Effect of Treatment with Microarc Oxidation Technology on Tribological Properties of Nonvalve Metal Low-Carbon Steel.

Steel is one of the most widely used alloys because of its excellent properties such as high toughness, good workability, and low cost. However, steel has weak wear resistance, which limits its range of applications and service life. We have used the microarc oxidation (MAO) technique to form an Al2O3 ceramic coating on the surface of nonvalve metal low-carbon steel, which is used to enhance the wear resistance of low-carbon steel. Tribological experiments have shown that the coefficient of friction is reduced by 26.9%, hardness is improved, and wear resistance is enhanced after MAO compared to the substrate. Through a series of characterizations, the wear mechanism of the MAO samples was found to be a complex friction mechanism including abrasive wear, adhesive wear, and friction oxidation. After MAO, the wear resistance of nonvalve metal low-carbon steel is improved. The use of steel can be extended and its service life can be prolonged. This innovative approach provides a viable solution for the development of low-carbon steel coatings.

Engineered Cellular Vesicles Displaying Glycosylated Nanobodies for Cancer Immunotherapy.

Immune checkpoint blockade targeting the CD47/SIRPα axis represents an alluring avenue for cancer immunotherapy. However, the compromised efficacy and safety concerns in vivo of conventional anti-CD47 antibodies impede their wide clinical applications. Here we introduced a single type of high-mannose glycans into the nanobodies against CD47 (HM-nCD47) and subsequently displayed HM-nCD47 on cellular vesicles (CVs) for enhanced cancer immunotherapy. In this platform, the CVs significantly improved the circulation time of HM-nCD47-CVs, the nCD47 enabled the blockade of the CD47/SIRPα axis, and the HM enhanced recognition of mannose-binding lectin, all synergistically activating the macrophage-mediated antitumor immunity. In both subcutaneous and metastatic murine tumor models, the HM-nCD47-CVs possessed significantly extended half-lives and increased accumulation at the tumor site, resulting in a remarkable macrophage-dependent inhibition of tumor growth, a transcriptomic remodeling of the immune response, and an increase in survival time. By integrating the chemical biology toolbox with cell membrane nanotechnology, the HM-nCD47-CVs represent a new immunotherapeutic platform for cancer and other diseases.

Kruppel-like Factors 3 Regulates Migration and Invasion of Gastric Cancer Cells Through NF-κB Pathway.

Context: The poorly understood regulatory mechanisms impede gastric cancer therapy. Kruppel-like factors (KLFs) are associated with the development of various tumors, The studies on the role of the KLF transcription factor 13 (KLF13) in gastric cancer progression haven't been studied. Objective: The current study aimed to investigate the role of KLF13 in the migration and invasion of gastric cancer and the regulatory mechanism of KLF13 in gastric cancer progression. Design: The research team performed a laboratory study. Setting: The study took place at the Zengcheng District People's Hospital of Guangzhou in Zengcheng, China. Participants: In addition to using normal gastric cells, GES1, and seven gastric cancer cell lines, the research team compared the fresh, gastric cancer tissues (T) and paired, adjacent, noncancerous gastric tissues (ANT) from eight patients undergoing surgical resection at the hospital. The research team also downloaded the data for 33 gastric cancer tissues and adjacent, normal gastric tissues from the Cancer Genome Atlas' TCGA database. Intervention: The research team used: (1) short hairpin RNAs (shRNAs) to knock down KLF13, (2) wound healing and transwell invasion analyses to determine the effects of KLF13 on the migration and invasion of gastric cancer, and (3) a Luciferase reporter assay to determine the effects of KLF13 on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity. Results: KLF13 was upregulated in gastric cancer cells and tissues, and the patients with a high KLF13 expression had poor outcome. Downregulation of KLF13 significantly inhibited the migration and invasion of gastric cancer cells. Mechanistically, downregulation of KLF13 significantly inhibited NF-κB activity, and its targets such as: (1) snail family transcriptional repressor 1 (SNAI1 or Snail), (2) snail family transcriptional repressor 2 (SNAI2 or Slug), (3) zinc finger e-box binding homeobox 1 (ZEB1), (4) Smad interacting protein 1 (Sip1), (5) twist family basic helix-loop-helix (BHLH) transcription factor (Twist), (6) matrix metallopeptidase 2 (MMP2), and (7) MMP9. Tumor necrosis factor alpha (TNF-α) can activate NF-κB. Treating with TNF-α can reverse the effects of KLF13 downregulation on migration and invasion, confirming that KLF13 promotes the migration and invasion of gastric cancer cells through activating the NF-κB pathway. Conclusions: KLF13 promoted the migration and invasion of gastric cancer cells through activating the NF-κB pathway, providing a new target for gastric cancer therapy.

