SnoN residue (1-366) attenuates hypertrophic scars through resistance to transforming growth factor-ß1-induced degradation.

Hypertrophic scars (HSs) are characterized by fibroblast hyperproliferation and excessive matrix deposition. During wound healing, transforming growth factor (TGF)-ß1/Smad signaling acts as a key regulator. As a transcriptional corepressor of TGF-ß1/Smads, SnoN is expressed at low levels in many fibrotic diseases due to TGF-ß1/Smad-induced degradation. SnoN residue (1-366; SR) is resistant to TGF-ß1-induced degradation. However, the expression and role of SR in HSs are unknown. Here, we inhibited TGF-ß1/Smad signaling via overexpression of SR to block fibroblast transdifferentiation, proliferation, and collagen deposition during HS formation. Our results showed that SnoN was downregulated in HS fibroblasts (HSFs) owing to TGF-ß1/Smad-induced degradation. Overexpression of SR in normal human dermal fibroblasts (NHDFs) and HSFs successfully blocked phosphorylation of Smad2 and Smad3, thereby inhibiting NHDF transdifferentiation and HSF proliferation and reducing type I collagen (ColI) and type III collagen (ColIII) production and secretion. In addition, we applied overexpressed full-length SnoN (SF) and SR to wound granulation tissue in a rabbit model of HSs. SR reduced wound scarring, improved collagen deposition and arrangement of scar tissue, and decreased mRNA and protein expression of ColI, ColIII, and α-smooth muscle actin (α-SMA) more effectively than SF in vivo. These results suggest that SR could be a promising therapy for the prevention of HS.

[Strategies of interventing complications in hemodialysis with classical prescriptions from clinical cases].

There are 400 thousand patients with long-term hemodialysis in China nowadays. Hemodialysis, as the most common alternative to renal replacement therapy, prolongs the life span of patients with end stage renal failure. However, there are still many complications of hemodialysis treatment. These complications reduce the quality of life of patients and may even endanger their life, and sometimes they are difficult to deal with. Classical prescriptions, commonly referred to as classical effective prescriptions in modern medicine, mainly indicating the formulas recorded in Treatise on Febrile Diseases and Synopsis of Golden Chamber, were relative to contemporary prescriptions emerging after Song and Yuan dynasties. Prescriptions corresponding to syndromes means one-to-one correspondence between syndromes and prescriptions, with many advantages and that is the key of clinical efficacy. Many complications of hemodialysis patients have typical clinical manifestations, which can match the syndromes corresponding to classical prescriptions, thus quickly relieving the symptoms of patients in clinical application. Six clinical cases of dialysis muscle spasm, disequilibrium syndrome, restless legs syndrome, uremic encephalopathy, post dialysis arrhythmia, and secondary hyperparathyroidism were used in this paper, to explore the intervention strategies for hemodialysis related complications.

[Expression of plasma miRNA-497 in children with sepsis-induced myocardial injury and its clinical significance].

OBJECTIVE: To study the expression of plasma miRNA-497 in children with sepsis-induced myocardial injury and its clinical significance. METHODS: A total of 148 children with sepsis were enrolled. According to the presence or absence of myocardial injury, these children were divided into myocardial injury group (n=58) and non-myocardial injury group (n=90). The two groups were compared in terms of the changes in plasma levels of miRNA-497, cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), N-terminal pro-brain natriuretic peptide (NT-proBNP), procalcitonin (PCT), and C-reactive protein (CRP) and left ventricular ejection fraction (LVEF). The receiver operating characteristic (ROC) curve was plotted to evaluate the value of plasma miRNA-497, cTnI, and CK-MB in the diagnosis of myocardial injury. A Pearson correlation analysis was used to determine the correlation of miRNA-497 with cTnI, CK-MB, NT-proBNP, PCT, CRP, and LVEF. RESULTS: Compared with the non-myocardial injury group, the myocardial injury group had significantly higher plasma levels of miRNA-497, cTnI, CK-MB, NT-proBNP, PCT, and CRP (P<0.05). Plasma miRNA-497, cTnI, and CK-MB when measured alone or in combination had an area under the ROC curve of 0.918, 0.931, 0.775, and 0.940 respectively. At the optimal cut-off value of 2.05, miRNA-497 had a sensitivity of 90.4% and a specificity of 91.2%. The correlation analysis showed that there was a good correlation between plasma miRNA-497 and cTnI in children with myocardial injury (r=0.728, P<0.01). CONCLUSIONS: Plasma miRNA-497 has a similar value as cTnI in the diagnosis of sepsis-induced myocardial injury in children and may be used as a potential marker for early diagnosis of myocardial injury.

