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2.
Anal Chim Acta ; 1188: 339167, 2021 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-34794583

RESUMO

ATP-sensitive potassium (KATP) channels couple intracellular metabolism to the electrical activity by regulating K+ flux across the plasma membrane, thus playing an important role in both normal and pathophysiology. To understand the mechanism of ATP regulating biological ion channels, developing an ATP-responsive artificial nanochannel is an appealing but challenging topic because KATP channel is a heteromultimer of two subunits (potassium channel subunit (Kir6.x) and sulfonylurea receptor (SUR)) and exhibit dynamic functions with adjustability and reversibility. Inspired by the structure of KATP channels, we designed a smart copolymer modified nanochannel that may address the challenge. In the tricomponent poly(N-isopropylacrylamide) (PNIPAAm, PNI)-based copolymer system, phenylthiourea was used to bind the phosphate units of nucleotides and phenylboronic acid was introduced to combine the pentose ring of the nucleoside unit. Besides, a -COOH group with electron-withdrawing property was added into the phenylthiourea units, which may promote the hydrogen-bond-donating ability of thiourea. Specially, the smart copolymer not only provided static binding sites for recognition but also translated the recognition of ATP into their dynamic conformational transitions by changing the hydrogen-bonding environments surrounding PNIPAAm chains, thus achieving the gating function of nanochannel, which resembled the integration and coordination of Kir6.x and SUR units in active KATP. The ATP-regulated ion channel exhibited excellent stability and reversibility. This study is the first example showing how to learn from nature to assemble the ATP-responsive artificial nanochannel and demonstrate the possible mechanism of ATP gating.


Assuntos
Trifosfato de Adenosina , Biomimética , Sítios de Ligação , Nucleotídeos , Receptores de Sulfonilureias
3.
Front Endocrinol (Lausanne) ; 12: 756137, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34803918

RESUMO

The association between polycystic ovary syndrome (PCOS) and endometrial cancer remains unclear. We aimed to investigate the causal association between genetically predicted PCOS and endometrial cancer risk in two ethnic groups through a two-sample Mendelian randomization (MR) approach. Our study includes 13 single nucleotide polymorphisms (SNPs) as instrumental variables (IVs) for PCOS in Europeans, and another 13 SNPs are used as IVs for PCOS in Asians. Outcome data were obtained from the largest published meta-GWAS of European ancestry to date, as well as from the BioBank Japan Project of Asian ancestry. Our study demonstrates that genetically predicted PCOS is not causally associated with the risk of overall endometrial cancer in either Europeans or Asians (odds ratio (OR) = 0.93, 95% confidence interval (CI) = 0.85-1.01, p = 0.09 and OR = 0.98, 95% CI 0.84-1.13, p = 0.75, respectively). Subgroup analyses according to histotype further illustrate that PCOS might not be associated with the risk of either endometrioid endometrial cancer or non-endometrioid endometrial cancer in European ancestry. No pleiotropy is found in our study, and a sensitivity analysis shows similar results. Our results indicate that genetically predicted PCOS might not be associated with the risk of endometrial cancer.

4.
Environ Res ; : 112398, 2021 Nov 17.
Artigo em Inglês | MEDLINE | ID: mdl-34800536

RESUMO

Bisphenol analogues (BPs) are heavily used and negatively affect the health of human beings, however, there is little knowledge regarding human exposure to BPs other than BPA. This study aims to assess human exposure to BPs through investigating pooled urine and wastewater samples. Twenty-four pooled urine samples were prepared from 960 specimens (classified by age and gender). Wastewater samples were collected from six major wastewater treatment plants (WWTPs) in Guangzhou, South of China. BPA, BPS, and BPAF were widely detected in urine samples, with a median concentration of 0.96, 0.42, and 0.15 µg/L, respectively. Median urinary levels of BPA and BPS were higher in males than females (p > 0.05). In addition, BPA and BPS urinary levels in young adults (15-30 years old) were greater than those in children (0-15 years old) (p > 0.05). Nevertheless, most of the BPs were detected in wastewater samples, of which BPA and BPS were predominant BPs, with a median concentration of 1.0 and 0.29 µg/L. The average per capital mass loads of ΣBPs on the weekdays of mix typed WWTP was much higher than those of the weekends. Nonetheless, the average loads of ΣBPs on the weekdays of domestic WWTP was slightly lower than those of the weekends. This indicated that important sources of BPs might include industrial wastewater and household cleaning products. Urinary BPA, BPS, and BPAF accounted for less than 5% per capital mass loads in wastewater, suggesting that much of the BPA, BPS, and BPAF in municipal wastewater originate non-human excretion. Hence, the wastewater-based epidemiology (WBE) approach based on parent compounds is not available for assessing human exposure to BPs, neither for other industrial chemicals with diverse sources in municipal wastewater. These results contributes to the development of an efficient surveillance system which can provide insight in the trends of human exposure of BPs.

