IL-1ß and CXCR4 as Potential Therapeutic Targets for Alzheimer's Disease.

BACKGROUND: Alzheimer's Disease (AD) is a highly prevalent form of age-related dementia. However, the underlying mechanisms of AD are largely unexplored. MATERIALS AND METHODS: In this study, bioinformatics analysis was performed to identify the possible therapeutic targets for AD. The GEO database was used to screen the Differentially Expressed Genes (DEGs). Enrichment analysis, protein-protein interaction network, and LASSO model analyses were successfully performed. Furthermore, an ELISA assay was also conducted to determine the expression of principal genes within the AD and control samples. RESULTS: A total of 416 differentially expressed genes (DEGs) were recognized based on the GSE48350 and GSE28146 datasets. The IL-1ß and CXCR4 levels were markedly elevated in the AD samples relative to the control. CONCLUSION: The IL-1ß and CXCR4 genes were identified as principal AD-related genes that can be targeted for anti-AD therapy.

Does childhood parental death impact late life health directly and indirectly? Evidence from a National Survey in China.

Despite growing interest in understanding the impact of childhood parental death, less is known about its long-term effects on older adults. We investigated the mediating role of poor health perception in the relationship between childhood parental loss and late life health. A cross-sectional study using data from the 2016 China Longitudinal Aging Social Survey was conducted. Our final sample featured 8,547 older adults. The prevalence of childhood parental death was 9.8%. Results indicated a significant direct impact of childhood parental death on depression and cognitive function. Mediating effects were observed, with older adults who experienced childhood parental loss perceiving their health status as significantly worse. This, in turn, predicted higher levels of objective physical impairment, greater depression, and lower levels of cognitive function. Our study offers the first empirical evidence of the enduring negative effects of childhood parental death as well as the pivotal mediating role of poor health perception.

"I never told my family I was grieving for my mom": The not-disclosing-grief experiences of parentally bereaved adolescents and young adults in Chinese families.

In bereavement literature, the significance of open communication within the family is often highlighted. However, in recent years, scholars have noticed the complexity of grief communication in the family, especially challenges and obstacles to sharing grief. Our study seeks to contribute to the research by offering a deeper understanding of the grief-sharing experiences of parentally bereaved adolescents and young adults from China, a family-centered society with strong traditions of treating bereavement and grief as taboo. We used a narrative approach to analyze 82 interviews with 44 participants. We found that almost all the participants, regardless of their gender, parent's gender, cause of death, or time since loss, indicated that they never shared grief with other family members. Specifically, three themes emerged from the analysis. "Holding back tears during the funeral" reflects participants' struggle to protect the family (especially the surviving parent) through hiding their grief during the family crisis. "Pretending no grief at all after loss" shows how participants intentionally avoided any grief conversations within the family to not trigger others' grief. In addition, "Keeping grief secret as a family rule" indicates how Chinese families powerfully guided and influenced participants in avoiding the open expression of their grief. Our findings have drawn attention to the not-disclosing-grief experiences of bereaved adolescents and young adults in the Chinese context and the role of the family in it, therefore, calling for further support for bereaved young people, either within the family or through professional services.

Effect of prior female SARS-CoV-2 infection on IVF outcomes: a prospective cohort study.

