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Abstract Background Canine enteric coronavirus (CECoV) is a prevalent infectious disease among dogs worldwide, yet its epidemiology in mainland China remains poorly understood. This systematic review and meta-analysis aimed to assess the prevalence of CECoV in mainland China and identify factors influencing its prevalence. Methods A comprehensive literature search was conducted across multiple databases for studies regarding CECoV epidemiology of China. PubMed, CNKI, Wanfang, and CQVIP were searched to obtain the studies. Eligible studies were selected based on predefined criteria, and data were extracted and synthesized. The quality the studies was assessed using the JBI assessment tool. Heterogeneity was checked using I2 test statistics followed by subgroup and sensitivity analysis. Subgroup analyses were performed to explore variations in CECoV prevalence by factors such as year, region, season, health status, social housing type, gender, age, and breed. Publication bias was assessed using a funnel plot and eggers test that was followed by trim and fill analysis. Results A total of 27 studies involving 21,034 samples were included in the meta-analysis. The overall pooled prevalence of CECoV in mainland China was estimated to be 0.30 (95% CI 0.24–0.37), indicating persistent circulation of the virus. Subgroup analyses revealed higher prevalence rates in younger dogs, multi-dog households, apparently healthy dogs, and certain regions such as southwest China. Seasonal variations were observed, with lower prevalence rates in summer. However, no significant differences in prevalence were found by gender. Conclusions This study provides valuable insights into the epidemiology of CECoV in mainland China, highlighting the persistent circulation of the virus and identifying factors associated with higher prevalence rates. Continuous monitoring and surveillance efforts, along with research into accurate detection methods and preventive measures, are essential for the effective control of CECoV and mitigation of its potential impact on animal and human health.

IntroductionGestational diabetes mellitus (GDM) is a form of gestational diabetes mellitus characterized by insulin resistance and abnormal function of pancreatic beta cells. In recent years, genomic association studies have revealed risk and susceptibility genes associated with genetic susceptibility to GDM. However, genetic predisposition cannot explain the rising global incidence of GDM, which may be related to the increased influence of environmental factors, especially the gut microbiome. Studies have shown that gut microbiota is closely related to the occurrence and development of GDM. This paper reviews the relationship between gut microbiota and the pathological mechanism of GDM, in order to better understand the role of gut microbiota in GDM, and to provide a theoretical basis for clinical application of gut microbiota in the treatment of related diseases.MethodsThe current research results on the interaction between GDM and gut microbiota were collected and analyzed through literature review. Keywords such as "GDM", "gut microbiota" and "insulin resistance" were used for literature search, and the methodology, findings and potential impact on the pathophysiology of GDM were systematically evaluated.ResultsIt was found that the composition and diversity of gut microbiota were significantly associated with the occurrence and development of GDM. Specifically, the abundance of certain gut bacteria is associated with an increased risk of GDM, while other changes in the microbiome may be associated with improved insulin sensitivity. In addition, alterations in the gut microbiota may affect blood glucose control through a variety of mechanisms, including the production of short-chain fatty acids, activation of inflammatory pathways, and metabolism of the B vitamin group.DiscussionThe results of this paper highlight the importance of gut microbiota in the pathogenesis of GDM. The regulation of the gut microbiota may provide new directions for the treatment of GDM, including improving insulin sensitivity and blood sugar control through the use of probiotics and prebiotics. However, more research is needed to confirm the generality and exact mechanisms of these findings and to explore potential clinical applications of the gut microbiota in the management of gestational diabetes. In addition, future studies should consider the interaction between environmental and genetic factors and how together they affect the risk of GDM.

AimTo report the global, regional, and national burden of type 2 diabetes mellitus (T2DM) in 2019, assess its trends in the past, and forecast its trends in the future.MethodsThe main data source was the Global Burden of Disease 2019 database. We assessed the changes in T2DM burden from 1990 to 2019 with joinpoint regression analysis. Age-period-cohort analysis was used to forecast the T2DM incidence and mortality rate from 2020 to 2034.ResultsThe burden of T2DM has increased from 1990 to 2019 generally. The low-middle socio-demographic index (SDI) region had the highest increase in age-standardized incidence rate (ASIR), age-standardized prevalence rate (ASPR), age-standardized mortality rate (ASMR), and age-standardized disability-adjusted life years (ASDR) due to T2DM. Nationally, the increase in ASIR (r=0.151, p=0.046) and the decrease in ASMR (r=0.355, p

In the dairy industry, Streptococcus uberis (S. uberis) is one of the most important pathogenic bacteria associated with mastitis in milk-producing cows, causing vast economic loss. To date, the only real effective method of treating and preventing streptococcal mastitis is antimicrobial therapy. In many inflammatory diseases, mesenchymal stem cells (MSCs) and angiotensin-converting enzyme 2 (ACE2) play an anti-inflammatory and anti-injurious role. Accordingly, we hypothesized that MSCs overexpressing ACE2 (MSC-ACE2) would ameliorate the inflammatory injury caused by S. uberis in mammary epithelial cells more efficiently than MSC alone. By activating the transcription 3/suppressor of cytokine signaling 3 (IL-10/STAT3/SOCS3) signaling pathway, MSC-ACE2 inhibited the NF-κB, MAPKs, apoptosis, and pyroptosis passways. Moreover, MSC-ACE2 overturned the downregulation of Occludin, Zonula occludens 1 (ZO-1), and Claudin-3 expression levels caused by S. uberis, suggesting that MSC-ACE2 promotes the repair of the blood-milk barrier. MSC-ACE2 demonstrated greater effectiveness than MSC alone, as expected. Based on these results, MSC-ACE2 effectively inhibits EpH4-Ev cell’s inflammatory responses induced by S. uberis, and would be an effective therapeutic tool for treating streptococcal mastitis.

OBJECTIVES:. The aim was to evaluate the effect of dihydropyridine calcium channel blocker on the prognosis for moderate-severe pulmonary acute respiratory distress syndrome in hypertension patients. DESIGN:. A retrospective, observational, multicenter cohort study. SETTING:. A total of 307 patients without propensity score matching and 186 adult inpatients with propensity score matching diagnosed with hypertension and moderate-severe pulmonary acute respiratory distress syndrome in five teaching hospitals in Jiangsu province, China, from December 2015 to December 2020 were enrolled. PATIENTS:. A total of 307 patients without propensity score matching and 186 patients with propensity score matching diagnosed with hypertension and moderate-severe pulmonary acute respiratory distress syndrome were included in the final analysis. INTERVENTIONS:. None. MEASUREMENTS AND MAIN RESULTS:. Demographic characteristics and clinical characteristics were recorded. The propensity score matching method was used to eliminate the difference between group with dihydropyridine calcium channel blocker and group without dihydropyridine calcium channel blocker. The primary outcome was in-hospital mortality. We used univariate and multivariate regression analyses for both patients with or without propensity score matching to assess the effect of these variables on mortality. In the subset of 186 patients with propensity score matching, in-hospital mortality was 53.2%. Inpatient mortality was significantly higher in patients treated with dihydropyridine calcium channel blocker than in those not treated with dihydropyridine calcium channel blocker of patients without propensity score matching (65.4% vs 40.4%; p < 0.01). Multivariate analysis for patients without propensity score matching showed that dihydropyridine calcium channel blocker (hazard ratio, 1.954; 95% CI, 1.415–2.699), lactate dehydrogenase greater than or equal to 600 U/L (hazard ratio, 3.809; 95% CI, 2.106–4.531), and lactate greater than or equal to 2 mmol/L (hazard ratio, 1.454; 95% CI, 1.041–2.029) were independently associated with in-hospital mortality. Based on univariate analysis for patients with propensity score matching, dihydropyridine calcium channel blocker (hazard ratio, 2.021; 95% CI, 1.333–3.064), lactate dehydrogenase greater than or equal to 600 U/L (hazard ratio, 4.379; 95% CI, 2.642–7.257), and lactate greater than or equal to 2 mmol/L (hazard ratio, 2.461; 95% CI, 1.534–3.951) were independently associated with in-hospital mortality. In contrast, patients not treated with dihydropyridine calcium channel blocker had a significant survival advantage over those treated with dihydropyridine calcium channel blocker in both patients without or with propensity score matching (p < 0.001; p = 0.001 by Kaplan-Meier analysis). CONCLUSIONS:. Dihydropyridine calcium channel blocker, lactate dehydrogenase greater than or equal to 600 U/L, and lactate greater than or equal to 2 mmol/L at admission were independent risk factors for patients with hypertension and moderate-severe pulmonary acute respiratory distress syndrome.

