Strengthened Surface Modification for High-Performance Inorganic Perovskite Solar Cells with 21.3% Efficiency.

Metal halide inorganic perovskites show excellent thermal stability compared to organic-inorganic perovskites. However, the performance of inorganic perovskite solar cells (PSCs) is far from theoretical values, together with unsatisfactory stability, mainly due to the poor interfacial properties. In this work, a facial but effective method is reported to realize high-performance inorganic PSCs by post-modifying the perovskite surface with 2-thiophene ethylamine (TEA). It is found that amine group from TEA can favorably interact with the undercoordinated Pb2+ via Lewis acid-based coordination, while thiophene ring with electron-rich sulfur assists such interaction by functioning as an electron donor. The synergetic interaction allows TEA to passivate perovskite film defects more efficiently, as compared to phenethylamine (PEA) with less electron-donating ability. Moreover, perovskite valence band is slightly upward shift to match with hole transport material and facilitate hole transfer. These combinations result in a reduced non-radiative charge recombination and improved charge carrier lifetime. Consequently, PSCs with TEA modification shows a drastic improvement of VOC by 54 mV, yielding a champion PCE of 21.3%, much higher than the control PSCs (19.3%), along with improved ambient stability. This work demonstrates that surface modifier with an electron-rich moiety is critical for achieving efficient and stable inorganic PSCs.

Ecological Effects of Predator Harvesting and Environmental Noises on Oceanic Coral Reefs.

Coral reefs provide refuge for prey and are important for the preservation of an oceanic ecosystem. However, they have been experiencing severe destruction by environmental changes and human activities. In this paper, we propose and analyze a tri-trophic food chain model consisting of coral, Crown-of-thorns starfish (CoTS), and triton in deterministic and stochastic environments. We investigate the effects of harvesting in the deterministic system and environmental noises in the stochastic system, respectively. The existence of possible steady states along with their stability is rigorously discussed. From the economic perspective, we examine the existence of the bionomic equilibrium and establish the optimal harvesting policy. Subsequently, the deterministic system is extended to a stochastic system through nonlinear perturbation. The stochastic system admits a unique positive global solution initiating from the interior of the positive quadrant. The long-time behaviors of the stochastic system are explored. Numerical simulations are provided to validate and complement our theoretical results. We show that over-harvesting of triton is not beneficial to coral reefs and modest harvesting of CoTS may promote sustainable growth in coral reefs. In addition, the presence of strong noises can lead to population extinction.

GATA-binding protein 4 promotes neuroinflammation and cognitive impairment in Aß1-42 fibril-infused rats through small nucleolar RNA host gene 1/miR-361-3p axis.

Aging with dysregulated metabolic and immune homeostasis stimulates pyroptosis, neuroinflammation, and cellular senescence, thus contributing to etiopathogenesis of Alzheimer's disease. GATA-binding protein 4 (GATA4) functions as a transcriptional factor in response to DNA damage, and is associated with neuroinflammation and cellular senescence. The role of GATA4 in Alzheimer's disease was investigated. GATA4 was elevated in hippocampus of Aß1-42 fibril-infused rats. Injection with shRNA targeting GATA4 reduced escape latency with increase of time in target quadrant and number of platform crossings in Aß1-42 fibril-infused rats. Moreover, knockdown of GATA4 ameliorated morphological changes of hippocampus and reduced amyloid plaque deposition in Aß1-42 fibril-infused rats. Silence of GATA4 repressed neuroinflammation and apoptosis in Aß1-42 fibril-infused rats. Loss of GATA4 in Aß1-42 fibril-infused rats reduced the expression of specificity protein 1 (Sp1) to downregulate long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) and upregulated miR-361-3p. Loss of SNHG1 ameliorated learning and memory impairments in Aß1-42 fibril-infused rats. Overexpression of Sp1 attenuated GATA4 silence-induced decrease of escape latency, increase of time in target quadrant, and number of platform crossings in Aß1-42 fibril-infused rats. In conclusion, silence of GATA4 ameliorated cognitive dysfunction and inhibited hippocampal inflammation and cell apoptosis through regulation of Sp1/SNHG1/miR-361-3p.

Layered Double Hydroxide-Based Micro "Chemical Factory" with Arsenic Processing and Screening Functions on Nitinol for Gallbladder Cancer Treatment.

