Preparation of Anti-Zearalenone IgY and Development of an Indirect Competitive ELISA Method for the Measurement of Zearalenone in Post-Fermented Tea.

Post-fermented tea (PFT) is one of the most commonly consumed beverages worldwide. Rapid microbial growth and significant changes in the microbial composition of PFT during processing and storage pose a potential risk of contamination with mycotoxins such as zearalenone (ZEN). Screening for ZEN contamination in a simple, rapid, and inexpensive manner is required to ensure that PFT is safe for consumption. To monitor ZEN in PFT, ZEN was conjugated with bovine serum albumin to prepare egg yolk immunoglobulins (IgY). A specific indirect competitive enzyme-linked immunosorbent assay (ic-ELISA) based on IgY was developed and validated. ZEN was extracted with acetonitrile and water (50:50, v/v) containing 5% acetic acid and purified using a mixture of primary and secondary amines and graphitized carbon black to remove matrix interference from the PFT samples. Under optimal conditions, the linear range of this assay was 13.8-508.9 ng mL-1, the limit of detection was 9.3 ng mL-1, and the half-maximal inhibitory concentration was 83.8 ng mL-1. Cross-reactivity was negligible, and the assay was specific for ZEN-related molecules. The recovery rate of ZEN in the control blanks of PFT samples spiked with a defined concentration of ZEN of 89.5% to 98.0%. The recovery and accuracy of the method were qualified for PFT matrices. No significant differences were evident between the results of the actual PFT samples analyzed by high-performance liquid chromatography and ic-ELISA. The collective data indicate that the developed ic-ELISA can be used for the rapid and simple detection of ZEN in PFT products.

B-Type Fumonisins in Post-Fermented Tea: Occurrence and Consumer Dietary Exposure in Guangxi, China.

Post-fermented tea (PFT), a commonly consumed beverage worldwide, is characterized by the rapid growth of its microbial groups and the substantial changes they undergo. Consequently, PFT may contain mycotoxins such as B-type fumonisins (FBs). This study aimed to assess the intake of FBs through the consumption of PFT among consumers in Guangxi, China. A novel quantitative method using high-performance liquid chromatography-mass spectrometry was used to determine the FB concentration in PFT products. Additionally, a PFT consumption survey was conducted using a face-to-face questionnaire, recording their body weight and PFT consumption patterns based on a three-day dietary recall method. Finally, hazard index was calculated to estimate the health risk of FBs from the consumption of PFT products in Guangxi. The results revealed that the occurrence of FBs in PFT was 20% (24/120), with a concentration ranging from 2.14 to 18.28 µg/kg. The results of the survey showed that the average daily consumption of PFT by consumers was 9.19 ± 11.14 g. The deterministic risk assessment revealed that only 0.026% of the provisional maximum tolerable daily intake of FBs was consumed through PFT, indicating that FB contamination in PFT is not a public health risk.

Identification of circ_0038632 as a Promoter of Breast Cancer through miR-520a-3p-Dependent Modulation of CDCA3.

OBJECTIVE: Emerging evidence proves the importance of circular RNAs (circRNAs) in many tumors, including breast cancer (BC). Here, we aimed to define a mechanism by which circ_0038632 regulates BC process. METHODS: To quantify the expression of circ_0038632, miR-520a-3p and cell division cycle associated 3 (CDCA3), a quantitative real-time PCR or immunoblotting method was utilized. The relationships of circ_0038632/miR-520a-3p and miR-520a-3p/CDCA3 in BC cells were determined using RNA immunoprecipitation (RIP) experiment and luciferase reporter assay. The effects of the circ_0038632/miR-520a-3p/CDCA3 cascade on cell biological phenotypes in vitro were examined by flow cytometry, EdU assay, cell counting kit 8 assay, transwell assay and wound healing assay. The function of circ_0038632 in tumorigenicity of BC cells in vivo was evaluated by xenograft experiments. RESULTS: Circ_0038632 and CDCA3 were highly expressed and miR-520a-3p expression was hindered in human BC. Depletion of circ_0038632 weakened cell growth, motility, and invasiveness while promoted cell apoptosis. In terms of mechanism, miR-520a-3p targeted CDCA3, and circ_0038632 involved the post-transcriptional modulation of CDCA3 expression by working as a miR-520a-3p sponge. Silencing of miR-520a-3p could reverse the inhibitory functions of circ_0038632 depletion in BC cell malignant phenotypes. Re-expression of CDCA3 also overturned the suppressive effects of miR-520a-3p on BC cell malignant phenotypes. In addition, circ_0038632 depletion inhibited the growth of xenograft tumors in vivo. CONCLUSION: Taken together, circ_0038632 promotes breast carcinogenesis through the miR-520a-3p/CDCA3 regulatory cascade, indicating that circ_0038632 may be a potential target for BC treatment.

