Search

Environmental awareness is currently significant caring in all industrial sectors, particularly in the animal industries. Animals are directly affected by environmental conditions and climate changes. Working dog is costly production in time and money to be successful. Health and temperament are key factors to be successful in training dog program. Working training dog school, NPUST is located in mountainous areas. The weather has frequently extreme change in temperature and humidity. The changes cause the heat in in-house and humidity in the air that may cause the dog illness. Therefore, working training dog school has to provide an appropriate kennel environment for all dogs throughout the training program. In order to secure the dogs, the automatic environmental sensing should be deployed. Web sensors and radio frequency identification (RFID) technologies were integrated, and have been implemented that are the weather sensing system and in-out control system, combining with health care management. Web based monitoring systems have provided based on user-friendly interface along with real-time information. In addition, it is very attractive use when the system operating via more convenient for computer and mobile communication devices. [ABSTRACT FROM AUTHOR]

Abstract: Nanomaterials can enhance the delivery and treatment efficiency of anticancer drugs, but the mechanisms of the tumor-reducing activity of ferrous-ferric oxide (Fe3O4) nanoparticles (NPs) with daunorubicin (DNR) have not been established. Here we investigate the synergistic effects of Fe3O4 NPs with DNR on the induction of apoptosis using K562 leukemia cells. Fe3O4 NPs increased the ability of DNR to induce apoptosis in both adriamycin-sensitive and adriamycin-resistant K562 cells through the caspase 8-poly(ADP-ribose) polymerase pathway. Fe3O4 NPs combined with DNR also effectively inhibited the tumor growth induced by the inoculation of K562 cells into nude mice. The increased cell apoptotic rate was closely correlated with the enhanced inhibition of tumor growth. Biodistribution studies in xenograft tumors indicated that Fe3O4 NPs could be potentially excreted from the body via the gastrointestinal system. In conclusion, our study suggests that Fe3O4 NPs combined with anticancer drugs could serve as a better alternative for targeted therapeutic approaches to cancer treatments.▪ From the Clinical Editor: In this paper, the synergistic effects on tumor growth of ferrous-ferric oxide nanoparticles with daunorubicin are investigated. The combined treatment was demonstrated to be superior in a leukemia cell line murine model in vivo. [Copyright &y& Elsevier]

10-Hydroxycamptothecin (HCPT) elicits strong anti-cancer effects and is less toxic than camptothecin (CPT), making it widely used in recent clinical trials. However, its low solubility limits its application as an effective anti-cancer therapy. In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated FeO nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway. We characterized the HCPT-loaded nanoparticles and determined their effects on lung cancer cell viability and apoptosis by using immunofluorescence light microscopy and SDS-PAGE/immunoblots. We found that HCPT-loaded nanoparticles elicited an anti-proliferative effect in a dose-dependent manner. HCPT-loaded nanoparticles reduced the expression of cell-cell junction protein claudins, E-cadherin and ZO-1, and transmission electron microcopy demonstrated a disrupted tight junction ultrastructure. Transepithelial electric resistance was also reduced, indicating the reduction of tight junction functions. The HCPT-loaded nanoparticles increased phosphorylation of p38 and SAPK/JNK while it showed no effects on p42/44 MAP kinase. Compared with void FeO nanoparticles or HCPT drug alone, HCPT drug-loaded nanoparticles evoked synergistic effects by increasing cell apoptosis with enhanced activation of the caspase-8 pathway. Therefore, our current study highlights the potential of HCPT drug-loaded nanoparticles as a chemotherapeutic agent for increasing anti-cancer drug efficacy. ( Cancer Sci 2011; 102: 1216-1222) [ABSTRACT FROM AUTHOR]

A simple, efficient, and cost-effective extended graphite as a supporting platform further supported the MnO2 growth for the construction of hierarchical flower-like MnO2/extended graphite. MnO2/extended graphite exhibited an increase in sp2 carbon bonds in comparison with that of extended graphite. It can be expected to display better electrical conductivity and further promote electron/ion transport kinetics for boosting the electrochemical performance in supercapacitors and glucose sensing. In supercapacitors, MnO2/extended graphite delivered an areal capacitance value of 20.4 mF cm−2 at 0.25 mA cm−2 current densities and great cycling stability (capacitance retention of 83% after 1000 cycles). In glucose sensing, MnO2/extended graphite exhibited a good linear relationship in glucose concentration up to about 5 mM, sensitivity of 43 μA mM−1cm−2, and the limit of detection of 0.081 mM. It is further concluded that MnO2/extended graphite could be a good candidate for the future design of synergistic multifunctional materials in electrochemical techniques. [ABSTRACT FROM AUTHOR]