Background and objective: Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline, behavioral changes, and functional impairments. Apathy, a common symptom in Alzheimer's disease, refers to a lack of motivation, interest, and emotional responsiveness. It can significantly impact patients' quality of life and increase caregiver burden. This study aimed to determine the effects of a diversified rehabilitation program combined with donepezil on apathy, cognitive function, and family caregiver burden of Alzheimer's disease patients. Methods: A total of 105 Alzheimer's disease patients treated at our hospital between January 2020 and January 2023 were selected and analyzed retrospectively. They were assigned to the control group (n = 50) or the observation group (n = 55). The two groups did not differ in terms of general data such as age and sex. All patients were treated with donepezil orally. The control group was given routine nursing, whereas the observation group was given a diversified rehabilitation program intervention, including cognitive training and emotional support. The Hasegawa's dementia scale, mini-mental state examination, and Montreal cognitive assessment scale were adopted to evaluate the cognitive function of the two groups before and after treatment. A caregiver burden scale, the Zarit Burden Interview (ZBI) and the Apathy Evaluation Scale Informant version (AES-I) were used to evaluate the caregiver burden and apathy of the two groups. Results: A significantly higher overall response rate to treatment was found in the observation group (94.55%) than in the control group (80.00%) (p = 0.024). After treatment, scores on the Hasegawa's dementia scale, mini-mental state examination, and Montreal cognitive assessment scale of the two groups increased to varying degrees, with greater increases in the observation group than in the control group (p < 0.05). The ZBI and AES-I scores of the two groups decreased to different degrees after treatment, with greater decreases in the observation group than in the control group (p < 0.05). Conclusion: A diversified rehabilitation program combined with donepezil can substantially alleviate the apathy of Alzheimer's disease patients, improve their cognitive function, and reduce the burden on their families. [ABSTRACT FROM AUTHOR]

Abstract Background Therapy in the latent period is favorable for retarding the process of epileptogenesis. Recently, we have discovered that the activated sigma‐1 receptor (Sig‐1R) attenuates the hippocampus pathological injury and memory impairment in the latent period of epileptogenesis. But the molecular mechanism needs further investigation. Methods PRE‐084 was utilized as a research tool to highly selectively activate Sig‐1R in epileptic mice. After the treatment of PRE‐084, the pro‐inflammatory cytokines, neuropathological traits, and the level of mitochondrial translocator assembly and maintenance 41 homolog (TAMM41) in the hippocampus were examined. The mode in which the Sig‐1R interacts with TAMM41 was explored. The role of TAMM41 in the protecting effect of PRE‐084 was established. Results PRE‐084 inhibited the growth of pro‐inflammatory cytokines, reduced the formation of gliosis, alleviated neuronal damage in the hippocampus, and attenuated memory impairment in the latent period of epileptogenesis. The protein level of TAMM41 decreased in the hippocampi of epileptic mice and increased in the PRE‐084‐treated mice. The Sig‐1R bound with TAMM41 directly, maintaining the stability of TAMM41. Knockdown of TAMM41 reversed the protective effect of PRE‐084, and overexpression of TAMM41 exhibited a similar protective action to that of PRE‐084. Conclusion We presented the concept of the “sigma‐1 receptor–TAMM41 axis” and proposed that augmenting this axis can attenuate neuroinflammation and memory impairment in the process of epileptogenesis.

Abstract Background Neurotrophic tyrosine receptor kinase (NTRK) rearranged spindle cell neoplasm is an emerging group of molecularly defined rare soft tissue tumors, often presenting with a monotonous spindle cell morphology, infiltrative growth, and co-expression of S-100 and CD34 proteins by immunohistochemistry (IHC). Accurate diagnosis necessitates the combination of morphology, immunohistochemistry, and molecular test results, with next-generation sequencing (NGS) as the gold standard. We present a rare case of NTRK rearranged spindle cell neoplasm of the uterine cervix and review the literature to highlight the current understanding of the diagnosis and treatment of this rare disease. Case presentation A 49-year-old perimenopausal woman presented with menorrhagia for more than a month. A biopsy of the cervix revealed a cervical spindle cell neoplasm with a tendency to be an isolated fibrous tumor. A total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed and the surgical pathology suggested NTRK rearranged spindle cell neoplasm, while NGS confirmed TFG-NTRK3 fusion gene. Postoperatively, the patient refused larotrectinib maintenance therapy for economic reasons and had no sign of recurrence or metastasis at 31 months of follow-up. Conclusion We presented the first case of cervical spindle cell neoplasm with TFG-NTRK3 gene rearrangement and retrieved 22 cases of NTRK rearranged spindle cell neoplasm of the uterine cervix from literature. The most prevalent type of gene fusion was TPM3-NTRK1, and almost all cases demonstrated S-100 and CD34 positivity by IHC. Surgery remains the initial treatment of choice and tyrosine receptor kinase (TRK) inhibitors may serve as a promising target therapy for patients with recurred or metastatic disease.

The United Nations Sustainable Development Goals (SDGs) establish a fresh global framework for evaluating the development agenda, emphasizing prosperity, growth, inclusivity, and transparency while safeguarding our planet Earth. Land Degradation Neutrality (LDN) represents a clear target for assessing the achievement of SDG 15.3. In response to the shortcomings of the African Great Green Wall initiative with respect to LDN monitoring, reporting, and intervention, we developed an online tool, the Great Green Wall Big Data Facilitator (GGW-BDF), based on earth observation data (e.g. SDGSAT-1), cutting-edge big data analysis technologies, and Chinese experience in combating desertification, to support the implementation of the African Great Green Wall initiative. The GGW-BDF comprises an LDN data portal, desertification control knowledge, and e-learning resources. This study highlights the functionality of this tool to support stakeholders across countries in monitoring LDN while providing the successful technoloiges to restore degraded or barren land. The contributions of the GGW-BDF are very useful in supporting the Pan-African Agency of the Great Green Wall (PAGGW), and will hopefully be continuously upgraded for being a part of the federated toolbox of the Group on Earth Observation (GEO) LDN Flagship.