Introduction: The clinical impact of SARS-CoV-2 infection on human reproduction remains controversial. This prospective cohort study aimed to assess the effect of prior female SARS-CoV-2 infection on subsequent in vitro fertilization (IVF) outcomes. Materials and methods: A total of 451 women who underwent fresh IVF treatment between December 1, 2022 and April 30, 2023 were included from an academic fertility center. Participants were divided into the infected group if they had a prior COVID-19 history before cycle initiation (n = 252), while the control group were those uninfected (n = 199). The primary outcomes were the number of oocytes retrieved and clinical pregnancy rate after fresh embryo transfer. Multivariate linear and logistic regression analyses were conducted to control for potential confounders. Results: The number of oocytes retrieved (11.4 ± 8.3 vs. 11.6 ± 7.7; P = 0.457) and clinical pregnancy rate (70.3% vs. 73.7%; P = 0.590) were similar between infected and uninfected groups, with a fully adjusted ß coefficient of 0 (95% confidence interval [CI]: -0.14-0.13) and odds ratio of 0.64 (95% CI: 0.20-2.07), respectively. Consistently, the two groups were comparable in cycle characteristics as well as other laboratory and pregnancy parameters. In both subgroup analyses and restricted cubic splines, different post-infection time intervals to IVF cycle initiation showed no significant associations with treatment outcomes. Conclusion: Prior SARS-CoV-2 infection in females had no adverse influence on subsequent IVF treatment, regardless of the time interval following infection. Our findings provide reassurance for infected women planning for assisted reproduction. Additional prospective cohort studies with larger datasets and longer follow-up are required to confirm the conclusion.

Efficacy of microsurgery for congenital neural tube defects in newborns.

OBJECTIVE: The purpose of this study was to investigate the clinical value of microsurgery in the treatment of congenital neural tube defect (CNTD) in newborns. METHODS: Eighty-five CNTD newborns withlipomyelomeningocele admitted to our hospital from March 2016 to December 2018 were retrospectively selected as study subjects. They were divided into a study group (SG, 43 cases, that received meningocele repair combined with tethered cord release within 6 h to 30 d after birth) and the control group (CG, 42 cases, that received meningocele repair combined with tethered cord release past 30 d after birth) according to the treatment regimen. Newborns in both groups were evaluated for short-term and long-term outcome of the surgery and the degree of postoperative untethering, and both groups were followed up dynamically to record changes in gross motor function and quality of life and assess risk factors. RESULTS: In terms of short-term outcomes, the total effective rate was 93.02% in SG and 85.71% in CG (P > 0.05); in terms of the long-term outcomes, the total effective rate was 88.37% in SG and 69.05% in CG (P < 0.05). The postoperative release of the newborns was evaluated according to the Kirollos grading system, which showed that SG had 40 (93.02%) cases of grade 1 untethering, 3 (6.98%) cases of grade 2 untethering, and 0 case of grade 3 untethering, and CG had 30 (71.43%) cases of grade 1 untethering, and 12 (28.57%) cases of grade 2 untethering. At 6 months postoperatively, there were no significant differences in gross motor function and quality of life scores between the two groups (P > 0.05), but at 1 year, 3 years and 4 years postoperatively, the gross motor function and quality of life scores of newborns in the SG were significantly higher than those in the CG (P < 0.05). Multivariate logistic regression analysis showed that age > 1 month was an independent risk factor for surgical outcome (P < 0.05). CONCLUSION: Microsurgery has better short-term and long-term outcomes for newborns with CNTD, and the newborns showed an improvement in the long-term postoperative motor function and quality of life.

Development and Validation of the Career and Life Development Hope (CLDH) Scale among Non-Engaged Youth in Hong Kong.

Increasing career and life development hope (CLDH) is critical for the career and life pursuits of non-engaged youths (NEY) who face various disadvantages in the school-to-work transition, especially considering current challenging labor market conditions and the impacts of the pandemic. Nevertheless, research that explores the assessment of CLDH among NEY is scarce. To address this gap, this study aimed to develop and validate a CLDH measurement instrument. A total of 1998 NEY aged 13-29 years in Hong Kong participated in our study. Exploratory factor analysis of the 20-item CLDH scale suggested a two-factor structure-career and life development pathways (CLDP) and career and life development agency (CLDA)-which accounted for 63.08% of the total variance. The confirmatory factor analysis results show a good model fit (CFI = 0.934, TLI = 0.926, RMSEA = 0.060, 90% CI [0.055, 0.065], SRMR = 0.042) and all the items significantly represented the corresponding sub-constructs. The results also demonstrate a satisfactory internal consistency for all subscales and the full scale (0.89-0.95). Sub-group consistency across subsamples categorized by gender, age, and years of residence in Hong Kong was indicated. Correlations between the CLDH scale and subscales with other career-related and social well-being outcomes (i.e., youth career development competency, career adaptability, civic engagement, social contribution, and social integration) showed good concurrent validity. Our results support that the CLDH scale is a valid and reliable tool for measuring NEY's hope for career and life development in the Hong Kong context. Theoretical and practical implications of the findings are also discussed.

