Resolution-increased fiber-optic strain sensor with a large dynamic range driven by white light.

The white light interferometer is advantageous for wavelength division multiplexing (WDM), but the excessive noise floor limits its application in practicality. In this Letter, we propose a fiber-optic sensor driven by a broadband light source, which uses a fiber-optic Fabry-Perot cavity and a reference interferometer to enhance strain resolution. In the experiment, the strain resolution of a 5.86 m resonant sensor is 18.5 fɛ/H z at 1.5 kHz, while the maximum detectable signal is over 230 rad at 1 kHz. With low cost, this method provides a new, to the best of our knowledge, solution for WDM sensing arrays with a large dynamic range.

MicroRNA-216a-5p Alleviates Acute Kidney Injury of Mice via Suppressing FAS Ligand Expression.

INTRODUCTION: The aim of this present work was to investigate the mechanism of the microRNA (miR)-216a-5p/FASL axis in mice with acute kidney injury (AKI). METHODS: Mice kidney ischemia/reperfusion (I/R) injury was used as AKI models in this study. I/R mice were injected with miR-216a-5p- and FASL-related constructs to investigate potential mechanisms of kidney protection. Kidney function, inflammation, oxidative stress, and kidney cell apoptosis were assessed after 24 h of reperfusion. In vitro, the hypoxia-reoxygenation (H/R) model was used with kidney tubular epithelial cells (TECs) to mimic kidney I/R injury. H/R-treated TECs were transfected with miR-216a-5p- and FASL-related constructs to detect cell viability, inflammation, and oxidative stress. MiR-216a-5p and FASL expression levels in mouse kidney tissues and in H/R-treated TECs were detected. RESULTS: MiR-216a-5p was downregulated and FASL was upregulated in kidney tissues of I/R mice and H/R-treated TECs. Upregulating miR-216a-5p attenuated kidney cell apoptosis and the damage of kidney function, and reduced inflammatory factor levels and oxidative stress response in kidney tissues of I/R mice. Upregulating miR-216a-5p advanced cell viability and reduced inflammatory factor levels and oxidative stress response in H/R-treated TECs. Downregulation of FASL effectively reversed the influences of downregulation of miR-216a-5p on kidney injury in mice and kidney TEC survival. CONCLUSION: Our study reveals that miR-216a-5p reduces I/R-induced pathological kidney damage in AKI via suppressing FASL.

Effects of dexmedetomidine administration on outcomes in critically ill patients with acute kidney injury: A propensity score-matching analysis.

PURPOSE: To evaluate the effects of dexmedetomidine (DEX) on outcomes of critically ill patients with acute kidney injury (AKI). MATERIALS AND METHODS: Data were extracted from the Medical Information Mart for Intensive Care III database (MIMIC III). Propensity score matching (PSM) analysis (1 : 3), Cox proportional hazards model, linear regression and logistic regression model were used to assess the effect of DEX on clinical outcomes. RESULTS: After PSM, 324 pairs of patients were matched between the patients with DEX administration and those without. DEX administration was associated with decreased in-hospital mortality (hazard ratio (HR) 0.287; 95% CI 0.151 - 0.542; p < 0.001) and 90-day mortality (HR 0.344; 95% CI 0.221 - 0.534; p < 0.001), and it was also associated with reduced length of stay (LOS) in ICU (4.54 (3.13,7.72) vs. 5.24 (3.15,10.91), p < 0.001) and LOS in hospital (11.63 (8.02,16.79) vs 12.09 (7.83,20.44), p = 0.002). Subgroup analysis showed that the above associations existed only in the mild and moderate AKI subgroups, but not in the severe AKI subgroup. Nevertheless, DEX administration was not associated with recovery of renal function (HR 1.199; 95% CI 0.851 - 1.688; p = 0.300). CONCLUSION: DEX administration improved outcomes in critically ill patients with mild and moderate AKI and could be a good choice of sedation.