Abstract Background Identifying new targets in triple negative breast cancer (TNBC) remains critical. REG3A (regenerating islet-derived protein 3 A), a calcium-dependent lectin protein, was thoroughly investigated for its expression and functions in breast cancer. Methods Bioinformatics and local tissue analyses were employed to identify REG3A expression in breast cancer. Genetic techniques were employed to modify REG3A expression, and the resulting effects on the behaviors of breast cancer cells were examined. Subcutaneous xenograft models were established to investigate the involvement of REG3A in the in vivo growth of breast cancer cells. Results Analysis of the TCGA database uncovered increased REG3A levels in human breast cancer tissues. Additionally, REG3A mRNA and protein levels were elevated in TNBC tissues of locally treated patients, contrasting with low expression in adjacent normal tissues. In primary human TNBC cells REG3A shRNA notably hindered cell proliferation, migration, and invasion while triggering caspase-mediated apoptosis. Similarly, employing CRISPR-sgRNA for REG3A knockout showed significant anti-TNBC cell activity. Conversely, REG3A overexpression bolstered cell proliferation and migration. REG3A proved crucial for activating the Akt-mTOR cascade, as evidenced by decreased Akt-S6K1 phosphorylation upon REG3A silencing or knockout, which was reversed by REG3A overexpression. A constitutively active mutant S473D Akt1 (caAkt1) restored Akt-mTOR activation and counteracted the proliferation inhibition and apoptosis induced by REG3A knockdown in breast cancer cells. Crucially, REG3A played a key role in maintaining mTOR complex integrity. Bioinformatics identified zinc finger protein 680 (ZNF680) as a potential REG3A transcription factor. Knocking down or knocking out ZNF680 reduced REG3A expression, while its overexpression increased it in primary breast cancer cells. Additionally, enhanced binding between ZNF680 protein and the REG3A promoter was observed in breast cancer tissues and cells. In vivo, REG3A shRNA significantly inhibited primary TNBC cell xenograft growth. In REG3A-silenced xenograft tissues, reduced REG3A levels, Akt-mTOR inhibition, and activated apoptosis were evident. Conclusion ZNF680-caused REG3A overexpression drives tumorigenesis in breast cancer possibly by stimulating Akt-mTOR activation, emerging as a promising and innovative cancer target.

As the main mechanism of extratropical cyclogenesis， moist baroclinic instability plays a central role in the study of cyclone thermodynamics， which can be further divided into four categories： dry baroclinic instability， moist instability， diabatic Rossby wave and Type C cyclogenesis （tropopause intrusion）.The '7·20' heavy rainstorm was caused by the eastward movement of a Yellow River cyclone into North China after its rapid formation on July 18， 2016.Compared with the mature stage of the cyclone， the mechanism of the initial stage is still unclear.This article uses ERA5 reanalysis data and WRF model to study the moist baroclinic instability of the cyclogenesis event numerically.The results show that mid-lower troposphere presented diabatic Rossby wave pattern， that is， the eastward movement of the system was mainly driven by the cycle of vertical motion and diabatic effect.The vertical motion on which the wave relied was more provided by vorticity advection.The PV sink and the ageostrophic wind in the upper layer delayed the eastward movement of the tropopause intrusion PV， maintaining the phase difference between upper and lower layers.Finally， a PV column formed throughout the troposphere in front of dry intrusion.Using piecewise PV inversion， several sensitivity runs are designed to remove unbalanced circulation， tropopause dry intrusion PV and lower-level diabatic-produced PV from the initial field， respectively.Combined with the analysis of generalized omega equation， it shows that the baroclinic wave in this process must be coupled with the diabatic process with the help of sufficient water vapor to develop strongly.The cyclogenesis was suppressed when the latent heat was turned off.Dry baroclinic instability cannot explain this process.The removal of initial unbalanced field did not affect the baroclinic instability but will delay development of the system.Limited by humidity and mesoscale circulation structure， the active area of lower-level unbalanced flow was controlled by dry baroclinic dynamics.In this case， the gradient of θbottom was too small to organize eastward diabatic Rossby wave by relying only on the initial lower-level PV.Nor can strong lower-level diabatic heating generate as in Type C cyclogenesis by tropopause intrusion.For this Yellow River cyclogenesis case， it is required the initial lower-level PV anomaly to be strong enough to counteract the suppression of the cooling subsidence in front of dry intrusion； on the other hand， it is also required that the dry intrusion， in an appropriate initial phase difference with the lower system， strengthened the ascending motion east of the low-level PV in form of vorticity advection through vertical penetration， so as to promote the eastward momentum of diabatic Rossby wave to enter north China with more saturated environment.None of dry baroclinic instability， diabatic Rossby wave and Type C cyclogenesis could independently explain this cyclogenesis event， which was an initial optimal perturbation growth under the combined effect of diabatic Rossby wave and tropopause dry intrusion.

Abstract The reduction of interfacial interaction and the deterioration of processing properties of aluminum hydrides (AlH3) is the main challenges preventing its practical application. Here, a simple and effective core–shell structure aluminum hydrides@polydopamine (AlH3@PDA) complex was constructed through in-situ polymerization. The evolution of element states on the surface of AlH3 conducted by X-ray photoelectron spectroscopy indicated the successful introduction of PDA to form the core@shell structure, the thickness of the PDA coated layer increased with the increasing PDA dosage from 0.1 to 1.6% in mass fraction, and the maximum of thickness is 50 nm in TEM testing. Py GC/MS results proved that the increase of dopamine concentration leads to higher proportions of self-assemble units, whereas lower dopamine concentrations favor higher levels of chemical bonded components. Regarding whether PDA is a covalent polymer or a noncovalent aggregate of some species, the formation of intermediates, such as dopaminechrome and 5,6-dihydroxyindole played an important role to coordination interaction with AlH3 in FTIR, Raman, and UV–Vis spectra testing. Compared with pure AlH3, the formation of organic PDA coating improved AlH3 heat resistance. The adhesion work with GAP adhesive was also improved from 107.02 J/m2 of pure AlH3 to 111.13 mJ/m2 of AlH3@PDA-5 complex. This paper provides well support for further practical application of AlH3 in solid propellants.

