Human amnion mesenchymal stem cells promote endometrial repair via paracrine, preferentially than transdifferentiation.

BACKGROUND: Intrauterine adhesion (IUA) is one of the most severe causes of infertility in women of childbearing age with injured endometrium secondary to uterine performance. Stem cell therapy is effective in treating damaged endometrium. The current reports mainly focus on the therapeutic effects of stem cells through paracrine or transdifferentiation, respectively. This study investigates whether paracrine or transdifferentiation occurs preferentially in treating IUA. METHODS: Human amniotic mesenchymal stem cells (hAMSCs) and transformed human endometrial stromal cells (THESCs) induced by transforming growth factor beta (TGF-ß1) were co-cultured in vitro. The mRNA and protein expression levels of Fibronectin (FN), Collagen I, Cytokeratin19 (CK19), E-cadherin (E-cad) and Vimentin were detected by Quantitative real-time polymerase chain reaction (qPCR), Western blotting (WB) and Immunohistochemical staining (IHC). The Sprague-Dawley (SD) rats were used to establish the IUA model. hAMSCs, hAMSCs-conditional medium (hAMSCs-CM), and GFP-labeled hAMSCs were injected into intrauterine, respectively. The fibrotic area of the endometrium was evaluated by Masson staining. The number of endometrium glands was detected by hematoxylin and eosin (H&E). GFP-labeled hAMSCs were traced by immunofluorescence (IF). hAMSCs, combined with PPCNg (hAMSCs/PPCNg), were injected into the vagina, which was compared with intrauterine injection. RESULTS: qPCR and WB revealed that FN and Collagen I levels in IUA-THESCs decreased significantly after co-culturing with hAMSCs. Moreover, CK19, E-cad, and Vimentin expressions in hAMSCs showed no significant difference after co-culture for 2 days. 6 days after co-culture, CK19, E-cad and Vimentin expressions in hAMSCs were significantly changed. Histological assays showed increased endometrial glands and a remarkable decrease in the fibrotic area in the hAMSCs and hAMSCs-CM groups. However, these changes were not statistically different between the two groups. In vivo, fluorescence imaging revealed that GFP-hAMSCs were localized in the endometrial stroma and gradually underwent apoptosis. The effect of hAMSCs by vaginal injection was comparable to that by intrauterine injection assessed by H&E staining, MASSON staining and IHC. CONCLUSIONS: Our data demonstrated that hAMSCs promoted endometrial repair via paracrine, preferentially than transdifferentiation.

IUA is the crucial cause of infertility in women of childbearing age, and no satisfactory treatment measures have been found in the clinic. hAMSCs can effectively treat intrauterine adhesions through paracrine and transdifferentiation mechanisms. This study confirmed in vitro and in vivo that amniotic mesenchymal stem cells preferentially inhibited endometrial fibrosis and promoted epithelial repair through paracrine, thus effectively treating intrauterine adhesions. The level of fibrosis marker proteins in IUA-THESCs decreased significantly after co-culturing with hAMSCs for 2 days in vitro. However, the level of epithelial marker proteins in hAMSCs increased significantly, requiring at least 6 days of co-culture. hAMSCs-CM had the same efficacy as hAMSCs in inhibiting fibrosis and promoting endometrial repair in IUA rats, supporting the idea that hAMSCs promoted endometrial remodeling through paracrine in vivo. In addition, GFP-labeled hAMSCs continuously colonized the endometrial stroma instead of the epithelium and gradually underwent apoptosis. These findings prove that hAMSCs ameliorate endometrial fibrosis of IUA via paracrine, preferentially than transdifferentiation, providing the latest insights into the precision treatment of IUA with hAMSCs and a theoretical basis for promoting the "cell-free therapy" of MSCs.

The function of NLRP3 in anti-infection immunity and inflammasome assembly of common carp (Cyprinus carpio L.).

