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1.
BMC Gastroenterol ; 20(1): 80, 2020 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-32228471

RESUMO

BACKGROUND: Hepatic angiosarcoma is a rare malignant tumor featured by highly aggressive behavior and poor prognosis. There are few reports about diffused hepatic angiosarcoma with Kasabach-Merritt syndrome till now. CASE PRESENTATION: A male patient with the chief complain of hepatic space-occupying lesion accompanied by disturbance of consciousness and jaundice. Hyperbilirubinemia, anemia, thrombocytopenia, prolonged prothrombin time, hypofibrinogenemia, decreased prothrombin activity, and increased fibrinogen degradation product and D-dimer were confirmed by blood analysis; multiple focal hypodense lesions in liver was detected by abdominal computed tomography. Liver failure and Kasabach-Merritt syndrome induced by hepatic hemangioma was diagnosed before operation and liver transplantation was performed. Hepatic angiosarcoma was finally proven by postoperative pathology. This patient died of tumor metastasis 2 months after operation. CONCLUSIONS: Hepatic angiosarcoma which can generate Kasabach-Merritt syndrome and even liver failure has an extremely poor prognosis; liver transplantation option should not be considered in hepatic angiosarcoma regardless of the reason.

2.
Chin J Integr Med ; 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32240473

RESUMO

OBJECTIVE: To study the sedative and hypnotic effects and underlying mechanisms of Polygala tenuifolia (PT) on treating aged insomnia rats. METHODS: Sixty Sprague-Dawley male rats were divided into 6 groups by a random number table, including control group, model group, diazepam group (0.92 mg/kg), as well as PT low-, medium- and high-dose groups (0.0875, 0.175, 0.35 g/kg, respectively), 10 rats in each group. Aged insomnia rat model was established with subcutaneous injection of D-galactose for 42 days and then intraperitoneal injection of para-chlorophenylalanine for 3 days. PT and diazepam were respectively given to aged insomnia rats by intragastric administration for 7 days after model establishment. Then the rats were investigated by body weight, Morris water maze test, pentobarbital test, enzyme-linked immunosorbent assay, and transcriptome sequencing. RESULTS: Compared with the model group, PT increased the body weight, improved memory ability, and prolonged pentobarbital-induced sleep time of aged insomnia rats (P<0.01 or P<0.05). The medium dose of PT also increased the neurotransmitter levels of 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA), and decreased the level of Glu in the hippocampus of aged insomnia rats (P<0.05 or P<0.01). Twenty-four differentially expressed genes (DEGs) were overlapped among model group, medium-dose PT group, and diazepam group in transcriptome analysis. Fuom and Pcp2 were down-regulated by the treatment of medium-dose PT (P<0.01 or P<0.05). The metabolic pathways of PT were relatively less than diazepam (91 vs. 104). CONCLUSIONS: The sedative and hypnotic effects of PT in aged insomnia rats might be related to neuro, metabolism pathways, especially through GABAergic signaling pathway. It provided more effective herb choice for the treatment of senile insomnia.

3.
Int Immunopharmacol ; 83: 106425, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32247266

RESUMO

Increasing evidence has demonstrated that the dysregulated expression of long noncoding RNAs (lncRNAs) has important roles in the progression of osteoarthritis (OA), but the function of the lncRNA SNHG15 remains unclear. In the present study, we observed that SNHG15 was downregulated in OA cartilage tissues and IL-1ß-induced chondrocytes. The lower expression of SNHG15 was negatively associated with the observed modified Mankin scale scores, extracellular matrix (ECM) degradation and chondrocyte apoptosis. Downregulated expression of SNHG15 increased chondrocyte viability and decreased chondrocyte apoptosis and ECM degradation in vitro and reduced damage to articular cartilage in vivo. Mechanistically, we demonstrated that SNHG15 overexpression promotes the expression of BCL2L13 by sponging miR-141-3p. The higher expression of miR-141-3p was negatively correlated with SNHG15 and BCL2L13 levels in OA cartilage tissues, and a positive correlation was also shown between SNHG15 and BCL2L13 levels. Furthermore, ectopic expression of miR-141-3p or knockdown of BCL2L13 expression could both reduce the effects of SNHG15 on chondrocyte proliferation, apoptosis and ECM degradation. Collectively, these findings reveal that SNHG15 inhibits OA progression by acting as an miR-141-3p sponge to promote BCL2L13 expression, suggesting that knockdown of SNHG15 expression in chondrocytes can be a potential therapeutic strategy to ameliorate OA progression.

