A simple and effective method to enrich endogenous DNA from mammalian faeces.

Utilization of faeces has long been a popular approach for genetic and ecological studies of wildlife. However, the success of molecular marker genotyping and genome resequencing is often unpredictable due to insufficient enrichment of endogenous DNA in the total faecal DNA that is dominated by bacterial DNA. Here, we report a simple and cheap method named PEERS to predominantly lyse animal cells over bacteria by using sodium dodecyl sulphate so as to discharge endogenous DNA into liquid phase before bacterial DNA. By brief centrifugation, total DNA with enriched endogenous fraction can be extracted from the supernatant using routine methods. Our assessments showed that the endogenous DNA extracted by PEERS was significantly enriched for various types of faeces from different species, preservation time and conditions. It significantly improves the genotyping correctness and efficiency of genome resequencing with the total additional cost of $ 0.1 and a short incubation step to treat a faecal sample. We also provide methods to assess the enrichment efficiency of mitochondrial and nuclear DNA and models to predict the usability of faecal DNA for genotyping of short tandem repeat, single-nucleotide polymorphism and whole-genome resequencing.

Fungal corneal ulcer after repair of an overhanging filtering bleb: A case report.

BACKGROUND: Overhanging filtering bleb is a common complication after trabeculectomy and surgical repair is an effective treatment when the patient presents with apparent symptoms. Filtering bleb relevant infection including in the filtering bleb itself and even endophthalmitis in some severe cases has been reported. However, corneal fungal infection after filtering bleb repair is rarely reported. CASE SUMMARY: A 57-year-old Chinese man who had sensations of redness and foreign body sensations in the left eye 3 wk after repair of overhanging filtering bleb. 3 wk ago, due to sensations of a foreign body in the left eye for 3 years with worsening for 3 mo. The patient was diagnosed as overhanging filtering bleb and underwent a repair of overhanging filtering bleb. Postoperative, the filtering bleb formed well and the intraocular pressure is normal. But the patient gradually develop redness, pain and a grey infiltrate of the cornea in the eye. Finally it developed into fungal corneal ulcer. Through asking the medical history, we found the patient had irregularly self-medicated for years with glucocorticoid eye drops for years to relieve the foreign body sensation in the eye caused by filtering bleb overhanging. Because the glucocorticoid eye drops he used years ago had provide normal sensation to the eye. After 3 mo of anti-fungal treatment, the inflammation was controlled. CONCLUSION: In addition to avoiding the development of overhanging filtering bleb after trabeculectomy, the present case report also suggests that clinicians should pay more attention to the patient's ocular self-medication history. Particularly in patients with a history of glaucoma or eye surgery. Because these patients may be exposed to more types of eye drops than other individuals, they may select the wrong medications for long-term use, based on their previous experience.

Mechanism of miRNA-141-3p in Calcium Oxalate-Induced Renal Tubular Epithelial Cell Injury via NLRP3-Mediated Pyroptosis.

BACKGROUND/AIMS: Renal calculi represent a prevalent disorder associated with mineral deposition in renal calyces and the pelvis. Aberrant microRNA (miRNA) expression is implicated in renal injury. This study investigated the mechanism of miR-141-3p in calcium oxalate (CaOx) crystal-induced renal tubular epithelial cell (RTEC) injury. METHODS: Human RTECs HK-2 cells were treated with CaOx crystals to induce RTEC injury. Cell viability was evaluated using Cell Counting Kit-8 assay, and apoptosis was measured using flow cytometry. The contents of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), interleukin (IL)-1ß, and IL-18 were measured using enzyme-linked immunosorbent assay kits. The expressions of NLRP3, cleaved caspase-1, and GSDMD-N were detected using Western blot. miR-141-3p and NLRP3 expressions were determined using reverse transcription quantitative polymerase chain reaction. The binding of miR-141-3p and NLRP3 was validated using a dual-luciferase assay. The role of NLRP3 in the protection of miR-141-3p on RTEC injury was verified using functional rescue experiments. RESULTS: CaOx crystals induced RTEC injury, manifested as attenuated cell viability, enhanced apoptosis, elevated intracellular LDH and MDA levels, and decreased SOD level. Pyroptosis of RTECs was enhanced by CaOx crystal induction, evidenced by elevated expressions of cleaved caspase-1, GSDMD-N, IL-1ß, and IL-18. miR-141-3p expression was reduced in CaOx crystal-induced RTECs. miR-141-3p overexpression alleviated CaOx crystal-induced RTEC injury and suppressed pyroptosis of RTECs. miR-141-3p bound to NLRP3 and thereby repressed NLRP3 expression. NLRP3 overexpression reversed the protective effect of miR-141-3p overexpression on RTECs. CONCLUSION: miR-141-3p repressed NLRP3-mediated pyroptosis by suppressing NLRP3 expression, thus protecting CaOx crystal-induced RTEC injury.

