Protonation of an Imine-linked Covalent Organic Framework for Efficient H2O2 Photosynthesis under Visible Light up to 700 nm.

Covalent organic frameworks (COFs) are promising photocatalysts for H2O2 production from water via oxygen reduction reactions (ORR). The design of COFs for efficient H2O2 production indubitably hinges on an in-depth understanding of their ORR mechanisms. In this work, taking an imine-linked COF as an example, we demonstrate that protonation of the functional units such as imine, amine, and triazine, is a highly efficient strategy to upgrade the activity levels for H2O2 synthesis. The protonation not only extends the light absorption of the COF but also provides proton sources that directly participate in H2O2 generation. Notably, the protonation simplifies the reaction pathways of ORR to H2O2, i.e. from an indirect superoxide radical ([[EQUATION]]) mediated route to a direct one-step two-electron route. Theoretical calculations confirm that the protonation favors H2O2 synthesis due to easy access of protons near the reaction sites that removes the energy barrier for generating *OOH intermediate. These findings not only extend the mechanistic insight into H2O2 photosynthesis but also provide a rational guideline for the design and upgradation of efficient COFs.

GBP2 inhibits pathological angiogenesis in the retina via the AKT/mTOR/VEGFA axis.

Pathological retinal angiogenesis is not only the hallmark of retinopathies, but also a major cause of blindness. Guanylate binding protein 2 (GBP2) has been reported to be associated with retinal diseases such as diabetic retinopathy and hypoxic retinopathy. However, GBP2-mediated pathological retinal angiogenesis remains largely unknown. The present study aimed to investigate the role of GBP2 in pathological retinal angiogenesis and its underlying molecular mechanism. In this study, we established oxygen-induced retinopathy (OIR) mice model for in vivo study and hypoxia-induced angiogenesis in ARPE-19 cells for in vitro study. We demonstrated that GBP2 expression was markedly downregulated in the retina of mice with OIR and ARPE-19 cells treated with hypoxia, which was associated with pathological retinal angiogenesis. The regulatory mechanism of GBP2 in ARPE-19 cells was studied by GBP2 silencing and overexpression. The regulatory mechanism of GBP2 in the retina was investigated by overexpressing GBP2 in the retina of OIR mice. Mechanistically, GBP2 downregulated the expression and secretion of vascular endothelial growth factor (VEGFA) in ARPE-19 cells and retina of OIR mice. Interestingly, overexpression of GBP2 significantly inhibited neovascularization in OIR mice, conditioned medium of GBP2 overexpressing ARPE-19 cells inhibited angiogenesis in human umbilical vein endothelial cells (HUVECs). Furthermore, we confirmed that GBP2 downregulated VEGFA expression and angiogenesis by inhibiting the AKT/mTOR signaling pathway. Taken together, we concluded that GBP2 inhibited pathological retinal angiogenesis via the AKT/mTOR/VEGFA axis, thereby suggesting that GBP2 may be a therapeutic target for pathological retinal angiogenesis.

Corn straw-saccharification fiber improved the reproductive performance of sows in the late gestation and lactation via lipid metabolism.

With the development of animal husbandry, the shortage of animal feedstuffs has become serious. Dietary fiber plays a crucial role in regulating animal health and production performance. The aim of this study was to investigate the effects of three kinds of corn straw-saccharification fibers (CSSF) such as high-fiber and low-saccharification (HFLS), medium-fiber and medium-saccharification (MFMS), low-fiber and high-saccharification (LFHS) CSSF on the reproductive performance of sows. Thirty-two primiparous Yorkshire sows were randomly assigned to 4 groups, 8 sows for each group. Group A was the basal diet as the control group; groups B - D were added with 6% HFLSCSSF, 6% MFMSCSSF and 6% LFHSCSSF to replace some parts of corn meal and wheat bran in the basal diet, respectively. The experimental period was from day 85 of gestation to the end of lactation (day 25 post-farrowing). The results showed that 6% LFHSCSSF addition significantly increased number of total born (alive) piglets, litter weight at birth (p < 0.05), whereas three kinds of CSSF significantly decreased backfat thickness of sows during gestation (p < 0.001), compared with the control group. Furthermore, CSSF improved the digestibility of crude protein, ether extract and fiber for sows. In addition, the levels of total cholesterol, total triglycerides, and high-density lipoprotein cholesterol in serum of sows were decreased by different kinds of CSSF. Further analysis revealed that CSSF regulated lipid metabolism through adjusting the serum metabolites such as 4-pyridoxic acid, phosphatidyl cholines and L-tyrosine. In summary, CSSF addition to the diets of sows during late gestation and lactation regulated lipid metabolism and improved reproductive performance of sows. This study provided a theoretical basis for the application of corn straw in sow diets.

