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1.
Medicine (Baltimore) ; 99(6): e19125, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32028438

RESUMO

Pain, the main symptom of osteoarthritis (OA), can lead to functional disability in patients with knee OA. Understanding the association factors related to knee pain is important since preventing OA-induced disabilities can be achieved by modifying these pain-associated issues. Therefore, this study was aimed to investigate the association factors for OA-induced knee pain in Taiwanese patients who received total knee replacements (TKR).In this retrospective study, 357 subjects who had undergone TKR at the Taipei Municipal Wan-Fang Hospital were recruited. The distribution of pain severity among patients with knee OA was evaluated. Demographic data and clinical parameters were analyzed to determine relationships between these variables and the severity of knee OA pain.Of the 357 patients studied, 54% and 33% had moderate and severe knee pain, respectively. Furthermore, a multivariate logistic regression analysis revealed that serum creatinine (>1.5 mg/dL) and an estimated glomerular filtration rate (eGFR) (<60 mL/min/1.73 m) were significantly associated with severe knee pain in OA patients. A significant correlation between severe knee pain and serum creatinine or eGFR was demonstrated by Pearson correlations.Taken together, the renal insufficiency defined by an elevated serum creatinine or a low eGFR in OA patients who required TKR was associated with severe knee pain. These variables must be considered while treating knee OA pain, especially in those patients with severe pain.


Assuntos
Artralgia/etiologia , Artroplastia do Joelho/efeitos adversos , Osteoartrite do Joelho/complicações , Insuficiência Renal/complicações , Idoso , Creatinina/sangue , Feminino , Taxa de Filtração Glomerular , Humanos , Masculino , Medição da Dor , Estudos Retrospectivos
2.
High Alt Med Biol ; 20(3): 293-302, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31329475

RESUMO

Background: This study aimed to explore the effects of netrin-1 on hypobaric hypoxia-induced lung injury in mice. Methods: We exposed 6-8-week-old C57BL/6 mice to hypobaric stress at 340 mmHg for 30 minutes followed by 260 mmHg for different periods (6, 12, 18, and 24 hours) to observe the severity of lung injury (O2 concentration, 21%; 54.6 mmHg). The wet/dry weight ratio and protein leakage from the mouse lung were used to determine the suitable exposure time. Netrin-1 was injected into the tail vein of mice before 18-hour decompression. Inflammatory cytokines, lung injury scores, and activity of nuclear factor κB were evaluated. The expression of apoptosis-related proteins was also examined. Results: Protein concentration in the bronchoalveolar lavage fluid was significantly higher in the 18-hour group (p < 0.05). Pulmonary pathology revealed neutrophil infiltration, alveolar septum thickening, and tissue edema. Injury score and macrophage inflammatory protein 2 levels were also increased. Intrinsic apoptosis pathway was activated. Hypoxia decreased the expression of Bcl2 protein, the number of active caspase-3-stained cells, and UNC5HB receptors. Pretreatment with netrin-1 reduced protein leakage, inhibited neutrophil migration, lowered the injury score, attenuated apoptosis, and increased UNC5HB receptor expression. Conclusion: Netrin-1 dampens hypobaric hypoxia-induced lung injury by inhibiting neutrophil migration and attenuating apoptosis.

3.
J Anesth ; 33(3): 463-477, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31076946

RESUMO

Over the last decade, considerable progress has been made regarding infraclavicular brachial plexus block (ICB) in adults, especially since the introduction of ultrasound guidance. The advancements in ICB have been attributed to the development of various approaches to improve the success rate and reduce complications. This has also necessitated a unified nomenclature system to facilitate comparison among different approaches. This review aimed to propose an anatomical nomenclature system by classifying ICB approaches into proximal and distal ones to aid future research and provide practice advisories according to recent updates. We also comprehensively discuss various aspects of this nomenclature system. Our review suggests that ultrasound-guided ICB should be categorized as an advanced technique that should be performed under supervision and dual guidance. For one-shot block, the conventional distal approach is still preferred but should be modified to follow ergonomic practice, with the arm in the proper position. For continuous ICB, the proximal approach is promising for reducing local anesthetic volume and increasing efficacy. Nevertheless, further studies are warranted in this direction. We provide practice advisories to maximize safety and minimize adverse events, and recommend designing future studies on ICB according to these findings based on the unified nomenclature system.