BackgroundThe compound 6:2 chlorinated polyfluorinated ether sulfonic acids (6:2 Cl-PFESA) has been demonstrated abilities of strong bioaccumulation and placental barrier penetration, and it can also cross the blood-brain barrier. However, the mechanism of its neurodevelopmental toxicity in offspring induced by early-life exposure is still unknown.ObjectiveTo explore effects of 6:2 Cl-PFESA on the growth and the α-amino-3-hydroxy-5-methylisoxazole-4-propionic (AMPA) receptor gene expression in the hippocampus of offspring mice by establishing a 6:2 Cl-PFESA exposure animal model.MethodsThirty Kunming pregnant mice were randomly divided into five groups: control group, and 2, 10, 50, and 250 μg·L−1 6:2 Cl-PFESA exposure groups. The treatment groups were exposed to designed doses of 6:2 Cl-PFESA through drinking water from the first day of gestation until the end of lactation. The pups were weaned on postnatal day (PND) 21, and continued to be exposed to 6:2 Cl-PFESA through drinking water. Birth weight and body length of the offspring were recorded. Offspring mice were anesthetized and sacrificed respectively on PND7, PND21, and PND35, then their hippocampus was peeled from harvested brain tissue. The ultrastructure of hippocampus was observed via transmission electron microscopy; and the expression of AMPA receptors GluR1, GluR2, and GluR3 in the hippocampus was evaluated by real-time reverse transcription polymerase chain reaction. The learning and memory ability of the PND35 mice was measured by Morris water maze test before they were sacrificed.ResultsThe birth weights and the lengths of the pups in the 10, 50, and 250 μg·L−1 6:2 Cl-PFESA exposure groups were (2.23±0.36), (1.92±0.20), (1.88±0.31) g, and (33.73±0.98), (32.91±1.30), (32.52±2.07) mm, respectively, which were lower than those in the control group, (2.78±0.35) g and (36.46±2.34) mm (P

The primary purpose of present study was to explore the effects of arsenic exposure on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear transcription factor-κB (NF-κB) signaling pathway in the hippocampus of offspring mice at different developmental stages. Sodium arsenite (NaAsO2) at doses of 0, 15, 30 or 60 mg/L administered to female mice and their pups. The nuclear translocation levels of NF-κB were assessed by EMSA. Real-time RT-PCR was used to measure Akt, NF-κB and PI3K mRNA levels. Protein expressions of PI3K, p-Akt, inhibitor kappa B kinase (IKK), p-NF-κB, protein kinase A (PKA), inhibitor kappa B (IκB), and cAMP response element-binding protein (CREB) were measured by Western blot. Results disclosed that exposure to 60 mg/L NaAsO2 could suppress NF-κB levels of nuclear translocation of postnatal day (PND) 20 and PND 40 mice. Arsenic downregulated the transcriptional and translational levels of PI3K, Akt and NF-κB. Additionally, protein expressions of p-IKK, p-IκB, PKA and p-CREB also reduced. Taken together, results of present study indicated that arsenic could downregulate the PI3K/Akt/NF-κB signaling pathway, particularly on PND 40, which might be involved in the cognitive impairments.

Abstract Background Previous studies have demonstrated that the glycolytic enzyme phosphoglycerate kinase 1 (PGK1) can promote tumor development. This study sought to investigate the specific role of PGK1 in bladder cancer (BLCA). Methods Public databases and immunohistochemistry assays were utilized to analyze the expression of PGK1 in BLCA and its prognostic significance. Cell proliferation was assessed through CCK‐8 and colony formation assays, while the level of metastasis was evaluated using transwell migration experiments. Additionally, IC50 experiments were conducted to assess the impact of PGK1 on cisplatin sensitivity. Results The mRNA and protein expression levels of PGK1 were significantly upregulated in BLCA. Cox proportional hazards model analysis revealed that PGK1 and T stage were independent prognostic factors for BLCA patients. Both CCK‐8 and colony assays demonstrated that PGK1 promotes proliferation. Furthermore, a positive correlation was observed between PGK1 and Ki67, a proliferation index. Transwell migration assays confirmed the ability of PGK1 to enhance metastasis. Finally, PGK1 increased the IC50 associated with cisplatin treatment in BLCA. Conclusion Collectively, these findings suggest that PGK1 may hold clinical value in predicting BLCA prognosis and improving the outcomes of this patient population.

Abstract Neural stem cells (NSCs) are critical for brain development and maintenance of neurogenesis. However, the molecular mechanisms that regulate NSC proliferation and differentiation remain unclear. Mysm1 is a deubiquitinase and is essential for the self-renewal and differentiation of several stem cells. It is unknown whether Mysm1 plays an important role in NSCs. Here, we found that Mysm1 was expressed in NSCs and its expression was increased with age in mice. Mice with Mysm1 knockdown by crossing Mysm1 floxed mice with Nestin-Cre mice exhibited abnormal brain development with microcephaly. Mysm1 deletion promoted NSC proliferation and apoptosis, resulting in depletion of the stem cell pool. In addition, Mysm1-deficient NSCs skewed toward neurogenesis instead of astrogliogenesis. Mechanistic investigations with RNA sequencing and genome-wide CUT&Tag analysis revealed that Mysm1 epigenetically regulated Id4 transcription by regulating histone modification at the promoter region. After rescuing the expression of Id4, the hyperproliferation and imbalance differentiation of Mysm1-deficient NSCs was reversed. Additionally, knockdown Mysm1 in aged mice could promote NSC proliferation. Collectively, the present study identified a new factor Mysm1 which is essential for NSC homeostasis and Mysm1-Id4 axis may be an ideal target for proper NSC proliferation and differentiation.

Camel whey protein (CWP) is a potent natural antioxidant, noted for its abundance of antioxidant amino acids. Despite its promising properties, the precise mechanisms underlying its effects remain inadequately explored. This study aims to investigate the impact of CWP on kidney damage induced by acute heat stress in rats, as well as to elucidate its mechanism of action. We assessed CWP’s influence on cytochrome P450 2J (CYP2J) activity during heat stress, measured oxidative stress levels, and evaluated renal injury using CYP2J knockout rats. Our findings indicate that acute heat stress reduces CYP2J expression, while CWP administration restores CYP2J activity and enhances PI3K/Akt signaling. However, CWP did not mitigate oxidative stress-induced kidney damage in CYP2J−/− rats, suggesting the necessity of CYP2J for its protective effects.

Land productivity is one of the sub-indicators for measuring SDG 15.3.1. Land Productivity Dynamics (LPD) is the most popular approach for reporting this indicator at the global scale. A major limitation of existing products of LPD is the coarse spatial resolution caused by remote sensing data input, which cannot meet the requirement of fine-scale land degradation assessment. To resolve this problem, this study developed a tool (HiLPD-GEE) to calculate 30 m LPD by fusing Landsat and MODIS data based on Google Earth Engine (GEE). The tool generates high-quality fused Normalized Difference Vegetation Index (NDVI) dataset for LPD calculation through gap filling and Savitzky–Golay filtering (GF-SG) and then uses the method recommended by the European Commission Joint Research Centre (JRC) to calculate LPD. The tool can calculate 30 m LPD in any spatial range within any time window after 2013, supporting global land degradation monitoring. To demonstrate the applicability of this tool, the LPD product was produced for African Great Green Wall (GGW) countries. The analysis proves that the 30 m LPD product generated by HiLPD-GEE could reflect the land productivity change effectively and reflect more spatial details. The results also provide an important insight for the GGW initiative.

Abstract CDK4/6 are important regulators of cell cycle and their inhibitors have been approved as anti-cancer drugs. Here, we report a STING-dependent anti-tumor immune mechanism responsible for tumor suppression by CDK4/6 blockade. Clinical datasets show that in human tissues, CDK4 and CDK6 are over-expressed and their expressions are negatively correlated with patients’ overall survival and T cell infiltration. Deletion of Cdk4 or Cdk6 in tumor cells significantly reduce tumor growth. Mechanistically, we find that Cdk4 or Cdk6 deficiency contributes to an increased level of endogenous DNA damage, which triggers the cGAS-STING signaling pathway to activate type I interferon response. Knockout of Sting is sufficient to reverse and partially reverse the anti-tumor effect of Cdk4 and Cdk6 deficiency respectively. Therefore, our findings suggest that CDK4/6 inhibitors may enhance anti-tumor immunity through the STING-dependent type I interferon response.