Zeolitic imidazolate framework-90 loaded with methylprednisolone sodium succinate effectively reduces hypertrophic scar in vivo.

Hypertrophic scar (HS) is characterized by an abnormal fibroblast-myofibroblast transformation; non-apoptosis of fibroblasts; and redundant expression of TGF-ß1, VEGF, α-SMA, and collagen I/III. An HS affects patients' physical and psychological quality of life, leading to joint dysfunction and skin cancer. However, there is currently no satisfactory drug to treat this disorder. In this study, we constructed methylprednisolone sodium succinate (MPSS) encapsulated ZIF-90 (MPSS@ZIF-90) for the effective treatment of an HS. The encapsulation of MPSS in ZIF-90 can achieve the controllable drug release of MPSS and prolong its effective treatment time. MPSS@ZIF-90 enhanced the apoptosis of human hypertrophic scar fibroblasts and downregulated the overexpression of TGF-ß1, VEGF, α-SMA, and collagen I/III both in vitro and in vivo. The instant injection of MPSS@ZIF-90 effectively intervened with the formation of the HS after 28 days. On the contrary, MPSS@ZIF-90 greatly reduced the HS with two injections and 14 days of treatment after the HS was formed. This work provides evidence of effective intervention in the formation of an HS and the therapeutic effectiveness of MPSS@ZIF-90 with short treatment periods in vivo. It suggests that MPSS@ZIF-90 can be used as a biomedical option in the treatment of skin wounds and may reveal the potential molecular basis for promising future antifibrotic agents against scarring.

Crystal Facet Engineering on SrTiO3 Enhances Photocatalytic Overall Water Splitting.

Single-crystal semiconductor-based photocatalysts exposing unique crystallographic facets show promising applications in energy and environmental technologies; however, crystal facet engineering through solid-state synthesis for photocatalytic overall water splitting is still challenging. Herein, we develop a novel crystal facet engineering strategy through solid-state recrystallization to synthesize uniform SrTiO3 single crystals exposing tailored {111} facets. The presynthesized low-crystalline SrTiO3 precursors enable the formation of well-defined single crystals through kinetically improved crystal structure transformation during solid-state recrystallization process. By employing subtle Al3+ ions as surface morphology modulators, the crystal surface orientation can be precisely tuned to a controlled percentage of {111} facets. The photocatalytic overall water splitting activity increases with the exposure percentage of {111} facets. Owing to the outstanding crystallinity and favorable anisotropic surface structure, the SrTiO3 single crystals with 36.6% of {111} facets lead to a 3-fold enhancement of photocatalytic hydrogen evolution rates up to 1.55 mmol·h-1 in a stoichiometric ratio of 2:1 than thermodynamically stable SrTiO3 enclosed with isotropic {100} facets.

Liquid metal-embraced photoactive films for artificial photosynthesis.

The practical applications of solar-driven water splitting pivot on significant advances that enable scalable production of robust photoactive films. Here, we propose a proof-of-concept for fabricating robust photoactive films by a particle-implanting technique (PiP) which embeds semiconductor photoabsorbers in the liquid metal. The strong semiconductor/metal interaction enables resulting films efficient collection of photogenerated charges and superior photoactivity. A photoanode of liquid-metal embraced BiVO4 can stably operate over 120 h and retain ~ 70% of activity when scaled from 1 to 64 cm2. Furthermore, a Z-scheme photocatalyst film of liquid-metal embraced BiVO4 and Rh-doped SrTiO3 particles can drive overall water splitting under visible light, delivering an activity 2.9 times higher than that of the control film with gold support and a 110 h stability. These results demonstrate the advantages of the PiP technique in constructing robust and efficient photoactive films for artificial photosynthesis.