Phosphatidylserine eversion regulated by phospholipid scramblase activated by TGF-ß1/Smad signaling in the early stage of kidney stone formation.

The mechanism underlying phosphatidylserine eversion in renal tubule cells following calcium oxalate-mediated damage remains unclear; therefore, we investigated the effects of TGF-ß1/Smad signaling on phosphatidylserine eversion in the renal tubule cell membrane during the early stage of kidney stone development. In a rat model of early stage of calcium oxalate stone formation, phosphatidylserine eversion on the renal tubular cell membrane was detected by flow cytometry, and the expression of TGF-ß1 (transforming growth factor-ß1), Smad7, and phospholipid scramblase in the renal tubular cell membrane was measured by western blotting. We observed that the TGF-ß1/Smad signaling pathway increased phosphatidylserine eversion at the organism level. The results of in vitro studies demonstrated that oxalate exposure to renal tubule cells induced TGF-ß1 expression, increasing phospholipid scramblase activity and phosphatidylserine eversion in the renal tubule cell membrane. These results indicate that TGF-ß1 stimulates phosphatidylserine eversion by increasing the phospholipid scramblase activity in the renal tubule cell membrane during the early stage of kidney stone development. The results of this study form a basis for further detailed research on the development of therapeutic agents that specifically treat urolithiasis and exert fewer adverse effects.

The Spatiotemporal Evolution Analysis of Ecosystem Pattern in Wenchuan (Magnitude 8.0) Earthquake Disaster Area, China.

The ecological system is the basis of human survival and global environmental protection. In the process of development, countries will pay close attention to the changing state of the ecosystem. Taking the ecosystem pattern as the research object, a three-layer analysis method was proposed. The transfer matrix and landscape index were used as the first layer to analyze the basic changes. Grey correlation, range-coupling coordination and relative priority were used as the second layer to analyze the reasons of the change. The interval-entropy weight, TOPSIS (Technique for Order Preference by Similarity to an Ideal Solution), was used as the third layer to evaluate the quality of the change. The ten counties in the worst-hit areas of the Wenchuan earthquake were analyzed from different angles, with county region, intensity zone and ecosystem as the objects, and the following results were obtained: (1) Taking Mianzhu City as an example, from 2000 to 2010 and 2018, the conversion ratio of forest, grassland and farmland is 54.24, 59.19, 17.21, 20.06, 37.39 and 52.86%, which were distributed in the north, central and southern parts, respectively. (2) Taking the ninth intensity zone as an example, the forest landscape fragmentation increased, disturbance decreased, and species diversity increased. There is a high influence and restriction relationship between ecosystem and landscape pattern in the total landscape area change. Additionally, the relationship between them tends to develop in a benign way. As of 2018, it is in the change state of moderate imbalance-ecosystem lag. (3) Taking the county ecosystem change as an example, urban type is the best in the counties of ecosystem change, of which Shifang is the best and Pingwu is the worst. The results show that this method can effectively compare and analyze the changes in the multi-regional ecosystem pattern, which has the characteristics of universality and can also be applied to the research of ecosystem pattern change in special regions.

EP4 activation ameliorates liver ischemia/reperfusion injury via ERK1/2­GSK3ß­dependent MPTP inhibition.