Abstract: Mutations in WNK4 have been linked to hypertension in PHAII. Paracellular ion transport has been reported to be involved in this disease process; however, the specific molecular target has not been identified. In this study, we found that TJ protein claudin-7 and WNK4 were partially co-localized in renal tubules of rat kidney and co-immunoprecipitated in kidney epithelial cells. The wild-type and PHAII-causing mutant, but not the kinase-dead mutant, phosphorylated claudin-7. We have identified ser206 in the COOH-terminus of claudin-7 as a putative phosphorylation site for WNK4. More importantly, disease-causing mutant enhanced claudin-7 phosphorylation and significantly increased paracellular permeability to Cl−. [Copyright &y& Elsevier]

Summary: δ-Catenin, or neural plakophilin-related armadillo protein, is a unique armadillo domain-containing protein in that it is neural-specific and primarily expressed in the brain. However, our recent analysis of the human genome revealed a consistent association of δ-catenin messenger RNA sequences with malignant cells, although the significance of these findings was unclear. In this study, we report that a number of δ-catenin epitopes were expressed in human prostate cancer cells. Western blot and tissue microarray revealed a close association between increased δ-catenin expression and human primary prostatic adenocarcinomas. The analyses of 90 human prostate cancer and 90 benign prostate tissue samples demonstrated that an estimated 85% of prostatic adenocarcinomas showed enhanced δ-catenin immunoreactivity. δ-Catenin expression increased with prognostically significant increased Gleason scores. By analyzing the same tumor cell clusters using consecutive sections, we showed that an increased δ-catenin immunoreactivity was accompanied by the down-regulation and redistribution of E-cadherin and p120ctn, major cell junction proteins whose inactivation is frequently associated with cancer progression. Furthermore, overexpression of δ-catenin in tumorigenic CWR-R1 cells that are derived from human prostate cancer xenograft resulted in reduced immunoreactivity for E-cadherin and p120ctn at the cell-cell junction. This is the first study comparing overexpression of δ-catenin with the E-cadherin/catenin system in cancer and shows that δ-catenin may be intimately involved in regulating E-cadherin/p120ctn cell-cell adhesion in prostate cancer progression. [Copyright &y& Elsevier]

In this study, nanostructured gold was successfully prepared on a bare Au electrode using the electrochemical deposition method. Nanostructured gold provided more exposed active sites to facilitate the ion and electron transfer during the electrocatalytic reaction of organophosphorus pesticide (methyl parathion). The morphological and structural characterization of nanostructured gold was conducted using field-emission scanning electron microscopy (FESEM), X-ray photoelectron spectroscopy (XPS), and X-ray diffraction (XRD), which was further carried out to evaluate the electrocatalytic activity towards methyl parathion sensing. The electrochemical performance of nanostructured gold was investigated by electrochemical measurements (cyclic voltammetry (CV) and differential pulse voltammetry (DPV)). The proposed nanostructured gold-modified electrode exhibited prominent electrochemical methyl parathion sensing performance (including two linear concentration ranges from 0.01 to 0.5 ppm (R2 = 0.993) and from 0.5 to 4 ppm (R2 = 0.996), limit of detection of 5.9 ppb, excellent selectivity and stability), and excellent capability in determination of pesticide residue in real fruit and vegetable samples (bok choy and strawberry). The study demonstrated that the presented approach to fabricate a nanostructured gold-modified electrode could be practically applied to detect pesticide residue in agricultural products via integrating the electrochemical and gas chromatography coupled with mass spectrometry (GC/MS-MS) analysis. [ABSTRACT FROM AUTHOR]

Investigates the ability of mutant occludin molecules to assemble in tight injunctions during the biogenesis of an epithelium in an organism, focusing on cell biology. Methodology used in the investigation; Importance of occludin to cells; Results from the investigation; Provision of statistical information.