4.
Diagn Pathol ; 15(1): 22, 2020 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-32164751

RESUMO

BACKGROUND: Extraovarian Brenner tumors (EOBTs) are extremely rare and can be observed incidentally in both female and male patients, raising concerns regarding the origin of Brenner tumors. CASE PRESENTATION: A 53-year-old postmenopausal woman presented with a nodular lesion in the left side of the corpus uteri, which was found at a routine health check. Macroscopically, the lesion appeared as a solid nodule with a yellowish-gray cut surface, approximately 6 cm in greatest diameter. Microscopically, the lesion consisted of well-defined epithelial nests and spindled stromal cells. Parenchymal cells expressed CK7, GATA3, CK5/6, 34ßE12, and p63. A single layer of cavity-lined cells with umbrella-like shape showed apical Uroplakin III positivity. Stromal cells were positive for SMA, ER, and PR. The final diagnosis was EOBT and the patient was followed for 2 months with no recurrence. CONCLUSIONS: We report here the third case of EOBTs in the uterus. The combination of morphologic and immunohistochemical results supported the involvement of urothelial metaplasia in the development of EOBTs. The similarities between EOBTs and Walthard nests made Müllerian epithelium an attractive candidate as the cellular origin. Changes of tissue structure or sex hormones imbalance may lead to the translocation of Müllerian remnants to distant organs, explaining the pathogenesis of EOBTs.

5.
Int Immunopharmacol ; 82: 106259, 2020 Mar 03.
Artigo em Inglês | MEDLINE | ID: mdl-32143000

RESUMO

Proteasome inhibitor bortezomib offers one more option for acute or chronic antibody-mediated rejection after kidney transplantation, but aggravated acute kidney injury (AKI) in some cases early after surgery using bortezomib bring new problem. Here, we evaluated the effects of bortezomib and ONX-0914 on renal tubule injury in a mouse model of ischemia-reperfusion injury. After treated with bortezomib, serum creatinine, usea nitrogen and tubular necrosis significantly increased compared with vehicle-treated mice, but decreased in ONX-0914 group mildly. Infiltration of neutrophil and macrophage were less in bortezomib and ONX-0914-treated mice than vehicle-treated group, and the same was observed on oxidative stress in the kidneys. Furthermore, the apoptosis of renal tubular epithelial cells increased in bortezomib-treated mice' kidneys compared with ONX-0914 and vehicle-treated controls. In vitro HK2 cell experiments also demonstrated the proapoptotic effect of bortezomib. The mRNA expression of several proapoptotic factors increased in kidneys of bortezomib-treated mice. In brief, bortezomib, as a proteasome inhibitor, shows a certain cytotoxicity to renal tubular epithelial cell during ischemia/reperfusion injury (IRI) through increased apoptosis. ONX-0914, as an immunoproteasome inhibitor, showed equal potency on anti-inflammation and oxidative stress relieving compared with bortezomib, while less cytotoxicity. The results render the immunoproteasome is a better target for anti-rejection and protecting kidney function in the field of organ transplantation.

