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Table of Content

    15 March 2011, Volume 2 Issue 1
    Review Article
    Management of upper gastrointestinal bleeding emergencies: evidence-based medicine and practical considerations
    Zongyu John Chen, Martin L Freeman
    2011, 2(1):  5-12. 
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    Acute upper gastrointestinal (GI) bleeding remains one of the most common encounters in emergency medicine. The increased use of non-steroid anti-inflammatory drugs by the general population and the increased prescription of anti-platelet agents and anti-coagulants after cardiovascular interventions and for prevention of cerebral vascular accidents may have aggravated the situation. Significant progress has been made in the past decade or so in the non-surgical management of acute upper GI bleeding emergencies. This article will review the current standard treatment of the most common upper GI bleeding emergencies in adults as supported by evidence-based medicine with practical considerations from the authors' own practice experience.

    Orginal Article
    Role of platelet TLR4 expression in pathogensis of septic thrombocytopenia
    Yong-qiang Wang, Bing Wang, Yong Liang, Shu-hua Cao, Li Liu, Xin-nv Xu
    2011, 2(1):  13-17. 
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    BACKGROUND: Infection-induced thrombocytopenia (TCP) is an independent risk factor for death of patients with sepsis, but its mechanism is unknown. This study aimed to explore the underlying mechanism of TCP based on the relationship between TLR4 expression and platelet activation in septic patients.
    METHODS: A total of 64 patients with sepsis were prospectively studied. Platelet count (PC), mean platelet volume (MPV), platelet distribution width (PDW), platelet TLR4 expression, platelet PAC-1 expression, sCD40L and TNF-α concentrations were compared between the healthy control group (15 volunteers) and sepsis group (64 patients) at admission and on the 3, 5, and 9 days after admission. The changes of MPV and PDW in the TCP and non-TCP subgroups of sepsis before and after treatment were recorded. Prognostic index was analyzed.
    RESULTS: PC was lower in the sepsis group (P=0.006), and MPV and PDW were higher in the sepsis group than those in the healthy control group (P=0.046, P=0.001). Platelet TLR4 and PAC-1 expressions, and sCD40L and TNF-α levels increased more significantly in the sepsis group (P<0.001). PAC-1 expression and TNF-α level were higher in the TCP group than in the non-TCP group before and after treatment (P=0.023, P=0.011). sCD40L concentration and platelet TLR4 expression were significantly higher in the treated TCP group than in the non-TCP group (P=0.047, P=0.001). Compared to the non-TCP group, the rate of bleeding was higher (P=0.024) and the length of ICU stay was longer (P=0.013). The APACHE II score and the 28-day mortality were higher in the TCP group (P<0.01, P=0.048).
    CONCLUSIONS: The elevation of platelet TLR4 expression in sepsis along with platelet activation is closely related to the incidence of thrombocytopenia. The occurrence of TCP is a sign of poor prognosis in sepsis patients.

    Clinical factors in patients with ischemic versus hemorrhagic stroke in East China
    Jing Zhang, Yao Wang, Gan-nan Wang, Hao Sun, Tao Sun, Jian-quan Shi, Hang Xiao, Jin-song Zhang
    2011, 2(1):  18-23. 
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    BACKGROUND: Stroke is one of the leading causes of mortality and morbidity of vascular diseases, and its incidence maintains at a high level around the world. In China, stroke has been a major public health problem. Because the pathogenesis of ischemic stroke is different from that of hemorrhagic stroke, their clinical factors would not be the same. Therefore to investigate the different effects of various effect factors on ischemic versus hemorrhagic stroke and then to enhance the prevention are crucial to decrease the incidence.
    METHODS: A total of 692 patients, consisting of 540 ischemic stroke patients and 152 hemorrhagic stroke patients from East China, were included in this study. The related factors of stroke subtypes were collected and analyzed.
    RESULTS: The factors significantly associated with ischemic stroke as opposed to hemorrhagic stroke were family history of stroke, obesity, atherosclerotic plaque of the common carotid artery, atrial fibrillation, hyperfibrinogenemia, transient ischemic attack (TIA), atherosclerotic plaque of the internal carotid artery, coronary heart, lower high-density lipoproteins (lower HDL), increasing age, diabetes mellitus, and gender (male) (P<0.05). Leukocytosis, hypertension and family history of hypertension were the significant factors associated with hemorrhagic stroke versus ischemic stroke. Smoking, drinking, kidney diseases and lower HDL-C were the significant factors contributing to ischemic stroke in man. Obesity, family history of hypertension, family history of stroke, hypercholesteremia and myocardial ischemia were the significant factors for females with ischemic stroke.
    CONCLUSIONS: The most prominent factors for overall stroke in East China were hypertension, followed by higher pulse pressure and hypercholesteremia. The factors for ischemic and hemorrhagic stroke are not the same. Different effects of risk factors on stroke are found in male and female patients.