Gallbladder cancer is a common malignant tumor of the biliary system with a high fatality rate. Nitinol (Ni-Ti) stents, a standard treatment for prolonging patients' lives, are susceptible to reocclusion and cannot inhibit tumor recurrence because they lack antitumor and antibacterial activity. Herein, an arsenic-loaded layered double-hydroxide film is constructed on Ni-Ti, forming a micro "chemical factory." The LDH plays the role of a "processer" which absorbs highly toxic trivalent arsenic (As(III)) and processes it into lowly toxic pentavalent arsenic (As(V)). It also acts as a "quality-inspector," confining As(III) in the interlayer and releasing only As(V) (the finished product) to the outside. This control mechanism minimizes the toxicity during contact with normal tissue. The acidic microenvironment and overexpression of glutathione in tumor tissues not only accelerates the release of arsenic from the platform but also triggers the in situ transformation of arsenic from lowly toxic As(V) to highly toxic As(III), exerting a strong arsenic-mediated antineoplastic effect. Such a microenvironment-responsive "chemical factory" with arsenic processing and screening functions is expected to prevent tumor overgrowth, metastasis, and bacterial infection and provide new insights into the design of Ni-Ti drug-eluting stents for gallbladder cancer treatment.

Hypercholesterolemia aggravates sevoflurane-induced cognitive impairment in aged rats by inducing neurological inflammation and apoptosis.

We aimed to explore the effects of hypercholesterolemia on sevoflurane-induced cognitive impairment in aged rats and the underlying mechanism(s). Aged rats were administrated with high-fat diet, sevoflurane, or both. Thereafter, the plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were evaluated. The Morris water maze task was performed to evaluate the spatial learning and memory ability of rats. Moreover, Nissl and Evans blue staining were conducted to test nerve damage and detect the blood-brain barrier permeability, respectively. The percentage of apoptotic cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The messenger RNA expression of inflammatory factors and protein expression of microglial activation markers and apoptosis-related proteins were tested by real-time polymerase chain reaction, enzyme-linked immunosorbent assay, or western blot analysis, respectively. High-fat diet induced high levels of TC, TG, and LDL but decreased levels of HDL. However, sevoflurane had no effects on these levels. In contrast, sevoflurane significantly induced the impairment of learning and memory, nerve damage, neuroinflammatory damage, and neuronal apoptosis. Hypercholesterolemia exacerbated the sevoflurane-induced impairment in aged rats. These results suggested that hypercholesterolemia aggravates sevoflurane-induced cognitive impairment in aged rats, possibly by inducing neurological inflammation and apoptosis.

Huaier shows anti-cancer activities by inhibition of cell growth, migration and energy metabolism in lung cancer through PI3K/AKT/HIF-1α pathway.

Huaier has been verified to have anti-cancer effects on many tumours. However, little information is available about the effects of Huaier on non-small cell lung cancer (NSCLC). We sought to probe the anti-cancer effects and related mechanisms of Huaier on lung cancer. A549 cells were pre-treated with 2, 4 and 8 mg/mL Huaier at different time points. Thereafter, cell viability was analysed by CCK-8 and the migration and invasion were detected by Scratch test and Transwell chamber migration assay. Moreover, ELISA, Western blot, shRNA transfection and RT-PCR were conducted to discover the related gene and protein expressions of energy metabolism and phosphatidylinositol 3-kinase (PI3K)/AKT/hypoxia-inducible factor 1α (HIF-1α) pathway. Furthermore, tumour xenografts were accomplished to inspect the anti-cancer effects of Huaier. Our consequences suggested that Huaier considerably repressed cell viability and migration in a dose-dependent way. In addition, Huaier statistically suppressed glycolysis, glucose transport and lactic acid (LA) accumulation. Besides, we detected that Huaier could inactivate the PI3K/AKT/HIF-1α pathway. The in vivo data confirmed that Huaier obviously decreased tumour volume and tumour growth, reduced the glycolysis, glucose transport and HIF-1α expression in the tumour-bearing tissues. Our results suggested Huaier revealed anti-tumour effects in both in vivo and in vitro possibly through PI3K/AKT/HIF-1α pathway.

A primate-specific RNA-binding protein (RBMXL3) is involved in glucocorticoid regulation of human pulmonary surfactant protein B (SP-B) mRNA stability.