6.
J Infect Dis ; 221(Supplement_2): S279-S287, 2020 Mar 16.
Artigo em Inglês | MEDLINE | ID: mdl-32176792

RESUMO

BACKGROUND: This prospective study compared pharmacokinetics (PK) and pharmacodynamics (PD) of linezolid in patients with sepsis receiving continuous venovenous hemofiltration (CVVH) with patients receiving extended daily hemofiltration (EDH). METHODS: Patients with sepsis treated with linezolid and CVVH or EDH were included. Serial blood samples were collected and linezolid concentrations measured. PKs were analyzed using Pmetrics. Monte Carlo simulations were used to evaluate PD target achievement. RESULTS: From 20 patients, 320 blood samples were collected for PK and PD analysis. PK profiles of linezolid were best described by a 2-compartment model. PK parameters were not significantly different between EDH and CVVH groups and were associated with body weight, renal replacement therapy (RRT) duration, and sequential organ failure assessment score. Monte Carlo simulations showed poor fractional target attainment for a minimum inhibitory concentration (MIC) of 2 mg/L with standard 600 mg intravenous administration every 12 hours. CONCLUSIONS: Patients with sepsis receiving RRT exhibited variability in PK/PD parameters for linezolid. PK parameters were not significantly different between CVVH- and EDH-treated patients. Higher probability of target attainment would be achievable at a MIC of 2 mg/L in EDH patients. Higher linezolid doses should be considered for patients on RRT to achieve adequate blood levels.

7.
Toxicol Appl Pharmacol ; 393: 114949, 2020 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-32147541

RESUMO

Acrylamide (ACR), a potential neurotoxin, is present in diet and drinking water. Dietary exposure contributes to cognitive impairment, but relevant mechanism information is limited. Neuroinflammation plays important roles in neurodegenerative disorders. This study aimed to explore whether chronic acrylamide exposure induced neuronal lesions, microglial activation, NLRP3 inflammasome-mediated neuroinflammation and cognitive impairment. For this purpose, 36 Sprague-Dawley (SD) rats were randomly divided into three groups (n = 12/group) and maintained on treated drinking water providing dosages of 0, 0.5, or 5 mg/kg/day ACR for 12 months. Chronic exposure to ACR caused gait abnormality and cognitive dysfunction, which was associated with neuronal lesions, decrease in synapse associated proteins including synapsin I (SYN1), synaptophysin (SYP) and postsynaptic density protein 95 (PSD95), neurogenesis suppression as shown by reduced brain derived neurotrophic factor (BDNF) and doublecortin (DCX) in the hippocampus and frontal cortex. ACR stimulated glial proliferation and microglial activation by increasing GFAP+, Iba-1+, Iba-1+CD68+ positive cells. ACR markedly upregulated the protein levels of NLRP3 inflammasome constituents NLRP3, caspase-1 and increased pro-IL-1ß and IL-1ß. ACR elevated the protein P62 to suppress NLPR3 inflammasome cleavage. Inflammatory cytokines including TNF-α, IL-6 and Cox-2 were also significantly increased after NF-κB pathway activation, which aggravated neuronal lesions and caused memory deficits. This work helped to propose the possible mechanism of chronic exposure of ACR-induced neurotoxicity.

8.
Drug Des Devel Ther ; 14: 845-854, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32161444

RESUMO

Background: Levodopa-carbidopa intestinal gel (LCIG) is a new type of administration that results in steadier levodopa plasma concentrations in advanced Parkinson's disease (PD) patients and effectively reduces poor mobility and dyskinesia. Methods: Electronic databases were searched up to January 1, 2018. The inclusion criteria for this review were as follows: LCIG vs oral medication in advanced PD patients. Results: Five trials, with a total of 198 patients, met all the inclusion criteria. The quality score of these studies ranged from 3 to 5. Two clinical trials showed that compared with oral medication, LCIG had a better treatment effect on on-time with troublesome dyskinesia (TSD) (p = 0.02) and on-time without TSD (p < 0.00001) in advanced PD patients. In addition, four of the 5 studies showed that the LCIG may have better efficacy than oral medication for improving the scores of the UPDRS, and two studies found that LCIG demonstrated better efficacy for improving the PDQ-39 scores. The video recording results indicated a potential decline in both dyskinesia and the "off" state in LCIG-treated patients. The incidence of adverse events was not significantly different between the LCIG and oral medication groups. Conclusion: Compared with oral treatment, LCIG exerts its effectiveness, mostly by reducing the time of on-time with TSD, increasing the time of on-time without TSD and scores of UPDRS and PDQ-39. It is suggesting that LCIG was likely to be a new type of administration used in clinical applications. However, due to methodological flaws, these findings should be viewed with caution, and more RCTs are needed in the field to complement our findings.

