Application of RhD Blood Group to Simulate Antibody Identification Test in Immunohematology Education.

BACKGROUND: Immunohematology skill education is an important part of the transfusion medicine professional training. We tried to solve the difficulty of obtaining suitable and sufficient positive samples in the immunohematology education. METHODS: Different identification panels and panel cells were created by RhD-positive red blood cells (RBCs) and RhD-negative RBCs, according to the underlying antibodies. Diluted anti-D reagent was used as simulated plasma for identification. RESULTS: The antibody identification of single antibody with dose-effect and two antibodies present at the same time were successfully simulated. CONCLUSIONS: It is a practical and cheap method for antibody identification training to use RhD blood group, especially when positive samples are short.

Analysis of the effect and influencing factors of a clinical competency-oriented prospective pre-job training programme on the comprehensive ability of new employees in the department of transfusion medicine.

BACKGROUND: The subject of pre-job training for transfusion service laboratory technicians is very important. The key is how to make a reasonable systematic training programme to improve the effectiveness of training. METHODS: A prospective training programme was conducted and an assessment was performed at enrollment (baseline) and reassessment after 3-months training, using the same tools with a validated questionnaire. RESULTS: Clinical competency-oriented prospective pre-job training significantly improves the clinical transfusion-related comprehensive skills of new employees. The post-training assessment score was significantly affected by undergraduate major. CONCLUSION: This study provided a clinical competency-oriented training programme for new employees in the department of transfusion medicine that could effectively enhance their comprehensive abilities.

Perceptions of attitudes toward statistics among medical undergraduates: insights from a regional medical college in China.

BACKGROUND: Among Chinese medical students, medical statistics is often perceived as a formidable subject. While existing research has explored the attitudes of Chinese postgraduate medical students towards statistics and its impact on academic performance, there is a scarcity of studies examining the attitudes of Chinese medical undergraduates on this subject. This study endeavors to scrutinize the attitudes of Chinese medical undergraduates towards statistics, assessing their ramifications on learning achievements, and delving into the influence of demographic factors. METHODS: 1266 medical undergraduates participated in this study, completing a questionnaire that included SATS-36 and additional queries. Furthermore, an examination was administered at the end of the medical statistics course. The analysis encompassed the SATS score and exam scores, examining both the overall participant population and specific demographic subgroups. RESULTS: Undergraduate medical students generally exhibit a favorable disposition towards statistics concerning Affect, Cognitive Competence, and Value components, yet harbor less favorable sentiments regarding the Difficulty component of SATS-36, aligning with previous research findings. In comparison to their postgraduate counterparts, undergraduates display heightened enthusiasm for medical statistics. However, they demonstrate a lower cognitive capacity in statistics and tend to underestimate both the value and difficulty of learning statistics. Despite these disparities, undergraduate medical students express a genuine interest in statistics and exhibit a strong dedication to mastering the subject. It is noteworthy that students' attitudes toward statistics may be influenced by their major and gender. Additionally, there exists a statistically significant positive correlation between learning achievement and the Affect, Cognitive Competence, Value, Interest, and Effort components of the SATS-36, while a negative correlation is observed with the Difficulty component. CONCLUSION: Educators should carefully consider the influence of attitudes toward statistics, especially the variations observed among majors and genders when formulating strategies and curricula to enhance medical statistics education.

Therapeutic plasma exchange-free treatment for first-episode TTP: A systematic review.

