Study on the development and usage of a cardiopulmonary resuscitation time point recorder.

BACKGROUND: To invent a novel cardiopulmonary resuscitation (CPR) time point recorder to synchronously and automatically record the time and to identify its effectiveness in humans. METHODS: A CPR time point recorder was invented after the doctors were familiar with the traditional Utstein recovery registration mode and mastered the registration time points required. The progress of CPR was simulated. The standard and correct times were recorded, and the doctors performing the recovery collected the data about the times using our CPR time point recorder or the memory registration mode. RESULTS: The deviation times were 21.4±24.7 seconds for the memory group and 3.57±4.58 seconds for CPR time point recorder group. The deviation of times increased significantly depending on the increase of the operation items in the memory group. A similar phenomenon was found in the timer group but with a smaller difference (P<0.01). CONCLUSION: A CPR time point recorder could reduce the deviation of operate-time, especially after a long-time operation, and for procedures with more operating items, compared with the memory mode. It was a more advantageous and accurate method for the Utstein registration.

Activation of autophagy improved the neurologic outcome after cardiopulmonary resuscitation in rats.

OBJECTIVE: Recent studies have shown the existence of autophagy in cerebral ischemia; however, there has been no research on the role of autophagy in cerebral injury after cardiopulmonary resuscitation (CPR). This study was conducted to determine the role of autophagy in an animal model of ventricular fibrillation (VF)/CPR. METHODS: Experiment 1: A total of 48 adult Wistar rats were untreated for 7 minutes after induction of VF using an external transthoracic alternating current, and subsequent CPR was performed to observe the existence of autophagy after the return of spontaneous circulation (ROSC). Experiment 2: A total of 72 rats were pretreated with intracerebroventricular injection of physiologic saline (control group), the autophagy inducer (rapamycin group), or the autophagy inhibitor 3-methyladenine (3-methyladenine group) before ROSC to evaluate the contribution of autophagy to neuronal injury after ROSC. RESULTS: The activation of autophagy was attenuated 2 to 4 hours after ROSC, which was related to the activity decrease of 5'-adenosine monophosphate-activated protein kinase after ROSC. Rapamycin treatment significantly increased the expressions of LC3-II and Beclin-1 after ROSC, attenuated the activation of caspase-3, promoted neuronal survival and decreased neuronal apoptosis, and improved the neurologic deficit score after CPR. CONCLUSIONS: The activation of autophagy after ROSC offered a remarkable tolerance to VF/CPR ischemic insult and improved the neurologic outcomes.

Prearrest hypothermia improved defibrillation and cardiac function in a rabbit ventricular fibrillation model.

BACKGROUND: Hypothermia when cardiopulmonary resuscitation begins may help achieve defibrillation and return of spontaneous circulation (ROSC), but few data are available. OBJECTIVE: The objective of this study was to determine whether prearrest hypothermia improved defibrillation and cardiac function in a rabbit ventricular fibrillation (VF) model. RESULTS: Thirty-six New Zealand rabbits were randomized equally to receive normothermia (Norm) (~39°C), post-ROSC hypothermia (~33°C), or prearrest hypothermia (~33°C). Ventricular fibrillation was induced by alternating current. After 4 minutes of VF, rabbits were defibrillated and given cardiopulmonary resuscitation until ROSC or no response (≥30 minutes). Hemodynamics and electrocardiogram were monitored; N-terminal pro-brain natriuretic peptideand troponin I were determined by enzyme-linked immunosorbent assay. Myocardial histology and echocardiographic data were evaluated. First-shock achievement of perfusion rhythm was more frequent in prearrest than normothermic animals (7/12 vs 1/12; P=.027). After ROSC, dp/dtmax was higher in prearrest than normothermic animals (P<.001). Left ventricular end-systolic pressure was higher in prearrest than normothermic animals (P=.001). At 240 minutes after ROSC, troponin I and N-terminal pro-brain natriuretic peptide were lower in prearrest than normothermic animals (15.74±2.26 vs 25.09±1.85 ng/mL and 426±23 vs 284±45 pg/mL, respectively), the left ventricular ejection fraction and cardiac output were lower in the Norm group than other 2 groups (P<.01). Myocardial histology was more disturbed in normothermic than post-ROSC and prearrest animals, but was not different in the latter 2 groups. CONCLUSIONS: Induction of hypothermia before VF led to improved cardiac function in a rabbit VF model through improving achievement of perfusing rhythm by first-shock defibrillation and facilitating resuscitation.