Living alone and the risk of depressive symptoms: a cross-sectional and cohort analysis based on the China Health and Retirement Longitudinal Study.

BACKGROUND: There were a few studies that examined the longitudinal association between living alone and depressive symptoms, and the vast majority of them were conducted in patients with certain diseases, such as heart failure, cancer, and glaucoma. This study aimed to examine the association between living alone and depressive symptoms in a large representative older Chinese population. METHODS: The China Health and Retirement Longitudinal Study (CHARLS) data from 2015 to 2018 were used. Living alone was defined as participants who did not live with others ever or more than 11 months in the past year at baseline. Depressive symptoms were measured using the 10-item Center for Epidemiological Studies-Depression Scale (CES-D10). The multivariate logistic regression was used to estimate the relationship between living alone and depressive symptoms. RESULTS: There were 5,311 and 2,696 participants ≥ 60 years old included in the cross-sectional and cohort analysis, respectively. The risk of depressive symptoms in participants who lived alone was significantly higher than those who lived with others in both cross-sectional (OR:1.33; 95%CI:1.14,1.54) and cohort analysis (OR:1.23; 95%CI:0.97,1.55). There was a significant interaction between financial support and living alone (Pinteraction = 0.008) on the risk of depressive symptoms. Stratified analyses showed that, compared to those who lived with others, the risk of depressive symptoms in participants who lived alone increased by 83% (OR:1.83; 95%CI:1.26,2.65) in participants receiving lower financial support. However, we did not find statistically significant associations in participants with medium (OR:1.10; 95%CI: 0.74,1.63) and higher financial support (OR: 0.87; 95%CI: 0.53,1.41). CONCLUSION: Living alone was associated with a higher risk of depressive symptoms in the Chinese older population, and this association was moderated by the receipt of financial support. Living alone may be an effective and easy predictor for early identification of high-risk populations of depression in the older population.

The effects of thioredoxin peroxidase from Cysticercus cellulosae excretory-secretory antigens on TGF-ß signaling pathway and Th17 cells differentiation in Jurkat cells by transcriptomics.

Thioredoxin peroxidase (TPx) protein from the excretory-secretory antigens (ESAs) of Cysticercus cellulosae (C. cellulosae) has been shown to regulate the differentiation of host Treg and Th17 cells, resulting in an immunosuppressive response dominated by Treg cells. However, the molecular mechanism by which TPx protein from the ESAs of C. cellulosae regulates the imbalance of host Treg/Th17 cell differentiation has not been reported. TPx protein from porcine C. cellulosae ESAs was used to stimulate Jurkat cells activated with PMA and ionomycin at 0, 24, 48, and 72 h. Transcriptomic analysis was performed to investigate the signaling pathways associated with Jurkat cells differentiation regulated by TPx protein from C. cellulosae ESAs. Gene Set Enrichment Analysis (GSEA) revealed that TPx protein from porcine C. cellulosae ESAs could induce upregulation of the TGF-ß signaling pathway and downregulation of Th17 cell differentiation in Jurkat cells. TPx protein from porcine C. cellulosae ESAs can activate the TGF-ß signaling pathway in Jurkat cells, thereby regulating the differentiation of Treg/Th17 cells and leading to an immunosuppressive response dominated by Treg cells, enabling evasion of the host immune attack. This study provides a foundation for further validation of these pathways and further elucidates the molecular mechanisms underlying immune evasion caused by porcine C. cellulosae.

Internalization of HMGB1 (High Mobility Group Box 1) Promotes Angiogenesis in Endothelial Cells.