5.
Nat Commun ; 12(1): 6486, 2021 11 10.
Artigo em Inglês | MEDLINE | ID: mdl-34759311

RESUMO

The hepatokine follistatin is elevated in patients with type 2 diabetes (T2D) and promotes hyperglycemia in mice. Here we explore the relationship of plasma follistatin levels with incident T2D and mechanisms involved. Adjusted hazard ratio (HR) per standard deviation (SD) increase in follistatin levels for T2D is 1.24 (CI: 1.04-1.47, p < 0.05) during 19-year follow-up (n = 4060, Sweden); and 1.31 (CI: 1.09-1.58, p < 0.01) during 4-year follow-up (n = 883, Finland). High circulating follistatin associates with adipose tissue insulin resistance and non-alcoholic fatty liver disease (n = 210, Germany). In human adipocytes, follistatin dose-dependently increases free fatty acid release. In genome-wide association study (GWAS), variation in the glucokinase regulatory protein gene (GCKR) associates with plasma follistatin levels (n = 4239, Sweden; n = 885, UK, Italy and Sweden) and GCKR regulates follistatin secretion in hepatocytes in vitro. Our findings suggest that GCKR regulates follistatin secretion and that elevated circulating follistatin associates with an increased risk of T2D by inducing adipose tissue insulin resistance.

6.
Artigo em Inglês | MEDLINE | ID: mdl-34769557

RESUMO

LPAR6 is the most recently determined G-protein-coupled receptor of the lysophosphatidic acid receptor, and very few of studies have demonstrated the performance of LPAR6 in cancers. Moreover, the relationship of LPAR6 to the potential of prognosis and tumor infiltration immune cells in different types of cancer are still unclarified. In this study, the mRNA expression of LPAR6 and its clinical characteristics were evaluated on various databases. The association between LPAR6 and immune infiltrates of various types of cancer were investigated via TIMER. Immunohistochemistry (IHC) for LPAR6 in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) tissue microarray with patients' information was detected. We constructed a systematic prognostic landscape in a variety of types of cancer base on the expression level of mRNA. We enclosed that higher LPAR6 mRNA expression level was associated with better overall survival in some types of malignancy. Moreover, LPAR6 significantly affects the prognostic potential of various cancers in The Cancer Genome Atlas Program (TCGA), especially in lung cancer. Tissue microarrays of lung cancer patient cohorts demonstrated that a higher protein level of LPAR6 was correlated to better overall survival of LUAD rather than LUSC cohorts. Further research indicated that the underlying mechanism of this phenome might be the mRNA expression level of LPAR6 was positively associated to infiltrating statuses of devious immunocytes in LUAD rather than in LUSC, that is, LPAR6 expression potentially contributes to the activation and recruiting of T cells (CD8+ T, naive T, effector T cell) and NK cells and inactivates Tregs, decreases T cell exhaustion and regulates T-helper (Th) cells in LUAD. Our discovery implies that LPAR6 is associated with prognostic potential and immune-infiltrating levels in LUAD. These discoveries imply that LPAR6 could be a promising novel biomarker for indicating the prognosis potential of LUAD patients.