Cantharidin Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing Autophagy and Inducing Apoptosis in Vitro and in Vivo.

BACKGROUND/AIMS: Cantharidin, a type of terpenoid secreted by the blister beetle Mylabris phalerata (Pallas), has attracted great attention in cancer therapy because of its potential anti-cancer activities. Here, we report the effects on apoptosis and autophagy in human triple-negative breast cancer (TNBC) cell lines after treatment with cantharidin and attempt to elucidate the underlying mechanisms. METHODS: MDA-MB-231 and MDA-MB-468 cells were treated with cantharidin and cell proliferation was examined using CCK-8 and clone formation assays. The expression of apoptosis- and autophagy-associated proteins was detected by western blotting. Cells were infected with lentivirus carrying the Beclin-1 gene, and MDA-MB-231-beclin1 (MB231-Bec) and MDA-MB-468-beclin-1(MB468-Bec) cells stably expressing Beclin-1 were established. Autophagic vacuoles in cells were observed with LC3 staining using fluorescence microscopy, and apoptotic cells were detected via flow cytometry. Tumor growth was assessed by subcutaneous inoculation of TNBC cells into BALB/c nude mice. RESULTS: Cantharidin inhibited the proliferation of MDA-MB-231 and MDA-MB-468 cells, and induced cell apoptosis. Cantharidin additionally inhibited the conversion of LC3 I to LC3 II and autophagosome formation by suppressing the expression of Beclin-1. Furthermore, overexpression of Beclin-1 in TNBC cells attenuated the cytotoxicity of cantharidin. In vivo, cantharidin inhibited the growth of MDA-MB-231 and MDA-MB-468 xenografts in nude mice by suppressing autophagy and inducing apoptosis, and Beclin-1 overexpression in TNBC cells reduced the efficacy of cantharidin. CONCLUSIONS: Cantharidin inhibits autophagy by suppressing Beclin-1 expression and inducing apoptosis of TNBC cells in vitro and in vivo, thereby representing a potential strategy for the treatment of TNBC.

Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo.