Prostaglandin E receptor subtype 4 (EP4) is widely distributed in the heart, but its role in hepatic ischemia/reperfusion (I/R), particularly in mitochondrial permeability transition pore (MPTP) modulation, is yet to be elucidated. In the present study, an EP4 agonist (CAY10598) was used in a rat model to evaluate the effects of EP4 activation on liver I/R and the mechanisms underlying this. I/R insult upregulated hepatic EP4 expression during early reperfusion. In addition, subcutaneous CAY10598 injection prior to the onset of reperfusion significantly increased hepatocyte cAMP concentrations and decreased serum ALT and AST levels and necrotic and apoptotic cell percentages, after 6 h of reperfusion. Moreover, CAY10598 protected mitochondrial morphology, markedly inhibited mitochondrial permeability transition pore (MPTP) opening and decreased liver reactive oxygen species levels. This occurred via activation of the ERK1/2­GSK3ß pathway rather than the janus kinase (JAK)2­signal transducers and activators of transcription (STAT)3 pathway, and resulted in prevention of mitochondria­associated cell injury. The MPTP opener carboxyatractyloside (CATR) and the ERK1/2 inhibitor PD98059 also partially reversed the protective effects of CAY10598 on the liver and mitochondria. The current findings indicate that EP4 activation induces ERK1/2­GSK3ß signaling and subsequent MPTP inhibition to provide hepatoprotection, and these observations are informative for developing new molecular targets and preventative therapies for I/R in a clinical setting.

Induction of cell-cycle arrest and apoptosis in human cholangiocarcinoma cells by pristimerin.

Pristimerin, a triterpenoid isolated from Celastraceae and Hippocrateaceae, is known to induce cytotoxicity in several cancer cell lines. However, whether pristimerin can induce apoptosis in cholangiocarcinoma cells and the underlying mechanism remain unexplored. We assessed the function of human cholangiocarcinoma QBC and RBE cell lines using various experimental methods such as the cell viability assay to elucidate the viability of cells, flow cytometry to detect the death rate of cells, and Western blot analysis to evaluate the expression of cell cycle-related proteins and autophagy-related proteins. Human cholangiocarcinoma QBC cells were transplanted to nude mice to establish an animal model, and the effect of pristimerin on tumor growth in this model was observed. QBC and RBE cell lines treated with pristimerin (0, 5, 10, and 20 µmol/L) demonstrated the induction of apoptosis in a dose-dependent manner. The cell viability assay revealed a reduction in the cell viability with an increase in the pristimerin concentration. Similarly, flow cytometry revealed a gradual increase in the cell death rate with an increase in the pristimerin concentration. In addition, pristimerin significantly lowered the expression of apoptosis-related proteins (Bcl-2, Bcl-xL, and procaspase-3), but increased the Bax expression. Furthermore, pristimerin resulted in the G0/G1 cell-cycle arrest, reducing the expression of cell cycle-related proteins (cyclin E, CDK2, and CDK4), and increased the expression of autophagy-related proteins (LC3) in QBC cell line. Treatment with pristimerin could inhibit tumor growth in the nude mouse model. Overall, this study suggests the potential effect of pristimerin on the cell-cycle arrest and apoptosis in human cholangiocarcinoma cells.

Suprapatellar versus infrapatellar intramedullary nailing for treatment of tibial shaft fractures in adults.

BACKGROUND: Numerous studies have compared suprapatellar (SP) nailing to infrapatellar (IP) nailing for treatment of tibial shaft fractures; however, the best strategy remains controversial. The aim of this meta-analysis is to assess whether SP or IP nailing is more effective for tibial shaft fractures in adults. METHODS: Literature searches of PubMed, Embase, OVID, Cochrane Library, Web of Science, Chinese Biomedical Literature, Wanfang, Weipu Journal, and CNKI databases were performed up to July 2017. Only randomized controlled trials (RCTs) comparing SP versus IP intramedullary nailing for tibial shaft fractures were included. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. RESULTS: Twelve RCTs were selected for analysis. SP intramedullary nailing reduced knee joint pain, visual analog score, fluoroscopy time, and sagittal angle, resulting in better Harris hip score, Lysholm knee score, short-form 36 questionnaire, range of motion, and rates of "excellent" and "good" outcome. There were no significant differences in operative time, blood loss, length of hospital stay, union time, and coronal angle between groups. CONCLUSION: The present meta-analysis indicates that SP intramedullary nailing has obvious advantages over IP intramedullary nailing for treatment of tibial shaft fractures in adults. However, owing to the low-quality evidence currently available, additional high-quality RCTs are needed to confirm these findings.

