Enhancing Pure Inertial Navigation Accuracy through a Redundant High-Precision Accelerometer-Based Method Utilizing Neural Networks.

The pure inertial navigation system, crucial for autonomous navigation in GPS-denied environments, faces challenges of error accumulation over time, impacting its effectiveness for prolonged missions. Traditional methods to enhance accuracy have focused on improving instrumentation and algorithms but face limitations due to complexity and costs. This study introduces a novel device-level redundant inertial navigation framework using high-precision accelerometers combined with a neural network-based method to refine navigation accuracy. Experimental validation confirms that this integration significantly boosts navigational precision, outperforming conventional system-level redundancy approaches. The proposed method utilizes the advanced capabilities of high-precision accelerometers and deep learning to achieve superior predictive accuracy and error reduction. This research paves the way for the future integration of cutting-edge technologies like high-precision optomechanical and atom interferometer accelerometers, offering new directions for advanced inertial navigation systems and enhancing their application scope in challenging environments.

High-Salt Diet Causes Defective Oocyte Maturation and Embryonic Development to Impair Female Fertility in Mice.

SCOPE: High salinity has been reported to induce many human disorders in tissues and organs to interfere with their normal physiological functions. However, it is unknown how salinity affects the development of female germ cells. This study suggests that a high-salt diet (HSD) may weaken oocyte quality to impair female fertility in mice and investigates the underlying mechanisms. METHODS AND RESULTS: C57BL/6 female mice are fed with a regular diet (Control) or a high-salt diet (HSD). Oocyte maturation, fertilization rate, embryonic development, and female fertility are evaluated. In addition, the spindle organization, actin polymerization, and kinetochore-microtubule attachment of oocytes are examined in both groups. Moreover, single-cell transcriptome data are used to demonstrate how HSD alters the transcript levels of genes. The observations confirm that HSD leads to female subfertility due to the deterioration of oocyte and embryo quality. The mechanism underlying reveals HSD compromises the oocytes' autophagy, apoptosis level, and mitochondrial function. CONCLUSION: The work illustrates that a high concentration of salt diet results in oocyte meiotic arrest, fertilization failure, and early developmental defection that embryos undergo to reduce female fertility in mice by perturbing the level of autophagy and apoptosis, mitochondrial function in oocytes.

The association between weight-adjusted-waist index and self-reported infertility among women of reproductive age in the United States.

AIM: This study aimed to determine whether the weight-adjusted-waist index (WWI) affected infertility in women of childbearing age in the United States. METHODS: In this study, a database from the 2013 to 2018 National Health and Nutrition Examination Survey (NHANES) was used. We analyzed 3374 participants' data cross-sectionally. The survey used WWI and fertility status as independent and dependent variables. To determine the effect of WWI, an analysis of the independent relationship between WWI and infertility was conducted using weighted multivariable logistic regression and a generalized additive mode (GAM). A smooth curve fitting test was used to calculate whether there was a linear association between WWI and the incidence rate of infertility, as well as subgroup analyses and interaction tests. RESULTS: The prevalence of infertility was 10.19% among 3374 participants. Higher WWI quartiles were associated with higher infertility rates. Based on a fully adjusted model, the effects of WWI on fertility were positive (odds ratio = 1.39, 95% confidence interval: 1.17-1.66). As a result of smooth curve fitting, the association was linear across the entire WWI. Different characteristics were associated with different risks of infertility in subgroup analysis. CONCLUSION: Among women of reproductive age in the United States, WWI levels were positively associated with infertility. This relationship needs to be confirmed by further studies.

Glutathione mitigates meiotic defects in porcine oocytes exposed to beta-cypermethrin by regulating ROS levels.

