Increased Yangtze finless porpoise presence in urban Wuhan waters of the Yangtze River during fishing closures.

Wuhan, a highly urbanized and rapidly growing region within China's Yangtze Economic Zone, has historically been identified as a gap area for the critically endangered Yangtze finless porpoise (Neophocaena asiaeorientalis asiaeorientalis) based on daytime visual surveys. However, there has been a noticeable increase in porpoise sightings since 2020. This study employed passive acoustic monitoring to investigate porpoise distribution in Wuhan between 2020 and 2022. Generalized linear models were used to explore the relationship between shipping, hydrological patterns, light intensity, and porpoise biosonar activity. Over 603 days of effective monitoring, the daily positive rate for porpoise biosonar detection reached 43%, with feeding-related buzz signals accounting for 55% of all porpoise biosonar signals. However, the proportion of minutes during which porpoise presence was detected was 0.18%, suggesting that while porpoises may frequent the area, their visits were brief and mainly focused on feeding. A significant temporal trend emerged, showing higher porpoise biosonar detection during winter (especially in February) and 2022. Additionally, periods without boat traffic correlated with increased porpoise activity. Hydrological conditions and light levels exhibited significant negative correlations with porpoise activity. Specifically, porpoise sonar detections were notably higher during the night, twilight, and new moon phases. It is highly conceivable that both fishing bans and COVID-19 pandemic-related lockdowns contributed to the heightened presence of porpoises in Wuhan. The rapid development of municipal transportation and shipping in Wuhan and resulting underwater noise pollution have emerged as a significant threat to the local porpoise population. Accordingly, it is imperative for regulatory bodies to effectively address this environmental stressor and formulate targeted protection measures to ensure the conservation of the finless porpoise.

Heterostructures Assembled from Bi2O2CO3 and MXene for Boosted Potassium-Ion Storage by Arousing the Built-in Electric Field.

Bismuth-based materials have been recognized as the appealing anodes for potassium-ion batteries (PIBs) due to their high theoretical capacity. However, the kinetics sluggishness and capacity decline induced by the structure distortion predominately retard their further development. Here, a heterostructure of polyaniline intercalated Bi2O2CO3/MXene (BOC-PA/MXene) hybrids is reported via simple self-assembly strategy. The ingenious design of heterointerface-rich architecture motivates significantly the interior self-built-in electric field (IEF) and high-density electron flow, thus accelerating the charge transfer and boosting ion diffusion. As a result, the hybrids realize a high reversible specific capacity, satisfying rate capability as well as long-term cycling stability. The in/ex situ characterizations further elucidate the stepwise intercalation-conversion-alloying reaction mechanism of BOC-PA/MXene. More encouragingly, the full cell investigation further highlights its competitive merits for practical application in further PIBs. The present work not only opens the way to the design of other electrodes with an appropriate working mechanism but also offers inspiration for built-in electric-field engineering toward high-performance energy storage devices.

Microglial ApoD-induced NLRC4 inflammasome activation promotes Alzheimer's disease progression.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disease with no effective therapies. It is well known that chronic neuroinflammation plays a critical role in the onset and progression of AD. Well-balanced neuronal-microglial interactions are essential for brain functions. However, determining the role of microglia-the primary immune cells in the brain-in neuroinflammation in AD and the associated molecular basis has been challenging. METHODS: Inflammatory factors in the sera of AD patients were detected and their association with microglia activation was analyzed. The mechanism for microglial inflammation was investigated. IL6 and TNF-α were found to be significantly increased in the AD stage. RESULTS: Our analysis revealed that microglia were extensively activated in AD cerebra, releasing sufficient amounts of cytokines to impair the neural stem cells (NSCs) function. Moreover, the ApoD-induced NLRC4 inflammasome was activated in microglia, which gave rise to the proinflammatory phenotype. Targeting the microglial ApoD promoted NSC self-renewal and inhibited neuron apoptosis. These findings demonstrate the critical role of ApoD in microglial inflammasome activation, and for the first time reveal that microglia-induced inflammation suppresses neuronal proliferation. CONCLUSION: Our studies establish the cellular basis for microglia activation in AD progression and shed light on cellular interactions important for AD treatment.