NLRP3 inflammasome can be activated by a variety of stimuli and plays an important role in protecting host from pathogen invasion and maintaining homeostasis. However, the activation mechanism of NLRP3 inflammasome in fish is still unclear. In the present study, the NLRP3 gene (CcNLRP3) was identified from common carp, which was 3069 bp in length and encoded a protein with five domains. Sequence analysis showed that NLRP3 was evolutionarily conserved, and CcNLRP3 was closely related to that in grass carp and zebrafish. Real-time PCR showed that CcNLRP3 was widely expressed in various immune-related tissues of healthy common carp, and significantly increased after stimulation with E. tarda, A. hydrophila and Cyprinus spring viremia virus (SVCV), suggesting that CcNLRP3 might be involved in the immune defense of common carp. The results of co-IP, spot formation, oligomerization and fluorescence localization showed that CcNLRP3 could interact with CcASC and assemble into inflammasome. The cytotoxicity assays showed that CcNLRP3 inflammasome was involved in the pyroptosis induced by CcGSDME. At the same time, CcNLRP3 could directly interact with CcCaspase-A/B and result in increased Caspase-B enzyme activity and LDH release, indicating that CcNLRP3 could also form inflammasome through ASC-independent pathway. Taken together, the results provide targets and theoretical basis for the prevention and control of infectious diseases in aquaculture.

The effects of art-making intervention on mind-body and quality of life in adults with cancer: a systematic review and meta-analysis.

PURPOSE: To investigate the effectiveness of art-making interventions on physical and psychological outcomes, as well as quality of life (QOL), in adult patients with cancer. METHODS: Seven English-language databases (PubMed, Academic Search Premier, EMBASE, CINAHL, PsycINFO, The Cochrane Library, and Web of Science) and three Chinese-language databases (CNKI, WanFang, and VIP) were searched up to and including May 1, 2023. We used the Cochrane Risk of Bias tool 2.0 and the Risk of Bias in Non-Randomized Studies-of Interventions to evaluate the certainty of evidence. The data were analyzed using Review Manager software 5.4. The study protocol was registered with PROSPERO (CRD42022321471). RESULTS: The studies predominantly focused on visual art (n = 21), two specifically used performing art (n = 2), and five integrated both forms of art-making (n = 5). The pooled results showed that art-making significantly improved anxiety (SMD = - 1.12, 95% CI [- 1.43, - 0.81], p < 0.01), depression (SMD = - 0.91, 95% CI [- 1.16, - 0.65], p < 0.01), distress (SMD = - 1.19, 95% CI [- 1.43, - 0.95], p < 0.01), psychological well-being (SMD = 0.41, 95% CI [0.02, 0.80], p = 0.04), societal well-being (SMD = 0.29, 95% CI [0.04, 0.54], p = 0.03), nausea (SMD = - 1.81, 95% CI [- 2.84, - 0.78], p < 0.01), physical well-being (SMD = 0.11, 95% CI [0.02, 0.20], p = 0.02), and QOL (SMD = 0.81, 95% CI [0.29, 1.33], p < 0.01). However, it did not significantly improve fatigue (SMD = - 0.28, 95% CI [- 0.75, 0.19], p = 0.24) and pain (SMD = - 0.18, 95% CI [- 1.97, 1.60], p = 0.84) in patients with cancer. CONCLUSIONS: Art-making interventions may boost psychological well-being, physical symptoms, and QOL among patients with cancer. More robust studies are necessary to overcome methodological limitations and promote wider adoption of these interventions. TRIAL REGISTRATION: Prospero registration number: CRD42022321471.

A latent class analysis of family resilience and its relationship with fear of recurrence in lung cancer patients: a cross-sectional study.

PURPOSE: Family resilience helps cancer-affected families overcome challenges and may influence an individual's fear of cancer recurrence (FCR). Identifying distinct classes of family resilience among lung cancer patients is crucial for tailored interventions. This study aimed to identify latent classes of family resilience in lung cancer patients and explore their relationships with FCR. METHODS: Three hundred ten lung cancer patients from three hospitals in Fujian were recruited from June to September 2021. Clinical data were extracted from medical records, while sociodemographic details, family resilience, and FCR were self-reported. A latent class analysis was performed to identify family resilience classes. RESULTS: A 4-class solution showed the best fit. Compared to Class 1, the patients who had no comorbidities (ORs = 3.480-16.005) had an increased likelihood of belonging to Class 2 and 3, while those who were not family breadwinners (ORs = 0.118-0.176) had a decreased likelihood. Further, the patients who (1) did not lack interest/pleasure in doing things during the past 2-week period (OR = 7.057), (2) were never smokers (OR = 6.230), and (3) were urban residents (OR = 8.985) had an increased likelihood of belonging to Class 4, while those who were (1) male (OR = 0.167), (2) not the family breadwinner (OR = 0.152), and (3) had none or only one child (OR = 0.203) had a decreased likelihood of belonging to Class 4. The FCR level differed significantly among these four classes. CONCLUSION: Our study identified four distinct classes of family resilience among Chinese lung cancer patients. FCR severity decreased with increasing levels of family resilience.