BACKGROUND/AIMS: Dachengqi decoction (DCQD) is a well-known traditional Chinese herbal drug with strong anti-inflammatory effects. Angiopoietin-1 (Ang-1) plays a vital role in maintaining the stability and integrity of the vascular wall and prevents vascular leakage due to inflammatory mediators. Our previous work found that DCQD protects against pancreatic injury in rats with severe acute pancreatitis (SAP). This study aims to investigate the effects of DCQD on intestinal endothelial damage in both damaged human umbilical vein endothelial cells (HUVECs) and SAP rats. METHODS: HUVECs were randomly divided into four groups: control group, TNF-α group, TNF-α plus Ang-1 group (Ang-1 group), and TNF-α plus DCQD group (DCQD group). Cells were incubated for 6 h, 12 h, and 24 h, before collection. The treatment concentration of DCQD was decided based on a Cell Counting Kit-8 (CCK-8) assay. The monolayer permeability of the HUVECs was assessed by measuring the transendothelial electrical resistance (TEER). Apoptosis was analyzed by flow cytometry. mRNA and protein expression of aquaporin 1 (AQP-1), matrix metalloproteinase 9 (MMP9), and junctional adhesion molecule-C (JAM-C) was evaluated by RT-PCR, immunocytofluorescence, and western blot. Forty male Sprague-Dawley rats were randomized into a control group, SAP group, SAP plus Ang-1 group (Ang-1 group), and SAP plus DCQD group (DCQD group). SAP was induced by intraperitoneal injection of cerulein and lipopolysaccharide (LPS), while the control group received 0.9% saline solution. Evans blue was injected through the penile vein and the rats were then sacrificed 12 h after modeling. Levels of serum amylase, TNF-α, IL-1ß, IL-2, and IL-6 were determined by using ELISA. Intestinal tissue was analysed by histology, and capillary permeability in the tissues was evaluated by Evans blue extravasation assay. Protein and mRNA expression of AQP-1, MMP9, and JAM-C were assessed by immunohistofluorescence, western blot, and RT-PCR. RESULTS: DCQD reduced the permeability of HUVEC induced by TNF-α in vitro. Furthermore, DCQD altered the mRNA and protein levels of JAM-C, MMP9, and AQP-1 in HUVECs after TNF-α induction. SAP intestinal injury induced by cerulein combined with lipopolysaccharides was concomitant with increased expression of JAM-C and MMP9, and reduced expression of AQP-1 in intestinal tissue. Pretreatment with DCQD attenuated SAP intestinal injury and lowered the levels of serum amylase, TNF-α, IL-1ß, IL-2, and IL-6 effectively. Our study demonstrated that DCQD decreased the expression of JAM-C and MMP9 and increased the expression of AQP-1 both in vitro and in vivo. CONCLUSION: DCQD can reduce capillary endothelial damage in acute pancreatitis-associated intestinal injury and the mechanism may be associated with the regulation of endothelial barrier function-associated proteins AQP-1, MMP9, and JAM-C.

Early prediction of intestinal mucosal barrier function impairment by elevated serum procalcitonin in rats with severe acute pancreatitis.

OBJECTIVES: The aim of this study was to evaluate serum procalcitonin (PCT) levels as a prognostic indicator of intestinal barrier function impairment in rats with severe acute pancreatitis (SAP). METHODS: Thirty-six male Sprague Dawley rats were randomly grouped into SAP group (injected sodium taurocholate via biliopancreatic duct), Gln group (gavaged with glutamine after modeling), and control group. Blood, pancreatic, and terminal ileum tissues were obtained from the rats after 6 h of modeling. Serum amylase (Amy) levels were determined using an automatic biochemical detector, while endotoxin (ET), diamine oxidase (DAO), and PCT levels were measured by ELISA test. The pathology of pancreatic and small intestine tissues were observed. PCT protein expression in intestinal tissues were detected by immunohistochemistry and western blot. RESULT: Pancreatic and intestinal injuries in Gln group were significantly lower than SAP group. Serum amylase, DAO, and PCT levels in SAP and Gln groups differed greatly and were significantly higher than control group. Immuno-histochemistry and western blot results showed that PCT protein expression levels in small intestine tissues of SAP group were higher than Gln group and control group. Serum PCT levels had a significant correlation with serum endotoxin, DAO levels and intestinal mucosal injury scores. CONCLUSION: PCT expression in serum and intestinal tissues in SAP rats increased significantly in the early stages of SAP, and was closely related to the onset and degree of intestinal barrier function impairment. Thus, our results showed that measuring serum PCT can be used to predict intestinal mucosal barrier function impairment in SAP rats.

Honokiol Prevents Intestinal Barrier Dysfunction in Mice with Severe Acute Pancreatitis and Inhibits JAK/STAT1 Pathway and Acetylation of HMGB1.