9.
J Infect Chemother ; 2020 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-32173284

RESUMO

The spread of carbapenemase-producing Enterobacteriaceae (CPE) is a major threat to public health. In the present study, we compared the difference between meropenem and imipenem disk for detecting carbapenemase-producing gram-negative bacilli using simplified carbapenem inactivation method (sCIM). 106 Enterobacteriaceae, including 74 CPE, 17 Pseudomonas aeruginosa including 10 carbapenemase-producing isolates and 36 Acinetobacter baumannii including 20 carbapenem-resistant isolates preserved in our laboratory were tested. Based on sCIM method, the test bacteria were tested with both meropenem and imipenem disk, respectively. In Enterobacteriaceae, the usage of both meropenem and imipenem disk showed high concordance (99.1%). Meropenem disk cannot identify positive isolates among the 10 P. aeruginosa and 20 A. baumannii isolates due to low carbapenem hydrolytic ability of the carbapenemase produced by these strains. Thus, meropenem disk was found to be similar to imipenem disk, presenting high specificity and sensitivity in the detection of carbapenemase in Enterobacteriaceae, but it cannot be used for the detection of carbapenemase in P. aeruginosa and A. baumannii.

10.
Environ Pollut ; 261: 114039, 2020 Feb 06.
Artigo em Inglês | MEDLINE | ID: mdl-32220747

RESUMO

Environmentally persistent free radicals (EPFRs) are easily generated in the combustion processes of municipal solid waste (MSW) and can cause adverse effects on human health. This study focuses on understanding the toxicity of EPFR particles (ZnO/MCB containing EPFRs) to human bronchial epithelial cell lines BEAS-2B and 16HBE, murine macrophages Raw264.7, and the lung of BALB/c mice after a short exposure (7 days). Exposure of BEAS-2B, 16HBE, and Raw264.7 cells to ZnO/MCB particles significantly increased the reactive oxygen species (ROS) production and perturbed levels of intracellular redox conditions (decreased the intracellular GSH level and the activity of cytosolic SOD, and stimulated oxidative stress related proteins such as HO-1 and Nrf2). EPFR particles decreased the mitochondrial membrane potential (MMP) and induced cell apoptosis, including the activation of Caspase-3, Bax, and Bcl-2 apoptotic signalling pathways. A signature inflammatory condition was observed in both cell models and the mouse model for lung lesions. Our data suggest that EPFRs in particles have greater toxicity to lung cells and tissues that are potential health hazards to human lung.