4.
J Bone Miner Res ; 34(7): 1275-1283, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30779856

RESUMO

The stiffness index (SI) from quantitative ultrasound measurements is a good indicator of BMD and may be used to predict the risk of osteoporotic fracture. We conducted a genomewide association study (GWAS) for SI using 7742 individuals from the Taiwan Biobank, followed by a replication study in a Korean population (n = 2955). Approximately 6.1 million SNPs were subjected to association analysis, and SI-associated variants were identified. We further conducted a meta-analysis of Taiwan Biobank significant SNPs with a Korean population-based cohort. Candidate genes were prioritized according to epigenetic annotations, gene ontology, protein-protein interaction, GWAS catalog, and expression quantitative trait loci analyses. Our results revealed seven significant single-nucleotide polymorphisms (SNPs) within three loci: 7q31.31, 17p13.3, and 11q14.2. Conditional analysis showed that three SNPs, rs2536195 (CPED1/WNT16), rs1231207 (SMG6), and rs4944661 (LOC10050636/TMEM135), were the most important signals within these regions. The associations for the three SNPs were confirmed in a UK Biobank estimated BMD GWAS; these three cytobands were replicated successfully after a meta-analysis with a Korean population cohort as well. However, two SNPs were not replicated. After prioritization, we identified two novel genes, RAB15 and FNTB, as strong candidates for association with SI. Our study identified three SI-associated SNPs and two novel SI-related genes. Overall, these results provide further insight into the genetic architecture of osteoporosis. Further studies in larger East Asian populations are needed. © 2019 American Society for Bone and Mineral Research.

5.
Phytomedicine ; 49: 41-51, 2018 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-30217261

RESUMO

BACKGROUND: Temozolomide (TMZ) is a first-line chemotherapeutic drug for malignant gliomas. Nonetheless, TMZ-induced side effects and drug resistance remain challenges. Our previous study showed the suppressive effects of honokiol on growth of gliomas. PURPOSE: This study was further aimed to evaluate if honokiol could enhance TMZ-induced insults toward malignant glioma cells and its possible mechanisms. METHODS: Human U87 MG glioma cells were exposed to TMZ, honokiol, and a combination of TMZ and honokiol. Cell survival, apoptosis, necrosis, and proliferation were successively assayed. Fluorometric substrate assays were conducted to determine activities of caspase-3, -6, -8, and -9. Levels of Fas ligand, Bax, and cytochrome c were immunodetected. Translocation of Bax to mitochondria were examined using confocal microscopy. Mitochondrial function was evaluated by assaying the mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and complex I enzyme activity. Caspase-6 activity was suppressed using specific peptide inhibitors. The honokiol-induced effects were further confirmed using human U373 MG and murine GL261 cells. RESULTS: Exposure of human U87 MG glioma cells to honokiol significantly increased TMZ-induced DNA fragmentation and cell apoptosis. Interestingly, honokiol enhanced intrinsic caspase-9 activity without affecting extrinsic Fas ligand levels and caspase-8 activity. Sequentially, TMZ-induced changes in Bax translocation, the MMP, mitochondrial complex I enzyme activity, intracellular ROS levels, and cytochrome c release were enhanced by honokiol. Consequently, honokiol amplified TMZ-induced activation of caspases-3 and -6 in human U87 MG cells. Fascinatingly, suppressing caspase-6 activity concurrently decreased honokiol-induced DNA fragmentation and cell apoptosis. The honokiol-involved improvement in TMZ-induced intrinsic apoptosis was also confirmed in human U373 MG and murine GL261 glioma cells. CONCLUSIONS: This study showed that honokiol can enhance TMZ-induced apoptotic insults to glioma cells via an intrinsic mitochondrion-dependent mechanism. Our results suggest the therapeutic potential of honokiol to attenuate TMZ-induced side effects.


Assuntos
Apoptose/efeitos dos fármacos , Compostos de Bifenilo/farmacologia , Dacarbazina/análogos & derivados , Medicamentos de Ervas Chinesas/farmacologia , Glioma/patologia , Lignanas/farmacologia , Mitocôndrias/fisiologia , Animais , Caspases/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Citocromos c/metabolismo , Fragmentação do DNA , Dacarbazina/farmacologia , Proteína Ligante Fas/metabolismo , Glioma/tratamento farmacológico , Humanos , Potencial da Membrana Mitocondrial , Camundongos , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Temozolomida
7.
Plants (Basel) ; 7(2)2018 Jun 19.
Artigo em Inglês | MEDLINE | ID: mdl-29921823