OBJECTIVE: To investigate the effect of honokiol (HON) and the role of high-mobility group protein B1 (HMGB1) on the pathogenesis of severe acute pancreatitis (SAP). METHODS: Thirty mice were numbered according to weight, and randomly divided into 5 groups using a random number table, including control, SAP, SAP and normal saline (SAP+NS), SAP and ethyl pyruvate (SAP+EP), or SAP+HON groups, 6 mice in each group. Samples of pancreas, intestine, and blood were collected 12 h after SAP model induction for examination of pathologic changes, immune function alterations by enzyme linked immunosorbent assay (ELISA), and Western blot. In vitro experiments, macrophages were divided into 5 groups, the control, lipopolysaccharide (LPS), LPS+DMSO (DMSO), LPS+anti-HMGB1 monoclonal antibody (mAb), and LPS+ HON groups. The tight connection level was determined by transmission electron microscopy and fluorescein isothiocyanate-labeled. The location and acetylation of HMGB1 were measured by Western blot. Finally, pyridone 6 and silencing signal transducer and activator of the transcription 1 (siSTAT1) combined with honokiol were added to determine whether the Janus kinase (JAK)/ STAT1 participated in the regulation of honokiol on HMGB1. The protein expression levels of HMGB1, JAK, and STAT1 were detected using Western blot. RESULTS: Mice with SAP had inflammatory injury in the pancreas, bleeding of intestinal tissues, and cells with disrupted histology. Mice in the SAP+HON group had significantly fewer pathological changes. Mice with SAP also had significant increases in the serum levels of amylase, lipase, HMGB1, tumor necrosis factor- α, interleukin-6, diamine oxidase, endotoxin-1, and procalcitonin. Mice in the SAP+HON group did not show these abnormalities (P<0.01). Studies of Caco-2 cells indicated that LPS increased the levels of occludin and claudin-1 as well as tight junction permeability, decreased the levels of junctional adhesion molecule C, and elevated intercellular permeability (P<0.01). HON treatment blocked these effects. Studies of macrophages indicated that LPS led to low nuclear levels of HMGB1, however, HON treatment increased the nuclear level of HMGB1 (P<0.01). HON treatment also inhibited the expressions of JAK1, JAK2, and STAT1 (P<0.01) and increased the acetylation of HMGB1 (P<0.05). CONCLUSION: HON prevented intestinal barrier dysfunction in SAP by inhibiting HMGB1 acetylation and JAK/STAT1 pathway.

[Efficacy of modified Roux-en-Y gastric bypass in the treatment of non-obese type 2 diabetes mellitus:one year follow-up].

OBJECTIVE: To evaluate the one year effect of modified Roux-en-Y gastric bypass (RYGP) in the treatment of non-obese type 2 diabetes and to investigate the reasonable indications for surgery. METHODS: Totally 72 patients diagnosed as type 2 diabetes underwent RYGP from May 2009 to June 2010. There were 45 male and 27 female patients, with an average age of (47 ± 10) years. Preoperative body mass index (BMI) of the patients was 18.69 to 31.22 kg/m(2), average (26 ± 4) kg/m(2). The follow-up data included fasting plasma glucose (FPG), 2 h plasma glucose after oral glucose challenge (2hPG), weight, BMI and medication usage in 1, 3, 6 and 12 months postoperative; hemoglobin A1c (HbA1c), fasting C-peptide (C-P), fasting serum insulin (Fins) and homeostasis model assessment of insulin resistance index (HOMA-IR) in 6 and 12 months postoperative, respectively. RESULTS: Compared with the preoperative, FPG, 2hPG, weight and BMI in 1, 3, 6 and 12 months after surgery were improved (t = 7.014 to 10.254, P = 0.000), while HbA1c, C-P and HOMA-IR in 6 and 12 months after surgery were improved (t = 1.782 to 7.789, P = 0.000 to 0.103) and there was no significant difference in Fins (P > 0.05). The rates of complete remission in 1, 3, 6 and 12 months after surgery were gradually improved to 22.2%, 27.8%, 36.1% and 60.6%, respectively, and the rate of remission in 1 year was 94.3%. The complete remission of 1 year after surgery was associated with normal C-P, insulin antibody and oral antidiabetic drugs (χ(2) = 11.730, P = 0.003; χ(2) = 7.131, P = 0.028;χ(2) = 6.149, P = 0.046). CONCLUSIONS: Modified RYGP is safely and effectively in the treatment of no-obese type 2 diabetes patients. The function of islet cells is significantly improved after operation. Especially for the patients of whom C-P is normal, insulin antibody is negative before surgery, the rate of complete remission after 1 year is better.

Tai Chi for spatiotemporal gait features and dynamic balancing capacity in elderly female patients with non-specific low back pain: A six-week randomized controlled trial.