Random Traffic Flow Simulation of Heavy Vehicles Based on R-Vine Copula Model and Improved Latin Hypercube Sampling Method.

The rationality of heavy vehicle models is crucial to the structural safety assessment of bridges. To establish a realistic heavy vehicle traffic flow model, this study proposes a heavy vehicle random traffic flow simulation method that fully considers the vehicle weight correlation based on the measured weigh-in-motion data. First, a probability model of the key parameters in the actual traffic flow is established. Then, a random traffic flow simulation of heavy vehicles is realized using the R-vine Copula model and improved Latin hypercube sampling (LHS) method. Finally, the load effect is calculated using a calculation example to explore the necessity of considering the vehicle weight correlation. The results indicate that the vehicle weight of each model is significantly correlated. Compared to the Monte Carlo method, the improved LHS method better considers the correlation between high-dimensional variables. Furthermore, considering the vehicle weight correlation using the R-vine Copula model, the random traffic flow generated by the Monte Carlo sampling method ignores the correlation between parameters, leading to a weaker load effect. Therefore, the improved LHS method is preferred.

Lysine Deprivation Regulates Npy Expression via GCN2 Signaling Pathway in Mandarin Fish (Siniperca chuatsi).

Regulation of food intake is associated with nutrient-sensing systems and the expression of appetite neuropeptides. Nutrient-sensing systems generate the capacity to sense nutrient availability to maintain energy and metabolism homeostasis. Appetite neuropeptides are prominent factors that are essential for regulating the appetite to adapt energy status. However, the link between the expression of appetite neuropeptides and nutrient-sensing systems remains debatable in carnivorous fish. Here, with intracerebroventricular (ICV) administration of six essential amino acids (lysine, methionine, tryptophan, arginine, phenylalanine, or threonine) performed in mandarin fish (Siniperca chuatsi), we found that lysine and methionine are the feeding-stimulating amino acids other than the reported valine, and found a key appetite neuropeptide, neuropeptide Y (NPY), mainly contributes to the regulatory role of the essential amino acids on food intake. With the brain cells of mandarin fish cultured in essential amino acid deleted medium (lysine, methionine, histidine, valine, or leucine), we showed that only lysine deprivation activated the general control nonderepressible 2 (GCN2) signaling pathway, elevated α subunit of eukaryotic translation initiation factor 2 (eIF2α) phosphorylation, increased activating transcription factor 4 (ATF4) protein expression, and finally induced transcription of npy. Furthermore, pharmacological inhibition of GCN2 and eIF2α phosphorylation signaling by GCN2iB or ISRIB, effectively blocked the transcriptional induction of npy in lysine deprivation. Overall, these findings could provide a better understanding of the GCN2 signaling pathway involved in food intake control by amino acids.

Chemical and olfactive impacts of organic matters on odor emission patterns from the simulated construction and demolition waste landfills.