RESUMO

Phi thickenings are specialized bands of secondary wall deposited around radial walls of root cortical cells. These structures have been reported in various species from the Brassicaceae, including Brassica oleracea, where previous reports using hydroponics indicated that they can be induced by exposure to salt. Using roots grown on agar plates, we show that both salt and sucrose can induce the formation of phi thickenings in a diverse range of species within the Brassicaceae. Within the genus Brassica, both B. oleracea and B. napus demonstrated the formation of phi thickenings, but in a strongly cultivar-specific manner. Confocal microscopy of phi thickenings showed that they form a complex network of reinforcement surrounding the inner root cortex, and that a delicate, reticulate network of secondary wall deposition can also variously form on the inner face of the cortical cell layer with phi thickenings adjacent to the endodermal layer. Results presented here indicate that phi thickenings can be induced in response to salt and water stress and that wide variation occurs in these responses even within the same species.

8.
Nutr Res ; 52: 87-97, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29525610

RESUMO

Arctigenin (ATG), a lignin extracted from Arctium lappa (L.), exerts antioxidant and anti-inflammatory effects. We hypothesized that ATG exerts a protective effect on hepatocytes by preventing nonalcoholic fatty liver disease (NAFLD) progression associated with lipid oxidation-associated lipotoxicity and inflammation. We established an in vitro NAFLD cell model by using normal WRL68 hepatocytes to investigate oleic acid (OA) accumulation and the potential bioactive role of ATG. The results revealed that ATG inhibited OA-induced lipid accumulation, lipid peroxidation, and inflammation in WRL68 hepatocytes, as determined using Oil Red O staining, thiobarbituric acid reactive substance assay, and inflammation antibody array assays. Quantitative RT-PCR analysis demonstrated that ATG significantly mitigated the expression of acetylcoenzyme A carboxylase 1 and sterol regulatory element-binding protein-1 and significantly increased the expression of carnitine palmitoyltransferase 1 and peroxisome proliferator-activated receptor alpha. The 40 targets of the Human Inflammation Antibody Array indicated that ATG significantly inhibited the elevation of the U937 lymphocyte chemoattractant, ICAM-1, IL-1ß, IL-6, IL-6sR, IL-7, and IL-8. ATG could activate the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and AMP-activated protein kinase (AMPK) pathways and could increase the phosphorylation levels of Akt and AMPK to mediate cell survival, lipid metabolism, oxidation stress, and inflammation. Thus, we demonstrated that ATG could inhibit NAFLD progression associated with lipid oxidation-associated lipotoxicity and inflammation, and we provided insights into the underlying mechanisms and revealed potential targets to enable a thorough understanding of NAFLD progression.


Assuntos
Arctium/química , Furanos/farmacologia , Lignanas/farmacologia , Fígado/efeitos dos fármacos , Hepatopatia Gordurosa não Alcoólica/prevenção & controle , Fosfatidilinositol 3-Quinase/metabolismo , Extratos Vegetais/farmacologia , Proteínas Quinases Ativadas por AMP/metabolismo , Acetil-CoA Carboxilase/metabolismo , Carnitina O-Palmitoiltransferase/metabolismo , Fígado Gorduroso/metabolismo , Fígado Gorduroso/prevenção & controle , Furanos/uso terapêutico , Células Hep G2 , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Humanos , Inflamação/metabolismo , Inflamação/prevenção & controle , Molécula 1 de Adesão Intercelular/metabolismo , Interleucinas/metabolismo , Lignanas/uso terapêutico , Fígado/citologia , Fígado/metabolismo , Fígado/patologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Ácido Oleico/metabolismo , Estresse Oxidativo/efeitos dos fármacos , PPAR alfa/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Fitoterapia , Extratos Vegetais/uso terapêutico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
9.
Oncotarget ; 9(1): 1169-1186, 2018 Jan 02.
Artigo em Inglês | MEDLINE | ID: mdl-29416685

