Objective To investigate atypical lymphocyte and lymphocyte subsets in children with infectious mononucleosis(IM)and its relationship with the clinical symptoms by retrospective method.Methods Two hundred and six children were diagnosed as infectious mononucleosis.Atypical types,lymphocyte subsets,and clinical symp-toms and their relationship were evaluated and analyzed.Results In the IM children CD +3 increased,CD +3 CD +4 decreased,CD +3 CD +8 increased and NK cells decreased.The control group was (64.23 ±6.26 )%,(32.96 ± 8.68)%,(20.25 ±7.45)%,(14.68 ±5.4)%,the IMgroup was (84.13 ±14.64)%,(18.45 ±5.14)%,(54.46 ± 16.82)%,(4.65 ±1.50)%,the difference was statistically significant(P <0.001).92.9% patients had more 10%atypical lymphocytes.The children with more than 20% atypical lymphocytes had higher CD +3 CD +v8 and NK cells decreased,(58.78 ±16.67)%,(3.28 ±1.57)%.The difference with the atypical cells more than 10% less than 20% and the group less than 10% has statistically sighnificant which were (54.53 ±15.12)%,(4.55 ±1.64)%, (50.25 ±14.23)%,(5.13 ±1.84)% (P <0.001).The serious type of IM children had higher ratio of increased CD +3 CD +8 and decreased NK cells and had statistically significant compared with the light group,which were (57.78 ± 15.45)%,(3.18 ±1.61)%,(51.09 ±12.26)%,(4.68 ±1.82)%,(20.25 ±7.45)%,(14.68 ±5.46)%(P <0.001).Conclusion The infectious mononucleosis can cause abnormal immune functions.The ratio of atypical lym-phocytes,CD +3 ,CD +3 CD +4 ,CD +3 CD +8 and NK cells numbers can be viewed as a monitoring index of the disease.

Problem-based learning (PBL) teaching method combined with formative evalua-tion was used in the teaching practice of pediatrics education. This method was implemented by four phases: courses designing, group-preparing, problems-organizing and teaching practice. The method was evaluated by students' feedback and survey results of patients, teachers and teaching councilors. It was showed that the teaching effects of PBL combined with formative evaluation was better than tra-ditional teaching method in pediatrics teaching.

The effects of ketamine on transient outward potassium current (I(to)) of isolated human atrial myocytes were investigated to understand the mechanism of part of its effects by whole-cell patch-clamp. Atrial myocytes were enzymatically isolated from specimens of human atrial appendage obtained from patients under going cardiac valve displacing. Ito is recorded in voltage-clamp modes using the patch-clamp technique at room temperature. Currents signals were recorded by an Axopatch 200B amplifier with the Digidata 1322A-pClamp 9.0 data acquisition system. Ketamine decreased I(to) of human atrial myocytes in a dose-dependent manner. The current-voltage curve was significantly lowered, 30, 100, 300, and 1000 micromol x L(-1) ketamine decreased respectively I(to) current density about (13.62 +/- 0.04)%, (38.92 +/- 0.05)%, (72.24 +/- 0.10)% and (83.84 +/- 0.05)% at the potential of 50 mV, with an IC50 of 121 micromol x L(-1). The I(to) activation curve, inactivation curve and the recovery curve were not altered by ketamine. So, ketamine concentration-dependently decreased I(to) of human atrial myocytes.

AIM: To investigate the primary culture method for coronary artery smooth muscle cells (CASMCs), and to establish the endoplasmic reticulum stress ( ERS) model in CASMCs of SD rats.METHODS:CASMCs were cultured by tissue explant method .The morphological characteristics were observed under optical micro-scope.The marker proteins of CASMCs , including α-SMA and SM-MHC, were identified by immunofluorescence tech-nique.The protein expression levels of BiP and CHOP , the marker molecules of ERS, were determined by Western blot . RESULTS:The spindle-shaped CASMCs climbed out from the edge of coronary artery tissues after 6 d, and formed the typical hill and valleygrowth pattern of CASMCs at 9~10 d.The result of immunofluorescence technique showed that α-SMA and SM-MHC were positively expressed .The results of Western blot showed that the protein expression of BiP and CHOP in TG ( 1 and 2 μmol/L ) treatment groups was increased compared with control group .Compared with control group, the protein expression of BiP and CHOP was significantly increased after 1 μmol/L TG treatment for 24 and 48 h. CONCLUSION:CASMCs can be successfully cultured by tissue explant method .ERS model of CASMCs was established by 1 μmol/L TG treatment for 24 h.

