Language and executive function in Mandarin-speaking deaf and hard-of-hearing children aged 3-5.

The study aimed to explore spoken language and executive function (EF) characteristics in 3-5-year-old prelingually deaf and hard-of-hearing (DHH) children, and evaluate the impact of demographic variables and EF on spoken language skills. 48 DHH children and 48 typically developing children who use auditory-oral communication were recruited. All participants underwent EF tests, including auditory working memory (WM), inhibitory control, cognitive flexibility, and the EF performance reported by parents. Using Mandarin Clinical Evaluation of Language for Preschoolers (MCELP), vocabulary comprehension, sentence comprehension, vocabulary naming, sentence structure imitation, and story narration were evaluated only in the DHH group, and their results were compared with the typical developmental level provided by MCELP. Results showed that DHH children exhibit deficiencies in different spoken language domains and EF components. While the spoken language skills of DHH children tend to improve as they age, a growing proportion of individuals fail to reach the typical developmental level. The spoken language ability in DHH children was positively correlated with age and EFs, and negatively correlated with aided hearing threshold, while auditory WM could positively predict their spoken language performance.

Lateral Open Wedge Osteotomy and Lateral Condyle Fusion In Situ for Children With Condyle Nonunion and Cubitus Valgus Deformity.

PURPOSE: Long-term nonunion of the lateral humeral condyle (LHC) can result in progressive cubitus valgus, elbow pain, instability, and delayed ulnar nerve palsy. Various techniques have been proposed for correction, each with its own advantages and disadvantages. The purpose of this study was to introduce a lateral open wedge osteotomy (LOWO) procedure combined with in situ osteosynthesis of nonunited LHC for the treatment of long-term LHC nonunion with cubitus valgus deformity. METHODS: We evaluated 18 pediatric patients who had a cubitus valgus deformity greater than 10 degrees after nonunion of the LHC for more than 2 years. The LHC was fixed in situ with 1 or 2 cancellous screws, and the LOWO was fixed with a locking plate. All patients underwent clinical and radiologic evaluation, and the pre- and postoperative carrying angle (CA), range of motion (ROM), and Mayo elbow performance score (MEPS) were analyzed. RESULTS: Eighteen patients, with a mean age of 9.9 ± 3.9 years, underwent treatment for LHC nonunion and cubitus valgus deformity after a mean interval of 61.6 ± 24.1 months from the initial injury. The mean follow-up period was 57.6 ± 22.8 months. Union of the LHC and LOWO was achieved in all patients. The mean CA decreased significantly from 31.6 ± 4.8 degrees before surgery to 10.4 ± 2.2 degrees after surgery (P<0.001). Surgery did not decrease elbow range of motion (P=0.202). The mean MEPS increased significantly from a preoperative value of 55 ± 4.9 to a postoperative value of 91.1 ± 5.6 (P<0.001). No significant complications were observed. CONCLUSIONS: LOWO combined with in situ fixation of nonunited LHC is an effective approach for treating long-term LHC nonunion associated with cubitus valgus deformity.

Synthesis of a deuterated disaccharide internal standard for LC-MS/MS quantitation of heparan sulfate in biological samples.

High levels of heparan sulfate (HS) are a marker for several mucopolysaccharidosis (MPS) disorders which are lysosomal storage diseases caused by genetic defects in HS-degrading enzymes. Quantitation of HS in biological samples is therefore critical for diagnosis and evaluating the efficacy of new therapies. Herein we present the efficient synthesis of a butylated GlcN-GlcA disaccharide and its deuterated derivative for use as an internal standard in a quantitative mass spectrometry-based assay for analysis of HS following butanolysis. The synthesis features the stereoselective 1,2-cis glycosylation of a GlcA acceptor with a 6-O-benzoyl-2-deoxy-2-azido thioglucoside donor.

Wide-ranging genetic variation in sensitivity to rapamycin in Drosophila melanogaster.

