小儿敌敌畏中毒延误诊治2例

例1男，4岁。因间断抽风12h，于1987-03—10以抽搐原因待查收住院。患儿不明原因突然发生抽搐，乡村医生给肌肉注射复方冬眠灵无效。入院时体温正常，脉搏95次／min，意识不清，精神萎靡，颈软，瞳孔2mm；心律整；两肺未闻干湿性罗音：腹软，肝肋下0．5cm，剑下1．0cm，脾肋下未及；病理反射(-)，初诊病毒性脑炎。予以抗生素、激素降低颅内压及对症等治疗12h后，患儿口吐白沫，皮肤苍白，出汗，抽搐呈持续状态。     

注射用头孢曲松致罕见迟发性过敏性休克1例

患儿,女,1岁2个月,因“呕吐2d,腹泻伴发热1d,抽搐1次”入院。诊断为急性腹泻并轻度脱水、急性咽炎和抽搐待查（颅内感染？电解质紊乱？）,入院前无药物过敏史。入院第1天经青霉素皮试阴性后,予注射用头孢他啶0．45givd,滴注约5min后颜面及躯干出现皮疹,伴潮红、痛痒,立即停用头孢他啶,皮疹很快消退。第2天开始,经注射用头孢曲松皮试液皮试阴性后,     

以反复抽搐诊断多发性大动脉炎一例

患儿男,14岁。以间歇性抽搐伴发热5d于2009年3月19日入院。抽搐时意识丧失,双眼上翻,牙关紧闭,颜面发绀,有时伴四肢强直,历时数秒至1min,发热,体温39．2℃,偶有咳嗽,无胸痛及呼吸困难,入院前曾予静脉滴注“头孢呋辛钠、利巴韦林”3d,抽搐加重1d遂收住人院。入院查体：体温38．7℃,脉搏90次／min,呼吸18次／min,     

脑瘤误诊为钩体脑病1例

患儿女，6岁。因左足跛行20d伴左手持物不稳入院。无头痛、发热、抽搐，无肢体疼痛及关节的肿痛。入院前2d出现轻咳及非喷射性呕吐。否认外伤史。体检；T36℃，P100次／min，R25次／min，BP12／8kPa。眼裂等大，双眼球稍有内斜．瞳孔等大等圆，鼻唇沟对称．口角无歪斜。颈软、心肺无异常、肝脾肋下未触及。     

伤寒并发胆囊穿孔1例报告

患者，男，15岁，因不规则发热10天伴头痛，全身乏力，食欲不振，大便溏稀2～3次／天，经庆大霉素、SMZco、氯霉素等治疗热不退而来院。查体：T39．5℃，P84次／分，BP12／8kPa，神情，瘦弱，表情淡漠，心肺（一）。腹平软，肝肋下2cm，脾肋下3．5cm。WBC4．8×109／L，N0.65，L0.35，嗜酸细胞计数0，肝、肾功能，胸透均正常，B超提示胆囊炎，肝、脾肿大，“H”与“O”抗体均为1：320，血培养第三次（＋）。入院后感上腹部阵发性疼痛伴呕吐，以氯霉素1．og／日，丁胺卡那霉素0．4g／日静滴，第八天腹痛加剧腹肌稍紧，腹腔穿刺两次均…     

苯妥英钠治疗癫痫致高热、皮疹2例

口服苯妥英纳治疗癫痫同时引起高热、皮疹、淋巴结及肝脾肿大、白细胞减少，临床较少见，现报告2例。例1，患儿林××，女，10岁，因发作性抽搐4个月，发热、皮疹2天入院。入院前13天，因抽搐在××医院就诊，脑电图示“癫痫样放电”，诊断为“癫痫大发作”，即给口服苯妥英钠0．1g，日2次，抽搐未能控制，其间发作2次。于治疗第11天出现高热，体温达39C～4iC，伴全身性皮疹。入院查体：T39C，R24次／min，BP13．5／8．skPa，全身皮肤可见散在红色斑丘疹，均匀分布。咽稍充血。血常规：Hbl03g／L，RBC38XIc””／L，WBC3．2X10‘／…     