BACKGROUND: Non-specific low back pain (NS-LBP) is a serious public health problem. Tai Chi is promising in reducing the risk of falls and alleviating symptoms in this population. OBJECTIVE: To investigate the effect of Tai Chi on gait and dynamic balance in elderly women with NS-LBP. METHODS: 20 women (age > 65 yr.) with NS-LBP were randomly assigned to a Tai Chi group (n= 10) or a control group (n= 10). The Tai Chi group practiced Tai Chi exercise 3 times a week for 6 weeks. Each session lasted 60 minutes. Pain, spatiotemporal gait features and dynamic balancing capacity were assessed at 0 and 6 weeks. RESULTS: Compared to the control group at 6 weeks, the Tai Chi group had a significant decrease in VAS (p= 0.027) and stride width (p= 0.019), significant improvement in gait velocity, stride length (p< 0.001). Regarding dynamic balance capacity, the Tai Chi group had significant improvements in anterior (Left: p= 0.001; Right: p= 0.038), postero-lateral (Left: p< 0.001; Right: p= 0.038), and postero-medial (Left: p= 0.015; Right: p= 0.018). CONCLUSION: 6-week Tai Chi can relieve pain and improve gait and dynamic balance in elderly women with NS-LBP, which suggests Tai Chi could be a promising rehabilitation intervention to reduce the risk of falls in this population.

[Resolvin E1 protects against ox-LDL-induced injury on vascular endothelial cells].

OBJECTIVE: To investigate whether Resolvin E1 (RvE1) could protect against ox-LDL-induced injury on human vein vascular endothelial cells and reveal related molecular mechanisms. METHODS: Human vein vascular endothelial cells were randomly assigned to six groups, which were treated with saline, RvE1, wortmanin, ox-LDL, ox-LDL and RvE1, ox-LDL and RvE1 and wortmanin, respectively. After 48 h, survival rates were determined by MTT, apoptosis rate of cells were determined by flow cytometry, TNF-α contents were assayed by ELISA, caspase 3 and 9 activities were measured by microplate reader, and the expression of p-AKT and LOX-1 were determined by Western blot. RESULT: Compared with normal saline group, survival rate was markedly decreased and apoptosis rate, TNF-α content, caspase 3 and 9 activities, and the expression of LOX-1 were significantly increased in ox-LDL group (P < 0.01). Survival rate was significantly increased and apoptosis rate, TNF-α content, caspase 3 and 9 activities, and the expression of LOX-1 were significantly decreased in ox-LDL + RvE1 group compared to ox-LDL group (P < 0.01), these beneficial effects of RvE1 could be blocked by PI3K inhibitor wortmanin (P < 0.05). CONCLUSION: The present data showed that RvE1 could effectively protect against ox-LDL-induced endothelial cell injury, which might be mediated by PI3K-AKT signaling pathway.

Joint effects of cadmium and copper on Apis mellifera forgers and larvae.

Honey bees (Apis mellifera L.) are important ecological and agricultural resources. They are among the most widely available pollinators and provide products as well as services. Unfortunately, honey bee populations are susceptible to several environmental threats, including heavy metal exposure. Honey bees can be exposed to heavy metals when foraging on contaminated honey and pollen resources, and in some cases by airborne exposure. We studied the joint acute and chronic effects of cadmium (Cd) and copper (Cu) on A. mellifera. A 1:1 solution of the two heavy metals increased larval developmental duration and the mortality of both larvae and foragers in a dose-dependent way, decreased forager feeding, increased body metal burdens, and disrupted the sucrose response behavior of foragers. In combination, Cd and Cu demonstrated a weakly synergistic effect on foragers, but for larvae an initially antagonistic effect at low doses changed to strongly synergistic response at higher concentrations. The sucrose response threshold of foragers decreased significantly when they were dosed with increasing concentrations of the metal mixtures. Overall, the fitness of honey bee larvae and foragers is detrimentally affected when these metals co-occur.

Characterization of midgut trypsinogen-like cDNA and enzymatic activity in Plutella xylostella parasitized by Cotesia vestalis or Diadegma semiclausum.