Social Isolation, Cognitive Function, and Depression Among Chinese Older Adults: Examining Internet Use as a Predictor and a Moderator.

Objectives: Despite the theoretical and practical interest in Internet use among older adults, evidence examining the impacts of Internet use on late-in-life health is limited. This study examines how Internet use affects depression and cognitive function in older adults and investigates if Internet use moderates the relationship between social isolation and depression/cognitive function. Method: We performed regression analyses using data came from the second wave of the China Longitudinal Aging Social Survey of 2016. Our final sample featured 8,835 older adults. Results: The results show 11.4% of Chinese older adults often used the Internet to engage in at least one activity. Internet use was negatively associated with depression, but it was positively related to cognitive function. Socially isolated older adults were more likely to have more depressive symptoms and higher level of cognitive function. There was also an interaction effect between Internet use and social isolation on depression/cognitive function. The negative effect of social isolation was stronger for older adults who used the Internet less. The moderating effect of Internet use was significant for both males and females. However, among those who used the Internet more, the depression levels of socially isolated male participants were much lower than female participants. Conclusions: Our results reveal the importance of considering Internet use in buffering the negative effects of social isolation and the associated health burdens for aging populations. Recommendations for service practice and future research are discussed.

Inhibition of translocator protein 18 kDa suppressed the progression of glioma via the ELAV-like RNA-binding protein 1/MAPK-activated protein kinase 3 axis.

Glioma is the most common primary malignant brain tumors in adults. Despite considerable advances in treatment, the clinical outcome remains dismal. Translocator protein 18 kDa (TSPO), an evolutionarily conserved transmembrane protein, has always been found to be elevated in glioma, which predicts a poor prognosis. However, studies on the regulatory network of TSPO in glioma are limited. The Cancer Genome Atlas (TCGA) and our research group cohorts demonstrated that TSPO expression was also highly expressed in glioma tissues and glioma cell lines. Inhibition of TSPO expression significantly reduced glioma cell proliferation and mobility in vitro. Suppression of TSPO decreased the expression of MAPK-activated protein kinase 3 (MAPKAPK3) and increased the degradation rate of its mRNA. TSPO directly interacts with ELAV1-like RNA-binding protein 1 (HUR) and promotes the nuclear-cytoplasmic shuttling of HUR. Inhibition of HUR decreased MAPKAPK3 expression and cell proliferation and mobility, whereas overexpression of MAPKAPK3 reversed the effects. Overexpression of HUR in TSPO-knockdown cells enhanced the mRNA stability of MAPKAPK3. Furthermore, rescue experiments show that the HUR/MAPKAPK3 axis accounts for the TSPO-mediated effects on glioma cell proliferation and mobility. Together, our present study indicated that TSPO may promote the nuclear-cytoplasmic shuttling of HUR, thus increasing the mRNA stability of MAPKAPK3 and promoting the proliferation and mobility of glioma cells. The HUR/MAPKAPK3 axis may be key targets for blocking the effects of TSPO and may contribute to glioma therapy.

Gender convergence or divergence in the relationship between late-life depression and multiple stressors: evidence from a national survey in China.

This study aimed to investigate gender convergence or divergence among older adults in China, a Confucian society with strong persistence of gender role differentiation. We examined how multiple stressors influence depression simultaneously, with gender comparison approach. The data were drawn from the China Longitudinal Aging Social Survey study (N = 8,097). Results indicated that older women reported significantly higher levels of depression than men, yet overall depressive symptoms showed many gender similarities. Surprisingly, our analyses supported the hypothesis of gender convergence in stressors predicting late-life depression. Recommendations for practice and further research priorities based on findings are discussed.