RESUMO

Estrogen deficiency usually leads to bone loss and osteoporosis in postmenopausal women. Osteoblasts play crucial roles in bone formation. However, osteoblast functions are influenced by mitochondrial bioenergetic conditions. In this study, we investigated the roles of the estrogen and estrogen receptor alpha (ERα) axis in mitochondrial energy metabolism and subsequent osteoblast mineralization. Exposure of rat calvarial osteoblasts to estradiol caused substantial improvements in alkaline phosphatase activities and cell calcification. In parallel, treatment of human osteoblast-like U2OS cells, derived from a female osteosarcoma patient, with estradiol specifically augmented ERα levels. Sequentially, estradiol stimulated translocation of ERα to nuclei in human osteoblasts and induced expressions of genomic respiratory chain complex NDUFA10, UQCRC1, cytochrome c oxidase (COX)8A, COX6A2, COX8C, COX6C, COX6B2, COX412, and ATP12A genes. Concurrently, estradiol stimulated translocation of ERα to mitochondria from the cytoplasm. A bioinformatic search found the existence of four estrogen response elements in the 5'-promoter region of the mitochondrial cox i gene. Interestingly, estradiol induced COX I mRNA and protein expressions in human osteoblasts or rat calvarial osteoblasts. Knocking-down ERα translation concurrently downregulated estradiol-induced COX I mRNA expression. Consequently, exposure to estradiol led to successive increases in the mitochondrial membrane potential, the mitochondrial enzyme activity, and cellular adenosine triphosphate levels. Taken together, this study showed the roles of the estradiol/ERα signaling axis in improving osteoblast maturation through upregulating the mitochondrial bioenergetic system due to induction of definite chromosomal and mitochondrial complex gene expressions. Our results provide novel insights elucidating the roles of the estrogen/ERα alliance in regulating bone formation.

10.
Biomed Res Int ; 2017: 8284363, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29226150

RESUMO

Purpose of Review: Transversus abdominis plane (TAP) block is a regional technique for analgesia of the anterolateral abdominal wall. This review highlights the nomenclature system and recent advances in TAP block techniques and proposes directions for future research. Recent Findings: Ultrasound guidance is now considered the gold standard in TAP blocks. It is easy to acquire ultrasound images; it can be used in many surgeries involving the anterolateral abdominal wall. However, the efficacy of ultrasound-guided TAP blocks is not consistent, which might be due to the use of different approaches. The choice of technique influences the involved area and block duration. To investigate the actual analgesic effects of TAP blocks, we unified the nomenclature system and clarified the definition of each technique. Although a single-shot TAP block is limited in duration, it is still the candidate of the analgesic standard for abdominal wall surgery because the use of the catheter technique and liposomal bupivacaine may overcome this limitation. Summary: Ultrasound-guided TAP blocks are commonly used. With the unified nomenclature and the development of catheter technique and/or liposomal local anesthetics, TAP blocks can be applied more appropriately to achieve better pain control.


Assuntos
Músculos Abdominais/efeitos dos fármacos , Bloqueio Nervoso/métodos , Parede Abdominal , Analgesia/métodos , Anestésicos Locais/administração & dosagem , Anestésicos Locais/química , Bupivacaína/administração & dosagem , Bupivacaína/química , Humanos , Lipossomos/administração & dosagem , Lipossomos/química , Manejo da Dor/métodos , Ultrassonografia de Intervenção/métodos
11.
Pain Pract ; 17(7): 879-885, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-27910248

RESUMO

BACKGROUND: Radiofrequency therapy (RFT) generates molecular motion and produces heat and electromagnetic effects on tissues, which attenuate pain sensation and thereby relieve pain. This study was to observe the altering trend of physiological parameters after RFT for chronic cervical or lumbar pain. METHODS: This study recruited 66 patients with chronic cervical or lumbar pain and recorded their physiological parameters before and after RFT using heart rate variability (HRV) and photoplethysmography (PPG) to explore the feasibility of RFT efficacy assessment. RESULTS: The patients' visual analog scale scores significantly decreased after RFT and the HRV parameters that represented parasympathetic activity significantly changed (HR decreased, and R-R interval and low- and high-frequency power increased significantly). Meanwhile, the PPG parameters that represented sympathetic activity also increased (PPG amplitude and autonomic nervous system state significantly decreased). CONCLUSIONS: This study showed significant efficacy of RFT in patients with chronic cervical or lumbar pain. The changes of HRV and PPG parameters may explain part of the mechanisms of RFT.


Assuntos
Dor Crônica/terapia , Frequência Cardíaca/fisiologia , Dor Lombar/terapia , Cervicalgia/terapia , Fotopletismografia/métodos , Tratamento por Radiofrequência Pulsada/métodos , Adulto , Idoso , Dor Crônica/diagnóstico por imagem , Dor Crônica/fisiopatologia , Feminino , Humanos , Dor Lombar/diagnóstico por imagem , Dor Lombar/fisiopatologia , Masculino , Pessoa de Meia-Idade , Cervicalgia/diagnóstico por imagem , Cervicalgia/fisiopatologia , Resultado do Tratamento
12.
Toxicology ; 368-369: 142-151, 2016 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-27638051