11.
Patient Educ Couns ; 2020 Feb 29.
Artigo em Inglês | MEDLINE | ID: mdl-32147306

RESUMO

OBJECTIVE: Patient delay in the recognition of and response to the symptoms of acute coronary syndrome (ACS) is a worldwide problem. A community education program about chest pain was implemented in China, and was aimed at providing better community intervention. In this study, the impact of this program on the time of symptom onset to the first medical contact (SO-to-FMC) in ACS patients was investigated, as was the incidence of major adverse cardiac and cerebrovascular events (MACCE) in these patients. METHODS: A total of 10 local communities were included in this study. A 9-month intensive community education program about chest pain was conducted in these communities. The data on the demographics, mode of transportation, procedures, clinical outcomes, and discharge diagnoses of all ACS patients in these communities were collected. RESULTS: The study communities had a combined population of 361,609, and all community population sizes ranged from 12,823 to 66,127. The average SO-to-FMC time of the control period was 510 min, whereas, following community intervention, the average SO-to-FMC time was 256 min (P <  0.001). Furthermore, comparative analyses revealed that, following discharge from the hospital, the 1.5-year MACCE-free survival rate was higher in the community intervention group than in the control group (95.0 % vs. 90.5 %, P =  0.025), and the 1.5-year mortality rate was lower in the community intervention group than in the control group (3.3 % vs. 6.3 %, P =  0.03). CONCLUSIONS AND PRACTICAL IMPLICATIONS: The Hangzhou Chest Pain Science Education Project(HCPSEP) was found to reduce the SO-to-FMC time and improve the outcome of ACS patients. This indicates that a scientific, educational program on chest pain can be effective in improving the knowledge and alertness of the local residents about chest pain. This type of program may be recognized and carried out in other regions.

12.
Int J Biol Macromol ; 154: 456-465, 2020 Mar 16.
Artigo em Inglês | MEDLINE | ID: mdl-32194105

RESUMO

To improve the yield and stability of VII-type cornstarch-lauric acid complexes and inhibit the digestibility of starch, debranched cornstarch was used to complex with lauric acid under a low complexation temperature and a high complexation temperature (DSL30 and DSL90). Debranching treatment raised the yield of the complexes and the melting enthalpy, which reached 51.4% and 14.26 J/g for the complex DSL90, respectively. Complexes formed at high complexation temperature showed high melting temperature ranged in 102.71 °C-120.30 °C, indicating high thermal stability. As the complexation temperature increased from 30 °C to 90 °C, the complexes transformed from VI-type to VII-type. The combination of debranching treatment and increasing complexation temperature decreased the in vitro digestibility of the complexes. The highest resistant starch content was found in the complex DSL90, which also exhibited a lamellar structure under the scanning electron microscopy. The root mean square deviation under the molecular dynamics simulations of the complexes was lower than that of single amylose, suggesting that the complexation with lauric acid could keep the conformation of the amylose chain stable. Debranching treatment combined with a high complexation temperature may be used as an applicable method to prepare VII-type starch-fatty acid complexes with high stability.

13.
Sci Transl Med ; 12(535)2020 Mar 18.
Artigo em Inglês | MEDLINE | ID: mdl-32188725

RESUMO

Acetaminophen/paracetamol (APAP) overdose is the leading cause of drug-induced acute liver failure (ALF) in the United States and Europe. The progression of the disease is attributed to sterile inflammation induced by the release of high mobility group box 1 (HMGB1) and the interaction with receptor for advanced glycation end products (RAGE). A specific, effective, and safe approach to neutralize the proinflammatory activity of HMGB1 is highly desirable. Here, we found that a heparan sulfate (HS) octadecasaccharide (18-mer-HP or hepatoprotective 18-mer) displays potent hepatoprotection by targeting the HMGB1/RAGE axis. Endogenous HS proteoglycan, syndecan-1, is shed in response to APAP overdose in mice and humans. Furthermore, purified syndecan-1, but not syndecan-1 core protein, binds to HMGB1, suggesting that HMGB1 binds to HS polysaccharide side chains of syndecan-1. Last, we compared the protection effect between 18-mer-HP and N-acetyl cysteine, which is the standard of care to treat APAP overdose. We demonstrated that 18-mer-HP administered 3 hours after a lethal dose of APAP is fully protective; however, the treatment of N-acetyl cysteine loses protection. Therefore, 18-mer-HP may offer a potential therapeutic advantage over N-acetyl cysteine for late-presenting patients. Synthetic HS provides a potential approach for the treatment of APAP-induced ALF.

