Background: Owing to the high prevalence and detrimental consequences, postpartum depression (PPD) has been identified as one of the severe global public health issues in the last decade. Prior research found that during disasters or events, the prevalence rates of mental disorders among postpartum women are significantly high. However, the effect of the coronavirus disease 2019 (COVID-19) pandemic on PPD and its risk factors remained unclear for postpartum women. Therefore, the present systematic review and meta-analysis aimed to estimate the influence of the COVID-19 pandemic on the prevalence of PPD and to summarize risk factors for PPD during the COVID-19 pandemic. Methods: Three electronic databases of MEDLINE, EMBASE, and Cochrane library databases were systematically searched for articles from their commencements until 1 November 2021. Quality assessment of included studies, random-effects meta-analysis, and sensitivity analysis were performed. Results: A total of eight studies with 6480 postpartum women during the COVID-19 pandemic were included, and most studies were conducted in developed countries. The pooled prevalence of PPD was 34% (95% CI: 21–46%) during the COVID-19 pandemic, much higher than the incident of previous research during the non-pandemic period. Risk factors for PPD during the COVID-19 pandemic were defined as socio-demographic and clinical characteristics, stress and anxiety, lack of various supports, and the COVID-19 related factors. Conclusion: The research findings indicated that the COVID-19 pandemic could make detrimental effects on maternal mental wellbeing among women after childbirth. Investigating the prevalence and risk factors of PPD among postpartum women could shed some light on their mental and emotional states; so that support measures and tailored interventions from health professionals and policymakers could be offered to improve the maternal and infant outcomes, especially during the COVID-19 pandemic. Much more research on maternal psychological wellbeing during the COVID-19 pandemic was strongly recommended to undertake in the middle and low-income countries.

Background: Airborne fine particulate matter (PM2.5) has been associated with lung cancer development and progression in never smokers. However, the molecular mechanisms underlying PM2.5-induced lung cancer remain largely unknown. The aim of this study was to explore the mechanisms by which PM2.5 regulated the carcinogenesis of non-small cell lung cancer (NSCLC). Methods: Paralleled ribosome sequencing (Ribo-seq) and RNA sequencing (RNA-seq) were performed to identify PM2.5-associated genes for further study. Quantitative real time-PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC) were used to determine mRNA and protein expression levels in tissues and cells. The biological roles of PM2.5 and PM2.5-dysregulated gene were assessed by gain- and loss-of-function experiments, biochemical analyses, and Seahorse XF glycolysis stress assays. Human tissue microarray analysis and ¹⁸F-FDG PET/CT scans in patients with NSCLC were used to verify the experimental findings. Polysome fractionation experiments, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assay were implemented to explore the molecular mechanisms. Results: We found that PM2.5 induced a translation shift towards glycolysis pathway genes and increased glycolysis metabolism, as evidenced by increased L-lactate and pyruvate concentrations or higher extracellular acidification rate (ECAR) in vitro and in vivo. Particularly, PM2.5 enhanced the expression of glycolytic gene DLAT, which promoted glycolysis but suppressed acetyl-CoA production and enhanced the malignancy of NSCLC cells. Clinically, high expression of DLAT was positively associated with tumor size, poorer prognosis, and SUVmax values of ¹⁸F-FDG-PET/CT scans in patients with NSCLC. Mechanistically, PM2.5 activated eIF4E, consequently up-regulating the expression level of DLAT in polysomes. PM2.5 also stimulated transcription factor Sp1, which further augmented transcription activity of DLAT promoter. Conclusions: This study demonstrated that PM2.5-activated overexpression of DLAT and enhancement in glycolysis metabolism contributed to the tumorigenesis of NSCLC, suggesting that DLAT-associated pathway may be a therapeutic target for NSCLC.

We have previously found that TdT-interacting factor 1 (TdIF1) is a potential oncogene expressed in non-small cell lung cancer (NSCLC) and is associated with poor prognosis. However, its exact mechanism is still unclear. The lysine-specific demethylase 1 (LSD1) is a crucial mediator of the epithelial–mesenchymal transition (EMT), an important process triggered during cancer metastasis. Here, we confirm that TdIF1 is highly expressed in NSCLC and related to lymph node metastasis through The Cancer Genome Atlas (TCGA) analysis of clinical samples. Silencing TdIF1 can regulate the expression of EMT-related factors and impair the migration and invasion ability of cancer cells in vitro. An analysis of tumor xenografts in nude mice confirmed that silencing TdIF1 inhibits tumor growth. Furthermore, we determined the interaction between TdIF1 and LSD1 using immunoprecipitation. Chromatin immunoprecipitation (ChIP) revealed that TdIF1 was enriched in the E-cadherin promoter region. The knockdown of TdIF1 repressed the enrichment of LSD1 at the E-cadherin promoter region, thereby regulating the level of promoter histone methylation and modulating E-cadherin transcription activity, ultimately leading to changes in EMT factors and cancer cell migration and invasion ability. The LSD1 inhibitor and TdIF1 knockdown combination showed a synergistic effect in inhibiting the growth, migration, and invasion of NSCLC cells. Taken together, this is the first demonstration that TdIF1 regulates E-cadherin transcription by recruiting LSD1 to the promoter region, thereby promoting EMT and tumor metastasis and highlighting the potential of TdIF1 as a therapeutic target for NSCLC.