OBJECTIVE: In patients with peripheral artery disease, blockages in arterioles <1 mm cannot be treated surgically, and there are currently few effective medicines. Studies have shown that inflammation in ischemic tissue is related to injury recovery and angiogenesis, but insufficient attention has been paid to this area. Studies have suggested that HMGB1 (high mobility group protein 1), which is released by ischemic tissue, promotes angiogenesis, but the mechanism is not entirely clear. In this study, we tested the internalization of HMGB1 in endothelial cells and investigated a novel proangiogenic pathway. Approach and Results: Using green fluorescent protein-tagged HMGB1 to stimulate endothelial cells, we demonstrated HMGB1 internalization via dynamin and RAGE (receptor for advanced glycation end products)-dependent signaling. Using a fluorescence assay, we detected internalized protein fusion to lysosomes, followed by activation of CatB (cathepsin B) and CatL (cathepsin L). The latter promoted the release of VEGF (vascular endothelial growth factor)-A and endoglin and upregulated the capacities of cell migration, proliferation, and tube formation in endothelial cells. We identified that the cytokine-induced fragment-a key functional domain in HMGB1-mediates the internalization and angiogenic function of HMGB1. We further confirmed that HMGB1 internalization also occurs in vivo in endothelial cells and promotes angiogenesis in mouse femoral artery ligation. CONCLUSIONS: In this study, we identified a novel pathway of HMGB1 internalization-induced angiogenesis in endothelial cells. This finding sheds light on the regulatory role of inflammatory factors in angiogenesis through cell internalization and opens a new door to understand the relationship between inflammation and angiogenesis in ischemic diseases.

The Essential Role of Bond Energetics in C-H Activation/Functionalization.

The most fundamental concepts in chemistry are structure, energetics, reactivity and their inter-relationships, which are indispensable for promoting chemistry into a rational science. In this regard, bond energy, the intrinsic determinant directly related to structure and reactivity, should be most essential in serving as a quantitative basis for the design and understanding of organic transformations. Although C-H activation/functionalization have drawn tremendous research attention and flourished during the past decades, understanding the governing rules of bond energetics in these processes is still fragmentary and seems applicable only to limited cases, such as metal-oxo-mediated hydrogen atom abstraction. Despite the complexity of C-H activation/functionalization and the difficulties in measuring bond energies both for the substrates and intermediates, this is definitely a very important issue that should be more generally contemplated. To this end, this review is rooted in the energetic aspects of C-H activation/functionalization, which were previously rarely discussed in detail. Starting with a concise but necessary introduction of various classical methods for measuring heterolytic and homolytic energies for C-H bonds, the present review provides examples that applied the concept and values of C-H bond energy in rationalizing the observations associated with reactivity and/or selectivity in C-H activation/functionalization.

Mechanism and Origins of Chemo- and Stereoselectivities of Aryl Iodide-Catalyzed Asymmetric Difluorinations of ß-Substituted Styrenes.

The mechanism of the aryl iodide-catalyzed asymmetric migratory geminal difluorination of ß-substituted styrenes ( Banik et al. Science 2016, 353, 51 ) has been explored with density functional theory computations. The computed mechanism consists of (a) activation of iodoarene difluoride (ArIF2), (b) enantiodetermining 1,2-fluoroiodination, (c) bridging phenonium ion formation via SN2 reductive displacement, and (d) regioselective fluoride addition. According to the computational model, the ArIF2 intermediate is stabilized through halogen-π interactions between the electron-deficient iodine(III) center and the benzylic substituents at the catalyst stereogenic centers. Interactions with the catalyst ester carbonyl groups (I(III)+···O) are not observed in the unactivated complex, but do occur upon activation of ArIF2 through hydrogen-bonding interactions with external Brønsted acid (HF). The 1,2-fluoroiodination occurs via alkene complexation to the electrophilic, cationic I(III) center followed by C-F bond formation anti to the forming C-I bond. The bound olefin and the C-I bond of catalyst adopt a spiro arrangement in the favored transition structures but a nearly periplanar arrangement in the disfavored transition structures. Multiple attractive non-covalent interactions, including slipped π···π stacking, C-H···O, and C-H···π interactions, are found to underlie the high asymmetric induction. The chemoselectivity for 1,1-difluorination versus 1,2-difluorination is controlled mainly by (1) the steric effect of the substituent on the olefinic double bond and (2) the nucleophilicity of the carbonyl oxygen of substrate.