头孢噻肟钠致严重过敏性休克及抢救体会1例

患儿男,6岁,主因“咳嗽半月,发热2d”入院,诊断“支气管肺炎”。入院查体：体温36．8℃,脉搏80次／min,呼吸20次／min,血压90／60mmHg,咽部充血,双肺呼吸音粗糙,未闻及干湿罗音。心率100次／min,律齐,心音有力,各瓣膜听诊区未闻及杂音。腹平软,肝脾肋下未触及。既往无药物过敏史,以往曾静脉滴注过青霉素及头孢噻肟钠。     

细辛脑过敏反应6例报告

病例1：患儿,男,2岁,因“咳喘3d”入院,体检：体重11kg,意识清,精神好,体温38．5℃,双肺呼吸音粗,可闻及湿哕音及哮鸣音,心率120次／min,律整,腹软,肝肋下1．5cm。血常规：WBC6．7×10^9／L、N78．3％、L18．4％、HB107g／L、PLT286×10^9／L;肝肾功正常;尿常规正常;胸片：双肺纹理增粗,可见小斑片状阴影。个人史及家族史无特殊。     

布洛芬过量致死亡1例

患儿，男，3个月。主因发热2d，嗜睡、大汗淋漓1d于2003年12月22日入院。患儿缘于2d前出现发热，达38．4℃，无大汗、抽搐，在当地肌注退热药物，具体用量不祥．热降后复升，又服用布洛芬(商品名：安瑞克，重庆产)，8h内服用0．38g，于1d前出现大汗淋漓、嗜睡，四肢无力．精神反应差，拒乳，无咳嗽、呕吐、腹泻及抽搐，在当地医院静点“菌必治”等药治疗，病情无好转来我院就诊。     

老年急性出血坏死性肠炎误诊分析

1病例介绍 1．1患者男，63岁，因发热、咳嗽、气喘10d，伴腹痛、腹泻4d，于2000年12月16日入院。病前无诱因，按“慢性支气管炎急性发作”在家中静脉滴注“氨苄青霉素和头孢曲松”等治疗7d，热退，但出现腹泻，2～3次／d，呈深色糊状，并有黑便1次，量不多，伴有腹痛。原有慢性支气管炎、肺气肿病史15年。体检：136℃，P80次／min，BP120／70mmHg（1mmHg=0．133kPa），精神差，全身散在少量出血性皮疹，下肢较多，眼睑无水种，巩膜无黄染，双肺闻及散在哮鸣音及湿哕音，心界不大，律齐，腹稍胀，满腹轻压痛，无肌紧张及反跳痛，肝肋下2em，脾肋下未触及，腹内无移动性浊音，肠鸣音活跃，双下肢Ⅱ度水肿。     

Allosteric activation mechanism of the cys-loop receptors

Binding of a neurotransmitter to its ionotropic receptor opens a distantly located ion channel, a process termed allosteric activation. Here we review recent advances in the molecular mechanism by which the cys-loop receptors are activated with emphasis on the best studied nicotinic acetylcholine receptors （nAChRs）. With a combination of affinity labeling, mutagenesis, electrophysiology, kinetic modeling, electron microscopy （EM）, and crystal structure analysis, the allosteric activation mechanism is emerging. Specifically, the binding domain and gating domain are interconnected by an allosteric activation network. Agonist binding induces conformational changes, resulting in the rotation of a β sheet of aminoterminal domain and outward movement of loop 2, loop F, and cys-loop, which are coupled to the M2-M3 linker to pull the channel to open. However, there are still some controversies about the movement of the channel-lining domain M2. Nine angstrom resolution EM structure of a nAChR imaged in the open state suggests that channel opening is the result of rotation of the M2 domain. In contrast, recent crystal structures of bacterial homologues of the cys-loop receptor family in apparently open state have implied an M2 tilting model with pore dilation and quaternary twist of the whole pentameric receptor. An elegant study of the nAChR using protonation scanning of M2 domain supports a similar pore dilation activation mechanism with minimal rotation of M2. This remains to be validated with other approaches including high resolution structure determination of the mammalian cys-loop receptors in the open state.     