Assessing the early changes of cerebral glucose metabolism via dynamic (18)FDG-PET/CT during cardiac arrest.

To study the changes of cerebral glucose metabolism (CGM) during the phase of return of spontaneous circulation (ROSC) after cardiac arrest (CA), we used 18-fluorodeoxyglucose-positron emission tomography/computed tomography ((18)FDG-PET/CT) to measure the CGM changes in six beagle canine models. After the baseline (18)FDG-PET/CT was recorded, ventricular fibrillation (VF) was induced for 6 min, followed by close-chest cardiopulmonary resuscitation (CPR) in conjunction with intravenous (IV) administration of epinephrine and external defibrillator shocks until ROSC was achieved, within 30 min. The (18)FDG was recorded prior to intravenous administration at 0 h (baseline), and at 4, 24, and 48 h after CA with ROSC. We evaluated the expression of two key control factors in canine CGM, hexokinase I (HXK I) and HXK II, by immunohistochemistry at the four above mentioned time points. Electrically induced VF of 6 min duration was successfully induced in the dogs. Resuscitation was then performed to maintain blood pressure stability. Serial (18)FDG-PET/CT scans found that the CGM decreased at 4 h after ROSC and remained lower than the baseline even at 48 h. The expression of HXK I and II levels were consistent with the changes in CGM. These data from our present work showed that (18)FDG-PET/CT imaging can be used to detect decreased CGM during CA and was consistent with the results of CMRgl. Furthermore, there were also concomitant changes in the expression of HXK I and HXK II. The decrease in CGM may be an early sign of hyperacute global cerebral ischemia.

A new species of Neobelocera Ding & Yang (Hemiptera: Delphacidae: Delphacinae: Tropidocephalini) from China, with a key to species of the genus.

Neobelocera medogensis sp. nov. (Hemiptera: Delphacidae: Delphacinae: Tropidocephalini) is described and illustrated from Mȇdog, Tibet, China. The new species can be easily separated from other known species in the genus Neobelocera by the color of tegmina and the form of the male genitalia. A key for separation of all known species of Neobelocera is also provided.

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation.

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde.

Enhanced external counterpulsation improves cerebral blood flow following cardiopulmonary resuscitation.

BACKGROUND: To investigate the therapeutic value of enhanced external counterpulsation (EECP) on recovery of cerebral blood flow following cardiac arrest (CA) and successful resumption of spontaneous circulation (ROSC) by cardiopulmonary resuscitation. METHODS: CA models were conducted using beagle dogs induced by alternating current. After successful ROSC by cardiopulmonary resuscitation, 16 dogs were randomly divided into the EECP and control group (n = 8 per group). Dogs underwent dynamic contrast-enhanced and diffusion-weighted magnetic resonance imaging at baseline prior to CA and during the 3 days following ROSC. Mean blood pressure, right common carotid artery blood flow, intracranial microcirculation and blood lactate levels were measured. Neurological outcome was assessed by the neurologic deficit score. Hematoxylin-eosin staining and transmission electron microscopy were performed for morphology and microconstruction of the cerebral cortex. RESULTS: The EECP group exhibited a significant elevation in right common carotid artery blood flow, intracranial microcirculation and a substantial decrease in blood lactate levels relative to the control group. Relative cerebral blood flow and volume were higher in the EECP group during the 3 days. Apparent diffusion coefficients were significantly higher in the EECP group on the first and third days. After ROSC, the neurologic deficit score was significantly higher in the control group compared to those in the EECP group during the three days of experiment. The cell swelling of neurons and increase of mitochondrial mass were more pronounced in the control group. CONCLUSION: EECP is beneficial for recovery of cerebral blood flow and attenuation of ischemic cerebral edema following CA and successful ROSC.