Beta-cypermethrin (ß-CYP) is a commonly used insecticide that is potentially toxic and has adverse effects on the health of both animals and humans. Studies have indicated that ß-CYP damages organs like the liver, thyroid, intestinal tract, and uterus. However, the underlying mechanisms that ß-CYP affects oocyte quality are poorly understood. According to our research, ß-CYP exposure led to the aberrant assembly of spindles and alignment of chromosomes, resulting in porcine oocytes' defective nuclear maturation. Concurrently, ß-CYP exposure perturbed the cytoplasmic maturation by disturbing the cortical granules (CGs), endoplasmic reticulum (ER), and mitochondrial integrity. It also led to accumulating reactive oxygen species (ROS) and apoptosis. We found that supplementation with glutathione (GSH) mitigated the meiotic defects induced by ß-CYP exposure via regulating ROS levels. Our observations illustrate that ß-CYP exposure adversely impacts oocyte meiotic maturation, and taking GSH supplementation is an effective strategy.

The Potential Role of PPARs in the Fetal Origins of Adult Disease.

The fetal origins of adult disease (FOAD) hypothesis holds that events during early development have a profound impact on one's risk for the development of future adult disease. Studies from humans and animals have demonstrated that many diseases can begin in childhood and are caused by a variety of early life traumas, including maternal malnutrition, maternal disease conditions, lifestyle changes, exposure to toxins/chemicals, improper medication during pregnancy, and so on. Recently, the roles of Peroxisome proliferator-activated receptors (PPARs) in FOAD have been increasingly appreciated due to their wide variety of biological actions. PPARs are members of the nuclear hormone receptor subfamily, consisting of three distinct subtypes: PPARα, ß/δ, and γ, highly expressed in the reproductive tissues. By controlling the maturation of the oocyte, ovulation, implantation of the embryo, development of the placenta, and male fertility, the PPARs play a crucial role in the transition from embryo to fetus in developing mammals. Exposure to adverse events in early life exerts a profound influence on the methylation pattern of PPARs in offspring organs, which can affect development and health throughout the life course, and even across generations. In this review, we summarize the latest research on PPARs in the area of FOAD, highlight the important role of PPARs in FOAD, and provide a potential strategy for early prevention of FOAD.

Role of Interleukin-1 family in bone metastasis of prostate cancer.

Prostate cancer (PCa) is one of the most fatal diseases in male patients with high bone metastatic potential. Bone metastasis severely shortens overall survival and brings skeletal-related events (SREs) which reduces the life quality of patients, and this situation is currently regarded as irreversible and incurable. The progression and metastasis of PCa are found to be closely associated with inflammatory cytokines and chemokines. As pivotal members of inflammatory cytokines, Interleukin-1 (IL-1) family plays a crucial role in this process. Elevated expression of IL-1 family was detected in PCa patients with bone metastasis, and accumulating evidences proved that IL-1 family could exert vital effects on the progression and bone metastasis of many cancers, while some members have dual effects. In this review, we discuss the role of IL-1 family in the bone metastasis of PCa. Furthermore, we demonstrate that many members of IL-1 family could act as pivotal biomarkers to predict the clinical stage and prognosis of PCa patients. More importantly, we have elucidated the role of IL-1 family in the bone metastasis of PCa, which could provide potential targets for the treatment of PCa bone metastasis and probable directions for future research.

Sex Differences at Early Old Stage in Glycolipid Metabolism and Fatty Liver in Offspring Prenatally Exposed to Chinese Great Famine.

