MR Lymphography of Lymphatic Vessels in Lower Extremity with Gynecologic Oncology-Related Lymphedema

Objective

To characterize lymphatic vessel morphology in lower extremity lymphedema using MR lymphography at 3T.

Study Design

Forty females with lower extremity lymphedema secondary to gynecologic carcinoma treatment underwent MR lymphography (MRL) at 3T. Lymphatic vessel morphology in normal and affected limbs was compared.

Results

The median diameter of the lymphatic vessels in swollen calf and thigh were significantly larger than that in the contralateral calf and thigh, respectively (p<0.05). The median number of lymphatic vessels visualized in normal calf was less than that in the lymphedematous calf (p<0.01), while no significant difference was found between the normal thigh and swollen thigh. Lymphatic vessel number in the affected calf was significantly greater than that in affected thigh and the mean diameter of affected calf was also significantly wider than that of affected thigh (p<0.01). Mean diameter of lymphatic vessels in the affected calf was significantly different between stage I and stage III (p<0.05), but not significantly different between stages I and II, and between stages II and III (p>0.05). The median number of lymphatic vessels for affected calf showed significant difference between stage I and stage III, and between stage II and stage III (p<0.05), but no significant difference between stage I and stage II (p>0.05). There was no significant difference in mean diameter or median number of lymphatic vessels in the affected thigh found between different stages (p>0.05).

Conclusion

There are significant differences in the number or diameter of lymphatic vessels between normal and affected limbs and there are significant differences for affected calf between early and late stages of lymphedema; therefore, MR lymphography can be helpful in diagnosis or clinical staging for lower extremity with gynecologic oncology-related lymphedema.     

Preliminary Study of MR Diffusion Tensor Imaging of the Liver for the Diagnosis of Hepatocellular Carcinoma

Objectives

To evaluate the feasibility of differentiating between hepatocellular carcinomas (HCC) and healthy liver using diffusion tensor imaging (DTI).

Material and Methods

All subjects underwent an abdominal examination on a 3.0T MRI scanner. Two radiologists independently scored the image quality (IQ). An optimal set of DTI parameters was obtained from a group of fifteen volunteers with multiple b-values (100, 300, 500, and 800 s/mm²) and various diffusion-encoding directions (NED = 6, 9, and 12)using two way ANOVA analysis. Eighteen Patients with HCC underwent DTI scans with the optimized parameters. Fractional anisotropy(FA) and average apparent diffusion coefficient (ADC) values were measured. The differences of FA and ADC values between liver healthy region and HCC lesion were compared through paired t tests.

Results

There were no significant changes in liver IQ and FA/ADC values with increased NED(P >0.05), whereas the liver IQ and FA/ADC values decreased significantly with increased b-values(P <0.05). Good IQ, acceptable scan time and reasonable FA/ADC values were acquired using NED = 9 with b-value of (0,300) s/mm². Using the optimized DTI sequence, ADC value of the tumor lesion was significantly lower than that of the healthy liver region (1.30 ± 0.34×10⁻³ vs 1.52 ± 0.27×10⁻³ mm²/s, P = 0.013), whereas the mean FA value of the tumor lesion (0.42 ± 0.11) was significantly higher than the normal liver region (0.32 ± 0.10) (P = 0.004).

Conclusion

Either FA or ADC value from DTI can be used to differentiate HCC from healthy liver. HCC lead to higher FA value and lower ADC value on DTI than healthy liver.     

Changes in short‐chain acyl‐coA dehydrogenase during rat cardiac development and stress

This study was designed to investigate the expression of short‐chain acyl‐CoA dehydrogenase (SCAD), a key enzyme of fatty acid β‐oxidation, during rat heart development and the difference of SCAD between pathological and physiological cardiac hypertrophy. The expression of SCAD was lowest in the foetal and neonatal heart, which had time‐dependent increase during normal heart development. In contrast, a significant decrease in SCAD expression was observed in different ages of spontaneously hypertensive rats (SHR). On the other hand, swim‐trained rats developed physiological cardiac hypertrophy, whereas SHR developed pathological cardiac hypertrophy. The two kinds of cardiac hypertrophy exhibited divergent SCAD changes in myocardial fatty acids utilization. In addition, the expression of SCAD was significantly decreased in pathological cardiomyocyte hypertrophy, however, increased in physiological cardiomyocyte hypertrophy. SCAD siRNA treatment triggered the pathological cardiomyocyte hypertrophy, which showed that the down‐regulation of SCAD expression may play an important role in pathological cardiac hypertrophy. The changes in peroxisome proliferator‐activated receptor α (PPARα) was accordant with that of SCAD. Moreover, the specific PPARα ligand fenofibrate treatment increased the expression of SCAD and inhibited pathological cardiac hypertrophy. Therefore, we speculate that the down‐regulated expression of SCAD in pathological cardiac hypertrophy may be responsible for ‘the recapitulation of foetal energy metabolism’. The deactivation of PPARα may result in the decrease in SCAD expression in pathological cardiac hypertrophy. Changes in SCAD are different in pathological and physiological cardiac hypertrophy, which may be used as the molecular markers of pathological and physiological cardiac hypertrophy.     