Abstract Plaque accumulation and microbial community changes are important causes of periodontal disease. Cleaned plaque microorganisms will reattach to form biofilms, but the recovery and outcome of plaque microbial communities in different periodontal health states remain unknown. In this study, we tracked the biofilm remodeling process in 206 dental plaque samples from 40 healthy periodontal, gingivitis and periodontitis volunteers at 6 time points before and after supragingival scaling. We found that microbial communities of different periodontal states changed asynchronously during the process, and the more severe the periodontal disease condition, the more lagged the recovery of plaque microorganisms to their original state after cleaning; this reflected a higher degree of plaque development in periodontitis samples. The plaque index and bleeding index were significantly correlated with plaque recovery, especially the recovery of bacteria such as Abiotrophia and Capnocytophaga. Meanwhile, we found that the microbial community structure of different periodontal health states was most similar at the Day 3 after plaque cleaning, and the communities gradually differentiated and developed in different directions. Abiotrophia and other bacteria might play an important role in determining the development trend of plaque biofilms. The discovery of specific time points and bacteria was of great value in clarifying the pathogenesis of periodontal disease and in seeking targets for prevention and treatment.

To enhance therapeutic approaches, we created a distinctive pattern utilizing the cell demise indicator (CDI) to predict the effectiveness of immunotherapy in individuals with bladder carcinoma (BLCA). Hub prognostic CDIs were identified from the TCGA database using differential gene expression and survival analysis, encompassing 763 genes across 13 death modes. The subtype assessment was employed to evaluate the impact of these genes on the prognosis and immunotherapeutic outcomes in patients with BLCA. The LASSO regression method was used to identify significant CDIs, while Cox regression and nomogram analyses were conducted to explore the impact of CDIs on prognosis. CHMP4C and GSDMB were selected as the hub genes for the following research. Subsequently, These two central genes underwent further investigation to explore their association with immunotherapy, followed by an analysis of their potential regulatory network. Subtype analysis showed that these CDIs were significantly associated with the prognosis and immunotherapy of BLCA patients. The regulatory network in BLCA was evaluated through the establishment of the lncRNA XIST/NEAT1-CDIs-miR-146a-5p/miR-429 axis. Immunohistochemical analysis revealed a significant up-regulation of CHMP4C in bladder cancer tissues, which was strongly associated with an unfavorable prognosis for BLCA patients. Moreover, our findings provide compelling evidence that CHMP4C plays a pivotal role in promoting BLCA progression through the activation of the epithelial-mesenchymal transition (EMT) pathway. These findings highlight the negative impact of CHMP4C on BLCA patient prognosis, while also providing insights into the oncogenic mechanisms and immunotherapy in which CHMP4C may be involved.

Ornithine is an arginine family amino acid and is not incorporated into protein. This study evaluated its role in growth, immune response and acute NH3 stress tolerance of Penaeus vannamei. Six diets with graded levels (0.6, 0.9, 1.2, 1.5, 1.8, 2.1 g kg−1) of L-ornithine were formulated, and fed the shrimp for 8 weeks. The growth of shrimp was significantly improved with the dietary ornithine levels increased from 0.6 to 1.5 g kg−1. Feed efficiency, protein efficiency ratio and protein productive value showed a similar trend to the growth performance of shrimp. Whole body protein and muscle lipid of shrimp were significantly increased in shrimp fed 1.8 g kg−1 ornithine compared to those fed 0.6 g kg−1 ornithine. The contents of several amino acids were increased with the dietary ornithine increased to 1.5 g kg−1. Elevated levels of ornithine increased the Nitric Oxide (NO) content and suppressed arginase activity in the hemolymph. The relative mRNA expression of superoxide dismutase, heat shock protein 70, dorsal and caspase 3 were increased with the dietary addition of ornithine, while the mRNA level of arginase was decreased with the increasing dietary ornithine levels. After 9 h acute NH3 stress, mortality of shrimp reduced with the increasing dietary ornithine levels. The relative mRNA levels of superoxide dismutase, heat shock protein 70, dorsal and catalase were increased with the dietary addition of ornithine after the acute NH3 stress. The second-order regression analysis of weight gain and survival after acute stress revealed that the suitable ornithine content in the shrimp diet was 1.4–1.5 g kg−1.

Little information is available on how exogenous phytosterol (PS) affect the growth performance and lipid homeostasis in fish. In the present study, an 8-week feeding trial were used to investigate the effects of PS on growth performance, serum biochemical indexes, cholesterol (CHO) metabolism and lipidomics of juvenile largemouth bass (Micropterus salmoides). The treatment diets (PS1-PS5) were formulated with supplementation of 0.01 %, 0.02 %, 0.03 %, 0.04 %, and 0.05 % PS on basis of the control diet (C, crude protein 48.39 %, crude lipid 11.65 %). Results showed that the final body weight and specific growth rate of largemouth bass increased as the levels of PS addition increased, reaching stability in the PS3 group. The concentration of high-density lipoprotein cholesterol was elevated and low-density lipoprotein cholesterol was reduced in serum were elevated following PS intervention at 0.03 %. PS treatment reduced the expression of genes associated with endogenous CHO anabolism, while increasing CHO catabolism and suppressing the corresponding negative transcriptional regulators. Lipidomics results showed that the composition patterns of lipid classes between the C and PS4 groups were similar. 7 of triglyceride (TG), 5 of phosphatidylcholine (PC), 2 of PE (phosphatidylethanolamine) and 1 of DG (diglyceride) lipid moleculars were identified as the potential lipid biomarkers in PS4 group. Furthermore, PS4 treatment enriched the pathway of ‘membrane component’ and ‘polyunsaturated fatty acid’. In conclusion, lipid and cholesterol metabolism were altered by the PS treatment, and the appropriate PS addition level was found to be 0.03 % based on the growth performance of the largemouth bass.

Digital economy is an important direction of the new round of technological revolution and a key driving force for realizing the “double control of carbon emissions”. This paper utilizes the panel data of 30 provincial-level administrative regions in China from 2011 to 2021 to measure the development level of the digital economy, total carbon emissions, and carbon emission intensity and explores the impact of the digital economy on the dual control of carbon emissions and the mechanism of its effect by applying the mediating and moderating effect models. The results show that the digital economy can play a significant inhibitory effect on total carbon emissions and carbon emissions intensity, and this conclusion is still robust after a series of tests. From the government level, there exists a transmission path of “digital economy → environmental regulation stringency → dual control of carbon emissions”; from the enterprise and research organization level, there also exists a transmission path of “digital economy → R&D intensity → dual control of carbon emissions”. From the perspective of regional imbalance, there are large regional differences in the impact of the digital economy on the dual control of carbon emissions, and there are also large differences in the impact of the various subdivided indicators of the digital economy on the dual control of carbon emissions. In addition, this paper also finds that the positive effect of the digital economy on the dual control of carbon emissions is more obvious in regions with a smaller proportion of SOEs. These findings add new evidence to the study of “the impact of the digital economy on the dual control of carbon emissions” and provide new ideas for accelerating the realization of green and sustainable development.

