Only in Titles

           Search results for: Brains    

paperclip

#32061194   // Save this To Up

Pathogenesis of obstructive sleep apnea in individuals with the COPD + OSA Overlap syndrome versus OSA alone.

Overlap syndrome (OVS) is the concurrence of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA), and is associated with poor outcomes. We hypothesized that physiological changes in COPD may affect the pathogenesis of OSA in important ways. We therefore sought to measure the anatomical and nonanatomical OSA traits in individuals with OVS and compare to those with OSA alone. Patients with established OVS were recruited, along with age, gender, and BMI matched OSA only controls. Smoking and relevant comorbidities or medications were excluded. Subjects underwent baseline polysomnography followed by an overnight physiological research study to measure the OSA traits (V , V , V , V , and loop gain). Fifteen subjects with OVS and 15 matched controls with OSA alone were studied (overall 66 ± 8 years, 20% women, BMI 31 ± 4 kg/m , apnea-hypopnea index 49 ± 36/hr). Mixed-modeling was used to incorporate each measurement (range 52-270 measures/trait), and account for age, gender, and BMI. There were no significant differences in the traits between OVS and OSA subjects, although OVS subjects potentially tolerated a lower ventilation before arousal (i.e., harder to wake; p = .06). Worsened lung function was significantly associated with worsened upper airway response and more unstable breathing (p < .05 for all). Consistent differences in key OSA traits were not observed between OVS and OSA alone. However, worse lung function does appear to exert an influence on several OSA traits. These findings indicate that a diagnosis of OVS should not generally influence the approach to OSA, but that lung function might be considered if utilizing OSA trait-specific treatment.

1323 related Products with: Pathogenesis of obstructive sleep apnea in individuals with the COPD + OSA Overlap syndrome versus OSA alone.



Related Pathways

paperclip

#   // Save this To Up


2031 related Products with:



Related Pathways

  •  
  • No related Items
paperclip

#32061171   // Save this To Up

Inhibition of MiR-122 Decreases Cerebral Ischemia-reperfusion Injury by Upregulating DJ-1-Phosphatase and Tensin Homologue Deleted on Chromosome 10 (PTEN)/Phosphonosinol-3 Kinase (PI3K)/AKT.

BACKGROUND Ischemia-reperfusion injury is caused by a blood reperfusion injury in ischemic brain tissue, and usually occurs in the treatment stage of ischemic disease, which can aggravate brain tissue injury. MiR-122 is closely related to ischemia-reperfusion injury in the myocardium, kidney, and liver; however, the role in cerebral ischemia-reperfusion injury has not been established. MATERIAL AND METHODS In this study, cerebral ischemia-reperfusion injury was established in a rat model, and the control group was a sham-operated group. After ischemia-reperfusion injury for 6, 12, and 24 hours, brain tissue specimens were collected and the expression of miR-122 and DJ-1 were determined using quantitative real-time polymerase chain reaction. Flow cytometry was used to determine the reactive oxygen species (ROS) content. The modified Neurological Severity Score (mNSS) scale was used to evaluate the sensory and motor function defects of the rats. The malondialdehyde (MDA), superoxide dismutase (SOD), and enzyme activity were determined. The rats in the cerebral ischemia-reperfusion injury model were divided into 2 groups (antagomir-NC group and antagomir miR-122 group). Brain neuron RN-c cells were divided into the following 4 groups: antagomir-NC, antagomir miR-122, pIRES2-blank, and pIRES2-DJ-1. Seventy-two hours after transfection, ischemia-reperfusion treatment was carried out and conventional cultured RN-c cells were used as the control group. Flow cytometry was used to detect apoptosis and western blot was used to detect the expression of DJ-1, PTEN, AKT, and p-AKT. RESULTS The expression of miR-122 increased significantly in the process of ischemia-reperfusion damage after cerebral infarction, while the expression of DJ-1 decreased significantly. Downregulation of miR-122 significantly increased the expression of DJ-1, enhanced the activity of the PTEN/PI3K/AKT pathway, reduced cell apoptosis, and alleviated cerebral ischemia-reperfusion injury. CONCLUSIONS Inhibition of miR-122 can decrease cerebral ischemia-reperfusion injury by upregulating DJ-1-PTEN/PI3K/AKT pathway.

1434 related Products with: Inhibition of MiR-122 Decreases Cerebral Ischemia-reperfusion Injury by Upregulating DJ-1-Phosphatase and Tensin Homologue Deleted on Chromosome 10 (PTEN)/Phosphonosinol-3 Kinase (PI3K)/AKT.



Related Pathways

paperclip

#32061154   // Save this To Up

Cytotoxic and apoptotic effects of ethanolic propolis extract on C6 glioma cells.

Propolis is a natural resinous substance obtained from beehives, and emerging evidence supports that it has antitumor, antiinflammatory, antioxidant, and antimicrobial activities. The aim of the study is to examine the cytotoxic, antioxidant, and apoptotic features of ethanolic propolis extract (PE) on C6 glioma cells. The cells were treated with ethanolic PE at various concentrations for 24 hours, after which the total antioxidant status (TAS) and total oxidant status; malondialdehyde, protein carbonyl, 8-hydroxy-2'-deoxyguanosine, and glutathione (GSH) levels; Cu/Zn-superoxide dismutase (Cu/Zn-SOD) activity; and apoptotic markers were measured. Ethanolic PE at 100, 250, and 500 μg/mL concentrations showed optimal activity on C6 glioma cells. TAS and GSH levels were significantly increased in C6 glioma cells treated with 100 and 500 μg/mL PE compared to control cells (P < .05). Similarly, the activity of Cu/Zn-SOD was higher in C6 glioma cells treated with 250 or 500 μg/mL ethanolic PE compared to control cells (P < .05), as was the caspase-3 mRNA expression level. The highest levels of caspase-8 and -9 expression were in C6 glioma cells treated with 500 μg/mL PE. Collectively, our results indicate that ethanolic PE has cytotoxic and apoptotic effects on C6 glioma cells. Furthermore, it may provide a protective role in the antioxidant defense system. PE shows potential for development as a natural antioxidant and apoptotic agent for the treatment of brain tumors.

2298 related Products with: Cytotoxic and apoptotic effects of ethanolic propolis extract on C6 glioma cells.

Mouse Anti-Mouse Natural Mouse Anti-Mouse NC1.1 (N AccuPrep Genomic DNA Extr Anti apoptotic marker in anti CD8 T cytotoxic supr Anti-apoptotic marker in Mouse Anti-Mouse NC1.1 (N AccuzolTM Total RNA Extra GFP Expressing Human Glom Chicken Red Blood Cells, Competent Cells for Cloni Nile Red, A lipophilic dy

Related Pathways