The explosive increase of construction and demolition waste (CDW) caused the insufficient source separation and emergency disposal at domestic waste landfills in many developing countries. Some organic fractions were introduced to the CDW landfill process and resulted in serious odor pollution. To comprehensively explore the impacts of organic matters on odor emission patterns, five CDW landfills (OIL), with organic matters/ inert CDW components (O/I) from 5% to 30%, and the control group only with inert components (IL) or organics (OL) were simulated at the laboratory. The chemical and olfactive characters of odors were evaluated using the emission rate of 94 odorants content (ERtotal), theory odor concentration (TOCtotal), and e-nose concentration (ERENC), and their correlations with waste properties were also analyzed. It was found that the main contributors to ERtotal (IL: 93.0% NH3; OIL: 41.6% sulfides, 31.0% NH3, 25.9% oxygenated compounds) and TOCtotal (IL: 64.1% CH3SH, 28.2% NH3; OIL: 71.7% CH3SH, 24.8% H2S) changed significantly. With the rise of O/I, ERtotal, TOCtotal, and ERENC increased by 10.9, 20.6, and 2.1 times, respectively. And the organics content in CDW should be less than 10% (i.e., DOC<101.3 mg/L). The good regressions between waste properties (DOC, DN, pH) and ERENC- (r=0.86, 0.86, -0.88, p<0.05), TOCtotal- (r=0.82, 0.79, -0.82, p<0.05) implied that the carbon sources and acidic substances relating to organics degradation might result in that increase. Besides, the correlation analysis results (ERENC-vs.TOCtotal-, r=0.96, p<0.01; vs.ERtotal-, r=0.86, p<0.05) indicated that e-nose perhaps was a reliable odor continuous monitoring tool for CDW landfills.

MAPRE1 promotes cell cycle progression of hepatocellular carcinoma cells by interacting with CDK2.

Targeting cyclin-dependent kinases (CDKs) is a promising method of therapy for cancer. Unfortunately, the efficacy of CDK inhibitors in hepatocellular carcinoma (HCC) is limited, due in part to incomplete understanding of cell cycle progression and a lack of specific biomarkers to adequately identify which patients may be responsive to CDK inhibitors. In the present study, we report that microtubule-associated protein RP/EB family member 1 (MAPRE1), a gene involved in cell cycle and microtubule regulation, is significantly increased in HCC tissue, promotes HCC cell proliferation, enhances in vitro tumorigenesis, and associates with poor prognosis of HCC. We demonstrate that MAPRE1 binds with CDK2, resulting in the hyperphosphorylation of the CDK2 Thr161 residue in HCC cells. Our findings reveal that targeting MAPRE1 might be an effective therapeutic strategy in HCC, and suggest that MAPRE1 expression might provide a promising biomarker to stratify patients with HCC who may benefit from treatment with CDK inhibitors.

Encapsulation of gemcitabine in RGD-modified nanoliposomes improves breast cancer inhibitory activity.

In this study, RGD coated GEM liposomes were prepared by the emulsification-solvent evaporation method. The in vitro and in vivo characterizations were done to evaluate the feasibility of application. The mean particle size of the prepared liposomes was found to be 165.6 ± 15.7 nm. The entrapment efficiency and drug loading of the formulation were 82.4% ± 7.2% and 10.1% ± 1.4%, respectively. The liposomes were negatively charged with a zeta potential of -25.8 mV. The surface morphology of RGD-GEM liposomes was spherical and smooth. After three months of storage at different conditions, lyophilized liposomes appeared to be stable since they showed no collapse or contraction. The Weibull model was the most appropriate kinetic model for RGD-GEM liposomes, showing that the release of GEM from the liposomes was in the manners of both dissolution and diffusion. In vivo, the additive cytotoxicity of RGD-GEM-LPs in our study was caused by the presence of RGD which is more effective in the treatment of breast cancer devoid of toxicity to normal cells. Liposomes could also significantly extend the role of GEM in vivo and showed higher bioavailability than solution.

Heterospecific alarm-call recognition in two warbler hosts of common cuckoos.

