Surgically treated reactive arthritis of the ankle after COVID-19 infection: A case report

A 37-year-old man developed right ankle pain and swelling six days after being diagnosed with coronavirus disease (COVID-19). Despite conservative treatment, his ankle symptoms persisted. Magnetic resonance imaging and computed tomography showed synovial hypertrophy and bone erosion in the ankle. Following arthroscopic synovectomy, performed 69 days after the COVID-19 diagnosis, the pain improved significantly. The clinical course was consistent with that of reactive arthritis following severe acute respiratory syndrome coronavirus 2 infection. The pathological findings resembled rheumatoid nodules. The bone erosion may have originated from the inflammatory pathway, which resembles the mechanism of rheumatoid arthritis.     

Supraclavicular lymphadenopathy following COVID-19 vaccination: an increasing presentation to the two-week wait neck lump clinic?

The first COVID-19 vaccination was given in December 2020 and there is an effort to vaccinate the international population on a massive scale. Common side effects from the vaccine include headache and tiredness. Regional lymphadenopathy has been described in relation to other vaccines. We describe two cases of supraclavicular reactive lymphadenopathy presenting in patients who had the COVID vaccination in the ipsilateral arm. Awareness of this diagnosis is important for patients presenting to the neck lump clinic.     

PTEN基因敲除降低辐射敏感性及其机制

目的 探讨PTEN基因敲除对辐射敏感性的影响及机制。方法 采用流式细胞术检测MEF1和MEF1/PTEN^－/－细胞内ROS水平;采用Western blot方法,检测H₂O₂和DPI预处理后AKT激酶的表达变化;采用细胞克隆形成率试验分析细胞对⁶⁰Co γ射线的敏感性。结果 PTEN基因敲除后细胞ROS水平增加,辐射敏感性降低。H₂O₂和DPI预处理后影响MEF1细胞AKT激酶活性,但对MEF1/Pten^－/－细胞无影响。 结论 PTEN基因敲除阻断了ROS对AKT的介导,AKT激酶持续活化,可能是辐射敏感性降低的重要原因。     

Hematopoietic turnover index in reactive and neoplastic bone marrow lesions: quantification by apoptosis and PCNA labeling

 In order to determine the dynamics of hematopoietic cell turnover, proliferative activity and incidence of apoptosis (programmed cell death) were evaluated in bone marrow trephine biopsies. Selection of patients (20 in each group) included in addition to a control group, idiopathic thrombocytopenia (ITP), reactive thrombocytosis (TH), secondary polycythemia-smokers' polyglobuly (PG), primary (essential-hemorrhagic) thrombocythemia (PTH), polycythemia vera (PV), and finally acute myeloid leukemia (AML). Apoptosis was demonstrated by the in situ end-labeling technique (ISEL) and proliferative activity by applying the monoclonal antibody PC10 raised against proliferating cell nuclear antigen (PCNA). To assess dynamic features of hematopoiesis, an index was calculated consisting of the ratio between PCNA-positive nuclei and the apoptotic cell fraction. This factor was termed the hematopoietic turnover index (HTI). Morphometric analysis revealed that the HTI was significantly increased in AML and PV. According to cell culture studies both disorders are characterized by either a prevalent proliferation of the myeloid or erythroid cell mass. On the other hand, PG, PTH, and TH showed no relevant enhancement of this index in comparison to the control specimen. In vitro experiment results are in keeping with the finding that PG and PTH are not associated with a significant expansion of the erythroid lineage (CFU-E). Similar to ITP and TH, in PTH megakaryocyte proliferation (CFU-MEG) is the predominant feature of cell turnover. Differences between PTH and TH are in line with the reduced in vitro formation of CFU-MEG in the latter disorder. In conclusion, our in situ study on turnover rates of the bone marrow in various neoplastic and reactive lesions extends previous experimental data on hematopoietic cell kinetics. Received: 10 March 1997 / Accepted: 18 May 1997     

Role of EDRF in the Regulation of Shear Rate in Large Coronary Arteries in Conscious Dogs

To determine whether dilation of large coronary arteries normalizes shear during increased flow following brief occlusion, six dogs were instrumented to measure aortic and left ventricular pressures, left circumflex coronary artery external diameter, and coronary blood flow. The coronary artery was occluded for 15 or 30 s. Data were obtained before and after blockade of EDRF synthesis with nitro-L-arginine. Internal coronary artery diameter and wall shear were calculated on a moment-to-moment basis and the area under the flow curve was measured. Peak flow and shear rate were unaffected by NLA or by the occlusion duration. Flow curve area increased with the duration of occlusion. Internal and external diameters increased significantly for 15 s occlusions before NLA (by 4 ± 1% in external diameter and by 11 ± 4% in internal diameter) and for 30 s occlusions before NLA (by 5 ± 1% in external diameter and by 14 ± 5% in internal diameter) but not after NLA. Adenosine infusions of 0.05, 0.10, 0.50, and 1.0 μmol/kg/min were also used to dilate the coronary arteries. With each infusion, flow, shear and diameter were allowed to reach steady state. Steady state shear was reduced only slightly and did not approach the baseline state. We conclude that increased shear rate causes an increase in coronary artery diameter which is EDRF dependent. Increased coronary artery diameter during reactive hyperemia and adenosine infusions did not normalize wall shear.     