RESUMO

Following brain injury, a sequence of mechanisms leads to disruption of the blood-brain barrier (BBB) and subsequent cerebral edema, which is thought to begin with activation of bradykinin. Our previous studies showed that ketamine, a widely used intravenous anesthetic agent, can suppress bradykinin-induced cell dysfunction. This study further aimed to evaluate the protective effects of ketamine against bradykinin-induced disruption of the mouse cerebrovascular endothelial cell (MCEC)-constructed tight junction barrier and the possible mechanisms. Exposure of MCECs to bradykinin increased intracellular calcium (Ca2+) concentrations in a time-dependent manner. However, pretreatment of MCECs with ketamine time- and concentration-dependently lowered the bradykinin-induced calcium influx. As to the mechanisms, although exposure of MCECs to ketamine induced bradykinin R1 receptor protein and mRNA expression, this anesthetic did not change levels of the bradykinin R2 receptor, a major receptor that responds to bradykinin stimulation. Bradykinin increased amounts of soluble occludin in MCECs, but pretreatment with ketamine alleviated this disturbance in occludin polymerization. Consequently, exposure to bradykinin decreased the transendothelial electronic resistance in the MCEC-constructed tight junction barrier. However, pretreatment with ketamine attenuated the bradykinin-induced disruption of the tight junction barrier. Taken together, this study shows that ketamine at a therapeutic concentration can protect against bradykinin-induced breakage of the BBB via suppressing calcium-dependent redistribution of occludin tight junctions. Thus, ketamine has the potential for maintaining the BBB in critically ill patients with severe brain disorders.


Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Bradicinina/toxicidade , Células Endoteliais/efeitos dos fármacos , Ketamina/farmacologia , Ocludina/metabolismo , Junções Íntimas/efeitos dos fármacos , Animais , Cálcio/metabolismo , Estado Terminal/terapia , Endotélio Vascular/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos ICR , Ocludina/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptor B1 da Bradicinina/genética , Receptor B1 da Bradicinina/metabolismo , Receptor B2 da Bradicinina/genética , Receptor B2 da Bradicinina/metabolismo
13.
PLoS One ; 10(10): e0140549, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26492493

RESUMO

Osteoporosis is a systemic skeletal disease characterized by a decreased bone mineral density that results in an increased risk of fragility fractures. Previous studies indicated that genetic factors are involved in the pathogenesis of osteoporosis. Polymorphisms of the FONG (FTCDNL1) gene (rs7605378) were reported to be associated with the risk of osteoporosis in a Japanese population. To assess whether polymorphisms of the FTCDNL1 gene contribute to the susceptibility and severity of osteoporosis in a Taiwanese population, 326 osteoporosis patients and 595 controls of a Taiwanese population were included in this study. Our results indicated that rs10203122 was significantly associated with osteoporosis susceptibility among female. Our findings provide evidence that rs10203122 in FTCDNL1 is associated with a susceptibility to osteoporosis.


Assuntos
Estudos de Associação Genética , Predisposição Genética para Doença , Hidroximetil e Formil Transferases/genética , Osteoporose/genética , Polimorfismo de Nucleotídeo Único/genética , Idoso , Densidade Óssea/genética , Osso e Ossos/patologia , Estudos de Casos e Controles , Demografia , Feminino , Haplótipos/genética , Humanos , Desequilíbrio de Ligação/genética , Masculino , Fatores de Risco
14.
Biomed Res Int ; 2015: 658928, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25710017

RESUMO

Propofol, an intravenous anesthetic agent, is widely used for inducing and maintaining anesthesia during surgical procedures and for sedating intensive care unit patients. In the clinic, rapid elimination is one of the major advantages of propofol. Meanwhile, the biotransformation and drug interactions of propofol in rat livers are still little known. In this study, we evaluated the ring-oxidative metabolism of propofol in phenobarbital-treated rat livers and possible drug interactions. Administration of phenobarbital to male Wistar rats significantly increased levels of hepatic cytochrome P450 (CYP) 2B1/2 and microsomal pentoxyresorufin O-dealkylase (PROD) activity. Analyses by high-performance liquid chromatography and liquid chromatography mass spectroscopy revealed that propofol was metabolized by phenobarbital-treated rat liver microsomes into 4-hydroxypropofol. In comparison, PROD activity and 4-hydroxy-propofol production from propofol metabolism were suppressed by orphenodrine, an inhibitor of CYP2B1/2, and a polyclonal antibody against rat CYP2B1/2 protein. Furthermore, exposure of rats to propofol did not affect the basal or phenobarbital-enhanced levels of hepatic CYP2B1/2 protein. Meanwhile, propofol decreased the dealkylation of pentoxyresorufin by phenobarbital-treated rat liver microsomes in a concentration-dependent manner. Taken together, this study shows that rat hepatic CYP2B1/2 plays a critical role in the ring-oxidative metabolism of propofol into 4-hydroxypropofol, and this anesthetic agent can inhibit CYP2B1/2 activity without affecting protein synthesis.