Dexmedetomidine reduces enteric glial cell injury induced by intestinal ischaemia-reperfusion injury through mitochondrial localization of TERT.

This study was performed to uncover the effects of dexmedetomidine on oxidative stress injury induced by mitochondrial localization of telomerase reverse transcriptase (TERT) in enteric glial cells (EGCs) following intestinal ischaemia-reperfusion injury (IRI) in rat models. Following establishment of intestinal IRI models by superior mesenteric artery occlusion in Wistar rats, the expression and distribution patterns of TERT were detected. The IRI rats were subsequently treated with low or high doses of dexmedetomidine, followed by detection of ROS, MDA and GSH levels. Calcein cobalt and rhodamine 123 staining were also carried out to detect mitochondrial permeability transition pore (MPTP) and the mitochondrial membrane potential (MMP), respectively. Moreover, oxidative injury of mtDNA was determined, in addition to analyses of EGC viability and apoptosis. Intestinal tissues and mitochondria of EGCs were badly damaged in the intestinal IRI group. In addition, there was a reduction in mitochondrial localization of TERT, oxidative stress, whilst apoptosis of EGCs was increased and proliferation was decreased. On the other hand, administration of dexmedetomidine was associated with promotion of mitochondrial localization of TERT, whilst oxidative stress, MPTP and mtDNA in EGCs, and EGC apoptosis were all inhibited, and the MMP and EGC viability were both increased. A positive correlation was observed between different doses of dexmedetomidine and protective effects. Collectively, our findings highlighted the antioxidative effects of dexmedetomidine on EGCs following intestinal IRI, as dexmedetomidine alleviated mitochondrial damage by enhancing the mitochondrial localization of TERT.

Demoralization profiles and their association with depression and quality of life in Chinese patients with cancer: a latent class analysis.

PURPOSE: The study aimed to identify latent classes of demoralization and examine their associations with depression and quality of life (QOL) among patients with cancer. METHODS: Cross-sectional data from 874 patients with cancer from three tertiary hospitals in Fujian province were collected using a convenience sampling method. Demoralization, depression, and QOL were assessed using the Chinese version of the Demoralization Scale-II, Patient Health Questionnaire-9, and McGill Quality of Life Questionnaire. Latent class analysis was performed on demoralization profiles. Binary logistic regression and multiple stepwise linear regression were used to examine the identified classes' associations with depression and QOL. RESULTS: Three latent classes of demoralization were identified: the "low demoralization and emotional disturbance" class (Class 1; 49.6%); "moderate demoralization and meaninglessness" class (Class 2; 29.1%); and "high demoralization and existential despair" class (Class 3; 21.3%). The severity of depression increased and the levels of QOL decreased with the three classes of demoralization. Patients with cancer being depressed in Classes 1 and 2 were 0.128 and 0.018 times that of Class 3, respectively, whereas the magnitudes of decrease in QOL scores for Classes 2 and 3 were 0.378 and 0.629, respectively. CONCLUSION: This study revealed three heterogeneous classes of demoralization in Chinese patients with cancer and indicated that increased classes were associated with more severe depression and decreased QOL. Targeted, step-by-step psychological interventions should be developed and implemented according to the characteristics of each class of demoralization to effectively promote psychological well-being among patients with cancer.

The α2AR/Caveolin-1/p38MAPK/NF-κB axis explains dexmedetomidine protection against lung injury following intestinal ischaemia-reperfusion.

Intestinal ischaemia-reperfusion (I/R) injury can result in acute lung injury due to ischaemia and hypoxia. Dexmedetomidine (Dex), a highly selective alpha2-noradrenergic receptor (α2AR) agonist used in anaesthesia, is reported to regulate inflammation in organs. This study aimed to investigate the role and mechanism of Dex in lung injury caused by intestinal I/R. After establishing a rat model of intestinal I/R, we measured the wet-to-dry specific gravity of rat lungs upon treatments with Dex, SB239063 and the α2AR antagonist Atipamezole. Moreover, injury scoring and histopathological studies of lung tissues were performed, followed by ELISA detection on tumour necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6 expression. Correlation of Caveolin-1 (Cav-1) protein expression with p38, p-p38, p-p65 and p65 in rat lung tissues was analysed, and the degree of cell apoptosis in lung tissues after intestinal I/R injury was detected by TUNEL assay. The lung injury induced by intestinal I/R was a dynamic process. Moreover, Dex had protective effects against lung injury by mediating the expression of Cal-1 and α2A -AR. Specifically, Dex promoted Cav-1 expression via α2A -AR activation and mitigated intestinal I/R-induced lung injury, even in the presence of Atipamezole. The protective effect of Dex on intestinal I/R-induced lung injury was also closely related to α2A -AR/p38 mitogen-activated protein kinases/nuclear factor-kappaB (MAPK/NF-κB) pathway. Dex can alleviate pulmonary inflammation after in intestinal I/R by promoting Cav-1 to inhibit the activation of p38 and NF-κB. In conclusion, Dex can reduce pulmonary inflammatory response even after receiving threats from both intestinal I/R injury and Atipamezole.