Species facing similar selection pressures should recognize heterospecific alarm signals. However, no study has so far examined heterospecific alarm-call recognition in response to parasitism by cuckoos. In this study, we tested whether two sympatric host species of the common cuckoo Cuculus canorus, Oriental reed warbler Acrocephalus orientalis (ORW, main host), and black-browed reed warbler Acrocephalus bistrigiceps (BRW, rare host), could recognize each other's alarm calls in response to cuckoos. Dummies of common cuckoo (parasite) and Eurasian sparrowhawk Accipiter nisus (predator) were used to induce and record alarm calls of the two warbler species, respectively. In the conspecific alarm-call playback experiments, ORW responded more strongly to cuckoo alarm calls than to sparrowhawk alarm calls, while BRW responded less strongly to cuckoo alarm calls than to sparrowhawk alarm calls. In the heterospecific alarm-call playback experiments, both ORW and BRW responded less strongly to cuckoo alarm calls than sparrowhawk alarm calls. BRW seemed to learn the association between parasite-related alarm calls of the ORW and the cuckoo by observing the process of ORW attacking cuckoos. In contrast, alarm calls of BRW to cuckoos were rarely recorded in most cases. BRW with low parasite pressure still developed recognition of heterospecific parasite-related alarm call. Unintended receivers in the same community should recognize heterospecific alarm calls precisely to extract valuable information.

[Correlation study on chemical constitutes of cardiac glycosides in Taxillus chinensis and its Nerium indicum host by UPLC-Q-TOF-MS/MS].

To build up an identification method on cardiac glycosides in Taxillus chinensis and its Nerium indicum host, and evaluate the influence on medicine quality from host to T. chinensis, ultra-performance liquid chromatography coupled with quadrupole-time-of-flight tandem mass-mass spectrometry(UPLC-Q-TOF-MS/MS)was applied. The samples of T. chinensis(harvested from N. indicum)and its N. indicum host were collected in field. The samples of T. chinensis(harvested from Morus alba)and its M. alba host was taken as control substance. All samples were extracted by ultrasonic extraction in 70% ethanol. Chromatographic separation was performed on an ACQUITY UPLC HSS T3 C_(18)(2.1 mm×100 mm,1.8 µm)column at 40 ℃. Gradient elution was applied, and the mobile phase was consisted of 0.1% formic acid water and acetonitrile. The 0.5 µL of sample solution was injected and the flow rate of the mobile phase was kept at 0.6 mL·min~(-1) in each run. It was done to identify cardiac glycosides and explore the chemical composition correlation in T. chinensis and its N. indicum host by analyzing positive and negative ion mode mass spectrometry data, elemental composition, cardiac glycoside reference substance and searching related literatures. A total of 29 cardiac glycosides were identified, 28 of it belonged to N. indicum host, 5 belonged to T. chinensis(harvested from N. indicum host), none of cardiac glycoside was identified in T. chinensis(harvested from M. alba host). The result could provide a reference in evaluating the influence in T. chinensis medicine quality from host. It was rapid, accurate, and comprehensive to identify cardiac glycosides in T. chinensis and its N. indicum host by UPLC-Q-TOF-MS/MS.

The lysosomal enzyme alpha-Galactosidase A is deficient in Parkinson's disease brain in association with the pathologic accumulation of alpha-synuclein.