Addictive evaluation of cholic acid-verticinone ester,a potential cough therapeutic agent with agonist action of opioid receptor

Aim： The purpose of this work was to search for potential drugs with potent antitussive and expectorant activities as well as a low toxicity, but without addictive properties. Cholic acid-verticinone ester （CA-Ver） was synthesized based on the clearly elucidated antitussive and expectorant activities of verticinone in bulbs of Fritillaria and different bile acids in Snake Bile. In our previous study, CA-Ver showed a much more potent activity than codeine phosphate. This study was carried out to investigate the central antitussive mechanism and the addictive evaluation of CA-Ver. Methods： Testing on a capsaicin-induced cough model of mice pretreated with naloxone, a non-selective opioid receptor antagonist, was performed for the observation of CA-Ver＇s central antitussive mechanism. We then took naloxone-induced withdrawal tests of mice for the judgment of CA-Ver＇s addiction. Lastly, we determined the opioid dependence of CA-Ver in the guinea pig ileum. Results： The test on the capsaicin-induced cough model showed that naloxone could block the antitussive effect of CA-Ver, suggesting the antitussive mechanism of CA-Ver was related to the central opioid receptors. The naloxone-urged withdrawal tests of the mice showed that CA-Ver was not addictive, and the test of the opioid dependence in the guinea pig ileum showed that CA-Ver had no withdrawal response. Conclusion： These findings suggested that CA-Ver deserved attention for its potent antitussive effects related to the central opioid receptors, but without addiction, and had a good development perspective.     

Nicotinic acetylcholine receptor α7 subunits with a C2 cytoplasmic loop yellow fluorescent protein insertion form functional receptors

Aim： Several nicotinic acetylcholine receptor （nAChR） subunits have been engineered as fluorescent protein （FP） fusions and exploited to illuminate features of nAChRs. The aim of this work was to create a FP fusion in the nAChR α7 subunit without compromising formation of functional receptors, Methods： A gene construct was generated to introduce yellow fluorescent protein （YFP）, in frame, into the otherwise unaltered, large, second cytoplamsic loop between the third and fourth transmembrane domains of the mouse nAChR α7 subunit （α7Y）. SH-EP1 cells were transfected with mouse nAChR wild type α7 subunits （α7） or with α7Y subunits, alone or with the chaperone protein, hRIC-3. Receptor function was assessed using whole-cell current recording. Receptor expression was measured with 125I-labeled α-bungarotoxin （I-Bgt） binding, laser scanning confocal microscopy, and total internal reflectance fluorescence （TIRF） microscopy. Results： Whole-cell currents revealed that α7Y nAChRs and α7 nAChRs were functional with comparable EC50 values for the α7 nAChR-selective agonist, choline, and IC50 values for the α7 nAChR-selective antagonist, methyllycaconitine. I-Bgt binding was detected only after co-expression with hRIC-3. Confocal microscopy revealed that α7Y had primarily intracellular rather than surface expression. TIRF microscopy confirmed that little α7Y localized to the plasma membrane, typical of α7 nAChRs. Conclusion： nAChRs composed as homooligomers of α7Y subunits containing cytoplasmic loop YFP have functional, ligand binding, and trafficking characteristics similar to those of α7 nAChRs, α7Y nAChRs may be used to elucidate properties of α7 nAChRs and to identify and develop novel probes for these receptors, perhaps in high-throughput fashion.     

The impact of extracellular and intracellular Ca2＋ on ethanol-induced smooth muscle contraction

Aim： To evaluate the impact of extracellular and intracellular Ca2＋ on contractions induced by ethanol in smooth muscle. Methods： Longitudinal smooth muscle strips were prepared from the gastric fundi of mice. The contractions of smooth muscle strips were recorded with an isometric force displacement transducer. Results： Ethanol （164 mmol/L） produced reproducible contractions in isolated gastric fundal strips of mice. Although lidocaine （50 and 100 μmol/L）, a local anesthetic agent, and hexamethonium （100 and 500 μmol/L）, a ganglionic blocking agent, failed to affect these contractions, verapamil （1-50 μmol/L） and nifedipine （1-50 pmol/L）, selective blockers of L-type Ca2＋ channels, significantly inhibited the contractile responses of ethanol. Using a Ca2＋-free medium nearly eliminated these contractions in the same tissue. Ryanodine （1-50 μmol/L） and ruthenium red （10-100 pmol/L）, selective blockers of intracellular Ca2＋ channels/ryanodine receptors; cyclopiazonic acid （CPA; 1-10 μmol/L）, a selective inhibitor of sarcoplasmic reticulum （SR） Ca2＋-ATPase; and caffeine （0.5-5 mmol/L）, a depleting agent of intracellular Ca2＋ stores, significantly inhibited the contractile responses induced by ethanol. In addition, the com- bination of caffeine （5 mmol/L） plus CPA （10 μmol/L）, and ryanodine （10 μmol/L） plus CPA （10 μmol/L）, caused further inhibition of contractions in response to ethanol. This inhibition was significantly different from those associated with caffeine, ryanodine or CPA. Furthermore the combination of caffeine （5 mmol/L）, ryanodine （10 μmol/L） and CPA（IO pmol/L） eliminated the contractions induced by ethanol in isolated gastric fundal strips of mice. Conclusion： Both extracellular and intracellular Ca2＋ may have important roles in regulating contractions induced by ethanol in the mouse gastric fundus.     

