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1.
徐凯 《华西医学》2010,(7):1289-1291
目的总结甲型H1N1流感病毒性肺炎患者的胸部X线和CT表现特征。方法回顾分析2009年3月-11月3例经临床表现及病原学检查证实的甲型H1N1流感病毒性肺炎的胸部X线、CT表现。结果肺部病灶多呈散在小片状高密度影,边缘模糊,邻近胸膜;病变最常累及肺基底段;病灶多有少量胸腔积液;病灶有扩散迅速,合理用药后消失较快的特点;病灶吸收落后于临床表现。结论甲型H1N1流感病毒性肺炎的X线、CT表现具有一定的特点,总结并掌握这些特点,有利于早期诊断。其确诊有赖于实验室检查和流行病学调查。  相似文献   

2.
目的 总结甲型H1N1流感肺炎影像学表现,提高对本病的认识。方法 回顾性分析17例确诊甲型H1N1流感肺炎患者胸部X线片及64层螺旋CT检查系列影像学资料。结果 17例甲型H1N1流感肺炎患者均有1次以上胸部计算机X线摄影术(CR)检查,其中8例接受CT检查。17例胸部X线及CT表现均以斑片或大片实变影合并磨玻璃密度影为主要表现。病变累及单侧肺野者4例,占23.53%;双侧肺野均受累者13例,占76.47%;随访病例均有不同程度的纤维化改变。结论 甲型H1N1流感肺炎X线及CT表现具有一定特征性。肺部病变以多叶段分布渗出性改变为其共有表现,病程后期两肺以纤维化表现为主。  相似文献   

3.
目的:探讨甲型H1N1流感首次胸部CT影像学特点.方法:回顾性分析临床确诊22例甲型H1N1流感患者的首次胸部CT表现.结果:22例患者中,男10例,女12例,年龄4~63岁,平均46岁.22例患者CT表现共有268个肺段病变,包括磨玻璃密度影218段、斑片状实变影30段、结节影20段.肺部病变分布在中外带17例,弥漫分布3例,内带2例.胸膜增厚15例,其中右侧12例、左侧10例、双侧7例.纵隔淋巴结肿大3例,胸腔积液2例.结论:甲型H1N1流感患者首次胸部CT表现特点为以双侧、多段、外带肺部磨玻璃密度影改变为主.  相似文献   

4.
目的 观察甲型H1N1流感患者的胸片及CT表现。 方法 回顾性分析51例甲型H1N1流感患者(实验室确诊47例,临床诊断4例)初始胸片及CT检查的病变表现形式、分布特点及病变程度。 结果 甲型H1N1流感患者的胸片及CT检查最主要表现是双侧或单侧多发磨玻璃密度影,伴或不伴单发或多发实变区。CT显示病变主要沿支气管血管周围中心肺区和(或)胸膜下区分布。 结论 影像学诊断甲型H1N1流感时,结合病史非常重要。  相似文献   

5.
目的:探讨甲型H1N1流感合并肺炎的影像学表现.方法:回顾分析经我院诊治的59例甲型H1N1流感合并肺炎患者的临床及影像资料.结果:59例患者中,单侧发病9例,双侧发病50例;病灶呈单发或少许散在分布的10例,多发分布的32例,弥漫广泛分布的16例.其中以胸膜下或者肺野后部为主的19例,病灶常多种影像改变并存.结论:甲型H1N1流感合并肺炎表现多样,以斑片状实变影以及磨玻璃样影为主,可伴有间质改变、胸腔积液,以胸膜下或者肺野后部好发,具有一定的特点.影像检查可以早期发现甲型H1N1流感的肺部改变,并对动态观察病情变化有重要价值.  相似文献   

6.
目的:研究甲型H1N1流感肺炎影像特点,为今后该病的诊断提供X线诊断依据.方法:回顾性分析研究30例临床诊断为甲型H1N1流感肺炎患者胸部影像学检查结果.结果:从发热到出现胸部X线异常影像平均为4.2 d,从出现异常影像到极期(X线影像最重的1d)平均为6.8 d,从极期到大部或基本吸收消散平均为10.5 d.有16例双侧中、下肺野出现不同程度的阴影,占53.3%;有13例早期表现为雾状、磨砂玻璃样浅淡阴影,占43.3%;全部病例均为多叶、多节段受损,占100%;有16例遗留条索状、网格状、蜂窝状阴影,占53.3%.结论:甲型H1N1流感肺炎发病后数天内胸片可无异常改变;大多数患者肺损害为多叶,多节段;胸片影像表现呈多种肺部炎性疾病影像表现;胸片阴影多发部位在中下2/3肺野;一部分患者遗留肺纤维化;胸部CT检查可早期发现病灶.  相似文献   