We have investigated the effects of temperature on the conductance and voltage-dependent kinetics of cardiac gap junction channels between pairs of seven-day embryonic chick ventricle myocytes over the range of 14-26 degrees C. Records of junctional conductance (Gj) and steady-state unit junctional channel activity were made using the whole-cell double patch-clamp technique while the bath temperature was steadily changed at a rate of about 4 degrees C/min. The decrease in Gj upon cooling was biphasic with a distinct break at 21 degrees C. In 12 cell pairs, Q10 was 2.2 from 26 to 21 degrees C, while between 21 and 14 degrees C it was 6.5. The mean Gj at 22 degrees C (Gj22) was 3.0 +/- 2.1 nS, ranging in different preparations from 0.24 to 6.4 nS. At room temperature, embryonic cardiac gap junctions contain channels with conductance states near 240, 200, 160, 120, 80 and 40 pS. In the present study, we demonstrate that cooling decreases the frequency of channel openings at all conductance levels, and at temperatures below 20 degrees C shifts the prevalence of openings from higher to lower conductance states: all 240 pS openings disappear below 20 degrees C; 200 pS openings are suppressed at 17 degrees C; below 16 degrees C 160 and 120 pS events disappear and only 80 and 40 pS states are seen. Temperature also affected the voltage-dependent kinetics of the channels. Application of a 6 sec, 80 mV voltage step across the junction (Vj80) caused a biexponential decay in junctional conductance. Decay was faster at lower temperatures, whereas the rate of recovery of Gj after returning to Vj0 was slowed. Cooling reduced the fast decay time constant, increased both recovery time constants, and decreased the magnitude of Gj decay, thus leaving a 10-16% larger residual conductance (Gss/Ginit, +/- 80 mV Vj) at 18 than at 22 degrees C. From these results we propose that embryonic chick cardiac gap junctions contain at least two classes of channels with different conductances and temperature sensitivities. [ABSTRACT FROM AUTHOR]

We used the double whole-cell voltage-clamp technique on ventricle cell pairs isolated from 7-day chick heart to measure the conductance of their gap junctions ( G) and junctional channels ( γ) with a steady-state voltage difference ( V) applied across the junction. Currents were recorded from single gap junction channels ( i) as symmetrical rectangular signals of equal size and opposite sign in the two cells, and γ was measured from i/ V. We observed channel openings at six reproducible conductance levels with means of 42.6, 80.7, 119.6, 157.7, 200.4 and 240.3 pS. More than half of all openings were to the 80-and 160-pS conductance levels. The probability that a high conductance event (e.g., 160 or 240 pS) results from the random simultaneous opening of several 40-pS channels is small, based on their frequency of occurrence and on the prevalence of shifts between small and large conductance states with no intervening 40-pS steps. Our results are consistent with three models of embryonic cardiac gap junction channel configuration: a homogeneous population of 40-pS channels that can open cooperatively in groups of up to six; a single population of large channels with a maximal conductance near 240 pS and five smaller substates; or several different channel types, each with its own conductance. G was determined from the junctional current ( I) elicited by rectangular pulses of applied transjunctional voltage as I/ V. It was highest near 0 V and was progressively reduced by application of V between 20 and 80 mV or −20 and −80 mV. In response to increases in V, G decayed in a voltage-and timedependent fashion. After a 6-sec holding period at 0 V, the initial conductance ( G) measured immediately after the onset of an 80-mV step in V was nearly the same as that measured by a 10-mV prepulse. However, during 6-sec pulses of V>±20 mV, G declined over several seconds from G to a steady-state value ( G). At potentials greater than ±20 mV the current decay could be fit with biexponential curves with the slow decay time constant ( τ) 5-20 times longer than τ. For the response to a step to 80 mV V, for example, τ=127 msec and τ=2.6 sec. The rate of current decay in response to smaller positive or negative steps in V was slower, the magnitude of the decline was smaller, and the ratio τ/ τ decreased. The relationship between G and V was approximately linear between 0 and 80 mV or −80 mV. whereas the relationship between G and V was nonlinear beyond ±20 mV. Upon returning to 0 V, G recovered with a biexponential time course, reaching its maximal value after several seconds; recovery time constants after a step in V from 80 to 0 mV were 225 msec and 1.9 sec. In the resting state, at low junctional voltage, high conductance channel activity (160-240 pS) is favored. Voltage-dependent decline of G results in part from a shift from high to lower conductance states. [ABSTRACT FROM AUTHOR]

The tight junction protein claudin‐7 is essential for tight junction function and intestinal homeostasis. Cldn7 deletion in mice leads to an inflammatory bowel disease‐like phenotype exhibiting severe intestinal epithelial damage, weight loss, inflammation, mucosal ulcerations, and epithelial hyperplasia. Claudin‐7 has also been shown to be involved in cancer metastasis and invasion. Here, we test our hypothesis that claudin‐7 plays an important role in regulating colonic intestinal stem cell function. Conditional knockout of Cldn7 in the colon led to impaired epithelial cell differentiation, hyperproliferative epithelium, a decrease in active stem cells, and dramatically altered gene expression profiles. In 3D colonoid culture, claudin‐7–deficient crypts were unable to survive and form spheroids, emphasizing the importance of claudin‐7 in stem cell survival. Inhibition of the Hippo pathway or activation of Notch signaling partially rescued the defective stem cell behavior. Concurrent Notch activation and Hippo inhibition resulted in restored colonoid survival, growth, and differentiation to the level comparable to those of wild‐type derived crypts. In this study, we highlight the essential role of claudin‐7 in regulating Notch and Hippo signaling–dependent colonic stem cell functions, including survival, self‐renewal, and differentiation. These new findings may shed light on potential avenues to explore for drug development in colorectal cancer. [ABSTRACT FROM AUTHOR]