Tunable optical forces enhanced by plasmonic modes hybridization in optical trapping of gold nanorods with plasmonic nanocavity.

The optomechanical interaction between a plasmonic nanocavity and a gold nanorod through optical forces is demonstrated. It is revealed that strong localized plasmon resonance mode hybridization induced by a gold nanorod results in the resonance mode of the nanocavity splitting into two different plasmon resonance modes (bonding plasmon resonance mode and antibonding plasmon resonance mode). When the whole system (gold nanorod and gold nanocavity) is excited at the antibonding plasmon mode, the gold nanorod can receive an optical pushing force and be pushed away from the gold nanocavity. On the other hand, an optical pulling force acts on the gold nanorod and the gold nanorod can be trapped by the gold nanocavity when the plasmonic tweezers work at the bonding mode. The optical pulling force acting on the gold nanorod can be enhanced by two orders of magnitude larger than that of the same sized dielectric nanorod, which benefits from the strong resonant nearfield interaction between the gold nanorod and the gold nanocavity. More importantly, the shape and the position of the optical potential can be tuned by tailoring the wavelength of the laser used in the optical trapping, which can be used to manipulate the gold nanorod within a nanoscale region. Our findings have important implications for optical trapping, manipulation, sorting, and sieving of plasmonic nanoparticles with plasmonic tweezers.

Propofol reduces hypoxia­induced autophagic cell death through downregulating HIF 1α in alveolar epithelial type II cells of rats.

Propofol (2,6­diisopropylphenol) exerts protective effects on alveolar epithelial type II (ATII) cells, partly through attenuating hypoxia­induced apoptosis. Autophagy is involved in the activation of apoptosis. Therefore, the present study investigated the modulating effect of propofol against autophagy in ATII cells under hypoxia. Western blot analysis was performed to detect the protein expression of the autophagy molecular marker, microtubule­associated protein 1 light chain 3 (LC3)­II, under various conditions. The effects of propofol on the accumulation of other autophagy­associated proteins and apoptosis­associated proteins were also determined using western blot analysis. The interactions between proteins were determined by co­immunoprecipitation. Apoptosis of the ATII cells was monitored using FITC­conjugated AV/PI staining. Furthermore, hypoxia­inducible factor 1α (HIF 1α) small interfering (si) RNA was designed to construct si­HIF 1α ATII cells. The efficiency of interference was measured using reverse transcription­quantitative polymerase chain reaction and western blot analyses. Following pre­treatment with propofol, the hypoxia­induced accumulation of LC3­II, HIF 1α and B­cell lymphoma­2 interacting protein 3 (Bnip3) were markedly decreased, accompanied with the activation of mammalian target of rapamycin. In addition, cleaved­poly ADP­ribose polymerase was suppressed, and hypoxia­induced autophagic cell death was inhibited by propofol pre­treatment. HIF 1α was inhibited by si­HIF 1α, which simultaneously suppressed Bnip3 and LC3­II under hypoxia. Taken together, propofol reduced hypoxia­induced autophagic cell death through reducing the expression of HIF 1α in ATII cells, indicating a novel strategy for modulating autophagy via propofol in hypoxic ATII cells.

Prognostic value of circulating tumor cells in esophageal cancer.

AIM: To perform a meta-analysis of the related studies to assess whether circulating tumor cells (CTCs) can be used as a prognostic marker of esophageal cancer. METHODS: PubMed, Embase, Cochrane Library and references in relevant studies were searched to assess the prognostic relevance of CTCs in patients with esophageal cancer. The primary outcome assessed was overall survival (OS). The meta-analysis was performed using the random effects model, with hazard ratio (HR), risk ratio (RR) and 95% confidence intervals (95%CIs) as effect measures. RESULTS: Nine eligible studies were included involving a total of 911 esophageal cancer patients. Overall analyses revealed that CTCs-positivity predicted disease progression (HR = 2.77, 95%CI: 1.75-4.40, P < 0.0001) and reduced OS (HR = 2.67, 95%CI: 1.99-3.58, P < 0.00001). Further subgroup analyses demonstrated that CTCs-positive patients also had poor OS in different subsets. Moreover, CTCs-positivity was also significantly associated with TNM stage (RR = 1.48, 95%CI: 1.07-2.06, P = 0.02) and T stage (RR = 1.44, 95%CI: 1.13-1.84, P = 0.003) in esophageal cancer. CONCLUSION: Detection of CTCs at baseline indicates poor prognosis in patients with esophageal cancer. However, this finding relies on data from observational studies and is potentially subject to selection bias. Prospective trials are warranted.