Background and objectivesThe prognosis of liver failure treated with non-bioartificial liver support systems is poor. Detecting its risk factors and developing relevant prognostic models still represent the top priority to lower its death risk.MethodsAll 215 patients with liver failure treated with non-bioartificial liver support system were retrospectively analyzed. Potential prognostic factors were investigated, and the Nomogram and the Random Survival Forests (RSF) models were constructed, respectively. Notably, we evaluated the performance of models and calculated the risk scores to divide patients into low-risk and high-risk groups.ResultsIn the training set, multifactorial Cox regression analysis showed that etiology, hepatic encephalopathy, total bilirubin, serum alkaline phosphatase, platelets, and MELD score were independent factors of short-term prognosis. The RSF model (AUC: 0.863, 0.792) performed better in prediction than the Nomogram model (AUC: 0.816, 0.756) and MELD (AUC: 0.658, 0.700) in the training and validation groups. On top of that, patients in the low-risk group had a significantly better prognosis than those in the high-risk group.ConclusionWe constructed the RSF model with etiology, hepatic encephalopathy, total bilirubin, serum alkaline phosphatase, platelets, and MELD score, which showed better prognostic power than the Nomogram model and MELD score and could help physicians make optimal treatment decisions.

BackgroundPituitary stalk interruption syndrome (PSIS) is a complex clinical syndrome characterized by varied pituitary hormone deficiencies, leading to severe manifestations across multiple systems. These include lifelong infertility, short stature, mental retardation, and potentially life-threatening pituitary crises if not promptly diagnosed and treated. Despite extensive research, the precise pathogenesis of PSIS remains unclear. Currently, there are two proposed theories regarding the pathogenic mechanisms: the genetic defect theory and the perinatal injury theory.MethodsWe systematically searched English databases (PubMed, Web of Science, Embase) and Chinese databases (CNKI, WanFang Med Online, Sinomed) up to February 24, 2023, to summarize studies on gene sequencing in PSIS patients. Enrichment analyses of reported mutated genes were subsequently performed using the Metascape platform.ResultsOur study included 37 articles. KEGG enrichment analysis revealed mutated genes were enriched in the Notch signaling pathway, Wnt signaling pathway, and Hedgehog signaling pathway. GO enrichment analysis demonstrated mutated genes were enriched in biological processes such as embryonic development, brain development, axon development and guidance, and development of other organs.ConclusionBased on our summary and analyses, we propose a new hypothesis: disruptions in normal embryonic development, partially stemming from the genetic background and/or specific gene mutations in individuals, may increase the likelihood of abnormal fetal deliveries, where different degrees of traction during delivery may lead to different levels of pituitary stalk interruption and posterior lobe ectopia. The clinical diversity observed in PSIS patients may result from a combination of genetic background, specific mutations, and variable degrees of traction during delivery.

The study aimed to estimate the feasibility of α-cyclodextrin (α-CD), β-cyclodextrin (β-CD), and γ-cyclodextrin (γ-CD) to encapsulate Mosla chinensis essential oil (EO) by ultrasonic-assisted method. The physical properties variations, stabilization mechanisms, and formation processes of the inclusion complexes (ICs) were investigated using experimental methods, molecular docking, and molecular dynamics (MD) simulation. Scanning electron microscopy, fourier transform infrared spectroscopy, thermogravimetric analysis, and gas chromatography–mass spectrometry showed that the ICs were successfully prepared, which differentially improved the thermal stability and retained the chemical composition of EO. The dissolution profile showed that the Peppas model can be used to describe the diffuse release mechanism of EO. Finally, molecular docking and MD simulation theoretically confirmed the interaction and conformational changes of carvacrol (the main active component of Mosla chinensis EO) inside the cavity of CDs. The results indicate that hydrogen bonding was the primary driving force for the carvacrol spontaneous access to the cavity. Further, a binding dynamic balance occurs between carvacrol and β-CD, whereas a bind and away dynamic balance occurs in the IC between carvacrol and α-CD, γ-CD. The comprehensive results show that the medium cavity size of β-CD is a suitable host molecule for Mosla chinensis EO of encapsulation, release, and stabilization. A combination of experimental and theoretical calculations is useful for the pinpoint targeted design and optimization of CD molecular encapsulation of small entity molecules. β-CD was rationally screened as a better candidate for stabilizing EO, which provides an option for a meaningful path to realistic EO applications.

Abstract Background Hippocampal damage caused by status epilepticus (SE) can bring about cognitive decline and emotional disorders, which are common clinical comorbidities in patients with epilepsy. It is therefore imperative to develop a novel therapeutic strategy for protecting hippocampal damage after SE. Mitochondrial dysfunction is one of contributing factors in epilepsy. Given the therapeutic benefits of mitochondrial replenishment by exogenous mitochondria, we hypothesized that transplantation of mitochondria would be capable of ameliorating hippocampal damage following SE. Methods Pilocarpine was used to induced SE in mice. SE‐generated cognitive decline and emotional disorders were determined using novel object recognition, the tail suspension test, and the open field test. SE‐induced hippocampal pathology was assessed by quantifying loss of neurons and activation of microglia and astrocytes. The metabolites underlying mitochondrial transplantation were determined using metabonomics. Results The results showed that peripheral administration of isolated mitochondria could improve cognitive deficits and depressive and anxiety‐like behaviors. Exogenous mitochondria blunted the production of reactive oxygen species, proliferation of microglia and astrocytes, and loss of neurons in the hippocampus. The metabonomic profiles showed that mitochondrial transplantation altered multiple metabolic pathways such as sphingolipid signaling pathway and carbon metabolism. Among potential affected metabolites, mitochondrial transplantation decreased levels of sphingolipid (d18:1/18:0) and methylmalonic acid, and elevated levels of D‐fructose‐1,6‐bisphosphate. Conclusion To the best of our knowledge, these findings provide the first direct experimental evidence that artificial mitochondrial transplantation is capable of ameliorating hippocampal damage following SE. These new findings support mitochondrial transplantation as a promising therapeutic strategy for epilepsy‐associated psychiatric and cognitive disorders.

Reference of the commented article: LI, H. Governance ideas in Kong-Zi Jia Yua and their contemporary values. Trans/Form/Ação: Revista de Filosofia da Unesp, v. 47, n. 1, e0240003, 2024.

Diffuse large B-cell lymphoma is the most common subtype of lymphoma, representing ∼25 % of non-Hodgkin lymphoid malignancies. EZH2 is highly expressed in Diffuse large B-cell lymphoma and ∼22 % of patients contain EZH2 mutations. EZH2 have been studied as a potential therapeutic target for a decade, but efficient inhibition of EZH2 did not robustly kill lymphoma cells. Here, we found that EZH2 mediates repression of oncogenic genes STAT3 and USP7 in Diffuse large B-cell lymphoma cells. Inhibition of EZH2 leads to upregulation of STAT3 and USP7 at both RNA and protein levels. Along with USP7 upregulation, MDM2 is upregulated and its ubiquitylation substrate, Tumor suppressor P53, is downregulated. Upregulation of STAT3 and downregulation of p53 can strength cell proliferation and prevent cells from apoptosis, which suggests resistance mechanisms by which cells survive EZH2 inhibition-induced cell death. Short-course co-inhibition of USP7 and EZH2 showed increased apoptosis and cell proliferation prevention with the concentration as low as 0.08 μM. In STAT3 and USP7 depleted cells, EZH2 inhibition shows superior efficacy of apoptosis, and in EZH2 depleted cells, USP7 inhibition also shows superior efficacy of apoptosis. Thus, our findings suggest a new precision therapy by combinational inhibition of EZH2 with STAT3 or USP7 for Diffuse large B-cell lymphoma.

