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1.
Anim Nutr ; 8(1): 135-143, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-34977383

RESUMO

Weaning stress can cause tight junctions damage and intestinal permeability enhancement, which leads to intestinal imbalance and growth retardation, thereby causing damage to piglet growth and development. Spermine can reduce stress. However, the mechanism of spermine modulating the intestinal integrity in pigs remains largely unknown. This study aims to examine whether spermine protects the intestinal barrier integrity of piglets through ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase C-γ1 (PLC-γ1) signaling pathway. In vivo, 80 piglets were categorised into 4 control groups and 4 spermine groups (10 piglets per group). The piglets were fed with normal saline or spermine at 0.4 mmol/kg BW for 7 h and 3, 6 and 9 d. In vitro, we investigated whether spermine protects the intestinal barrier after a tumor necrosis factor α (TNF-α) challenge through Rac1/PLC-γ1 signaling pathway. The in vivo study found that spermine supplementation increased tight junction protein mRNA levels and Rac1/PLC-γ1 signaling pathway gene expression in the jejunum of piglets. The serum D-lactate content was significantly decreased after spermine supplementation (P < 0.05). The in vitro study found that 0.1 µmol/L spermine increased the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability (P < 0.05). Further experiments demonstrated that spermine supplementation enhanced the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability compared with the NSC-23766 and U73122 treatment with spermine after TNF-α challenge (P < 0.05). Collectively, spermine protects intestinal barrier integrity through Rac1/PLC-γ1 signaling pathway in piglets.

2.
HGG Adv ; 3(1): 100078, 2022 Jan 13.
Artigo em Inglês | MEDLINE | ID: mdl-35047863

RESUMO

Pancreatic cancer is a deadly disease that accounts for approximately 5% of cancer deaths worldwide, with a dismal 5-year survival rate of 10%. Known genetic risk factors explain only a modest proportion of the heritable risk of pancreatic cancer. We conducted a whole-exome case-control sequencing study in 1,591 pancreatic cancer cases and 2,134 cancer-free controls of European ancestry. In our gene-based analysis, ATM ranked first, with a genome-wide significant p value of 1 × 10-8. The odds ratio for protein-truncating variants in ATM was 24, which is substantially higher than prior estimates, although ours includes a broad 95% confidence interval (4.0-1000). SIK3 was the second highest ranking gene (p = 3.84 × 10-6, false discovery rate or FDR = 0.032). We observed nominally significant association signals in several genes of a priori interest, including BRCA2 (p = 4.3 × 10-4), STK11 (p = 0.003), PALB2 (p = 0.019), and TP53 (p = 0.037), and reported risk estimates for known pathogenic variants and variants of uncertain significance (VUS) in these genes. The rare variants in established susceptibility genes explain approximately 24% of log familial relative risk, which is comparable to the contribution from established common susceptibility variants (17%). In conclusion, this study provides new insights into the genetic susceptibility of pancreatic cancer, refining rare variant risk estimates in known pancreatic cancer susceptibility genes and identifying SIK3 as a novel candidate susceptibility gene. This study highlights the prominent importance of ATM truncating variants and the underappreciated role of VUS in pancreatic cancer etiology.

4.
Transl Oncol ; 17: 101340, 2022 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-35021150

RESUMO

Long noncoding RNA urothelial cancer associated 1 (UCA1), initially identified in bladder cancer, is associated with multiple cellular processes, including metabolic reprogramming. However, its characteristics in the anaplerosis context of bladder cancer (BLCA) remain elusive. We identified UCA1 as a binding partner of heterogeneous nuclear ribonucleoproteins (hnRNPs) I and L, RNA-binding proteins (RBPs) with no previously known role in metabolic reprogramming. UCA1 and hnRNP I/L profoundly affected glycolysis, TCA cycle, glutaminolysis, and proliferation of BLCA. Importantly, UCA1 specifically bound to and facilitated the combination of hnRNP I/L to the promoter of glutamic pyruvate transaminase 2 (GPT2), an enzyme transferring glutamate to α-ketoglutarate, resulting in upregulated expression of GPT2 and enhanced glutamine-derived carbons in the TCA cycle. We also systematically confirmed the influence of UCA1 and hnRNP I/L on metabolism and proliferation via glutamine-driven anaplerosis in BLCA. Our study revealed the critical role of UCA1-mediated mechanisms involved in glutamine-driven anaplerosis and provided novel evidence that lncRNA regulates metabolic reprogramming in tumor cells.