OBJECTIVE: Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy (TMA), and therapeutic plasma exchange (TPE) is currently the standard treatment. However, TPE sometimes cannot be implemented. The aim of this study was to systematically review patients with a first TTP episode who were treated without TPE. METHOD: The PubMed, Embase, Web of Science and Cochrane Library databases were searched by two investigators independently to collect case reports and clinical studies on TTP patients treated without TPE. After removing duplicate records and records that did not meet the inclusion criteria, the patients' data of eligible studies, including the basic characteristics, treatment regimens, and outcomes were extracted for further analysis. RESULTS: A total of 5338 potentially relevant original studies were identified, from which 21 studies, including 14 cases, 3 case series and 4 retrospective studies, met eligibility requirements and were included. Treatment regimens in the absence of TPE were found to vary based on individual information. Most patients recovered, with normal platelet counts and ADAMT13 activity at discharge. In the meta-analysis of retrospective studies, the TPE-free group had no higher mortality than the TPE-treated group. CONCLUSION: Our study shows that TPE-free treatment may not increase the mortality of TTP patients, which provides a new treatment concept for patients with first episodes of TTP. However, the current evidence is not high due to the lack of randomized controlled trials, so more well-designed prospective clinical trials are warranted to investigate the safety and efficacy of TPE-free treatment regimens in TTP patients.

Expression and role of anti-oxidative damage factors in the placenta of preterm infants with premature rupture of membranes. / æŠ—æ°§åŒ–æŸä¼¤å› å­åœ¨èƒŽè†œæ—©ç ´æœªè¶³æœˆå„¿èƒŽç›˜ä¸­çš„è¡¨è¾¾åŠä½œç”¨.

OBJECTIVES: To study the association of the anti-oxidative damage factors nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) with preterm premature rupture of membranes (PPROM). METHODS: A prospective study was conducted. The neonates who were hospitalized in Yanbian Hospital from 2019 to 2020 were enrolled as subjects, among whom there were 30 infants with PPROM, 32 infants with term premature rupture of membranes (TPROM), and 35 full-term infants without premature rupture of membranes (PROM). Hematoxylin and eosin staining was used to observe the inflammatory changes of placental tissue. Immunohistochemical staining was used to measure the expression of Nrf2, HO-1, and NQO1 in placental tissue. Western blot was used to measure the protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue. RESULTS: Compared with the PPROM group, the TPROM group and the non-PROM full-term group had significantly higher positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue (P<0.05). There were no significant differences in the positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue between the TPROM and non-PROM full-term groups (P>0.05). CONCLUSIONS: The low expression levels of Nrf2, HO-1, and NQO1 in placental tissue may be associated with PPROM, suggesting that anti-oxidative damage is one of the directions to prevent PPROM.

Deficiency in the function of inhibitory interneurons contributes to glutamate-associated central sensitization through GABABR2-SynCAM1 signaling in chronic migraine rats.

The occurrence of pain has always been closely related to a break in the balance between excitatory and inhibitory systems, and the internal relationship between these two systems has not been studied in the pathogenesis of chronic migraine (CM). In this study, we explored how inhibitory interneurons specifically modulate the glutamate-induced hyperexcitability in the periaqueductal gray (PAG) of CM rats. The CM model was established by repeated dural infusion of inflammatory soup (IS) in rats. Then, Baclofen, a gamma-aminobutyric acid type B receptor (GABABR) agonist; CGP35348, a GABABR antagonist; H89, a protein kinase A (PKA) inhibitor; and 8-Bromo-cAMP, a PKA agonist, were applied by intraventricular injection to investigate the detailed CM mechanism. Our results showed that GABABR2 mRNA and protein levels were significantly downregulated (P < .01) in the PAG of CM rats. Similarly, gamma-aminobutyric acid (GABA) and its synthetase glutamate decarboxylase 65/67 (GAD65/67) seriously decreased (P < .01), implying a deficit in the function of inhibitory interneurons in the PAG of CM rats. Afterward, the application of Baclofen and H89 alleviated the IS-evoked hyperalgesia and extenuated vesicular glutamate transporter 2 (VGLUT2), glutamate, calcitonin gene-related peptide (CGRP), and c-Fos expression by regulating the GABABR2/PKA/SynCAM1 pathway in the PAG of CM rats, while the application of CGP35348 and 8-Bromo-cAMP exactly exerted the opposite effect. Importantly, CGP35348 induced an elevation of CGRP, and VGLUT2 expression was relieved by H89. These data suggest that the loss in the function of inhibitory interneurons contributes to glutamate-associated central sensitization through the GABABR2/PKA/SynCAM1 pathway in the PAG of CM rats.