Protein digestion in insects is a result of the action of a complex of proteinases present in the midgut. In this report we describe the cloning and sequencing of a trypsin cDNA from larvae of the lepidopteran herbivore Plutella xylostella. We investigated the expression of this gene and enzymatic activity of its translation product with N-a-benzoyl-l-arginine p-nitroanilide (BApNA) as substrate in P. xylostella larvae that were either unparasitized or parasitized by Cotesia vestalis or Diadegma semiclausum parasitoids. The full cDNA sequence consisted of an open reading frame (ORF) encoding 273 amino acid residues including 23 residues of a signal peptide, and the predicted mature trypsinogen-like enzyme had a molecular mass of 26.5 kDa. The amino acid sequence of this trypsinogen-like enzyme protein and phylogenetic relationship with other published trypsin enzyme proteins suggested that it may be a new proteinase in the trypsin protein family. Parasitism of D. semiclausum did not significantly change the mRNA transcript level or BApNAase activity in host larvae. By contrast, parasitization by C. vestalis induced higher transcript levels coupled with a higher level of BApNAase activity. The BApNAase activity in the midgut of nonparasitized or parasitized P. xylostella larvae increased to a maximum level at pH 12, and the parasitism by both C. vestalis and D. semiclausum increased sensitivity of the enzyme to pH values ranging from 2 to 9.5. These parasitoid-induced changes may represent host manipulation by the developing parasitoid larva.

Characterization of an IkappaB-like gene in Cotesia vestalis polydnavirus.

Cotesia vestalis (Braconidae, Hymenoptera) depends mainly on 3 regulatory factors to manipulate its host's development and immune response, including polydnavirus, venom, and teratocytes, among which polydnavirus plays a key role in suppressing the host immune system. In the present work, we cloned the full sequence of gene CvBV-ank2, encoding an IkappaB-like protein in C. vestalis polydnavirus (CvBV). The full sequence of CvBV-ank2 is 955 bp, encoding 162 amino acids with a calculated molecular mass of 18,355 Da. CvBV-ank2 shares high similarity with the exon I and exon II of CvBV-ank1, which is on the same segment with CvBV-ank2. This result suggests that gene duplication might occur in CvBV-ank1 and CvBV-ank2. Phylogenetic analysis indicated that CvBV-ank2 and CvBV-ank1, both on segment CvBV-S2, are, respectively, closely related with CcBV-26.3 and CcBV-26.2, both on segment Circle26 of C. congregata polydnavirus (CcBV). BLAST search using the sequence of segment CvBV-S2 as a query revealed that segment CvBV-S2 shares 90% max identity with segment Circle26 of CcBV over 67% query coverage. These results demonstrate that there is not only gene similarity, but also segment similarity between CvBV and CcBV. Transcripts of CvBV-ank2 were detected as early as 0.5 h post-parasitization and continued to be detected for 6 days, indicating that CvBV-ank2 might be involved in the early protection of the parasitoid egg.

Effects of venom/calyx fluid from the endoparasitic wasp Cotesia plutellae on the hemocytes of its host Plutella xylostella in vitro.

Crude venom and calyx fluid from Cotesia plutellae (Hymenoptera Braconidae) were assayed for biological activity toward hemocytes of Plutella xylostella (Lepidoptera Plutellidae). Venom from C. plutellae displayed high activity toward the spreading of plasmatocytes of P. xylostella early in the incubation period, and the inhibition was more severe as the concentration of venom increased. However, most inhibited hemocytes spread normally after being incubated for 4h. No effects were found toward granular cells from the host. Additionally, the venom from C. plutellae had some lethal effects on hemocytes of P. xylostella at high concentrations. In contrast, when incubated with different concentrations of calyx fluid, the spreading of some hemocytes was inhibited, some began to disintegrate, and some were badly damaged with only the nucleus left. After 4h, the majority of hemocytes died. The same results were observed when hemocytes were incubated in calyx fluid together with venom. These results show that calyx fluid from C. plutellae may play a major role in the suppression of the host immune system, whereas venom from C. plutellae has a limited effect on hemocytes and probably synergizes the effect of calyx fluid or polydnavirus.