Background: About 50 years ago, Chinese Great Famine (CGF) affected the entire population in China, and its long-term influence on the offspring has attracted significant attention for research. However, information on possible metabolic differences between sexes is limited. This study explored whether there might be sex differences in the risks of development of glucolipid metabolic dysfunction and fatty liver following prenatal exposure to CGF. Materials and Methods: There were 11,417 subjects around 55 years of age (6,661 women and 4,756 men). They were divided as the exposed group in which the fetal stage was in CGF, and the unexposed group included those born after CGF. Analysis focused on comparisons between sexes. Results: Compared to the unexposed group, the BMI and triglyceride (P < 0.05) in men were higher in exposed group, while waist circumference and blood sugar (P < 0.05) in the exposed women were significantly higher. With the ages being properly balanced, the risks of glycolipid metabolic dysfunction were significantly higher in both men and women in the exposed than in the unexposed group (P < 0.001). Prenatal exposure to CGF significantly increased risks of abnormal BMI (P < 0.001, 95% CI: 2.305-2.93), blood sugar (P < 0.05, 95% CI: 1.050-1.401), triglycerides (P < 0.05, 95% CI: 1.006-1.245), and fatty liver (P < 0.001, 95% CI: 1.121-1.390) in men, and increased risks of abnormal blood sugar (P < 0.05, 95% CI: 1.024-1.689) and positive urine sugar (P < 0.05, 95% CI: 1.062-6.211) in women. Height and body weight were either the same or higher in the exposed subjects compared with the unexposed ones, regardless of sexes. Conclusion: This study is the first to identify sex differences in the long-term effects of CGF on metabolism and fatty liver. Importance of the findings include the benefits of prescribing medicine for the early prevention of certain diseases for each sex before aging based on the differences revealed. This study also shows "catch-up growth" in the offspring prenatally exposed to CGF as possible mechanisms underlying the long-term effects.

Prenatal hypoxia induced ETBR activation and abnormal ROS signalling in pulmonary artery cells of rat offspring.

Pulmonary arterial hypertension is a progressive disorder characterized by remodeling and increased small pulmonary arteries resistance. Endothelin-1 (ET-1) was related to PAH and ET-1 receptors were up-regulated selectively in the lung when exposed to toxic factor hypoxia. However, the role of ET-1 signaling in the pathogenesis of prenatal hypoxia-induced pulmonary abnormalities remains to be elucidated. Pregnant rats were divided into prenatal hypoxia (10.5 % O2 from gestational day 4-21) and control group. Their three-month-old offspring male rats were tested for vascular functions and molecular analysis, DNA methylation was assessed for cellular hypoxia. Functional testing showed that ET-1-mediated vasoconstriction was enhanced, and the expressions of endothelin A receptor/B receptor (ETAR/ETBR), inositol 1,4,5-trisphosphate receptor, type 1, and the sensitivity of calcium channels were increased in the small pulmonary arteries following prenatal hypoxia. q-PCR and DHE staining showed that the expressions of NADPH oxidase 1/4 (Nox1/4) were up-regulated, along with the increased production of superoxide anion. Furthermore, superoxide anion promoted ET-1-mediated pulmonary artery contraction. In the pulmonary artery smooth muscle cell experiments, q-PCR, Western Blot, CCK8 and DHE staining showed that the expressions of ETBR, Nox1/4, and superoxide anion were increased by hypoxia, along with promoted cell proliferation. 2,2,6,6-Tetramethyl-1-piperidinyloxy reversed hypoxia-induced cell proliferation. ETBR antagonist BQ788 inhibited hypoxia-increased expressions of Nox1/4, superoxide anion production, and proliferation of cells. Moreover, methylation analysis indicated that hypoxia decreased the methylation levels of the ETBR promoter in the pulmonary artery smooth muscle cells. The results indicated that prenatal toxic factor hypoxia resulted in abnormal ETBR activation, which enhanced ET-1-mediated vasoconstriction of pulmonary arteries and pulmonary artery smooth muscle cell proliferation through ETBR/Nox1/4-derived ROS pathway.

Hic-5 in pancreatic stellate cells affects proliferation, apoptosis, migration, invasion of pancreatic cancer cells and postoperative survival time of pancreatic cancer.