Claudin-7 knockout (CLDN7−/−) mice display renal salt wasting and dehydration phenotypes. To address the role of CLDN7 in kidneys, we established collecting duct (CD) cell lines from CLDN7+/+ and CLDN7−/− mouse kidneys. We found that deletion of CLDN7 increased the transepithelial resistance (TER) and decreased the paracellular permeability for Cl− and Na+ in CLDN7−/− CD cells. Inhibition of transcellular Cl− and Na+ channels has no significant effect on TER or dilution potentials. Current-voltage curves were linear in both CLDN7+/+ and CLDN7−/− CD cells, indicating that the ion flux was through the paracellular pathway. The impairment of Cl− and Na+ permeability phenotype can be rescued by CLDN7 re-expression. We also found that WNK4 (its mutations lead to hypertension) expression, but not WNK1, was significantly increased in CLDN7−/− CD cell lines as well as in primary CLDN7−/− CD cells, suggesting that the expression of WNK4 was modulated by CLDN7. In addition, deletion of CLDN7 upregulated the expression level of the apical epithelial sodium channel (ENaC), indicating a potential cross-talk between paracellular and transcellular transport systems. This study demonstrates that CLDN7 plays an important role in salt balance in renal CD cells and modulating WNK4 and ENaC expression levels that are vital in controlling salt-sensitive hypertension. [ABSTRACT FROM AUTHOR]

Background: Barrett's esophagus (BE) is a premalignant condition with increased incidence worldwide both in old and young individuals. However, the role of certain potential risk factors remains unclear in young adults (< 50 years). We aimed to determine the risk factors of BE in young adults. Methods: A total of 4943 young adults who underwent upper gastrointestinal endoscopy at our health check-up center were enrolled. The diagnosis of BE was based on histological confirmation. We analyzed demographic factors, laboratory data, potential risk factors such as smoking, alcohol consumption, presence of gastroesophageal reflux disease (GERD) symptoms, and metabolic syndrome for the risk of BE by using binary logistic regression analysis. Results: The prevalence of BE was 1.8% (88/4943). Male sex, the presence of GERD symptoms, and smoking were three significant risk factors related to BE. Furthermore, participants who had smoked for 10 pack-years or more had increased risk of BE with dose-dependent phenomenon (p trend < 0.001). The proportion of BE in male participants with both GERD symptoms and a smoking history of 10 pack-years or more was as high as 10.3% (16/155). Conclusions: Significant risk factors of BE in young adults are male sex, the presence of GERD symptoms, and smoking. The risk also increases with an increase in cumulative exposure to smoking. [ABSTRACT FROM AUTHOR]

Background: Necrotizing enterocolitis (NEC) is a leading cause of death in preterm infants. Neonates weighing <1500 grams are at the highest risk for acquiring NEC, with a prevalence of nearly 7-10%, mortality up to 30%, and several long-term complications among survivors. Despite advancements in neonatal medicine, this disease remains a challenge to treat. The aim of this study is to investigate the effect of NEC on gut epithelial tight junctions and its barrier function using a NEC mouse model.Methods: Three-day old C57BL/6 mouse pups were fed with Esbilac formula every 3 hours and then subjected to hypoxia twice daily followed by cold stress. Dam fed pups from the same litters served as controls. Pups were observed and sacrificed 96 hours after the treatments and intestines were removed for experiments. The successful induction of NEC was confirmed by histopathology. Changes in tight junction proteins in NEC intestines were studied by western blotting and immunofluorescent microscopy using specific protein markers. The gut leakage in NEC was visualized using biotin tracer molecules.Results: Our study results demonstrate that we induced NEC in >50% of experimental pups, pups lost nearly 40% of weight and their intestines showed gross changes and microscopic changes associated with NEC. There were inflammatory changes with loss of tight junction barrier function and disruption of tight junction claudin proteins in the intestines of NEC mouse model. We have demonstrated for the first time that NEC intestines develop increased leakiness as visualized by biotin tracer leakage.Conclusions: NEC leads to breakdown of epithelial barrier due to changes in tight junction proteins with increased leakiness which may explain the transmigration of microbes and microbial products from the gut lumen into the blood stream leading to sepsis like signs clinically witnessed. [ABSTRACT FROM AUTHOR]