    Five-year mortality and coronary heart disease development after normal coronary angiogram
    Jason T McMullan, Christopher J Lindsell, Andra L Blomkalns
    2011, 2(1):  24-29. 
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    BACKGROUND: Previous studies depict low cardiac event and mortality rates in patients with angiographically normal coronary arteries. These studies, however, are limited by small sample sizes, short follow-up intervals, and selection biases. This study was undertaken to determine the natural five-year course of a diverse cohort of subjects with documented normal coronary arteries with respect to coronary heart disease development, revascularization need, and all-cause mortality.
    METHODS: Consecutive adult patients with angiographically normal coronary arteries were followed up for 5 years through medical record review. Patients with any degree of angiographic abnormality, including minimal luminal irregularity or non-critical stenosis, were excluded. Patients were not excluded based on age, co-morbidities (except cardiac transplant and structural heart disease), indication for angiogram, or initial hospitalization status.
    RESULTS: Normal coronary arteries were found in 182 (31.3%) of 582 patients; 129 met all inclusion criteria. The mean age was (49.1±12.5) years; 47 (36.7%) were male and 75 (58.1%) were caucasian. The most common indication for angiography was cumulative risk factors (60.5%). Within 5 years of a normal angiogram, 13 of 129 patients died (10.1%; 95 CI 5.7%-16.9%). Six (40%; 95 CI 19.8% to 64.3%) of 15 patients undergoing repeat angiogram within five years developed new coronary heart disease, with one requiring revascularization. Of traditional risk factors of coronary heart disease, only diabetes was associated with a higher risk of death.
    CONCLUSION: The natural five-year course of a diverse cohort of patients with documented normal coronary arteries suggests that there is significant risk for death and development of coronary heart disease.

    Nebulized lidocaine inhalation in the treatment of patients with acute asthma
    Zu-ming Lv, Li Chen, Jie Tang
    2011, 2(1):  30-32. 
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    BACKGROUND: Lidocaine can promote the apoptosis of eosinophils, which is normally delayed by IL-5; it has a good effect on serious steroid resistant asthma (SRA). The study aimed to explore the effect of nebulized lidocaine inhalation on asthma.
    METHODS: It was a randomized, double-blind, placebo-controlled and prospective study. A total of 36 patients with acute asthma were divided into groups A1, A2, B1 and B2, with 9 patients in each group. The patients of groups A1 and A2 had steroid resistant asthma (SRA) and those of groups B1 and B2 had steroid sensitive asthma (SSA). Patients in groups A2 and B1 were administered nebulized lidocaine in addition to routine treatment, while patients in groups A1 and B2 were given nebulized normal saline apart from routine treatment and served as placebo-controlled groups.
    RESULTS: There were significant differences in heart rate, respiratory rate, and peak flow rate and forced expiratory volume in one second between the experimental groups and the placebo-controlled groups. There was no significant difference between groups A2 and B1, and between A1 and B2.
    CONCLUSION: Inhaled lidocaine is beneficial to asthma patients, especially those with steroid-resistant asthma.