CD14-CD10-CD45+HLA-DR-SSC+ neutrophils may be granulocytic myeloid-derived suppressor cell-like cells and relate to disease progression in non-Hodgkin's lymphoma patients.

We explored the frequency of CD14-CD10-CD45+HLA-DR-SSC++ neutrophils (CD10- neutrophils) in patients with non-Hodgkin's lymphoma (NHL), and their immunologic characteristics and clinical significance. Patients with NHL who were newly diagnosed (NDP; n = 33), in remission (RMP; n = 28) and relapsed (RLP; n = 29) were included, and 47 volunteers were recruited as healthy controls (HCs). The frequency of CD10- neutrophils in the peripheral blood from HC and patients with NHL was detected. CD10- and CD10+ neutrophils were sorted, and their cytology was analyzed. CD3+ T cells were also isolated and cultured with the autologous CD10- or CD10+ neutrophils, after which the proliferation and death rates of T cells were determined. The levels of arginase-1 (Arg-1) and reactive oxygen species (ROS) in CD10+ or CD10- neutrophils were examined. Few CD10- neutrophils were detected in HCs but were significantly elevated in patients with NHL, especially in NDP and RLP. In addition, CD10- neutrophils in NDP with advanced stage and high risk were markedly higher than those in NDP with limited stage and low risk. In RMP and RLP, the relapse-free survival and overall survival in patients with high CD10- neutrophils were shorter than those with low CD10- neutrophils. CD10- neutrophils from patients with NHL, which mainly consist of immature neutrophils, inhibit T-cell proliferation and facilitate T-cell death. Furthermore, a significant increase was observed in Arg-1 expression, along with an increase to a certain extent in ROS. CD10- neutrophils in patients with NHL have characteristics of myeloid-derived suppressor cells and may be related to disease progression and poor prognosis.

TIMP1/CHI3L1 facilitates glioma progression and immunosuppression via NF-κB activation.

Gliomas are highly heterogeneous brain tumours that are resistant to therapies. The molecular signatures of gliomas play a high-ranking role in tumour prognosis and treatment. In addition, patients with gliomas with a mesenchymal phenotype manifest overpowering immunosuppression and sophisticated resistance to treatment. Thus, studies on gene/protein coexpression networks and hub genes in gliomas holds promise in determining effective treatment strategies. Therefore, in this study, we aimed to. Using average linkage hierarchical clustering, 13 modules and 224 hub genes were described. Top ten hub genes (CLIC1, EMP3, TIMP1, CCDC109B, CASP4, MSN, ANXA2P2, CHI3L1, TAGLN2, S100A11), selected from the most meaningful module, were associated with poor prognosis. String analysis, co-immunoprecipitation and immunofluorescence revealed a significant correlation between TIMP1 and CHI3L1. Furthermore, we found, both in vivo and in vitro, that TIMP1 promoted gliomagenesis via CHI3L1 overexpression as well as NF-κB activation. TIMP1 expression correlated with tumour immune infiltration and immune checkpoint-related gene expression. In addition, TIMP1 resulted in immunosuppressive macrophage polarization. In summary, TIMP1/CHI3L1 might be perceived as a diagnostic marker and an immunotherapy target for gliomas.

FUS-Mediated CircFGFR1 Accelerates the Development of Papillary Thyroid Carcinoma by Stabilizing FGFR1 Protein.

Papillary thyroid carcinoma (PTC) is the most prevalent type of thyroid cancer and its incidence is rising globally. The molecular mechanisms of PTC progression remain unclear, hindering the development of effective treatments. This study focuses on hsa_circ_0008016 (circFGFR1), a circular RNA significantly up-regulated in PTC cells. Silencing circFGFR1 inhibited PTC cell proliferation and increased cell apoptosis, suggesting its role in PTC progression. The RNA-binding protein FUS was identified as a promoter of circFGFR1 formation. While circFGFR1 does not influence FGFR1 mRNA translation, it inhibits ubiquitination and degradation of FGFR1 protein, prolonging its half-life. CircFGFR1 also interacts with protein CBL, inhibiting CBL-mediated ubiquitination of FGFR1 proteins. Rescue assays confirmed circFGFR1 promotes PTC cell growth through mediating FGFR1. This study highlights the potential of circFGFR1 as a therapeutic target, offering insights into PTC's molecular mechanisms, and paving the way for novel treatment strategies.