Claudins are a family of tight junction proteins, and serve important roles in epithelial barrier, selective ion transports and cancer metastasis. Although the exact role of claudin-7 in human lung cancer has not been completely elucidated, recent clinical studies have demonstrated that claudin-7 is associated with the survival of patients with lung cancer. Our previous studies have demonstrated that claudin-7 forms a protein complex with integrin β1 in human lung cancer cells. The knockdown (KD) of claudin-7 by short hairpin RNA (shRNA) reduced integrin β1 expression and increased the cell proliferative rate, whereas claudin-7 re-expression in the KD cells decreased the cell proliferation. It is unknown as to whether claudin-7 and integrin β1 regulate cell proliferation and invasion synergistically or independently. In the present study, it was observed that ectopic expression of integrin β1 in claudin-7 KD lung cancer cells did not reduce the cell proliferation. However, integrin β1-transfected cells migrated more effectively in wound healing and cell invasion assays and were more adhesive in a cell attachment assay when compared with those of claudin-7 KD cells. This indicates that claudin-7 controls cell proliferation, while cell attachment and motility were regulated partially through integrin β1. Additionally, claudin-7 overexpression in claudin-7 KD cells resulted in an improved ability to attach to the surface of cell culture plates and a higher expression of focal adhesion proteins when compared with claudin-7 non-KD control cells, which supports the role of claudin-7 in cell adhesion and motility. Taken together, these data suggest that claudin-7 regulates cell motility through integrin β1, providing additional insight into the roles of claudins in carcinogenesis and cancer cell metastasis. [ABSTRACT FROM AUTHOR]

The present study examined the effectiveness of the method of inversing the distal clavicle anatomic locking plate to treat medial-end clavicle fractures. This involved retrospectively analyzing six cases of medial-end clavicle fractures treated using the method of inversing the distal clavicle anatomic locking plate between September 2013 and December 2015. These cases included five men and one woman with an average age of 46.3±10.6 years old and a range of 24–66 years old. Among these cases, one was type A, two were type C, and three were type D, based on the Throckmorton type classification. All patients had fresh closed fractures, which were caused by direct injury. A regular postoperative follow-up was performed and the therapeutic efficacy was evaluated systematically with reference to the Rockwood and Disability of the Arm, Shoulder and Hand (DASH) score standards. All six cases had a follow-up visit, which was between 10 and 14 months with an average of 12.0±2.2 months. All patients exhibited osseous healing and functional recovery without incision infection, nerve vascular injury, chest injury, fracture nonunion, or other complications. According to the Rockwood and DASH score standards, evaluation of the curative effect showed that five cases were excellent and one case was good, and the associated rate for achieving good or excellent outcomes was 100%. All of the DASH scores were <10. These results indicated that the effect of the treatment of medial-end clavicle fractures by the method of inversing the distal clavicle anatomic locking plate was reliable, and the functional recovery of patients was good, making this method worthy of clinical promotion. [ABSTRACT FROM AUTHOR]

Epithelial cells are polarized with defined apical tight junctions (TJs), lateral adherens junctions (AJs), and basal integrin–matrix interactions. However, it is increasingly recognized that resident cell junction proteins can be found in varying locations and with previously unrecognized functions. Our study here presents the nanoarchitecture and nanocolocalization of cell junction proteins in culture and tissue by stochastic optical reconstruction microscopy (STORM). The Z‐axial view of noncancerous MDCK‐II and PZ‐HPV‐7 cell–cell junctions resolved β‐catenin and p120ctn localizations to TJs and AJs, with p120ctn apical to β‐catenin and colocalizing with TJ protein claudin‐7. More basally, p120ctn and β‐catenin become colocalized. This topography was lost in isogenic Ras‐transformed MDCK cells and cancerous PC3 cells, where p120ctn becomes basally localized in relation to β‐catenin. Claudin‐7 gene conditional knockout (cKO) in mice also have altered polarity of p120ctn relative to β‐catenin, like that seen in normal‐to‐cancer cell phenotypic transformation. Additionally, claudin‐7 cKO resulted in redistribution and relocalization of other cell junction proteins, including claudin‐1, zonula occludens‐1, integrin α2, epithelial cell adhesion molecule, and focal adhesion kinase (FAK); specifically, integrin α2 and FAK were observed at the apical–lateral compartment. Our data show that STORM reveals regional cellular junction nanoarchitecture previously uncharacterized, providing new insight into potential trans‐compartmental modulation of protein functions. [ABSTRACT FROM AUTHOR]