The progress made in aging research using laboratory organisms is undeniable. Yet, with few exceptions, these studies are conducted in a limited number of isogenic strains. The path from laboratory discoveries to treatment in human populations is complicated by the reality of genetic variation in nature. To model the effect of genetic variation on the action of the drug rapamycin, here we use the growth of Drosophila melanogaster larvae. We screened 140 lines from the Drosophila Genetic References Panel for the extent of developmental delay and found wide-ranging variation in their response, from lines whose development time is nearly doubled by rapamycin, to those that appear to be completely resistant. Sensitivity did not associate with any single genetic marker, nor with any gene. However, variation at the level of genetic pathways was associated with rapamycin sensitivity and might provide insight into sensitivity. In contrast to the genetic analysis, metabolomic analysis showed a strong response of the metabolome to rapamycin, but only among the sensitive larvae. In particular, we found that rapamycin altered levels of amino acids in sensitive larvae, and in a direction strikingly similar to the metabolome response to nutrient deprivation. This work demonstrates the need to evaluate interventions across genetic backgrounds and highlights the potential of omic approaches to reveal biomarkers of drug efficacy and to shed light on mechanisms underlying sensitivity to interventions aimed at increasing lifespan.

In Situ Lattice-Resolution Revelation of the Origins of Unexplored Anisotropic Sodiation Kinetics and Phase Transition in the Niobium Sulfide Anode.

Layered transition metal dichalcogenides (TMDs) have exhibited huge potential as anode materials for sodium-ion batteries. Most of them usually store sodium via an intercalation-conversion mechanism, but niobium sulfide (NbS2) may be an exception. Herein, through in situ transmission electron microscopy, we carefully investigated the insertion behaviors of Na ions in NbS2 and directly visualized anisotropic sodiation kinetics. Lattice-resolution imaging coupled with density functional theory calculations reveals the preferential diffusion of Na ions within layers of NbS2, accompanied by observable interlayer lattice expansion. Impressively, the Na-inserted layers can still withstand in situ mechanical testing. Further in situ observation vertical to the a/b plane of NbS2 tracked the illusive conversion reaction, which could result from interlayer gliding or wrinkling associated with stress accumulation. In situ electron diffraction measurements ruled out the possibility of such a conversion mechanism and identified a phase transition from pristine 3R-NbS2 to 2H-NaNbS2. Therefore, the NbS2 anode stores Na ions via only the intercalation mechanism, which conceptually differs from the well-known intercalation-conversion mechanism of typical TMDs. These findings not only decipher the whole sodiation process of the NbS2 anode but also provide valuable reference for unraveling the precise sodium storage mechanism in other TMDs.

Synthesis and anti-proliferative effect of novel 4-Aryl-1, 3-Thiazole-TPP conjugates via mitochondrial uncoupling process.

With the advent of mitochondrial targeting moiety such as triphenlyphosphonium cation (TPP+), targeting mitochondria in cancer cells has become a promising strategy for combating tumors. Herein, a series of novel 4-aryl-1,3-thiazole derivatives linked to TPP+ moiety were designed and synthesized. The cytotoxicity against a panel of four cancer cell lines was evaluated by CCK-8 assay. Most of these compounds exhibited moderate to good inhibitory activity over HeLa, PC-3 and HCT-15 cells while MCF-7 cells were less sensitive to most compounds. Among them, compound 12a exhibited a significant anti-proliferative activity against HeLa cells, and prompted for further investigation. Specifically, 12a decreased mitochondrial membrane potential and enhanced levels of reactive oxygen species (ROS). The flow cytometry analysis revealed that compound 12a could induce apoptosis and cell cycle arrest at G0/G1 phase in HeLa cells. In addition, mitochondrial bioenergetics assay revealed that 12a displayed mild mitochondrial uncoupling effect. Taken together, these findings suggest the therapeutic potential of compound 12a as an antitumor agent targeting mitochondria.

Calixarene-Based Supramolecular Sensor Array for Pesticide Discrimination.