Brazilin Inhibits the Invasion and Metastasis of Breast Cancer.

This study aimed to determine the effect of brazilin on the invasion and metastasis of breast cancer. The breast cancer MDA-MB-231 and 4T1 cells were treated with brazilin to investigate proliferation and invasion using cell proliferation assay, wound healing assay, transwell assay. BALB/C mice were randomized into normal, model, positive control, and Sappan L. extract groups (n = 6/group). The mice were injected with 4T1 cells via caudal veins to establish a lung metastasis model and via subcutaneous injection to establish a xenograft model. Metastatic nodules on the lung surface, survival rates and visceral indices were evaluated. Subcutaneous tumor volumes and weights were measured. Brazilin inhibited the proliferation of breast cancer cells and significantly inhibited the wound healing, migration, and invasion of MDA-MB-231 and 4T1 cells. Compared with the normal group, the average survival days and spleen index in the model group were significantly decreased, but the lung index and number of pulmonary metastatic nodules were significantly increased. Compared with the model group, the average survival and spleen index of dose groups were significantly increased, and the lung index, the number of pulmonary metastatic nodules, and tumor volume and weight were significantly decreased. Brazilin significantly inhibits the proliferation and metastasis of breast cancer. This study might suggest a new therapeutic agent for breast cancer.

LPCAT1 is transcriptionally regulated by FOXA1 to promote breast cancer progression and paclitaxel resistance.

Bioinformatics analysis indicates that lysophosphatidylcholine acyltransferase 1 (LPCAT1) and forkhead box A1 (FOXA1) are highly expressed in breast cancer tissues and their expression levels are correlated. Therefore, the aim of the present study was to investigate their involvement in the malignant progression and drug resistance of breast cancer. The clinical significance of LPCAT1 was analyzed using The Cancer Genome Atlas data. The enrichment of LPCAT1 in breast cancer cells was determined and the effects of LPCAT1 knockdown on cell proliferation, colony formation, migration, invasion and paclitaxel (PTX) resistance were evaluated. The association between LPCAT1 and FOXA1 was verified using luciferase reporter and chromatin immunoprecipitation assays. Thereafter, the ability of FOXA1 overexpression to regulate LPCAT1 regulation was evaluated. The results revealed that a high LPCAT1 level was associated with poor overall survival in patients with breast cancer. Furthermore, LPCAT1 was found to be highly expressed in breast cancer cells, and its knockdown resulted in suppressed proliferation, colony formation, migration and invasion, and weakened PTX resistance. Furthermore, FOXA1 overexpression attenuated the effects of LPCAT1 knockdown on cells, indicating that FOXA1 transcriptionally regulates LPCAT1. In summary, the present study reveals that LPCAT1 is transcriptionally regulated by FOXA1, which influences breast cancer cell proliferation, metastatic potential and PTX resistance.

Efficacy of virtual reality-based interventions for patients with breast cancer symptom and rehabilitation management: a systematic review and meta-analysis.

