Objective System of pressure breathing for +Gz (PBG) has been incorporated into service in the high performance fighter aircraft,but there were significant differences among PBG pressure schedules used in different countries.The purpose of this study was to define an optimal pressure schedule in PBG system.Method Five male subjects wearing GZ-2 anti-G suit and medium-sized bladder vest,plus PBG with 1.6,2.4,and 3.2 kPa/G pressure schedules,respectively,were exposed to rapid onset (3.0 G/s) centrifuge +Gz runs.+Gz protection of PBG with each of the three pressure schedules were measured and the subjective ratings were collected.Result The +Gz protection afforded by PBG with 1.60,2.40,and 3.20 kPa/G pressure schedules were 2.00±0.31,2.54±0.32,and 2.44±0.31 G,respectively.Subjective ratings showed that the PBG with 2.40 kPa/G pressure schedule was better than the other two.Conclusion Our data suggest that a PBG pressure schedule of 2.4 kPa/G in PBG system is optimal.It not only assures the anti-G performance of PBG,but also reduces its side effects.

BACKGROUND: Aldosterone is an important pathogenic factor of left ventricular hypertrophy. There has been evidence that the extract of red sage root (a Chinese herb) can intervene the synthesis of aldosterone.OBJECTIVE: To investigate the effects of tanshinone Ⅱ A on expression of genes related to aldosterone synthesis in myocardium. DESIGN:A randomized and controlled trial. SETTING :Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS:The experiment was performed at the laboratory of Emergency Department, Tongji Hospital Affiliated to Tongji Medical College,Huazhong University of Science and Technology from November 2002 to March 2004. Totally 20 male 12-week-old rats with spontaneous hypertension were randomly divided as hypertension group and tanshinone Ⅱ A group. METHODS:Rats in each group were injected tanshinone Ⅱ A or distilled water in the same volume respectively through caudal vein. After 12-week administration,the rats were put to death by decapitation, and the samples of myocardium were prepared. The expressions of CYP11B1mRNA and CYP11B2 mRNA, or myocardial genes related to aldosterone synthesis were examined with reverse transcriptase polymerase chain reaction (RTPCR) and referring to the amplification primers of glyceraldehydes 3-phosphate dehydrogenase (GAPDH) gene. MAIN OUTCOME MEASURES:The levels of CYP11B1 and CYP11B2 mRNA related to aldosterone synthesis in myocardium.RESULTS :Totally 20 rats were involved in the trial and all entered in the final result analysis without any loss of value. ① Quantitative analysis of expression of myocardial CYP11B1 and CYP11B2 genes in rats of two groups: Taking 100bp Plus Ladder as Marker,clear amplified strands could be seen at 440bp,461bp and 336bp sites,DNA sequencing proved they were the encoding gene segments of CYP11B1,YP11B2 and GAPDH. ②Qualitative analysis of expression of myocardial CYP11B1 and CYP11B2 genes in rats of two groups:The expressive levels of CYP11B1 and CYP1 1B2 mRNA contents in tanshinone Ⅱ A group were significantly lower than those in hypertension group (0.924±0.121 vs 1.343±0.132,P ＜ 0.05;1.017±0.119 vs 1.675±0.126,P 0.01). CONCLUSION:Tanshinone Ⅱ A could directly down-regulate the expression of CYP1 1B1 and CYP1 1B2 mRNA, the genes related to aldosterone syn thesis, so that it inhibited the biological synthesis of aldosterone in myocardinm, thus playing a role to resist hypertensive left ventricular hypertrophy.