5.
J Sci Food Agric ; 102(2): 496-504, 2022 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-34145905

RESUMO

BACKGROUND: Heat stress (HS) has a negative impact on the intestinal barrier and immune function of pigs. Selenium (Se) may improve intestinal health through affecting selenoproteins. Thus we investigate the protective effect of new organic Se (2-hydroxy-4-methylselenobutanoic acid, HMSeBA) on jejunal damage in growing pigs upon HS and integrate potential roles of corresponding selenoproteins. RESULTS: HS decreased the villus height and increased (P < 0.05) the protein abundance of HSP70, and downregulated (P < 0.05) protein levels of tight junction-related proteins (CLDN-1 and OCLD). HS-induced jejunal damage was associated with the upregulation of four inflammation-related genes and ten selenoprotein-encoding genes, downregulation (P < 0.05) of four selenoprotein-encoding genes and decreased (P < 0.05) the protein abundance of GPX4 and SELENOS. Compared with the HS group, HMSeBA supplementation not only elevated the villus height and the ratio of V/C (P < 0:05), but also reduced (P < 0.05) the protein abundance of HSP70 and MDA content, and increased (P < 0.05) the protein abundance of OCLD. HMSeBA supplementation downregulated the expression of seven inflammation-related genes, changed the expression of 12 selenoprotein-encoding genes in jejunum mucosa affected by HS, and increased the protein abundance of GPX4, TXNRD1 and SELENOS. CONCLUSION: Organic Se supplementation beyond nutritional requirement alleviates the negative effect of HS on the jejunum of growing pigs, and its protective effect is related to the response of corresponding selenoproteins. © 2021 Society of Chemical Industry.


Assuntos
Transtornos de Estresse por Calor/veterinária , Mucosa Intestinal/imunologia , Jejuno/imunologia , Substâncias Protetoras/administração & dosagem , Selênio/administração & dosagem , Doenças dos Suínos/prevenção & controle , Animais , Suplementos Nutricionais/análise , Proteínas de Choque Térmico HSP70/genética , Proteínas de Choque Térmico HSP70/imunologia , Transtornos de Estresse por Calor/genética , Transtornos de Estresse por Calor/imunologia , Transtornos de Estresse por Calor/prevenção & controle , Resposta ao Choque Térmico/efeitos dos fármacos , Mucosa Intestinal/efeitos dos fármacos , Jejuno/efeitos dos fármacos , Selenoproteínas/genética , Selenoproteínas/imunologia , Suínos , Doenças dos Suínos/genética , Doenças dos Suínos/imunologia
6.
Pestic Biochem Physiol ; 180: 105006, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34955180

RESUMO

Pyraoxystrobin is a new QoI fungicide developed in China. The present study was aimed at determining the baseline sensitivity of M. oryzae to pyraoxystrobin and investigating the potential resistance risk and resistance mechanism of pyraoxystrobin in M. oryzae. The results showed that the mean EC50 of 109 M. oryzae isolates to pyraoxystrobin was 0.0094 µg/mL and the sensitivity exhibited a unimodal distribution. The established baseline sensitivity could provide critical data for monitoring sensitivity changes of M. oryzae to pyraoxystrobin in rice fields. The potential resistance risk was assessed by investigating the biological characteristics of the resistant mutants obtained by fungicide adaptation. The results indicated that the resistance risk of pyraoxystrobin in M. oryzae was medium to high with positive cross-resistance between pyraoxystrobin and azoxystrobin, but without cross resistance between pyraoxystrobin and carbendazim, isoprothiolane, and prochloraz. Further investigation revealed that the pyraoxystrobin-resistant mutants had a G143S mutation in the cyt b protein. Molecular docking confirmed that the G143S substitution conferred high resistance to pyraoxystrobin in M. oryzae. Collectively, the results of this study provided essential data for monitoring the emergence of resistance and developing resistance management strategies for pyraoxystrobin.