Assuntos
Hidrocarboneto de Aril Hidroxilases/metabolismo , Citocromo P-450 CYP2B1/metabolismo , Fígado/metabolismo , Fenobarbital/administração & dosagem , Propofol/farmacocinética , Espécies Reativas de Oxigênio/metabolismo , Esteroide Hidroxilases/metabolismo , Animais , Biotransformação , Interações Medicamentosas , Ativação Enzimática/efeitos dos fármacos , Fígado/efeitos dos fármacos , Masculino , Oxirredução/efeitos dos fármacos , Fenobarbital/farmacocinética , Propofol/administração & dosagem , Ratos , Ratos Wistar
15.
J Clin Monit Comput ; 29(6): 801-6, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25708672

RESUMO

Heart rate variability (HRV) is a well-known method for the assessment of autonomic nervous function of the heart. Previous study suggested that pulse rate variability (PRV) determined by photoplethysmography could be used instead of HRV to more simply assess autonomic nervous function. However, most research studies included healthy subjects. Thus, the aim of this study was to investigate the feasibility for PRV as a surrogate index for patients with chronic pain. This study investigated the correlation coefficient (by Pearson correlation) and agreement (by Bland-Altman analysis) between PRV and HRV in chronic pain patients in the clinical setting. The results showed high significant correlations (p < 0.001, r > 0.86) between all the HRV and PRV parameters and good agreements (ratio < 0.1) between the parameters in terms of HR, mean RR, VLF, LF, nLF, nHF, and SD1/SD2. Our study suggests that HRV can also be reliably estimated using the photoplethysmography-based PP interval in elderly patients with chronic pain.


Assuntos
Dor Crônica/fisiopatologia , Frequência Cardíaca/fisiologia , Fotopletismografia/métodos , Adulto , Análise de Variância , Eletrocardiografia/estatística & dados numéricos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fotopletismografia/estatística & dados numéricos
16.
J Agric Food Chem ; 62(15): 3466-75, 2014 Apr 16.
Artigo em Inglês | MEDLINE | ID: mdl-24694235

RESUMO

The blood-brain barrier (BBB) maintains brain microenvironment. Our previous study showed that oxidized low-density lipoprotein (oxLDL) can damage the BBB by inducing apoptosis of cerebrovascular endothelial cells. This study was aimed at evaluating the effects of resveratrol on high-fat diet-induced insults to the BBB and brain neurons. Exposure of mice to a high-fat diet for 8 weeks increased levels of serum total cholesterol (146 ± 13) and LDL (68 ± 8), but resveratrol decreased such augmentations (119 ± 6; 45 ± 8). Permeability assays showed that a high-fat diet induced breakage of the BBB (88 ± 21). Meanwhile, resveratrol alleviated this interruption (16 ± 6). Neither resveratrol nor a high-fat diet caused the death of cerebrovascular endothelial cells. Instead, exposure to a high-fat diet disrupted the polymerization of occludin and zonula occludens (ZO)-1, but resveratrol significantly attenuated those injuries. Neither a high-fat diet nor resveratrol changed the levels of occludin or ZO-1 in brain tissues. Resveratrol protected brain neurons against high-fat diet-induced caspase-3 activation and genomic DNA fragmentation. This study shows that resveratrol can attenuate the high-fat diet-induced disruption of the BBB via interfering with occludin and ZO-1 tight junctions, and protects against apoptotic insults to brain neurons.