The ability of pulmonary surfactant to reduce alveolar surface tension requires adequate levels of surfactant protein B (SP-B). Dexamethasone (DEX) increases human SP-B expression, in part, through increased SP-B mRNA stability. A 30-nt-long hairpin element (RBE) in the 3'-untranslated region of human SP-B mRNA mediates both DEX-induced and intrinsic mRNA stabilities, but the mechanism is unknown. Proteomic analysis of RBE-interacting proteins identified a primate-specific protein, RNA-binding motif X-linked-like-3 (RBMXL3). siRNA directed against RBMXL3 reduces DEX-induced SP-B mRNA expression in human bronchoalveolar cells. Human SP-B mRNA stability, measured by our dual cistronic plasmid assay, is unaffected by DEX in mouse lung epithelial cells lacking RBMXL3, but DEX increases human SP-B mRNA stability when RBMXL3 is expressed and requires the RBE. In the absence of DEX, RBE interacts with cellular proteins, reducing intrinsic SP-B mRNA stability in human and mouse lung epithelial cells. RBMXL3 specifically binds the RBE in vitro, whereas RNA immunoprecipitation and affinity chromatography analyses indicate that binding is enhanced in the presence of DEX. These results describe a model where intrinsic stability of human SP-B mRNA is reduced through binding of cellular mRNA decay factors to RBE, which is then relieved through DEX-enhanced binding of primate-specific RBMXL3.

An internal amino-terminal FLAG-tag octapeptide alters oligomerization of expressed surfactant protein-A.

Pulmonary surfactant protein-A (SP-A) is expressed by lung alveolar and bronchiolar epithelial cells and plays a critical role in innate immunity of the lung. Exposure of the lung to various environmental insults alters SP-A homeostasis. To investigate the cellular mechanisms involved in these alterations, we added the FLAG octapeptide (DYKDDDDK) to the carboxy-terminus (SP-A/C-FLAG) or near the amino-terminus (SP-A/N-FLAG) of mouse SP-A (WT-SP-A) to tag specific pools of protein. We hypothesized that addition of FLAG would have negligible effects on SP-A expression, oligomerization and secretion. Analysis of Chinese hamster ovary cells expressing these proteins indicated that tagged SP-A mRNA could be distinguished from WT-SP-A by northern analysis and RT-PCR using sequence-specific oligonucleotides. Tagged SP-A protein could be differentiated from WT-SP-A by western analysis using antibodies specific for the FLAG epitope. Subcellular fractionation and immunocytochemistry indicated the majority of each protein was present in punctuate (presumably endocytic) vesicles, and all forms of SP-A protein were secreted. These results suggest that a FLAG epitope added to the carboxy-terminus or inserted into the amino-terminus of the mature SP-A protein has little effect on its expression and cellular processing. However, disruptions of the amino-terminal end of SP-A prevents proper oligomerization, suggesting that this region of mature SP-A is critical in proper oligomeric assembly and is not useful for studies intended to define mechanisms underlying SP-A homeostasis.

The Median Effective Dose of One Intravenous Bolus of Oxycodone for Postoperative Analgesia After Myomectomy and Hysterectomy With Local Ropivacaine Wound Infiltration: An Up-Down Dose-Finding Study.