14.
Cell Death Dis ; 11(2): 83, 2020 Feb 03.
Artigo em Inglês | MEDLINE | ID: mdl-32015327

RESUMO

Although dietary α-linolenic acid (ALA) or linolenic acid (LA) intake was reported to be epidemiologically associated with a lower prevalence of hypertension, recent clinical trials have yielded conflicting results. Comparable experimental evidence for the roles of these two different fatty acids is still lacking and the underlying mechanisms need to be further elucidated. Our data showed that ALA but not LA supplementation alleviated systolic blood pressure elevation and improved ACh-induced, endothelium-dependent vasodilation in both spontaneously hypertensive rats (SHRs) and AngII-induced hypertensive mice. In addition, SHRs displayed reduced vascular Sirtuin 3 (SIRT3) expression, subsequent superoxide dismutase 2 (SOD2) hyperacetylation and mitochondrial ROS overproduction, all of which were ameliorated by ALA but not LA supplementation. In primary cultured endothelial cells, ALA treatment directly inhibited SIRT3 reduction, SOD2 hyperacetylation, mitochondrial ROS overproduction and alleviated autophagic flux impairment induced by AngII plus TNFα treatment. However, these beneficial effects of ALA were completely blocked by silencing SIRT3. Restoration of autophagic flux by rapamycin also inhibited mitochondrial ROS overproduction in endothelial cells exposed to AngII plus TNFα. More interestingly, SIRT3 KO mice developed severe hypertension in response to a low dose of AngII infusion, while ALA supplementation lost its anti-hypertensive and endothelium-protective effects on these mice. Our findings suggest that ALA but not LA supplementation improves endothelial dysfunction and diminishes experimental hypertension by rescuing SIRT3 impairment to restore autophagic flux and mitochondrial redox balance in endothelial cells.

15.
Acta Biomater ; 106: 387-395, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32058079

RESUMO

Ti-6Al-4V alloys with cellular structure fabricated by additive manufacturing are currently of significant interest because their modulus is comparable to bone and the cellular structure allows the cells to penetrate and exchange nutrients, promoting osseointegration. We describe here a unique simulation device that replaces the traditional steady electrochemistry approach, enabling in-situ study of variation of ion concentration and surface potential with pore depth for cellular structured Ti-6Al-4V alloys fabricated by electron beam melting (EBM) in phosphate buffered saline (PBS). This approach addresses the scientific gap on the electrochemical behavior of cellular structured titanium alloys. The study indicated that concentration of H+ and Cl- increased with the increase of pore depth, while the surface potential decreased. The exposed surface of inner cellular structure was not corroded but passivated after immersing in PBS at 37 °C for 14 days, which was independent of pore depth. Furthermore, X-ray photoelectron spectroscopy (XPS) and Mott-Schottky (M-S) studies suggested that a thinner passive film containing a greater donor density was formed on the surface of cellular structured Ti-6Al-4V alloy at the deepest pore depth. This is attributed to insufficient oxygen supply and Cl-adsorption on the surface inside the pores. STATEMENT OF SIGNIFICANCE: Porous titanium alloys are promising implants in biomedical applications. However, it is a challenge to accurately characterize the corrosion behavior of porous titanium alloys with complex pore structure using traditional electrochemical methods. In this study, we have adopted a special device to simulate the environment within the pore structure. The variation in ion concentration and surface potential of Ti-6Al-4V fabricated by EBM with pore depth was in-situ monitored. After immersing in PBS for 14 days, Ti-6Al-4V exhibited good corrosion properties and the samples with less than 60 mm pore depth were not corroded but passivated. Also, we analyzed the difference in corrosion property at different pore depth. This type of in-situ corrosion performance monitoring in EBM-produced Ti-6Al-4V has not been previously studied.