Objective To explore the transitions of different blood pressure states based on a multistate Markov model among the Chinese elderly population. Setting A community health centre in Xiamen, China. Participants 1833 elderly Chinese people. Methods A multistate Markov model was built based on 5001 blood pressure measurements from 2015 to 2020. Research was conducted to explore the process of hypertension progression, providing information on the transition probability, HR and the mean sojourn time in three blood pressure states, namely normal state, elevated state and hypertensive state. Results Probabilities of moving from the normal state to the hypertensive state in the first year were 16.97% (female) and 21.73% (male); they increased dramatically to 47.31% (female) and 51.70% (male) within a 3-year follow-up period. The sojourn time in the normal state was 1.5±0.08 years. Elderly women in the normal state had a 16.97%, 33.30% and 47.31% chance of progressing to hypertension within 1, 2 and 3 years, respectively. The corresponding probabilities for elderly men were 21.73%, 38.56% and 51.70%, respectively. For elderly women starting in the elevated state, the probabilities of developing hypertension were 25.07%, 43.03% and 56.32% in the next 1, 2 and 3 years, respectively; while the corresponding changes for elderly men were 20.96%, 37.65% and 50.86%. Increasing age, body mass index (BMI) and glucose were associated with the probability of developing hypertension from the normal state or elevated state. Conclusions Preventive actions against progression to hypertension should be conducted at an early stage. More awareness should be paid to elderly women with elevated state and elderly men with normal state. Increasing age, BMI and glucose were critical risk factors for developing hypertension. The derived transition probabilities and sojourn time can serve as a significant reference for making targeted interventions for hypertension progression among the Chinese elderly population.

Background: Postpartum depression (PPD) has been recognized as a severe public health problem worldwide due to its high incidence and the detrimental consequences not only for the mother but for the infant and the family. However, the pattern of natural transition trajectories of PPD has rarely been explored. Methods: In this research, a quantitative longitudinal study was conducted to explore the PPD progression process, providing information on the transition probability, hazard ratio, and the mean sojourn time in the three postnatal mental states, namely normal state, mild PPD, and severe PPD. The multi-state Markov model was built based on 912 depression status assessments in 304 Chinese primiparous women over multiple time points of six weeks postpartum, three months postpartum, and six months postpartum. Results: Among the 608 PPD status transitions from one visit to the next visit, 6.2% (38/608) showed deterioration of mental status from the level at the previous visit; while 40.0% (243/608) showed improvement at the next visit. A subject in normal state who does transition then has a probability of 49.8% of worsening to mild PPD, and 50.2% to severe PPD. A subject with mild PPD who does transition has a 20.0% chance of worsening to severe PPD. A subject with severe PPD is more likely to improve to mild PPD than developing to the normal state. On average, the sojourn time in the normal state, mild PPD, and severe PPD was 64.12, 6.29, and 9.37 weeks, respectively. Women in normal state had 6.0%, 8.5%, 8.7%, and 8.8% chances of progress to severe PPD within three months, nine months, one year, and three years, respectively. Increased all kinds of supports were associated with decreased risk of deterioration from normal state to severe PPD (hazard ratio, HR: 0.42–0.65); and increased informational supports, evaluation of support, and maternal age were associated with alleviation from severe PPD to normal state (HR: 1.46–2.27). Conclusions: The PPD state transition probabilities caused more attention and awareness about the regular PPD screening for postnatal women and the timely intervention for women with mild or severe PPD. The preventive actions on PPD should be conducted at the early stages, and three yearly; at least one yearly screening is strongly recommended. Emotional support, material support, informational support, and evaluation of support had significant positive associations with the prevention of PPD progression transitions. The derived transition probabilities and sojourn time can serve as an importance reference for health professionals to make proactive plans and target interventions for PPD.

Object: Clinically, the effective treatment options available to thyroid cancer (THCA) patients are very limited. Elucidating the features of tumor suppressor genes (TSGs) and the corresponding signal transduction cascade may provide clues for the development of new strategies for targeted therapy of THCA. Therefore, this paper aims to explore the mechanism of ZNF24 underlying promoting THCA cell senescence at molecular level.Methods: We performed RT-PCR and Western Blotting for evaluating associated RNA and protein expression. CCK8, colony forming, wound healing and Transwell chamber assays were conducted to examine THCA cell proliferation, invasion and migration. β-galactosidase staining assay was performed to detect THCA cells senescence. The size and volume of xenotransplanted tumors in nude mice are calculated to asses ZNF24 effect in vivo.Results: Ectopic expression of ZNF24 significantly inhibited the cell viability, colony forming, migration and invasion abilities of THCA cell lines (K1/GLAG-66i and BCPAPi) (P < 0.05). ZNF24 induced BCPAPi cells senescence through regulating Wnt signaling pathway. ZNF24 inhibited Wnt signaling pathway activition by competitively binding β-catenin from LEF1/TCF1-β-catenin complex. In nude mice, both Ectopic expression of ZNF24 and 2,4-Da (the strong β-catenin/Tcf-4 inhibitor) treatment significantly decreased both the size and weight of xenotransplanted tumors when compared with control mice (P < 0.05).Conclusion: Results obtained in vivo and in vitro reveal the role of ZNF24 in significantly suppressing THCA tumorigenesis and invasion by regulating Wnt signaling pathway.