Assuntos
Magnaporthe , Oryza , Acrilatos , Ascomicetos , Citocromos b/genética , Magnaporthe/genética , Simulação de Acoplamento Molecular , Doenças das Plantas , Mutação Puntual , Pirazóis
7.
J Nutr Biochem ; 99: 108859, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34517095

RESUMO

The aim of this study was to investigate the effect of dietary L-theanine supplementation on skeletal muscle fiber type transition in mice. Our data indicated that dietary 0.15% L-theanine supplementation significantly increased the mRNA expression levels of muscle fiber type related genes (MyHC I, MyHC IIa, PGC-1α, Sirt1, Tnnt1, Tnnc1, Tnni1, MEF2C) and the protein expression levels of MyHC IIa, myoglobin, PGC-1α, Sirt1 and Troponin I-SS, but significantly decreased the mRNA and protein expression levels of MyHC IIb. Dietary 0.15% L-theanine supplementation significantly increased the activities of SDH and MDH and decreased the activity of LDH. Furthermore, immunofluorescence demonstrated that dietary 0.15% L-theanine supplementation significantly increased the percentage of type I fibers, and significantly decreased the percentage of type II fibers. In addition, we found that dietary 0.15% L-theanine supplementation increased the fatigue-resistant, antioxidant capacity, mitochondrial biogenesis, and function in skeletal muscle of mice. Furthermore, dietary 0.15% L-theanine supplementation significantly increased the mRNA levels of prox1, CaN and NFATc1, the protein levels of prox1, CNA and NFATc1 and the activity of CaN in GAS muscle when compared with the control group. These results indicated that dietary L-theanine supplementation promoted skeletal muscle fiber transition from type II-type I, which might be via activation of CaN and/or NFATc1 signaling pathway.

8.
Spectrochim Acta A Mol Biomol Spectrosc ; 267(Pt 1): 120490, 2022 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-34688061

RESUMO

The oxygen sensing enhancement based on room temperature phosphorescence (RTP) of Gd-HMME adjusted by imidazole was studied. The phosphorescence intensity IP0 and the Stern-Volmer equations under different imidazole concentration were obtained, and the physical mechanism of imidazole regulating the oxygen quenching constant KSV was analyzed. It was found that the KSV value increased by ∼46 folds in the range of 12.4(1)-576.1(5) kPa-1, and the large-scale variation of KSV is conducive to the realization of high precision oxygen concentration measurement in a wide range. In addition, the standard deviation σ of continuous measurement results was given, and the limit of detection (LOD) was determined to be 6.6 ppm.


Assuntos
Medições Luminescentes , Oxigênio , Temperatura
9.
Front Plant Sci ; 12: 739671, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34868124

RESUMO

In all organisms, splicing occurs through the formation of spliceosome complexes, and splicing auxiliary factors are essential during splicing. U2AF65 is a crucial splicing cofactor, and the two typical RNA-recognition motifs at its center recognize and bind the polypyrimidine sequence located between the intron branch site and the 3'-splice site. U2AF65A is a member of the U2AF65 gene family, with pivotal roles in diseases in mammals, specifically humans; however, few studies have investigated plant U2AF65A, and its specific functions are poorly understood. Therefore, in the present study, we systematically identified U2AF65A in plant species from algae to angiosperms. Based on 113 putative U2AF65A sequences from 33 plant species, phylogenetic analyses were performed, followed by basic bioinformatics, including the comparisons of gene structure, protein domains, promoter motifs, and gene expression levels. In addition, using rice as the model crop, we demonstrated that the OsU2AF65A protein is localized to the nucleus and cytoplasm, and it is involved in responses to various stresses, such as drought, high salinity, low temperature, and heavy metal exposure (e.g., cadmium). Using Arabidopsis thaliana and rice mutants, we demonstrated that U2AF65A is involved in the accumulation of plant biomass, growth of hypocotyl upon thermal stimulation, and reduction of tolerance of high temperature stress. These findings offer an overview of the U2AF65 gene family and its stress response functions, serving as the reference for further comprehensive functional studies of the essential specific splicing cofactor U2AF65A in the plant kingdom.

10.
Front Med (Lausanne) ; 8: 773471, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34869492

RESUMO

Electrical impedance tomography (EIT) is a non-invasive, radiation-free and bedside imaging tool that is widely used for real-time monitoring of lung ventilation. Recently, it has been proposed for use in quantitative assessment of regional lung perfusion with hypertonic saline bolus injection and consequently for pulmonary embolism (PE) detection. Here, we present a case of high-risk PE in a postoperative patient, in which EIT monitoring provided us with useful information for diagnosis and decision-making, especially with the challenge of anticoagulation and risk of bleeding.