OBJECTIVES: To determine the effectiveness of virtual reality (VR)-based intervention on the symptoms and rehabilitation management in patients with breast cancer. DESIGN: Systematic review and meta-analysis. STUDY SELECTION: We included all eligible randomised controlled trials and quasi-experimental studies (published in English and Chinese). PARTICIPANTS: Patients with breast cancer (≥18 years) undergoing cancer treatment. INTERVENTIONS: Any intervention administered to improve the symptoms and rehabilitation of patients with breast cancer. The control group was given conventional care. OUTCOMES: All outcomes were as follows: pain, fatigue, anxiety, depressive symptoms, cognitive function, and range of motion of upper limb in patients with breast cancer. DATA SOURCES: We searched PubMed, Embase, CENTRAL and SinoMed, four electronic databases, covering the database establishment period to January 2022. REVIEW METHODS: Two reviewers independently extracted content and data consistent with the prespecified framework and assessed risk bias. Random-effects meta-analysis was used to pool data across trials. Meta-analysis was performed using Review Manager V.5.4. RESULTS: A total of eight studies met the eligibility criteria and were included in this study. The combined effect size showed that VR was positive for improving patients' anxiety(standard mean differenc (SMD)=-2.07, 95% CI= (-3.81 to -0.34), I2=95%) and abduction of upper limbs (MD=15.54, 95% CI= (12.79 to 18.29), I2=0%), but fatigue (SMD=-0.92, 95% CI= (-4.47 to 2.62), I2=99%) was not. Qualitative analysis showed VR improved patients' depressive symptoms, pain and cognitive function. CONCLUSIONS: VR technology has a good effect on symptoms and rehabilitation management of patients with breast cancer, but the quality of evidence is low, and the sample size is small. To date, there are few intervention studies, therefore, giving precise recommendation or conclusion is difficult. We have a favourable view of this, and more clinical studies are needed in the future to improve the credibility of the results.

Relationship between marital status and survival in patients with lung adenocarcinoma: A SEER-based study.

ABSTRACT: Numerous studies have focused on whether the marital status has an impact on the prognosis in patients with non-small cell lung cancer, but none have focused on lung adenocarcinoma.We selected 61,928 eligible cases with lung adenocarcinoma from the Surveillance, Epidemiology, and End Results database from 2004 to 2016 and analyzed the impact of marital status on cancer-specific survival (CSS) using Kaplan-Meier and Cox regression analyses.We confirmed that sex, age, race, cancer TNM stage and grade, therapeutic schedule, household income, and marital status were independent prognostic factors for lung adenocarcinoma CSS. Multivariate Cox regression showed that widowed patients had worse CSS (hazard ratio 1.26, 95% confidence interval 1.20-1.31, P < .001) compared with married patients. Subgroup analysis showed consistent results regardless of sex, age, cancer grade, and TNM stage. However, the trend was not significant for patients with grade IV cancer.These results suggest that marital status is first identified as an independent prognostic factor for CSS in patients with lung adenocarcinoma, with a clear association between widowhood and a high risk of cancer-specific mortality. Psychological and social support are thus important for patients with lung adenocarcinoma, especially unmarried patients.

Knockdown of TRIM66 in MDA-MB-468 triple negative breast cancer cell line suppresses proliferation and promotes apoptosis through EGFR signaling.

Triple negative breast cancer (TNBC) is one of the most common malignant tumors in women and the tripartite motif 66 (TRIM66) is closely associated with the behaviors of wide variety of cancer. Thus, in this study, we aimed to explore the effect of TRIM66 in MDA-MB-468 TNBC cell line. Western blot and RT-PCR assays were used to detect the expression level of TRIM66 in human normal mammary cells and human breast cancer cell lines. We silenced its expression in MDA-MB-468 cells by transient siRNA transfection to ascertain the function of TRIM66 in MDA-MB-468 cells. CCK8 and clonogenicity assays were used to evaluate the ability of cell proliferation. Wound healing and Transwell were used to detect cell invasion and migration. TUNEL was applied to detect the apoptosis level. Western blotting was used to detect the expression of related proteins. TRIM66 was observed markedly elevated in breast cancer cell line. Knockdown of TRIM66 inhibited the expression of EGFR, P-Jak2, P-STAT3, JAK2, and STAT3 in MDA-MB-468 cells through regulating the epidermal growth factor receptor (EGFR) signaling. Knockdown of TRIM66 suppresses proliferation, invasion and migration of MDA-MB-468 cell line and promotes apoptosis in these cells through EGFR signaling.

Severe Case of Rickettsiosis Identified by Metagenomic Sequencing, China.

A case of Rickettsia sibirica subspecies sibirica BJ-90 infection in China was identified by metagenomic analysis of an eschar biopsy specimen and confirmed by nested PCR. Seroprevalence of spotted fever group Rickettsia was ≈17.4% among the local population. This report highlights the threat of rickettsioses to public health in the Qinghai-Tibet Plateau.