Cellular p32 Is a Critical Regulator of Porcine Circovirus Type 2 Nuclear Egress.

Circoviruses are the smallest DNA viruses known to infect mammalian and avian species. Although circoviruses are known to be associated with a range of clinical diseases, the details of circovirus DNA release still remain unknown. Here, we identified p32 as a key regulator for porcine circoviral nuclear egress. Upon porcine circovirus type 2 (PCV2) infection, p32 was recruited into the nucleus by the viral capsid (Cap) protein; simultaneously, protein kinase C isoform δ (PKC-δ) was phosphorylated at threonine 505 by phospholipase C (PLC)-mediated signaling at the early stage of infection, which was further amplified by Jun N-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK) signaling at the late infection phase. p32 functioned as an adaptor to recruit phosphorylated PKC-δ and Cap to the nuclear membrane to phosphorylate lamin A/C, resulting in a rearrangement of nuclear lamina and thus facilitating viral nuclear egress. Consistent with these findings, knockout (KO) of p32 in PCV2-infected cells markedly reduced the phosphorylation of PKC-δ and impeded the recruitment of p-PKC-δ and Cap to the nuclear membrane, hence abolishing the phosphorylation of lamin A/C and the rearrangement of nuclear lamina. As a result, p32 depletion profoundly impaired the production of cell-free viruses during PCV2 infection. We further identified the N-terminal 24RRR26 of Cap to be crucial for binding to p32, and mutation of these three arginine residues significantly weakened the replication and pathogenesis of PCV2 in vivo In summary, our findings highlight a critical role of p32 in the activation and recruitment of PKC-δ to phosphorylate lamin A/C and facilitate porcine circoviral nuclear egress, and they certainly help understanding of the mechanism of PCV2 replication.IMPORTANCE Circovirus infections are highly prevalent in mammalian and avian species. Circoviral capsid protein is the only structural protein of the virion that plays an essential role in viral assembly. However, the machinery of circovirus nuclear egress is currently unknown. In this work, we identified p32 as a key regulator of porcine circovirus type 2 (PCV2) nuclear egress that forms a complex with the viral capsid (Cap) protein to enhance protein kinase C isoform δ (PKC-δ) activity; this resulted in a recruitment of phosphorylated PKC-δ to the nuclear membrane, which further phosphorylates lamin A/C to promote the rearrangement of nuclear lamina and facilitate viral nuclear egress. Notably, we found that the N-terminal 24RRR26 of Cap, a highly conserved motif among circovirus species, was required for interacting with p32, and that mutation of this motif markedly impeded PCV2 nuclear egress. These data indicate that p32 is a critical regulator of PCV2 nuclear egress and reveal the importance of this finding in circovirus replication.

Concealed object enhancement using multi-polarization information for passive millimeter and terahertz wave security screening.

Passive millimeter and terahertz wave imaging has become a significant potential technique for human security check and scene monitoring. Due to the small difference of the brightness temperatures between human body and concealed objects, the temperature sensitivity and spatial resolution of radiometers are always the key performance indexes which are difficult to improve. Therefore, when the hardware performance is given, improving detectivity becomes a pressing need. In this paper, a physically-based concealed object enhancement method using multi-polarization information is presented. The polarization model and polarization property of human body and concealed objects have been analyzed. By fusing multiple polarization images, we can obtain a complete polarization image in which the contrast between human body and concealed objects is enhanced and stable. The experimental results of simulation and measurement demonstrate the enhancement performance, and Differential Signal Noise Ratio (DSNR) is obviously improved by using the proposed method.

Porcine Circovirus Type 2 Suppresses IL-12p40 Induction via Capsid/gC1qR-Mediated MicroRNAs and Signalings.