Dexmedetomidine inhibits mitochondria damage and apoptosis of enteric glial cells in experimental intestinal ischemia/reperfusion injury via SIRT3-dependent PINK1/HDAC3/p53 pathway.

BACKGROUND: Intestinal ischemia/reperfusion (I/R) injury commonly occurs during perioperative periods, resulting in high morbidity and mortality on a global scale. Dexmedetomidine (Dex) is a selective α2-agonist that is frequently applied during perioperative periods for its analgesia effect; however, its ability to provide protection against intestinal I/R injury and underlying molecular mechanisms remain unclear. METHODS: To fill this gap, the protection of Dex against I/R injury was examined in a rat model of intestinal I/R injury and in an inflammation cell model, which was induced by tumor necrosis factor-alpha (TNF-α) plus interferon-gamma (IFN-γ) stimulation. RESULTS: Our data demonstrated that Dex had protective effects against intestinal I/R injury in rats. Dex was also found to promote mitophagy and inhibit apoptosis of enteric glial cells (EGCs) in the inflammation cell model. PINK1 downregulated p53 expression by promoting the phosphorylation of HDAC3. Further studies revealed that Dex provided protection against experimentally induced intestinal I/R injury in rats, while enhancing mitophagy, and suppressing apoptosis of EGCs through SIRT3-mediated PINK1/HDAC3/p53 pathway in the inflammation cell model. CONCLUSION: Hence, these findings provide evidence supporting the protective effect of Dex against intestinal I/R injury and its underlying mechanism involving the SIRT3/PINK1/HDAC3/p53 axis.

H2Bub1 Regulates RbohD-Dependent Hydrogen Peroxide Signal Pathway in the Defense Responses to Verticillium dahliae Toxins.

Histone H2B monoubiquitination (H2Bub1) plays critical roles in regulating growth and development as well as stress responses in Arabidopsis (Arabidopsis thaliana). In this study, we used wild-type and HUB1 and HUB2 loss-of-function Arabidopsis plants to elucidate the mechanisms involved in the regulation of the plant's defense responses to Verticillium dahliae toxins (Vd-toxins). We demonstrated that HUB-mediated H2Bub1 regulates the expression of the NADPH oxidase RbohD by enhancing the enrichment of histone H3 trimethylated on Lys-4 in response to Vd-toxins. RbohD-dependent hydrogen peroxide (H2O2) signaling is a critical modulator in the defense response against Vd-toxins. Moreover, H2Bub1 also affects posttranscriptional mitogen-activated protein kinase (or MPK) signaling. H2Bub1 was required for the activation of MPK3 and MPK6. MPK3 and MPK6 are involved in regulating RbohD-mediated H2O2 production. MPK3 and MPK6 are associated with protein tyrosine phosphatases (PTPs), such as Tyr-specific phosphatase1 and mitogen-activated protein kinases phosphatase1, which negatively regulated H2O2 production. In addition, H2Bub1 is involved in regulating the expression of WRKY33 WRKY33 directly binds to RbohD promoter and functions as a transcription factor to regulate the expression of RbohD Collectively, our results indicate that H2Bub1 regulates the NADPH oxidase RbohD-dependent H2O2 production and that the PTP-MPK3/6-WRKY pathway plays an important role in the regulation of RbohD-dependent H2O2 signaling in defense responses to Vd-toxins in Arabidopsis.

Dexmedetomidine protects intestinal ischemia-reperfusion injury via inhibiting p38 MAPK cascades.