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, ...

Comparing percutaneous coronary intervention and thrombolysis in patients with return of spontaneous circulation after cardiac arrest.

OBJECTIVE: To evaluate the effects of percutaneous coronary intervention and thrombolysis after restoration of spontaneous circulation in cardiac arrest patients with ST-elevation myocardial infarction using meta-analysis. METHODS: We performed a meta-analysis of clinical studies indexed in the PUBMED, MEDLINE and EMBASE databases and published between January 1995 and October 2012. In addition, we compared the hospital discharge and neurological recovery rates between the patients who received percutaneous coronary intervention and those who received thrombolysis. RESULTS: Twenty-four studies evaluating the effects of percutaneous coronary intervention or thrombolysis after restoration of spontaneous circulation in cardiac arrest patients with ST-elevation myocardial infarction were included. Seventeen of the 24 studies were used in this meta-analysis. All studies were used to compare percutaneous coronary intervention and thrombolysis. The meta-analysis showed that the rate of hospital discharge improved with both percutaneous coronary intervention (p<0.001) and thrombolysis (p<0.001). We also found that cardiac arrest patients with ST-elevation myocardial infarction who received thrombolysis after restoration of spontaneous circulation did not have decreased hospital discharge (p = 0.543) or neurological recovery rates (p = 0.165) compared with those who received percutaneous coronary intervention. CONCLUSION: In cardiac arrest patients with ST-elevation myocardial infarction who achieved restoration of spontaneous circulation, both percutaneous coronary intervention and thrombolysis improved the hospital discharge rate. Furthermore, there were no significant differences in the hospital discharge and neurological recovery rates between the percutaneous coronary intervention-treated group and the thrombolysis-treated group.

Ulinastatin improved cardiac dysfunction after cardiac arrest in New Zealand rabbits.

OBJECTIVE: The present study was designed to evaluate the effects of ulinastatin (UTI) on cardiac dysfunction after cardiopulmonary resuscitation (CPR). METHODS: A total of 48 healthy adult male New Zealand rabbits were untreated for 8 minutes after the induction of ventricular fibrillation (VF) by an external transthoracic alternating current and then treated by CPR. These rabbits were then randomly divided into the control and UTI groups after the return of spontaneous circulation (ROSC) and were observed for 8 hours after the ROSC. Before CPR and after ROSC at 2, 4, and 8 hours, blood samples were collected to determine the levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), cardiac troponin I (cTnI), and N-terminal probrain natriuretic peptide (NT-proBNP), and the left ventricular ejection fraction (EF) was measured by echocardiography. RESULTS: Nineteen of 24 rabbits in the control group and 18 of 24 in the UTI group were successfully resuscitated. The plasma levels of TNF-α, IL-6, MDA, cTnI, and NT-proBNP were significantly increased, accompanying a deceased EF in the control group, but the cotreatment with UTI decreased the plasma levels of TNF-α, IL-6, MDA, cTnI, and NT-proBNP (P < .05), attenuating the myocardial injury and improving the EF in the UTI group. Only 9 of 19 animals in the control group but 14 of 18 animals in the UTI group survived longer than 8 hours (P = .011). CONCLUSIONS: The progression of proinflammatory responses, oxidative stress, and myocardial injury have been linked to the reduced EF after VF/CPR, and the administration of UTI at a cardioprotective dosage preserved the cardiac function after VF/CPR.

Early enhanced external counter pulsation improves neurological recovery after the return of spontaneous circulation in a mongrel dog cardiac arrest model*.