Assuntos
Adenocarcinoma de Pulmão , Neoplasias Pulmonares , Adenocarcinoma de Pulmão/genética , Biomarcadores Tumorais/genética , Humanos , Neoplasias Pulmonares/genética , Linfócitos do Interstício Tumoral , Receptores de Ácidos Lisofosfatídicos/genética , Microambiente Tumoral
7.
Artigo em Inglês | MEDLINE | ID: mdl-34760016

RESUMO

Background: Sinomenine has been reported to effectively repress the progression of lung cancer and breast cancer. However, the effects of sinomenine in bladder cancer are not well understood. The purpose of this study was to evaluate the effects of sinomenine in bladder cancer. Methods: The mRNA expression of HEIH in bladder cancer cells was measured by RT-qPCR. T24 and SW780 cells were treated with sinomenine for 24 hours. Cell viability was detected by the MTT assay. Cell migration and invasion were detected by the transwell assay. Western blotting assay was performed to assess the protein expression of Bcl-2, Bax, and caspase-3. Results: Sinomenine significantly suppressed cell viability in T24 and SW780 cells. Moreover, cell migration and invasion were significantly inhibited by sinomenine. Sinomenine accelerated the expression of Bax and caspase-3 but decreased the expression of Bcl-2. HEIH was upregulated in bladder cancer cells compared with normal bladder epithelial cells. Besides this, we noticed that HEIH knockdown blocked cell proliferation, migration, and invasion but facilitated cell apoptosis in bladder cancer cells. Additionally, HEIH reversed the suppression of the progression induced by sinomenine. Conclusion: Sinomenine was observed to suppress cell progression of bladder cancer cells by inhibiting HEIH expression. Our findings suggested that the use of sinomenine might be an effective treatment for bladder cancer.

8.
J Am Chem Soc ; 143(44): 18643-18651, 2021 Nov 10.
Artigo em Inglês | MEDLINE | ID: mdl-34726407

RESUMO

Although great progress has been made in artificial enzyme engineering, their catalytic performance is far from satisfactory as alternatives of natural enzymes. Here, we report a novel and efficient strategy to access high-performance nanozymes via direct atomization of platinum nanoparticles (Pt NPs) into single atoms by reversing the thermal sintering process. Atomization of Pt NPs into single atoms makes metal catalytic sites fully exposed and results in engineerable structural and electronic properties, thereby leading to dramatically enhanced enzymatic performance. As expected, the as-prepared thermally stable Pt single-atom nanozyme (PtTS-SAzyme) exhibited remarkable peroxidase-like catalytic activity and kinetics, far exceeding the Pt nanoparticle nanozyme. The following density functional theory calculations revealed that the engineered P and S atoms not only promote the atomization process from Pt NPs into PtTS-SAzyme but also endow single-atom Pt catalytic sites with a unique electronic structure owing to the electron donation of P atoms, as well as the electron acceptance of N and S atoms, which simultaneously contribute to the substantial enhancement of the enzyme-like catalytic performance of PtTS-SAzyme. This work demonstrates that thermal atomization of the metal nanoparticle-based nanozymes into single-atom nanozymes is an effective strategy for engineering high-performance nanozymes, which opens up a new way to rationally design and optimize artificial enzymes to mimic natural enzymes.

