Women with preeclampsia may have reduced risk of breast cancer: a meta-analysis of cohort studies with 7.8 million participants

This review pooled data from the literature to examine the association between preeclampsia (PE) and subsequent risk of breast cancer in women. Cohort studies published in the databases of PubMed, Embase, Scopus, and Web of Science up to 18 July 2023 were searched. Adjusted data were pooled to obtain the risk ratio (RR). Eleven studies with 15 cohorts and a cumulative sample size of 7,838,693 women were included. Meta-analysis of all studies demonstrated a reduced risk of breast cancer in women with PE as compared to those without PE (RR: 0.89 95% CI: 0.83, 0.95 p 2 = 50%). Follow-up ranged from 8 to 29.2 years. Results did not change during sensitivity analysis. Outcomes varied on subgroup analysis based on location, study type, data extraction method, incidence of breast cancer, and follow-up. To conclude, women with PE may have a reduced risk of breast cancer later in life. However, the risk reduction is minimal and may not have much clinical significance. The evidence is also limited by high inter-study heterogeneity and lack of adjustment of all possible confounders.</p

Additional file 1 of Secretory clusterin promotes hepatocellular carcinoma progression by facilitating cancer stem cell properties via AKT/GSK-3β/β-catenin axis

Additional file 1: Fig. S1. sCLU regulated the expression of CSC markers of HCC cells. A, the expression of CSC markers in HCCLM3 cells transfected with NC or sh-sCLU were detected by western blotting. B, relative protein intensities in A were detected by Image J software. C, the expression of CSC markers in HepG2 cells transfected with NC or OE-sCLU were detected by western blotting. D, relative protein intensities in C were detected by Image J software. GAPDH was used as a loading control. **P < 0.01; *P < 0.05. Fig. S2. The expression features of sCLU and β-catenin in HCC tissues. A, sCLU staining scores in HCC and para-cancerous tissues. B, β-catenin staining scores in HCC and para-cancerous tissues. C, positive ratio of sCLU and β-catenin expression in HCC tissues at different TNM stages. *P < 0.05, **P < 0.01. TNM, tumor-node-metastasis

Data_Sheet_1_Household air pollution and childhood stunting in China: A prospective cohort study.DOCX

BackgroundExposure to air pollution, especially indoor air pollution, was associated with an increased risk of childhood stunting. However, few longitudinal studies have explored the long-term impacts of indoor air pollution from household solid fuel use on child growth. We aimed to investigate the association between household air pollution (HAP) from solid fuel use and childhood stunting in Chinese children.MethodThe longitudinal data from the Chinese Family Panel Study over 2010–2018 were included in this study with a total of 6,013 children aged 0–15 years enrolled at baseline. Exposure to HAP was measured as solid fuel use for cooking, while solid fuel was defined as coal and firewood/straw according to the questionnaire survey. Stunting was defined as−2SD below the height-for-age z-score (HAZ) of the reference children. Logistic regression and Cox proportional hazards models with time-varying exposures were employed to estimate the association between childhood stunting and HAP exposure.ResultsAt baseline, children with exposure to HAP from combusting solid fuels had a relatively higher risk of stunting [OR (95%CI): 1.42 (1.24–1.63)]. Among children without stunning at baseline, those living in households with solid fuel use had a higher stunting risk over an 8-year follow-up [HR (95%CI): 2.05 (1.64–2.57)]. The risk of childhood stunting was increased for those with HAP exposure from firewood/straw combustion or with longer exposure duration [HR (95%CI): 2.21 (1.74–2.79) and 3.01 (2.23–4.08), respectively]. Meanwhile, this risk was significantly decreased among children from households switching from solid fuels to clean fuels [HR (95%CI): 0.53 (0.39–0.70)]. Solid fuel use was suggested to be a mediator of the relationship between poor socioeconomic factors (i.e., household income and parental education level) and childhood stunning, with a mediation effect ranging from 11.25 to 14.26%.ConclusionsHAP exposure from solid fuel use was associated with childhood stunting. Poor parental education and low household income might be socioeconomic factors contributing to solid fuel use. Therefore, household energy policies to facilitate access to clean fuels are urgently needed, especially for low-income and low-educated households.</p

Correlation between CPT II activity and β-oxidation/ATP production at 41°C and 37°C in CPT II-deficient fibroblasts.

<p>(●) control, (■) V368I (homozygous), (△) F352C (heterozygous) + V368I (homozygous). CPT II activity, β-oxidation, and ATP production are expressed as % of control values of control fibroblasts at 37°C. Data areand means of five separate experiments: 0.53 nmol/min/mg protein of CPT II activity; 14.5 nmol of released CO₂/h/10⁶ cells; 8.12 nmol of ATP/10⁶ cells. The average of three independent experiments is shown ± SEM.</p

Pulse-chase (left) and half-lives (right) of control and variant CPT II in fibroblasts.

<p>Cultured fibroblasts were pulse-labeled with L-[³⁵S] methionine for 2 h and chased for 0, 6, 12, and 18 h. CPT II from fibroblast lysates was immunoprecipitated with anti-CPT II antibodies, then subjected to SDS-PAGE followed by autoradiography. (●) control, (■) V368I (homozygous), (▲) F352C (heterozygous) + V368I (homozygous). The average of three independent experiments is shown ± SEM.</p

Cell apoptosis analysis of <i>CPT II</i> variants in fibroblasts.

<p>(A) Apoptotic fibroblasts were measured by flow cytometry. Fibroblasts incubated with DMSO were used as a control. (B) LDH assay of control and <i>CPT II</i> variants in fibroblasts. (C) Apoptotic factor release was analyzed by Western Blotting with antibodies against caspase-3, caspase-8, cytochrome c, and Bid for control and variant CPT IIs in control and CPT II-deficient fibroblasts. CPT II proteins are expressed relative to β-actin. Data are means of three separate experiments. The average of three independent experiments is shown ± SEM (*P<0.05).</p

MOESM3 of Regulators of Salmonella-host interaction identified by peripheral blood transcriptome profiling: roles of TGFB1 and TRP53 in intracellular Salmonella replication in pigs

Additional file 3. Differentially expressed transcripts. The full list of differentially expressed transcripts

MOESM4 of Regulators of Salmonella-host interaction identified by peripheral blood transcriptome profiling: roles of TGFB1 and TRP53 in intracellular Salmonella replication in pigs

Additional file 4. Over-represented pathways. The significantly over-represented pathways in cluster A, C, D, E, and F

Reduction of mitochondrial membrane potential of control and variant CPT IIs in cultured fibroblasts.

<p>Control (A, D), V368I (homozygous) (B, E), and F352C (heterozygous) + V368I (homozygous) (C, F) fibroblasts were cultured at 37°C and 41°C. Mitochondrial depolarization was monitored by 15 min treatment with 10 μM of JC-1 in the dark and visualized under a fluorescence microscope. Scale bars, 100 μm.</p

MOESM8 of Regulators of Salmonella-host interaction identified by peripheral blood transcriptome profiling: roles of TGFB1 and TRP53 in intracellular Salmonella replication in pigs

Additional file 8. Salmonella intracellular salmonella growth assay. Details of the Salmonella intracellular salmonella growth assay