    Transition to computed radiography: can emergency medicine doctors accurately predict the need of film printing to facilitate optimal patient care?
    Siu Ming Yang, Chor Man Lo
    2011, 2(1):  33-37. 
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    BACKGROUND: This study aimed to evaluate emergency medicine doctors' accuracy in predicting the need of film printing in a simulated setting of computed radiography and assess whether this can facilitate optimal patient care.
    METHODS: Cross sectional study was conducted from 20 March 2009 to 3 April 2009 in 1334 patients. After clinical assessment of those patients who needed X-ray examination, doctors in the emergency department would indicate whether film printing was necessary for subsequent patient care in a simulated computed radiography setting. The final discharge plan was then retrieved from each patient record. Accuracy of doctors' prediction was calculated by comparing the initial request for radiographic film printing and the final need of film. Doctors with different level of emergency medicine experience would also be analyzed and compared.
    RESULTS: The sensitivity of predicting film printing was 84.5% and the specificity of predicting no film printing was 91.2%. Positive predictive value was 88.4% while negative predictive value was 88.2%. The overall accuracy was 88.2%. The accuracy of doctors stratified into groups of fellows, higher trainees and basic trainees were 85.4%, 90.5% and 88.5% respectively (P=0.073).
    CONCLUSIONS: Our study showed that doctors can reliably predict whether film printing is needed after clinical assessment of patients, before actual image viewing. Advanced indication for film printing at the time of imaging request for selected patients can save time for all parties with minimal wastage.

    Bcl-2 in suppressing neuronal apoptosis after spinal cord injury
    Ying Wang, Zhi-yang Sun, Kui-ming Zhang, Guo-qiang Xu, Guang Li
    2011, 2(1):  38-44. 
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    BACKGROUND: Apoptosis plays an important role in central neural diseases and trauma. B-cell lymphoma/Leukemia-2 (Bcl-2) can inhibit apoptosis in a wide variety of cells including neurons. In this experiment, by studying Bcl-2 over-expression transgenic (TG) mice subjected to spinal cord injury (SCI), we investigated whether Bcl-2 could reduce posttraumatic neuronal apoptosis, reduce the range of damage, and improve the behavioral functional recovery after contusive SCI.
    METHODS: Nine Bcl-2 TG mice and nine control mice were subjected to SCI of moderate severity at T10, with the use of weight dropping (WD) method (impact force 2.5×3.0 g/cm). At times up to 1 day, 7 days and 14 days after SCI, functional deficits were evaluated with Basso, Beattie, and Bresnahan (BBB) scales, and apoptosis of neurons was investigated by using the TUNEL method. Another three control mice only underwent lamina opening, but were not subjected to SCI, to provide blank comparison.
    RESULTS: The mean functional scores for the control mice (5.05 ±0.35) were lower than those for the Bcl-2 TG mice (5.45 ±0.15), although the unpaired T-test revealed no significant difference (P=0.67). On the other hand, the number of TUNEL positive neurons and integrated option density (IOD) scores for the Bcl-2 TG mice were both significantly lower than those for the control mice (P<0.05).
    CONCLUSIONS: This experiment suggests that overexpression of Bcl-2 may suppress neuronal apoptosis after SCI. Bcl-2 may be an important factor within the central nervous system that can relieve the damage after trauma.