12.
Front Cell Infect Microbiol ; 11: 790422, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34900762

RESUMO

Patients with Coronavirus Disease 2019 (COVID-19), due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection mainly present with respiratory issues and related symptoms, in addition to significantly affected digestive system, especially the intestinal tract. While several studies have shown changes in the intestinal flora of patients with COVID-19, not much information is available on the gut virome of such patients. In this study, we used the viromescan software on the latest gut virome database to analyze the intestinal DNA virome composition of 15 patients with COVID-19 and investigated the characteristic alternations, particularly of the intestinal DNA virome to further explore the influence of COVID-19 on the human gut. The DNA viruses in the gut of patients with COVID-19 were mainly crAss-like phages (35.48%), Myoviridae (20.91%), and Siphoviridae (20.43%) family of viruses. Compared with healthy controls, the gut virome composition of patients with COVID-19 changed significantly, especially the crAss-like phages family, from the first time of hospital admission. A potential correlation is also indicated between the change in virome and bacteriome (like Tectiviridae and Bacteroidaceae). The abundance of the viral and bacterial population was also analyzed through continuous sample collection from the gut of patients hospitalized due to COVID-19. The gut virome is indeed affected by the SARS-CoV-2 infection, and along with gut bacteriome, it may play an important role in the disease progression of COVID-19. These conclusions would be helpful in understanding the gut-related response and contribute to the treatment and prevention strategies of COVID-19.


Assuntos
COVID-19 , Microbioma Gastrointestinal , DNA , Humanos , SARS-CoV-2 , Viroma
13.
Front Immunol ; 12: 748497, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34745120

RESUMO

Background: Impaired intestinal barrier integrity plays a crucial role in the development of many diseases such as obesity, inflammatory bowel disease, and type 2 diabetes. Thus, protecting the intestinal barrier from pathological disruption is of great significance. Tryptophan can increase gut barrier integrity, enhance intestinal absorption, and decrease intestinal inflammation. However, the mechanism of tryptophan in decreasing intestinal barrier damage and inflammatory response remains largely unknown. The objective of this study was to test the hypothesis that tryptophan can enhance intestinal epithelial barrier integrity and decrease inflammatory response mediated by the calcium-sensing receptor (CaSR)/Ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase Cγ1 (PLC-γ1) signaling pathway. Methods: IPEC-J2 cells were treated with or without enterotoxigenic Escherichia coli (ETEC) K88 in the absence or presence of tryptophan, CaSR inhibitor (NPS-2143), wild-type CaSR overexpression (pcDNA3.1-CaSR-WT), Rac1-siRNA, and PLC-γ1-siRNA. Results: The results showed that ETEC K88 decreased the protein concentration of occludin, zonula occludens-1 (ZO-1), claudin-1, CaSR, total Rac1, Rho family member 1 of porcine GTP-binding protein (GTP-rac1), phosphorylated phospholipase Cγ1 (p-PLC-γ1), and inositol triphosphate (IP3); suppressed the transepithelial electrical resistance (TEER); and enhanced the permeability of FITC-dextran compared with the control group. Compared with the control group, 0.7 mM tryptophan increased the protein concentration of CaSR, total Rac1, GTP-rac1, p-PLC-γ1, ZO-1, claudin-1, occludin, and IP3; elevated the TEER; and decreased the permeability of FITC-dextran and contents of interleukin-8 (IL-8) and TNF-α. However, 0.7 mM tryptophan+ETEC K88 reversed the effects induced by 0.7 mM tryptophan alone. Rac1-siRNA+tryptophan+ETEC K88 or PLC-γ1-siRNA+tryptophan+ETEC K88 reduced the TEER, increased the permeability of FITC-dextran, and improved the contents of IL-8 and TNF-α compared with tryptophan+ETEC K88. NPS2143+tryptophan+ETEC K88 decreased the TEER and the protein concentration of CaSR, total Rac1, GTP-rac1, p-PLC-γ1, ZO-1, claudin-1, occludin, and IP3; increased the permeability of FITC-dextran; and improved the contents of IL-8 and TNF-α compared with tryptophan+ETEC K88. pcDNA3.1-CaSR-WT+Rac1-siRNA+ETEC K88 and pcDNA3.1-CaSR-WT+PLC-γ1-siRNA+ETEC K88 decreased the TEER and enhanced the permeability in porcine intestine epithelial cells compared with pcDNA3.1-CaSR-WT+ETEC K88. Conclusion: Tryptophan can improve intestinal epithelial barrier integrity and decrease inflammatory response through the CaSR/Rac1/PLC-γ1 signaling pathway.