Enhancing regenerative medicine: the crucial role of stem cell therapy.

Stem cells offer new therapeutic avenues for the repair and replacement of damaged tissues and organs owing to their self-renewal and multipotent differentiation capabilities. In this paper, we conduct a systematic review of the characteristics of various types of stem cells and offer insights into their potential applications in both cellular and cell-free therapies. In addition, we provide a comprehensive summary of the technical routes of stem cell therapy and discuss in detail current challenges, including safety issues and differentiation control. Although some issues remain, stem cell therapy demonstrates excellent potential in the field of regenerative medicine and provides novel tactics and methodologies for managing a wider spectrum of illnesses and traumas.

Untargeted metabolomics yields insight into extramammary Paget's disease mechanisms.

Background: Extramammary Paget's disease (EMPD) is a rare cutaneous malignancy, commonly affecting the external genitalia and perianal area of the elderly with unclear pathogenesis. Metabolomics provides a novel perspective for uncovering the metabolic mechanisms of a verity of cancers. Materials and methods: Here, we explored the metabolome of EMPD using an untargeted strategy. In order to further investigate the potential relationship between metabolites and gene expression, we re-analyzed the gene expression microarray data (GSE117285) using differential expression analysis and functional enrichment analyses. Results: Results showed that a total of 896 metabolites were identified and 87 metabolites including 37 upregulated and 50 downregulated significantly in EMPD were sought out. In the following feature selection analyses, four metabolites, namely, cyclopentyl fentanyl-d5, LPI 17:0, guanosine-3',5'-cyclic monophosphate, kynurenine (KYN, high in EMPD) were identified by both random forest and support vector machine analyses. We then identified 1,079 dysfunctional genes: 646 upregulated and 433 downregulated in EMPD. Specifically, the tryptophan-degrading enzyme including indoleamine-2,3-dioxygenase-1 (IDO1) and tryptophan 2,3-dioxygenase (TDO2) were also increased. Generally, cancers exhibit a high expression of IDO1 and TDO2 to catabolize tryptophan, generating abundant KYN. Moreover, we also noticed the abnormal activation of sustaining proliferative signaling in EMPD. Conclusion: In conclusion, this study was the first to reveal the metabolome profile of EMPD. Our results demonstrate that IDO1/TDO2-initialized KYN metabolic pathway may play a vital role in the development and progression of EMPD, which may serve as a potential therapeutic target for treating EMPD.

Chlorogenic acid attenuates deoxynivalenol-induced apoptosis and pyroptosis in human keratinocytes via activating Nrf2/HO-1 and inhibiting MAPK/NF-κB/NLRP3 pathways.

Deoxynivalenol (DON) is a common mycotoxic contaminant, frequently found in food and feed, causing a severe threat to human and animal health. Because of the widespread contamination of DON, humans involved in agricultural practices may be directly exposed to DON through the skin route. Chlorogenic acid (CGA) is a phenolic acid, which has anti-inflammatory and antioxidant properties. However, it is still unclear whether CGA can protect against DON-induced skin damage. Here, the effect of CGA on mitigating damage to human keratinocytes (HaCaT) triggered by DON, as well as its underlying mechanisms were investigated. Results demonstrated that DON exposure significantly decreased cell viability, and induced excessive mitochondrial reactive oxygen species (mtROS) generation, mitochondrial damage, oxidative stress, cell apoptosis and pyroptosis. However, CGA pretreatment for 2 h significantly increased cell viability and reversed DON-induced oxidative stress by improving antioxidant enzyme activities such as superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), reducing mtROS generation and enhancing mitochondrial function through activating Nrf2/HO-1 pathway. Moreover, CGA significantly increased the Bcl-2 protein expression, decreased the protein expressions of Bax and cleaved Caspase-3, and suppressed the phosphorylated of ERK, JNK, NF-κB. Further experiments revealed that CGA could also inhibit the pyroptosis-related protein expressions including NLRP3, cleaved Caspase-1, GSDMD-N, cleaved IL-1ß and IL-18. In conclusion, our results suggest that CGA could attenuate DON-induced oxidative stress, inflammation, and apoptosis by activating the Nrf2/HO-1 pathway and inhibiting MAPK/NF-κB/NLRP3 pathway. CGA might be a novel promising therapeutic agent for alleviating the dermal damage triggered by DON.