    Imaging in detecting sites of pulmonary fibrosis induced by paraquat
    Xiao-li Xu, Wei Wang, Zu-jun Song, Hong Ding, Xiao-hong Duan, Huan-cheng Meng, Jian Chong
    2011, 2(1):  45-49. 
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    BACKGROUND: The most common cause of death from paraquat (PQ) poisoning is respiratory failure from pulmonary fibrosis, which develops through pathological overproduction of extracellular matrix proteins such as collagens. In this study, a MicroCT system was used to observe dynamic changes of pulmonary fibrosis in rats with PQ poisoning, and find the characteristics of interstitial lung diseases via density-based and texture-based analysis of CT images of the lung structure.
    METHODS: A total of 15 male SD rats were randomly divided into a control group (n=5) and a PQ poisoning group (n=10). The rats in the poisoning group were intraperitoneally administered with 4 mg/ mL PQ at 14 mg/kg, and the rats in the control group were administered with the same volume of saline. The signs of pulmonary fibrosis observed by the MicroCT included ground-glass opacity, nodular pattern, subpleural interstitial thickening, consolidation honeycomb-like shadow of the lung.
    RESULTS: Compared with the control group, the rats with acute PQ poisoning had different signs of pulmonary fibrosis. Ground-glass opacity and consolidation of the lung appeared at the early phase of pulmonary fibrosis, and subpleural interstitial thickening and honeycomb-like shadow developed at the middle or later stage. MicroCT images showed that fibrotic lung tissues were denser than normal lungs, and their density was up-regulated with pulmonary fibrosis. There was no difference in the progress of pulmonary fibrosis between the right lung and the left lung (P>0.05), but there were differences in fibrosis degree at different sites in the lung (P<0.05 or P<0.01). Pulmonary fibrosis was mainly seen in the exterior area of the middle-lower part of the lung.
    CONCLUSION: Imaging can show the development of pulmonary fibrosis in PQ poisoning rats, and this method may help to administer drugs more reasonably in treating pulmonary fibrosis.

    Pathological changes in the lung and brain of mice during heat stress and cooling treatment
    Zhi-feng Liu, Bing-ling Li, Hua-sheng Tong, You-qing Tang, Qiu-lin Xu, Jin-qiang Guo, Lei Su
    2011, 2(1):  50-53. 
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    BACKGROUND: Heatstroke often leads to multiple organ dysfunction syndrome (MODS) with a death rate of 40% or a neurological morbidity of 30%. These high rates in patients with heatstroke are largely due to the progression of heat stress to MODS, resulting in no specific treatment available. This study aimed to develop a mouse model of heat stress and determine the pathological changes in the lung and brain during heat stress and cooling treatment.
    METHODS: A mouse model of heat stress was established in a pre-warmed incubator set at 35.5 ± 0.5°C and with a relative humidity of 60% ± 5%. Rectal temperature was monitored, and at a temperature of 39 °C, 40 °C, 41 °C, or 42 °C, the mice were sacrificed. The remaining animals were removed from the incubator and cooled at an ambient temperature of 25 ± 0.5 °C and a humidity of 35% ± 5% for 12 or 24 hours at a temperature of 41 °C or for 6 hours at a temperature of 42 °C. The control mice were sham-heated at a temperature of 25 ± 0.5 °C and a humidity of 35% ± 5%. The lungs and brains of all animals were isolated. Hematoxylin and eosin staining and light microscopy were performed to detect pathological changes.
    RESULTS: All mice demonstrated a uniform response to heat stress. A low degree of heat stress induced marked pathological changes of the lungs. With the rise of the temperature to 42°C, progressively greater damage to the lungs with further congestion of the lung matrix, asystematic hemorrhage of alveolar space, abscission of alveolar epithelial cells, and disappearance of pulmonary alveolus tissue structure were detected. However, absorption of congestion and hemorrhage as well as recovery of pulmonary alveolus tissue structure was observed following cooling treatment at an ambient temperature. With a low degree of heat stress, the brain only showed moderate edema. Neuronal denaturation and necrosis were detected at a temperature of 42°C. Interestingly, the lesions in the brain were further aggravated at 42 °C regardless of cooling treatment, but recovery was observed after cooling treatment at 41 °C.
    CONCLUSIONS: The pathological changes of the lungs and brain of mice showed distinctive lesions following heat stress and cooling treatment, and they were correlated with the time and duration of cooling treatment. The results of this study are helpful for further study of the mechanisms linking heatstroke.