Objective To introduce inhaled inactivated-mycobacterium phlei on prevention and treatment of moderate bronchial asthma to observe the clinical effect. Method This study was a prospective and controlled study. The patients diagnosed with asthma in our out-patient from March 2009 to December 2010 were collected, who met the following conditions were included in the study: age≥ 14 years; met the criteria of moderate chronic persistent bronchial asthma in Global Initiative for Asthma (GINA) in 2008; suspended receiving systemic corticosteroids, Montelukast, ketotifen and other anti-inflammatory and anti-allergic drugs in one month; no significant respiratory tract infections; and other serious illnesses or abnormalities known.A total of 100 patients with asthma were selected, including 37 males and 63 females, age (32.11 ± 12.95 )years. The patients were randomly(random number) divided into two groups: A group(treatment group; 16males and 34 females, age 33.56 ± 14.23 years) and B group (control group; 21 males and 29 females,age 30.66 ± 11.50 years); 50 in each group. No significant difference was noted between the two groups on age and gender composition. The patients in A group were treated with inhaled inactivated-mycobacterium phlei F. U. 36 Injection 1.72 μg/mL × 2 that adding 3 mL normal saline, once a day for 5 days. The patients in B group were treated with salmeterol xinafoate and fluticasone propionate powder for inhalation (50/100 μg), twice daily for sustainable use. The patients in the two groups were observed for one month. During this course, the patients in the two groups could inhale the salbutamol sulphate aerosol as need to relieve symptoms. And the number of using was recorded. Pulmonary function test and asthma provocative test were carried out on the Day O, 6 and 31. ACT scores were measured before and after the treatment. Results On Day 6 and 31 after treatment, the negative conversion rates of asthma provocative test of the patients in A group were 82% and 78% respectively, B group were 84% and 90% respectively. Provocative test of the patients in the two groups were negative conversion significantly before and after treatment. There was no significant difference between the two groups by chi-square test (P ＞ 0. 05 ). Completely random designed data was analyzed by analysis of variance. The analysis showed that the accumulated doses of methacholine of the patients in the two group increased significantly ( P ＜ 0. 05 ), but no difference between the two groups.There was a improvement trend on forced expiratory volume in one second( FEV1 )of the patients in A group after treatment, but no difference. FEV1 of the patients in B group increased significantly higher ( P ＜0.05), which was significantly higher than A group on the 31th day (P ＜0. 05); Peak expiratory flow (PEF) of the patients in the two group increased significantly on Day 6 and 31 after treatment (P ＜0.05 ).On Day 31, B group was significantly higher than A group ( P ＜ 0. 05 ); Scores of asthma control test (ACT)of the patients in the two group were significantly increased, and the number of using of salbutamol sulfate aerosol was significantly reduced (P ＜0.01 ). B group was obvious than group A (P ＜0.05 ). During treatment, there were only two adverse reaction cases of transient low fever; most obvious was on the third day.Conclusions Inhaled inactivated-mycobacterium phlei would inhibit the airway hyperresponsiveness of the patients with moderate bronchial asthma in short time, improve the symptoms, reduce the acute exacerbation, and reduce the use of rescue medication, which has the roles of prevention and treatment of moderate asthma in a certain period of time.

OBJECTIVETo investigate the reactivity of intrapulmonary arterial rings to vasoactive substances as thromboxane A2 and endothelin-1 in patients with chronic obstructive pulmonary disease (COPD).

METHODSIntrapulmonary arterial rings isolated from patients with normal lung function and COPD were mounted in a Multi Myograph system to determine the reactivity of the intrapulmonary arterial rings to 60 mmol/L KCl, thromboxane A2 analogue U46619 and endothelin-1 before and after preconditioning with the COX synthase inhibitor indomethacin.

RESULTSThe reactivity of intrapulmonary arterial rings to U46619 and endothelin-1 was significantly decreased in patients with COPD. The reactivity to U46619 was dramatically decreased in patients with normal lung function after application of indomethacin.