Porcine circovirus (PCV) type 2 (PCV2), an immunosuppression pathogen, is often found to increase the risk of other pathogenic infections. Yet the relative immune mechanisms determining the susceptibility of PCV2-infected animals remain unclear. In this study, we confirmed that PCV2 infection suppressed IL-12p40 expression and host Th1 immune response, leading to a weakened pathogenic clearance upon porcine reproductive respiratory syndrome virus (PRRSV) or Haemophilus parasuis infection. PCV2 infection suppressed pathogens, LPS/IFN-γ, or LPS/R848-induced IL-12p40 expression in porcine alveolar macrophages. PCV2 capsid (Cap) was the major component to suppress IL-12p40 induction by LPS/IFN-γ, LPS/R848, PRRSV, or H. parasuis Either wild-type PCV2 or mutants PCV2-replicase 1 and PCV type 1-Cap2, which contained PCV2 Cap, significantly decreased IL-12p40 levels and increased the replication of PRRSV and H. parasuis in the lung tissues relative to mock or PCV type 1 infection. gC1qR, a Cap binding protein, was not involved in IL-12p40 induction but mediated the inhibitory effect of PCV2 Cap on IL-12p40 induction. PCV2 also activated PI3K/Akt1 and p38 MAPK signalings to inhibit IL-12p40 expression via inhibition of NF-κB p65 binding to il12B promoter and upregulation of miR-23a and miR-29b. Knockdown of Akt1 and p38 MAPK downregulated miR-23a and miR-29b and increased IL-12p40 expression. Inhibition of miR-23a and miR-29b attenuated the inhibitory effect of PCV2 on IL-12p40 induction, resulting in an increased IL-12p40 expression and Th1 cell population and reduced susceptibility to PRRSV or H. parasuis Taken together, these results demonstrate that PCV2 infection suppresses IL-12p40 expression to lower host Th1 immunity to increase the risk of other pathogenic infection via gC1qR-mediated PI3K/Akt1 and p38 MAPK signaling activation.

Metabotropic glutamate receptor 5 regulates synaptic plasticity in a chronic migraine rat model through the PKC/NR2B signal.

BACKGROUND: The mechanism of chronic migraine (CM) is complex, central sensitization is considered as one of the pathological mechanism. Synaptic plasticity is the basis of central sensitization. Metabotropic glutamate receptor 5 (mGluR5) plays a vital role in the synaptic plasticity of the central nervous system. However, whether mGluR5 can promote the central sensitization by regulating synaptic plasticity in CM is unknown. METHODS: Male Wistar rats were used to establish a CM rat model, and the expression of mGluR5 mRNA and protein were detected by qRT-PCR and western blot. The allodynia was assessed by mechanical and thermal thresholds, and central sensitization was assessed by expression of the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) at Serine 133(pCREB-S133) and c-Fos. The synaptic-associated protein postsynaptic density protein 95 (PSD), synaptophysin (Syp), and synaptophysin-1(Syt-1), synaptic ultrastructure, and dendritic spines were detected to explore synaptic plasticity. The expression of PKC, total NR2B(tNR2B), and phosphorylation of NR2B at Tyr1472(pNR2B-Y1472) were detected by western blot. RESULTS: We found that the expression of mGluR5 was upregulated in CM rats. Downregulated the mGluR5 with MPEP alleviated the allodynia and reduced the expression of CGRP, pCREB-S133, c-Fos, PSD, Syp and Syt-1 and synaptic transmission. Moreover, the administration of MPEP inhibited the upregulation of PKC and pNR2B-Y1472. CONCLUSIONS: These results indicate that mGluR5 contributes to central sensitization by regulating synaptic plasticity in CM through the PKC/NR2B signal, which suggests that mGluR5 may be a potential therapeutic candidate for CM.

Porcine MKRN1 Modulates the Replication and Pathogenesis of Porcine Circovirus Type 2 by Inducing Capsid Protein Ubiquitination and Degradation.