Pancreatic cancer is one of the most severe types of tumors, with a 5-year survival rate of less than 7%. The prognosis and treatment of pancreatic cancer are largely limited by the extent of tumor invasion and the presence of lymph node and distant metastases. Therefore, exploring the biological behavior of pancreatic cancer cells (PCCs) is extremely important for the understanding, diagnosis, and treatment of pancreatic cancer. Current studies have shown that pancreatic stellate cells (PSCs) regulate the biological behavior of PCCs, such as their proliferation, apoptosis, invasion, and migration, by remodeling the extracellular matrix. Though Hic-5 is an important gene in PSCs, no study has investigated the regulation of PCCs by Hic-5. Here, we demonstrate that Hic-5 expression is upregulated in pancreatic cancer and that siRNA transfection can effectively inhibit Hic-5 expression. Compared to the control group, Hic-5 inhibition significantly reduced proliferation, increased apoptosis, and reduced invasion and migration of PCCs. Moreover, the inhibition of Hic-5 expression simultaneously reduced matrix metalloproteinase-9 (MMP-9) expression. Statistical analysis revealed that Hic-5 expression was higher among the pancreatic cancer group than among the normal group and was negatively correlated with postoperative survival time among patients with pancreatic cancer. These results have important clinical significance for further exploring the molecular mechanism involved in Hic-5-mediated invasion and metastasis of pancreatic cancer and ameliorating the prognosis of patients with pancreatic cancer.

FSH modulates the expression of inhibin-alpha and the secretion of inhibins via orphan nuclear receptor NUR77 in ovarian granulosa cells.

It has been previously reported that follicle-stimulating hormone (FSH) regulates the expression of inhibin-alpha in human granulosa cells, but the precise molecular pathway remains unknown. In the present study, we investigated the role of the orphan nuclear receptor, NUR77, in both the transcriptional regulation of the inhibin α-subunit gene and the secretion of inhibins. Our results showed that in a human granulosa cell tumor-derived cell line (KGN) and in human granulosa-lutein cells (hGL), FSH induced the expression of NUR77 and inhibin-alpha, although inhibin-alpha expression did not increased following FSH treatment if NUR77 was knocked down. Furthermore, simply overexpressing or reducing NUR77 levels affected inhibin-alpha expression, while NUR77 overexpression improved the secretion of inhibin A and B from human granulosa cells. In addition, chromatin immunoprecipitation-PCR, avidin-biotin-conjugated DNA precipitation, and luciferase reporter assays confirmed that NUR77 directly regulated the transcription of the inhibin-alpha gene through the specific NGFI-B response element located within its promoter. In the ovarian granulosa cells of the Nur77 knockout mice, the mRNA levels of inhibin-alpha were decreased relative to wild-type mice. These data indicate a role of NUR77 in the regulation of inhibin-alpha in ovarian granulosa cells.

Orphan nuclear receptor Nur77 regulates androgen receptor gene expression in mouse ovary.

The androgen receptor (AR) is a nuclear receptor that is expressed in growing follicles and involved in folliculogenesis and follicle growth. The orphan nuclear receptor, Nur77, also has an important role in steroid signaling and follicle maturation. We hypothesized that AR levels and androgen signaling through AR are regulated by Nur77 in the ovary. In the ovaries of Nur77 knockout mice (n = 5), real-time PCR results showed that the mRNA levels of AR and an androgen signaling target gene, Kitl, were decreased by 35% and 24%, respectively, relative to wild-type mice (n = 5), which suggested transcriptional regulation of AR by Nur77 in vivo. In cultured mouse granulosa cells and a steroidogenic human ovarian granulosa-like tumor cell line, KGN, mRNA and protein expression levels of AR were increased by overexpressing Nur77 but decreased by knocking down endogenous Nur77. Consistent with increased AR expression, chromatin immunoprecipitation showed that Nur77 bound to the NGFI-B response element (NBRE) in the AR promoter sequence. AR promoter activity was stimulated by Nur77 in HEK293T cells and attenuated in Nur77 knockout mouse granulosa cells (luciferase assay). Overexpression of Nur77 enhanced the androgenic induction of Kitl (200 nM; 48h), while knockout of Nur77 attenuated this induction. These results demonstrate that AR is regulated by Nur77 in the ovaries, and they suggest that the participation of Nur77 in androgen signaling may be essential for normal follicular development.