with more than 3 kinds of antibiotics (OR = 8.03), endotracheal intubation (OR = 4.10) or tracheotomy (OR = 50.29) and mechanical ventilation (OR = 7.95) were risk factors for hospital-acquired lower respiratory tract infection by Stenotrophomonas maltophilia. Multivariate logistic regression showed that variables such as APACHE-II score (OR = 8.39), kinds of antibiotics used (OR = 5.96) and tracheotomy (OR = 28.92) were independent risk factors (P < 0.01). CONCLUSIONS: Underlying diseases, the severity of diseases, tracheotomy, mechanical ventilation, and the use of wide-spectrum antibiotics are important risk factors for lower respiratory tract infection by Stenotrophomonas maltophilia in MICU. To identify these factors and take preventive measures earlier may be useful for decreasing Stenotrophomonas maltophilia infection-related mortality.