应用荧光探针H2DCF-DA检测光照致细胞内活性氧产生的初步研究

目的应用荧光显微镜及新型荧光探针H2DCF-DA检测在光源照射过程中人脐静脉血管内皮细胞(ECV304)内活性氧的产生情况。方法将ECV304细胞接种于35mm培养皿中,24h后加入H2DCF-DA,使其终浓度为10μmol/L,孵育30min。利用荧光显微镜的激发光源作为照射光源,在采集荧光图像的同时完成光源照射,光源输出波长范围为460～490nm,功率密度约为100mW/cm2。连续采集DCF的荧光图,观察细胞内DCF荧光的变化情况,采用计算机图像处理和分析技术,求得细胞内不同照射时间点DCF平均荧光强度,进而得到平均荧光强度-时间曲线。另外,使用线粒体特异标记探针MitoFluorRed589与H2DCF-DA共同孵育细胞,分别采集同一细胞的DCF的荧光图和MitoFluorRed589的荧光图,并利用像素-荧光强度分析方法来确定DCF荧光在细胞内的分布位置。结果在光源照射的开始阶段,ECV304细胞内的DCF荧光强度迅速增加,在第10s时便上升至第2s时的2.2倍,但是随着照射时间逐渐延长,荧光强度增幅逐渐变小,到第60s时上升至第2s时的4.7倍。观察时间进一步延长,DCF的荧光强度的变化似乎进入平台期,继而开始出现下降。考察DCF荧光在ECV304细胞内的分布位置主要通过比较细胞内不同区域的I1/I2值,通过图像分析与计算得到线粒体区、细胞核区以及细胞质非线粒体区内I1/I2值分     

Mediastinal lymphadenopathy: a variant of incomplete Kawasaki disease

A 14-month-old girl presented with a 4-d history of fever and generalized exanthema. Four characteristic symptoms of incomplete Kawasaki disease (KD) were present on admission (fever, rash, non-purulent conjunctival injection, oropharyngeal changes) and then followed by oedema of the hands and feet and mild plantar desquamation. The typical laboratory features of KD, such as elevated erythrocyte sedimentation rate, leukocytosis, thrombocytosis, and positive C-reactive protein were also seen. Ultrasound examination of the mediastinum revealed the presence of a lymph node, 30 mm in diameter, below the tracheal carina. Thoracic CT scan confirmed the mediastinal lymph node. The patient was treated with aspirin and intravenous γ -globulin. Ultrasound study of the mediastinum, which was carried out 6 weeks after hospital discharge, showed that the lymph node had disappeared. This case illustrates that lymph nodes other than cervical lymphadenopathy should be sought when the diagnosis of classical or atypical KD is suspected.     

去甲肾上腺素对心肌细胞NF-κB活性的影响

目的:探讨去甲肾上腺素(NE)对心肌细胞核因子-κB(NF-κB)活性的影响及机制。方法:采用乳鼠心肌细胞培养模型,分别加入NE和哌唑嗪、普萘洛尔及维生素E等刺激,观察心肌细胞内活性氧水平和NF-κB核结合活性的改变。结果:NE刺激后,心肌细胞活性氧生成明显增加、NF-κB活性增强,维生素E、哌唑嗪和普萘洛尔可不同程度减少心肌细胞活性氧含量、降低NF-κB活性。结论:NE对心肌细胞的作用部分通过激活NF-κB实现,这与NE通过肾上腺素能受体介导活性氧过量产生有关。     

Nitric oxide neurotoxicity

Derangements in glutamate neurotransmission have been implicated in several neurodegenerative disorders including, stroke, epilepsy, Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). Activation of the N-methyl- -aspartate (NMDA) receptor subtype of glutamate receptors results in the influx of calcium which binds calmodulin and activates neuronal nitric oxide synthase (nNOS), to convent -arginine to citrulline and nitric oxide (NO). NO has many roles in the central nervous system as a messenger molecule, however, when generated in excess NO can be neurotoxic. Excess NO is in part responsible for glutamate neurotoxicity in primary neuronal cell culture and in animal models of stroke. It is likely that most of the neurotoxic actions of NO are mediated by peroxynitrite (ONOO−), the reaction product from NO and superoxide anion. In pathologic conditions, peroxynitrite and oxygen free radicals can be generated in excess of a cell antioxidant capacity resulting in severe damage to cellular constitutents including proteins, DNA and lipids. The inherent biochemical and physiological characteristis of the brain, including high lipid concentrations and energy requirements, make it particularly susceptible to free radical and oxidant mediated insult. Increasing evidence indicates that many neurologic disorders may have components of free radical and oxidative stress induced injury.