Establishing the Trifluoromethylthio Radical Donating Abilities of Electrophilic SCF3-Transfer Reagents.

The recent recognition of the novel application of a few traditional electrophilic trifluoromethylthiolating reagents as SCF3 radical sources offers a remarkable new opportunity for the development of radical trifluoromethylthiolation reactions. Herein, the first trifluoromethylthio radical donating ability (Tt•DA) scale of electrophilic SCF3-transfer reagents has been developed. This scale is based on Y-SCF3 bond dissociation energies, which were obtained by density functional calculations (M06-2X). Single electron transfer is revealed to exhibit a substantial Y-SCF3 bond-weakening effect, thus significantly facilitating the SCF3 radical (•SCF3) release. The results may aid in future novel radical SCF3-transfer reagent design and new reaction development.

SIRT1 plays a neuroprotective role in traumatic brain injury in rats via inhibiting the p38 MAPK pathway.

Traumatic brain injury (TBI) is a major cause of disability and death in patients who experience a traumatic injury. Mitochondrial dysfunction is one of the main factors contributing to secondary injury in TBI-associated brain damage. Evidence of compromised mitochondrial function after TBI has been, but the molecular mechanisms underlying the pathogenesis of TBI are not well understood. Silent information regulator family protein 1 (SIRT1), a member of the NAD+-dependent protein deacetylases, has been shown to exhibit neuroprotective activities in animal models of various pathologies, including ischemic brain injury, subarachnoid hemorrhage and several neurodegenerative diseases. In this study, we investigated whether SIRT1 also exert neuroprotective effect post-TBI, and further explored the possible regulatory mechanisms involved in TBI pathogenesis. A lateral fluid-percussion (LFP) brain injury model was established in rats to mimic the insults of TBI. The expression levels of SIRT1, p-p38, cleaved caspase-9 and cleaved caspase-3 were all markedly increased and reached a maximum at 12 h post-TBI. In addition, mitochondrial function was impaired, evidenced by the presence of swollen and irregularly shaped mitochondria with disrupted and poorly defined cristae, a relative increase of the percentage of neurons with low ΔΨm, the opening of mPTP, and a decrease in neuronal ATP content, especially at 12 h post-TBI. Pretreatment with the SIRT1 inhibitor sirtinol (10 mg/kg, ip) induced p-p38 activation, exacerbated mitochondrial damage, and promoted the activation of the mitochondrial apoptosis pathway. In contrast, pretreatment with the p38 inhibitor SB203580 (200 µg/kg, ip) significantly attenuated post-TBI-induced expression of both cleaved caspase-9 and cleaved caspase-3 and mitochondrial damage, whereas it had no effects on SIRT1 expression. Together, these results reveal that the 12 h after TBI may be a crucial time at which secondary damage occurs; the activation of SIRT1 expression and inhibition of the p38 MAPK pathway may play a neuroprotective role in preventing secondary damage post-TBI. For this reason, both SIRT1 and p38 are likely to be important targets to prevent secondary damage post-TBI.

Mechanism and Origin of the Unexpected Chemoselectivity in Fluorocyclization of o-Styryl Benzamides with a Hypervalent Fluoroiodane Reagent.

The mechanism and origin of the unexpected chemoselectivity in fluorocyclization of o-styryl benzamide with a cyclic hypervalent fluoroiodane reagent were explored with DFT calculations. The calculations suggested an alternative mechanism that is broadly similar to, but also critically different from, the previously proposed mechanism for the formation of an unexpected structurally novel seven-membered 4-fluoro-1,3-benzoxazepine. The amide group of o-styryl benzamide was revealed to be crucial for activating the fluoroiodane reagent and facilitating C-F bond formation. In contrast to the popular electrophilic N-F reagent Selectfluor, the F atom in the fluoroiodane reagent is nucleophilic, and the I(III) atom is the most electrophilic site, thus inducing a completely different reactivity pattern. The insights reported here will be valuable for the further development of new reactions based on the hypervalent fluoroiodane reagent.