This study aimed to construct recombinant adenovirus expressing Epstein-Barr nuclear antigen 1 (EBNA1) against nasopharyngeal carcinoma (NPC). The C-terminal region fragment of the ebna1 gene of Epstein-Barr virus was amplified from the standard strain B95-8 by polymerase chain reaction (PCR). The gene fragment was inserted into the pDC316 shuttle plasmid using the EcoRI and BgIII restriction enzyme sites. The pDC316-ebna1 shuttle plasmid and pBHG helper plasmid were cotransfected into HEK293 cells after sequencing. The soluble protein was extracted from HEK293 cells, which caused apparent cytopathic effects. The transcription and expression of the ebna1 gene were confirmed using flow cytometry and Western blotting. rAd-ebna1 titers were measured by the TCID50. rAd-ebna1 was injected into BALB/c mice at a dose of 2 x 10(8) VP per mouse, EBNA1 epitope-specific responses were measured at 1st, 2nd, 4th and 8th weeks post-immunization. The target fragment of ebna1 (939 bp) was obtained by PCR, and was in consensus with the sequence from the standard strain B95-8. Cytopathic effects were observed after the pDC316-ebna1 shuttle plasmid and pBHG helper plasmid were cotransfected into HEK293 cells. rAd-ebna1 was successfully recombined in HEK293 cells. EBNA1 protein was detected in HEK293 cells, rAd-ebna1 titers reached 10(8) TCID50/mL. Specific responses to CD4+ epitopes of EBNA1 were detected in the immunized mice. In conclusion, rAd-ebna1 was successfully constructed and induced specific responses to CD4+ epitopes of EBNA1 in immunized mice.
Adenoviridae ; genetics ; immunology ; Animals ; CD4-Positive T-Lymphocytes ; immunology ; virology ; Epstein-Barr Virus Infections ; immunology ; prevention & control ; virology ; Epstein-Barr Virus Nuclear Antigens ; administration & dosage ; genetics ; immunology ; Genetic Vectors ; genetics ; immunology ; Herpesvirus 4, Human ; genetics ; immunology ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Viral Proteins ; administration & dosage ; genetics ; immunology

Objective To investigate the effects of penehyclidine hydrochloride (PHC) on acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats.Methods Forty male SpragueDawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 4 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma combined with hemorrhagic shock and resuscitation group (group THSR),PHC for prevention group (group P1)and PHC for treatment group (group P2).ALI was induced by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs in anesthetized rats in THSR,P1 and P2 groups.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In P1 group,PHC 2 mg/kg was injected intravenously at 30 min before blunt chest trauma.In P2 group,PHC 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,arterial blood samples were obtained for blood gas analysis and for measurement of concentrations of interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum by ELISA.Oxygenation index (OI) was calculated.The animals were sacrificed and bronchoalveolar lavage fluid (BALF) was collected for determination of white blood cell count and protein concentrations.Lungs were removed for examination of pathological changes and ultrastructure and for determination of Toll-like receptor (TLR4) and phosphor-p38 mitogen activated protein kinase (p-p38MAPK) expression (by Western blot).Results Compared with group S,PaO2 and OI were significantly decreased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-1β concentrations in serum were increased,and TLR4 and p-p38MAPK expression was up-regulated in THSR,P1 and P2 groups.Compared with group THSR,PaO2 and OI were significantly increased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-lβ concentrations in serum were decreased,TLR4 and p-p38MAPK expression was down-regulated in P1 and P2 groups.No significant differences were found in the parameters mentioned above between P1 and P2 groups.Conclusion PHC can mitigate acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats,and inhibited activation of TLR4/ p38MAPK signaling pathway and attenuated inflammatory responses are involved in the mechanism.

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

Objective To investigate the effects of penehyclidine hydrochloride on Fas/FasL expression during acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male SPF Sprague-Dawley rats, aged 8 weeks, weighing 245-275 g, were randomly assigned into 3 equal groups using a random number table: sham operation group (group Sham) , blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloric group (group PHCD).The model of acute lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until mean arterial pressure was decreased to 35-45 mmHg within 15 min, and maintained at this level for 60 min, followed by resuscitation.In PHCD group, PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established, the rats were sacrificed, the lungs were then removed for microscopic examination of pathologic changes and for determination of Fas, FasL and caspase-8 expression, and interleukin-6 (IL-6) and IL-1β contents in lung tissues.Apoptotic index was calculated.Results Compared with group Sham, the expression of Fas, FasL and caspase-8 was significantly up-regulated, and AI and contents of IL-6 and IL-1β were increased in THSR and PHCD groups (P＜O.05).Compared with group THSR, the expression of Fas, FasL and caspase-8 was significantly down-regulated,and AI and contents of IL-6 and IL-1β were decreased in group PHCD (P＜0.05).The pathologic changes of lungs were significantly reduced in group PHCD compared with group THSR.Conclusion The mechanism by which penehyclidine hydrochloride inhibits lung cell apoptosis induced by blunt chest trauma-HSR is associated with inhibition of Fas/FasL expression in rats.