The identification and detection of pesticides is crucial to protecting both the environment and human health. However, it can be challenging to conveniently and rapidly differentiate between different types of pesticides. We developed a supramolecular fluorescent sensor array, in which calixarenes with broad-spectrum encapsulation capacity served as recognition receptors. The sensor array exhibits distinct fluorescence change patterns for seven tested pesticides, encompassing herbicides, insecticides, and fungicides. With a reaction time of just three minutes, the sensor array proves to be a rapid and efficient tool for the discrimination of pesticides. Furthermore, this supramolecular sensing approach can be easily extended to enable real-time and on-site visual detection of varying concentrations of imazalil using a smartphone with a color scanning application. This work not only provides a simple and effective method for pesticide identification and quantification, but also offers a versatile and advantageous platform for the recognition of other analytes in relevant fields.

CD28 costimulation augments CAR signaling in NK cells via the LCK/CD3Z/ZAP70 signaling axis.

Multiple factors in the design of a chimeric antigen receptor (CAR) influence CAR T-cell activity, with costimulatory signals being a key component. Yet, the impact of costimulatory domains on the downstream signaling and subsequent functionality of CAR-engineered natural killer (NK) cells remains largely unexplored. Here, we evaluated the impact of various costimulatory domains on CAR-NK cell activity, using a CD70-targeting CAR. We found that CD28, a costimulatory molecule not inherently present in mature NK cells, significantly enhanced the antitumor efficacy and long-term cytotoxicity of CAR-NK cells both in vitro and in multiple xenograft models of hematologic and solid tumors. Mechanistically, we showed that CD28 linked to CD3Z creates a platform that recruits critical kinases, such as LCK and ZAP70, initiating a signaling cascade that enhances CAR-NK cell function. Our study provides insights into how CD28 costimulation enhances CAR-NK cell function and supports its incorporation in NK-based CARs for cancer immunotherapy.

Oroxylin A-induced Trained Immunity Promotes LC3-associated Phagocytosis in Macrophage in Protecting Mice Against Sepsis.

Sepsis is defined as a dysregulated host response to infection that leads to multiorgan failure. Innate immune memory, i.e., "trained immunity", can result in stronger immune responses and provide protection against various infections. Many biological agents, including ß-glucan, can induce trained immunity, but these stimuli may cause uncontrolled inflammation. Oroxylin A (OA) is an active flavonoid compound that is derived from Scutellaria baicalensis. OA is an agonist for inducing trained immunity in vivo and in vitro, and ß-glucan was used as a positive control. The protective effects of OA-induced trained immunity were evaluated in mouse models that were established by either lipopolysaccharide (LPS) administration or caecal ligation and puncture (CLP). The expression of inflammatory factors and signaling pathway components involved in trained immunity was evaluated in vitro using qRT‒PCR, western blotting (WB) and enzyme-linked immunosorbent assay (ELISA). Flow cytometry and confocal microscopy were used to examine reactive oxygen species (ROS) levels and phagocytosis in trained macrophages. A PCR array was used to screen genes that were differentially expressed in trained macrophages. Here, we revealed that OA alleviated sepsis via trained immunity. OA-treated macrophages displayed increased glycolysis and mTOR phosphorylation, and mTOR inhibitors suppressed OA-induced trained immunity by effectively reprogramming macrophages. The PCR array revealed key genes in the mTOR signaling pathway in OA-treated macrophages. Furthermore, OA targeted the Dectin-1-syk axis to promote LC3-associated phagocytosis (LAP) by trained macrophages, thereby enhancing the ability of these macrophages to protect against infection. This ability could be transferred to a new host via the adoptive transfer of peritoneal macrophages. This study is the first to provide new insights into the potential of OA-induced trained immunity to be used as a strategy to protect mice against sepsis by promoting LAP by macrophages.

Amphiregulin secreted by umbilical cord multipotent stromal cells protects against ferroptosis of macrophages via the activating transcription factor 3-CD36 axis to alleviate endometrial fibrosis.