CONCLUSIONThe reactivity of intrapulmonary arterial rings is significantly decreased in patients with COPD.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ; pharmacology ; Aged ; Endothelin-1 ; metabolism ; Female ; Humans ; In Vitro Techniques ; Indomethacin ; pharmacology ; Male ; Middle Aged ; Pulmonary Artery ; metabolism ; Pulmonary Disease, Chronic Obstructive ; metabolism ; Thromboxane A2 ; metabolism

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from 10–300 µM). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations (10–100 µM) followed by secondary relaxation (at 100–300 µM). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed CaCl₂-induced constriction in the 60 mM K⁺-containing Ca²⁺-free solution in a dose-dependent manner. Fluorescent imaging of Ca²⁺ using fluo-4 showed that a 10 min incubation with propofol (10–300 µM) inhibited the Ca²⁺ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM K⁺-containing Ca²⁺-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ; Arteries ; Calcium ; Calcium Channels ; Constriction ; Endothelium ; Humans* ; Indomethacin ; Myocytes, Smooth Muscle ; Propofol* ; Prostaglandin-Endoperoxide Synthases ; Pulmonary Artery* ; Relaxation ; Vasoconstriction* ; Vasodilation

AIM:To investigate whether the association of connexin 43 ( Cx43 ) and L-type calcium channel involved in the pathogenesis of atrial fibrillation ( AF) .METHODS:The biochemical assays and whole-cell patch-clamp technique were used to study the expression of Cx43 in human atrial tissue.The co-localization of Cx43 and L-type calcium channel, and the regulation of L-type calcium current in atrial myocytes were investigated.RESULTS:The expression of Cx43 at mRNA and protein levels was decreased in human atrial tissues of AF patients.In cultured atrium-derived myocytes ( HL-1 cells) , knockdown of Cx43 significantly inhibited the mRNA expression of L-type calcium channelα1c subunit, as well as L-type calcium current.Co-localization of Cx43 with L-type calcium channel α1c subunit in mouse atrial myocytes was observed.CONCLUSION:The decrease in Cx43 is involved in the pathogenesis of AF, probably through reducing the L-type calcium current in atrial myoctyes by co-localization with L-type calcium channel, thus representing the potential pathogenesis in atrial fibrillation.

AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .

OBJECTIVETo investigate the effect of dexmedetomidine on 5-HT-induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms.

METHODSLung tissue was obtained from patients undergoing surgery for lung carcinoma. Intrapulmonary arteries were dissected and cut into rings, which were mounted in a Multi Myograph system to determine the effect of dexmedetomidine (0.3-3 nmol/L) on 5-HT-induced vasoconstrictions. The influences of the endothelium removal and various drugs including L-NAME, yohimbine and indomethacin were tested on the effects of dexmedetomidine.

RESULTSDexmedetomidine (0.1-100 nmol/L) did not obviously affect the resting tension of endothelium-intact human intrapulmonary arteries. 5-HT induced concentration-dependent contraction in endothelium-intact intrapulmonary arteries [pD2: 6.11∓0.05, Emax: (102.10∓1.96)%]. In the rings with intact endothelium, dexmedetomidine (0.3-3 nmol/L) significantly attenuated the Emax and pD2 of 5-HT-induced vasoconstriction [pD2: 5.94∓0.03, Emax: (79.96∓1.31)%]. 5-HT also induced concentration-dependent contraction in endothelium-denuded intrapulmonary arteries [pD2: 6.10∓0.07, Emax: (107.40∓3.20)%]. Dexmedetomidine produced no significant effects on the rings with denuded endothelium. The effects of dexmedetomidine on 5-HT-induced vasoconstriction was suppressed by L-NAME and yohimbine, but not by indomethacin.

CONCLUSIONDexmedetomidine can inhibit 5-HT-induced vasoconstriction of isolated human intrapulmonary arteries probably through α2-adrenergic acceptor and NO released from the endothelium.

Adult ; Aged ; Dexmedetomidine ; pharmacology ; Female ; Humans ; In Vitro Techniques ; Male ; Middle Aged ; Pulmonary Artery ; drug effects ; Serotonin ; pharmacology ; Vasoconstriction ; drug effects