Abstract The June‐July Yangtze flooding in 1998 and 2020 drew incredible attention owing to the extreme precipitation events and devastating societal/economic damages. However, the quantitative estimation of the moisture transport mechanism is intensely discussed but still unresolved. Here we investigated two events from a unique perspective of Eulerian atmospheric water tracers that tries to explain the two events from model physics. The results showed that the moisture supplies from the Northwest Pacific decreased despite of different inducements, whereas the southwest summer monsoon (SWSM)‐related moisture supplies exhibited conspicuous enhancements in both events, suggesting that the SWSM‐related moisture supplies controlled the occurrence of Yangtze flooding. The physical processes of the two events were further compared. The 2020 flooding was more severe than the 1998 event, which was related to the stronger advective convergences and in‐stratus condensations of the SWSM‐related moisture.

Feline viral diseases, such as feline panleukopenia, feline infectious peritonitis, and feline coronaviral enteritis, seriously endanger the health of cats, and restrict the development of pet industry. Meanwhile, there is a current lack of effective vaccines to protect against feline viral diseases. Thus, effective therapeutic agents are highly desirable. Interferons (IFNs) are important mediators of the antiviral host defense in animals, particularly type I IFNs. In this study, a novel feline IFN omega (feIFN-ω) gene was extracted from the cat stimulated with feline parvovirus (FPV) combined with poly(I:C), and following codon optimization encoding the feIFN-ω, the desired gene (feIFN-ω’) fragment was inserted into plasmid pPICZαA, and transformed into Pichia pastoris GS115, generating a recombinant P. pastoris GS115 strain expressing the feIFN-ω’. After induction, we found that the expression level of the feIFN-ω’ was two times more than that of feIFN-ω (p

Bovine viral diarrhoea virus (BVDV) is the etiologic agent of bovine viral diarrhea-mucosal disease, one of the most important viral diseases in cattle, with inflammatory diarrhea, enteritis, and mucosa necrosis as the major clinical manifestations. NF-κB is an important transcription complex that regulates the expression of genes involved in inflammation and immune responses. NLRP3 inflammasome plays a key role in the development of inflammatory diseases. However, whether the activation of NF-κB is crucial for BVDV infection-induced inflammatory responses remains unclear. The results of our present study showed that BVDV infection significantly activated the NF-κB pathway and promoted the expression of NLRP3 inflammasome components (NLRP3, ASC, pro-caspase 1) as well inflammatory cytokine pro-IL-1β in BVDV-infected bovine cells, resulting in the cleavage of pro-caspase 1 and pro-IL-1β into active form caspase 1 and IL-1β. However, the levels of the NLRP3 inflammasome components and inflammatory cytokines were obviously inhibited, as well the cleavage of pro-caspase 1 and pro-IL-1β in the pre-treated bovine cells with NF-κB-specific inhibitors after BVDV infection. Further, cytopathic biotype BVDV (cpBVDV) Erns and NS5A proteins with their key functional domains contributed to BVDV-induced inflammatory responses via activating the NF-κB pathway were confirmed experimentally. Especially, the NS5A can promote cholesterol synthesis and accelerate its augmentation, further activating the NF-κB signalling pathway. Conclusively, our data elucidate that the activation of NF-κB signaling pathway plays a crucial role in cpBVDV infection-induced inflammatory responses.

Esophageal squamous cell carcinoma (ESCC) is a major histological subtype of esophageal cancer with a poor prognosis. Although several serum metabolomic investigations have been reported, ESCC tumor-associated metabolic alterations and predictive biomarkers in sera have not been defined. Here, we enrolled 34 treatment-naive patients with ESCC and collected their pre- and post-esophagectomy sera together with the sera from 34 healthy volunteers for a metabolomic survey. Our comprehensive analysis identified ESCC tumor-associated metabolic alterations as represented by a panel of 12 serum metabolites. Notably, postoperative abrosia and parenteral nutrition substantially perturbed the serum metabolome. Furthermore, we performed an examination using sera from carcinogen-induced mice at the dysplasia and ESCC stages and identified three ESCC tumor-associated metabolites conserved between mice and humans. Notably, among these metabolites, the level of pipecolic acid was observed to be progressively increased in mouse sera from dysplasia to cancerization, and it could be used to accurately discriminate between mice at the dysplasia stage and healthy control mice. Furthermore, this metabolite is essential for ESCC cells to restrain oxidative stress-induced DNA damage and cell proliferation arrest. Together, this study revealed a panel of 12 ESCC tumor-associated serum metabolites with potential for monitoring therapeutic efficacy and disease relapse, presented evidence for refining parenteral nutrition composition, and highlighted serum pipecolic acid as an attractive biomarker for predicting ESCC tumorigenesis.

Abstract Background Traumatic brain injury (TBI) leads to cell and tissue impairment, as well as functional deficits. Stem cells promote structural and functional recovery and thus are considered as a promising therapy for various nerve injuries. Here, we aimed to investigate the role of ectoderm-derived frontal bone mesenchymal stem cells (FbMSCs) in promoting cerebral repair and functional recovery in a murine TBI model. Methods A murine TBI model was established by injuring C57BL/6 N mice with moderate-controlled cortical impact to evaluate the extent of brain damage and behavioral deficits. Ectoderm-derived FbMSCs were isolated from the frontal bone and their characteristics were assessed using multiple differentiation assays, flow cytometry and microarray analysis. Brain repairment and functional recovery were analyzed at different days post-injury with or without FbMSC application. Behavioral tests were performed to assess learning and memory improvements. RNA sequencing analysis, immunofluorescence staining, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to examine inflammation reaction and neural regeneration. In vitro co-culture analysis and quantification of glutamate transportation were carried out to explore the possible mechanism of neurogenesis and functional recovery promoted by FbMSCs. Results Ectoderm-derived FbMSCs showed fibroblast like morphology and osteogenic differentiation capacity. FbMSCs were CD105, CD29 positive and CD45, CD31 negative. Different from mesoderm-derived MSCs, FbMSCs expressed the ectoderm-specific transcription factor Tfap2β. TBI mice showed impaired learning and memory deficits. Microglia and astrocyte activation, as well as neural damage, were significantly increased post-injury. FbMSC application ameliorated the behavioral deficits of TBI mice and promoted neural regeneration. RNA sequencing analysis showed that signal pathways related to inflammation decreased, whereas those related to neural activation increased. Immunofluorescence staining and qRT-PCR data revealed that microglial activation and astrocyte polarization to the A1 phenotype were suppressed by FbMSC application. In addition, FGF1 secreted from FbMSCs enhanced glutamate transportation by astrocytes and alleviated the cytotoxic effect of excessive glutamate on neurons. Conclusions Ectoderm-derived FbMSC application significantly alleviated neuroinflammation, brain injury, and excitatory toxicity to neurons, improved cognition and behavioral deficits in TBI mice. Therefore, ectoderm-derived FbMSCs could be ideal therapeutic candidates for TBI which mostly affect cells from the same embryonic origins as FbMSCs.