SRRM2 may be a potential biomarker and immunotherapy target for multiple myeloma: a real-world study based on flow cytometry detection.

Serine/arginine repetitive matrix 2 (SRRM2) has been implicated in tumorigenesis, cancer development, and drug resistance through aberrant splicing; however, its correlation with multiple myeloma (MM) has not been reported. We investigated the potential of SRRM2 as a biomarker and immunotherapeutic target in MM by examining its expression in MM cells using flow cytometry. Our study included 95 patients with plasma cell disease, including 80 MM cases, and we detected SRRM2 expression on plasma cells and normal blood cells to analyze its relationship with clinical profiles. We found widespread positive expression of SRRM2 on plasma cells with little expression on normal blood cells, and its expression on abnormal plasma cells was higher than that on normal plasma cells. Comparative analysis with clinical data suggests that SRRM2 expression on plasma cells correlates with MM treatment response. MM patients with high SRRM2 expression had higher levels of serum ß2-mg and LDH, ISS staging, and plasma cell infiltration, as well as high-risk mSMART 3.0 stratification and cytogenetic abnormalities, particularly 1q21 amplification. In patients with previous MM, high SRRM2 expression on plasma cells was associated with higher plasma cell infiltration, high-risk mSMART 3.0 risk stratification, cytogenetic abnormalities, more relapses, and fewer autologous stem cell transplant treatments. In summary, SRRM2 may serve as a novel biomarker and immunotherapeutic target for MM. Its expression level on plasma cells can help in risk stratification of MM and monitoring of treatment response.

TET1-mediated epigenetic regulation of tumor necrosis factor-α in trigeminal ganglia contributes to chronic temporomandibular joint pain.

Chronic temporomandibular joint (TMJ) pain profoundly affects patients' quality of life. Trigeminal tumor necrosis factor-α (TNFα) plays a pivotal role in mediating TMJ pain in mice, yet the underlying epigenetic mechanisms remain enigmatic. To unravel these epigenetic intricacies, we employed a multifaceted approach. Hydroxymethylated DNA immunoprecipitation (hMeDIP) and chromatin immunoprecipitation (ChIP) followed by qPCR were employed to investigate the demethylation of TNFα gene (Tnfa) and its regulation by ten-eleven translocation methylcytosine dioxygenase 1 (TET1) in a chronic TMJ pain mouse model. The global levels of 5-hydroxymethylcytosine (5hmc) and percentage of 5hmc at the Tnfa promoter region were measured in the trigeminal ganglia (TG) and spinal trigeminal nucleus caudalis (Sp5C) following complete Freund's adjuvant (CFA) or saline treatment. TET1 knockdown and pain behavioral testing were conducted to ascertain the role of TET1-mediated epigenetic regulation of TNFα in the pathogenesis of chronic TMJ pain. Our finding revealed an increase in 5hmc at the Tnfa promoter region in both TG and Sp5C of CFA-treated mice. TET1 was upregulated in the mouse TG, and the ChIP result showed TET1 direct binding to the Tnfa promoter, with higher efficiency in the CFA-treated group. Immunofluorescence revealed the predominant expression of TET1 in trigeminal neurons. TET1 knockdown in the TG significantly reversed CFA-induced TNFα upregulation and alleviated chronic TMJ pain. In conclusion, our study implicates TET1 as a vital epigenetic regulator contributing to chronic inflammatory TMJ pain via trigeminal TNFα signaling. Targeting TET1 holds promise for epigenetic interventions in TMJ pain management.

Composite poly(ethylene oxide)-based solid electrolyte with consecutive and fast ion transport channels constructed by upper-dimensional MIL-53(Al) nanofibers.