Dodecahedral W@WC Composite as Efficient Catalyst for Hydrogen Evolution and Nitrobenzene Reduction Reactions.

Core-shell composites with strong phase-phase contact could provide an incentive for catalytic activity. A simple, yet efficient, H2O-mediated method has been developed to synthesize a mesoscopic core-shell W@WC architecture with a dodecahedral microstructure, via a one-pot reaction. The H2O plays an important role in the resistance of carbon diffusion, resulting in the formation of the W core and W-terminated WC shell. Density functional theory (DFT) calculations reveal that adding W as core reduced the oxygen adsorption energy and provided the W-terminated WC surface. The W@WC exhibits significant electrocatalytic activities toward hydrogen evolution and nitrobenzene electroreduction reactions, which are comparable to those found for commercial Pt/C, and substantially higher than those found for meso- and nano-WC materials. The experimental results were explained by DFT calculations based on the energy profiles in the hydrogen evolution reactions over WC, W@WC, and Pt model surfaces. The W@WC also shows a high thermal stability and thus may serve as a promising more economical alternative to Pt catalysts in these important energy conversion and environmental protection applications. The current approach can also be extended or adapted to various metals and carbides, allowing for the design and fabrication of a wide range of catalytic and other multifunctional composites.

Loss of the Opa interacting protein 5 inhibits breast cancer proliferation through miR-139-5p/NOTCH1 pathway.

Opa interacting protein 5 (OIP5) has been reported to be over-expressed in several kinds of human cancer. However, the biological function and clinical significance of OIP5 in human breast cancer remains unknown. In this study, we found that OIP5 was notably over-expressed in breast cancer tissues compared with their corresponding nontumorous tissues. Statistical analysis showed a significant correlation of OIP5 expression with advanced clinical stage. Ablation OIP5 inhibited the proliferation of breast cancer cells. OIP5 over-expression inhibited hsa-miR-139-5p expression, antagonized its functions and led to the de-repression of its endogenous target NOTCH1, which was a core oncogene in promoting breast cancer progression. Our results suggested that OIP5 is a potential diagnosis biomarker and therapeutic target for breast cancer.

Using rare earth elements to constrain particulate organic carbon flux in the East China Sea.

Fluxes of particulate organic carbon (POC) in the East China Sea (ECS) have been reported to decrease from the inner continental shelf towards the outer continental shelf. Recent research has shown that POC fluxes in the ECS may be overestimated due to active sediment resuspension. To better characterize the effect of sediment resuspension on particle fluxes in the ECS, rare earth elements (REEs) and organic carbon (OC) were used in separate two-member mixing models to evaluate trap-collected POC fluxes. The ratio of resuspended particles from sediments to total trap-collected particles in the ECS ranged from 82-94% using the OC mixing model, and 30-80% using the REEs mixing model, respectively. These results suggest that REEs may be better proxies for sediment resuspension than OC in high turbidity marginal seas because REEs do not appear to undergo degradation during particle sinking as compared to organic carbon. Our results suggest that REEs can be used as tracers to provide quantitative estimates of POC fluxes in marginal seas.

SHCBP1 is over-expressed in breast cancer and is important in the proliferation and apoptosis of the human malignant breast cancer cell line.

BACKGROUND: SHC SH2-binding protein 1, a member of Src homolog and collagen homolog (Shc) family, has been recently identified in different contexts in unbiased screening assays. It has been reported to be over-expressed in several malignant cancers. METHODS: Immunohistochemistry of SHCBP1 on 128 breast cancer tissues and adjacent normal tissues were used to evaluate the prognostic significance of SHCBP1. Survival analyses were performed by Kaplan-Meier method. CRISPR/CAS9 method was used to knockout SHCBP1 expression. CRISPR/CAS9 technology was used to knockout SHCBP1 in 2 breast cancer cell lines. MTT assay, BrdU assay, colony formation assay, cell cycle assay and apoptosis analysis in MCF-7 and MDA-MB-231 cell lines were carried out to evaluate the effects of SHCBP1 on breast cancer in vitro. RESULTS: Immunohistochemical analysis revealed SHCBP1 was significantly up-regulated in breast cancer tissues compared with adjacent normal tissues (82 of 128, 64%). Over-expressed SHCBP1 was correlated with advanced clinical stage and poorer survival. Ablation of SHCBP1 inhibited the proliferation in vitro. SHCBP1 knockout increased cyclin-dependent kinase inhibitor p21, and decreased the Cyclin B1 and CDK1. CONCLUSION: Our study suggests SHCBP1 is dysregulated expressed in breast cancer and plays a critical role in cancer progression, which can be a potential prognosis predictor of breast cancer.