BACKGROUND: Oxycodone has been shown to be an effective analgesic for early postoperative analgesia, especially for abdominal operations associated with severe visceral pain. However, the dose needed varies depending on the operation and application of multimodal analgesia, such as local ropivacaine wound infiltration. Therefore, we conducted this study to estimate the median effective dose (ED50) of oxycodone that provides analgesia for hysterectomy and myomectomy with local ropivacaine wound infiltration. METHODS: In this dose-finding study, the ED50 of oxycodone for postoperative analgesia was estimated separately for laparoscopic hysterectomy, transabdominal hysterectomy, laparoscopic myomectomy, and transabdominal myomectomy. We used the sequential allocation designed by Dixon. Trials were conducted simultaneously in the 4 surgical type groups. A predefined dose of oxycodone was injected 30 minutes before the end of the operation with an initial dose of 0.1 mg/kg. A series of trials were performed following the rule of a relative 10% increase in dose after inadequate analgesia and a relative 10% decrease in dose after adequate analgesia. The study was conducted until the collection of 7 crossover points was achieved. Local ropivacaine wound infiltration was administered during abdominal stitching. The mean blood pressure (MBP) and heart rate (HR) were analyzed to assess the hemodynamic changes associated with oxycodone administration. RESULTS: A total of 113 patients were included in the estimation of ED50: 28 each in the laparoscopic hysterectomy group and transabdominal myomectomy group, 27 in the transabdominal hysterectomy group, and 30 in the laparoscopic myomectomy group. The estimated oxycodone ED50 (95% confidence interval [CI]) after laparoscopic hysterectomy, transabdominal hysterectomy, laparoscopic myomectomy, and transabdominal myomectomy was 0.060 mg/kg (0.053-0.068), 0.079 mg/kg (0.072-0.086), 0.060 mg/kg (0.051-0.071), and 0.092 mg/kg (0.086-0.098), respectively, for postoperative analgesia with local ropivacaine wound infiltration. The ED50 of oxycodone was different between laparoscopic surgeries and transabdominal surgeries (P < .001). The MBP and HR before and after oxycodone injection were different, regardless of surgical type. CONCLUSIONS: The oxycodone ED50 for postoperative analgesia was lower for laparoscopic hysterectomy (0.060 mg/kg) and laparoscopic myomectomy (0.060 mg/kg) than for transabdominal hysterectomy (0.079 mg/kg) and transabdominal myomectomy (0.092 mg/kg) when combined with local ropivacaine wound infiltration. A single intravenous injection of oxycodone is associated with an acceptable decrease in MBP and HR within a short time.

IMRT combined with S-1 concurrent chemoradiotherapy in locally advanced nasopharyngeal carcinoma: a prospective phase II study.

Purpose The current standard treatment for locally advanced nasopharyngeal carcinoma (LANPC) is intensity-modulated radiation therapy (IMRT) plus cisplatin concurrent chemoradiotherapy (CCRT). However, this regimen has well-known hematological and gastrointestinal toxicities. Many studies have reported that S-1 was effective in the treatment of multiple solid cancers with mild toxicities. However, knowledge regarding IMRT plus S-1 CCRT in LANPC is lacking. Therefore, we conducted this prospective phase II trial to evaluate the efficacy and safety of this regimen in LANPC. Patients and Methods Eligible patients with histologically confirmed LANPC were enrolled in this study. IMRT was given in 30-32 fractions five times per week. Concurrently, S-1 was administrated twice per day orally based on the body surface area (BSA < 1.25 m2, 30 mg; BSA: 1.25-1.5 m2, 40 mg; BSA > 1.5 m2, 50 mg). The primary endpoints were progression-free survival (PFS) and adverse events. Results From August 1, 2013, to December 15, 2017, 131 patients were enrolled in this study. The distribution of disease stages among the patients was as follows: 21 patients were in stage II (16.0%), 42 patients were in stage III (32.0%), and 68 patients were in stage IV (52.0%). After CCRT, the 3-year PFS, overall survival (OS), local recurrence-free survival (LRFS) and distant metastasis-free survival (DMFS) rates were 87.4%, 95.7%, 94.7%, and 91.5%, respectively. The severity of most toxicities was mild. Approximately two-thirds of patients had no hematological toxicity. Grade 2 hematological toxicities included leukopenia (11.5%), anemia (1.5%), and thrombocytopenia (0.8%). Grade 3 hematological toxicities were rarely observed. Conclusion The results demonstrated that IMRT plus S-1 CCRT was effective with mild toxicity for patients with LANPC.

Deregulated MYC expression induces dependence upon AMPK-related kinase 5.

Deregulated expression of the MYC oncoprotein contributes to the genesis of many human tumours, yet strategies to exploit this for a rational tumour therapy are scarce. MYC promotes cell growth and proliferation, and alters cellular metabolism to enhance the provision of precursors for phospholipids and cellular macromolecules. Here we show in human and murine cell lines that oncogenic levels of MYC establish a dependence on AMPK-related kinase 5 (ARK5; also known as NUAK1) for maintaining metabolic homeostasis and for cell survival. ARK5 is an upstream regulator of AMPK and limits protein synthesis via inhibition of the mammalian target of rapamycin 1 (mTORC1) signalling pathway. ARK5 also maintains expression of mitochondrial respiratory chain complexes and respiratory capacity, which is required for efficient glutamine metabolism. Inhibition of ARK5 leads to a collapse of cellular ATP levels in cells expressing deregulated MYC, inducing multiple pro-apoptotic responses as a secondary consequence. Depletion of ARK5 prolongs survival in MYC-driven mouse models of hepatocellular carcinoma, demonstrating that targeting cellular energy homeostasis is a valid therapeutic strategy to eliminate tumour cells that express deregulated MYC.