Novel structural designs for metal organic frameworks (MOFs) are expected to improve ion-transport behavior in composite solid electrolytes. Herein, upper-dimensional MIL-53(Al) nanofibers (MNFs, MIL-53 belongs to the MIL (Material Institute Lavoisier) group) with flower-like nanoflake structures have been designed and constructed via modified hydrothermal coordination. The optimized MNFs with high surface area and porosity can form abundant interfaces with poly(ethylene oxide) (PEO) matrix. The plasticization of MNFs to the PEO matrix will facilitate segmental movement of PEO chains to facilitate Li+ conduction. The unsaturated open metal centers of MNFs can effectively capture bis(trifluoromethanesulfonyl)imide anions (TFSI-) to deliver more free lithium ions for transfer. Moreover, the upper-dimensional nanofiber structure endows lithium ions with a long-range and consecutive transport pathway. The obtained composite solid electrolyte (MNFs@PEO) presents a high ionic conductivity of 4.1 × 10-4 S cm-1 and a great Li+ transference number of 0.4 at 60 °C. The electrolyte also exhibits a stable Li plating/stripping behavior over 1000 h at 0.1 mA cm-1 with inhibited Li dendrite growth. Furthermore, the Li/LiFePO4 and Li/LiNi0.8Mn0.1Co0.1O2 batteries with MNFs@PEO as electrolytes both display great cycling stabilities with high-capacity retention, indicating their potential applications in lithium metal batteries. The study will put forward new inspirations for designing advanced MOF-based composite solid electrolytes.

Involvement of spinal NADPH oxidase 4 and endoplasmic reticulum stress in morphine-tolerant rats.

Morphine tolerance (MT) is currently a challenging issue related to intractable pain treatment. Studies have shown that reactive oxygen species (ROSs) derived from NADPH oxidase (NOX) and produced in response to endoplasmic reticulum (ER) stress participate in MT development. However, which NOX subtype initiates ER stress during MT development is unclear. NOX4 is mainly expressed on intracellular membranes, such as the ER and mitochondrial membranes, and its sole function is to produce ROS. Whether NOX4 is activated during MT development and the mechanisms underlying the association between NOX4 and ER stress during this process still need to be confirmed. In our study, we used the classic morphine-tolerant rat model and evaluated the analgesic effect of intrathecally injected morphine through a hot water tail-flick assay. Our research demonstrated for the first time that chronic morphine administration upregulates NOX4 expression in the spinal cord by activating three ER stress sensors, protein kinase RNA-like ER kinase (PERK), inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6), subsequently leading to the activation of microtubule-associated protein 1 light chain 3 b (LC3B) and P62 (a well-known autophagy marker) in GABAergic neurons. Our results may suggest that regulating NOX4 and the key mechanism underlying ER stress or autophagy may be a promising strategy to treat and prevent MT development.

A Fully Elastic Wearable Electrochemical Sweat Detection System of Tree-Bionic Microfluidic Structure for Real-Time Monitoring.

Fresh sweat contains a diverse range of physiological indicators that can effectively reflect changes in the body. However, existing wearable sweat detection systems face challenges in efficiently collecting and detecting fresh sweat in real-time. Additionally, they often lack the necessary deformation capabilities, resulting in discomfort for the wearer. Here, a fully elastic wearable electrochemical sweat detection system is developed that integrates a sweat-collecting microfluidic chip, a multi-parameter electrochemical sensor, a micro-heater, and a sweat detection elastic circuit board system. The unique tree-bionic structure of the microfluidic chip significantly enhances the efficiency of fresh sweat collection and discharge, enabling real-time detection by the electrochemical sensors. The sweat multi-parameter electrochemical sensor offers high-precision and high-sensitivity measurements of sodium ions, potassium ions, lactate, and glucose. The electronic system is built on an elastic circuit board that matches perfectly to wrinkled skin, ensuring improved wearing comfort and enabling multi-channel data sampling, processing, and wireless transmission. This state-of-the-art system represents a significant advancement in the field of elastic wearable sweat detection and holds promising potential for extending its capabilities to the detection of other sweat markers or various wearable applications.

Immune characteristics and prognostic implications of mucosal-associated invariant T cells in acute myeloid leukemia.

