Caesarean section and respiratory system disorders in newborns.

Cesarean section (C-section) delivery is associated with a higher risk of respiratory problems in newborns, particularly if performed electively at 37 weeks. This risk is greater than with spontaneous or induced labor but diminishes as gestation advances. To lower the incidence of respiratory issues in newborns, it is vital to promote natural labor, avoid unnecessary C-sections, and offer thorough prenatal care. Healthcare providers and expectant mothers should assess the risks and benefits of elective C-sections carefully. By advocating for natural labor and reducing unnecessary C-sections, the occurrence of respiratory problems in newborns can be decreased. Adequate prenatal care and monitoring are crucial for identifying and managing potential risk factors for respiratory diseases in newborns. It is crucial for healthcare professionals to educate expectant mothers about the risks of elective C-sections and the advantages of allowing labor to progress naturally. By fostering transparent communication and collaborative decision-making between healthcare providers and pregnant women, well-informed choices can be made that prioritize the health of both the mother and the baby. Furthermore, ongoing research and advancements in medical technology can improve our understanding of how delivery methods affect newborn respiratory health, ultimately leading to better outcomes and care practices in the future.

A Comprehensive Consolidation of Data on the Relationship Between Surfactant Protein-B (SFTPB) Polymorphisms and Susceptibility to Bronchopulmonary Dysplasia.

BACKGROUND: This meta-analysis aims to evaluate the potential link between common variations in the Surfactant Protein-B (SFTPB) gene and the risk of bronchopulmonary dysplasia (BPD) in preterm neonates. METHODS: All pertinent articles published prior to February 1, 2024, in PubMed, Web of Science, EMBASE, CNKI, and Scopus databases were reviewed. RESULTS: Nineteen case-control studies involving 1149 BPD cases and 1845 non-BPD controls, were analyzed. Combined data indicated a significant link between SFTPB -18 A > C and Intron 4 VNTR polymorphisms with increased BPD susceptibility, while the 1580 C > T polymorphism provides a protective impact on BPD initiation. CONCLUSIONS: Pooled data indicated a significant association between SFTPB -18 A > C and Intron 4 VNTR polymorphisms with increased BPD risk, whereas the 1580 C > T polymorphism confers protection. These findings suggest a genetic susceptibility to BPD, underscoring the complex interplay of different genetic elements in its development.

The interaction of breastfeeding and genetic factors on childhood obesity.

Childhood obesity represents a pressing global public health concern due to its widespread prevalence and its close connection to early-life exposure to risk factors. The onset of obesity is contingent upon the interplay of genetic composition, lifestyle choices, and environmental as well as nutritional elements encountered during both fetal development and early childhood. This paper critically examines research discoveries in this area and concisely outlines the influence of breastfeeding on genetic predispositions associated with childhood obesity. Studies have demonstrated that breastfeeding has the potential to reduce childhood obesity by impacting anthropometric indicators. Moreover, the duration of breastfeeding is directly correlated with the degree to which it alters the risk of childhood obesity. Current explorations into the link between genetic factors transmitted through breast milk and childhood obesity predominantly focus on genes like FTO, Leptin, RXRα, PPAR-γ, and others. Numerous research endeavors have suggested that an extended period of exclusive breastfeeding is tied to a diminished likelihood of childhood obesity, particularly if sustained during the initial six months. The duration of breastfeeding also correlates with gene methylation, which could serve as the epigenetic mechanism underpinning breastfeeding's preventative influence against obesity. In summary, the thorough evaluation presented in this review underscores the intricate nature of the association between breastfeeding, genetic factors, and childhood obesity, providing valuable insights for future research efforts and policy formulation.

A Comprehensive Compilation of Data on the Relationship Between Surfactant Protein-B (SFTPB) Polymorphisms and Susceptibility to Neonatal Respiratory Distress Syndrome.

BACKGROUND: This study aims to explore the association between variations in the Surfactant Protein-B (SFTPB) gene and the risk of neonatal respiratory distress syndrome (NRDS). METHODS: A comprehensive literature search was conducted across PubMed, Scopus, EMBASE, and CNKI databases up to February 10, 2024, to identify pertinent studies. RESULTS: A total of seventeen studies examining the +1580 C/T polymorphism (2,058 cases and 2,596 controls) and five studies investigating the -18 A/C polymorphism (680 cases and 739 controls) were included in the analysis. The pooled data indicated that the +1580 C/T polymorphism confers a protective effect against NRDS in various populations and ethnic groups. Conversely, the -18 A/C polymorphism did not demonstrate a significant association either globally or among Asian neonates. CONCLUSIONS: The +1580 C/T variant appears to be protective against NRDS, whereas the -18 A/C polymorphism shows minimal impact on the disease's progression.