A systematic review was undertaken, including studies that evaluated the incidence of the blood system adverse events of Tripterygium wilfordii (TWP). Medline, Embase and the Cochrane library were searched for relevant studies, including RCT, cohort studies and case series, of patients treated with TWP published in English and Chinese from inception up until May 25th, 2013 with the keywords including "Tripterygium wilfordii", "toxicity", "reproductive", "side effect", "adverse", "safety" and "tolerability". Relevant information was extracted and the incidence of the blood system adverse events was pooled with MetaAnalyst software. Besides, subgroup and sensitivity analyses were performed based on age, mode of medicine, observation time and disease system. According to inclusion and exclusion criteria, a total of 49 articles were included in the meta-analysis, they were split into 54 researches incorporated in the analysis. There is a large degree of heterogeneity among the studies, so data was analyzed using random-effects model and the summary estimates of incidence of the blood system adverse events was 6.1%. The weighted combined incidence of three major blood system adverse events were white-blood cells decreasing 5.6% (95% CI, 4.3% - 7.3%), hemoglobin decreasing 1.7% (95% CI, 0.5% - 5.0%) and platelet decreasing 1.8% (95% CI, 1.0% - 3.1%), respectively . Sensitivity analyses based on 45 studies with high quality showed the combined value was close to the summary estimate of total 54 studies. The current evidence indicates that the incidence of the blood system adverse events induced by TWP was high; attentions should be paid on to the prevention and treatment of the blood system adverse events.
Blood Cells ; drug effects ; Hemoglobins ; analysis ; Humans ; Tripterygium ; adverse effects

Objective To investigate the relationship between high-sensitivity C-reactive protein(hsCRP), pulse pressure(PP) and microalbuminuria(MAU) in patients with essential hypertension.Methods Consecutive 60 patients with essential hypertension were classified based on the MAU level:patients with MAU(n=30) and the group of patients with normoalbuminuria(NMAU,n=30) with 30 healthy subjects as control.MAU,hsCRP,PP were determined.Results The level of hsCRP and pulse pressure in MAU group were higher than those in NMAU patients and healthy subjects (P

Abstract: Objective　To analyze the laboratory indexes of patients infected with malaria patients and COVID-19, so as to provide reliable evidence for the diagnosis of mixed infection of both. Methods　The routine clinical laboratory items such as routine blood, biochemistry and lymphocyte subsets were tested in three cases of COVID-19 complicated with falciparum malaria who admitted to Guangzhou Eighth People's Hospital Affiliated to Guangzhou Medical University from July to December 2020 were tested. Laboratory data were stage-wise analyzed in conjunction with changes in the course of disease. Results　Three patients confirmed COVID-19 infection recruited all had malaria infection history. Fever, headache, and other symptoms emerged on the 4rd to 11th day after admission. Malaria parasite was detected by malaria parasite antigen testing and blood smear testing, and all three patients had re-ignition of malaria after being confirmed COVID-19 infection. In the early stage of malaria relapse, lymphocytes decreased, CRP and SAA increased, and gradually returned to normal level after antimalarial treatment. Interestingly, we only found one patient at the initial stage of malaria detection showed PLT decreased, no other unnormal changes in other routine blood results (WBC, ESO) and liver function results (ALT, AST, GGT, TBIL, DBIL, CG) were found from the beginning to end course of the disease. Conclusion　COVID-19 infection may promote the resurgence of malaria, so the relapse of malaria should be monitored especially for the patient with malaria infection history who begin to develop fever and other symptoms a few days after the diagnosis of COVID-19. The inflammatory indicators would be worth able as an auxiliary judgment basis for the effective treatment of the two combined infection.

No abstract available.
Angiography* ; Glomus Tumor* ; Multidetector Computed Tomography*