7.
首发重症及危重症甲型H1N1流感6例   总被引:1,自引:1,他引:0  
甲型H1N1流感患者的胸部影像学改变出现早、分布广、变化快,认识其特征及动态变化,密切结合临床表现及实验室检查对早期确诊和有效治疗有积极的指导作用.本文对我院2009年收治首批确诊的6例散发重症及危重症甲型H1N1流感患者的临床、实验室、影像学表现进行回顾性分析.  相似文献   

8.
目的探讨重症型甲型H1N1流感的X线平片与CT特征。方法回顾性分析9例临床确诊的重症型甲型H1N1流感的X线与CT表现。结果首次X线胸部平片示双肺受累8例,单肺受累1例,8例行CT检查两肺均受累,1例死亡未行CT检查。受累肺叶3~5叶,受累肺段5~8个。9例均表现在两肺多叶,以中外带及下叶为甚,2例病变进展迅速,1例死亡。结论重症型甲型H1N1流感的主要影像学表现为:(1)病变主要发生在肺的外周;(2)两肺多叶受累,下肺野多于上肺野;(3)病变变化迅速;(4)两肺出现磨玻璃影、大片实变影,可见支气管气相,伴有胸膜增厚或少量胸水;(5)CT比胸片能更好地显示肺内病变特征。熟悉其影像学表现,密切结合临床和实验室检查可以做出明确诊断。  相似文献   

9.
目的 分析甲型H1N1流感肺炎的肺CT特点及其与临床转归相关性.方法 将73例甲流肺炎患者分为呼吸衰竭组和非呼吸衰竭组,比较两组胸部影像学的差异及影像学严重程度与临床转归的相关性.结果 73例患者中,呼吸衰竭组32例,非呼吸衰竭组41例.两组患者胸部影像学比较病变形态差别不大,但病变范围上有明显差别,呼吸衰竭组患者病变范围大于非呼吸衰竭组.结论 影像学严重程度可以作为判断甲型H1N1流感病情严重程度和预后的指标.  相似文献   

10.
重症甲型H1N1流感肺部的影像学表现   总被引:2,自引:0,他引:2  
目的:探讨重症甲型H1N1流感患者的胸部X线和CT表现特征,以期提高对甲型H1N1流感的认识。方法:搜集我院2009年6月~2010年3月住院确诊重症甲型H1N1流感的患者11例,对其临床及影像学资料进行回顾性总结分析。结果:重症甲型H1N1流感临床的主要特征是持续高热、咳嗽,部分出现呼吸衰竭和神志改变。肺部影像学特点是:①早期最常见影像学表现为斑片状磨玻璃影;②发病后1~3天达到高峰,重症患者肺部病变变化较快且易反复;③治疗后患者肺部大部分病变可完全吸收,部分可见肺间质的改变。④肺部影像学表现与临床表现基本一致。结论:重症甲型H1N1流感患者的影像学表现可以反映病情变化,对指导临床治疗及判断预后具有重要的参考价值。  相似文献   

11.
Human immunodeficiency virus (HIV) type 1 Vpu is an integral membrane protein with a unique affinity for betaTrCP (TrCP), a key member of the SkpI-Cullin-F-box E3 ubiquitin ligase complex that is involved in the regulated degradation of cellular proteins, including IkappaB. Remarkably, Vpu is resistant to TrCP-mediated degradation and competitively inhibits TrCP-dependent degradation of IkappaB, resulting in the suppression of nuclear factor (NF)-kappaB activity in Vpu-expressing cells. We now report that Vpu, through its interaction with TrCP, potently contributes to the induction of apoptosis in HIV-infected T cells. Vpu-induced apoptosis is specific and independent of other viral proteins. Mutation of a TrCP-binding motif in Vpu abolishes its apoptogenic property, demonstrating a close correlation between this property of Vpu and its ability to inhibit NF-kappaB activity. The involvement of NF-kappaB in Vpu-induced apoptosis is further supported by the finding that the levels of antiapoptotic factors Bcl-xL, A1/Bfl-1, and TNF receptor-associated factor (TRAF)1, all of which are expressed in an NF-kappaB-dependent manner, are reduced and, at the same time, levels of active caspase-3 are elevated. Thus, Vpu induces apoptosis through activation of the caspase pathway by way of inhibiting the NF-kappaB-dependent expression of antiapoptotic genes.  相似文献   

