Acute Disease ; Adult ; Altitude Sickness ; blood ; pathology ; Bronchoalveolar Lavage Fluid ; chemistry ; Case-Control Studies ; Humans ; Inflammation Mediators ; metabolism ; Male

Animals ; Blood Gas Analysis ; Endothelin-1 ; blood ; Hypertension, Pulmonary ; pathology ; Hypoxia ; blood ; physiopathology ; therapy ; Male ; Oxygen ; administration & dosage ; therapeutic use ; Oxygen Inhalation Therapy ; Swine

AIMTo explore whether hypoxic response and breath holding at sea level could predict acute mountain sickness (AMS).

METHODS113 men aged (19 +/- 1) years took part in this study. Blood oxygen saturation (SaO2), heart rate and blood pressure were measured during the course of breathing 10% O2 for 10 minutes and breath holding. Two days later after reaching Lasa (3 658 m altitude) by air, the symptomatic scores of AMS were evaluated. Then the relations between them were analyzed.

RESULTSThe SaO2 reduced progressively and the heart rate speeded up, while the blood pressure represented increase at first and then decrease within 10 min during the short-term hypoxia. The heart rate was lower during short-term hypoxia in subjects who developed AMS than in subjects doing well. But significant reverse correlation existed only between AMS scores and heart rate at 7th min after hypoxic breathing (r = -0.176).

CONCLUSIONLimited information can be gained on AMS score by assessing physiological responses to short-term hypoxia and breath holding at sea level.

Acute Disease ; Adolescent ; Altitude Sickness ; diagnosis ; physiopathology ; Breath Holding ; Humans ; Hypoxia ; diagnosis ; physiopathology ; Inhalation ; Male ; Pulmonary Gas Exchange ; Young Adult

[Objective]To explore the distribution and expression changes of tight junctional protein JAM-1 in rat models after intracerebral hemorrhage (ICH) and their significance.[Methods]One hundred and twenty-eighty healthy male SD rats were randomly divided into normal control group (n=16) and ICH group (n=112),and the ICH models were induced by stereotactically injecting 75 uL autologous blood into the right caudate nucleus.Seven time points after ICH (6,12,24 and 48 h,and 3,7 and 14 d after ICH,16 rats for each time point) were chosen.BBB permeability was evaluated by Evans blue dye extravasation.The distribution and expression of JAM-1 were detected by immunofluorescence and real-time quantitative PCR.[Results] As compared with that in the normal control group,BBB permeability in the ICH group significantly increased at 24 and 48 h,and 3 and 7 d after ICH (P＜0.05).JAM-1 expression decreased at blood vessels at 12,24 and 48 h after ICH,and JAM-1 expressed at the circulatingleukocytes3 dafterlCH,and abundant JAM-1 positive cells around hematoma were noted in the ED-l-positve macrophages 7 d after ICH.JAM-I mRNA significantly decreased at 12,24 and 48 h after ICH,and significantly increased 7 d after ICH as compared with that in the normal control group (P＜0.05).[Conclusion] JAM-1 experssion changes not only participate in regulation of BBB permeability but also play roles in inflammatory insult after ICH.

Marsdeniae tenacissimae extract (MTE), commonly known as Xiao-Ai-Ping in China, is a traditional Chinese herb medicine capable of inhibiting proliferation and metastasis and boosting apoptosis in various cancer cells. However, little is known about the contribution of MTE towards tumor angiogenesis and the underlying mechanism. The present study aimed to evaluate the effects of MTE on the proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) and the molecular mechanism. 3-(4,5-dimethylthiazol-2-yl)-5(3-carboxymethoxyphenyl)-2-(4-sulfopheny)-2H-tetrazolium, inner salt (MTS) and PI-stained flow cytometry assays revealed that MTE dose-dependently reduced the proliferation of HUVECs by arresting cell cycle at S phase (P < 0.05). Annexin V-FITC/PI-stained flow cytometry confirmed that MTE (160 μL·L) enhanced the apoptosis of HUVECs significantly (P < 0.001). Real-time quantitative RT-PCR and Western blot analyses showed an increase in Bax expression and a sharply decline in Bcl-2 expression; caspase-3 was activated simultaneously in a dose-dependent manner (P < 0.05). Further study observed the dose-dependent down-regulation of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2), P2Y6 receptor (P2Y6R), and chemokine (C-C motif) ligand 2 (CCL-2), along with the activation of PKC Δ and up-regulation of p53 in a dose-dependent manner in MTE-treated selected cells (P < 0.05). Collectively, the results from the present study suggested that MTE suppressed the proliferation by attenuating CCL-2-mediated VEGF/VEGFR2 interactions and promoted the apoptosis through PKCΔ-induced p53-dependent mitochondrial pathway in HUVECs, supporting that MTE may be developed as a potent anti-cancer medicine.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Human Umbilical Vein Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Marsdenia ; chemistry ; Plant Extracts ; pharmacology ; Protein Kinase C ; genetics ; metabolism ; Signal Transduction ; drug effects ; Vascular Endothelial Growth Factor A ; genetics ; metabolism ; Vascular Endothelial Growth Factor Receptor-2 ; genetics ; metabolism