Sevoflurane Exacerbates Cognitive Impairment Induced by Aß 1-40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus.

OBJECTIVE: This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event. METHODS: Thirty-two rats were randomly divided into four groups of normal saline (NS) + O2, NS + sevoflurane (sevo), amyloid-ß peptide (Aß) + O2, and Aß + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or Aß. The treated hippocampus was harvested after inhaling 30% O2 or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an Aß 1-42 level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR. RESULTS: Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of Aß 1-42 of the brain in the Aß-treated group. Sevoflurane inhalation but not O2 significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in Aß-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled O2 and sevoflurane in Aß-treated groups (all P < 0.05). Interleukin- (IL-) 1ß, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) mRNA expression increased after the rats inhaled sevoflurane in the Aß-treated group (both P < 0.01). There were no significant differences in the change of GFAP, IBA1, Bcl-xL, caspase-9, RAGE, BDNF, IL-1ß, NF-κB, and iNOS in the NS + O2 and NS + sevo group (all P > 0.05). CONCLUSION: Sevoflurane exacerbates cognitive impairment induced by Aß 1-40 in rats through initiating neurotoxicity, neuroinflammation, and neuronal apoptosis in rat hippocampus.

Hydrogen-Rich Saline Attenuates Brain Injury Induced by Cardiopulmonary Bypass and Inhibits Microvascular Endothelial Cell Apoptosis Via the PI3K/Akt/GSK3ß Signaling Pathway in Rats.

BACKGROUND/AIMS: Cardiopulmonary bypass (CPB) is prone to inducing brain injury during open heart surgery. A hydrogen-rich solution (HRS) can prevent oxidation and apoptosis, and inhibit inflammation. This study investigated effects of HRS on brain injury induced by CPB and regulatory mechanisms of the PI3K/Akt/GSK3ß signaling pathway. METHODS: A rat CPB model and an in vitro cell hypoxia model were established. After HRS treatment, Rat behavior was measured using neurological deficit score; Evans blue (EB) was used to assess permeability of the blood-brain barrier (BBB); HE staining was used to observe pathological changes; Inflammatory factors and brain injury markers were detected by ELISA; the PI3K/Akt/GSK3ß pathway-related proteins and apoptosis were assessed by western blot, immunohistochemistry and qRT -PCR analyses of brain tissue and neurons. RESULTS: After CPB, brain tissue anatomy was disordered, and cell structure was abnormal. Brain tissue EB content increased. There was an increase in the number of apoptotic cells, an increase in expression of Bax and caspase-3, a decrease in expression of Bcl2, and increases in levels of Akt, GSK3ß, P-Akt, and P-GSK3ß in brain tissue. HRS treatment attenuated the inflammatory reaction ,brain tissue EB content was significantly reduced and significantly decreased expression levels of Bax, caspase-3, Akt, GSK3ß, P-Akt, and P-GSK3ß in the brain. After adding the PI3K signaling pathway inhibitor, LY294002, to rat cerebral microvascular endothelial cells (CMECs), HRS could reduce activated Akt expression and downstream regulatory gene phosphorylation of GSK3ß expression, and inhibit CMEC apoptosis. CONCLUSION: The PI3K/Akt/GSK3ß signaling pathway plays an important role in the mechanism of CPB-induced brain injury. HRS can reduce CPB-induced brain injury and inhibit CMEC apoptosis through the PI3K/Akt/GSK3ß signaling pathway.

Relationship between mammalian target of rapamycin and autophagy in lipopolysaccharide-induced lung injury.