9.
Front Neurosci ; 15: 737874, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34630023

RESUMO

Background: People with chronic pain (CP) sometimes report impaired cognitive function, including a deficit of attention, memory, executive planning, and information processing. However, the association between CP and cognitive decline was still not clear. Our study aimed to assess the association of CP as a risk factor with cognitive decline among adults. Methods: We included data from clinical studies. Publications were identified using a systematic search strategy from PubMed, Embase, and Cochrane Library databases from inception to October 10, 2020. We used the mean cognitive outcome data and the standard deviations from each group. The standardized mean difference (SMD) or odds ratio (OR), and 95% confidence intervals (CI) were performed for each cognitive decline outcome. I 2-values were assessed to quantify the heterogeneities. Results: We included 37 studies with a total of 52,373 patients with CP and 80,434 healthy control participants. Because these studies used different evaluative methods, we analyzed these studies. The results showed CP was associated with cognitive decline when the short-form 36 health survey questionnaire (SF-36) mental component summary (SMD = -1.50, 95% CI = -2.19 to -0.81), the Montreal cognitive assessment (SMD = -1.11, 95% CI = -1.60 to -0.61), performance validity testing (SMD = 3.05, 95% CI = 1.74 to 4.37), or operation span (SMD = -1.83, 95% CI = -2.98 to -0.68) were used. However, we got opposite results when the studies using International Classification of Diseases and Related Health Problems classification (OR = 1.58, 95% CI = 0.97 to 2.56), the Mini-Mental State Examination (SMD = -0.42, 95% CI = -0.94 to 0.10; OR = 1.14, 95% CI = 0.91 to 1.42), and Repeatable Battery for the Assessment of Neuropsychological Status memory component (SMD = -0.06, 95% CI = -0.37 to 0.25). Conclusion: There may be an association between CP and the incidence of cognitive decline when some cognitive, evaluative methods were used, such as short-form 36 health survey questionnaire, Montreal cognitive assessment, performance validity testing, and operation span.

10.
J Virol ; : JVI0169521, 2021 Oct 13.
Artigo em Inglês | MEDLINE | ID: mdl-34643429

RESUMO

The replication of coronaviruses, including severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is closely associated with the endoplasmic reticulum (ER) of infected cells. The unfolded protein response (UPR), which is mediated by ER stress (ERS), is a typical outcome in coronavirus-infected cells and is closely associated with the characteristics of coronaviruses. However, the interaction between virus-induced ERS and coronavirus replication is poorly understood. Here, we demonstrated that infection with the betacoronavirus porcine hemagglutinating encephalomyelitis virus (PHEV) induced ERS and triggered all three branches of the UPR signaling pathway both in vitro and in vivo. In addition, ERS suppressed PHEV replication in mouse neuro-2a (N2a) cells primarily by activating the protein kinase R-like ER kinase (PERK)-eukaryotic initiation factor 2α (eIF2α) axis of the UPR. Moreover, another eIF2α phosphorylation kinase, IFN-induced double-stranded RNA-dependent protein kinase (PKR), was also activated and acted cooperatively with PERK to decrease PHEV replication. Furthermore, we demonstrated that the PERK/PKR-eIF2α pathways negatively regulated PHEV replication by attenuating global protein translation. Phosphorylated eIF2α also promoted the formation of stress granule (SG), which in turn repressed PHEV replication. In summary, our study presents a vital aspect of the host innate response to invading pathogens and reveals attractive host targets (e.g., PERK, PKR and eIF2α) for antiviral drugs. IMPORTANCE Coronavirus diseases are caused by different coronaviruses of importance in humans and animals, and specific treatments are extremely limited. ERS, which can activate the UPR to modulate viral replication and the host innate response, is a frequent occurrence in coronavirus-infected cells. PHEV, a neurotropic ß-coronavirus, causes nerve cell damage, which accounts for the high mortality rates in suckling piglets. However, it remains incompletely understood whether the highly developed ER in nerve cells plays an antiviral role in ERS and how ERS regulates viral proliferation. In this study, we found that PHEV infection induced ERS and activated the UPR both in vitro and in vivo and that the activated PERK/PKR-eIF2α axis inhibited PHEV replication through attenuating global protein translation and promoting SG formation. A better understanding of coronavirus-induced ERS and UPR activation may reveal the pathogenic mechanism of coronavirus and facilitate the development of new treatment strategies for these diseases.

11.
Adv Mater ; : e2105120, 2021 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-34713511

RESUMO

To develop wearable and implantable bioelectronics accommodating the dynamic and uneven biological tissues and reducing undesired immune responses, it is critical to adopt batteries with matched mechanical properties with tissues as power sources. However, batteries available cannot reach the softness of tissues due to high Young's moduli of components (e. g., metals, carbon materials, conductive polymers or composite materials). The fabrication of tissue-like soft batteries thus remains a challenge. Here we report the first ultrasoft batteries totally based on hydrogels. The ultrasoft batteries exhibited Young's moduli of 80 kPa, perfectly matching skin and organs (e. g., heart). The high specific capacities of 82 mAh·g-1 in all-hydrogel lithium-ion batteries and 370 mAh·g-1 in all-hydrogel zinc-ion batteries at a current density of 0.5 A·g-1 were achieved. Both high stability and biocompatibility of the all-hydrogel batteries has been demonstrated upon the applications of wearable and implantable. This work illuminates a pathway for designing power sources for wearable and implantable electronics with matched mechanical properties. This article is protected by copyright. All rights reserved.