PAK4 Phosphorylates p53 at Serine 215 to Promote Liver Cancer Metastasis.

PAK4 kinase contributes to signaling pathways controlling cancer cell transformation, invasion, and survival, but its clinicopathological impact has begun to emerge only recently. Here we report that PAK4 overexpression in hepatocellular carcinoma (HCC) conveys aggressive metastatic properties. A novel nuclear splice isoform of PAK4 lacking exon 2 sequences was isolated as part of our studies. By stably overexpressing or silencing PAK4 in HCC cells, we showed that it was critical for their migration. Mechanistic investigations in this setting revealed that PAK4 directly phosphorylated p53 at S215, which not only attenuated transcriptional transactivation activity but also inhibited p53-mediated suppression of HCC cell invasion. Taken together, our results showed how PAK4 overexpression in HCC promotes metastatic invasion by regulating p53 phosphorylation. Cancer Res; 76(19); 5732-42. ©2016 AACR.

Advantages of Pure Platelet-Rich Plasma Compared with Leukocyte- and Platelet-Rich Plasma in Treating Rabbit Knee Osteoarthritis.

BACKGROUND Concentrated leukocytes in leukocyte- and platelet-rich plasma (L-PRP) may deliver increased levels of pro-inflammatory cytokines to activate the NF-κB signaling pathway, to counter the beneficial effects of growth factors on osteoarthritic cartilage. However, to date no relevant studies have substantiated that in vivo. MATERIAL AND METHODS Autologous L-PRP and pure platelet-rich plasma (P-PRP) were prepared, measured for componential composition, and injected intra-articularly after 4, 5, and 6 weeks post-anterior cruciate ligament transection. Caffeic acid phenethyl ester (CAPE) was injected intraperitoneally to inhibit NF-κB activation. All rabbits were sacrificed after 8 weeks postoperative. Enzyme-linked immunosorbent assays were performed to determine interleukin 1ß (IL-1ß) and prostaglandin E2 (PGE2) concentrations in the synovial fluid, Indian ink staining was performed for gross morphological assessment, and hematoxylin and eosin staining and toluidine blue staining were performed for histological assessment. RESULTS Compared with L-PRP, P-PRP injections achieved better outcomes regarding the prevention of cartilage destruction, preservation of cartilaginous matrix, and reduction of IL-1ß and PGE2 concentrations. CAPE injections reversed the increased IL-1ß and PGE2 concentrations in the synovial fluid after L-PRP injections and improved the outcome of L-PRP injections to a level similar to P-PRP injections, while they had no influence on the therapeutic efficacy of P-PRP injections. CONCLUSIONS Concentrated leukocytes in L-PRP may release increased levels of pro-inflammatory cytokines to activate the NF-κB signaling pathway, to counter the beneficial effects of growth factors on osteoarthritic cartilage, and finally, result in a inferior efficacy of L-PRP to P-PRP for the treatment of osteoarthritis.

Association between Apolipoprotein E polymorphism and myocardial infarction risk: A systematic review and meta-analysis.

Published data regarding the association between Apolipoprotein E (ApoE) genetic variation and myocardial infarction (MI) risk were not always consistent. Therefore, the current meta-analysis was conducted to derive a more precise estimation of the association between ApoE polymorphism and MI risk. PubMed and Web of Science were searched to identify relevant studies. Summary odds ratio (ORs) and 95% confidence intervals (CIs) were calculated using random-effect or fixed-effect models based on the heterogeneity of included studies. All the tests were performed using Stata 11.0. A total of 22 eligible studies were identified in this meta-analysis. The results show that ApoE ε2 and ε4 alleles were associated with MI risk. The study suggests that there is close association between ApoE polymorphism and MI risk. It shows that ApoE ε2 allele is a protective factor of MI, while ε4 allele is a risk factor of MI, especially in Caucasian and Asian population. Nevertheless, well-designed, unbiased and larger sample size studies are required to confirm the results.