BACKGROUND: To investigate the relationship between the mammalian target of rapamycin (mTOR) signaling pathway and autophagy in lung tissue cells in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. MATERIALS AND METHODS: Thirty-two male C57BL/6 mice were randomly assigned to four different treatment groups: control (C), LPS (L), rapamycin (R), and LPS + rapamycin (LR). Optical and electron microscopy were used to detect lung injury and autophagy. Tumor necrosis factor alpha, interleukin 6, and p62 in lung tissues and IgM concentrations and total protein in bronchoalveolar lavage fluid were evaluated using enzyme-linked immunosorbent assay. LC3Ⅱ, LC3Ⅰ, ribosomal protein p70S6 kinase1 (p70S6K1), and phosphorylation of ribosomal protein p70S6 kinase1(P-p70S6K1) in lung tissues were measured by Western blot. RESULTS: The L group had an increased ALI index (P < 0.05) compared with the C group, but there were no differences between the L and the LR groups or the C and R groups (all P > 0.05). According to the index of autophagy, the L, the R and C groups, the level of autophagy were in descending order (P < 0.05), there were no differences between the L and the LR groups (P > 0.05). The expression of P-p70S6K1 declined after rapamycin treatment, showing that the signaling pathway of mTOR is inhibited by rapamycin. CONCLUSIONS: LPS could trigger the mTOR signaling pathway and autophagy of lung tissue cells in LPS-induced ALI in mice; The mTOR signaling pathway did not play a major role in lung injury and autophagy of lung tissue cells induced by LPS.

Effects of hydrogen-rich saline on aquaporin 1, 5 in septic rat lungs.

Aquaporin 1(AQP1) and AQP5 have an important role in eliminating extravascular lung water, an increase of which contributes to lung injury in patients with sepsis and its consequent mortality. It has been reported that hydrogen-rich saline (HRS) has protective effects against sepsis-related lung injury. In this study, we hypothesized that the protective effect occurred by preserving the expression of AQP1 and AQP5. To test this hypothesis, male Sprague-Dawley rats received intratracheal administration of lipopolysaccharide (LPS) followed by intraperitoneal injection of HRS. Lung function, wet-to-dry weight ratio, and histopathology scores were determined. The expression of AQP1 and AQP5 at the messenger RNA and protein levels, as well as the involved pathways, was explored by quantitative polymerase chain reaction and Western blot. LPS significantly impaired lung function and downregulated the expression of AQP1 and AQP5 in the rat lung, all of which were attenuated by HRS treatment. Moreover, HRS treatment inhibited LPS-induced activation of p38 mitogen-activated protein kinase and jun N-terminal kinase, which is associated with LPS-induced downregulation of AQP1 and AQP5.

Observation of the excretion pattern of a precocious line of Eimeria necatrix and the strengthening of immune homogeneity.

The excretion frequencies of cecal and intestinal droppings of Chinese Lingnan yellow chickens were observed for 10 consecutive days. The chickens were then orally inoculated with a precocious line of Eimeria necatrix, and the oocysts present in the cecal and intestinal droppings were separately collected and monitored using the McMaster method. The results showed that the excretion frequency of cecal droppings was significantly lower than that of intestinal droppings, and the oocysts of E. necatrix were distributed primarily in the cecal droppings. This distribution affects the homogeneity of the second and third generation of oocysts ingested by the chickens and therefore affects the immune effect observed during E. necatrix immunization. To artificially strengthen the immunologic homogeneity against E. necatrix, a method of artificially strengthening the second immunization was applied, and the immune effect was evaluated based on oocyst excretion, body weight gain, fecal scores, intestinal lesion scores and survival percentages. The results showed that no significant intestinal damage was caused by immunization reactions in the chickens. In addition, the number of excreted oocysts in the immunized chicken groups could be significantly increased, and the immunologic homogeneity of the immunized chickens could be improved by artificially strengthening the second immunization, which could in turn improve the immune protective effect.

Effective methods for extracting extracellular polymeric substances from Shewanella oneidensis MR-1.

Extracellular polymeric substances (EPS) play crucial roles in bio-aggregate formation and survival of bacterial cells. To develop an effective but harmless method for EPS extraction from Shewanella oneidensis MR-1, five extraction methods, i.e. centrifugation (control), heating (40, 45, 50, and 60 °C), and treatments with H2SO4, ethylenediaminetetraacetic acid (EDTA) and NaOH, were examined, respectively. Results from scanning electron microscope and flow cytometric analyses indicate that MR-1 cells were severely broken by H2SO4, NaOH and heating temperature ≥45 °C. Proteins and polysaccharides in EPS extracted by heating at 40 °C were 7.12 and 1.60 mg g-1 dry cell, respectively. Although EDTA treatment had a relatively lower yield of EPS (proteins and polysaccharides yields of 5.15 and 1.30 mg g-1 dry cell, respectively), cell lysis was barely found after EPS extraction. Three peaks were identified from the three-dimensional excitation-emission matrix spectrum of each EPS sample, suggesting the presence of protein-like substances. Furthermore, the peak intensity was in good accordance with protein concentration measured by the chemical analysis. In short, heating (40 °C) and EDTA treatments were found the most suitable methods for EPS extraction considering the cell lysis and EPS content, composition and functional groups together.