The aberrant accumulation of alpha-synuclein (α-syn) is believed to contribute to the onset and pathogenesis of Parkinson's disease (PD). The autophagy-lysosome pathway (ALP) is responsible for the high capacity clearance of α-syn. ALP dysfunction is documented in PD and pre-clinical evidence suggests that inhibiting the ALP promotes the pathological accumulation of α-syn. We previously identified the pathological accumulation of α-syn in the brains of mice deficient for the soluble lysosomal enzyme alpha-Galactosidase A (α-Gal A), a member of the glycosphingolipid metabolism pathway. In the present study, we quantified α-Gal A activity and levels of its glycosphingolipid metabolites in postmortem temporal cortex specimens from control individuals and in PD individuals staged with respect to α-syn containing Lewy body pathology. In late-state PD temporal cortex we observed significant decreases in α-Gal A activity and the 46kDa "active" species of α-Gal A as determined respectively by fluorometric activity assay and western blot analysis. These decreases in α-Gal A activity/levels correlated significantly with increased α-syn phosphorylated at serine 129 (p129S-α-syn) that was maximal in late-stage PD temporal cortex. Mass spectrometric analysis of 29 different isoforms of globotriaosylceramide (Gb3), a substrate of α-Gal A indicated no significant differences with respect to different stages of PD temporal cortex. However, significant correlations were observed between increased levels of several Gb3 isoforms and with decreased α-Gal A activity and/or increased p129S-α-syn. Deacylated Gb3 (globotriaosylsphingosine or lyso-Gb3) was also analyzed in PD brain tissue but was below the limit of detection of 20pmol/g. Analysis of other lysosomal enzymes revealed a significant decrease in activity for the lysosomal aspartic acid protease cathepsin D but not for glucocerebrosidase (GCase) or cathepsin B in late-stage PD temporal cortex. However, a significant correlation was observed between decreasing GCase activity and increasing p129S-α-syn. Together our findings indicate α-Gal A deficiency in late-stage PD brain that correlates significantly with the pathological accumulation of α-syn, and further suggest the potential for α-Gal A and its glycosphingolipid substrates as putative biomarkers for PD.

Dynamics and Correlates of CD8 T-Cell Counts in Africans with Primary Human Immunodeficiency Virus Type 1 Infection.

In individuals with HIV-1 infection, depletion of CD4+ T cells is often accompanied by a malfunction of CD8+ T cells that are persistently activated and/or exhausted. While the dynamics and correlates of CD4 counts have been well documented, the same does not apply to CD8 counts. Here, we examined the CD8 counts in a cohort of 497 Africans with primary HIV-1 infection evaluated in monthly to quarterly follow-up visits for up to 3 years in the absence of antiretroviral therapy. Statistical models revealed that (i) CD8 counts were relatively steady in the 3- to 36-month period of infection and similar between men and women; (ii) neither geography nor heterogeneity in the HIV-1 set-point viral load could account for the roughly 10-fold range of CD8 counts in the cohort (P > 0.25 in all tests); and (iii) factors independently associated with relatively high CD8 counts included demographics (age ≤ 40 years, adjusted P = 0.010) and several human leukocyte antigen class I (HLA-I) alleles, including HLA-A*03:01 (P = 0.013), B*15:10 (P = 0.007), and B*58:02 (P < 0.001). Multiple sensitivity analyses provided supporting evidence for these novel relationships. Overall, these findings suggest that factors associated with the CD8 count have little overlap with those previously reported for other HIV-1-related outcome measures, including viral load, CD4 count, and CD4/CD8 ratio. IMPORTANCE: Longitudinal data from 497 HIV-1 seroconverters allowed us to systematically evaluate the dynamics and correlates of CD8+ T-cell counts during untreated primary HIV-1 infection in eastern and southern Africans. Our findings suggest that individuals with certain HLA-I alleles, including A*03 (exclusively A*03:01), persistently maintain relatively high CD8 counts following HIV-1 infection, a finding which may offer an intriguing explanation for the recently reported, negative association of A*03 with HIV-1-specific, broadly neutralizing antibody responses. In future studies, attention to HLA-I genotyping data may benefit in-depth understanding of both cellular and humoral immunity, as well as the intrinsic balances of these types of immunity, especially in settings where there is emerging evidence of antagonism between the two arms of adaptive immunity.

Doxycycline affects gene expression profiles in aortic tissues in a rat model of vascular calcification.