Increasing evidence suggests that mucosal-associated invariant T cells (MAITs) play a crucial role in anti-tumor responses against various cancers. In this study, we investigated the immune characteristics of MAIT cells in patients with acute myeloid leukemia (AML). Using multi-parameter flow cytometry, we performed phenotypic and functional analysis of MAITs in peripheral blood or bone marrow samples collected from 131 patients with AML including 99 newly diagnosed, 18 remission, and 14 relapsed cases, as well as 69 healthy controls. We found that MAITs exhibit signs of aging and exhaustion, particularly in CD8+ MAITs subset, at newly diagnosis. MAITs exhibit an effector memory or terminally differentiated phenotype. Frequency and number of MAITs reflect AML cell genetic features, tumor burden, disease status, and treatment responsiveness. Moreover, MAITs exhibit a highly activated or even exhausted state, as indicated by upregulation of PD-1. Furthermore, impaired production of Th1-type cytokines and increased secretion of Th17-type cytokines, granzyme B, and perforin were observed in MAITs from AML patients. Additionally, MAITs shifted toward producing cytokines that promote tumor progression, such as IL-8. Lower frequency of MAITs was associated with poorer overall survival (OS), and multivariate analysis revealed that MAITs frequency < 2.12% was an independent prognostic factor affecting OS. Collectively, our findings suggest that MAITs may play a role in immune deficiency in AML, emphasizing their potential importance in AML pathogenesis and treatment. These discoveries provide a theoretical basis for the development of novel immunotherapeutic strategies in AML.

Idiopathic multicentric castleman's disease mimicking immunoglobulin G4-related disease responding well to Bortezomib: a case report.

BACKGROUND: Castleman's disease (CD) is a rare disease that has clinical and pathological similarities to lymphoma and is characterized by a high frequency of associated immunological dysfunction. ImmunoglobulinG4-related disease (IgG4-RD) is a collection of systemic disorders that affect numerous organs and are also referred to as IgG4-associated sclerosing diseases. CD and IgG4-RD are difficult to separate because they may manifest similar commin clinical features. CASE PRESENTATION: This case describes a 53-year-old female who, during routine medical check-up, exhibited a progressive increase in serum globulin levels and a simultaneous worsening of anemia symptoms, raising concern for a clonal plasma cell disease such as myeloma. However, bone marrow punctures did not reveal any abnormal plasma cells. Also, serum and urine immunofixation electrophoresis demonstrated no abnormal monoclonal protein bands. In addition, several laboratory findings excluded chronic liver disease, chronic infections caused by bacteria or viruses. Later, we found elevated serum IgG4 levels (10,700 mg/L), and identified multiple enlarged lymph nodes throughout the patient's body. Axillary lymph node aspiration revealed no abnormal lymphocytes, ruling out the possibility of lymphoma. Pathological morphology of the axillary lymph revealed a large number of plasma cells in the lymphatic follicles. In addition, there was a reduction in lymphatic follicle size and apoptosis of the germinal centres. Immunohistochemistry revealed IgG4+/IgG + in > 40% of cells, and more than 100 IgG4 + cells per high powered field (HPF) of specimen. As of now, finding strongly suggested IgG4-RD. This patient was treated with glucocorticoids and various immunosuppressive drugs, such as prednisone, cyclosporine, methotrexate, cyclophosphamide, mycophenolate mofetil, azathioprine and hydroxychloroquine. Unfortunately, the patient did not recover. Ultimately, idiopathic multicentric Castleman disease (iMCD) was diagnosed in relation to the patient's clinical presentation and laboratory tests, and after combination chemotherapy (VCD: Bortezomib, Cyclophosphamide and Dexamethasone), durable remission was achieved without serious adverse effects. During the follow-up period of one year and ten months, the patient remained stable. CONCLUSION: The diagnosis of Castleman must be distinguished from other disorders such as IgG4-RD, malignant lymphoma, reactive hyperplasia of various lymph nodes (mostly caused by viral infections), plasmacytoma, advanced HIV and rheumatic diseases. Besides observing systemic symptoms, laboratory tests such as immunoglobulin levels, complement levels, interleukin levels, and C-reactive protein levels should also be performed in order to determine a diagnosis.

Novel ADAMTS13 mutations in a patient with congenital thrombotic thrombocytopenic purpura.