Biological characteristics of Chinese precocious strain of eimeria acervulina and its immune efficacy against different field strains.

In this study, the biologic characteristics of one experimental precocious strain of Eimeria acervulina and seven field isolates from different geographic locations in China were compared, and the immune efficacy of two precocious strains against coccidiosis in chickens was assessed to explore their potential use as coccidiosis vaccines. All the different strains were purified by single oocyst separation and their monospecificity was confirmed using E acervulina-specific PCR assays. The average sizes of E. acervulina oocysts were 18.28-20.19 X 14.09-14.79 microm and the shape indexes were from 1.28 to 1.40. The prepatent periods ranged from 93 to 115 hr, except for the Heyuan precocious strain (HYP; 75 hr). Chickens infected with Huadu field strain (GHD) produced the highest oocyst output whereas HYP induced the lowest level. When inoculated with 50,000 sporulated oocysts or more, the average weight gains of infected chickens were reduced, with apparent clinical symptoms. To assess the immunogenicity of precocious strains HYP and Baoding (BDP), birds were orally immunized and challenged with seven different field strains of E. acervulina. Body weight gain, fecal oocyst output, and gut lesion scores were compared to evaluate their vaccine potential. The results showed that the average body weight gains of chickens in all the vaccinated and challenged groups were higher than those of nonvaccinated and challenged groups. In general, oocyst shedding was reduced 34.39%-95.31% and gut lesion scores decreased 31.03%-86.21% compared with unvaccinated and challenged control chickens. In summary, this study indicated that the precocious strains of E. acervulina could induce a protective immune effect with various responses against coccidiosis caused by different field strains.

Polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) in water samples from the middle reaches of the Yangtze River, China.

Few studies have been conducted to investigate the polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) in freshwater since the volume of water needed for dioxin analysis is large. In this study, 19 water samples from the middle reaches of the Yangtze River were analysed for the levels of PCDD/Fs and dioxin-like PCBs (dl-PCBs). The results showed that the concentration ranges of PCDD/Fs and dl-PCBs were 0.6-8.5 and 2.0-15.8 pg/L, respectively, which were relatively low compared with those reported in the literature. The WHO-TEQ concentration range of dioxins was 0.002-0.040 pg/L. The PCA results indicated that the main sources of PCDD/Fs may be the applications of pentachlorophenol or sodium pentachlorophenate and domestic wood and coal burning. For dl-PCBs, domestic wood burning and coal burning were the main sources.

PFKFB3 Regulates the Growth and Migration of Ovarian Cancer Cells through Pyroptosis and Warburg Effect Progression.

Ovarian cancer is one of the most common malignant tumors in female reproductive organs. Its incidence rate is second only to uterine body cancer and cervical cancer, posing a serious threat to women's health. Herein, we explored that PFKFB3 in cancer progression of ovarian cancer and its underlying mechanism. All the serum samples from ovarian cancer were collected by our hospital. PFKFB3 mRNA expressions in patients with ovarian cancer and ovarian cancer cell lines were up-regulated. PFKFB3 protein expressions in ovarian cancer cells were induced. ovarian cancer patients with high PFKFB3expression had lower survival rate. The PFKFB3gene promoted cell proliferation and EDU cells, and increased cell metastasis of ovarian cancer. Si-PFKFB3 reduced cell proliferation and EDU cells, and decreased cell metastasis of ovarian cancer. PFKFB3 gene up-regulation reduced caspase-3/9 activity levels of ovarian cancer. Si-PFKFB3 also promoted caspase-3/9 activity levels of ovarian cancer. PFKFB3 gene promoted Warburg effect progression of ovarian cancer. PFKFB3 gene reduced NLRP3-induced pyroptosis of ovarian cancer. PFKFB3 suppressed NLRP3 expression. NLRP3 was one target spot for PFKFB3 on pyroptosis of ovarian cancer. Taken together, we conclude that PFKFB3 suppressed NLRP3 axis to reduce pyroptosis and increase Warburg effect progression of ovarian cancer, and provide molecular insight into the mechanisms by which the PFKFB3 regulates pyroptosis of ovarian cancer.