Endometrium fibrosis is the leading cause of uterine infertility. Macrophages participated in the occurrence and development of endometrial fibrosis. We previously reported that human umbilical cord multipotent stromal cells (hUC-MSCs) exerted their therapeutic effect in a macrophage-dependent manner in endometrial fibrosis. However precise mechanisms by which hUC-MSCs may influence macrophages in endometrial fibrosis remain largely unexplored. Here, we demonstrated that abnormal iron and lipid metabolism occurred in patients with intrauterine adhesions (IUA) and murine models. Ferroptosis has been proven to contribute to the progression of fibrotic diseases. Our results revealed that pharmacological activation of ferroptosis by Erastin aggravated endometrial fibrosis, while inhibition of ferroptosis by Ferrostatin-1 ameliorated endometrial fibrosis in vivo. Moreover, ferroptosis of macrophages was significantly upregulated in endometria of IUA murine models. Of note, transcriptome profiles revealed that CD36 gene expression was significantly increased in patients with IUA and immunofluorescence analysis showed CD36 protein was mainly located in macrophages. Silencing CD36 in macrophages could reverse cell ferroptosis. Dual luciferase reporter assay revealed that CD36 was the direct target of activation transcription factor 3 (ATF3). Furthermore, through establishing coculture system and IUA murine models, we found that hUC-MSCs had a protective role against macrophage ferroptosis and alleviated endometrial fibrosis related to decreased CD36 and ATF3. The effect of hUC-MSCs on macrophage ferroptosis was attributed to the upregulation of amphiregulin (AREG). Our data highlighted that macrophage ferroptosis occurred in endometrial fibrosis via the ATF3-CD36 pathway and hUC-MSCs protected against macrophage ferroptosis to alleviate endometrial fibrosis via secreting AREG. These findings provided a potential target for therapeutic implications of endometrial fibrosis.

Real-time imaging reveal anisotropic dissolution behaviors of silver nanorods.

The morphology and size control of anisotropic nanocrystals are critical for tuning shape-dependent physicochemical properties. Although the anisotropic dissolution process is considered to be an effective means to precisely control the size and morphology of nanocrystals, the anisotropic dissolution mechanism remains poorly understood. Here, usingin situliquid cell transmission electron microscopy, we investigate the anisotropic etching dissolution behaviors of polyvinylpyrrolidone (PVP)-stabilized Ag nanorods in NaCl solution. Results show that etching dissolution occurs only in the longitudinal direction of the nanorod at low chloride concentration (0.2 mM), whereas at high chloride concentration (1 M), the lateral and longitudinal directions of the nanorods are dissolved. First-principles calculations demonstrate that PVP is selectively adsorbed on the {100} crystal plane of silver nanorods, making the tips of nanorods the only reaction sites in the anisotropic etching process. When the chemical potential difference of the Cl-concentration is higher than the diffusion barrier (0.196 eV) of Cl-in the PVP molecule, Cl-penetrates the PVP molecular layer of {100} facets on the side of the Ag nanorods. These findings provide an in-depth insight into the anisotropic etching mechanisms and lay foundations for the controlled preparation and rational design of nanostructures.

Alleviating Recombinant Tissue Plasminogen Activator-induced Hemorrhagic Transformation in Ischemic Stroke via Targeted Delivery of a Ferroptosis Inhibitor.

Intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) is the primary treatment for ischemic stroke. However, rtPA treatment can substantially increase blood-brain barrier (BBB) permeability and susceptibility to hemorrhagic transformation. Herein, the mechanism underlying the side effects of rtPA treatment is investigated and demonstrated that ferroptosis plays an important role. The ferroptosis inhibitor, liproxstatin-1 (Lip) is proposed to alleviate the side effects. A well-designed macrocyclic carrier, glucose-modified azocalix[4]arene (GluAC4A), is prepared to deliver Lip to the ischemic site. GluAC4A bound tightly to Lip and markedly improved its solubility. Glucose, modified at the upper rim of GluAC4A, imparts BBB targeting to the drug delivery system owing to the presence of glucose transporter 1 on the BBB surface. The responsiveness of GluAC4A to hypoxia due to the presence of azo groups enabled the targeted release of Lip at the ischemic site. GluAC4A successfully improved drug accumulation in the brain, and Lip@GluAC4A significantly reduced ferroptosis, BBB leakage, and neurological deficits induced by rtPA in vivo. These findings deepen the understanding of the side effects of rtPA treatment and provide a novel strategy for their effective mitigation, which is of great significance for the treatment and prognosis of patients with ischemic stroke.