Vitamin D3-induced vascular calcification (VC) in rats shares many phenotypical similarities with calcification occurring in human atherosclerosis, diabetes mellitus and chronic kidney disease, thereby it is a reliable model for identifying chemopreventive agents. Doxycycline has been shown to effectively attenuated VC. This study aimed to explore the effects of doxycycline on gene expression profiles in VC rats. The model of VC in rats was established by subcutaneous injection of vitamin D3 for 3days. Doxycycline at 120mgkg-1day-1 was given via subcutaneous injection for 14days. Rat pathological changes, calcium deposition and calcium content in aortic tissues were measured by Hematoxylin-eosin, von Kossa staining and colorimetry, respectively. The gene change profile of aortic tissues after doxycycline treatment was assessed by Gene Microarray analysis using the Agilent Whole Rat Genome Oligo Microarray. The results showed that doxycycline significantly decreased the deposition of calcium, reduced the relative calcification area and alleviated pathological injury in aortic tissues. In addition, doxycycline treatment altered 88 gene expressions compared with untreated VD group. Of these, 61 genes were down-regulated and 27 genes were up-regulated. The functions of differentially expressed (DE) genes were involved in neutrophil chemotaxis, chronic inflammatory response, negative regulation of apoptotic process, cellular response to mechanical stimulus and immune response, etc. In conclusions, this study might provide the potential novel insights into the molecular mechanisms of doxycycline on VC.

PPFIA1 is upregulated in liver metastasis of breast cancer and is a potential poor prognostic indicator of metastatic relapse.

Although the oncogenic role of PPFIA1 (liprin-α1) in breast cancer has been reported, whether its dysregulation is associated with metastasis risk or survival outcomes in breast cancer patients is not clear. Our primary data showed that PPFIA1 expression was significantly higher in liver metastatic breast tumors than in the primary tumors. Then, we tried to pool previous annotated genomic data to assess the prognostic value of PPFIA1 in distant metastasis-free survival, the risk of metastatic relapse, and metastatic relapse-free survival in breast cancer patients by data mining in two large databases, Kaplan-Meier plotter and bc-GenExMiner 4.0. Results from Kaplan-Meier plotter showed that although high PPFIA1 expression was generally associated with decreased distant metastasis-free survival in estrogen receptor+ patients, subgroup analysis only confirmed significant association in estrogen receptor+/N- (nodal negative) group (median survival, high PPFIA1 group vs low PPFIA1 cohort: 191.21 vs 236.22 months; hazard ratio: 2.23, 95% confidence interval: 1.42-3.5, p < 0.001), but not in estrogen receptor+/N+ (nodal positive) group (hazard ratio: 1.63, 95% confidence interval: 0.88-3.03, p = 0.12). In estrogen receptor- patients, there was no association between PPFIA1 expression and distant metastasis-free survival, no matter in Nm (nodal status mixed), N-, or N+ subgroups. In bc-GenExMiner 4.0, Nottingham Prognostic Index- and Adjuvant! Online-adjusted analysis validated the independent prognostic value of PPFIA1 in metastatic risks in estrogen receptor+/N- patients. Based on these findings, we infer that high PPFIA1 expression might be an independent prognostic indicator of increased metastatic relapse risk in patients with estrogen receptor+/N- breast cancer, but not in estrogen receptor+/N+ or estrogen receptor- patients.

Influence of CYP2C9 and COX-2 Genetic Polymorphisms on Clinical Efficacy of Non-Steroidal Anti-Inflammatory Drugs in Treatment of Ankylosing Spondylitis.

BACKGROUND The aim of this study was to evaluate the relationships of CYP2C9 and COX-2 genetic polymorphisms with therapeutic efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) in treatment of ankylosing spondylitis (AS). MATERIAL AND METHODS We enrolled 130 AS inpatients and outpatients in the Arthritis and Rheumatism Department of Peking University First Hospital and 106 healthy people getting routine check-ups between September 2013 and July 2014. CYP2C9 and COX-2 genetic polymorphisms were detected by PCR-RFLP. All AS patients underwent medical treatment and 12-week follow-up treatment. Score differences of BASDAI, ASAS20, ASAS50, and ASAS70 for AS patients with different genotypes before and after treatment were compared. RESULTS In terms of COX-2-1290A/G and -1195G/A gene polymorphism genotype and allele frequency, the case group and control group were obviously different (all P<0.05), but CYP2C9*3 polymorphism genotype and allele frequency were not statistically different between the 2 groups (P>0.05). AS patients had improved BASDAI, ASAS20, ASAS50, and ASAS70 scores after they received NSAID treatment (all P<0.05). Furthermore, the efficacy of NSAID in treatment of AS and COX-2 gene -1290A/G and -1195G/A polymorphism were associated (all P<0.05), but it is not associated with CYP2C9 *3 polymorphism (all P>0.05). CONCLUSIONS COX-2-1290A/G and -1195G/A polymorphism may increase AS risk and they both can be considered as biological indicators for prediction of efficacy of NSAIDs in treatment of AS.