    Effects of Hemin on neuroglobin expression after cardiopulmonary resuscitation in rats
    Ai-wen He, Ting Yang, Shou-quan Chen, Zhang-ping Li, Hui-ping Li, Wei-jia Huang, Jun-yan Cheng, Jie Zhang, Ping Yang, Wan-tie Wang
    2011, 2(1):  54-58. 
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    BACKGROUND: Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin (NGB) is an oxygen-binding heme protein found in the brain with a protection role against ischemic-hypoxic brain injury. Hemin is an effective activator of neuroglobin. This study was undertaken to assess the effect of hemin on expression of neuroglobin (NGB) in the cerebral cortex, neuro-deficit score (NDS) and pathological changes after cardiopulmonary resuscitation (CPR) in rats.
    METHODS: A total of 120 male Sprague-Dawley (SD) rats were randomly divided into a control group (A), a CPR group (B) and a Hemin group (C). The animal model of cardiac arrest (CA) induced by asphyxia and CPR was established. NGB expression in the cerebral cortex with immunohistochemistry, NDS and pathological changes in the cerebral cortex were examined at 3, 6, 12, 24 hours after recovery of spontaneous circulation (ROSC) in each group. Experimental data were treated as one-factor analysis of variance and the Tukey test.
    RESULTS: In comparison with group A, NGB expression was increased significantly at 12 and 24 hours after ROSC (P<0.05 or P<0.01), NDS was decreased significantly at each time point after ROSC (P<0.01), and pathological changes were severe at each time point after ROSC in group B. In comparison with group A, NGB expression was increased significantly at 6, 12, 24 hours after ROSC (P<0.05 or P<0.01), NDS was decreased significantly at 3, 6, 12 hours after ROSC (P<0.01) in group C. In comparison with group B, NGB expression was increased significantly at 12 and 24 hours after ROSC, NDS was increased significantly at 12 and 24 hours after ROSC, and pathological changes were milder in group C.
    CONCLUSION: There were increased NGB expression in the cerebral cortex, decreased NDS, and severe pathological changes after CPR in rats. Hemin treatment up-regulated expression of NGB, improved NDS, mitigated pathological changes, and alleviated cerebral injury after CPR.

    Role of corticotrophin releasing hormone in cerebral infarction-related gastrointestinal barrier dysfunction
    Ye-cheng Liu, Zhi-wei Qi, Shi-gong Guo, Zhong Wang, Xue-zhong Yu, Sui Ma
    2011, 2(1):  59-65. 
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    BACKGROUND: Corticotrophin releasing hormone (CRH) is believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response, and studies on CRH in physical stress are few. This study was undertaken to investigate whether CRH plays an important role in cerebral infarction-related gastrointestinal barrier dysfunction.
    METHODS: Thirty male Wistar rats were randomly divided into a pseudo-operation group (group C, n=10), a cerebral infarction group (group I, n=10), and a cerebral infarction + ic α-helical-CRH (9-41) group (group Aic, n=10). Urine samples were collected to determine the levels of epinephrine, norepinephrine, cortisol, and sucrose. At 24 hours after establishment of the models, blood samples were taken to determine the activity of diamine oxidase (DAO) and the concentration of D-lactic acid (D-lac). The stomach was taken to determine gastric Guth score, and the hypothalamus was also taken to determine tissue CRH protein expression using Western blotting.
    RESULTS: The hypothalamus CRH protein, the indicators of stress, the plasma DAO activity and plasma D-lac, urine sucrose exertion and gastric Guth score in group I were higher than those in groups Aic and C.
    CONCLUSIONS: After cerebral infarction, CRH in the hypothalamus was increased, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system were activated, gastrointestinal permeability was increased, and gastrointestinal barrier function was destroyed. CRH receptor antagonist alleviated the gastrointestinal barrier function.