TGF-ß1-509C/T polymorphism and the risk of ESCC in a Chinese Han population.

BACKGROUND: The studies investigating whether transforming growth factor (TGF)-ß1-509C/T polymorphism is associated with the risk of ESCC is inconsistent. METHODS: The TGF-ß1-509C/T genotypes were determined by using a polymerase chain reaction (PCR)-restriction fragment length polymorphism assay and DNA sequencing analysis. The differences in demographic variables and genotype distributions of TGF-ß1-509C/T polymorphism between ESCC patients and controls were calculated by Pearson's Chi square test. Associations between TGF-ß1-509C/T polymorphism genotypes and ESCC risk were estimated by OR and their 95% CIs computed using unconditional logistic regression model. RESULTS: There was a significant difference of TGF-ß1-509C/T polymorphism genotype distribution between ESCC group and control group (P<0.001). With the CC genotype as reference, the adjusted OR for CT genotype reached to 0.78 (95% CI: 0.65-0.89; P=0.041), and the adjusted OR for TT homozygous carriers was 0.52 (95% CI: 0.33-0.78; P=0.017). The T allele carriage also presented a lower risk for ESCC (adjusted OR=0.43; 95% CI, 0.29-0.71; P=0.009). CONCLUSION: TGF-ß1-509C/T polymorphism may contributes to ESCC susceptibility in Chinese population.

Fabricating Hexagonal Al-Doped LiCoO2 Nanomeshes Based on Crystal-Mismatch Strategy for Ultrafast Lithium Storage.

In the designed synthesis, low crystal-mismatch strategy has been applied in the synthesis of ion-doped LiCoO2 materials, and a good success of single crystal property has been achieved between the precursor and the final sample for the first time. The hexagonal LiCo0.8Al0.26O2 (LCAO) nanomesh possesses several advantages in morphology and crystal structure, including mesoporous structure, single crystal, atomic even distribution, high exposing surface area as (100) or their equivalent planes, and shortened Li ions diffusion distance. All the merits are beneficial to the application in Li-ion batteries (LIBs) cathode, for example, accelerating Li ions diffusion rate, improving the Li ions shuttle between the LCAO nanomesh and electrolyte, and reducing the Li ions capacitive behavior during Li intercalation. Hence, our research adopts Al-contained precursor with morphology of hexagonal nanoplates to fabricate designed Al-doped LiCoO2 nanomeshes and greatly improves the cathode performance in LIBs.

Nobiletin inhibited hypoxia-induced epithelial-mesenchymal transition of lung cancer cells by inactivating of Notch-1 signaling and switching on miR-200b.

Epithelial-mesenchymal transition (EMT) is an early step in the process of tumor metastasis. It is well known that tumor microenvironment affects malignancy in various carcinomas; in particular, that hypoxia induces EMT. Deregulated notch signaling also contributes a lot to the development of EMT in lung cancer. In this study, we investigated the use of Notch-1-inhibiting compound as novel therapeutic candidates to regulate hypoxia-induced EMT in lung cancer cells. According to previous screening, nobiletin was selected as a Notch-1 inhibitor. Hypoxia-induced EMT was characteristic of increased N-cadherin & vimentin expressions and decreased E-cadherin expressions. Treatment with nobiletin notably attenuated hypoxia-induced EMT, invasion and migration in H1299 cells, accompanied with reduced Notch-1, Jagged1/2 expressions and its downstream genes Hey-1 and Hes-1. Nobiletin treatment also promoted tumorsuppressive miR-200b level. Moreover, notch-1 siRNA prevented hypoxia-mediated cell migration and decreased Twist1, Snail1, and ZEB1/2 expressions, which are key EMT markers. Re-expression of miR-200b blocked hypoxia-induced EMT and cell invasion. Our findings suggest that downregulation of Notch-1 and reexpression of miR-200b by nobiletin might be a novel remedy for the therapy of lung cancer.