12.
Front Endocrinol (Lausanne) ; 12: 731569, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34646235

RESUMO

Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic diseases among women of reproductive age. Inflammation may be involved in the pathogenesis of PCOS, but its exact relationship with PCOS remains unclear. Herein, we investigate the causal association between systemic inflammatory regulators and PCOS risk through a two-sample Mendelian randomization (MR) approach based on the latest and largest genome-wide association study (GWAS) of 41 systemic inflammatory regulators in 8293 Finnish participants and a GWAS meta-analysis consisting of 10,074 PCOS cases and 103,164 controls of European ancestry. Our results suggest that higher levels of IL-17 and SDF1a, as well as lower levels of SCGFb and IL-4, are associated with an increased risk of PCOS (OR = 1.794, 95% CI = 1.150 - 2.801, P = 0.010; OR = 1.563, 95% CI = 1.055 - 2.315, P = 0.026; OR = 0.838, 95% CI = 0.712 - 0.986, P = 0.034; and OR = 0.637, 95% CI = 0.413 - 0.983, P = 0.042, respectively). In addition, genetically predicted PCOS is related to increased levels of IL-2 and VEGF (OR = 1.257, 95% CI = 1.022 - 1.546, P = 0.030 and OR = 1.112, 95% CI = 1.006 - 1.229, P = 0.038, respectively). Our results indicate the essential role of cytokines in the pathogenesis of PCOS. Further studies are warranted to assess the possibility of these biomarkers as targets for PCOS prevention and treatment.

13.
Plant Dis ; 2021 Oct 18.
Artigo em Inglês | MEDLINE | ID: mdl-34661446

RESUMO

Colletotrichum horii is a main causal agent of persimmon (Diospyros kaki Thunb.) anthracnose and distributed widely in persimmon producing areas of the world. Here, we report the first high-quality draft genome sequence of C. horii strain SD010. This will provide a reference for understaning adaptive evolution of genome structure, genes and population diversity among C. gloeosporioides species complex, and also help understand the mechanisms of host-pathogen interaction and improve management strategies of anthracnose.

14.
Crit Rev Food Sci Nutr ; : 1-17, 2021 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-34672229

RESUMO

Folic acid, a water-soluble vitamin B nutrient, plays an important role not only in maintaining a healthy pregnancy but also in offspring brain development and function, however, it remains unclear whether maternal folic acid (FA) supplementation associated with the risk of different postnatal neurodevelopmental outcomes. Here, we performed a systematic review and meta-analysis on the impact of maternal FA supplementation on a wide range of postnatal neurodevelopmental outcomes which include intellectual development, risk of autistic traits, ADHD, behavior, language, and psychomotor problems, using studies extracted from the following databases, including MEDLINE, Web of Science, Cochrane Library, Scopus, EMBASE, and PsychInfo. Thirty-two cohort studies and seven case-control studies were included in this meta-analysis. In the present study, we found that prenatal FA supplementation had a positive impact on offspring's neurodevelopmental outcomes, including improved intellectual development and reduced risk of autism traits, ADHD, behavioral, and language problems. We also found that FA over-supplementation was not associated with an improvement in offspring's brain development, and may have a negative impact on offspring's neurodevelopmental outcomes. This study proved the first panoramic review on the relationship of FA supplementation with offspring's neurodevelopment. Further studies focusing on different dosages and periods of FA supplementation are needed.Supplemental data for this article is available online at https://doi.org/10.1080/10408398.2021.1993781 .