Coexistence of an aberrant right subclavian artery and anomalous origins of bilateral vertebral arteries: A case report.

RATIONALE: Anatomical variations in aortic arch (AA) branching are not unusual. Generally, these variations are asymptomatic and are diagnosed incidentally. Here, we report a rare case of a middle-aged female patient with an aberrant right subclavian artery (ARSA) associated with anomalous origins of the bilateral vertebral arteries (VAs). PATIENT CONCERNS: The patient treated for urolithiasis complained of repeated dizziness for several years. DIAGNOSES: Echocardiography and computed tomography angiography (CTA) confirmed arterial variations. Moreover, mild stenosis was found in the left common carotid artery (LCCA), which was considered to be the cause of dizziness. INTERVENTIONS: Congenital anomalous arteries were not necessary to intervene urgently, but aspirin and atorvastatin were administered to prevent potential thrombosis attributed to vascular stenosis after completing the operation for urolithiasis. OUTCOMES: Whether the symptoms will be alleviated or not should be continuously followed up, and the patient may accept interventional therapy in the future if necessary. LESSONS: Here, we report the rare variation of AA branches and highlight the importance of preoperative vascular assessment in surgical or interventional procedures for the affected body regions.

Transmission center and driving factors of hand, foot, and mouth disease in China: A combined analysis.

Hand, foot, and mouth disease (HFMD) has become a major public health issue in China. The disease incidence varies substantially over time and across space. To understand the heterogeneity of HFMD transmission, we compare the spatiotemporal dynamics of HFMD in Qinghai and Shanghai by conducting combined analysis of epidemiological, wavelet time series, and mathematical methods to county-level data from 2009 to 2016. We observe hierarchical epidemic waves in Qinghai, emanating from Huangzhong and in Shanghai from Fengxian. Besides population, we also find that the traveling waves are significantly associated with socio-economic and geographical factors. The population mobility also varies between the two regions: long-distance movement in Qinghai and between-neighbor commuting in Shanghai. Our findings provide important evidence for characterizing the heterogeneity of HFMD transmission and for the design and implementation of interventions, such as deploying optimal vaccine and changing local driving factors in the transmission center, to prevent or limit disease spread in these areas.

An Exploratory Study of Influenza Vaccination Coverage in Healthcare Workers in a Western Chinese City, 2018-2019: Improving Target Population Coverage Based on Policy Interventions.

Objectives: To evaluate a policy-based intervention to increase seasonal-influenza-vaccination coverage in healthcare workers in Xining, a city in Western China. Methods: From October 2018 to March 2019, we implemented a free vaccination policy in healthcare workers in Xining. A face-to-face interview with the head of the infection control department and an online survey for medical staff in four tertiary medical facilities was conducted to understand both the implementation of the free policy and influenza vaccination coverage. Possible factors for influenza vaccination among healthcare workers (physician, nurses working on the front-line, HCWs) were investigated by multivariate-logistic regression. Results: Coverage in two hospitals that implemented the free vaccination policy was 30.5% and 25.9%, respectively, which was statistically different to hospitals that did not implement the free policy (7.2% and 8.7%, respectively) (χ2 = 332.56, p < 0.0001). Among vaccinated healthcare workers, 65.5% and 48.6% reported their main reasons for vaccination were a convenient vaccination service and awareness of the free vaccination policy. The reasons for not being vaccinated among the 3389 unvaccinated healthcare workers included: the inconvenient vaccination service (33.8%), believing vaccination was unnecessary (29.7%), concerns about adverse reactions to the vaccine (28.8%), and having to pay for the vaccine (25.6%). Conclusions: Implementing the free vaccination policy, combined with improving the accessibility of the vaccination service, increased seasonal-influenza vaccination-coverage in healthcare workers in Xining.

Epidemiological features and spatial clusters of hand, foot, and mouth disease in Qinghai Province, China, 2009-2015.