    Effect of glucocorticoid on MIP-1α and NF-кb expressing in the lung of rats undergoing mechanical ventilation with a high tidal volume
    Zhi-hong Liu, Xin-ri Zhang, Xiao-yun Hu, Meng-yu Cheng, Jian-ying Xu, Yong-cheng Du
    2011, 2(1):  66-69. 
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    BACKGROUND: Ventilator induced lung injury (VILI) is a serious complication in the treatment of mechanical ventilating patients, and it is also the main cause that results in exacerbation or death of patients. In this study, we produced VILI models by using glucocorticoid in rats with high tidal volume mechanical ventilation, and observed the content of macrophage inflammatory protein-1α (MIP-1α) in plasma and bronchoalveolar lavage fluid (BALF) and the expression of MIP-1α mRNA and nuclear factor-kappa B (NF-кB) p65 mRNA in the lung so as to explore the role of glucocorticoid in mechanical ventilation.
    METHODS: Thirty-two healthy Wistar rats were randomly divided into a control group, a ventilator induced lung injury (VILI) group, a dexamethasone (DEX) group and a budesonide (BUD) group. The content of MIP-1a in plasma and BALF was measured with ELISA and the level of MIP-1α mRNA and NF-кBp65 mRNA expressing in the lung of rats were detected by RT-PCR. The data were expressed as mean±SD and were compared between the groups.
    RESULTS: The content of MIP-1α in plasma and BALF and the level of MIP-1α mRNA and NF-кBp65 mRNA in the lung in the DEX and BUD groups were significantly lower than those in the VILI group (P<0.001). Although the content of MIP-1α in plasma and BALF and the level of MIP-1α mRNA and NF-кBp65 mRNA in the lung in the BUD group were higher than those in the DEX group, there were no significant differences between them (P>0.05).
    CONCLUSIONS: Glucocorticoid could down-regulate the expression of MIP-1α by inhibiting the activity of NF-кB in the lung and may exert preventive and therapeutic effects on VILI to some extent. The effect of local use of glucocorticoid against VILI is similar to that of systemic use, but there is lesser adverse reaction.

    Case Reports
    Acute myocardial infarction in a child with myocardial bridge
    Xiao-dong Liu, Chun-lei Sun, Su-ping Mu, Xiao-mei Qiu, Hai-ying Yu
    2011, 2(1):  70-72. 
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    BACKGROUND: Myocardial infarction (MI) is rare in children, and Kawasaki disease is now recognized as the main cause for MI. In this report, we present a child with MI caused by myocardial bridge (MB).
    METHODS: A 7.5-year-old boy was admitted to Weifang People’s Hospital on September 16, 2008 for heart disease. By electrocardiogram, coronary CT angiography, emission computed tomography, and other examinations, he was initially diagnosed as having (1) acute inferior myocardial infarction and extensive anterior myocardial infarction; (2) fulminant myocarditis; or (3) coronary myocardial bridge. He was treated with oxygen, thrombolysis, myocardial nutrition, vitamin C (4.0 g per time), dexamethasone (7.5 mg per time), a large dose of gamma globulin, and interferon.
    RESULTS: Myocardial enzymes, liver function, C-reactive protein, and troponin-I returned to normal at 21 days after treatment. At 29 days, electrocardiogram indicated that II, III, aVF, V4 - V6 leads had abnormal Q wave, and ST-T changed. The patient was discharged.
    CONCLUSION: Myocardial bridge may be one of the causes of MI in children.

    Treatment of vitamin K-dependent coagulation factor deficiency and subarachnoid hemorrhage
    Hai-fei Chen, Tian-qin Wu, Ling-juan Jin, Jie-qing Tang, Jing-jing Zhu, Ying-chao Ge, Zheng-yang Li, Hong-shi Shen, Long-mei Qin, Zi-qiang Yu, Zhao-yue Wang
    2011, 2(1):  73-76. 
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    BACKGROUND: In adults, vitamin K-dependent coagulation factor deficiency (VKCFD) increases in the recent years. We treated a VKCFD patient with subarachnoid hemorrhage, with favorable outcomes.
    METHODS: A 19-year-old male student with VKCFD was treated at our hospital. The initial treatment was injection of a large dose of vitamin K and fresh plasma, and then with oral high dose of vitamin K4.
    RESULTS: At 4 weeks after admission, the focus of hemorrhage subsided, neurological examination was normal, and the patient was discharged.
    CONCLUSIONS: VKCFD is rare and its diagnosis should be based on the history of the patient and the results of laboratory examinations. A large dose of vitamin K is the first choice of treatment.

    Instructions for Authors
    Instructions for Authors
    2011, 2(1):  77-80. 
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