14.
Cell Biosci ; 11(1): 187, 2021 Nov 02.
Artigo em Inglês | MEDLINE | ID: mdl-34727974

RESUMO

Mesenchymal stem/stromal cell (MSC)-based therapeutics is already available for treatment of a range of diseases or medical conditions. Autologous or allogeneic MSCs obtained from self or donors have their own advantages and disadvantages in their medical practice. Therapeutic benefits of using autologous vs. allogeneic MSCs are inconclusive. Transplanted MSCs within the body interact with their physical microenvironment or niche, physiologically or pathologically, and such cells in a newly established tissue microenvironment may be impacted by the pathological harmful environmental factors to alter their unique biological behaviors. Meanwhile, a temporary microenvironment/niche may be also altered by the resident or niche-surrounding MSCs. Therefore, the functional plasticity and heterogeneity of MSCs caused by different donors and subpopulations of MSCs may result in potential uncertainty in their safe and efficacious medical practice. Acknowledging a connection between MSCs' biology and their existing microenvironment, donor-controlled clinical practice for the long-term therapeutic benefit is suggested to further consider minimizing MSCs potential harm for MSC-based individual therapies. In this review, we summarize the advantages and disadvantages of autologous vs. allogeneic MSCs in their therapeutic applications. Among other issues, we highlight the importance of better understanding of the various microenvironments that may affect the properties of niche-surrounding MSCs and discuss the clinical applications of MSCs within different contexts for treatment of different diseases including cardiomyopathy, lupus and lupus nephritis, diabetes and diabetic complications, bone and cartilage repair, cancer and tissue fibrosis.

15.
Poult Sci ; 100(12): 101462, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34731734

RESUMO

This study was conducted to investigate the influence of zinc (Zn) supplementation on growth performance, intestinal development and intestinal barrier function in Pekin ducks. A total of 480, one-day-old male Pekin ducks were divided into 6 groups with 8 replicates: 0 mg/kg Zn, 0 mg/kg Zn +0.5 mg/kg lipopolysaccharide (LPS), 30 mg/kg Zn, 30 mg/kg Zn +0.5 mg/kg LPS, 120 mg/kg Zn, 120 mg/kg Zn +0.5 mg/kg LPS. The duck primary intestinal epithelial cells (DIECs) were divided into 6 groups: D-Zn (Zinc deficiency, treated with 2 µmol/L zinc Chelator TPEN), A-Zn (Adequate Zinc, basal medium), H-Zn (High level of Zn, supplemented with 20 µmol/L Zn), D-Zn + 20 µg/mL LPS, A-Zn + 20 µg/mL LPS, H-Zn + 20 µg/mL LPS. The results were as follows: in vivo, with Zn supplementation of 120 mg/kg reduced LPS-induced decrease of growth performance and intestine damage (P < 0.05), and increased intestinal digestive enzyme activity of Pekin ducks (P < 0.05). In addition, Zn supplementation also attenuated LPS-induced intestinal epithelium permeability (P < 0.05), inhibited LPS-induced the expression of proinflammatory cytokines and apoptosis-related genes (P < 0.05), as well as reduced LPS-induced the intestinal stem cells mobilization of Pekin ducks (P < 0.05). In vitro, 20 µmol/L Zn inhibited LPS-induced expression of inflammatory factors and apoptosis-related genes (P < 0.05), promoted the expression of cytoprotection-related genes, and attenuated LPS-induced intestinal epithelium permeability in DIECs (P < 0.05). Mechanistically, 20 µmol/L Zn enhanced tight junction protein markers including CLDN-1, OCLD, and ZO-1 both at protein and mRNA levels (P < 0.05), and also increased the level of phosphorylation of TOR protein (P < 0.05) and activated the TOR signaling pathway. In conclusion, Zn improves growth performance, digestive enzyme activity, and intestinal barrier function of Pekin ducks. Importantly, Zn also reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins and activating the TOR signaling pathway.


Assuntos
Patos , Lipopolissacarídeos , Animais , Galinhas , Suplementos Nutricionais , Mucosa Intestinal , Masculino , Zinco
16.
J Agric Food Chem ; 69(47): 14278-14286, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34797979

RESUMO

Magnesium (Mg) plays important roles in photosynthesis, sucrose partitioning, and biomass allocation in plants. However, the specific mechanisms of tea plant response to Mg deficiency remain unclear. In this study, we investigated the effects of Mg deficiency on the quality constituents of tea leaves. Our results showed that the short-term (7 days) Mg deficiency partially elevated the concentrations of polyphenols, free amino acids, and caffeine but decreased the contents of chlorophyll and Mg. However, long-term (30 days) Mg-deficient tea displayed decreased contents of these constituents. Particularly, Mg deficiency increased the index of catechins' bitter taste and the ratio of total polyphenols to total free amino acids. Moreover, the transcription of key genes involved in the biosynthesis of flavonoid, caffeine, and theanine was differentially affected by Mg deficiency. Additionally, short-term Mg deficiency induced global transcriptome change in tea leaves, in which a total of 2522 differentially expressed genes were identified involved in secondary metabolism, amino acid metabolism, and chlorophyll metabolism. These results may help to elucidate why short-term Mg deficiency partially improves the quality constituents of tea, while long-term Mg-deficient tea may taste more bitter, more astringent, and less umami.