Enhancement of NK cells proliferation and function by Shikonin.

CONTEXT: Shikonin is a kind of naphthoquinone compound found mainly in Lithospermum erythrorhizon Sieb,et Zucc. Previous studies have shown that Shikonin has anti-tumor, anti-inflammatory and extensive pharmacological effects. According to new studies, Shikonin could also modulate the immune system function, but the effect to NK (nature killer) cells is yet unknown. OBJECTIVE: To investigate the effect and mechanism of Shikonin on NK cells proliferation and cytotoxicity to colon cancer cell line (Caco-2). METHODS: The proliferation and cytotoxicity of NK cells cultured with Shikonin were detected with CCK-8 assay. The expressions of perforin, GranB and IFN-γ were examined with FCM. The content of TNF-alpha was disclosed with ELISA kit. p-ERK1/2 and p-Akt expression of NK cells were detected with western blot. RESULTS: With CCK-8 assay, it is found that Shikonin could significantly enhance NK cells proliferation and cytotoxicity to colon cancer cells. With FCM assay, it is found that Shikonin could improve the expression of perforin and GranB in a dose-dependent manner. Shikonin had no effect on TNF-alpha and IFN-γ expression. In mechanism, the study shows that Shikonin could enhance the expression of p-ERK1/2 and p-Akt. CONCLUSIONS: Shikonin enhances NK cells proliferation and cytotoxicity via the improvement of perforin, GranB, p-ERK1/2 and p-Akt expression.

Recompression in new levels after percutaneous vertebroplasty and kyphoplasty compared with conservative treatment.

STUDY DESIGN: A prospective clinical study assessing new vertebral compression fracture after previous treatment. OBJECTIVE: The purpose of this study was to investigate the incidence and associated risk factors of new symptomatic osteoporotic vertebral compression fractures (OVCFs) in patients treated by percutaneous vertebroplasty (PVP) and kyphoplasty (PKP) versus conservative treatment, and to elucidate our findings. There are a lot of reports concerning the feasibility and efficacy of this minimally invasive procedure compared with conservative treatment, especially in pain soothing. However, it is still unclear whether the risk of subsequent fracture has increased among operative treatment patients in the long term. METHODS: From November 2005 to July 2009, 290 consecutive patients with 363 OVCFs were randomly selected for PVP/PKP or conservative treatment and evaluated with a mean follow-up of 49.4 months (36-80 months). Some parameters were characterized and statistically compared in this study. Telephone questionnaires, clinical reexamine, and plain radiographs were performed in the follow-up. RESULTS: Thirty-one of 290 (10.7%) patients had experienced 42 newly developed symptomatic secondary OVCFs. Among 169 operation (53.3% vertebroplasty, 46.7% kyphoplasty) and 121 comparison patients, there is no significant statistical difference of new OVCFs incidence between the two groups calculated by patient proportion. However, in separate, the rate of secondary adjacent fractures calculated by vertebral refracture number is significantly higher than non-adjacent levels in PVP/PKP group but no significant statistical difference was observed in conservative group. The time interval of recompression after operative procedure was much shorter than that for comparison group (9.7 ± 17.8 versus 22.4 ± 7.99 months, p = 0.017). In addition, older age, gender, fracture times, location of original fracture segment, the amount of cement, cement leakage, operation modality (PVP or PKP),and initial number of OVCFs were documented, but these were not the influencing factors in this study (p > 0.05). CONCLUSIONS: Patients who had experienced PVP/PKP were not associated with an increased risk of recompression in new levels. However, recompression in new levels of PVP/PKP group occurred much sooner than that of conservative group in the follow-up period. The incidence of new vertebral fractures observed at adjacent levels was substantially higher but no sooner than at distant levels in PVP/PKP group. No major risk factors involving new OVCFs have been found in this study and augmentation for sandwich situation is not necessary.