Intestinal ischemia-reperfusion (I/R) is a life-threatening condition associated with high morbidity and mortality. Dexmedetomidine (DEX), an agonist of α2-adrenoceptor with sedation and analgesia effect, has recently been identified with protective function against I/R injury in multiple organs. However, the mechanism underlying the beneficial effect of DEX on intestine after I/R injury remained poorly understood. In the present study, using in both in vitro and in vivo models, we found that intestinal I/R injury was associated with the activation of p38 MAPK cascade, while DEX was capable of deactivating p38 MAPK and thus protect intestinal cells from apoptosis by inhibiting p38 MAPK-mediated mitochondrial depolarization and cytochrome c (Cyto C) release. Moreover, through inhibiting p38 MAPK activity, the downstream production of pro-inflammatory cytokines-regulated by NF-κB was also suppressed by DEX treatment, leading to the resolution of I/R-induced inflammation in intestine. In general, our study provided evidence that DEX protected intestine from I/R injury by inhibiting p38 MAPK-mediated mitochondrial apoptosis and inflammatory response.

An Interpenetrating Alginate/Gelatin Network for Three-Dimensional (3D) Cell Cultures and Organ Bioprinting.

Crosslinking is an effective way to improve the physiochemical and biochemical properties of hydrogels. In this study, we describe an interpenetrating polymer network (IPN) of alginate/gelatin hydrogels (i.e., A-G-IPN) in which cells can be encapsulated for in vitro three-dimensional (3D) cultures and organ bioprinting. A double crosslinking model, i.e., using Ca2+ to crosslink alginate molecules and transglutaminase (TG) to crosslink gelatin molecules, is exploited to improve the physiochemical, such as water holding capacity, hardness and structural integrity, and biochemical properties, such as cytocompatibility, of the alginate/gelatin hydrogels. For the sake of convenience, the individual ionic (i.e., only treatment with Ca2+) or enzymatic (i.e., only treatment with TG) crosslinked alginate/gelatin hydrogels are referred as alginate-semi-IPN (i.e., A-semi-IPN) or gelatin-semi-IPN (i.e., G-semi-IPN), respectively. Tunable physiochemical and biochemical properties of the hydrogels have been obtained by changing the crosslinking sequences and polymer concentrations. Cytocompatibilities of the obtained hydrogels are evaluated through in vitro 3D cell cultures and bioprinting. The double crosslinked A-G-IPN hydrogel is a promising candidate for a wide range of biomedical applications, including bioartificial organ manufacturing, high-throughput drug screening, and pathological mechanism analyses.

KDM4B promotes DNA damage response via STAT3 signaling and is a target of CREB in colorectal cancer cells.

Resistance to radiotherapy is a major limitation for the successful treatment of colorectal cancer (CRC). Recently, accumulating evidence supports a critical role of epigenetic regulation in tumor cell survival upon irradiation. Lysine Demethylase 4B (KDM4B) is a histone demethylase involved in the oncogenesis of multiple human cancers but the underlying mechanisms have not been fully elucidated. Here we show that KDM4B is overexpressed in human colorectal cancer (CRC) tumors and cell lines. In CRC cells, KDM4B silencing induces spontaneous double-strand breaks (DSBs) formation and potently sensitizes tumor cells to irradiation. A putative mechanism involved suppression of Signal Transducer and Activator of Transcription 3 (STAT3) signaling pathway, which is essential for efficient repair of damaged DNA. Overexpression of STAT3 in KMD4B knockdown cells largely attenuates DNA damage triggered by KDM4B silencing and increases cell survival upon irradiation. Moreover, we find evidence that transcription factor CAMP Responsive Element Binding Protein (CREB) is a key regulator of KMD4B expression by directly binding to a conserved region in KMD4B promoter. Together, our findings illustrate the significance of CREB-KDM4B-STAT3 signaling cascade in DNA damage response, and highlight that KDM4B may potentially be a novel oncotarget for CRC radiotherapy.

Associations of the MTHFR rs1801133 polymorphism with coronary artery disease and lipid levels: a systematic review and updated meta-analysis.