Widowhood and depression among Chinese older adults: examining coping styles and perceptions of aging as mediators and moderators.

Objectives: Based on the stress-coping framework, this study examined the role of coping styles and perceptions of aging in the relationship between widowhood and depression through two alternative pathways-mediation and moderation-with a national probability sample of older adults in China.Method: The data came from the baseline wave of the China Longitudinal Aging Social Survey of 2014. Our final sample featured 8,404 older adults.Results: The results of structural equation modeling showed a good fit for the total sample (NFI = .909, IFI = .916, GFI = .963, RMSEA = .038) and indicated the significant direct impact of widowhood on depression among Chinese older adults. Moreover, the findings of mediating effects found compared with a married group, widowed older adults used less problem-focused coping and had more negative perceptions of aging, which in turn, predicted higher depression; they were also more likely to use emotion-focused coping, which in turn, predicted lower depression. The results of moderation analysis demonstrated that a higher level of negative perceptions of aging significantly worsened the adverse effects of widowhood on depression.Conclusion: Overall, our findings highlight the importance of a cognitive approach to targeting programs for widowed older adults in China, with a focus on strengthening their abilities to alter maladaptive copings styles and reauthor their life narratives.

Effect of physical frailty on elder mistreatment in a national survey: examining psychological vulnerability, housework involvement, and financial independence as mediators.

OBJECTIVES: To explore the prevalence of EM in an older Chinese population and examine the mediating role of three psychosocial variables - psychological vulnerability, housework involvement, and financial independence - in the relationship between physical frailty and EM. DESIGN: Cross-sectional analysis. SETTING: The data source was the Third Survey on Chinese Women's Social Status (SCSSW), which is a nationwide decennial survey conducted in 2010. PARTICIPANTS: Community-dwelling adults aged 60 and older who participated in SCSSW (N = 3516). MEASUREMENTS: The past-year prevalence of EM and its seven subtypes, physical frailty, psychological vulnerability, housework involvement, financial independence, and demographic characteristics. RESULTS: The past-year prevalence of EM was 4% among Chinese older adults, with psychological abuse being the most common subtype (3.9%). A higher level of physical frailty had a direct influence on EM. Older adults with higher levels of physical frailty were more likely to have higher levels of psychological vulnerability (anxiety, loneliness, and uselessness) and lower levels of housework involvement, which further correlated with increased risk of EM. Frail Chinese older adults were less likely to have financial independence, which in turn, surprisingly predicted a lower probability of EM. CONCLUSIONS: In this nationally representative sample, we provided the first evidence of the prevalence of EM among Chinese older adults and expanded the global understanding of EM by examining the mediating role of three psychosocial variables. Future studies are warranted to corroborate our findings and identify factors contributing to the complex mechanism of EM.

Validating the evaluation capacity scale among practitioners in non-governmental organizations.

The growing emphasis on demonstrating the effectiveness of social services through evaluation has heightened demand for nongovernmental organization (NGO) practitioners to enhance evaluation capacity. However, a lack of validated instruments in the NGO context has hampered efforts to assess NGO practitioners' current evaluation capacity and understand how capacity-building activities could be tailored to meet NGO practitioners' actual needs and enhance their evaluation capacity. Hence, this study aims to develop the Evaluation Capacity Scale (ECS), a self-reporting instrument of NGO practitioners' capacity to conduct an effective evaluation of their service programs. Validation data was derived from 439 NGO practitioners who attended the Jockey Club MEL Institute Project in Hong Kong, China. Exploratory factor analysis of the ECS revealed three factors-evaluation mindset, evaluation implementation, and evaluation communication-and confirmatory factor analysis further validated this three-factor structure. Moreover, MANCOVA analysis demonstrated the ECS's predictive validity. Overall, the ECS demonstrated satisfactory convergent validity, high internal consistency reliability, and predictive validity, and its factor structure was supported in subgroups based on gender, age, and level of education. Theoretical and practical implications of the findings are discussed.

Systemic immune-inflammation index acts as a novel diagnostic biomarker for postmenopausal osteoporosis and could predict the risk of osteoporotic fracture.