Assuntos
Apoptose/efeitos dos fármacos , Barreira Hematoencefálica/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Dieta Hiperlipídica/efeitos adversos , Arteriosclerose Intracraniana/prevenção & controle , Neurônios/citologia , Estilbenos/administração & dosagem , Animais , Barreira Hematoencefálica/metabolismo , Encéfalo/citologia , Encéfalo/metabolismo , Gorduras na Dieta/metabolismo , Humanos , Arteriosclerose Intracraniana/tratamento farmacológico , Arteriosclerose Intracraniana/metabolismo , Arteriosclerose Intracraniana/fisiopatologia , Masculino , Camundongos , Camundongos Endogâmicos ICR , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Resveratrol
17.
Biomed Res Int ; 2014: 980657, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24689067

RESUMO

BACKGROUND: Traumatic brain injuries (TBIs) are a major health care problem worldwide. Approximately 1.5 million new TBI cases occur annually in the United States, with mortality rates ranging between 35% and 40% in severe patients. Despite the incidence of these injuries and their substantial socioeconomic implications, no specific pharmacological intervention is available for clinical use. Several studies have indicated that 300 mg/kg or 400 mg/kg of valproate (VPA) exhibits neuroprotective effects in animal models. However, humans cannot tolerate high doses of VPA. This study aims to investigate whether 30 mg/kg of VPA administered to rats affects TBIs. METHODS: We used a rat model to test the effects of 30 mg/kg of VPA on TBIs. Molecular identifications for histone acetylation and phosphorylation of cAMP response element-binding protein (CREB) and phosphorylated extracellular signal regulated kinase (ERK) were performed. RESULTS: The results indicated that treating adult rats with VPA after TBIs significantly decreased the contusion volume and recovery of contusion-related skilled forelimb reaching deficits. Applying VPA also increased histone acetylation, p-ERK, and p-CREB expression in the brain. Furthermore, applying VPA reduced inflammation, glial fibrillary acidic protein activation, and apoptosis. Conclusion. This study found that 30 mg/kg of VPA assists in treating TBIs in rat models.


Assuntos
Lesões Encefálicas/tratamento farmacológico , Lesões Encefálicas/fisiopatologia , Atividade Motora/efeitos dos fármacos , Ácido Valproico/administração & dosagem , Ácido Valproico/uso terapêutico , Acetilação/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Lesões Encefálicas/metabolismo , Lesões Encefálicas/patologia , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Relação Dose-Resposta a Droga , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Proteína Glial Fibrilar Ácida/metabolismo , Histonas/metabolismo , Humanos , Inflamação/patologia , Masculino , Fosforilação/efeitos dos fármacos , Ratos Sprague-Dawley , Ácido Valproico/farmacologia
18.
Br J Nutr ; 111(1): 55-63, 2014 Jan 14.
Artigo em Inglês | MEDLINE | ID: mdl-23829885

RESUMO

Oestrogen and oestrogen receptors (ER) play critical roles in the maintenance of bone remodelling. Genistein, structurally similar to 17ß-oestradiol, is a phyto-oestrogen that may be beneficial for treating osteoporosis. In the present study, we evaluated the effects of genistein on the regulation of ERα gene expression and osteoblast mineralisation using MC3T3-E1 cells and primary rat calvarial osteoblasts as our experimental models. Exposure of MC3T3-E1 cells and primary rat osteoblasts to genistein at ≤ 10 µm for 24 h did not affect the cell morphology or viability. However, treatment of MC3T3-E1 cells with 10 µm-genistein enhanced the phosphorylation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase 1/2 in a time-dependent manner. Sequentially, genistein increased the translocation of NF-κB and c-Jun from the cytoplasm to the nucleus. Consequently, exposure of MC3T3-E1 cells to genistein induced ERα mRNA expression in concentration- and time-dependent manners. In parallel, the amounts of cytosolic and nuclear ERα in MC3T3-E1 cells were increased following genistein administration. Additionally, genistein also increased the levels of ERα mRNA and nuclear ERα protein in rat calvarial osteoblasts. A bioinformatic search revealed that there are several ERα-specific DNA-binding elements in the 5'-promoter regions of the bone morphogenetic protein-6, collagen type I and osteocalcin genes. As a result, genistein could induce the expressions of these osteoblast differentiation-related genes in primary rat osteoblasts. Co-treatment with genistein and traditional differentiation reagents synergistically increased osteoblast mineralisation. Therefore, the present study showed that genistein can induce ERα gene expression via the activation of MAPK/NF-κB/activator protein-1 and accordingly stimulates differentiation-related gene expressions and osteoblast mineralisation.