BACKGROUND: The associations of the 5,10-methylenetetrahydrofolate reductase gene (MTHFR) rs1801133 polymorphism with coronary artery disease (CAD) and plasma lipid levels have been widely investigated, but the results were inconsistent and inconclusive. This meta-analysis aimed to clarify the relationships of the rs1801133 polymorphism with CAD and plasma lipid levels. METHODS: By searching in PubMed, Google Scholar, Web of Science, Cochrane Library, Wanfang, VIP and CNKI databases, 123 studies (87,020 subjects) and 65 studies (85,554 subjects) were identified for the CAD association analysis and the lipid association analysis, respectively. Odds ratio (OR) and standardized mean difference (SMD) were used to determine the effects of the rs1801133 polymorphism on CAD risk and lipid levels, respectively. RESULTS: The variant T allele of the rs1801133 polymorphism was associated with increased risk of CAD under allelic model [OR = 1.11, 95% confidence interval (CI) = 1.06-1.17, P < 0.01], additive model (OR = 1.25, 95% CI = 1.14-1.37, P < 0.01), dominant model (OR = 1.11, 95% CI = 1.04-1.17, P < 0.01), and recessive model (OR = 1.22, 95% CI = 1.12-1.32, P < 0.01). The T carriers had higher levels of total cholesterol (TC) (SMD = 0.04, 95% CI = 0.01-0.07, P = 0.02) and low-density lipoprotein cholesterol (LDL-C) (SMD = 0.07, 95% CI = 0.01-0.12, P = 0.01) than the non-carriers. CONCLUSIONS: The meta-analysis suggested that the T allele of the rs1801133 polymorphism is a risk factor for CAD, which is possibly and partly mediated by abnormal lipid levels.

[Associations of the MicroRNA-143/145 Polymorphisms with Cardiovascular Risk Factors and the Severity of Coronary Heart Disease].

Objective To explore the possible effects of the microRNA(miR)-143/145 polymorphisms on cardiovascular risk factors and the severity of coronary heart disease(CHD) in Chinese Han people. Methods Polymerase chain reaction-restriction fragment length polymorphism analysis was employed to identify the genotypes of the rs353292 and rs4705343 polymorphisms for 380 patients with CHD and 163 CHD-free controls. The physiological and biochemical parameters between the genotypes were compared in the CHD patients and in controls,and the incidence of myocardial infarction(MI) was also compared between the genotypes in the CHD patients. Results The subjects with the rs353292 TT genotype had higher serum levels of triglycerides(F=3.00,P=0.05) and glucose(F=9.91,P<0.001) than the C carriers,and the subjects with the rs4705343 TT genotype had significantly higher prevalence of hypertension(Χ2=6.35,P=0.04) than the C carriers in the control group. The patients with the rs353292 TT genotype had significantly higher serum levels of hypersensitive C-reactive protein(hs-CRP)(F=8.43,P<0.001) than the C carriers in the CHD group,and the frequency of MI was significantly higher in the patients with the rs353292 TT genotype than that in the C carrier patients(Χ2=5.29,P=0.02). Conclusion The T allele of the rs353292 polymorphism is associated with serum hs-CRP levels in CHD patients,and it may affect the occurrence and development of MI by up-regulation of CRP gene through miR-143/145. The rs4705343 polymorphism is not related to the risk and severity of CHD.

Histone H2B monoubiquitination regulates salt stress-induced microtubule depolymerization in Arabidopsis.

Histone H2B monoubiquitination (H2Bub1) is recognized as a regulatory mechanism that controls a range of cellular processes. We previously showed that H2Bub1 was involved in responses to biotic stress in Arabidopsis. However, the molecular regulatory mechanisms of H2Bub1 in controlling responses to abiotic stress remain limited. Here, we report that HISTONE MONOUBIQUITINATION1 (HUB1) and HUB2 played important regulatory roles in response to salt stress. Phenotypic analysis revealed that H2Bub1 mutants confer decreased tolerance to salt stress. Further analysis showed that H2Bub1 regulated the depolymerization of microtubules (MTs), the expression of PROTEIN TYROSINE PHOSPHATASE1 (PTP1) and MAP KINASE PHOSPHATASE (MKP) genes - DsPTP1, MKP1, IBR5, PHS1, and was required for the activation of mitogen-activated protein kinase3 (MAP kinase3, MPK3) and MPK6 in response to salt stress. Moreover, both tyrosine phosphorylation and the activation of MPK3 and MPK6 affected MT stability in salt stress response. Thus, the results indicate that H2Bub1 regulates salt stress-induced MT depolymerization, and the PTP-MPK3/6 signalling module is responsible for integrating signalling pathways that regulate MT stability, which is critical for plant salt stress tolerance.

Synthesis and antioxidant ability of 6,6'-diamino-6,6'-dideoxytrehalose.