BACKGROUND: Postmenopausal osteoporosis (PMOP) is a bone metabolism disorder involving systematic inflammation activation. Blood routine examination is easily available in clinical practice and contains abundant information reflecting the systematic inflammation level. Thus, it is attractive to achieve early diagnosis of PMOP and predict osteoporotic fracture risk just based on the biomarkers in blood routine examination. METHODS: A multi-centric prospective cohort study was designed and enrolled postmenopausal women from two independent institutions. All participants underwent the dual-energy X-ray absorptiometry (DEXA) scanning for diagnosing PMOP. Blood routine examination was conducted, and the key inflammatory biomarkers such as neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII) were calculated. PMOP patients were followed up to observe osteoporotic fracture and identify the related risk predictors. RESULTS: A total of 92 participants out of 238 enrolled postmenopausal women were diagnosed with PMOP, with a prevalence of 38.66%. The main risk factors identified for PMOP included older age (OR = 2.06, 95% CI = 1.14-3.72), longer menopause duration (OR = 3.14, 95% CI = 2.06-4.79), higher NLR (OR = 2.11, 95% CI = 1.37-3.25), and higher SII (OR = 3.02, 95% CI = 1.98-4.61). Besides age and menopause duration, SII ≥834.89 was newly identified as a prominent risk factor for discriminating osteoporotic fracture risk in PMOP patients (HR = 3.66, 95% CI = 1.249-10.71). CONCLUSION: As an easy and economical biomarker calculated from blood routine examination, SII not only acts as a good risk predictor for PMOP diagnosis but also well discriminates the osteoporotic fracture risk, which deserves further investigation and application in clinical practice.

Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK-Mfn1 pathway.

The pathogenesis of cerebral ischaemia reperfusion injury (IRI) has not been fully described. Accordingly, there is little effective drug available for the treatment of cerebral IRI. The aim of our study was to explore the exact role played by Mfn1-mediated mitochondrial protection in cerebral IRI and evaluate the beneficial action of resveratrol on reperfused brain. Our study demonstrated that hypoxia-reoxygenation (HR) injury caused N2a cell apoptosis and this process was highly affected by mitochondrial dysfunction. Decreased mitochondrial membrane potential, increased mitochondrial oxidative stress, and an activated mitochondrial apoptosis pathway were noted in HR-treated N2a cells. Interestingly, resveratrol treatment could attenuate N2a cell apoptosis via sustaining mitochondrial homeostasis. Further, we found that resveratrol modulated mitochondrial performance via activating the Mfn1-related mitochondrial protective system. Knockdown of Mfn1 could abolish the beneficial effects of resveratrol on HR-treated N2a cells. Besides, we also report that resveratrol regulated Mfn1 expression via the AMPK pathway; inhibition of AMPK pathway also neutralized the anti-apoptotic effect of resveratrol on N2a cells in the setting of cerebral IRI. Taken together our results show that mitochondrial damage is closely associated with the progression of cerebral IRI. In addition we also demonstrate the protective action played by resveratrol on reperfused brain and show that this effect is achieved via activating the AMPK-Mfn1 pathway.

TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt-Parkin pathway.

