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排序方式: 共有232条查询结果,搜索用时 31 毫秒
31.
SARS: ventilatory and intensive care 总被引:2,自引:0,他引:2
Severe acute respiratory syndrome (SARS) is an emerging infection caused by a novel coronavirus. It is characterised by a highly infectious syndrome of fever and respiratory symptoms, and is usually associated with bilateral lung infiltrates. The clinical syndrome of SARS often progresses to varying degrees of respiratory failure, with about 20% of patients requiring intensive care. Despite concern about potential aerosol generation, non-invasive ventilation (NIV) has been reported to be efficacious in the treatment of SARS-related ARF without posing infection risks to health care workers (HCW). Spontaneous pneumomediastinum and pneumothorax in SARS is common. The incidence of NIV-associated barotrauma ranged from 6.6% to 15%. Patients who fail to tolerate NIV or fail NIV with progressive dyspnoea, tachypnoea and hypoxaemia should be intubated and mechanically ventilated. Mortality rates in intensive care units for SARS patients were high: 34–53% at 28 days, when some patients were still being ventilated. Strict adherence to infection control measures including isolation, use of appropriate personal protective equipment and negative pressure environment had been reported to eliminate cross-infection to HCW. 相似文献
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Chen YC; Wang CH; Su IJ; Hu CY; Chou MJ; Lee TH; Lin DT; Chung TY; Liu CH; Yang CS 《Blood》1989,74(1):388-394
Among 354 adult patients with either hematological malignancy or aplastic anemia, eight were positive for anti-HTLV-I antibodies; six of eight had received multiple transfusions. There was an approximately 3.5-fold increase (P less than .001) of HTLV-I seropositivity in the patients with hematologic disease (8 of 354, 2.23%) compared to the healthy adults older than 20 years (34 of 5252, .65%). Two hematological patients, one with Hodgkin's disease and one with acute promyelocytic leukemia, were found to be positive for HTLV-I, and developed and died of adult T-cell leukemia/lymphoma (ATL) subsequently. Both were long-term survivors of the primary disease and had received multiple transfusions. The latent period from blood transfusion to onset of ATL was 6 months and 11 years, respectively. Immunocompromised patients, who were seropositive for HTLV-I, may be at increased risk for ATL compared to healthy carriers of HTLV-I, and the latent period may be shorter. 相似文献
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Jad El‐Hoss Kate Sullivan Tegan Cheng Nicole YC Yu Justin D Bobyn Lauren Peacock Kathy Mikulec Paul Baldock Ian E Alexander Aaron Schindeler David G Little 《Journal of bone and mineral research》2012,27(1):68-78
Neurofibromatosis type 1 (NF1) is a common genetic condition caused by mutations in the NF1 gene. Patients often suffer from tissue‐specific lesions associated with local double‐inactivation of NF1. In this study, we generated a novel fracture model to investigate the mechanism underlying congenital pseudarthrosis of the tibia (CPT) associated with NF1. We used a Cre‐expressing adenovirus (AdCre) to inactivate Nf1 in vitro in cultured osteoprogenitors and osteoblasts, and in vivo in the fracture callus of Nf1flox/flox and Nf1flox/? mice. The effects of the presence of Nf1null cells were extensively examined. Cultured Nf1null‐committed osteoprogenitors from neonatal calvaria failed to differentiate and express mature osteoblastic markers, even with recombinant bone morphogenetic protein‐2 (rhBMP‐2) treatment. Similarly, Nf1null‐inducible osteoprogenitors obtained from Nf1 mouse muscle were also unresponsive to rhBMP‐2. In both closed and open fracture models in Nf1flox/flox and Nf1flox/? mice, local AdCre injection significantly impaired bone healing, with fracture union being <50% that of wild type controls. No significant difference was seen between Nf1flox/flox and Nf1flox/? mice. Histological analyses showed invasion of the Nf1null fractures by fibrous and highly proliferative tissue. Mean amounts of fibrous tissue were increased upward of 10‐fold in Nf1null fractures and bromodeoxyuridine (BrdU) staining in closed fractures showed increased numbers of proliferating cells. In Nf1null fractures, tartrate‐resistant acid phosphatase–positive (TRAP+) cells were frequently observed within the fibrous tissue, not lining a bone surface. In summary, we report that local Nf1 deletion in a fracture callus is sufficient to impair bony union and recapitulate histological features of clinical CPT. Cell culture findings support the concept that Nf1 double inactivation impairs early osteoblastic differentiation. This model provides valuable insight into the pathobiology of the disease, and will be helpful for trialing therapeutic compounds. © 2012 American Society for Bone and Mineral Research 相似文献
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对强效镇痛剂羟甲芬太尼的两个光学异构体体cis-(3R,4S,2′R)-羟甲芬太尼(I)和trans-(3R,4R,2′S)-羟甲芬太尼(Ⅱ)进行了X-射线衍射晶体结构分析。两个异构体均有一个sp3N(l)原子和一个sp2N(7)原子。哌啶环呈椅式构象,顺式异构体I的3-甲基处于直立键,4-N-苯基丙酰胺基处于平伏键;反式异构体II的3-甲基与4-N-苯基丙酰胺基均处于平伏键。在I分子中,C(4)原子与4-丙酰胺基组成的平面与N-苯环平面近似相互垂直,而在II中,两平面的二面角近似为100℃。两异构体分子中均存在分子内氢键O(1)一H…N(1),反式异构体II还存在分子间氢键O(1)一H(A)…O(2)(B)。 相似文献
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6-(αα-二苯基乙酰哌嗪基苯基)-4,5-二氢-5-甲基-3(2H)-哒嗪酮对兔血小板聚集及TXB2,cAMP的影响 总被引:4,自引:0,他引:4
6-(αα-二苯基乙酰哌嗪基苯基)-4,5-二氢-5-甲基-3(2H)-哒嗪酮(简称DMDP)是我院新合成的哒嗪酮的衍生物。DMDP可以显著抑制由花生四烯酸(AA(?),ADP和血小板活化因子(PAF)诱导的免血小板聚集,其IC50分别为1.12±0.1.4.19±0.5和2.97±0.1μmol/L。实验还表明DMDP在1~500 μmol/L浓度范围内呈剂量依赖性地抑制兔血小板内血栓素B2含量,但升高兔血小板内环腺苷酸水平,这可能是其抑制血小板聚集的作用机理之一。 相似文献