Deoxynivalenol exposure induces oxidative stress and apoptosis in human keratinocytes via PI3K/Akt and MAPK signaling pathway.

Deoxynivalenol (DON) is a mycotoxin frequently occurring in human and animal food worldwide, which raises increasing public health concerns. In the present study, we used human keratinocytes (HaCaT cells) as an in vitro model to explore the cytotoxic effect of DON. The results showed that the cells exhibited varying degrees of damage, including decreased cell number and viability, cell shrinkage and floating, when treated with 0.125, 0.25, and 0.5 µg/mL DON for 6, 12, and 24 h, respectively. Furthermore, exposure to DON for 24 h significantly increased the lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS), and prominently decreased the superoxide dismutase (SOD) and catalase (CAT) activity. Additionally, DON exposure induced mitochondrial damage and cell apoptosis through reducing mitochondrial membrane potential. Then, we performed RNA-sequencing to investigate the molecular changes in HaCaT cells after DON exposure. The RNA-sequencing results revealed that DON exposure altered the gene expression involved in apoptosis, MAPK signaling pathway, and PI3K/Akt signaling pathway. Moreover, DON exposure significantly decreased the mRNA and protein expression of Bcl-2, and increased the mRNA and protein expression of Bax, Caspase 3 and COX-2, the protein expression of PI3K, and the phosphorylation levels of Akt, ERK, p38, and JNK. Taken together, these findings suggest that DON exposure could induce cell damage, oxidative stress, and apoptosis in HaCaT cells through the activation of PI3K/Akt and MAPK pathways.

Dissecting neural circuits from rostral ventromedial medulla to spinal trigeminal nucleus bidirectionally modulating craniofacial mechanical sensitivity.

Chronic craniofacial pain is intractable and its mechanisms remain unclarified. The rostral ventromedial medulla (RVM) plays a crucial role in descending pain facilitation and inhibition. It is unclear how the descending circuits from the RVM to spinal trigeminal nucleus (Sp5) are organized to bidirectionally modulate craniofacial nociception. We used viral tracing, in vivo optogenetics, calcium signaling recording, and chemogenetic manipulations to investigate the structure and function of RVM-Sp5 circuits. We found that most RVM neurons projecting to Sp5 were GABAergic or glutamatergic and facilitated or inhibited craniofacial nociception, respectively. Both GABAergic interneurons and glutamatergic projection neurons in Sp5 received RVM inputs: the former were antinociceptive, whereas the latter were pronociceptive. Furthermore, we demonstrated activation of both GABAergic and glutamatergic Sp5 neurons receiving RVM inputs in inflammation- or dysfunction-induced masseter hyperalgesia. Activating GABAergic Sp5 neurons or inhibiting glutamatergic Sp5 neurons that receive RVM projections reversed masseter hyperalgesia. Our study identifies specific cell types and projections of RVM-Sp5 circuits involved in facilitating or inhibiting craniofacial nociception respectively. Selective manipulation of RVM-Sp5 circuits can be used as potential treatment strategy to relieve chronic craniofacial muscle pain.

Relationship between illness perception and family resilience in gynecologic cancer patients: the mediating role of couple illness communication.

OBJECTIVE: To analyze the current family resilience levels of Chinese patients with gynecologic cancer and explore the mediating role of couple illness communication between illness perception and family resilience to facilitate patient adaptation to cancer. METHODS: A total of 310 patients with gynecologic cancer were selected from the gynecology ward of a tertiary care hospital in Jinan, Shandong Province, China. All participants provided their demographic and clinical information and completed the Brief Illness Perception Questionnaire (BIPQ), Couples' Illness Communication Scale (CICS), and Family Hardiness Index (FHI). The mediating effect of couple illness communication was analyzed using SPSS26.0 and Amos21.0. RESULTS: The family resilience score of patients with gynecologic cancer was moderate (55.78 ± 8.65). Illness perception was negatively correlated with couple illness communication(p < 0.05) and family resilience(p < 0.01), while couple illness communication was positively correlated with family resilience (p < 0.01). Couple illness communication mediated the relationship between illness perception and family resilience [ß = - 0.071; 95% confidence interval: (- 0.127)-(- 0.013)]. CONCLUSIONS: The family resilience of patients with gynecologic cancer must be further improved. Since couple illness communication mediates the relationship between illness perception and family resilience in this population, it is important to improve patients' illness perceptions and couple illness communication to enhance their family resilience.