Tribological properties of MAO ceramic coatings with annulus array texture on disposable surgical gloves.

Introduction: In recent research, the expansion in the use of Mg alloys for biomedical applications has been approached by modifying their surfaces in conjunction with micro-arc oxidation (MAO) techniques which enhance their abrasion and corrosion resistance. Methods: In this study, combining laser texturing and MAO techniques to produce the dense ceramic coatings with microstructures. On the surface of the AZ31 Mg alloy, a micro-raised annulus array texture has been designed in order to increase the surface friction under liquid lubrication and to improve the operator's grip when holding the tool. For this work, the micro-morphology of the coatings was characterised, and the friction properties of the commonly used scalpel shank material 316 L, the untextured surface and the textured surface were comparatively analysed against disposable surgical gloves. Results and discussion: The results show that the Laser-MAO ceramic coating grows homogenous, the porosity decreases from 14.3% to 7.8%, and the morphology after friction indicates that the coating has good wear resistance. More specifically, the average coefficient of friction (COF) of the three types of gloves coated with Laser-MAO ceramic was higher than that of the 316 L and MAO ceramic coatings under the action of the annulus-integrated texture under the lubrication conditions of physiological saline and defatted sheep blood, which achieved the goal of increasing friction for the purpose of helping to prevent the problem of tool slippage from the hand.

Corrigendum: Tribological properties of MAO ceramic coatings with annulus array texture on disposable surgical gloves.

[This corrects the article DOI: 10.3389/fbioe.2024.1397050.].

Association between lactate metabolism­related molecules and venous thromboembolism: A study based on bioinformatics and an in vitro model.

Venous thromboembolism (VTE) is characterized by a high recurrence rate and adverse consequences, including high mortality. Damage to vascular endothelial cells (VECs) serves a key role in VTE and lactate (LA) metabolism is associated with VEC damage. However, the pathogenesis of VTE and the role of lactate metabolism-related molecules (LMRMs) remain unclear. Based on the GSE48000 dataset, the present study identified differentially expressed (DE-)LMRMs between healthy individuals and those with VTE. Thereafter, LMRMs were used to establish four machine learning models, namely, the random forest, support vector machine and generalized linear model (GLM) and eXtreme gradient boosting. To verify disease prediction efficiency of the models, nomograms, calibration curves, decision curve analyses and external datasets were used. The optimal machine learning model was used to predict genes involved in disease and an in vitro oxygen-glucose deprivation (OGD) model was used to detect the survival rate, LA levels and LMRM expression levels of VECs. A total of four DE-LMRMs, solute carrier family 16 member 1 (SLC16A1), SLC16A7, SLC16A8 and SLC5A12 were obtained and GLM was identified as the best performing model based on its ability to predict differential expression of the embigin, lactate dehydrogenase B, SLC16A1, SLC5A12 and SLC16A8 genes. Additionally, SLC16A1, SLC16A7 and SLC16A8 served key roles in VTE and the OGD model demonstrated a significant decrease in VEC survival rate as well as a significant increase and decrease in intracellular LA and SLC16A1 expression levels in VECs, respectively. Thus, LMRMs may be involved in VTE pathogenesis and be used to build accurate VTE prediction models. Further, it was hypothesized that the observed increase in intracellular LA levels in VECS was associated with the decrease in SLC16A1 expression. Therefore, SLC16A1 expression may be an essential target for VTE treatment.