Congenital thrombotic thrombocytopenic purpura (TTP) is a rare autosomal recessive genetic disorder caused by mutations in the ADAMTS13 gene. Approximately 200 mutations of the ADAMTS-13 gene have been identified, although only a few have been characterized through in vitro expression studies. We conducted an investigation on a male congenital TTP patient with reduced plasma levels of ADAMTS13 activity. DNA sequence analysis revealed two mutations on chromosome 9 (1.9q34.2) in the patient's ADAMTS13 gene. One mutation was a non-synonymous mutation (exon 5: c.A530G: p.Y177C), while the other was a nonsense mutation (exon 21: c.G2651A: p.W884X). Both mutations were found to be heterozygous. The patient's parents had no history of thrombocytopenia or neurological symptoms. DNA sequence analysis showed the patient's father was a heterozygote for the nonsense mutation of the ADAMTS13 gene (exon 21: c.G2651A: p.W884X), while the mother was a heterozygote for the non-synonymous mutation of the ADAMTS13 gene (exon 5: c.A530G: p.Y177C). To investigate the mechanism behind ADAMTS13 deficiency in this patient, wild type (WT), ADAMTS13 p.Y177C, and ADAMTS13 p.W884X were transiently expressed in 293-6E cells. Expression studies revealed a significant reduction in enzyme activity and secretion, although the protease was detected within the cells. The 3D structures of the natural and mutated ADAMTS-13 proteins were partially reconstructed using the Phyre2 web server. The mutation that replaces the tyrosine residue at amino acid position 177 with cysteine may result in decreased steric hindrance and a looser structure. This mutation affects the binding of calcium ions and the secretion of the enzyme from intracellular to extracellular compartments.

Patients' Perceptions of Biosimilars: A Systematic Review.

OBJECTIVE: To systematically summarize and evaluate the findings of existing studies about patients' perceptions of biosimilars by assessing their attitudes and knowledge. METHODS: We conducted a systematic review of published studies concerning patients' perceptions of biosimilars, using databases of China National Knowledge Infrastructure, SinoMed, Web of Science, PubMed, Embase, and Cochrane Library. Two independent reviewers screened a total of 2197 Chinese or English papers published between 1 January 2018, and 1 October 2022. We assessed the quality of the included studies by applying the Joanna Briggs Institute appraisal tools. RESULTS: Forty-three studies were included in the review, with the majority originating from Europe (n = 22) and North America (n = 10). Of these studies, 37 were cross-sectional quantitative studies, three were quasi-experimental studies, and the remaining three were qualitative studies based on semi-structured interviews. The sample sizes of the included studies ranged from 9 to 6554 patients. Twenty-two out of 31 studies investigating patients' acceptance of biosimilars found that most participants expressed satisfaction with treatment using biosimilars. However, doubts about the clinical effects and regulatory approval pathway could negatively influence patients' attitudes. The majority of patients understood the economic advantages of biosimilars; however, some incorrectly connected lower prices with lower quality. Patients generally lacked knowledge about biosimilars. There were 6-51% of participants who were familiar with biosimilars, and 25-58% thought they did not know enough about biosimilars. Physicians, pharmacists, medicines agencies, academia, and patient associations were identified as the main sources of information on biosimilars for patients. Healthcare providers not informing or advising patients about switching may hinder patients from acquiring enough knowledge. CONCLUSIONS: The majority of patients expressed satisfaction with treatment using biosimilars, but limited knowledge continued to impede their perceptions. Doubts about the clinical effects and regulatory approval pathway were identified as major factors that negatively influenced patients' attitudes towards biosimilars, while the impact of a price advantage was mixed. It is essential to maintain a focus on educating healthcare professionals about biosimilars, including their clinical outcomes and the regulatory pathway, which equips them to provide comprehensive and informed guidance to patients.

Multifunctional hydrogel/platelet-rich fibrin/nanofibers scaffolds with cell barrier and osteogenesis for guided tissue regeneration/guided bone regeneration applications.