Hardy-Weinberg Equilibrium in Meta-Analysis Studies and Large-Scale Genomic Sequencing Era.

The Hardy-Weinberg Equilibrium (HWE) is a fundamental principle employed in the analysis of genetic data, encompassing studies of meta-analysis and genomic sequencing. It has been demonstrated that HWE possesses the property of transitivity, wherein a multi-allelic polymorphism in equilibrium will persist in its equilibrium state even when alleles are deleted or combined. Nonetheless, the practice of filtering loci that do not adhere to HWE has been observed to impact the inference of population genetics within RADseq datasets. In response to this concern, the Robust Unified Test for HWE (RUTH) has been devised to consider population structure and genotype uncertainty, thereby offering a more precise evaluation of the quality of genotype data. Furthermore, deviations from HWE, such as extreme heterozygote excess, can be effectively utilized to identify genotyping errors or to pinpoint the presence of rare recessive disease-causing variants. In summary, it is evident that HWE holds immense significance in the field of genetic analysis, and its application in meta-analysis studies and genomic sequencing can yield invaluable insights into the intricacies of population structure and the genetics of diseases.

Comprehensive data on the relationship between KCNJ11 polymorphisms and gestational diabetes mellitus predisposition: a meta-analysis.

Purpose: The genetic aspect of gestational diabetes mellitus (GDM) is influenced by multiple causal genetic variants, each with different effect sizes. The KCNJ11 gene is particularly noteworthy as a potential contributor to the risk of GDM due to its role in regulating glucose-induced insulin secretion. To evaluate the association between KCNJ11 polymorphisms and GDM, a comprehensive meta-analysis was conducted to review the existing literature and quantitatively assess the correlation. Methods: A thorough search was performed on the PubMed, EMBASE, Scopus, and CNKI databases until December 25, 2023, using precise terms and keywords related to Gestational Diabetes, KCNJ11 gene, and polymorphism. Odds ratios and 95% confidence intervals were used to evaluate the relationships. The statistical analysis was conducted using Comprehensive Meta-Analysis software, and the Cochrane risk of bias assessment tool was used to determine bias presence. Results: The meta-analysis comprised 9 studies with 3108 GDM cases and 5374 controls for the rs5219 polymorphism, and 3 studies with 1209 GDM cases and 1438 controls for the rs5210 polymorphism. The pooled data indicated a noteworthy link between the rs5219 polymorphism and GDM globally and among various ethnic groups, notably in Caucasian and Asian populations. However, no substantial association was observed between the rs5210 polymorphism and GDM. Conclusions: Pooled data showed a correlation between the KCNJ11 rs5219 polymorphism and GDM susceptibility, but no association was found for the rs5210 polymorphism. Future research with larger sample sizes and more diverse populations is needed to improve result generalizability. Supplementary Information: The online version contains supplementary material available at 10.1007/s40200-024-01428-0.

A Comprehensive Integration of Data Regarding the Correlation of TNF-α rs1800629 Polymorphism with Susceptibility to Cervical Cancer.

BACKGROUND: Cervical cancer, globally, ranks as the runner-up among the most prevalent forms of cancer affecting women. The role of the tumor necrosis factor alpha (TNF-α) polymorphism in the susceptibility to cervical cancer has been a subject of interest. However, the current evidence regarding this association remains inconclusive. METHODS: To address this uncertainty, eligible studies were systematically searched and retrieved from various databases including Cochrane Library, EMBASE, PubMed, Web of Science, CNKI, and Wanfang database. The search was conducted until September 01, 2023. The collected literature was then subjected to independent analysis by two authors. The pooled odds ratio along with the corresponding 95% confidence interval was calculated using different genetic models. Additionally, sensitivity and cumulative analyses were performed to assess the stability of the obtained results. RESULTS: A total of 29 case-control studies involving 8850 cases and 9286 controls were included in the present analysis. The findings revealed that the TNF-α rs1800629 polymorphism increased the risk of cervical cancer under the allele genetic model (A vs. G: OR = 1.277, 95% CI = 1.104-1.477, P = 0.001) in the general population. Subgroup analysis based on ethnicity demonstrated that this polymorphism was associated with an increased risk of cervical cancer in Caucasian and African women, but not in Asians. Furthermore, subgroup analysis based on country of origin indicated a significant correlation between the TNF-α rs1800629 polymorphism and an increased risk of cervical cancer in American and Chinese women, but not in Iranian women. CONCLUSIONS: The findings from this meta-analysis suggest that the TNF-α rs1800629 polymorphism is a risk factor for cervical cancer in the general population, particularly in Caucasian and African women. However, further well-designed studies are warranted to validate these findings.