Pivotal effects of phosphodiesterase inhibitors on myocyte contractility and viability in normal and ischemic hearts

Phosphodiesterases （PDEs） are enzymes that degrade cellular cAMP and cGMP and are thus essential for regulating the cyclic nucleotides. At least 11 families of PDEs have been identified, each with a distinctive structure, activity, expression, and tissue distribution. The PDE type-3, -4, and -5 （PDE3, PDE4, PDE5） are localized to specific regions of the cardiomyocyte, such as the sarcoplasmic reticulum and Z-disc, where they are likely to influence cAMP/cGMP signaling to the end effectors of contractility. Several PDE inhibitors exhibit remarkable hemodynamic and inotropic properties that may be valuable to clinical practice. In particular, PDE3 inhibitors have potent cardiotonic effects that can be used for short-term inotropic support, especially in situations where adrenergic stimulation is insufficient. Most relevant to this review, PDE inhibitors have also been found to have cytoprotective effects in the heart. For example, PDE3 inhibitors have been shown to be cardioprotective when given before ischemic attack, whereas PDE5 inhibitors, which include three widely used erectile dysfunction drugs （sildenafil, vardenafil and tadalafil）, can induce remarkable cardioprotection when administered either prior to ischemia or upon reperfusion. This article provides an overview of the current laboratory and clinical evidence, as well as the cellular mechanisms by which the inhibitors of PDE3, PDE4 and PDE5 exert their beneficial effects on normal and ischemic hearts. It seems that PDE inhibitors hold great promise as clinically applicable agents that can improve cardiac performance and cell survival under critical situations, such as ischemic heart attack, cardiopulmonary bypass surgery, and heart failure.     

The peroxisome proliferator-activated receptor-α （PPAR-α） agonist,AVE8134, attenuates the progression of heart failure and increases survival in rats

Aim： To investigate the efficacy of the peroxisome proliferator-activated receptor-α （PPARa） agonist, AVE8134, in cellular and experimental models of cardiac dysfunction and heart failure.
Methods： In Sprague Dawley rats with permanent ligation of the left coronary artery （post-MI）, AVE8134 was compared to the PPARy agonist rosiglitazone and in a second study to the ACE inhibitor ramipril. In DOCA-salt sensitive rats, efficacy of AVE8134 on cardiac hypertrophy and fibrosis was investigated. Finally, AVE8134 was administered to old spontaneously hypertensive rats （SHR） at a nonblood pressure lowering dose with survival as endpoint. In cellular models, we studied AVE8134 on hypertrophy in rat cardiomyocytes nitric oxide signaling in human endothelial cells （HUVEC） and LDL-uptake in human MonoMac-6 cells.
Results： In post-MI rats, AVE8134 dose-dependently improved cardiac output, myocardial contractility and relaxation and reduced lung and left ventricular weight and fibrosis. In contrast, rosiglitazone exacerbated cardiac dysfunction. Treatment at AVE8134 decreased plasma proBNP and arginine and increased plasma citrulline and urinary NOx/creatinine ratio. In DOCA rats, AVE8134 prevented development of high blood pressure, myocardial hypertrophy and cardiac fibrosis, and ameliorated endothelial dysfunction. Compound treatment increased cardiac protein expression and phosphorylation of eNOS. In old SHR, treatment with a low dose of AVE8134 improved cardiac and vascular function and increased life expectancy without lowering blood pressure. AVE8134 reduced phenylephrine-induced hypertrophy in adult rat cardiomyocytes. In HUVEC, Ser-1177-eNOS phosphorylation but not eNOS expression was increased. In monocytes, AVE8134 increased the expression of CD36 and the macrophage scavenger receptor 1, resulting in enhanced uptake of oxidized LDL.
Conclusion： The PPARa agonist AVE8134 prevents post-MI myocardial hypertrophy, fibrosis and cardiac dysfunction. AVE8134 has beneficial effects against hy     