[Construction and identification of the Bifidobacterium expression system pGEX-TSOL18/B. longum of Taenia solium].

The TSOL18 gene of Taenia solium was synthesized and cloned into Escherichia coli-Bifidobacteria shuttle vector pGEX-1lambdaT. The recombinant plasmid pGEX-TSOL18 was transformed into Bifidobacterium longum with electroporation. The recombinant plasmid containing TSOL18 gene was identified by restriction endonuclease analysis, PCR and DNA sequencing. The length of synthesized TSOL18 gene was 393 bp. The results indicated that the Bifidobacteria expression system pGEX-TSOL18/B. longum was successfully constructed.

Dexmedetomidine attenuates ferroptosis by Keap1-Nrf2/HO-1 pathway in LPS-induced acute kidney injury.

Previous research has demonstrated that Dexmedetomidine (DEX), an α2 adrenergic agonist commonly used for its sedative and analgesic properties, can attenuate lipopolysaccharide (LPS)-induced acute kidney injury (AKI). This study explores the possibility that DEX's protective effects in LPS-induced AKI are mediated through the inhibition of ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, and the activation of the antioxidant response through the Keap1/Nrf2/HO-1 signaling pathway. We induced AKI in 42 mice using LPS and divided them into six groups: saline control, LPS, LPS + DEX, LPS + Ferrostatin-1 (LPS + Fer-1; a ferroptosis inhibitor), LPS + DEX with α2-receptor antagonist Altipamizole (LPS + DEX + ATI), and LPS + DEX with Nrf2 inhibitor ML385 (LPS + DEX + ML385). After 24 h, we analyzed blood and kidney tissues. LPS exposure resulted in AKI, with increased serum creatinine, BUN, and cystatin C, and tubular damage, which DEX and Fer-1 ameliorated. However, Altipamizole and ML385 negated these improvements. The LPS group exhibited elevated oxidative stress markers and mitochondrial damage, reduced by DEX and Fer-1, but not when α2-adrenergic or Nrf2 pathways were blocked. Nrf2 and HO-1 expression declined in the LPS group, rebounded with LPS + DEX and LPS + Fer-1, and fell again with inhibitors; inversely, Keap1 expression varied. Our results demonstrate that DEX may protect against LPS-induced AKI, at least partially by regulating ferroptosis and the α2-adrenergic receptor/Keap1/Nrf2/HO-1 pathway, suggesting a potential therapeutic role for DEX in AKI management by modulating cell death and antioxidant defenses.

Long-Term Visit-to-Visit Blood Pressure Variability and Cognitive Decline Among Patients With Hypertension: A Pooled Analysis of 3 National Prospective Cohorts.

BACKGROUND: A limited number of studies investigated the association between blood pressure variability (BPV) and cognitive impairment in patients with hypertension. This study aimed to identify the longitudinal association between BPV and cognitive decline and the role of blood pressure (BP) control in this association. METHODS AND RESULTS: Participants with hypertension from the HRS (Health and Retirement Study), the ELSA (English Longitudinal Study of Ageing), and the CHARLS (China Health and Retirement Longitudinal Study) were included. Variation independent of the mean (VIM) was adopted to measure BPV. Cognitive function was measured by standard questionnaires, and a standardized Z score was calculated. Linear mixed-model and restricted cubic splines were adopted to explore the association between BPV and cognitive decline. The study included 4853, 1616, and 1432 eligible patients with hypertension from the HRS, ELSA, and CHARLS, respectively. After adjusting for covariates, per-SD increment of VIM of BP was significantly associated with global cognitive function decline in Z scores in both systolic BP (pooled ß, -0.045 [95% CI, -0.065 to -0.029]) and diastolic BP (pooled ß, -0.022 [95% CI, -0.040 to -0.004]) among hypertensive patients. Similar inverse associations were observed in patients with hypertension taking antihypertensive drugs and in patients with hypertension with well-controlled BP. CONCLUSIONS: High BPV was independently associated with a faster cognitive decline among patients with hypertension, even those with antihypertensive medications or well-controlled BP. Further studies are needed to confirm our results and determine whether reducing BPV can prevent or delay cognitive decline.