15.
Opt Express ; 29(17): 27661-27673, 2021 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-34615178

RESUMO

Quantum digital signatures (QDSs) promise information-theoretic security against repudiation and forgery of messages. Compared with currently existing three-party QDS protocols, multiparty protocols have unique advantages in the practical case of more than two receivers when sending a mass message. However, complex security analysis, numerous quantum channels and low data utilization efficiency make it intractable to expand three-party to multiparty scenario. Here, based on six-state non-orthogonal encoding protocol, we propose an effective multiparty QDS framework to overcome these difficulties. The number of quantum channels in our protocol only linearly depends on the number of users. The post-matching method is introduced to enhance data utilization efficiency and make it linearly scale with the probability of detection events even for five-party scenario. Our work compensates for the absence of practical multiparty protocols, which paves the way for future QDS networks.

17.
iScience ; 24(10): 103133, 2021 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-34632332

RESUMO

Immune transcripts are essential for depicting onco-immunologic interactions. However, whether cancer cells mimic immune transcripts to reprogram onco-immunologic interaction remains unclear. Here, single-cell transcriptomic analyses of 7,737 normal and 37,476 cancer cells reveal increased immune transcripts in cancer cells. Cells gradually acquire immune transcripts in malignant transformation. Notably, cancer cell-derived immune transcripts contribute to distinct prognoses of immune gene signatures. Optimized immune response signature (oIRS), obtained by excluding cancer-related immune genes from immune gene signatures, and offers a more reliable prognostic value. oIRS reveals that antigen presentation, NK cell killing and T cell signaling are associated with favorable prognosis. Patients with higher oIRS expression are associated with favorable responses to immunotherapy. Indeed, CD83+ cell infiltration, which indicates antigen presentation activity, predicts favorable prognosis in breast cancer. These findings unveil that immune mimicry is a distinct cancer hallmark, providing an example of cancer cell plasticity and a refined view of tumor microenvironment.

18.
Phytomedicine ; 92: 153749, 2021 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-34601220

RESUMO

BACKGROUND: MicroRNA-155(miR-155) is closely associated with diabetic peripheral neuropathy (DPN). Astragaloside IV (AST) is a significant extract of Astragalus membranaceus, which has been found to be effective in the treatment of DPN. However, whether astragaloside IV alleviate DPN via regulating miR-155-mediated autophagy remains unclear. PURPOSE: This study was designed to evaluate the effects of AST on DPN myelin Schwann cells injury and explore the mechanism of AST in treating DPN for the first time. METHODS: GK rats fed with high-fat diet and RSC96 cells cultured in high glucose were used to establish DPN Schwann cells injury in vivo and in vitro model. The effects of AST on DPN were explored through blood glucose detection, nerve function detection, pathological detection and the expression of Neuritin detected by immunohistochemical. To study the effect of AST on the DPN Schwann cells autophagy and the upstream PI3K/Akt/mTOR pathway, the expressions of beclin-1 and LC3 were detected by western blot (WB) in sciatic nerves and by immunofluorescence (IFC) in RSC96 cells. The real-time polymerase chain reaction (RT-PCR) was applied to detect the expressions of miR-155, ATG5, ATG12 both in vivo and in vitro. The binding effect of miR-155 and target gene PI3KCA was verified by luciferase reporter gene assay. The expressions of PI3K, p-Akt/Akt, p-mTOR/mTOR were detected by WB and the expressions of PI3KCA were detected by RT-PCR in vitro. The apoptosis was detected by flow cytometry. Meanwhile, the influence of miR-155 overexpression and knocked down on the above indicators was also detected in RSC96 cells. At last, further mechanism experiments were conducted to verify the mechanism of AST regulating the autophagy and apoptosis of RSC96 cells. RESULTS: AST reduced blood glucose levels, alleviated peripheral nerve myelin sheath injury, and improved neurological function in DPN rats. In addition, AST enhanced the autophagy activity and alleviated the apoptosis in RSC96 cell. Mechanism study shown that AST promote autophagy via regulating miR-155-mediated PI3K/Akt/mTOR signaling pathways. AST reduced RSC96 cells apoptosis by promoting autophagy. CONCLUSION: AST alleviate the myelin sheath injury of DPN caused by the apoptosis of Schwann cells via enhancing autophagy, which was attributed to inhibiting the activation of the PI3K/Akt/mTOR signaling pathway by upregulating miR-155 expression.