16.
Chin Med J (Engl) ; 133(5): 530-536, 2020 Mar 05.
Artigo em Inglês | MEDLINE | ID: mdl-32049744

RESUMO

BACKGROUND: Texture features were the intrinsic properties of the human tissues and could efficiently detect the subtle functional changes of involved tissue. The pathologic changes of the lateral pterygoid muscle (LPM) were significantly correlated with the temporomandibular disc displacement. However, the occult functional changes of LPM could not be detected by the naked eye on the medical images. The current study was aimed to evaluate the functional changes of the LPM in the patients with temporomandibular disorders (TMDs) using texture analysis. METHODS: Twenty-nine patients with TMD were performed with magnetic resonance (MR) imaging on a 3.0T MR scanner, who were consecutively recruited from the TMD clinic of Hainan Hospital of Chinese People's Liberation Army General Hospital from February 2019 to September 2019. The patients were classified into three groups according to the disc displacement: disc without displacement (DWoD), disc displacement with reduction (DDWR) and disc displacement without reduction (DDWoR). The gray-level co-occurrence matrix method was applied with the texture analysis of LPM on the axial T2-weighted imaging. The texture features included angular second moment, contrast, correlation, inverse different moment, and entropy. One-way analysis of variance was used for grouped comparisons and receiver operating characteristics (ROC) curve analysis was applied to evaluate the diagnostic efficacy of the texture parameters. RESULTS: Texture contrast of LPM presented significantly lower in DDWoR (46.30 [35.03, 94.48]) than that in DWoD (123.85 [105.06, 143.23]; test statistic = 23.05; P < 0.001). Texture entropy of LPM showed significant differences among DWoD (7.62 ±â€Š0.33), DDWR (6.76 ±â€Š0.35), and DDWoR (6.46 ±â€Š0.39) (PDWoD-DDWR < 0.001, PDWoD-DDWoR < 0.001, and PDDWR-DDWoR = 0.014). Area under the ROC curve (AUC) demonstrated that texture entropy had an excellent diagnostic accuracy for DWoD-DDWR (AUC = 0.96) and DWoD-DDWoR (AUC = 0.98). CONCLUSION: The texture contrast and entropy could identify the altered functional status of LPM in patients with TMD and could be considered as the effective imaging biomarker to evaluate the functional changes of LPM in TMD.

17.
Int J Biol Macromol ; 152: 199-206, 2020 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-32088231

RESUMO

Hyaluronic acid (HA) is a major glycosaminoglycan, a family of structurally complex, linear, anionic hetero-co-polysaccharides. HA is important in various anatomical structures including the eyes, joints, heart and myriad intricate tissues, and is currently widely used in the therapeutics and cosmetics areas. The synthesis of HA of well-defined and uniform chain lengths is of major interest for the development of safer and more reliable drugs and to gain a better understanding of its structure-activity relationships. However, HA has received less attention from the synthetic carbohydrate community compared with other members of the glycosaminoglycan family. In this review, we examine the remarkable progress that has been made in the chemical and chemoenzymatic synthesis of HA, providing a broad spectrum of options to access HA of well controlled chain lengths.

18.
Artigo em Inglês | MEDLINE | ID: mdl-32100232

RESUMO

The aim of this study was to explore whether or not acetylresveratrol as a potential substitute for resveratrol dragged the toxic aldehyde to inhibit the mutation of mitochondrial DNA. The results revealed that the acetylresveratrol shifted ultraviolet peak of trans-crotonaldehyde from 316 to 311 nm. In mitochondria, the acetylresveratrol split the ultraviolet peak at 311 nm of trans-crotonaldehyde into 311 nm and 309 nm; the aldehyde Raman band of trans-crotonaldehyde was red shifted by the acetylresveratrol from 1689 to 1686 cm-1 with obvious band decline; Raman bands at 1149 cm-1, 1168 cm-1, and 1325 cm-1 of acetylresveratrol disappeared. In aldehyde dehydrogenase, the aldehyde Raman band of trans-crotonaldehyde was red shifted by the acetylresveratrol from 1689 to 1684 cm-1 with band decline; Raman bands at 1150 cm-1, 1168 cm-1, and 1324 cm-1 of acetylresveratrol declined. The weak acidic microenvironment was the best, for the acetylresveratrol dragged the toxic aldehyde of trans-crotonaldehyde. Compared with the resveratrol, the effect of the acetylresveratrol on the toxic aldehyde of trans-crotonaldehyde was very similar to that of the resveratrol. The acetylresveratrol is very suitable as a potential substitute for resveratrol dragged the toxic aldehyde to inhibit the mutation of mitochondrial DNA. Graphical Abstract In mitochondria, the Raman band of the toxic -CH=O of trans-crotonaldehyde (TCA) dragged by the Acetyl-Res from 1689 to 1686 cm-1 with obvious band decline, while the Raman bands at 1149 cm-1, 1168 cm-1, and 1325 cm-1 of the Acetyl-Res disappeared, respectively. The Acetyl-Res is very suitable as a potential substitute, for the Res dragged the toxic -CH=O of TCA to inhibit the mutation of mitochondrial DNA for anticancer.