Selective Exposure of Robust Perovskite Layer of Aurivillius-Type Compounds for Stable Photocatalytic Overall Water Splitting.

Aurivillius-type compounds ((Bi2 O2 )2+ (An -1 Bn O3 n +1 )2- ) with alternately stacked layers of bismuth oxide (Bi2 O2 )2+ and perovskite (An -1 Bn O3 n +1 )2- are promising photocatalysts for overall water splitting due to their suitable band structures and adjustable layered characteristics. However, the self-reduction of Bi3+ at the top (Bi2 O2 )2+ layers induced by photogenerated electrons during photocatalytic processes causes inactivation of the compounds as photocatalysts. Here, using Bi3 TiNbO9 as a model photocatalyst, its surface termination is modulated by acid etching, which well suppresses the self-corrosion phenomenon. A combination of comprehensive experimental investigations together with theoretical calculations reveals the transition of the material surface from the self-reduction-sensitive (Bi2 O2 )2+ layer to the robust (BiTiNbO7 )2- perovskite layer, enabling effective electron transfer through surface trapping and effective hole transfer through surface electric field, and also efficient transfer of the electrons to the cocatalyst for greatly enhanced photocatalytic overall water splitting. Moreover, this facile modification strategy can be readily extended to other Aurivillius compounds (e.g., SrBi2 Nb2 O9 , Bi4 Ti3 O12 , and SrBi4 Ti4 O15 ) and therefore justify its usefulness in rationally tailoring surface structures of layered photocatalysts for high photocatalytic overall water-splitting activity and stability.

Descending serotonergic modulation from rostral ventromedial medulla to spinal trigeminal nucleus is involved in experimental occlusal interference-induced chronic orofacial hyperalgesia.

BACKGROUND: Dental treatment associated with unadaptable occlusal alteration can cause chronic primary myofascial orofacial pain. The serotonin (5-HT) pathway from the rostral ventromedial medulla (RVM) exerts descending modulation on nociceptive transmission in the spinal trigeminal nucleus (Sp5) and facilitates chronic pain. The aim of this study was to investigate whether descending 5-HT modulation from the RVM to the Sp5 is involved in the maintenance of primary myofascial orofacial hyperalgesia after persistent experimental occlusal interference (PEOI) or after delayed removal of experimental occlusal interference (REOI). METHODS: Expressions of 5-HT3A and 5-HT3B receptor subtypes in the Sp5 were assessed by immunofluorescence staining and Western blotting. The release and metabolism of 5-HT in the Sp5 were measured by high-performance liquid chromatography. Changes in the pain behavior of these rats were examined after specific pharmacologic antagonism of the 5-HT3 receptor, chemogenetic manipulation of the RVM 5-HT neurons, or selective down-regulation of 5-HT synthesis in the RVM. RESULTS: Upregulation of the 5-HT3B receptor subtype in the Sp5 was found in REOI and PEOI rats. The concentration of 5-HT in Sp5 increased significantly only in REOI rats. Intrathecal administration of Y-25130 (a selective 5-HT3 receptor antagonist) dose-dependently reversed the hyperalgesia in REOI rats but only transiently reversed the hyperalgesia in PEOI rats. Chemogenetic inhibition of the RVM 5-HT neurons reversed the hyperalgesia in REOI rats; selective down-regulation of 5-HT in advance also prevented the development of hyperalgesia in REOI rats; the above two manipulations did not affect the hyperalgesia in PEOI rats. However, chemogenetic activation of the RVM 5-HT neurons exacerbated the hyperalgesia both in REOI and PEOI rats. CONCLUSIONS: These results provide several lines of evidence that the descending pathway from 5-HT neurons in the RVM to 5-HT3 receptors in the Sp5, plays an important role in facilitating the maintained orofacial hyperalgesia after delayed EOI removal, but has a limited role in that after persistent EOI.