Lactobacillus rhamnosus GR-1 stimulates colony-stimulating factor 3 (granulocyte) (CSF3) output in placental trophoblast cells in a fetal sex-dependent manner.

Bacterial vaginosis is associated with a 1.4-fold increased risk of preterm birth. We have shown previously that Lactobacillus rhamnosus GR-1 supernatant up-regulates interleukin 10 and down-regulates tumor necrosis factor-alpha output in lipopolysaccharide (LPS)-treated human primary placenta cultures in a fetal sex-dependent manner. We hypothesize that lactobacilli also exert their anti-inflammatory effect by up-regulation of colony-stimulating factor 3 (granulocyte) (CSF3), which is secreted from both immune and placental trophoblast cells, and that this activity is dependent on the sex of the fetus. Placental trophoblast cells were isolated from term elective cesarean section placentae using a Percoll gradient and separated from CD45(+) cells using magnetic purification. Cells were treated with LPS in the presence or absence of pretreatments with L. rhamnosus GR-1 supernatant or chemical inhibitors of the intracellular signaling pathways. Phosphorylations of mitogen-activated protein kinase 14 (MAPK14, previously known as p38) and signal transducer and activator of transcription (STAT) 3 were measured by Western blot analysis, and levels of CSF3 were determined by ELISA. CSF3 output was increased only in the placental trophoblast cells of female fetuses treated with LPS, GR-1 supernatant, and a combination of both treatments. The GR-1 supernatant up-regulated the phosphorylation of STAT3 and MAPK14. CSF3 output was inhibited by both Janus kinases (JAK) and MAPK14 inhibitors. None of the treatments was able to increase CSF3 output in either the pure trophoblast or the CD45(+) cell preparations alone. These results suggest an underlying mechanism for the sex difference in incidence of preterm birth and provide potential evidence for a therapeutic benefit of lactobacilli in reducing the risk of preterm labor.

Lactobacillus rhamnosus GR-1-induced IL-10 production in human placental trophoblast cells involves activation of JAK/STAT and MAPK pathways.

Intrauterine infection/inflammation complicates 25% to 40% of preterm births (PTB). The human vagina is normally populated by Lactobacillus species, some of which upregulate interleukin 10 (IL-10) output in lipopolysaccharide (LPS)-treated human placental trophoblast cells. We hypothesize that a probiotic strain, L rhamnosus GR-1 exerts its anti-inflammatory effect through activation of the Janus Kinases/Signal Transducers and Activators of Transcription (JAK/STAT) and mitogen-activated protein kinase (MAPK) pathways. Placental trophoblasts from term healthy pregnancies were treated with LPS in the presence or absence of pretreatments with GR-1 supernatant and/or chemical inhibitors of the intracellular signaling pathways. Phosphorylation of STAT3 and p38 was measured by Western Blot analysis, and output of IL-10 was determined by enzyme-linked immunosorbent assay (ELISA). Phosphorylation of STAT-3 and p38 was upregulated by GR-1 supernatant alone or in combination with LPS, while IL-10 output was inhibited by both JAK and p38 inhibitors. These data provide an underlying intracellular mechanism for cytokine regulation in the human placenta by L rhamnosus GR-1 and potential prevention of infection/inflammation-mediated PTB.

Effect of Lactobacillus rhamnosus GR-1 supernatant and fetal sex on lipopolysaccharide-induced cytokine and prostaglandin-regulating enzymes in human placental trophoblast cells: implications for treatment of bacterial vaginosis and prevention of preterm labor.

OBJECTIVE: The objective of the study was to determine the effect of fetal sex on the output of cytokines and prostaglandin-regulating enzymes in lipopolysaccharide (LPS) and probiotic lactobacilli-treated placental trophoblast cells. STUDY DESIGN: We examined the effect of LPS and Lactobacillus rhamnosus GR-1 supernatant in placental trophoblast cells on tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-10 using enzyme-linked immunosorbent assay and on prostaglandin-endoperoxide synthase 2 (PTGS2), 15-hydroxy prostaglandin dehydrogenase (PGDH), and toll-like receptor-4 (TLR-4) using Western blotting. Comparisons were performed using one-way analysis of variance and Student t test. RESULTS: LPS increased the output of TNF-alpha, IL-10, and PTGS2 with a greater response in male placentae. L rhamnosus GR-1 supernatant inhibited the LPS-stimulated TNF-alpha and increased IL-10. It also up-regulated expression of PGDH in female placentae and partially reduced the LPS-stimulated PTGS2 in male placentae. There was no change in IL-1beta. Expression of TLR-4 was greater in placentae of male fetuses. CONCLUSION: These findings suggest an underlying mechanism for the sex difference in the incidence of preterm birth and provide potential evidence for a therapeutic benefit of lactobacilli in reducing preterm labor.