19.
Glia ; 2020 Feb 10.
Artigo em Inglês | MEDLINE | ID: mdl-32039516

RESUMO

Microglia are implicated in the pathophysiology of several neurodegenerative disorders, including Alzheimer's disease. While the role of microglia and peripheral macrophages in regulating amyloid beta pathology has been well characterized, the impact of these distinct cell subsets on tau pathology remains poorly understood. We and others have recently demonstrated that monocytes can engraft the brain and give rise to long-lived parenchymal macrophages, even under nonpathological conditions. We undertook the current study to investigate the regulation of tau pathology by microglia and peripheral macrophages using hTau transgenic mice, which do not exhibit microglial activation/pathology or macrophage engraftment. To assess the direct impact of microglia on tau pathology we developed a protocol for long-term microglial depletion in Cx3cr1CreER R26DTA mice and crossed them with hTau mice. We then depleted microglia up to 3 months in both young and old mice, but no net change in forebrain soluble oligomeric tau or total or phosphorylated levels of aggregated tau was recorded. To investigate the consequence of peripherally-derived parenchymal macrophages on tau aggregation we partially repopulated the hTau microglial pool with peripheral macrophages, but this also did not affect levels of tau oligomers or insoluble aggregates. Our study questions the direct involvement of microglia or peripheral macrophages in the development of tau pathology in the hTau model.

20.
BMC Neurol ; 20(1): 65, 2020 Feb 22.
Artigo em Inglês | MEDLINE | ID: mdl-32087674

RESUMO

BACKGROUND: Inflammation plays an important role in atherosclerosis but the contribution of neutrophils to this process is unclear. We sought to assess whether neutrophil count is associated with intracranial atherosclerotic stenosis (ICAS). METHODS: A total of 2847 individuals were included in our study, including 1363 with acute ischemic stroke and 1484 normal controls without stroke. The presence of ICAS was confirmed by magnetic resonance angiography. The association between neutrophil count and ICAS was evaluated by multivariable logistic regression analysis. RESULTS: Among 2847 individuals included in this study, individuals with ICAS had higher neutrophil counts than those without ICAS in groups with and without stroke (P <  0.0001 for stroke group, P = 0.0097 for group without stroke). The multivariable logistic regression analysis showed that the third and fourth quartiles were independent predictors of ICAS in all the subjects (Q3: OR 1.81, 95% CI 1.39-2.37, Q4: OR 2.29, 95% CI 1.70-3.10) and patients in the fourth quartile had a higher risk for the occurrence of ICAS in stroke group (Q4: OR 2.82, 95% CI 1.79-4.48). However, there was no significant association between neutrophil count and ICAS in the group without stroke. CONCLUSIONS: The levels of circulating neutrophils were associated with the presence of ICAS. Our findings suggest that neutrophils may play a role in the pathogenesis of stroke related to ICAS and emphasize the need to develop proper strategies to control neutrophil response for the treatment of ICAS.

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