12.
The coronavirus SARS-CoV-2, the aetiological agent of COVID-19 disease, is representing a worldwide threat for the medical community and the society at large so that it is being defined as “the twenty-first-century disease”. Often associated with a severe cytokine storm, leading to more severe cases, it is mandatory to block such occurrence early in the disease course, to prevent the patients from having more severe, sometimes fatal, outcomes. In this framework, early detection of “danger signals”, possibly represented by alarmins, can represent one of the most promising strategies to effectively tailor the disease and to better understand the underlying mechanisms eventually leading to death or severe consequences. In light of such considerations, the present article aims at evaluating the role of alarmins in patients affected by COVID-19 disease and the relationship of such compounds with the most commonly reported comorbidities. The conducted researches demonstrated yet poor literature on this specific topic, however preliminarily confirming a role for danger signals in the amplification of the inflammatory reaction associated with SARS-CoV-2 infection. As such, a number of chronic conditions, including metabolic syndrome, gastrointestinal and respiratory diseases, in turn, associated with higher levels of alarmins, both foster the infection and predispose to a worse prognosis. According to these preliminary data, prompt detection of high levels of alarmins in patients with COVID-19 and co-morbidities could suggest an immediate intense anti-inflammatory treatment.

Key message

  • Alarmins have a role in the amplification of the inflammatory reaction associated with SARS-CoV-2 infection
  • a prompt detection of high levels of alarmins in patients with COVID-19 could suggest an immediate intense anti-inflammatory treatment
  相似文献   

13.
The essential trace element selenium has long been considered to exhibit anti-diabetic and insulin-mimetic properties, but recent epidemiological studies indicated supranutritional selenium intake and high plasma selenium levels as possible risk factors for development of type 2 diabetes, pointing to adverse effects of selenium on carbohydrate metabolism in humans. However, increased plasma selenium levels might be both a consequence and a cause of diabetes. We summarize current evidence for an interference of selenium compounds with insulin-regulated molecular pathways, most notably the phosphoinositide-3-kinase/protein kinase B signaling cascade, which may underlie some of the pro- and anti-diabetic actions of selenium. Furthermore, we discuss reports of hyperinsulinemia, hyperglycemia and insulin resistance in mice overexpressing the selenoenzyme glutathione peroxidase 1. The peroxisomal proliferator-activated receptor gamma coactivator 1α represents a key regulator for biosynthesis of the physiological selenium transporter, selenoprotein P, as well as for hepatic gluconeogenesis. As proliferator-activated receptor gamma coactivator 1α has been shown to be up-regulated in livers of diabetic animals and to promote insulin resistance, we hypothesize that dysregulated pathways in carbohydrate metabolism and a disturbance of selenium homeostasis are linked via proliferator-activated receptor gamma coactivator 1α.  相似文献   

14.
目的与背景 本研究旨在检测长链非编码RNA DBH-AS1在胰腺癌中的表达情况,探讨DBH-AS1在胰腺癌进展中的潜在分子作用。方法 采用实时定量PCR检测基因表达。细胞增殖、成克隆生长和迁移侵袭能力分别通过CCK-8、克隆形成和transwell检测。蛋白质水平用免疫印迹法测定。结果GEPIA数据库和定量PCR结果证实,DBH-AS1在胰腺癌组织中表达下调,与癌旁正常胰腺组织相比差异均有统计学意义(P 均<0.05)。在胰腺癌肿瘤组织中DBH-AS1的低表达与肿瘤分化差、TNM分期晚期、淋巴结转移、以及预后不良(无瘤生存时间和总体生存时间)有关(P均<0.05)。DBH-AS1基因敲除可促进胰腺癌细胞的增殖、克隆形成、迁移和侵袭能力,与对照组相比差异均有统计学意义(P均<0.05)。机制研究表明,在胰腺癌中DBH-AS1通过下调AKT1表达抑制mTOR信号通路。结论DBH-AS1通过降低AKT1的表达抑制胰腺癌的进展。  相似文献   

15.
GD3, a ganglioside expressed on human melanoma, can be recognized by the humoral immune system. In this paper, we demonstrate that immunizing mice with the human melanoma cell line SK-MEL-28 (GD3+ GM2- CD1-) or with syngeneic APCs loaded with GD3 can induce a GD3-reactive natural killer T (NKT) cell response. GD3-reactive NKT cells were detected among splenocytes of immunized mice at frequencies of approximately 1:2000 both by ELISPOT and GD3-loaded mouse CD1d tetramer analysis. GD3-reactive NKT cells did not react with GM2, a closely related ganglioside, and were not detectable in unimmunized mice. GD3-reactive NKT cells initially produced IL-4 and IFN-gamma followed by IL-10. They were CD1d restricted in that reactivity was abrogated when APCs were blocked with anti-CD1d monoclonal antibody before being loaded with GD3 or when APCs from CD1d knockout mice were used. Because SK-MEL-28 does not express any isoform of human CD1, GD3 must be cross-presented by murine APCs in vivo. This is the first analysis of a natural ligand for mouse NKT cells and the first definitive paper of cross-presentation to NKT cells. This could be a mechanism for NKT cell recognition of tumor gangliosides in CD1- tumors.  相似文献   

16.
17.