The objectively measured walking speed and risk of hypertension in Chinese older adults: a prospective cohort study.

This study aims to investigate the longitudinal association between objectively measured walking speed and hypertension and to explore the potential effect modification of obesity on this association in Chinese older adults. The data from the Chinese Health and Retirement Prospective Cohort Study (CHARLS) during 2011-2015 was used. Walking speed was assessed by measuring the participants' usual gait in a 2.5 m course, and it was divided into four groups according to the quartiles (Q1, Q2, Q3, and Q4). A total of 2733 participants ≥60 years old were eligible for the analyses. After a follow-up of 4 years, 26.9% occurred hypertension. An inverse association was observed between walking speed and the risk of hypertension. There was an interaction between body mass index (BMI) and walking speed for the hypertension risk (P = 0.010). the association of walking speed with hypertension was stronger in overweight and obese participants (Q2, OR: 0.54, 95%CI = 0.34-0.85, P = 0.009; Q3, OR: 0.69, 95%CI = 0.44-1.08, P = 0.106; Q4, OR: 0.62, 95%CI = 0.39-0.98, P = 0.039). However, this association was not significant among lean ones. A similar trend was observed for systolic and diastolic blood pressure. In conclusion, higher walking speed was longitudinally associated with a lower risk of hypertension in Chinese older adults, especially among overweight and obese participants.

Association between prescription opioid use and heart failure: Cohort studies and Mendelian randomization analysis.

BACKGROUND: Prescription opioid use (POU) has been shown to lead to cardiovascular disease (CVD), but its association with heart failure has not been well studied. We investigated the potential causal association between POU and HF using cohort studies and Mendelian Randomization (MR) analysis. METHODS: Initially, we examined the longitudinal association between POU and HF using the data from the Health and Retirement Study (HRS) and the UK biobank. Next, we employed a two-sample MR analysis using summary statistics from genome-wide association studies (GWAS) to assess the potential causal associations between POU and HF. RESULTS: During a median of 3.8 and 13.8 years of follow-up, there were 441(8.04 per 1000 person-year) and 16,170 (3.96 per 1000 person-year) HF cases in the HRS and the UK biobank, respectively. After adjusting for covariates, participants who used prescription opioids had a 32% increased risk of developing HF, compared with non-users (HR = 1.32, 95%CI: 1.26-1.38, P < 0.001). In the MR analysis, summary statistics for POU were obtained from 78,808 UK Biobank study participants, and summary data for HF were obtained from 218,792 participants of a European population. A causal effect of genetic liability for POU on an increased risk of HF (OR = 1.16, 95% CI = 1.06, 1.27, P = 0.001) was suggested. The results were generally consistent in the sensitivity analysis, and no pleiotropy or heterogeneity were observed. CONCLUSIONS: POU is associated with a high risk of HF. Our findings provide new insight into prescription opioid use among populations at risk of heart failure. More studies are needed to validate our results and further investigate the underlying mechanisms.

[Cloning, expression of TSO45W-4B gene from Taenia solium and preparation of its polyclonal antibody].