Co-Assembled Nanoparticles toward Multi-Target Combinational Therapy of Alzheimer's Disease by Making Full Use of Molecular Recognition and Self-Assembly.

The complex pathologies in Alzheimer's disease (AD) severely limit the effectiveness of single-target pharmic interventions, thus necessitating multi-pronged therapeutic strategies. While flexibility is essentially demanded in constructing such multi-target systems, for achieving optimal synergies and also accommodating the inherent heterogeneity within AD. Utilizing the dynamic reversibility of supramolecular strategy for conferring sufficient tunability in component substitution and proportion adjustment, amphiphilic calixarenes are poised to be a privileged molecular tool for facilely achieving function integration. Herein, taking ß-amyloid (Aß) fibrillation and oxidative stress as model combination pattern, a supramolecular multifunctional integration is proposed by co-assembling guanidinium-modified calixarene with ascorbyl palmitate and loading dipotassium phytate within calixarene cavity. Serial pivotal events can be simultaneously addressed by this versatile system, including 1) inhibition of Aß production and aggregation, 2) disintegration of Aß fibrils, 3) acceleration of Aß metabolic clearance, and 4) regulation of oxidative stress, which is verified to significantly ameliorate the cognitive impairment of 5×FAD mice, with reduced Aß plaque content, neuroinflammation, and neuronal apoptosis. Confronted with the extremely intricate clinical realities of AD, the strategy presented here exhibits ample adaptability for necessary alterations on combinations, thereby may immensely expedite the advancement of AD combinational therapy through providing an exceptionally convenient platform.

Blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner.

Targeting C5aR1 modulates the function of infiltrated immune cells including tumor-associated macrophages (TAMs). The gut microbiome plays a pivotal role in colorectal cancer (CRC) tumorigenesis and development through TAM education. However, whether and how the gut flora is involved in C5aR1 inhibition-mediated TAMs remains unclear. Therefore, in this study, genetic deletion of C5ar1 or pharmacological inhibition of C5aR1 with anti-C5aR1 Ab or PMX-53 in the presence or absence of deletion Abs were utilized to verify if and how C5aR1 inhibition regulated TAMs polarization via affecting gut microbiota composition. We found that the therapeutic effects of C5aR1 inhibition on CRC benefited from programming of TAMs toward M1 polarization via driving AKT2-mediated 6-phosphofructokinase muscle type (PFKM) stabilization in a TLR5-dependent manner. Of note, in the further study, we found that C5aR1 inhibition elevated the concentration of serum IL-22 and the mRNA levels of its downstream target genes encoded antimicrobial peptides (AMPs), leading to gut microbiota modulation and flagellin releasement, which contributed to M1 polarization. Our data revealed that high levels of C5aR1 in TAMs predicted poor prognosis. In summary, our study suggested that C5aR1 inhibition reduced CRC growth via resetting M1 by AKT2 activation-mediated PFKM stabilization in a TLR5-dependent manner, which relied on IL-22-regulated gut flora.

Radiologic, clinical, and functional evaluation of children with displaced T-condylar fractures treated by closed reduction and percutaneous fixation using the Mayo Elbow Performance Score.

