Objective:To investigate the role of conjunctival impression cytology in the diagnosis of Sj?gren's syndrome (SS) and the immunological factors influencing conjunctival lesions.Methods:A total of 57 patients complaining about dry eye were collected, including 38 patients with primary Sj?gren's syndrome (pSS) and 19 patients with non-SS. Conjunctival impression cytology tests were performed for all patients, and they were scored by the Nelson method. Thirty-one patients with SS underwent serological tests such as autoantibodies, immunoglobulins, and complement. The correlation between the relevant data was compared using the t test and the rank sum test. Results:The Nelson grade ≥2 is the positive cut-off value for the diagnosis of SS. The sensitivity was 68.4%, and the specificity was 89.5%, and the area under the receiver operating characteristic curve (ROC) was 0.767. In patients with SS, there was statistical correlation between the results of conjunctival impression cytology and antinuclear antibody (ANA) ( χ2=4.664, P=0.031), anti-SSA antibody ( χ2=8.58, P<0.01), anti-SSB antibody ( χ2=6.13, P=0.013), anti-SSA-52 antibody ( χ2=6.48, P=0.011), immunoglobulin (Ig)G ( t=-4.344, P<0.01) and rheumatoid factor (RF) ( U=25.0, P<0.01). Conclusion:Con-junctival impression cytology has certain value in the diagnosis of SS and can be used to evaluate conjunctival lesions in SS. Serum ANA, anti-SSA antibody, anti-SSB antibody, anti-SSA-52 antibody, IgG, and RF levels are significantly associated with the degree of conjunctival lesions, and can be considered as an indirect evidence of conjunctival involvement in SS.

Cell Nucleus ; Cellular Senescence/genetics* ; CRISPR-Cas Systems/genetics*

BACKGROUNDCardiopulmonary bypass (CPB) has been shown to be associated with systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a novel, minimally invasive rat model of normothermic CPB model without blood priming.

METHODSTwenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into CPB group (n = 10) and control group (n = 10). All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and further transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. The volume of the priming solution, composed of 6% HES 130/0.4 and 125 IU heparin, was less than 12 ml. The surface of the hollow fiber oxygenator was 0.075 m(2). CPB was conducted for 60 minutes at a flow rat of 100-120 ml × kg (-1)× min(-1) in CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg.

RESULTSAll CPB processes were successfully achieved. Blood gas analysis and hemodynamic parameters of each time point were in accordance with normal ranges. The vital signs of all rats were stable.

CONCLUSIONSThe establishment of CPB without blood priming in rats can be achieved successfully. The nontransthoracic model should facilitate the investigation of pathophysiological processes concerning CPB-related multiple organ dysfunction and possible protective interventions. This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.

Animals ; Cardiopulmonary Bypass ; methods ; Lung Injury ; surgery ; Male ; Rats ; Rats, Sprague-Dawley

Aging poses a major risk factor for cardiovascular diseases, the leading cause of death in the aged population. However, the cell type-specific changes underlying cardiac aging are far from being clear. Here, we performed single-nucleus RNA-sequencing analysis of left ventricles from young and aged cynomolgus monkeys to define cell composition changes and transcriptomic alterations across different cell types associated with age. We found that aged cardiomyocytes underwent a dramatic loss in cell numbers and profound fluctuations in transcriptional profiles. Via transcription regulatory network analysis, we identified FOXP1, a core transcription factor in organ development, as a key downregulated factor in aged cardiomyocytes, concomitant with the dysregulation of FOXP1 target genes associated with heart function and cardiac diseases. Consistently, the deficiency of FOXP1 led to hypertrophic and senescent phenotypes in human embryonic stem cell-derived cardiomyocytes. Altogether, our findings depict the cellular and molecular landscape of ventricular aging at the single-cell resolution, and identify drivers for primate cardiac aging and potential targets for intervention against cardiac aging and associated diseases.
Aged ; Animals ; Humans ; Aging/genetics* ; Forkhead Transcription Factors/metabolism* ; Myocytes, Cardiac/metabolism* ; Primates/metabolism* ; Repressor Proteins/metabolism* ; Transcriptome ; Macaca fascicularis/metabolism*