In order to study the influence of amino group on antioxidant activity of oligosaccharides, an amino disaccharide, 6,6'-diamino-6,6'-dideoxytrehalose (DAMDT) was successfully prepared in this paper, and its antioxidant activities against DPPH, superoxide, hydrogen peroxide, and hydroxyl radicals, and reducing power were evaluated, respectively. The results indicated that DAMDT had better antioxidant activity than trehalose at any tested concentration. The influence of amino group on antioxidant activity of disaccharides is positive based on the results in this paper, and amination should be an effective method to improve the bioactivity of saccharides.

Hydrogen-rich water induces aluminum tolerance in maize seedlings by enhancing antioxidant capacities and nutrient homeostasis.

The ameliorative effect of H2 on aluminum (Al)-induced stress remains poorly understood. We treated maize seedlings with Al and hydrogen-rich water (HRW) to determine the roles of H2 in the alleviation of Al toxicity. Our results demonstrated that Al stress triggered damage to the photosynthetic apparatus, plant growth inhibition, and reactive oxygen species (ROS) production, and boosted lipid peroxidation. However, the addition of HRW at 75% saturation markedly alleviated Al toxicity symptoms through the promotion of root elongation. These responses were related to the significantly increased activities of typical antioxidant enzymes (CAT, APX, SOD, and POD). In vivo imaging of plasma membrane integrity, lipid peroxidation, and the level of ROS provided further evidence that HRW could improve Al tolerance. Our results also indicate that 100% HRW mitigated Al toxicity less than 75% HRW. Moreover, different concentrations of HRW significantly improved photosynthesis and increased nutrient uptake. We conclude that exogenous H2 supplementation could enhance Al tolerance by reestablishing redox homeostasis and maintaining nutrient homeostasis.

Functional Analyses of a Novel CITED2 Nonsynonymous Mutation in Chinese Tibetan Patients with Congenital Heart Disease.

CITED2 gene is an important cardiac transcription factor that plays a fundamental role in the formation and development of embryonic cardiovascular. Previous studies have showed that knock-out of CITED2 in mice might result in various cardiac malformations. However, the mechanisms of CITED2 mutation on congenital heart disease (CHD) in Chinese Tibetan population are still poorly understood. In the present study, 187 unrelated Tibetan patients with CHD and 200 unrelated Tibetan healthy controls were screened for variants in the CITED2 gene; we subsequently identified one potential disease-causing mutation p.G143A in a 6-year-old girl with PDA and functional analyses of the mutation were carried out. Our study showed that the novel mutation of CITED2 significantly enhanced the expression activity of vascular endothelial growth factor (VEGF) under the role of co-receptor hypoxia inducible factor 1-aipha (HIF-1A), which is closely related with embryonic cardiac development. As a result, CITED2 gene mutation may play a significant role in the development of pediatric congenital heart disease.

Preparation and Characterization of Novel Cationic Chitosan Derivatives Bearing Quaternary Ammonium and Phosphonium Salts and Assessment of Their Antifungal Properties.

Chitosan is an abundant and renewable polysaccharide, its derivatives exhibit attractive bioactivities and the wide applications in various biomedical fields. In this paper, two novel cationic chitosan derivatives modified with quaternary phosphonium salts were successfully synthesized via trimethylation, chloride acetylation, and quaternization with tricyclohexylphosphine and triphenylphosphine. The structures and properties of synthesized products in the reactions were characterized by FTIR spectroscopy, ¹H-NMR, 31P-NMR, elemental and thermogravimetric analysis. The antifungal activities of chitosan derivatives against four kinds of phytopathogens, including Phomopsis asparagi, Watermelon fusarium, Colletotrichum lagenarium, and Fusarium oxysporum were tested using the radial growth assay in vitro. The results revealed that the synthesized cationic chitosan derivatives showed significantly improved antifungal efficiency compared to chitosan. It was reasonably suggested that quaternary phosphonium groups enabled the obviously stronger antifungal activity of the synthesized chitosans. Especially, the triphenylphosphonium-functionalized chitosan derivative inhibited the growth of Phomopsis asparagi most effectively, with inhibitory indices of about 80% at 0.5 mg/mL. Moreover, the data demonstrated that the substituted groups with stronger electron-withdrawing ability relatively possessed greater antifungal activity. The results suggest the possibility that cationic chitosan derivatives bearing quaternary phosphonium salts could be effectively employed as novel antifungal biomaterials for application in the field of agriculture.