Glycyrrhinic acid and probiotics alleviate deoxynivalenol-induced cytotoxicity in intestinal epithelial cells.

Deoxynivalenol (DON) is one of the most prevalent mycotoxin contaminants, which posing a serious health threat to animals and humans. Previous studies have found that individually supplemented probiotic or glycyrrhinic acid (GA) could degrade DON and alleviate DON-induced cytotoxicity. The present study investigated the effect of combining GA with Saccharomyces cerevisiae (S. cerevisiae) and Enterococcus faecalis (E. faecalis) using orthogonal design on alleviating IPEC-J2 cell damage induced by DON. The results showed that the optimal counts of S. cerevisiae and E. faecalis significantly promoted cell viability. The optimal combination for increasing cell viability was 400 µg/mL GA, 1 × 106 CFU/mL S. cerevisiae and 1 × 106 CFU/mL E. faecalis to make GAP, which not only significantly alleviated the DON toxicity but also achieved the highest degradation rate of DON (34.7%). Moreover, DON exposure significantly increased IL-8, Caspase3 and NF-κB contents, and upregulated the mRNA expressions of Bax, Caspase 3, NF-κB and the protein expressions of Bax, TNF-α and COX-2. However, GAP addition significantly reduced aforementioned genes and proteins. Furthermore, GAP addition significantly increased the mRNA expressions of Claudin-1, Occludin, GLUT2 and ASCT2, and the protein expressions of ZO-1, Claudin-1 and PePT1. It was inferred that the combination of GA, S. cerevisiae, and E. faecalis had the synergistic effect on enhancing cell viability and DON degradation, which could protect cells from DON-induced damage by reducing DON cytotoxicity, alleviating cell apoptosis and inflammation via inhibiting NF-κB signaling pathway, improving intestinal barrier function, and regulating nutrient absorption and transport. These findings suggest that GAP may have potential as a dietary supplement for livestock or humans exposed to DON-contaminated food or feed.

Gene therapy: an emerging therapy for hair cells regeneration in the cochlea.

Sensorineural hearing loss is typically caused by damage to the cochlear hair cells (HCs) due to external stimuli or because of one's genetic factors and the inability to convert sound mechanical energy into nerve impulses. Adult mammalian cochlear HCs cannot regenerate spontaneously; therefore, this type of deafness is usually considered irreversible. Studies on the developmental mechanisms of HC differentiation have revealed that nonsensory cells in the cochlea acquire the ability to differentiate into HCs after the overexpression of specific genes, such as Atoh1, which makes HC regeneration possible. Gene therapy, through in vitro selection and editing of target genes, transforms exogenous gene fragments into target cells and alters the expression of genes in target cells to activate the corresponding differentiation developmental program in target cells. This review summarizes the genes that have been associated with the growth and development of cochlear HCs in recent years and provides an overview of gene therapy approaches in the field of HC regeneration. It concludes with a discussion of the limitations of the current therapeutic approaches to facilitate the early implementation of this therapy in a clinical setting.

Combination of glycyrrhizic acid and compound probiotics alleviates deoxynivalenol-induced damage to weaned piglets.