Intracellular receptor EPAC regulates von Willebrand factor secretion from endothelial cells in a PI3K-/eNOS-dependent manner during inflammation

Coagulopathy is associated with both inflammation and infection, including infections with novel severe acute respiratory syndrome coronavirus-2, the causative agent Coagulopathy is associated with both inflammation and infection, including infection with novel severe acute respiratory syndrome coronavirus-2, the causative agent of COVID-19. Clot formation is promoted via cAMP-mediated secretion of von Willebrand factor (vWF), which fine-tunes the process of hemostasis. The exchange protein directly activated by cAMP (EPAC) is a ubiquitously expressed intracellular cAMP receptor that plays a regulatory role in suppressing inflammation. To assess whether EPAC could regulate vWF release during inflammation, we utilized our EPAC1-null mouse model and revealed increased secretion of vWF in endotoxemic mice in the absence of the EPAC1 gene. Pharmacological inhibition of EPAC1 in vitro mimicked the EPAC1-/- phenotype. In addition, EPAC1 regulated tumor necrosis factor-α–triggered vWF secretion from human umbilical vein endothelial cells in a manner dependent upon inflammatory effector molecules PI3K and endothelial nitric oxide synthase. Furthermore, EPAC1 activation reduced inflammation-triggered vWF release, both in vivo and in vitro. Our data delineate a novel regulatory role for EPAC1 in vWF secretion and shed light on the potential development of new strategies to control thrombosis during inflammation.     

Autophagy facilitates age-related cell apoptosis—a new insight from senile cataract

Age-related cell loss underpins many senescence-associated diseases. Apoptosis of lens epithelial cells (LECs) is the important cellular basis of senile cataract resulted from prolonged exposure to oxidative stress, although the specific mechanisms remain elusive. Our data indicated the concomitance of high autophagy activity, low SQSTM1/p62 protein level and apoptosis in the same LEC from senile cataract patients. Meanwhile, in primary cultured LECs model, more durable autophagy activation and more obvious p62 degradation under oxidative stress were observed in LECs from elder healthy donors, compared with that from young healthy donors. Using autophagy-deficiency HLE-B3 cell line, autophagy adaptor p62 was identified as the critical scaffold protein sustaining the pro-survival signaling PKCι-IKK-NF-κB cascades, which antagonized the pro-apoptotic signaling. Moreover, the pharmacological inhibitor of autophagy, 3-MA, significantly inhibited p62 degradation and rescued oxidative stress-induced apoptosis in elder LECs. Collectively, this study demonstrated that durable activation of autophagy promoted age-related cell death in LECs. Our work contributes to better understanding the pathogenesis of senescence-associated diseases.Subject terms: Macroautophagy, Apoptosis, Senescence, Diseases     

Human retinal pigment epithelial cells

''Human retinal pigment epithelial cells'' is the first set of guidelines on human retinal pigment epithelial cells in China, jointly drafted and agreed upon by experts from the Chinese Society for Stem Cell Research. This standard specifies technical requirements, test methods, inspection rules, instructions for usage, labelling requirements, packaging requirements, storage requirements and transportation requirements and waste disposal requirements for human retinal pigment epithelial cells, which is applicable to quality control during the process of manufacturing and testing of human retinal pigment epithelial cells. It was originally released by the Chinese Society for Cell Biology on 9 January 2021. We hope that publication of these guidelines will promote institutional establishment, acceptance and execution of proper protocols and accelerate the international standardization of human retinal pigment epithelial cells for applications.     

Requirements for human haematopoietic stem/progenitor cells

‘Requirements for human haematopoietic stem/progenitor cells’ is the first set of guidelines on human haematopoietic stem/progenitor cells in China, jointly drafted and agreed upon by experts from the Chinese Society for Stem Cell Research. This standard specifies the technical requirements, inspection methods, inspection rules, instructions for usage, labelling requirements, packaging requirements, storage requirements and transportation requirements for human haematopoietic stem/progenitor cells, which is applicable to the quality control for human haematopoietic stem/progenitor cells. We hope that publication of these guidelines will promote institutional establishment, acceptance and execution of proper protocols, and accelerate the international standardization of human haematopoietic stem/progenitor cells for applications.     

鉴定隶属于糖苷水解酶13家族(glycoside hydrolase family 13, GH13)的潮滩发光杆菌的β-半乳糖苷酶

【背景】糖苷水解酶13家族(glycoside hydrolase family 13, GH13)是已知最大的α-淀粉酶家族,不含有半乳糖苷酶。【目的】对海洋细菌潮滩发光杆菌(Photobacterium gaetbulicola)的一个蛋白BgalPg进行鉴定。【方法】通过保守位点分析和系统发育树确定BgalPg蛋白的家族分类;通过克隆、表达和纯化测定重组BgalPg蛋白的酶学性质并鉴定功能。【结果】BgalPg的蛋白序列新颖,与已知的碳水化物酶无同源性。序列分析结果表明该蛋白具有GH13家族的典型特性,并且隶属于GH13＿38亚家族。BgalPg对α-淀粉酶家族酶的相关底物均无催化活性,却能水解含有β-半乳糖苷键的底物p NP-β-Gal [(2.8±0.4) U/mg]和o NP-β-Gal [(1.4±0.3) U/mg],并且能水解乳糖[(0.40±0.01) U/mg],表现出典型的β-半乳糖苷酶活性。同时,该酶在pH 7.0–8.5稳定性好,60℃的半衰期为1.5 h。【结论】发现隶属于GH13家族的β-半乳糖苷酶。