A chemical study of the 80% aqueous acetone extract of aerial parts of Setaria viridis led to the isolation of three new naphthol rhamnosides, 8-O-α-L-rhamnosyl-β-sorigenin ( 1), 6-hydroxy-8-O-α-L-rhamnosyl-β-sorigenin ( 2), and 6-methoxy-8-O-α-L-rhamnosyl-β-sorigenin ( 3), together with nine ( 4-12) known compounds. Their structures were established on the basis of spectroscopic data, including IR, MS, 1D, and 2D NMR. All the 12 compounds were tested for their antioxidant activity against 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, as well as antimicrobial activity. Compounds 1-3 exhibited strong antioxidant activity with IC values of 10.5, 13.8, and 15.3 μM, respectively, and modest activity against Staphylococcus aureus (ATCC 29213). [ABSTRACT FROM AUTHOR]

Abstract: A series of cyclometalated platinum complexes with diverse coordination patterns and geometries were screened for their anticancer activity. It was discovered that the N^C^N-coordinated platinum complex based on 1,3-di(pyridyl)benzene displayed much higher cytotoxicity against human lung cancer cells NCI-H522, HCC827, and NCI-H1299, and human prostate cancer cell RV1 than cisplatin. In a sharp contrast, the C^N^N-coordinated platinum complex based on 6-phenyl-2,2′-bipyridine was ineffective on these cancer cells. This remarkable difference in cytotoxicity displayed by N^C^N- and C^N^N-coordinated platinum complexes was related to the trans effect of the carbon donor in the cyclometalated platinum complexes, which played a crucial role in facilitating the dissociation of the chloride ligand to create an active binding site. The DNA binding was studied for the N^C^N-coordinated platinum complex using electrophoresis and emission titration. The cellular uptake observed by fluorescent microscope showed that the complex is largely concentrated in the cytoplasm. The possible pathways for the cell apoptosis were studied by western blot analysis and the activation of PARP via caspase 7 was observed. [Copyright &y& Elsevier]

Summary: The expression of the melanoma-associated antigen (MAGE) genes consists of variables in all tumor types, such as lung cancer, which are relevant to be silent in all normal tissues except germ cells. They are considered as tumor-specific antigens, and are ideal targets for cancer immunotherapy. A complete MAGE genes differential expression profile analysis of lung cancer can provide this study not only various target genes for immunotherapy, but also valuable markers for further diagnosis and prognosis. This research has constructed a membrane array, which was consisted 32 MAGE genes, to detect whether the differential expression profile occurred in 52 pairs of non-small-cell lung cancer (NSCLC) samples. Nearly 32 MAGE genes have been differential expressed in NSCLC except MAGE-B1 and -E2. MAGE-B, -C, -D, and subgroup -B6, -D4 have showed prominences in lung adenocarcinoma. High-frequent expression of MAGE-D, and subgroup -A2, -D2 has also been discovered in non-metastasis group (p <0.05). However, there is no significant difference of MAGE genes differential expression shown among different primary tumor (T), nodal involvement (N) and overall stages. Several MAGE subgroup genes, such as MAGE-A5, -A7, -A8, -A9, -A11, -B3, -B4, -B10, -D2, -D3, -F1, -G1, -H1, and -L2, have been first discovered to show differential expression in NSCLC. Although the small size of the sample may limit the diagnostic and prognostic value of MAGE genes, the function of the membrane array can provide this study a high-throughput method to detect the whole MAGE genes differential expression profile. [Copyright &y& Elsevier]

Background: The Maastricht V/Florence Consensus Report recommends amoxicillin‐fluoroquinolone triple or quadruple therapy as a second‐line treatment for Helicobacter pylori infection. An important caveat of amoxicillin‐fluoroquinolone rescue therapy is poor eradication efficacy in the presence of fluoroquinolone resistance. The study aimed to investigate the efficacies of tetracycline‐levofloxacin (TL) quadruple therapy and amoxicillin‐levofloxacin (AL) quadruple therapy in the second‐line treatment of H. pylori infection. Methods: Consecutive H. pylori‐infected subjects after the failure of first‐line therapies were randomly allocated to receive either TL quadruple therapy (tetracycline 500 mg QID, levofloxacin 500 mg QD, esomeprazole 40 mg BID, and tripotassium dicitrato bismuthate 300 mg QID) or AL quadruple therapy (amoxicillin 500 mg QID, levofloxacin 500 mg QD, esomeprazole 40 mg BID, and tripotassium dicitrato bismuthate 300 mg QID) for 10 days. Post‐treatment H. pylori status was assessed 6 weeks after the end of therapy. Results: The study was early terminated after an interim analysis. In the TL quadruple group, 50 out of 56 patients (89.3%) had successful eradication of H. pylori infection. Cure of H. pylori infection was achieved only in 39 of 52 patients (69.6%) receiving AL quadruple therapy. Intention‐to‐treat analysis showed that TL quadruple therapy achieved a markedly higher eradication rate than AL quadruple therapy (95% confidence interval: 4.8% to 34.6%; p = 0.010). Further analysis revealed that TL quadruple therapy had a high eradication rate for both levofloxacin‐susceptible and resistant strains (100% and 88.9%). In contrast, AL quadruple therapy yielded a high eradication for levofloxacin‐susceptible strains (90.9%) but a poor eradication efficacy for levofloxacin‐resistant strains (50.0%). The two therapies exhibited comparable frequencies of adverse events (37.5% vs 21.4%) and drug adherence (98.2% vs 94.6%). Conclusions: Ten‐day TL quadruple therapy is more effective than AL quadruple therapy in the second‐line treatment of H. pylori infection in a population with high levofloxacin resistance. [ABSTRACT FROM AUTHOR]