Periodontal defect seriously affects people's life health and quality. Guided tissue regeneration (GTR) and guided bone regeneration (GBR) have made great progress in periodontal disease treatment, but some deficiencies existed in commercial materials of GTR and GBR. For obtaining better therapeutic effects, multifunctional composite scaffolds containing different biological macromolecules were developed in this study. Chitosan/poly (γ-glutamic acid)/nano-hydroxyapatite hydrogels (CP/nHA) made by electrostatic interactions and lyophilization were filled in the bone defects to achieve osteogenesis. Platelet-rich fibrin (PRF) extracted from blood could accelerate bone formation by releasing various bioactive substances as middle layer of composite scaffolds. Polycaprolactone/gelatin nanofibers (PG) prepared by electrospinning were attached to the junction of soft and hard tissue, which could prevent fibrous tissue from infiltrating into bone defects. The composite scaffolds showed good morphology, biocompatibility, cell barriers and osteogenic differentiation in vitro. The excellent ability of bone formation was verified by implantation of triple-layered composite scaffolds into alveolar bone defects in rabbit in vivo. The hierarchical structure was conducive to personalized customization to meet the needs of different defects. All in all, the multifunctional scaffolds could play important roles of GTR and GBR in alveolar bone regeneration and provide good application prospect for bone repair in clinic.

Efficacy of Acellular Dermal Matrix Versus Connective Tissue Graft for Root Coverage in Patients with Gingival Recession: A Meta-Analysis.

This study aimed to compare the efficacy of acellular dermal matrix (ADM) versus connective tissue graft (CTG) for root coverage in patients with gingival recession. Randomized controlled trials (RCTs) on the comparison of ADM with CTG in adult patients with gingival recession were searched in multiple databases updated on 15th May 2020. The quality of studies was evaluated using the upgraded Jadad scale. Included studies were assessed for percent root coverage (PRC), clinical attachment level (CAL), keratinized tissue (KT), probing depth (PD), recession width (RW) and recession depth (RD). Weighted mean difference (WMD) was used as the statistics for measurement data and the effect sizes were expressed as 95% confidence intervals (CI). Totally 24 RCTs were eligible for the final analysis. The patients accepting ADM had a higher gain in CAL (WMD: 0.250, 95%CI: 0.030-0.470, P=0.026) but a smaller gain in KT width (WMD: -0.440, 95%CI: -0.629--0.252, P<0.001) than those receiving CTG. No significant differences were found between the patients accepting ADM and those undergoing CTG in PRC (WMD: -1.608, 95%CI: -3.491-0.275, P=0.094), PD (WMD: 0.066, 95%CI: -0.005-0.137, P=0.067), RW (WMD: 0.065, 95%CI: -0.098-0.228, P=0.437) and RD (WMD: 0.109, 95%CI: -0.095-0.314, P=0.294). Overall, the ADM treatment for patients with gingival recession may be superior to CTG in gaining CAL, but CTG has a significant advantage over ADM in gaining KT width.

Anthropogenic activity, hydrological regime, and light level jointly influence temporal patterns in biosonar activity of the Yangtze finless porpoise at the junction of the Yangtze River and Poyang Lake, China.

Under increasing anthropogenic pressure, species with a previously contiguous distribution across their ranges have been reduced to small fragmented populations. The critically endangered Yangtze finless porpoise ( Neophocaena asiaeorientalis asiaeorientalis), once commonly observed in the Yangtze River-Poyang Lake junction, is now rarely seen in the river-lake corridor. In this study, static passive acoustic monitoring techniques were used to detect the biosonar activities of the Yangtze finless porpoise in this unique corridor. Generalized linear models were used to examine the correlation between these activities and anthropogenic impacts from the COVID-19 pandemic lockdown and boat navigation, as well as environmental variables, including hydrological conditions and light levels. Over approximately three consecutive years of monitoring (2020-2022), porpoise biosonar was detected during 93% of logged days, indicating the key role of the corridor for finless porpoise conservation. In addition, porpoise clicks were recorded in 3.80% of minutes, while feeding correlated buzzes were detected in 1.23% of minutes, suggesting the potential existence of localized, small-scale migration. Furthermore, both anthropogenic and environmental variables were significantly correlated with the diel, lunar, monthly, seasonal, and annual variations in porpoise biosonar activities. During the pandemic lockdown period, porpoise sonar detection showed a significant increase. Furthermore, a significant negative correlation was identified between the detection of porpoise click trains and buzzes and boat traffic intensity. In addition to water level and flux, daylight and moonlight exhibited significant correlations with porpoise biosonar activities, with markedly higher detections at night and quarter moon periods. Ensuring the spatiotemporal reduction of anthropogenic activities, implementing vessel speed restrictions (e.g., during porpoise migration and feeding), and maintaining local natural hydrological regimes are critical factors for sustaining porpoise population viability.

