Disaster Medicine ; Earthquakes ; Emergency Medicine ; General Surgery ; Humans ; Relief Work ; Wounds and Injuries ; surgery

The risk factors of traffic crash include drinking/drunk drive, accident proneness, fatigue driving, speeding, and poor vehicle quality. This article introduces the protection, emergency treatment, and basic scientific research of road traffic injury (RTI). As a public health issue, RTI is preventable, and personal factor is a key problem. It is important to establish an accurate and comprehensive RTI database, which may provide necessary information for the epidemiological research and crash prevention. The author also gives some suggestions on road traffic safety development in our country.
Accidents, Traffic ; prevention & control ; Databases, Factual ; Epidemiologic Research Design ; Humans ; Wounds and Injuries ; prevention & control ; therapy

Child, Preschool ; Dental Restoration, Permanent ; Dentition, Permanent ; Humans ; Infant ; Root Canal Therapy ; Tooth Avulsion ; therapy ; Tooth Crown ; injuries ; Tooth Extraction ; Tooth Fractures ; therapy ; Tooth Injuries ; therapy ; Tooth, Deciduous ; injuries ; Tooth, Impacted ; etiology

Humans ; Physicians ; organization & administration

Accidents, Traffic ; prevention & control ; Global Health ; Humans ; World Health Organization

Child ; Dental Restoration, Permanent ; Dentition, Permanent ; Humans ; Incisor ; diagnostic imaging ; injuries ; Male ; Orthodontic Appliances ; Orthodontic Extrusion ; Orthodontics, Corrective ; Radiography ; Tooth Avulsion ; classification ; diagnostic imaging ; therapy ; Tooth Eruption

In the recent years,the earthquake occured frequently in the whole world which caused the increased incidence of crush syndrome (CS). The four limbs and torso will be bleeding and swelling when they are prounded and crushed from the heavy objects. The necrosis of muscular tissue causes massive production of toxin which leads to a series of symptoms including hypotension ,kidney dysfunction and so on. The serious acute kidney injury (AKI) will be vital. When CS-AKI ,the ascending velocity of urea nitrogen and K+ levels in the blood is quicker than those of general AKI;many kinds of immune cells are activated to engender a great deal of inflammatory mediators;the blood dynamics is often unstable. Therefore, it is advocated that the blood purification treatment should be carried early to eliminate excessive metabolic produces in vivo,to reduce the cardiovascular complication occurrence, and to avoid the irreversible change of the kidney function.

Objective To investigate the effects of substance P (SP) pretreatment on the expression of β1-adrenoreceptor(β1-R) induced by norepinephrine (NE) in cultured neonatal rat cardiomyecytes.Methods The cardiomyocytes obtained from 1-3 day old SD rats were cultured for 72 h.The experiment was performed in 2 parts.In part 1 the cells were seeded in 15 well plate and randomly divided into 5 groups (n=3 wells each):control group (C1)and 4 NE groups were exposed to NE 10-9, 10-8,10-7,10-6 mol/L respectively (NE1,2,3,4).In part Ⅱ the.cells were seeded in 12 well plate and randomly divided into 4 groups (n=3 wells each): group I control (C2): group II NE 10-7 tool/L; group Ⅲ (SN)was pretreated with SP 10-6 mol/L 30 minbefore NE 10-7 mol/L and group IV (NSN)was treated with NK-1 receptor antagonist (NK-1 tachykinin receptor antagonist,S3144) 30 min before SP pretreatment.After exposure to NE for 3 h the expression of β1-R in the rat cardiomyecytes was detected using flow cytometry.Results In part Ⅰ the expression of β1-R was significantly higher in group NE1-3 than in control group (C1),with the highest expression in group NF3.In part Ⅱ the expression of β1-R was significantly higher in group Ⅱ (NE) than in control group (C2) while lower in group Ⅲ (SN) than in control group Ⅱ.(NE).There was no significant difference in the expression of β1-R between group Ⅰ (C2) and group Ⅲ and Ⅳ (NSN).Conclusion Substance P pretreatment can inhibit the up-regulation of β1-R expression in cultured rat cardiomyocytes induced by norepinephrine through activating NK-1 receptor.