Recently, carbon quantum dots (CQDs) have become popular because of their simple synthesis and potential applications. Although CQDs have high biocompatibility, their biotoxicity must be verified to reduce the possible risks associated with large-scale application. In this study, the hepatotoxicity of three CQD types, namely diammonium citrate (AC)-based (CQDs-AC), spermidine trihydrochloride (Spd)-based (CQDs-Spd), and AC- and Spd-based CQDs (CQDs-AC/Spd), were evaluated in vivo and in vitro. It was observed in vivo that CQDs-Spd and CQDs-AC/Spd, but not CQDs-AC, caused histopathological damage, including liver steatosis and mild mixed inflammatory cell infiltration; however, reduced liver function was only observed in CQD-Spd–treated mice. The in vitro results revealed that only CQDs-Spd significantly decreased the number of viable HepG2 cells (NADH depletion) and induced oxidative stress (heme oxygenase-1 activation) after 24 h of exposure, which promoted inflammatory factor secretion (NF-κB activation). Additionally, decreasing zonula occludens-2 and α1-antitrypsin protein expression in HepG2 cells suggested that CQD-Spd exposure increases the risk of liver diseases. Our results revealed that CQDs-Spd had greater hepatotoxic potential than CQDs-AC and CQDs-AC/Spd, which might be attributable to their high positive surface charge. Overall, the risk of CQD-induced hepatotoxic risk must be considered when applying positively charged CQDs. [Display omitted] • CQDs-Spd can induce histopathological harm and impair liver function. • CQDs-Spd initiates pronounced oxidative cytotoxicity. • CQDs-Spd triggers heightened inflammatory responses. • CQDs-Spd may accelerate the initial stages of liver disease. • Exposure to positively charged surface CQDs can impact hepatic well-being. [ABSTRACT FROM AUTHOR]

Background and Aim: Concomitant therapy is a recommended first‐line treatment for Helicobacter pylori infection in most national or international consensuses. Reverse hybrid therapy is a modified 14‐day concomitant therapy without clarithromycin and metronidazole in the final 7 days. This study aims to test whether 14‐day reverse hybrid therapy is non‐inferior to 14‐day concomitant therapy in the first‐line treatment of H. pylori infection. Methods: Helicobacter pylori‐infected adult patients were randomly assigned to receive either reverse hybrid therapy (dexlansoprazole 60 mg o.d. plus amoxicillin 1 g b.d. for 14 days, and clarithromycin 500 mg plus metronidazole 500 mg b.d. for initial 7 days) or concomitant therapy (dexlansoprazole 60 mg once o.d. plus amoxicillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg b.d. for 14 days). H. pylori status was assessed 6 weeks after the end of treatment. Results: Helicobacter pylori‐infected participants (n = 248) were randomized to receive either 14‐day reverse hybrid therapy (n = 124) or 14‐day concomitant therapy (n = 124). Intention‐to‐treat analysis demonstrated that the two therapies had comparable eradication rate (95.2% vs 93.5%; 95% confidence interval, −4.0% to 7.4%; P = 0.582). However, reverse hybrid therapy had a much lower frequency of adverse events than concomitant therapy (20.2% vs 38.7%, P = 0.001). The two therapies exhibited comparable drug adherence (93.5% vs 87.9%, P = 0.125). Conclusions: Fourteen‐day reverse hybrid therapy and 14‐day concomitant therapy are equivalent in efficacy for the first‐line treatment of H. pylori infection. However, reverse hybrid therapy has fewer adverse events compared with concomitant therapy. [ABSTRACT FROM AUTHOR]