OBJECTIVES: The aim of this study was to investigate whether early enhanced external counter pulsation therapy after cardiopulmonary resuscitation improved neurological outcome in a mongrel dog cardiac arrest model. DESIGN: Randomized, animal study. SETTING: Assisted circulation laboratory. SUBJECTS: Twenty-four healthy male adult dogs (12-14 kg). INTERVENTIONS: After minutes of untreated ventricular fibrillation followed by 2 minutes of cardiopulmonary resuscitation, the dogs were randomized to receive 4 hours of enhanced external counter pulsation therapy, to receive 4 hours of hypertension with over 140 mm Hg or to be a control. MEASUREMENTS: Blood pressure and left ventricular ejection fraction were recorded. Cerebral flow was assessed using magnetic resonance imaging. Arterial blood gases and endothelium-derived vasoactive substances were assessed before cardiac arrest and 4 hours after the return of spontaneous circulation. Neurological outcome was assessed by the neurologic deficit score and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. RESULTS: Enhanced external counter pulsation significantly improved the left ventricular ejection fraction and increased common carotid artery blood flow and shear stress. Enhanced external counter pulsation increased both relative cerebral blood volume (RCBV, p = 0.043) and relative cerebral blood flow (RCBF, p = 0.012) in animals 4 hours after return of spontaneous circulation. Enhanced external counter pulsation therapy promoted the production of nitric oxide and tissue plasminogen activator and decreased the release of endothelin-1 (p = 0.013) after return of spontaneous circulation. Treatment with norepinephrine in the high mean artery pressure also increased common carotid artery blood flow and shear stress. However, no effects on the left ventricular ejection fraction, the production of nitric oxide and tissue plasminogen activator, or the release of endothelin-1 were found. The neurologic deficit scores of the animals were significantly lower at 24, 48, 72, and 96 hours in the enhanced external counter pulsation group, as well as at 24, 72, and 96 hours compared with animals in the control group after return of spontaneous circulation. Fewer apoptotic neurons were observed in the animals in the enhanced external counter pulsation group compared with the animals in the control and hypertension groups. CONCLUSIONS: These data indicated that the treatment of early enhanced external counter pulsation improved neurological outcome by both increasing cerebral blood flow and improving the recovery of microcirculation after return of spontaneous circulation. The treatment of early enhanced external counter pulsation can be a good option for protecting the brain after return of spontaneous circulation.

Comparing percutaneous coronary intervention and thrombolysis in patients with return of spontaneous circulation after cardiac arrest

OBJECTIVE: To evaluate the effects of percutaneous coronary intervention and thrombolysis after restoration of spontaneous circulation in cardiac arrest patients with ST-elevation myocardial infarction using meta-analysis. METHODS: We performed a meta-analysis of clinical studies indexed in the PUBMED, MEDLINE and EMBASE databases and published between January 1995 and October 2012. In addition, we compared the hospital discharge and neurological recovery rates between the patients who received percutaneous coronary intervention and those who received thrombolysis. RESULTS: Twenty-four studies evaluating the effects of percutaneous coronary intervention or thrombolysis after restoration of spontaneous circulation in cardiac arrest patients with ST-elevation myocardial infarction were included. Seventeen of the 24 studies were used in this meta-analysis. All studies were used to compare percutaneous coronary intervention and thrombolysis. The meta-analysis showed that the rate of hospital discharge improved with both percutaneous coronary intervention (p<0.001) and thrombolysis (p<0.001). We also found that cardiac arrest patients with ST-elevation myocardial infarction who received thrombolysis after restoration of spontaneous circulation did not have decreased hospital discharge (p = 0.543) or neurological recovery rates (p = 0.165) compared with those who received percutaneous coronary intervention. CONCLUSION: In cardiac arrest patients with ST-elevation myocardial infarction who achieved restoration of spontaneous circulation, both percutaneous coronary intervention and thrombolysis improved the hospital discharge rate. Furthermore, there were no significant differences in the hospital discharge and neurological recovery rates between the percutaneous coronary intervention-treated group and the thrombolysis-treated group. .

The effect of an NgR1 antagonist on the neuroprotection of cortical axons after cortical infarction in rats.