Deoxynivalenol (DON) can affect health and growth performance of pigs, resulting in significant economic losses in swine production. The aim of this study was to investigate the effect of glycyrrhizic acid combined with compound probiotics, i.e. Enterococcus faecalis plus Saccharomyces cerevisiae (GAP) on improving growth performance, intestinal health and its fecal microbiota composition change of piglets challenged with DON. A total of 160 42-day-old weaned piglets (Landrace × Large White) were used and the experimental period was 28 d. The results showed that supplementing GAP in the diet significantly improved the growth performance of piglets challenged with DON and alleviate DON-induced intestinal damage by reducing ALT, AST and LDH concentrations in serum, increasing the morphological parameters of jejunum, and decreasing DON residues in serum, liver and feces. Moreover, GAP could significantly decrease the expressions of inflammation and apoptosis genes and proteins (IL-8, IL-10, TNF-α, COX-2, Bax, Bcl-2 and Caspase 3), and increase the expressions of tight-junction proteins and nutrient transport factor genes and proteins (ZO-1, Occludin, Claudin-1, ASCT2 and PePT1). In addition, it was also found that GAP supplementation could significantly increase the diversity of gut microbiota, maintain microbial flora balance and promote piglet growth by significantly increasing the abundance of beneficial bacterium such as Lactobacillus and reducing the abundance of harmful bacterium such as Clostridium_sensu_stricto_1. In conclusion, GAP addition to piglet diets contaminated with DON could significantly promote the health and growth performance of piglets though alleviating DON-induced hazards. This study provided a theoretical basis for the application of GAP to alleviate DON toxicity for animals.

Couple communication quality and family resilience among Chinese gynecologic cancer patients and their spouses: a dyadic study.

PURPOSE: The purpose of this study was to explore the couple communication process for gynecologic cancer (GC) patients and their spouses. Particular attention was given to examining the relationship between couple communication quality and family resilience for GC dyads. METHODS: In this cross-sectional study, 354 dyads were recruited from a gynecology ward of a public hospital in China. The patients and their spouses completed the Couples' Communication Quality Scale and the Family Hardiness Index. This study used the actor-partner interdependence model (APIM) to examine the effect of couple communication quality on family resilience in distinguishable GC dyads. RESULTS: Both GC patients and their spouses reported a moderate level of couple communication quality and family resilience, but spouses reported better couple communication and family resilience than patients. With the exception of perceived response, for which only a patient actor effect was observed, the factors of couple communication quality had significant actor effects on family resilience for both patients and spouses. Additionally, four significant partner effects were found: spouse self-disclosure, stress coping, and productive action positively predicted patients' family resilience, while patient normalcy crafting positively predicted spouses' family resilience. CONCLUSION: This study not only highlights the need for couple-based communication strategies for developing family resilience but also identifies differences in the experiences of patients and their partners, which provides a direction for future intervention research. Through the development of interventions at a dyadic level, spouses can be encouraged to actively engage in communication, which may promote mutual family resilience in a larger sense.

Triptolide Induces Apoptosis and Autophagy in Cutaneous Squamous Cell Carcinoma via Akt/mTOR Pathway.

BACKGROUND: Tripterygium wilfordii Hook F provided the source of the first diterpenoid triepoxide lactone, Triptolide, identified as the primary constituent causing the anticancer activity. So far, it has not been reported whether triptolide has a therapeutic effect on cutaneous squamous cell carcinoma (cSCC). OBJECTIVE: This study investigates the triptolide's therapeutic impact on cSCC both in vitro and in vivo and investigates the triptolide's potential involvement in signaling pathways. METHODS: The CCK-8 assays, wound healing assays, and colony formation assays were used to assess the effects of triptolide on the proliferation and migration of cSCC cells. The alteration in gene expression following triptolide treatment was shown by RNA sequencing. Flow cytometry was then applied to evaluate cell apoptosis. Western blot was used to find the associated proteins' expressions. The effectiveness of triptolide was then evaluated in vivo using a xenograft model, and histological staining was employed to determine the visceral toxicity. RESULTS: Triptolide greatly reduces the migratory and proliferative capacity of cSCC cells. Triptolide dramatically decreased cell viability and migration in the A431 and SCL-1 cells compared to the control group, according to the CCK8 assay, wound healing assay, and colony formation assay. Flow cytometry demonstrated that treatment with 10- 40 nM triptolide increased apoptosis in a concentration-dependent manner, with a statistically significant difference. Furthermore, mice given triptolide had smaller tumor sizes than those in the control group. Triptolide treatment drastically altered the expression of autophagic and apoptotic proteins. The considerable reduction in the proteins Akt and mTOR levels further illustrated the critical function of triptolide in cSCC. CONCLUSION: Triptolide caused cSCC cells to engage in autophagy and apoptosis by inhibiting the Akt/mTOR signaling pathways. Triptolide may be a possible antitumor agent for the treatment of cSCC.