Assuntos
Diabetes Mellitus , Neuropatias Diabéticas , MicroRNAs , Animais , Apoptose , Autofagia , Neuropatias Diabéticas/tratamento farmacológico , MicroRNAs/genética , Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-akt , Ratos , Saponinas , Células de Schwann , Triterpenos
19.
Pain Physician ; 24(7): E955-E971, 2021 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-34704707

RESUMO

BACKGROUND: Several minimally invasive nonsurgical treatments have been widely applied for plantar fasciitis (PF). To date, controversy still exists regarding the effectiveness of these approaches for treating PF. OBJECTIVE: The purpose of this study was to perform a comprehensive comparison of the currently available invasive nonsurgical treatments for PF regarding short- and mid-term reductions in pain using a network meta-analysis (NMA). STUDY DESIGN: NMA of randomized controlled trials (RCTs) for minimally invasive nonsurgical treatments of PF. METHODS: The EMBASE, PubMed, and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched for eligible studies. Patients were adults age >= 18 years with PF. The outcome measures were the visual analog scale (VAS) scores at 3-6 weeks and 4-6 months. Pairwise meta-analysis and NMA based on a Bayesian analysis were performed, and all potential comparisons and rank of probabilities were calculated. RESULTS: Thirty RCTs were included in the NMA. The trials investigated 20 treatments or combined treatments, including autologous whole blood, botulinum toxin A (BTA), ultrasound-guided gastrocnemius injection of botulinum toxin (BTA in the gastrocnemius), corticosteroid (CS), miniscalpel-needle (MSN), placebo, platelet-rich plasma (PRP), and the ultrasound-guided technique and peppering technique (PEP). The MSN treatment may be the best choice. LIMITATIONS: Some treatments were investigated in only one study or at one follow-up period and were separated from the network at 4-6 months. Other limitations include the inconformity of the treatment schedule and dose. CONCLUSIONS: The MSN treatment should be recommended as the best therapy, followed by BTA in the gastrocnemius and BTA. CS and PRP are common medications that remain valuable in clinical practice. PEP can be performed after the injection of medication.

20.
Bone ; 154: 116221, 2021 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-34600161

RESUMO

OBJECTIVE: To establish serological biomarker models composed of bone turnover markers (BTMs), vitamin D (Vit D), and estradiol (E2) and to explore their auxiliary diagnostic value in girls with idiopathic central precocious puberty (ICPP). METHODS: Ninety-three girls with ICPP and 93 healthy girls were included in the ICPP group and the control group, respectively. The serum levels of total procollagen type 1 N-terminal propeptide (P1NP), N-terminal midfragment of osteocalcin (N-MID), ß-C-terminal telopeptide of type 1 collagen (ß-CTX), Vit D, E2, and other biochemical parameters were detected in all participants. Serological biomarker models for assistance with ICPP diagnosis were established by logistic regression analyses. RESULTS: Serum P1NP, ß-CTX, Vit D, and E2 levels differed significantly between the two groups (p < 0.05). Three models were established. Model 1 consisted of P1NP and ß-CTX, and had an area under curve (AUC) of 0.764, sensitivity of 74.19%, and specificity of 72.04%. Model 2 consisted of P1NP, ß-CTX, and Vit D, and had an AUC of 0.840, sensitivity of 83.87%, and specificity of 72.04%. Model 3 consisted of P1NP, ß-CTX, Vit D, and E2, and had an AUC of 0.917, sensitivity of 82.80%, and specificity of 86.02%. CONCLUSIONS: Serum P1NP, ß-CTX, Vit D, and E2 levels may be effective indicators for auxiliary diagnosis of ICPP. Serological biomarker models composed of P1NP, ß-CTX, Vit D, and E2 (models 1, 2, and 3) may have auxiliary diagnostic value for ICPP.

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