Objective To investigate the effects of calcitonin gene-related peptide (CGRP) combined with norepinephrine (NE) on L-type calcium current (LCa-l) in rat ventricular myocytes. Methods Ventricular myocytes were isolated from SD rats (weighing 260-280 g) by retrograde perfusion of the heart via the aorta with an enzyme-containing solution as previously described. Whole-cell patch-clamp recording was made using Axopatch 200B amplifier. The cells were perfused for 1 min with Tyrode solution containing CGRP 1 × 10-7 mol/L (group CGRP) , NE 1 × 10-6 mol/L (group NE), or CGRP 1 × 10-7 mol/L + NE 1 × 10-6 mol/L (group CN) and again washed with Tyrode solution. ICa-L was recorded 1 min before and 1 min after the cells were perfused and 1 min after the cells were washed. I-V curve of ICa-L was made after the cells were perfused with solution containing CGRP or NE alone. Results CGRP significantly inhibited the peak of ICa-L, while NE significantly promoted the peak of ICa-L(P < 0.05) . The peak of ICa-L was significantly decreased 1 min after the cells were perfused in group CGRP,while increased 1 min after the cells were perfused in group NE compared with group CN ( P < 0.05). CGRP made the I-V curve of ICa-L move up-ward, while NE made the I-V curve of ICa-L move down-ward. Conclusion CGRP can weaken the promotion of ICa-L induced by NE in rat ventricular myocytes.

Objective To investigate the effects of tramadol hydrechloride pretreatment on the expression of calcitonin gene-related peptide (CGRP) in ischemic and non-ischemic myocardium following acute myocardial is-chemia in the rats. Method Eighteen adult male SD rats weighing 270 to 300 g were randomly divided into three groups(n = 6, in each): group Ⅰ ,sham operation; group Ⅱ , myocardial isehemia, and group Ⅲ, tramadol hydrochloride pretreatment. The anterior descending branch of left coronary artery was occluded(CAO)for 3 hours in rats of group Ⅱ and Ⅲ. In group Ⅲ, tramadol hydrochloride 12.5 mg·kg~(-1) was injected through caudal vein 15 minutes before CAO. At 3 hours after myocardial ischemia, the hearts were removed for determination of CGRP protein content in ischemic and non-ischemie myocardium by immuno-histochemistry and enzyme immunometric as-say, and the expression of CGRPmRNA by RT-PCR. One-way ANOVA was used for statistical analysis. ResultsOnly β-CGRPmRNA was found in rats myocardium. In the ischemic myocardium, the average light density of CGRP(0.215 ± 0. 100), positive unit (36.95 ± 1.70), concentration (39.06 ± 1.86) and expression of β-CGRP mRNA 0. 946 ± 0. 019) were significantly increased in group Ⅱ compared with those in group Ⅰ (0. 139 ± 0.006), (25.01 ± 1.03), (20.80± 1.24), (0.734±0.025) (P <0.05), and decreased markedly in group Ⅲ(0.158+0.008),(28.53±1.21),(28.58±2.10),(0.872±0.024) (P < 0.05) In the non-ischemic my-ocardium, the average hght density of CGRP(0.156 ± 0.017), positive unit(28.57 ± 2.23), concentration (28.58 ± 1.12) and expression of β-CGRP mRNA(0.810 ± 0.021) were significantly increased in group Ⅱ com-pared with those in group Ⅰ (0.109+0.013, 20.91 ～2.14, 17.35+2.72, 0.701 ～0.018) (P < 0.05), and decreased markedly in group Ⅲ(0.120±0.008), (22.58±1.18), (23.26±2.41), (0.779±0.022) (P < 0.05). Conclusions Tramadol hydrochloride pretreatment can significantly inhibit increase in CGRP expression in myocardium elicited by CAO, which might imply that tramadol hydrochloride might take part in protection of my-ocardium against acute myocardial ischemia by means of pain-relief.