BACKGROUND: Hand, Foot, and Mouth Disease (HFMD) is most frequently caused by Enterovirus71 (EV-A71) or Coxsackie virus A16 (CV-A16), infants and young children are at greatest risk. Describing the epidemiology of HFMD can help develop and better target interventions, including the use of pediatric EV-A71 vaccination. METHODS: We obtained data from the national surveillance system for HFMD cases with onset dates from 2009 to 2015. We defined probable cases as patient with skin papular or vesicular rashes on the hands, feet, mouth, or buttocks and confirmed cases as patients with the above symptoms along with laboratory-based enterovirus detection. We generated overall and age-specific annual incidence rates and described the temporal variability and seasonality of HFMD in Qinghai Province. We identified spatial clustering of HFMD incidence at the county level using the Local Indicator of Spatial Associationand an alpha level of 0.05. RESULTS: During the study period, 14,480 HFMD probable or confirmed cases were reported in Qinghai Province. Of the 2158 (14.9%) with laboratory confirmation, 924 (42.6%) were caused by CV-A16 and 830 (38.2%) were caused by EV-A71. The majority (89%) of all case-patients were ≤ 5 years of age and male (61.5%). The overall mean annual HFMD incidence rate was 36.4 cases per 100,000 populations, while the incidence rate for children ≤5 years of age was 379.5 cases per 100,000. Case reports peaked during the months of May through July. HFMD was predominantly caused by EV-A71, except in 2010 and 2014 when CV-A16 was the predominant causative agent. High incidence rates of HFMD were clustered (Moran's I = 0.59, P < 0.05) in the eastern region of the province. CONCLUSION: HFMD remains an important cause of childhood disease in Qinghai Province, occurring in an acyclical pattern of increased incidence, primarily due to CV-A16 circulation every three years. Incidence is also seasonal and tends to spatially cluster in the eastern region of the province. Since approximately 40% of confirmed HFMD cases were due to EV-A71, EV-A71 vaccination is likely to have a positive impact on the HFMD disease burden. Routine analysis of local surveillance data is crucial for describing disease occurrence and changes in etiology.

Diacerein inhibits the pro-atherogenic & pro-inflammatory effects of IL-1 on human keratinocytes & endothelial cells.

We investigated IL-1-induced regulation of genes related to inflammation and atherogenesis in human keratinocytes and endothelial cells, and if 'diacerein', an oral IL-1 inhibiting drug currently approved for use in osteoarthritis, would reverse IL-1's effects on these cells. Primary human keratinocytes and coronary artery endothelial cells were treated with either IL-1α or IL-1ß, with and without diacerein. Using PCR-array, we assessed differential gene-expression regulated by IL-1 and diacerein. We identified 34 pro-atherogenic genes in endothelial cells and 68 pro-inflammatory genes in keratinocytes significantly (p<0.05) regulated at least 2-fold by IL-1, in comparison to control. Diacerein completely or partially reversed this regulation on almost all genes. Using ELISA, we confirmed diacerein's ability to reverse IL-1-driven gene-regulation of 11 selected factors, at the protein level. The results support a novel idea that diacerein acts as an inhibitor of the pro-atherogenic and pro-inflammatory effects of IL-1. Diacerein may have therapeutic applications to diminish IL-1-induced skin inflammation in psoriasis and attenuate IL-1-induced development of atherosclerosis. Further investigation into diacerein's effect on skin inflammation, atherogenesis and cardiovascular risk in animal models or humans is warranted.

Interleukin-4 Downregulation of Involucrin Expression in Human Epidermal Keratinocytes Involves Stat6 Sequestration of the Coactivator CREB-Binding Protein.

Skin barrier defects play an important role in atopic dermatitis (AD). Involucrin, an important barrier protein suppressed in human AD, is downregulated by interleukin-4 (IL-4). However, the molecular mechanism for IL-4 downregulation of involucrin has not been delineated, and especially how Stat6, a transcriptional activator, represses involucrin expression is unknown. Since Stats usually recruit p300/CBP in the general transcription machinery of their target genes and involucrin expression also involves p300/CBP, we hypothesize that Stat6 activated by IL-4 may sequestrate p300/CBP from the involucrin transcription complex, thus suppressing involucrin expression in keratinocytes. Using IL-4 transgenic mice, an AD mouse model, we find that involucrin expression is similarly downregulated as in human AD. In HaCat cells, the Jak inhibitor and dominant negative studies indicate that the Jaks-Stat6 pathway is involved in IL-4 downregulation of involucrin. Next, we transfected HaCat cells with an involucrin promoter-luciferase construct and then treated them with IL-4. IL-4 greatly suppresses the promoter activity, which is totally abolished by cotransfecting the CREB-binding protein (CBP) expression vector, indicating that IL-4 cannot downregulate involucrin in the presence of excess CBP. Finally, chromatin immunoprecipitation assay demonstrates that IL-4 decreases CBP binding to the involucrin transcription complex. For the first time, we defined a molecular mechanism for IL-4 downregulation of involucrin in keratinocytes, which may play an important role in the pathogenesis of AD.