Response of mesenchymal stem cells to shear stress in tissueengineered vascular grafts

Aim： Recent studies have demonstrated that mesenchymal stem cells （MSCs） can differentiate into endothelial cells. The effect of shear stress on MSC differentiation is incompletely understood, and most studies have been based on two-dimensional systems. We used a model of tissue-engineered vascular MSC differentiation. grafts （TEVGs） to investigate the effects of shear stress on Methods： MSCs were isolated from canine bone marrow. The TEVG was constructed by seeding MSCs onto poly-ε- caprolactone and lactic acid （PCLA） scaffolds and subjecting them to shear stress provided by a pulsatile bioreactor for four days （two days at 1 dyne/cm^2 to 15 dyne/cm^2 and two days at 15 dyne/cm^2）. Results： Shear stress significantly increased the expression of endothelial cell markers, such as platelet-endothelial cell adhesion molecule-1 （PECAM-1）, VE-cadherin, and CD34, at both the mRNA and protein levels as compared with static control cells. Protein levels of alpha-smooth muscle actin （α-SMA） and calponin were substantially reduced in shear stresscultured cells. There was no significant change in the expression of α-SMA, smooth muscle myosin heavy chain （SMMHC） or calponin at the mRNA level. Conclusion： Shear stress upregulated the expression of endothelial cell-related markers and downregulated smooth muscle-related markers in canine MSCs. This study may serve as a basis for further investigation of the effects of shear stress on MSC differentiation in TEVGs.     

Central cholinergic regulation of respiration： nicotinic receptors

Nicotinic acetylcholine receptors （nAChRs） are expressed in brainstem and spinal cord regions involved in the control of breathing. These receptors mediate central cholinergic regulation of respiration and effects of the exogenous ligand nicotine on respiratory pattern. Activation of α4＊ nAChRs in the preBotzinger Complex （preBotC）, an essential site for normal respiratory rhythm generation in mammals, modulates excitatory glutamatergic neurotransmission and depolarizes preBotC inspiratory neurons, leading to increases in respiratory frequency, nAChRs are also present in motor nuclei innervating respiratory muscles. Activation of post- and/or extra-synaptic α4＊ nAChRs on hypoglossal （XII） motoneurons depolarizes these neurons, potentiating tonic and respiratory-related rhythmic activity. As perinatal nicotine exposure may contribute to the pathogenesis of sudden infant death syndrome （SIDS）, we discuss the effects of perinatal nicotine exposure on development of the cholinergic and other neurotransmitter systems involved in control of breathing. Advances in understanding of the mechanisms underlying central cholinergic/nicotinic modulation of respiration provide a pharmacological basis for exploiting nAChRs as therapeutic targets for neurological disorders related to neural control of breathing such as sleep apnea and SIDS.     

Expression pattern of neural synaptic plasticity marker-Arc in different brain regions induced by conditioned drug withdrawal from acute morphine-dependent rats

Aim： The immediate early gene Arc （activity-regulated cytoskeletal-associated protein） mRNA and protein are induced by strong synaptic activation and rapidly transported into dendrites, where they localize at active synaptic sites. Thus, the Arc mRNA and protein are proposed as a marker of neuronal reactivity to map the neural substrates that are recruited by various stimuli. In the present study, we examined the expression of Arc protein induced by conditioned naloxone-precipitated drug withdrawal in different brain regions of acute morphine-dependent rats. The objective of the present study was to address the specific neural circuits involved in conditioned place aversion （CPA） that has not yet been well characterized. Methods： Place aversion was elicited by conditioned naloxone-precipitated drug withdrawal following exposure to a single dose of morphine. An immunohistochemical method was employed to detect the expression of Arc, which was used as a plasticity marker to trace the brain areas that contribute to the formation of the place aversion. Results： Marked increases in Arc protein levels were found in the medial and lateral prefrontal cortex, the sensory cortex, the lateral striatum and the amygdala. This effect was more pronounced in the basolateral amygdala （BLA）, the central nucleus of the amygdala （CeA）, and the bed nucleus of the striatal terminals （BNST） when compared with the control group. Conclusion： Our results suggest that these brain regions may play key roles in mediating the negative motivational component of opiate withdrawal.