Assuntos
Receptor alfa de Estrogênio/genética , Genisteína/farmacologia , Proteínas Quinases Ativadas por Mitógeno/metabolismo , NF-kappa B/metabolismo , Osteoblastos/efeitos dos fármacos , Osteogênese/efeitos dos fármacos , Fator de Transcrição AP-1/metabolismo , Células 3T3 , Animais , Proteína Morfogenética Óssea 6/genética , Proteína Morfogenética Óssea 6/metabolismo , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/genética , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Relação Dose-Resposta a Droga , Receptor alfa de Estrogênio/metabolismo , Fabaceae/química , Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Camundongos , Osteoblastos/metabolismo , Osteocalcina/genética , Osteocalcina/metabolismo , Osteogênese/genética , Fosforilação , Fitoestrógenos/farmacologia , Extratos Vegetais/farmacologia , Regiões Promotoras Genéticas , RNA Mensageiro/metabolismo , Ratos
19.
PLoS One ; 8(8): e72404, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23940812

RESUMO

Lipopolysaccharide (LPS) is a critical factor for inducing acute lung injury. GATA-2, a transcription factor, contributes to the control of cell activity and function. Exposure of RAW 264.7 cells to LPS induced interleukin (IL)-1ß mRNA and protein expression and GATA-2 translocation from the cytoplasm to nuclei in concentration- and time-dependent manners. A bioinformatic search revealed that GATA-2-specific binding elements exist in the 5'-promoter region of the il-1ß gene. LPS could enhance the transactivation activity of GATA-2 in macrophages. Knocking-down translation of GATA-2 mRNA using RNA interference significantly alleviated LPS-induced IL-1ß mRNA and protein expression. As to the mechanism, transfection of toll-like receptor (TLR) 4 small interfering (si)RNA into macrophages concurrently decreased LPS-caused increases in nuclear GATA-2 levels. Sequentially, treatment with myeloid differentiation factor 88 (MyD88) siRNA decreased LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs) kinase 1/2 and subsequent translocation of GATA-2. Reducing MAPK activities using specific inhibitors simultaneously decreased GATA-2 activation. Furthermore, exposure of primary macrophages to LPS significantly increased the transactivation activities of GATA-2 and IL-1ß mRNA and protein expression. Transfection of GATA-2 siRNA inhibited LPS-induced IL-1ß mRNA expression. Results of this study show that LPS induction of il-1ß gene expression in macrophages is mediated by GATA-2 via activation of TLR4, MyD88, and MAPKs.


Assuntos
Fator de Transcrição GATA2/fisiologia , Interleucina-1beta/genética , Lipopolissacarídeos/farmacologia , Macrófagos Peritoneais/efeitos dos fármacos , Fator 88 de Diferenciação Mieloide/fisiologia , Receptor 4 Toll-Like/fisiologia , Animais , Células Cultivadas , Fator de Transcrição GATA2/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Interleucina-1beta/metabolismo , Sistema de Sinalização das MAP Quinases/fisiologia , Macrófagos Peritoneais/metabolismo , Camundongos , Transporte Proteico/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia
20.
Respir Res ; 13: 88, 2012 Oct 03.
Artigo em Inglês | MEDLINE | ID: mdl-23031213

RESUMO

BACKGROUND: Lipoteichoic acid (LTA), a gram-positive bacterial outer membrane component, can cause septic shock. Our previous studies showed that the gram-negative endotoxin, lipopolysaccharide (LPS), could induce surfactant protein-A (SP-A) production in human alveolar epithelial (A549) cells. OBJECTIVES: In this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms. METHODS: A549 cells were exposed to LTA. Levels of SP-A, nuclear factor (NF)-κB, extracellular signal-regulated kinase 1/2 (ERK1/2), and mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1 were determined. RESULTS: Exposure of A549 cells to 10, 30, and 50 µg/ml LTA for 24 h did not affect cell viability. Meanwhile, when exposed to 30 µg/ml LTA for 1, 6, and 24 h, the biosynthesis of SP-A mRNA and protein in A549 cells significantly increased. As to the mechanism, LTA enhanced cytosolic and nuclear NF-κB levels in time-dependent manners. Pretreatment with BAY 11-7082, an inhibitor of NF-κB activation, significantly inhibited LTA-induced SP-A mRNA expression. Sequentially, LTA time-dependently augmented phosphorylation of ERK1/2. In addition, levels of phosphorylated MEK1 were augmented following treatment with LTA. CONCLUSIONS: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway.


Assuntos
Células Epiteliais Alveolares/metabolismo , Lipopolissacarídeos/farmacologia , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , NF-kappa B/metabolismo , Proteína A Associada a Surfactante Pulmonar/biossíntese , Ácidos Teicoicos/farmacologia , Células Epiteliais Alveolares/efeitos dos fármacos , Técnicas de Cultura de Células , Sobrevivência Celular/efeitos dos fármacos , Humanos , Immunoblotting , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais
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