Porcine circovirus type 2 (PCV2) capsid protein (Cap) is a unique structure protein that plays pivotal roles in the process of viral replication and pathogenesis. Herein, we characterized a putative porcine Makorin RING finger protein 1 (pMKRN1) variant, an N-terminal-truncated variant of putative full-size porcine MKRN1 which has a unique expression pattern resulting from the porcine mkrn1 gene and which interacts with PCV2 Cap. A domain mapping assay showed that the C terminus of pMKRN1 and fragments (amino acids 108 to 198) of Cap are required for this interaction. PCV2 transiently upregulated pMKRN1 in PK-15 cells, but persistent viral infection downregulated pMKRN1 in major pathological tissues of PCV2-infected piglets. Overexpression of pMKRN1 significantly inhibited the generation of progeny PCV2 via ubiquitination and degradation of Cap, whereas knockout of pMKRN1 blocked Cap degradation and promoted progeny virus replication. pMKRN1 specifically targeted PCV2 Cap lysine residues 164, 179, and 191 to induce polyubiquitination and subsequent degradation. Mutation of either of the three lysine residues in the Cap protein or mutation of the histidine at residue 243 within the RING finger domain of pMKRN1 abrogated the E3 ligase activity of pMKRN1, rendering cells incapable of inducing Cap ubiquitination and degradation. Consistent with this finding, a Cap ubiquitination-deficient PCV2 strain showed enhanced virus replication and produced severe histological lesions in the lung and lymph node tissues compared with wild-type PCV2. Taken together, the results presented here suggest that PCV2 downregulates the pMKRN1 variant to avoid pMKRN1-mediated Cap ubiquitination and degradation, thus promoting viral replication and pathogenesis in its targeted tissues.IMPORTANCE Porcine circovirus type 2 is the pathogen to which pigs are the most susceptible, causing immense economic losses in the global swine industry, but whether host cells have developed some strategies to prevent viral replication is still unclear. Here, we found that porcine MKRN1 (pMKRN1) was upregulated in the early stage of PCV2 infection and mediated the polyubiquitination and degradation of Cap protein to block PCV2 replication, yet persistent PCV2 infection downregulated pMKRN1 levels to avoid degradation, promoting viral replication and pathogenesis in its targeted tissues. These data present new insight into the molecular mechanisms underlying the antiviral effects of pMKRN1 E3 ligase during PCV2 infection and also suggest potential new control measures for PCV2 outbreaks.

CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers.

BACKGROUND: Multiple factors, including co-exposure between lifestyle and environmental risks, are important in susceptibility to oxidative DNA damage. However, the underlying mechanism is not fully understood. This study was undertaken to evaluate whether Cytochrome P4501A1 (CYP1A1) methylation can mediate the co-exposure effect between smoking and occupational polycyclic aromatic hydrocarbons (PAH) in development of oxidative DNA damage. METHODS: We explored the associations between smoking and occupational PAH co-exposure effect, CYP1A1 methylation and oxidative DNA damage among 500 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (1-hydroxypyrene, 1-OHP; 2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; and 9-hydroxyphenanthren, 9-PHE) and a marker of oxidative DNA damage (8-hydroxy- 2'- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. CYP1A1 methylation was measured by pyrosequencing. Finally, mediation analysis was performed to investigate whether CYP1A1 methylation mediated smoking and occupational PAH co-exposure effect on oxidative DNA damage. RESULTS: We observed significant associations of smoking and 1-OHP co-exposure with CYP1A1 hypomethylation (OR: 1.87, 95% CI: 1.01-3.47) and high 8-OHdG (OR: 2.13, 95% CI: 1.14-3.97). There was a significant relationship between CYP1A1 hypomethylation and high 8-OHdG (1st vs. 3rd tertile = 1.58, 95% CI: 1.01-2.47, P for trend = 0.046). In addition, mediation analysis suggested CYP1A1 hypomethylation could explain 13.6% of effect of high 8-OHdG related to smoking and 1-OHP co-exposure. CONCLUSIONS: Our findings suggested that the co-exposure effect of smoking and occupational PAH could increase the risk of oxidative DNA damage by a mechanism partly involving CYP1A1 hypomethylation.

[Impact of subchronic exposure to low-dose nano-nickel oxide on the reproductive function and offspring of male rats].