Decreased Level of IgE is Associated with Breast Cancer and Allergic Diseases.

BACKGROUND The aim of this study was to explore the prevalence of type I allergic diseases in patients with breast cancer by carrying out a questionnaire survey and IgE detection in a healthy population and in patients with breast cancer. MATERIAL AND METHODS There were 309 patients enrolled and they were further divided into the type I allergic disease group, the newly diagnosed breast cancer with type I allergic disease group, the re-visit breast cancer with type I allergic disease group, and the re-visit breast cancer without type I allergic disease group, as well as a healthy control group. Serum total IgE level was detected by immunoassay. RESULTS The IgE value in the healthy population with type I allergic diseases (89.3±51.4 IU/ml) was significantly higher than in those without type I allergic diseases (45.6±65.1 IU/ml). There was no significant difference between IgE values in the re-visit breast cancer patients with type I allergic disease (25.1±65.1 IU/ml) and those without type I allergic disease (23.0±45.9 IU/ml). The area under the ROC curve was 0.618±0.04, sensitivity was 78%, specificity was 47.1%, Youden index was 0.251, and IgE threshold was 32.6 IU/ml. CONCLUSIONS The patients with newly diagnosed breast cancer were susceptible to type I allergic disease at about the same levels as in the healthy population. There was no correlation between breast cancer and type I allergic disease.

Differential expression of inflammation-related genes in IL-4 transgenic mice before and after the onset of atopic dermatitis skin lesions.

IL-4 plays an important role in the pathogenesis of atopic dermatitis (AD), a common chronic inflammatory skin disease. We have generated IL-4 transgenic (Tg) mice by over-expressing IL-4 in the epidermis. These mice spontaneously develop chronic pruritic inflammatory skin lesions, which meet the clinical and histological diagnostic criteria for human AD. Systemic survey of immune-related genes in this mouse model, however, has not been performed. In this study, we utilize PCR array technique to examine hundreds of inflammation-related genes in the IL-4 Tg mice before and after the onset of skin lesions as well as in their wild type (WT) littermates. Only those genes with at least 2-fold up-regulation or down-regulation and with a P-value of less than 0.05 in comparison to WT controls were identified and analyzed. In the skin lesions, many chemokines, pro-inflammatory cytokines, and other AD-related factors are dysregulated compared to the wild type mice. Particularly, CXCL5, IL-1ß, IL-24, IL-6, oncostatin M, PTGS2, FPR1 and REG3γ are up-regulated several hundred-fold. In the pre-lesional group that shows no obvious skin abnormality on clinical observation, 30 dysregulated genes are nevertheless identified though the fold changes are much less than that of the lesional group, including CCL6, CCL8, CCL11, CCL17, CXCL13, CXCL14, CXCR3 and IL-12Rß2. Finally using ELISA, we demonstrate that 4 most dramatically up-regulated factors in the skin are also elevated in the peripheral blood of the IL-4 Tg mice. Taken together, our data have identified hundreds of dysregulated factors in the IL-4 Tg mice before and after the onset of skin lesions. Future detailed examination of these factors will shed light on our understanding of the development and progression of AD and help to discover important biomarkers for clinical AD diagnosis and treatment.

Varying levels of 6-keto-prostaglandin F1α and thromboxane B2 in serum and endothelialization and hyperplasia in small-diameter grafts seeded with CD34+ bone marrow cells in canines.