This study investigated the kinetics of estimated glomerular filtration rate (eGFR) and quantitative hepatitis B surface antigen (qHBsAg) in telbivudine (LdT)-treated chronic hepatitis B (CHB) patients whose treatment was subsequently adjusted with the adding on adefovir or by switching to tenofovir disoproxil fumarate (TDF) as rescue. Of 295 CHB patients initially treated with LdT, 102 of them who subsequently receiving either adding-on adefovir (group A, n = 58) or switching to TDF (group B, n = 44) for more than 24 months were enrolled. Serial eGFR and qHBsAg levels (3 to 6 monthly) in both LdT monotherapy and rescue therapy periods were analyzed retrospectively. Subsequent decline of qHBsAg especially in rescue therapy period were noted (p<0.001 and p = 0.068 in group A and B). However, patients in group B achieved a significant increase of eGFR (p = 0.010) in LdT monotherapy period but had a significant decline of eGFR (p<0.001) in rescue therapy period. In contrast, patients in group A maintained eGFR levels in both periods. Meanwhile, switch to TDF (hazard ratio: 3.036; 95% confidence interval: 1.040–8.861; p = 0.042) was the sole factor related to the decrease of eGFR>20% from baseline. Both rescue therapies achieved subsequent declines of qHBsAg over time but caused different changes in eGFR. LdT-based rescue therapy maintained eGFR but TDF switching therapy descended eGFR. Therefore, it is essential to monitor patient's renal function intensively when switching from LdT to TDF as a rescue strategy. [ABSTRACT FROM AUTHOR]

Purpose: Evidence has shown that propofol may cause widespread apoptotic neurodegeneration. Hypoxic preconditioning has been demonstrated to provide neuroprotection and brain recovery from both acute and chronic neurodegeneration in several cellular and animal models. However, the mechanism has not been well elucidated. Therefore, the present study was designed to investigate the expression of glucose transporters (GLUT1 and GLUT3) and mitochondrial division and fusion (Drp1 and Mfn2) proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity. Methods: Propofol (100 mg/kg) was given to 7-day-old Sprague-Dawley rats; in some rats, hypoxic preconditioning was administered before intraperitoneal propofol injection by subjecting rats to five cycles of 10 min of hypoxia (8% O2) and 10 min of normoxia (21% O2). Then, the rats were allowed to breathe room air for 2 h. Neuronal mitochondrial morphology was observed by transmission electron microscopy. ATP content was detected using an ATP assay kit. The expression levels of GLUT1, GLUT3, pDrp1, Drp1 and Mfn2 were detected by Western blot, and the expression levels of GLUT1 and GLUT3 were further examined by immunohistochemistry. Results: Propofol damaged mitochondria, and decreased ATP content and GLUT3 and pDrp1 protein expression. However, our results suggested that hypoxic preconditioning could attenuate propofol neurotoxicity by reducing mitochondrial damage and increasing ATP content and pDrp1, GLUT1 and GLUT3 protein expression. Conclusion: Hypoxic preconditioning reduced propofol-induced damage in the hippocampus of neonatal rats by attenuating the increase in mitochondrial division and decrease in GLUT3 expression. [ABSTRACT FROM AUTHOR]

Background and Aims: Anti‐Helicobacter pylori therapy may lead to the growth of pathogenic or antibiotic‐resistant bacteria in the gut. The study aimed to investigate the short‐term and long‐term impacts of H. pylori eradication with reverse hybrid therapy on the components and macrolide resistance of the gut microbiota. Methods: Helicobacter pylori‐related gastritis patients were administered a 14‐day reverse hybrid therapy. Fecal samples were collected before treatment and at the end of week 2, week 8, and week 48. The V3–V4 region of the bacterial 16S rRNA gene in fecal specimens was amplified by polymerase chain reaction and sequenced on Illumina MiSeq platform. Additionally, amplification of erm(B) gene (encoding erythromycin resistance methylase) was performed. Results: Reverse hybrid therapy resulted in decreased relative abundances of Firmicutes (from 62.0% to 30.7%; P < 0.001) and Actinobacteria (from 3.4% to 0.6%; 0.032) at the end of therapy. In contrast, the relative abundance of Proteobacteria increased from 10.2% to 49.1% (0.002). These microbiota alterations did not persist but returned to the initial levels at week 8 and week 48. The amount of erm(B) gene in fecal specimens was comparable with the pretreatment level at week 2 but increased at week 8 (0.025) and then returned to the pretreatment level by week 48. Conclusions: Helicobacter pylori eradication with reverse hybrid therapy can lead to short‐term gut dysbiosis. The amount of erm(B) gene in the stool increased transiently after treatment and returned to the pretreatment level at 1‐year post‐treatment. [ABSTRACT FROM AUTHOR]