PURPOSE: T-condylar (T-C) fractures of the distal humerus are rare in children. There is no accepted treatment for such an injury, and there is a lack of reports evaluating the outcome of T-C fractures treated by closed reduction and percutaneous fixation. The aim of this study was to evaluate the feasibility of closed reduction and percutaneous K-wire and screw (CRPKS) fixation in patients with type II and III T-C fractures according to the Toniolo-Wilkins classification modified by Canavese et al. (TWC classification). METHODS: The clinical data of 12 consecutive patients (8 males, 4 females) who were younger than 14 years of age and who had a T-C fracture that was managed by CRPKS were retrospectively evaluated. Fractures were classified according to the TWC classification. The baseline information of the patients, carrying angle (CA) and Mayo Elbow Performance Score (MEPS) were used to evaluate clinical and functional outcomes; related complications were recorded. Statistical analysis was performed. RESULTS: The mean age at the time of injury was 11.6 ± 1.8 years (range, 8-14). The time from injury to surgical treatment was 1.5 ± 1.0 days (range, 0-3), and the mean follow-up duration was 33.7 ± 12.3 months (range, 18-61). Surgery lasted 45.7 ± 7.6 min on average (range, 35-58). All fractures healed in 4.9 ± 1.0 weeks on average (range, 4-7). At the last follow-up visit, the CA was 12.6° ± 5.8° on the injured side and 13.8° ± 1.8° on the uninjured side (p=0.432). The MEPS was 100 (95, 100) on the injured side and 100 (100, 100) on the uninjured side (p=0.194). Three complications were recorded. CONCLUSION: Good functional and radiological outcomes can be expected in pediatric patients with type II and III T-C fractures treated by CRPKS. The technique is relatively simple to perform and has a lower rate of complications.

Molecular Recognition with Macrocyclic Receptors for Application in Precision Medicine.

ConspectusMacrocyclic receptors can serve as alternatives to natural recognition systems as recognition tools. They provide effectively preorganized cavities to encapsulate guests via host-guest interactions, thereby affecting the physiochemical properties of the guests. Macrocyclic receptors exhibit chemical and thermal stabilities higher than those of natural receptors and thus are expected to resist degradation inside the body. This reduces the risk of harmful degradation byproducts and ensures optimal levels of effectiveness. Macrocyclic receptors have precise molecular weights and well-defined structures; this ensures their batch-to-batch reproducibility, which is critical for ensuring quality and effectiveness levels. Moreover, macrocyclic receptors exhibit broad modification tunabilities, rendering them adaptable to various guests. Molecular recognition is the basis of numerous biological processes. Macrocyclic receptors may display considerable potential for application in diagnosing and treating diseases, depending on the host-guest recognition of bioactive molecules. However, the binding affinities and selectivities of macrocyclic receptors toward bioactive molecules are generally insufficient, which may lead to problems such as low diagnosis accuracies, off-target leaking, and interference with normal functions. Therefore, addressing the challenge of the strong and specific complexation of bioactive molecules and macrocyclic receptors is imperative.To overcome this challenge, we proposed the innovative strategies of longitudinal cavity extension and coassembled heteromultivalent recognition for application in the recognition of small molecules and biomacromolecules, respectively. The deepened cavity provides a stronger hydrophobic effect and a larger interaction area while maintaining the framework rigidity. By coassembling two macrocyclic amphiphiles into one ensemble, we achieved the desired heteromultivalent recognition. This strategy affords the necessary binding properties while preventing the requirement of tedious steps and site mismatch in covalent synthesis. Using these two strategies, we achieved specific and strong binding of macrocyclic receptors to various bioactive molecules including biomarkers, drugs, and disease-related peptides/proteins. We then applied these macrocyclic receptor-based recognition systems in biosensing and bioimaging, drug delivery, and therapeutics.In this Account, we summarize the strategies we used in the recognition of small molecules and biomacromolecules. Thereafter, we discuss their applications in precision medicine, involving the (1) sensing of biomarkers and imaging of lesion sites, which are critical in the early screening of diseases and accurate diagnoses; (2) precise loading and targeted delivery of drugs, which are crucial in improving their therapeutic efficacies and reducing their side effects; and (3) capture and removal of disease-related biomacromolecules, which are significant for precise intervention in life processes. Finally, we propose recommendations for the further development of macrocyclic receptor-based recognition systems in biomedicine. Macrocyclic receptors exhibit considerable potential for research, and continued investigation may not only expand the applications of supramolecular chemistry but also open novel avenues for the development of precision medicine.