We investigated the effect of the soluble Nogo66 receptor (sNgR-Fc) on the protection of cortical axons after cortical infarction in rats. The cortical infarction was induced by photothrombotic cortical injury (PCI) in Sprague-Dawley rats, after which sNgR-Fc was injected into the lateral ventricle. The ipsilesional cortices were harvested for analyses using histochemical and transmission-electron microscope techniques. The involved signaling pathways, which include RhoA, JNK, c-JUN and ATF-2, were detected by Western blot. Serious pathologies were found in the brains of the rats after injury, including edemas in the axoplasms of axons that have no medulla sheath and a thickening or shrinkage in the sheath of the axons that have medulla sheathes. However, these pathologies improved after sNgR-Fc treatment. The levels of GTP-RhoA, p-JNK, p-c-JUN and p-ATF-2 in the PCI group were increased when compared with their levels in the sham-operation group (P < 0.05), and animals receiving the sNgR-Fc treatment showed lower expression levels of these proteins when compared with the sham-operation group (P < 0.05). Our results suggest that sNgR-Fc can alleviate the pathological changes of axons following cortical infarction via decreasing the activation of RhoA/JNK signaling pathways.

Comparing the diagnostic values of circulating microRNAs and cardiac troponin T in patients with acute myocardial infarction.

OBJECTIVE: Recent studies have shown that circulating microRNAs might be useful, novel biomarkers for the diagnosis of acute myocardial infarction. The aims of this study were to evaluate the expression of cardiac-specific miRNAs (miR-1, -133a, -208b, and -499) in patients with acute myocardial infarction and to compare the diagnostic values of these miRNAs with that of cardiac troponin T. METHODS: Sixty-seven plasma samples obtained from patients with acute myocardial infarction and 32 plasma specimens collected from healthy volunteers were analyzed in this study. The levels of cardiac-specific miRNAs (miR-1, -133a, -208b, and -499) were measured by quantitative reverse transcription-polymerase chain reaction, and the concentrations of plasma cardiac troponin T were measured using electrochemiluminescence-based methods and an Elecsys 2010 Immunoassay Analyzer. RESULTS: The levels of plasma miR-1, -133a, -208b, and -499 were significantly higher in acute myocardial infarction patients (all p<0.001) than in healthy volunteers. The expression of the cardiac-specific miRNAs in acute myocardial infarction patients decreased to close to the baseline levels at the time of hospital discharge (all p>0.05). There were no correlations between the levels of the four circulating miRNAs and the clinical characteristics of the study population (all p>0.05). Furthermore, receiver operating characteristic curve analyses showed that the four plasma miRNAs were not superior to cardiac troponin T for the diagnosis of acute myocardial infarction (all p>0.05). CONCLUSION: Our results demonstrate that circulating miR-1, -133a, -208b, and -499 may be useful biomarkers in acute myocardial infarction patients but that these miRNAs are not superior to cardiac troponin T for the diagnosis of acute myocardial infarction.

Comparing the diagnostic values of circulating microRNAs and cardiac troponin T in patients with acute myocardial infarction

OBJECTIVE: Recent studies have shown that circulating microRNAs might be useful, novel biomarkers for the diagnosis of acute myocardial infarction. The aims of this study were to evaluate the expression of cardiac-specific miRNAs (miR-1, -133a, -208b, and -499) in patients with acute myocardial infarction and to compare the diagnostic values of these miRNAs with that of cardiac troponin T. METHODS: Sixty-seven plasma samples obtained from patients with acute myocardial infarction and 32 plasma specimens collected from healthy volunteers were analyzed in this study. The levels of cardiac-specific miRNAs (miR-1, -133a, -208b, and -499) were measured by quantitative reverse transcription-polymerase chain reaction, and the concentrations of plasma cardiac troponin T were measured using electrochemiluminescence-based methods and an Elecsys 2010 Immunoassay Analyzer. RESULTS: The levels of plasma miR-1, -133a, -208b, and -499 were significantly higher in acute myocardial infarction patients (all p<0.001) than in healthy volunteers. The expression of the cardiac-specific miRNAs in acute myocardial infarction patients decreased to close to the baseline levels at the time of hospital discharge (all p>0.05). There were no correlations between the levels of the four circulating miRNAs and the clinical characteristics of the study population (all p>0.05). Furthermore, receiver operating characteristic curve analyses showed that the four plasma miRNAs were not superior to cardiac troponin T for the diagnosis of acute myocardial infarction (all p>0.05). CONCLUSION: Our results demonstrate that circulating miR-1, -133a, -208b, and -499 may be useful biomarkers in acute myocardial infarction patients but that these miRNAs are not superior to cardiac troponin T for the diagnosis of acute myocardial infarction.