Solid adsorbents that simultaneously have high selectivity and uptake capacity are highly promising as alternatives to conventional cryogenic distillation of propene/propane (C3H6/C3H8) separation. Coordinatively unsaturated metal sites (CUS) plays a vital role in selective adsorption of olefins over paraffins. Ultrathin poly (triazine imide) (PTI) nanosheets can reach rapid gas adsorption equilibrium, due to its large surface-to-volume ratio. In this work, combining the advantages of the CUS and the PTI nanosheets, Li CUSs were introduced into the PTI nanosheets for C3H6/C3H8 separation. Density functional theory (DFT) calculations demonstrated the thermodynamic feasibility of incorporating Li CUSs into the PTI nanosheets. These highly exposed Li CUSs were predicted to have a higher adsorption affinity toward C3H6 than C3H8. Using the DFT-derived force field parameters, we further performed grand canonical Monte Carlo (GCMC) simulations to investigate C3H6/C3H8 adsorption on the Li–PTI complexes slit pore model with different pore widths (H). We found that the Li–PTI complexes display considerable C3H6/C3H8 selectivity (4.2–7.9) under relevant conditions. Moreover, the Li–PTI complexes slit pore have large C3H6 working capacities (1.5–4.0 mmol g−1), superior to those calculated for the most of adsorbent materials that have been reported. The Li–PTI complexes with slit pore architecture show potential as C3H6/C3H8 separation materials.

Bartonellae are considered to be emerging opportunistic pathogens. The bacteria are transmitted by blood-sucking arthropods, and their hosts are a wide range of mammals including humans. After a protective barrier breach in mammals, Bartonella colonizes endothelial cells (ECs), enters the bloodstream, and infects erythrocytes. Current research primarily focuses on investigating the interaction between Bartonella and ECs and erythrocytes, with recent attention also paid to immune-related aspects. Various molecules related to Bartonella’s pathogenicity have been identified. The present review aims to provide a comprehensive overview of the newly described molecular and immune responses associated with Bartonella’s pathogenicity.

Abstract Background The homeostasis of mesenchymal stem cells (MSCs) is modulated by both their own intracellular molecules and extracellular milieu signals. Hematopoiesis in the bone marrow is maintained by niche cells, including MSCs, and it is indispensable for life. The role of MSCs in maintaining hematopoietic homeostasis has been fully elucidated. However, little is known about the mechanism by which hematopoietic cells reciprocally regulate niche cells. The present study aimed to explore the close relationship between MSCs and hematopoietic cells, which may be exploited for the development of new therapeutic strategies for related diseases. Methods In this study, we isolated cells from the offspring of Tie2Cre + and Ptenflox/flox mice. After cell isolation and culture, we investigated the effect of hematopoietic cells on MSCs using various methods, including flow cytometry, adipogenic and osteogenic differentiation analyses, quantitative PCR, western bloting, and microCT analysis. Results Our results showed that when the phosphatase and tensin homolog deleted on chromosome 10 (Pten) gene was half-deleted in hematopoietic cells, hematopoiesis and osteogenesis were normal in young mice; the frequency of erythroid progenitor cells in the bone marrow gradually decreased and osteogenesis in the femoral epiphysis weakened as the mice grew. The heterozygous loss of Pten in hematopoietic cells leads to the attenuation of osteogenic differentiation and enhanced adipogenic differentiation of MSCs in vitro. Co-culture with normal hematopoietic cells rescued the abnormal differentiation of MSCs, and in contrast, MSCs co-cultured with heterozygous null Pten hematopoietic cells showed abnormal differentiation activity. Co-culture with erythroid progenitor cells also revealed them to play an important role in MSC differentiation. Conclusion Our data suggest that hematopoietic cells function as niche cells of MSCs to balance the differentiation activity of MSCs and may ultimately affect bone development.

Objective: The objective of this study was to assess the expression of serum complement component 1q tumor necrosis factor-related protein 3 (CTRP3) and CTRP9 in rheumatoid arthritis (RA) patients, and further explore their correlation with disease activity and the predictive value of RA. Methods: RA group (n = 60) and healthy group (n = 60) were enrolled in Beijing Luhe Hospital, Capital Medical University. We collected the clinical data, including the basic information, laboratory parameters as well as the Disease Activity Score using 28 joint counts (DAS28) scores, and measured the expression of serum CTRP3 and CTRP9 in two groups by enzyme-linked immunosorbent assay. To analyze the correlation between serum CTRP3 and CTRP9 and RA. We explored the predictive value of the serum CTRP3 and CTRP9 for RA. Results: Compared to the healthy group, the expression of serum CTRP3 and CTRP9 was higher in the RA group (P < 0.05). Except rheumatoid factor (serum CTRP9: r = −0.310, P = 0.018), and immunoglobulin (serum CTRP9: r = 0.338, P = 0.010), platelet, erythrocyte sedimentation rate, C-reactive protein, DAS28, anti-cyclic citrullinated peptide antibody, triglyceride, total cholesterol, high-density lipoprotein, low-density lipoprotein, etc., of RA patients were not related to the levels of serum CTRP3 and CTRP9. The best cutoff value of serum CTRP3 and CTRP9 was 31.66 and 34.39 ng/ml, respectively. In terms of sensitivity, negative predictive value, and accuracy, compared with single detection of serum CTRP3 or CTRP9, combined detection has more predictive value for RA. Conclusion: CTRP3 and CTRP9 may become two candidate biomarkers for RA. The serum CTRP3 and CTRP9 may have certain predictive values for RA.

This article investigates the climatic characteristics of Meiyu over the Yangtze-Huaihe River Basin and the primary impact system based on Meiyu onset data from 1954 to 2020, precipitation during the Meiyu Period, NCEP/NCAR reanalysis data, sea surface temperature (SST) data of NOAA, and western Pacific subtropical high (sub-high) data provided by the National Climate Center. The main analytical method used is synthetic analysis. The results indicate that the Meiyu onset date has enormous interannual variation. The date of the earliest Meiyu emergence is 27 days prior to the latest. There is a strong relationship between the duration of Meiyu and rainfall. The start of Meiyu correlates with the northward motion of the South Asia High, the northward jump of the westerly jet, the northward jump of the subtropical high, and the northward motion of the low-level jet. In the early Meiyu years featured in this study, the northward jump of the aforementioned systems occurred earlier and the position of the westerly jet shifted from 34–35°N to 38–40°N, which is much further north than its position under typical climatic circumstances. From late May to early June, the subtropical high was extraordinarily powerful, the ridgeline reached 20°N, and its position was further to the north. In years with a late Meiyu onset, the position of the westerly jet and the ridgeline were further south than the climatological average from early to late June; the jump to the north was not evident until late June. In addition, SST anomalies of the Indian Ocean and Pacific Ocean are significant external forcing variables that influence the Meiyu start date. The high SST of the equatorial Indian Ocean and the equatorial tropical eastern Pacific in the autumn of the preceding year and the high SST of the equatorial Indian Ocean in the spring of that year are prophase indicators of an early Meiyu start in the Yangtze-Huaihe River Basin.