Predictive value of hepatitis B serological indicators for mortality among cancer survivors and validation in a gastric cancer cohort.

Hepatitis B virus (HBV) infection has gradually been considered to associate with cancer development and progression. This study aimed to explore the associations of serological indicators of HBV infection with mortality risk among cancer survivors and further validated using a gastric cancer (GC) cohort from China, where HBV infection is endemic. National Center for Health Statistics' National Health and Nutrition Examination Survey (NHANES) data were used in this study. Individuals with positive results of hepatitis B core antigen (anti-HBc) were considered to have current or past HBV infection. Serological indicators were positive only for hepatitis B surface antibodies (anti-HBs), indicating vaccine-induced immunity, whereas negativity for all serologic indicators was considered to indicate the absence of HBV infection and immunity to HBV. The GC cohort included patients from the First Hospital of Jilin University, China. The median follow-up time of the NHANES was 10 years; during the follow-up, 1505 deaths occurred. The results revealed that anti-HBs-positive cancer survivors had a 39% reduced risk of mortality (hazard ratio [HR] 0.61, 95% confidence interval [CI] 0.44-0.85). Men and individuals aged <65 years old with past exposure to HBV had higher mortality risk (HR 1.52, 95% CI 1.09-2.13; HR 2.07, 95% CI 1.13-3.83). In this GC cohort, individuals who were only anti-HBs-positive showed a reduced risk of mortality (HR 0.77, 95% CI 0.62-0.95). Thus, anti-HBs positivity was a significant factor of decreased mortality among cancer survivors. More rigorous surveillance is necessary for cancer survivors with anti-HBc positivity, particularly men, and younger individuals.

In situ rapid synthesis of ionic liquid/ionic covalent organic framework composites for CO2 fixation.

IL/ICOF composites were in situ synthesized via a one-pot route in half an hour under ambient conditions for catalytic cycloaddition of CO2 with epoxides into cyclic carbonates. The prepared composites feature a decent CO2 adsorption capacity of 1.63 mmol g-1 at 273 K and 1 bar and exhibit excellent catalytic performance in terms of yield and durability. This work may pave a new way to design and construct functionalized porous organic frameworks as heterogeneous catalysts for CO2 capture and conversion.

Risk-stratified approach by aMAP score for community population infected with hepatitis B and C to guide subsequent liver cancer screening practice: A cohort study with 10-year follow-up.

The aim of this study was to determine whether the age-Male-ALBI-Platelet (aMAP) score is applicable in community settings and how to maximise its role in risk stratification. A total of thousand five hundred and three participants had an aMAP score calculated at baseline and were followed up for about 10 years to obtain information on liver cancer incidence and death. After assessing the ability of aMAP to predict liver cancer incidence and death in terms of differentiation and calibration, the optimal risk stratification threshold of the aMAP score was explored, based on absolute and relative risks. The aMAP score achieved higher area under curves (AUCs) (almost all above 0.8) within 10 years and exhibited a better calibration within 5 years. Regarding absolute risk, the risk of incidence of and death from liver cancer showed a rapid increase after an aMAP score of 55. The cumulative incidence (5-year: 8.3% vs. 1.3% and 10-year: 20.9% vs. 3.6%) and mortality (5-year: 6.7% vs. 1.1% and 10-year: 17.5% vs. 3.1%) of liver cancer in individuals with an aMAP score of ≥55 were significantly higher than in those with a score of <55 (Grey's test p < .001). In terms of relative risk, the risk of death from liver cancer surpassed that from other causes after an aMAP score of ≥55 [HR = 1.38(1.02-1.87)]. Notably, the two types of death risk had opposite trends between the subpopulation with an aMAP score of ≥55 and < 55. To conclude, this study showed the value of the aMAP score in community settings and recommends using 55 as a new risk stratification threshold to guide subsequent liver cancer screening.