4.Research and thinking on road traffic injury.
Acta Academiae Medicinae Sinicae 2007;29(4):455-458
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
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prevention & control
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Databases, Factual
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Epidemiologic Research Design
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Humans
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Wounds and Injuries
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prevention & control
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therapy
5.Effects of tramadol hydrochloride pretreatment on expression of calcitonin gene-related peptide in myocardium following acute myocardial ischemia in rats
Chinese Journal of Emergency Medicine 2009;18(11):1165-1168
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.
6.The clinical features and Correlative Analysis of Hyperlipidemic acute Pancreatitis
Chinese Journal of Primary Medicine and Pharmacy 2009;16(9):1552-1553
Objective To study the clinical features of hyperlipidemic acute pancreatitis(HL-AP)and to en-hyance the awareness of diagnosis and treatment of HL-AP. Methods To Retrospective analyse 159 cases with acute pancreatitis (AP), of which 18 cases of HL-AP(HL-AP group), 141 cases of other causes of AP(non-HL-AP group),to compare the age, triglyceride (TG), calcium (Ca2+) levels, blood glucose (GLU), CT severity index (CTSI), acute physiology and chronic health evaluation (APACHE Ⅱ) and the the incidence of combined diabetic ketoacidosis (DKA) in two groups,correlative analysis between TG in HL-AP group and the above-mentioned indicators was car-rird out. Results In addition to significantly decreased Ca22+ , TG, APACHEⅡ score, CTSI points, GLU, and the combined incidence of DKA were significantly increased (both P < 0. 05) in HL-AP group when compared with the control group,TG and APACHE Ⅱ score, CTSI score were positively correlated(P < 0. 05),TG and the Ca2+ was negatively correlated (r = - 0. 795, P < 0. 01). Conclusion HL-AP is not uncommon, mainly patients are young and middle-aged with positively correlated between serum TG levels and the HL-AP lesions, and the condition is more seri-ous and,we should pay attention to the early diagnosis and treatment of HL-AP, main treatment is non-surgical treat-ment.
7.Treatment of spinal giant cell tumor of bone
Orthopedic Journal of China 2006;0(07):-
Spinal giant cell tumor of bone (GCTB) is a kind of primary benign bone tumors in the spine. It is rich in blood supply,aggressive,and easily recurring and lung metastasizing. So the benign GCTBs of the spine remains a challenge to treat.This article reviews the therapeutic methods in spinal GCTBs,including surgery,radiation therapy,arterial embolization. The treatment for the tumor with lung metastasis is also covered in this review. It is established that En bloc resection with wide margins is the most effective method to spinal GCTBs. To eliminate the residual tumor cells,adjuvant radiation should be done when complete resection is not available. Arterial embolization can be used to treat the huge sacral GCTBs.For those with lung metatasis,they can be controlled by lobectomy and /or chemotherapy.
8.SPATIO-TEMPORAL EXPRESSION OF CONNEXIN 43 IN THE CULTURED VENTRICULAR MYOCARDIAL CELLS OF NEONATAL RATS
Acta Anatomica Sinica 1954;0(02):-
Objective To investigate the spatio-temporal expression of connexin 43(Cx43) in the cultured ventricular myocardial cells of neonatal rats. Methods The techniques of Immunocytochemistry(ICC) and immuno-electron microscopy were used to detect the Cx43 expression in the cultured rat ventricular myocardial cells on the(2nd),(4th),(8th),(10th),(12th),(16th),(20th,)(26th) and(30th) days. Results Cx43 expression was detected in the cultured ventricular myocardial cells on the 2(nd) day,and the Cx43 granules were located largely in the cellular cytoplasm and membrane.The punctiform granule of the cellular cytoplasm decreased and the expression of Cx43 was located mainly in cellular membrane junction on the 4(th) day.The expression of Cx43 increased in cellular membrane junction on the 10(th) day,and the morphology of Cx43 expression was chain-and strip-like.There were not obvious changes in the following days.The expression of Cx43 on the 30(th) day was derangement.Conclusion The spatio-temporal expression of Cx43 in the cultured ventricular myocardial cells of neonatal rats changed with the cultural time in terms of location and quantity.It was in accordance with the growth and development of the cultured ventricular myocardial cells.
9.Effects of midazolam on the response of parafascicular nucleus to noxious stimuli
Chinese Journal of Anesthesiology 1994;0(01):-
Objective To investigate the effect of intravenous midazolam on the response of parafascicular nucleus(Pf) to noxious stimuli in rats. Methods Twenty SD rats of both sexes weighing 260-300g were used in the study. The animals were anesthetized with intraperitoneal urethane(1.2 g/kg) . A hole was drilled in the skull. Under stereomicroscope micro-glass electrode was inserted into Pf nucleus and the characteristic discharge of nociceptive neurons was recorded. The experiment was then performed in four steps. The discharge was recorded in the basal state (A), when hind paw was pinched by a pair of strong forceps: noxious stimuli (B) , 2 min after midazolam 0.2 mg/kg was given intravenously , step B was repeated (C) and flumazenil 0.05mg was given iv and 2 min later step B was repeated (D) . There was a pause of 5 min after each step. Results The characteristic discharge of nociceptive neurons was recorded only in 9 animals and the data from 6 animals were complete and could be analyzed. Noxious stimuli induced significant increase in spike of discharge of nociceptive neurons. Midazolam significantly depressed the response of nociceptive neurons to noxious stimuli. There was no significant difference in the mean spikes of discharge of nociceptive neurons between step A and C. After flumazenil the mean spike of discharge increased again in response to noxious stimuli. Conclusion Midazolam can inhibit the activity of the nociceptive neurons located in Pf nucleus, probably through GABA-BZ receptor.
10.The antinociceptive effect of fentanyl on the discharges of the neurons in the parafascicular nucleus evoked by coronary artery occlusion
Chinese Journal of Anesthesiology 1996;0(07):-
Objective The purpose of this study was to determine if parafascicular nucleus of thalamus is involved in the nociceptive stimulation evoked by coronary artery occlusion-induced acute myocardial ischemia and to investigate the effect of fentanyl on this nociceptive stimulation. Methods Male SD rats weighing 260-300 g were operated upon under general anesthesia with intraperitoneal urethane (1.2 g ? kg -1 ) and local infiltration of the skin incision. The discharges of pain-sensitive neurons (PSN) were recorded for 20 seconds every 5 min using single-barrel glass electrode before and after the coronary artery occlusion ( CAO) . The study was divided into 3 groups: group Ⅰ CAO alone ( n = 9); group Ⅱ CAO + fentanyl ( n = 6) : fentanyl 0.01 mg ?kg-1 was administered iv 15 min after CAO; group Ⅲ CAO + fentanyl + naloxone ( n = 6) : naloxone 0.04 mg? kg-1 was administered iv 15 min after intravenous fentanyl administration. Results The discharge frequency was significantly increased following CAO and peaked within 5-10 min after CAO and maintained for 60 min. The increased frequency of nociceptive discharge was significantly inhibited within 10 min after fentanyl and intravenous naloxone could completely antagonize the inhibitory effect of fentanyl. Conclusion Visceral pain can be evoked by acute myocardial ischemia induced by coronary artery occlusion. Thalamic parafascicular nucleus is involved in the perception of nociception in CNS. Opioid receptors play a critical role in the modulation of the nociception.