The aim of the present study was to investigate the serum levels of 6-keto-prostaglandin (PG)F1α and thromboxane (TX)B2, as well as the endothelialization and hyperplasia of polytetrafluoroethylene (PTFE) and Dacron prostheses seeded with CD34+ cells in medium-term observation. A total of 24 crossbred dogs were randomly distributed into PTFE or Dacron groups. CD34+ cells were isolated from bone marrow aspirate and collected using an immunomagnetic bead-based system. The PTFE or Dacron prostheses were implanted into the abdominal aortic artery and inferior vena cava of the dogs. In each group, 8 dogs were implanted with prostheses that had been seeded with CD34+ cells, while 4 dogs were implanted with prostheses that had been seeded with autogenous blood as a control. Serum concentrations of 6-keto-PGF1α and TXB2 were determined at days 0, 10, 30 and 60 following surgery. The grafts were removed and examined at days 10, 30, 60 and 100 following surgery. Finally, CD34 factor staining was used to identify endothelial cells, while light and electron microscopy were applied to examine endothelialization and patency. The results revealed that confluent endothelial cells appeared on the neointima of prostheses seeded with CD34+ cells at day 30 following surgery. In the control groups compared with the experimental groups, there were fewer endothelial cells and the neointima was significantly thicker in the arterial (PTFE, 174±1.41 vs. 117±2.83 µm, respectively; P=0.001; Dacron, 187.5±3.5 vs. 100±1.41 µm, respectively; P<0.001) and venous (PTFE, 230.5±6.36 vs. 135±5.66 µm, respectively; P=0.001; Dacron, 249±2.83 vs. 121.5±3.54 µm, respectively; P<0.001) prostheses. In the experimental groups, intimal hyperplasia in the venous prostheses (PTFE, 135±5.66 µm; Dacron, 121.5±3.54 µm) was more severe compared with that in the arterial prostheses (PTFE, 117±2.83 µm; Dacron, 100±1.41 µm) at day 60. Compared with the 6-keto-PGF1α concentrations in the experimental groups, those in the control groups were significantly lower on day 10 (PTFE, 135±6.01 vs. 80.5±4.35 pg/l, respectively; P=0.001; Dacron, 145±6.54 vs. 81.2±5.10 pg/l, respectively; P<0.001) and were then maintained at a lower level. By contrast, the TXB2 concentration, following marked increases on day 10 in the experimental and control groups (PTFE, 635±32.8 vs. 1,256±63.5 pg/l, respectively; P<0.001; Dacron, 652±30.9 vs. 1,136±53.2 pg/l, respectively; P=0.001), remained at a high level in the control groups. Therefore, the results of the present study indicate that it is possible to achieve rapid endothelialization in PTFE or Dacron prostheses by implanting CD34+ cells. Endothelialization inhibited the reduction in the concentration of 6-keto-PGF1α and the increase in the concentration of TXB2. In addition, endothelialization inhibited excessive intimal hyperplasia and thrombosis. Thus, CD34+ cell seeding provides a theoretical basis for the clinical application of artificial vessel endothelialization.

The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis.

Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by inflammatory cell skin infiltration. The JAK-STAT pathway has been shown to play an essential role in the dysregulation of immune responses in AD, including the exaggeration of Th2 cell response, the activation of eosinophils, the maturation of B cells, and the suppression of regulatory T cells (Tregs). In addition, the JAK-STAT pathway, activated by IL-4, also plays a critical role in the pathogenesis of AD by upregulating epidermal chemokines, pro-inflammatroy cytokines, and pro-angiogenic factors as well as by downregulating antimicrobial peptides (AMPs) and factors responsible for skin barrier function. In this review, we will highlight the recent advances in our understanding of the JAK-STAT pathway in the pathogenesis of AD.

[Determination of bifenthrin residue in plant-based foods using gas chromatography-mass spectrometry].

A method was established for the determination of bifenthrin residue in 8 plant-based foods using gas chromatography-mass spectrometry (GC-MS). The grain was extracted by acetonitrile and cleaned up with gel permeation chromatography (GPC) combined with a Florisil solid-phase extraction (SPE) cartridge, while the vegetables and fruits were extracted by ethyl acetate and cleaned up only with a Florisil SPE cartridge. Most of the lipids in the extract for the grain were eliminated by GPC, prior to SPE cleanup. The cleaned extract was analyzed by GC-MS with electron impact (EI) source in selective ion monitoring (SIM) mode. The detection limit was 5 microg/kg (S/N = 10). There was a good linearity within the range of 0.005 -0.5 mg/L with the correlation coefficient of 0.999 9. The recoveries were between 74% - 99% with the relative standard derivations of less than 13% at the spiking levels of 0.005, 0.04 and 0.1 mg/kg.