OBJECTIVE: To investigate the influence of subchronic exposure to low-dose subchronic nano-nickel oxide (NNO) on the reproductive function of male rats and embryonic development of the pregnant rats. METHODS: Fifty normal healthy male SD rats weighing 180－220 g were randomly divided into five groups of equal number, negative control, 4 mg/ml micro-nickel oxide (MNO), and 0.16, 0.8 and 4 mg/ml NNO, those of the latter four groups exposed to MNO or NNO by non-contact intratracheal instillation once every 3 days for 60 days, and then all mated with normal adult female rats in the ratio of 1∶2. After the female animals were confirmed to be pregnant, the males were sacrificed and the weights of the body, testis and epididymis obtained, followed by calculation of the visceral coefficients, determination of epididymal sperm concentration and viability and the nickel contents in the blood and semen by atomic fluorescence spectrometry. The female rats were killed on the 20th day of gestation for counting of the implanted fertilized eggs and live, dead and resorbed fetuses. RESULTS: After 60 days of exposure, the rats of the NNO groups showed no statistically significant differences from those of the negative control and MNO groups in the weights of the body, testis and epididymis or visceral coefficients. Compared with the negative control group, the animals of the 0.8 and 4 mg/ml NNO groups exhibited markedly decreased sperm concentration (ï¼»9.36 ± 0.98ï¼½ vs ï¼»7.49 ± 1.46ï¼½ and ï¼»6.30 ± 1.36ï¼½ ×106/ml, P < 0.05) and viable sperm (ï¼»85.35 ± 9.16ï¼½% vs ï¼»68.26 ± 16.63ï¼½% and ï¼»65.88 ± 14.68ï¼½ %, P < 0.05), increased morphologically abnormal sperm (ï¼»8.30 ± 2.47ï¼½% vs ï¼»13.99 ± 4.87ï¼½% and ï¼»15.38 ± 8.86ï¼½ %, P < 0.05), and elevated rate of dead and resorbed fetuses (1.18% vs 6.89% and 7.37%, P < 0.05), blood nickel content (ï¼»0.13 ± 0.16ï¼½ vs ï¼»0.52 ± 0.34ï¼½ and ï¼»0.82 ± 0.44ï¼½ mg/L, P < 0.05) and semen nickel content (ï¼»0.08 ± 0.13ï¼½ vs ï¼»0.35 ± 0.23ï¼½ and ï¼»0.63 ± 0.61ï¼½ mg/L, P < 0.05). The nickel level in the semen was correlated significantly with that in the blood (r = 0.912, P <0.01), negatively with the rate of viable sperm (r = －0.879, P <0.01) and positively with the percentage of morphologically abnormal sperm (r = －0.898, P <0.01). CONCLUSIONS: Sixty-day exposure to nano-nickel oxide at 0.8 and 4 mg/ml can produce reproductive toxicity in male rats and result in fetal abnormality in the females, while that at 0.16 mg/ml has no significant toxic effect on the reproductive function of the males.

Circular RNA circPVT1 Promotes Proliferation and Invasion Through Sponging miR-125b and Activating E2F2 Signaling in Non-Small Cell Lung Cancer.