Neuronal death caused by inflammatory cytokine-mediated neuroinflammation is being extensively explored. Thioredoxin reductase (TrxR) 2 is a novel mediator of inflammation response. In the current study, we focus on the mechanisms of TrxR2 overexpression in inflammation-mediated neuronal death. LPS was used to induce neuroinflammation in N2a cells in vitro. Adenovirus-loaded TrxR2 was transfected into N2a cells to up-regulate TrxR2 expression. Then, cell viability was determined via MTT assay and TUNEL assay. Apoptosis was measured via western blotting and ELISA. Oxidative stress was detected via ELISA and flow cytometry. A pathway inhibitor was used to verify the role of the Akt-Parkin pathway in the LPS-mediated N2a cell death in the presence of TrxR2 overexpression. With the help of immunofluorescence assay and western blotting, we found that TrxR2 expression was significantly reduced in response to LPS treatment, and this effect was associated with N2a cell death via apoptosis. At the molecular level, TrxR2 overexpression elevated the activity of the Akt-Parkin pathway, as evidenced by the increased expression of p-Akt and Parkin. Interestingly, inhibition of the Akt-Parkin pathway abolished the regulatory effect of TrxR2 on LPS-treated N2a cells, as evidenced by the decreased cell viability and increased apoptotic ratio. Besides, TrxR2 overexpression also reduced oxidative stress, inflammation factor transcription and mitochondrial apoptosis. However, inhibition of Akt-Parkin axis abrogated the protective effects of TrxR2 on redox balance, mitochondrial performance and cell survival. LPS-mediated neuronal death was linked to a drop in TrxR2 overexpression and the inactivation of the Akt-Parkin pathway. Overexpression of TrxR2 sustained mitochondrial function, inhibited oxidative stress, repressed inflammation response, and blocked mitochondrial apoptosis, finally sending a pro-survival signal for the N2a cells in the setting of LPS-mediated inflammation environment.

HucMSCs-Derived miR-206-Knockdown Exosomes Contribute to Neuroprotection in Subarachnoid Hemorrhage Induced Early Brain Injury by Targeting BDNF.

Early brain injury (EBI) is the most important potentially treatable cause of mortality and morbidity following subarachnoid hemorrhage (SAH). Apoptosis is one of the main pathologies of SAH-induced EBI. Numerous studies suggest that human umbilical cord derived mesenchymal stem cells (hucMSCs) may exert neuroprotective effect through exosomes instead of transdifferentiation. In addition, microRNA-206 (miR-206) targets BDNF and plays a critical role in brain injury diseases. However, the therapy effect of miR-206 modified exosomes on EBI after SAH and its regulatory mechanism have not been elucidated. Here, to identify whether hucMSCs-derived miR-206-knockdown exosomes have a better neuroprotective effect, we established SAH rat model and treated it with the exosomes to research the mechanism of miR-206 in EBI after SAH. We found that treatment with hucMSCs-derived miR-206-knockdown exosomes has a greater neuroprotective effect on SAH-induced EBI compared to treatment with simple exosomes. The miR-206-knockdown exosomes could significantly improve neurological deficit and brain edema and suppress neuronal apoptosis by targeting BDNF. Moreover, the BDNF/TrkB/CREB pathway was activated following treatment with miR-206 modified exosomes in vivo. In summary, these findings indicate that the hucMSCs-derived miR-206-knockdown exosomes prevent early brain injury by inhibiting apoptosis via BDNF/TrkB/CREB signaling. This may serve as a novel therapeutic target for treatment of SAH-induced EBI.

Migration of a Distal Ventriculoperitoneal Shunt Catheter Into the Pulmonary Vasculature: a Report of an Unusual Case and a Review of the Literature.

The authors report an unusual case of distal ventriculoperitoneal shunt catheter into the pulmonary vasculature. The migrated catheter was extracted through a thoracotomy and venotomy, with the cooperation of Neuroneurosurgery and Cardiovascular team. This rare complication after ventriculoperitoneal shunt surgery should be paid enough attention. There were 2 possible mechanisms. To solve the problem, multidisciplinary cooperation should be applied.

Sirt3 inhibits cerebral ischemia-reperfusion injury through normalizing Wnt/ß-catenin pathway and blocking mitochondrial fission.