17.
Materials (Basel) ; 14(22)2021 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-34832295

RESUMO

Surface friction is currently the most common metric for evaluating the performance of high friction surface treatment (HFST). However, friction test methods such as the locked wheel skid tester (LWST) commonly provide a spot measurement. Large variations may arise in the LWST testing on curves. Based on 21 actual HFST projects, a study was performed to use a macrotexture metric, i.e., the mean profile depth (MPD) to evaluate HFST's performance and improve its quality control (QC)/quality assurance (QA) procedures. The material properties were presented to understand the aspects of HFST. The method for calculating MPD was modified to account for the variations of macrotexture measurements. A vehicle-based test system was utilized to measure MPD periodically over an 18-month period since HFST installation. Statistical analysis was performed on the MPD measurements to identify the effects of influencing factors. Compared with the friction from LWST, MPD was equally effective in evaluating HFST performance. However, the use of MPD eliminated the errors as arisen in LWST testing and made it possible to detect surface distresses, including aggregate loss, delamination, and cracking. The expected overall MPD may be calculated by combining the MPD measurements made three months after installation at different HFST sites and used as a metric for evaluating HFST performance and QC/QA.

18.
Artigo em Inglês | MEDLINE | ID: mdl-34781405

RESUMO

BACKGROUND: Microvascular decompression (MVD) has become accepted as an effective therapeutic option for hemifacial spasm (HFS); however, the curative rate of MVD for HFS varies widely (50-98%) in different medical centers. This study could contribute to the improvement of the MVD procedure. METHODS: We retrospectively analyzed 32 patients in whom initial MVD failed in other hospitals and who underwent a second MVD at our center. The clinical characteristics, operative findings, outcome of the second MVD, and complications were recorded. RESULTS: There were 18 women and 14 men (56.3 and 43.7%, respectively). The left-to-right ratio was 19:13. The mean age of the patients was 59.8 years. We found an undiscovered conflict site located in zone 4 in 10 patients and in the root entry zone in 8 patients. The initial MVD failed in nine patients because of ignorance of the arterioles that originate from the anterior inferior cerebellar artery. There were no special findings in four patients. No Teflon felts were found in the whole surgical field in one patient. CONCLUSION: Omission of the offending vessel is the most common cause of an unsuccessful MVD. Intraoperative abnormal muscle response associated with the Z-L response is a good measure to correctly identify the involved arterioles.

19.
Anim Biotechnol ; : 1-14, 2021 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-34762003

RESUMO

This study aimed to test the hypothesis that the calcium-sensing receptor (CaSR) can protect intestinal epithelial barrier integrity and decrease inflammatory response mediated by the Ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase Cγ1 (PLC-γ1) signaling pathway. IPEC-J2 monolayers were treated without or with TNF-α in the absence or presence of CaSR antagonist (NPS 2143), CaSR overexpression, and Rac1 silencing, PLCγ1 silencing or spermine. Results showed that spermine increased transepithelial electrical resistance (TER), tight junction protein levels, the protein concentration of Rac1/PLC-γ1 signaling pathway, and decreased paracellular permeability in the presence of TNF-α. NPS2143 inhibited spermine-induced change in above-mentioned parameters. CaSR overexpression increased TER, the levels of tight junction proteins and the protein concentration of CaSR, phosphorylated PLCγ1, Rac1, and IP3, and decreased paracellular permeability and contents of interleukin-8 (IL-8) and TNF-α after TNF-α challenge. Rac1 and PLCγ1 silencing inhibited CaSR-induced increase in barrier function and the protein concentration of phosphorylated PLCγ1, Rac1, and IP3, and decrease in contents of IL-8 and TNF-α after TNF-α challenge. These results suggest that CaSR activation protects intestinal integrity and alleviates the inflammatory response by activating Rac1 and PLCγ1 signaling after TNF-α challenge, and spermine can maintain barrier function via CaSR/Rac1/PLC-γ1 pathway.

20.
Aging (Albany NY) ; 13(20): 23435-23436, 2021 10 26.
Artigo em Inglês | MEDLINE | ID: mdl-34700298
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