BACKGROUND/AIMS: Circular RNAs (circRNAs) are key regulators in the development and progression of human cancers, however its role in non-small cell lung cancer (NSCLC) tumorigenesis is not well understood. The aim of this study is to identify the expression level of circPVT1 in NSCLC and further investigated its functional relevance with NSCLC progression both in vitro and in vivo. METHODS: Quantative real-time PCR was used for the measurement of circPVT1 in NSCLC specimens and cell lines. Fluorescence in situ hybridization analysis (FISH) assay was used for the identification of sublocation of circPVT1 in NSCLC cells. Bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) were performed to verify the binding of c-Fos at circPVT1 promoter region, and the direct interaction between circPVT1 and miR-125b. Gain- or loss-function assays were performed to evaluate the effects of circPVT1 on cell proliferation and invasion. Western blot and immunohistochemistry assays were performed to detect the protein levels involved in E2F2 pathway. RESULTS: We found that circPVT1 was upregulated in NSCLC specimens and cells. The transcription factor c-Fos binded to the promoter region of circPVT1, resulting in the overexpression of circPVT1 in NSCLC. Knockdown of circPVT1 suppressed NSCLC cell proliferation, migration and invasion, and increased apoptosis. In addition, circPVT1 mediated NSCLC progression via the regulation of E2F2 signaling pathway. More importantly, circPVT1 was predominantly abundant in the cytoplasm of NSCLC cells, and circPVT1 could serve as a competing endogenous RNA to regulate E2F2 expression and tumorigenesis in a miR-125b-dependent manner, which is further verified by using an in vivo xenograft model. CONCLUSION: circPVT1 promotes NSCLC cell growth and invasion, and may serve as a promising therapeutic target for NSCLC patients. Therefore, silence of circPVT1 could be a future direction to develop a novel treatment strategy.

High-Stacking-Density, Superior-Roughness LDH Bridged with Vertically Aligned Graphene for High-Performance Asymmetric Supercapacitors.

The high-performance electrode materials with tuned surface and interface structure and functionalities are highly demanded for advanced supercapacitors. A novel strategy is presented to conFigure high-stacking-density, superior-roughness nickel manganese layered double hydroxide (LDH) bridged by vertically aligned graphene (VG) with nickel foam (NF) as the conductive collector, yielding the LDH-NF@VG hybrids for asymmetric supercapacitors. The VG nanosheets provide numerous electron transfer channels for quick redox reactions, and well-developed open structure for fast mass transport. Moreover, the high-stacking-density LDH grown and assembled on VG nanosheets result in a superior hydrophilicity derived from the tuned nano/microstructures, especially microroughness. Such a high stacking density with abundant active sites and superior wettability can be easily accessed by aqueous electrolytes. Benefitting from the above features, the LDH-NF@VG can deliver a high capacitance of 2920 F g-1 at a current density of 2 A g-1 , and the asymmetric supercapacitor with the LDH-NF@VG as positive electrode and activated carbon as negative electrode can deliver a high energy density of 56.8 Wh kg-1 at a power density of 260 W kg-1 , with a high specific capacitance retention rate of 87% even after 10 000 cycles.

Graphene-Based Tunable Dual-Frequency Terahertz Sensor.

A tunable dual-band terahertz sensor based on graphene is proposed. The sensor consists of a metal bottom layer, a middle dielectric layer, and single-layer graphene patterned with four strips on the top. The numerical simulations results show that the proposed sensor exhibits two significant absorption peaks at 2.58 THz and 6.07 THz. The corresponding absorption rates are as high as nearly 100% and 98%, respectively. The corresponding quality factor (Q) value is 11.8 at 2.58 THz and 29.6 at 6.07 THz. By adjusting the external electric field or chemical doping of graphene, the positions of the dual-frequency resonance peak can be dynamically tuned. The excitation of plasma resonance in graphene can illustrate the mechanism of the sensor. To verify the practical application of the device, the terahertz response of different kinds and different thicknesses of the analyte is investigated and analyzed. A phenomenon of obvious frequency shifts of the two resonance peaks can be observed. Therefore, the proposed sensor has great potential applications in terahertz fields, such as material characterization, medical diagnosis, and environmental monitoring.

Association of lifestyles and multimorbidity with mortality among individuals aged 60 years or older: Two prospective cohort studies.