Revision of the subgenus Cosmiomorpha (Cosmiomorpha)(Coleoptera: Scarabaeidae: Cetoniinae).

A taxonomic revision of the subgenus Cosmiomorpha (Cosmiomorpha) Saunders is presented. Seven species are recognized, including four described herein, C. fortis new species, C. nigripedis new species, C. maolanensis new species, and C. cheni new species all from China. Cosmiomorpha baryi Bourgoin and C. squamulosa Schürhoff are placed as junior synonyms of C. decliva Janson, and C. angulosa Fairmaire as a synonym of C. decliva is also confirmed. Lectotypes are designated for C. decliva Janson, C. angulosa Fairmaire, and C. squamulosa Schürhoff. Color photographs and diagnoses of all species are provided, with comments on intraspecific variations. A key to males is also presented. Localities of "Siào-Lòu" and "Se Pin-Lou Chan" are discussed with a map. 

Drug associated vanishing bile duct syndrome combined with hemophagocytic lymphohistiocytosis.

A 28-year-old woman with untreated autoimmune disorder, demonstrated skin rash and fever after taking Amoxicillin-clavulanate and developed progressive jaundice. A bone marrow aspiration indicated an increased number of macrophages with hemophagocytosis and liver biopsy showed pure centrilobular cholestasis with necrosis and some absence of portal bile ducts. Furthermore, a serological test for Epstein-Barr virus was positive. Under treatment by liver dialysis and administration of steroids led to rapidly defervescence and clinical improvement. However, liver enzymes were still markedly elevated with persistent anemia, even after immunosuppressive treatment. The patient is currently waiting for liver transplantation. This is the first description of vanishing bile duct syndrome combined with hemophagocytic lymphohistiocytosis, with underlying causes including infection, drug-induced factors and untreated autoimmune disorder.

[Treatment of contracture of achilles tendon with minimally invasive achilles tendon lengthening and system rehabilitation].

OBJECTIVE: To investigate the safety and efficacy of minimally invasive achilles tendon lengthening and system rehabilitation for the treatment of contracture of achilles tendon. METHODS: From January 2002 to December 2010, 27 patients (31 feet) with contracture of achilles tendon were treated with minimally invasive achilles tendon lengthening and system rehabilitation. There were 11 males and 16 females with an average age of 35.5 years (ranged 3 to 65 years). Right foot was in 13 cases, left foot was in 10 cases, both feet were in 4 cases. Course of disease was from 1 to 5 years with an average of 2.3 years. The cause of contracture included postoperative complication of tibia fractures treated with intramedullary nailing in 7 feet, sequelae of lower leg compartment syndrome in 11 feet, congenital talipes equinovarus in 13 feet (both feet in 4). Before operation, all the patients walked with limping, plantar flexion anomaly was from 15 degrees to 50 degrees with an average of 35.5 degrees. The strength of quadriceps muscle of thigh was grade V in 27 feet, grade IV in 4 feet, the strength of musculus triceps surae was grade V in 24 feet, grade IV in 7 feet. RESULTS: All the patients were followed-up for 6-24 months with an average of 11.3 months. According to standard of Arner-Lindholm to evaluate function of ankle joint, 29 feet obtained excellent results and 2 feet good. No infection, re-rupture or re-contracture was found. CONCLUSION: Minimally invasive achilles tendon lengthening and system rehabilitation in treating contracture of achilles tendon has advantage such as simple operation, less complication, lower recurrence rate, which is favourable for thoroughly rehabilitation of patients. But, the case in which the strength of quadriceps muscle of thigh or musculus triceps surae still less than grade III after preoperative rehabilitation care should not choose the method.