OBJECTIVE: To clone and express TSO45W-4B gene of Taenia solium, and prepare the rabbit antiserum against the recombinant protein TSO45W-4B. METHODS: The gene encoding TSO45W-4B antigen was synthesized and cloned into the expression vector pGEX-1lambdaT. The recombinant plasmid was transformed into Escherichia coli ArcticExpress (DE3), and followed by the expression of the protein induced by IPTG. The recombinant protein was purified by GST affinity chromatography and analyzed by SDS-PAGE. The rabbits were immunized with the purified recombinant protein. The titer of the antibody against TSO45W-4B was detected by ELISA. The specificity of anti-TSO45W-4B antibody was determined by Western blotting. RESULTS: It was demonstrated that TSO45W-4B gene (351 bp) was synthesized. The gene was inserted into pGEX-1lambdaT and confirmed by restriction enzyme digestion and DNA sequencing. SDS-PAGE analysis showed that the relative molecular mass (M(r)) of the expressed recombinant protein was approximately 40 000. The purity of the recombinant protein with an affinity chromatography column was about 90%. The titer of the antibody against TSO45W-4B was 1: 512 000. The recombinant protein reacted with the anti-TSO45W-4B antibody by Western blotting. CONCLUSION: The TSO45W-4B gene of Taenia solium is efficiently expressed in E. coli. The recombinant protein TSO45W-4B and its rabbit antiserum are successfully prepared.

Associations of pyrethroid exposure with skeletal muscle strength and mass.

This study aimed to examine the associations of pyrethroid exposure with handgrip strength and skeletal muscle mass and potential modification effects in US adults. The data from the National Health and Nutrition Examination Survey was used. Handgrip strength was determined with a handgrip dynamometer, and we quantified muscle mass by using the appendicular skeletal muscle index (ASMI). Urinary 3-Phenoxybenzoic Acid (3-PBA), a validated biomarker for pyrethroid exposure, was used in the primary analysis. After adjusting for other covariates, participants exposed to the highest tertile of 3-PBA exposure had significantly lower handgrip strength (ß = -1.88, 95% CI: -3.29, -0.23, P = 0.026) than those exposed to the lowest tertile of 3-PBA. Similarly, the 3-PBA exposure was marginally significantly associated with ASMI (Tertile 3 vs. Tertile 1: ß = -0.07, 95% CI: -0.14, -0.01, P = 0.056). Significant interactions were found between 3-PBA and body mass index (BMI) on handgrip strength and ASMI (P interaction < 0.05), which indicated a potential moderation effect of BMI on the associations. In conclusion, pyrethroid exposure was adversely associated with handgrip strength and skeletal muscle mass, especially in overweight and obese populations. Further studies are warranted to confirm our results and to explore the potential mechanisms.

Effects of Cysticercus cellulosae Excretory-Secretory Antigens on the TGF-ß Signaling Pathway and Th17 Cell Differentiation in Piglets, a Proteomic Analysis.

Excretory-secretory antigens (ESAs) of Cysticercus cellulosae can directly regulate the proliferation and differentiation of host T regulatory (Treg) cells, thus inhibiting host immune responses. However, previous studies have only focused on this phenomenon, and the molecular mechanisms behind the ways in which C. cellulosae ESAs regulate the differentiation of host Treg/Th17 cells have not been reported. We collected CD3+ T cells stimulated by C. cellulosae ESAs through magnetic bead sorting and used label-free quantification (LFQ) proteomics techniques to analyze the signaling pathways of C. cellulosae ESAs regulating Treg/Th17 cell differentiation. Through gene set enrichment analysis (GSEA), we found that C. cellulosae ESAs could upregulate the TGF-ß signaling pathway and downregulate Th17 cell differentiation in piglet T cells. Interestingly, we also found that the IL-2/STAT5 signaling pathway also affects the downregulation of Th17 cell differentiation. C. cellulosae ESAs activate the TGF-ß signaling pathway and the IL-2/STAT5 signaling pathway in host T cells to further regulate the differentiation of Treg/Th17 cells in order to evade host immune attack. This study lays the foundation for the subsequent verification of these pathways, and further clarifies the molecular mechanism of C. cellulosae-mediated immune evasion.