Cartilage Oligomeric Matrix Protein-Angiopoietin-1 Has a Protective Effect of Vascular Endothelial Barrier in Rat With Acute Necrotizing Pancreatitis.

OBJECTIVE: To investigate the protective effect of angiopoietin-1 (Ang-1) from capillary endothelial damage in rats with acute necrotizing pancreatitis (ANP). METHODS: 96 male Sprague-Dawley rats were randomly averaged and divided into control group, ANP group, Si-Ang-1 group, and COMP (cartilage oligomeric matrix protein)-Ang-1 group. Animals were killed at 6, 12, and 24 hours after molding. Levels of serum amylase, porcine endothelin 1, C-reactive protein, and Ang-1 were detected; histopathological changes in the pancreas were observed; capillary permeability and Ang-1 expression of the pancreatic tissue were detected by Evans Blue extravasation assay, immunohistochemistry, Western blot, and quantitative polymerase chain reaction. RESULTS: (1) Levels of serum amylase, C-reactive protein, and porcine endothelin-1 increased and level of Ang-1 decrease in the ANP group and Si-Ang-1 group compared with the control group, whereas COMP-Ang-1 group could improve the changes. (2) The order of pancreas pathological changes (mild to severe) is: control group, COMP-Ang-1 group, ANP group, and Si-Ang-1 group. (3) Capillary permeability of the pancreatic tissue in the COMP-Ang-1 group was lower than that in the ANP group. (4) Ang-1 mRNA and protein expression in the COMP-Ang-1 group was significantly higher than in the ANP group. CONCLUSIONS: COMP-Ang-1 can upregulate the expression of Ang-1 protein to promote angiogenesis and improve early inflammatory and pathological damage in ANP group.

[Expression of miR-16 in patients with T lymphoblastic lymphoma/acute lymphoblastic leukemia].

This study was purposed to investigate the expression of miR-16 in T lymphoblastic lymphoma/acute lymphoblastic leukemia (T-LBL/ALL) and its relation with target therapy and prognosis. The CD3, cCD3, CD10, CD20, CD34, CD43, CD99, TdT, PAX-5, BCL-2 and Ki67 in paraffin samples from 38 cases of T-LBL/ALL were detected by immunohistochemical labeling; the miR-16 expression level was detected by real-time RT-PCR. Fifteen cases of reactive hyperplasia of lymph nodes were selected as control. The results indicated that among 38 cases of T-LBL/ALL the positive rate of TdT was highest (94.7%), the positive rate of CD34 was lowest (22.1%), the PAX-5 and CD20 were found to be negative. The Ki67 expression level in 39.5% cases exceeded 80%. As compared with reactive hyperplasia of lymph node, the miR-16 expression in T-LBL/ALL was up-regulated, ant its expression level was 4.87-fold of reactive hyperplasia of lymph node (P < 0.05). The overall survival rate in group of miR-16 high expression decreased (P < 0.05). The prognosis of T-LBL/ALL patients with BCL-2 positive expression was better than that of patients with BCL-2 negative expression (P < 0.05). The miR-16 expression correlated with BCL-2 protein (r = 0.51, P < 0.05). It is concluded that the overall survival rate in miR-16 high expression group is higher than that in miR-16 low expression group, suggesting possible relation of miR-16 with prognosis. Moreover, the prognosis in BCL-2 positive expression group is better than that in negative expression group, which may be a factor influencing prognosis.