Background

Detection of cardiac fibrosis based on endogenous magnetic resonance (MR) characteristics of the myocardium would yield a measurement that can provide quantitative information, is independent of contrast agent concentration, renal function and timing. In ex vivo myocardial infarction (MI) tissue, it has been shown that a significantly higher T is found in the MI region, and studies in animal models of chronic MI showed the first in vivo evidence for the ability to detect myocardial fibrosis with native T-mapping. In this study we aimed to translate and validate T-mapping for endogenous detection of chronic MI in patients.

Methods

We first performed a study in a porcine animal model of chronic MI to validate the implementation of T-mapping on a clinical cardiovascular MR scanner and studied the correlation with histology. Subsequently a clinical protocol was developed, to assess the feasibility of scar tissue detection with native T-mapping in patients (n = 21) with chronic MI, and correlated with gold standard late gadolinium enhancement (LGE) CMR. Four T-weighted images were acquired using a spin-lock preparation pulse with varying duration (0, 13, 27, 45 ms) and an amplitude of 750 Hz, and a T-map was calculated. The resulting T-maps and LGE images were scored qualitatively for the presence and extent of myocardial scarring using the 17-segment AHA model.

Results

In the animal model (n = 9) a significantly higher T relaxation time was found in the infarct region (61 ± 11 ms), compared to healthy remote myocardium (36 ± 4 ms) . In patients a higher T relaxation time (79 ± 11 ms) was found in the infarct region than in remote myocardium (54 ± 6 ms). Overlap in the scoring of scar tissue on LGE images and T-maps was 74%.

Conclusion

We have shown the feasibility of native T-mapping for detection of infarct area in patients with a chronic myocardial infarction. In the near future, improvements on the T -mapping sequence could provide a higher sensitivity and specificity. This endogenous method could be an alternative for LGE imaging, and provide additional quantitative information on myocardial tissue characteristics.  相似文献   

18.
Hemofiltrate C-C chemokine (HCC)-1 is a recently cloned C-C chemokine that is structurally similar to macrophage inflammatory protein (MIP)-1α. Unlike most chemokines, it is constitutively secreted by tissues and is present at high concentrations in normal human plasma. Also atypical for chemokines, HCC-1 is reported not to be chemotactic for leukocytes. In this paper, we have investigated the chemokine receptor usage and downstream signaling pathways of HCC-1. Cross-desensitization experiments using THP-1 cells suggested that HCC-1 and MIP-1α activated the same receptor. Experiments using a panel of cloned chemokine receptors revealed that HCC-1 specifically activated C-C chemokine receptor (CCR)1, but not closely related receptors, including CCR5. HCC-1 competed with MIP-1α for binding to CCR1-transfected cells, but with a markedly reduced affinity (IC50 = 93 nM versus 1.3 nM for MIP-1α). Similarly, HCC-1 was less potent than MIP-1α in inducing inhibition of adenylyl cyclase in CCR1-transfected cells. HCC-1 induced chemotaxis of freshly isolated human monocytes, THP-1 cells, and CCR1-transfected cells, and the optimal concentration for cell migration (100 nM) was ∼100-fold lower than that of MIP-1α (1 nM). These data demonstrate that HCC-1 is a chemoattractant and identify CCR1 as a functional HCC-1 receptor on human monocytes.  相似文献   

19.
20.
Dendritic cell (DC) maturation is an innate response that leads to adaptive immunity to coadministered proteins. To begin to identify underlying mechanisms in intact lymphoid tissues, we studied alpha-galactosylceramide. This glycolipid activates innate Valpha14(+) natural killer T cell (NKT) lymphocytes, which drive DC maturation and T cell responses to ovalbumin antigen. Hours after giving glycolipid i.v., tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma were released primarily by DCs. These cytokines induced rapid surface remodeling of DCs, including increased CD80/86 costimulatory molecules. Surprisingly, DCs from CD40(-/-) and CD40L(-/-) mice did not elicit CD4(+) and CD8(+) T cell immunity, even though the DCs exhibited presented ovalbumin on major histocompatibility complex class I and II products and expressed high levels of CD80/86. Likewise, an injection of TNF-alpha up-regulated CD80/86 on DCs, but CD40 was required for immunity. CD40 was needed for DC interleukin (IL)-12 production, but IL-12p40(-/-) mice generated normal ovalbumin-specific responses. Therefore, the link between innate and adaptive immunity via splenic DCs and innate NKT cells has several components under distinct controls: antigen presentation in the steady state, increases in costimulatory molecules dependent on inflammatory cytokines, and a distinct CD40/CD40L signal that functions together with antigen presentation ("signal one") and costimulation ("signal two") to generate functioning CD4(+) T helper cell 1 and CD8(+) cytolytic T lymphocytes.  相似文献   

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