Unusual Hybrid Magnesium Storage Mechanism in a New Type of Bi2O2CO3 Anode.

Bismuth and bismuth-based compounds have been extensively studied as anodes as prospective candidates for rechargeable magnesium batteries (rMBs). However, the unsatisfactory magnesium-storage capability caused by the typical alloying reaction mechanism severely restricts the practical option for anodes in rMBs. Herein, polyaniline intercalated Bi2O2CO3 nanosheets are prepared by an effective interlayer engineering strategy to fine-tune the layer structure of Bi2O2CO3, achieving enhanced magnesium-storage capacity, rate performance, as well as long cycle life. Excitedly, a stepwise insertion-conversion-alloying reaction is aroused to stabilize the performance, which is elucidated by in/ex situ investigations. Moreover, first-principles calculations confirm that the coupling of Bi2O2CO3 and polyaniline not only increases the conductivity induced by the strong density of states and the interior self-built-in electric field but also significantly reduces the energy barrier of Mg shuttles. Our findings shed light on exploring new electrode materials with an appropriate working mechanism toward high-performance rechargeable batteries.

[Prognostic Value of CD56 Expression in Newly Diagnosed Multiple Myeloma Patients and Its Related Factors].

OBJECTIVE: To analyze the effect of CD56 expression on the prognosis of newly diagnosed multiple myeloma (MM) patients and explore the relationship between CD56 with clinical characteristics. METHODS: In this retrospective study, the clinical data and laboratory parameters of 175 newly diagnosed MM patients from February 2015 to December 2020 in the Second Hospital of Anhui Medical University were collected. The patients were divided into CD56+ and CD56- groups based on the expression of CD56, and the general data and laboratory parameters of the two groups were compared. The patients were followed up to June 30, 2021, and progression-free survival (PFS) and overall survival (OS) were recorded. PFS and OS curves of the two groups were plotted respectively, and the survival differences were compared. Univariate and multivariate Cox regression analyses were performed to analyze the effect of CD56 on the prognosis of newly diagnosed MM patients. RESULTS: In 175 newly diagnosed MM patients, 57(32.6%) cases were in the CD56-group and 118 (67.4%) cases in the CD56+ group. There was significant correlation between CD56 expression and ISS stage, ECOG score, platelets, ß2-microglobulin, creatinine, and extramedullary disease (all P <0.05). The incidence of extramedullary disease in the CD56- group was significantly higher than that in the CD56+ group (29.8% vs 12.7%, P =0.006). The median follow-up time of the whole cohort was 23.6 (1.0-78.6) months. The median PFS of patients in CD56+ group and CD56- group were 18.6 (1.2-77.6) and 12.2 (1.0-49.0) months, respectively, and the median OS of the two groups were 27.6 (1.4-77.7) and 19.7 (1.0-78.6) months, respectively. The 2-year PFS rate in the CD56+ group was significantly higher than that in the CD56- group (57.6% vs 36.8%, P =0.010), and the 2-year OS rate in the CD56+ group was higher than that in the CD56- group, but it didn't reach statistical significance (74.6% vs 64.9%, P =0.158). The results of univariate Cox regression analysis showed that the PFS was significantly shorter in newly diagnosed MM patients with advanced age, type IgG, high ECOG score, decreased platelet count, increased lactate dehydrogenase level, extramedullary disease, and CD56- (all P <0.05), the OS was significantly shorter in patients with high ECOG score, decreased platelet count, increased lactate dehydrogenase level, extramedullary disease, and CD56- (all P <0.05). The results of multivariate Cox regression analysis showed that advanced age, type IgG, elevated lactate dehydrogenase level, extramedullary disease, and CD56- were independent prognostic factors for poor PFS (all P <0.05); and decreased platelet count, elevated lactate dehydrogenase level, and extramedullary disease were independent adverse prognostic factors for OS (all P <0.05), while there was no significant independent correlation between CD56 and OS (P >0.05). CONCLUSION: Most of the newly diagnosed MM patients have positive expression of CD56. Loss of CD56 expression was associated with unfavorable biological and clinical parameters and poor prognosis, suggesting that CD56 has important clinical value in the prognosis of newly diagnosed MM patients.