The relationship between platelet endothelial cell adhesion molecule-1 and paraquat-induced lung injury in rabbits.

BACKGROUND: Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is mainly distributed in vascular endothelial cells. Studies have shown that PECAM-1 is a very significant indicator of angiogenesis, and has been used as an indicator for vascular endothelial cells. The present study aimed to explore the relationship between the expression of PECAM-1 and the degree of acute lung injury (ALI) and fibrosis in paraquat (PQ) induced lung injury in rabbits. METHODS: Thirty-six adult New Zealand rabbits were randomly divided into three groups (12 rabbits in each group) according to PQ dosage: 8 mg/kg (group A), 16 mg/kg (group B), and 32 mg/kg (group C). After PQ infusion, the rabbits were monitored for 7 days and then euthanized. The lungs were removed for histological evaluation. Masson staining was used to determine the degree of lung fibrosis (LF), and semi-quantitative immune-histochemistry analysis to determine the expression of PECAM-1. Pearson's product-moment correlation analysis was performed to evaluate the relationship between the expression of PECAM-1 and the extent of lung injuries expressed by ALI score and degree of LF. RESULTS: Rabbits in the three groups showed apparent poisoning. The rabbits survived longer in group A than in groups B and C (6.47±0.99 days vs. 6.09±1.04 days vs. 4.77±2.04 days) (P<0.05). ALI score was lower in group A than in groups B and C (8.33±1.03 vs. 9.83±1.17 vs. 11.50±1.38) (P<0.05), and there was statistically significant difference between group B and group C (P=0.03). LF was slighter in group A than in groups B and C (31.09%±2.05 % vs. 34.37%±1.62 % vs. 36.54%±0.44%) (P<0.05), and there was statistically significant difference between group B and group C (P=0.026). The PEACAM-1 expression was higher in group A than in groups B and C (20.31%±0.70% vs. 19.34%±0.68% vs. 18.37%±0.46%) (P<0.05), and there was statistically significant difference between group B and group C (P=0.017). Pearson's correlation analysis showed that the expression of PECAM-1 was negatively correlated to both ALI score (Coe=-0.732, P=0.001) and degree of LF (Coe=-0.779, P<0.001). CONCLUSIONS: The PECAM-1 expression significantly decreases in New Zealand rabbits after PQ poisoning, and the decrease is dose-dependent. The PECAM-1 expression is negatively correlated with ALI score and LF, showing a significant role in the development of lung injuries induced by PQ.

The changes of brain water diffusion and blood flow on diffusion-weighted and perfusion-weighted imaging in a canine model of cardiac arrest.

OBJECTIVE: To study the changes of brain water diffusion and cerebral haemodynamics of cortical areas using magnetic resonance imaging (MRI) in canine models of cardiac arrest (CA) and restoration of spontaneous circulation (ROSC). The secondary study objective was to evaluate whether MRI can be used to observe haemodynamic disorders in brain microcirculation. METHODS: CA was induced in six beagle dogs using electrical stimulation followed by resuscitation to spontaneous circulation 3 min later. The dogs were scanned using MRI for echo planar, diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) with injection of Gd-diethylene triamine pentaacetic acid (DTPA) prior to induction of CA and 3 days after ROSC. The arterial blood pressure, unilateral common carotid artery flow and intracranial microcirculation were recorded. RESULTS: All dogs successfully underwent electric-induced ventricular fibrillation which lasted 3 min and were resuscitated to maintain blood pressure stability. Serial MRI scans found that cerebral blood flow (RCBF) decreased in day 1 after ROSC and returned to baseline on day 3. Apparent diffusion coefficient (ADC), however, decreased on day 1 and remained lower than baseline on day 3, with 765.8±82.5×10(-6) mm(2) s(-1) on day 1 and 770.4±59.4×10(-6) mm(2) s(-1) on day 3 comparing to 855.8±43.4×10(-6) mm(2) s(-1) on baseline. CONCLUSIONS: These data provide the evidence that early MRI can be used to observe acute haemodynamic disorders in brain microcirculation in a canine model of cardiac arrest.