Photodynamic therapy mediated by 5-aminolevulinic acid suppresses gliomas growth by decreasing the microvessels.

Although 5-aminolevulinic acid (5-ALA)-mediated photodynamic therapy (PDT) has been demonstrated to be a novel and effective therapeutic modality for some human malignancies, its effect and mechanism on glioma are still controversial. Previous studies have reported that 5-ALA-PDT induced necrosis of C6 rat glioma cells in vitro. The aim of this study was to further investigate the effect and mechanism of 5-ALA-PDT on C6 gliomas implanted in rats in vivo. Twenty-four rats bearing similar size of subcutaneously implanted C6 rat glioma were randomly divided into 3 groups: receiving 5-ALA-PDT (group A), laser irradiation (group B), and mock procedures but without any treatment (group C), respectively. The growth, histology, microvessel density (MVD), and apoptosis of the grafts in each group were determined after the treatments. As compared with groups B and C, the volume of tumor grafts was significantly reduced (P<0.05), MVD was significantly decreased (P<0.001), and the cellular necrosis was obviously increased in group A. There was no significant difference in apoptosis among the three groups. The in vivo studies confirmed that 5-ALA-PDT may be an effective treatment for gliomas by inhibiting the tumor growth. The mechanism underlying may involve increasing the cellular necrosis but not inducing the cellular apoptosis, which may result from the destruction of the tumor microvessels.

Correlation of the structure and applications of dealloyed nanoporous metals in catalysis and energy conversion/storage.

Nanoporous metals produced by dealloying have shown great promise in many areas such as catalysis/electrocatalysis, energy conversion/storage, sensing/biosensing, actuation, and surface-enhanced Raman scattering. Particularly, nanoscale metal ligaments with high electronic conductivity, tunable size and rich surface chemistry make nanoporous metals very promising as catalysts/electrocatalysts for energy conversion applications such as fuel cells and also as versatile three-dimensional substrates for energy-storage in supercapacitors and lithium ion batteries. In this review, we focus on the recent developments of dealloyed nanoporous metals in both catalysis/electrocatalysis and energy storage. In particular, based on the state-of-the-art electron microscopy characterization, we explain the atomic origin of the high catalytic activity of nanoporous gold. We also highlight the recent advances in rationally designing nanoporous metal-based composites and hierarchical structures for enhanced energy storage. Finally, we conclude with some outlook and perspectives with respect to future research on dealloyed nanoporous metals in catalysis- and energy-related applications.

Effects of sevoflurane and propofol on right ventricular function and pulmonary circulation in patients undergone esophagectomy.

OBJECT: Sevoflurane and propofol are both widely used in clinical anesthesia. The aim of this study is to compare the effects of sevoflurane and propofol on right ventricular function and pulmonary circulation in patients receiving esophagectomy. METHODS: Forty adult patients undergoing an elective open-chest thoracotomy for esophagectomy were randomized to receive either propofol (n=20) or sevoflurane (n=20) as the main anesthetic agent. The study was performed in Changzheng Hospital. Hemodynamic data were recorded at specific intervals: before the surgery (T0), BIS values reaching 40 after anesthesia induction (T1), two-lung ventilation (T2), ten minutes after one-lung ventilation (T3), the end of the operation (T4) using PiCCO2 and Swan-Ganz catheter. RESULTS: CI, RVEF, RVSWI and RVEDVI were significantly smaller in propofol group than those in sevoflurane group throughout the surgery (P<0.05). However, SVRI was significantly greater in propofol group than that in sevoflurane group (P<0.05). Compared with the patients in propofol group, the patients who received sevoflurane had a greater reduction in OI and increase in Os/Ot (P<0.05). And, PVRI was significantly smaller in sevoflurane group than in propofol group (P<0.05). CONCLUSION: Anesthesia with sevoflurane preserved better right ventricular function than propofol in patients receiving esophagectomy. However, propofol improved oxygenation and shunt fraction during one-lung ventilation compared with sevoflurane anesthesia. To have the best effect, anesthesiologists can choose the two anesthetics flexibly according to the monitoring results.