Cerebral ischemia-reperfusion injury (IRI) potentiates existing brain damage and increases mortality and morbidity via poorly understood mechanisms. The aim of our study is to investigate the role of Sirtuin 3 (Sirt3) in the development and progression of cerebral ischemia-reperfusion injury with a focus on mitochondrial fission and the Wnt/ß-catenin pathway. Our data indicated that Sirt3 was downregulated in response to cerebral IRI. However, the overexpression of Sirt3 reduced the brain infarction area and repressed IRI-mediated neuron apoptosis. Functional assays demonstrated that IRI augmented mitochondrial fission, which induced ROS overproduction, redox imbalance, mitochondrial pro-apoptotic protein leakage, and caspase-9-dependent cell death pathway activation. However, the overexpression of Sirt3 blocked mitochondrial fission and induced pro-survival signals in neurons subjected to IRI. At the molecular level, our data further illustrated that the Wnt/ß-catenin pathway is required for the neuroprotection exerted by Sirt3 overexpression. Wnt/ß-catenin pathway activation via inhibiting ß-catenin phosphorylation attenuates mitochondrial fission and mitochondrial apoptosis. Collectively, our data show that cerebral IRI is associated with Sirt3 downregulation, Wnt/ß-catenin pathway phosphorylated inactivation, and mitochondrial fission initiation, causing neurons to undergo caspase-9-dependent cell death. Based on this, strategies for enhancing Sirt3 activity and activating the Wnt/ß-catenin pathway could be therapeutic targets for treating cerebral ischemia-reperfusion injury.

Rapid determination of carbendazim in complex matrices by electrospray ionization mass spectrometry with syringe filter needle.

The determination of pesticide residues is an indispensable task in controlling food safety and environment protection. Carbendazim is one of the extensive uses of pesticides in the agricultural industry. In this study, a simple method utilizing syringe filter has been applied as electrospray ionization emitter for mass spectrometric identification and quantification of carbendazim in complex matrices including soil, natural water, and fruit juice samples, which contain many insoluble materials. With online syringe filter of the complex samples, most of insoluble materials such as soil were excluded in spray ionization process due to the filter effect, and analytes were subsequently sprayed out from syringe needle for mass spectrometric detection. The pore sizes of filters and diameters of syringe needles also were investigated. The analytical performances, including the linear range (1-200 ng·mL-1 ), limit of detection (0.2-0.6 ng·mL-1 , S/N > 3), limit of quantitation (3.5-8.6 ng·mL-1 , S/N > 10), reproducibility (6.4%-12.5%, n = 6), and recoveries (72.1%-91.0%, n = 6) were well acceptable for direct analysis of raw samples. Matrix effect for detection of carbendazim in soil samples also was experimentally investigated. This study demonstrated that syringe filter needle coupled with electrospray ionization mass spectrometry is a simple, efficient, and sensitive method for detection of pesticide residues in water, soil, and fruit juice for risk assessment.

Elevated plasma levels of lysophosphatidic acid and aberrant expression of lysophosphatidic acid receptors in adenomyosis.

BACKGROUND: Given the important roles of the receptor-mediated lysophosphatidic acid (LPA) signaling in both reproductive tract function and gynecological cancers, it will be informative to investigate the potential role of LPA in the development of adenomyosis. The objective of this study was to evaluate the levels of LPA in plasma and the expression of six LPA receptors in the endometrial tissue collected from women with and without adenomyosis. METHODS: Plasma and endometrial tissue samples were collected form women with and without adenomyosis. The levels of LPA in plasma were determined by using high-performance liquid chromatography electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS). Immunohistochemistry was performed to evaluate the expression of six LPA receptors (LPA1-6) in endometrial tissue samples. The effects of LPA on IL-8 production, VEGF production and cell proliferation in human endometrial stromal cells (ESCs) were also assessed. RESULTS: LPA1 staining was localized to the cytoplasm, membrances of the epithelial cells of the endometrial glands, and there was little staining in the stromal cells. LPA2-5 staining were localized to the nuclei of stromal and glandular cells. Plasma levels of LPA were increased in adenomyosis. LPA1, LPA4 and LPA5 immunoreactivity were significantly higher in the adenomyosis group than in the control group, while LPA2 and LPA3 immunoreactivity were significantly lower in the adenomyosis group than in the control group. LPA6 was undetectable in the endometria. LPA induced the release of IL-8 from ESCs but did not affect cell proliferation and VEGF production. CONCLUSION: These results indicate that elevated plasma levels of LPA and aberrant expression of LPA receptors in the endometria may be associated with the development of adenomyosis.