Lifestyles are associated with all-cause mortality, yet limited research has explored the association in the elderly population with multimorbidity. We aim to investigate the impact of adopting a healthy lifestyle on reducing the risk of all-cause mortality in older individuals with or without multimorbidity in both China and UK. This prospective study included 29,451 and 173,503 older adults aged 60 and over from Chinese Longitudinal Healthy Longevity Survey (CLHLS) and UK Biobank. Lifestyles and multimorbidity were categorized into three groups, respectively. Cox proportional hazards regression was used to estimate the Hazard Ratios (HRs), 95% confidence intervals (95% CIs), and dose-response for all-cause mortality in relation to lifestyles and multimorbidity, as well as the combination of both factors. During a mean follow-up period of 4.7 years in CLHLS and 12.14 years in UK Biobank, we observed 21,540 and 20,720 deaths, respectively. For participants with two or more conditions, compared to those with an unhealthy lifestyle, adopting a healthy lifestyle was associated with a 27%-41% and 22%-42% reduction in mortality risk in the CLHLS and UK Biobank, respectively; Similarly, for individuals without multimorbidity, this reduction ranged from 18% to 41%. Among participants with multimorbidity, individuals with an unhealthy lifestyle had a higher mortality risk compared to those maintaining a healthy lifestyle, with HRs of 1.15 (95% CI: 1.00, 1.32) and 1.27 (95% CI: 1.16, 1.39) for two conditions, and 1.24 (95% CI: 1.06, 1.45) and 1.73 (95% CI: 1.56, 1.91) for three or more conditions in CLHLS and UK Biobank, respectively. Adherence to a healthy lifestyle can yield comparable mortality benefits for older individuals, regardless of their multimorbidity status. Furthermore, maintaining a healthy lifestyle can alleviate the mortality risks linked to a higher number of diseases.

Association of Combined Healthy Lifestyle Factors With Incident Dementia in Participants With and Without Multimorbidity: A Large Population-Based Prospective Cohort Study.

BACKGROUND: The effect of a healthy lifestyle on dementia associated with multimorbidity is not well understood. Our objective is to examine whether the adoption of a healthy lifestyle could potentially reduce the elevated risk of dementia in individuals with and without multimorbidity. METHODS: We utilized data from the UK Biobank cohort. A comprehensive healthy lifestyle score, ranging from 0 to 6, was generated. Cox proportional hazards models were used to examine the associations between multimorbidity, the healthy lifestyle score, and the incidence risk of dementia. RESULTS: Over a median follow-up period of 12.5 years, 5 852 all-cause dementia were recorded. Multimorbidity including cardiovascular, metabolic, neuropsychiatric, and inflammation-related diseases was associated with a higher risk of subsequent dementia. Each additional chronic disease was associated with a hazard ratio (HR) of 1.38 (95% CI: 1.33, 1.44). Compared to individuals without multimorbidity and a healthy lifestyle score of 5-6, patients with multimorbidity and a lifestyle score of 0-1 had a significantly higher risk of dementia (HR: 3.13; 95% CI: 2.64, 3.72), but the risk was markedly attenuated among those with multimorbidity and a lifestyle score of 5-6. Among patients with 3 or more diseases, the HR for dementia was 0.53 (95%CI: 0.42, 0.68) when comparing a lifestyle score of 5-6 to 0-1. And we observed more pronounced association between them among people younger than 60 years old. CONCLUSIONS: Adherence to a combination of healthy lifestyle factors, especially at a young age, was associated with a significantly lower risk of dementia among participants with multimorbidity.

Antidepressant-like and anxiolytic-like effects of hydrogen sulfide in behavioral models of depression and anxiety.

Depression is a common and debilitating mental illness and is often comorbid with anxiety disorders. Altered synaptic plasticity is considered to be an important mechanism underlying antidepressant drug action. It has been reported that hydrogen sulfide (H2S), the third gaseous transmitter, facilitates the induction of hippocampal long-term potentiation and augments synaptic neurotransmission, involved in the regulation of synaptic plasticity. The aim of this study was to clarify the antidepressant-like and anxiolytic-like effects of H2S. H2S (NaHS, 1.68 or 5.6 mg/kg, intraperitoneally, for 7 days) exerts a specific antidepressant-like effect in the forced swimming test of mice and rats and the tail suspension test of mice, and reduces the anxiety-like behaviors of both mice and rats in the elevated plus-maze test. These results reveal a unique antagonistic action of H2S in depressive-like and anxiety-like behaviors and suggest that elevating H2S signaling in the brain may represent a novel approach for the treatment of depressive and anxiety disorders.