The implantation of mesenchymal stem cells (MSC) has been reported as a new technique to restore renal tubular structure and improve renal function in acute kidney injury (AKI). Vascular endothelial growth factor (VEGF) plays an important role in the renoprotective function of MSC. Whether upregulation of VEGF by a combination of MSC and VEGF gene transfer could enhance the protective effect of MSC in AKI is not clear. We investigated the effects of VEGF-modified human embryonic MSC (VEGF-hMSC) in healing cisplatin-injured renal tubular epithelial cells (TCMK-1) with a coculture system. We found that TCMK-1 viability declined 3 days after cisplatin pretreatment and that coculture with VEGF-hMSC enhanced cell protection via mitogenic and antiapoptotic actions. In addition, administration of VEGF-hMSC in a nude mouse model of cisplatin-induced kidney injury offered better protective effects on renal function, tubular structure, and survival as represented by increased cell proliferation, decreased cellular apoptosis, and improved peritubular capillary density. These data suggest that VEGF-modified hMSC implantation could provide advanced benefits in the protection against AKI by increasing antiapoptosis effects and improving microcirculation and cell proliferation.

Objective To investigate the alternative spliced isoforms of Fibronectin (FN) in the stroma of radicular cysts and analyze the associations between these isoforms and the osteoclastogenic effects of fibroblasts. Methods and materials The specimens of radicular cysts were stained with immunohistochemistry, and the associations between each FN isoform and clinical parameters were assessed. The fibroblasts isolated from cysts or jaw bone were cultured to induce the Trap + MNCs. In the conditioned medium, the Fibronectin containing extra domain A (EDA + FN) was neutralized by antibody IST‐9, and the EDA exon of fibroblasts was knockout by CRISPR/Cas system, for assessing the osteoclastogenic effects. The mRNA level of FN isoforms and the osteoclastogenesis‐related genes were analyzed by quantitive PCR. Results EDA + FN staining was positively associated with the size of the lesions (p < 0.05). In contrast with the controls, the ratio of EDA + FN/total FN in the fibroblasts from radicular cysts was significantly higher (p < 0.05), and positively associate with Trap + MNCs counting, it was consistent with increased expression of COX‐2, IL‐6, IL‐17, and the RANKL/OPG (p < 0.05). The Trap + MNCs counting and osteoclastogenesis‐related genes were decreased by IST‐9 blocking and EDA exon knockout in fibroblasts, but the blockage of the interaction between EDA + FN and pre‐osteoclasts exhibited little effects on Trap + MNCs formation. Conclusion The microenvironment of the fibrous capsule of radicular cysts facilitates the splicing of EDA exon, it endues EDA + FN with autocrine effects on fibroblast itself, and it increases the expression of osteoclastogenesis‐related genes, by which the osteoclastogenesis in radicular cysts could be initiated.

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Advances in research relating to pulmonary embolisms (PE) can assist physicians in selecting the best management strategies for PE patients. However, the symptoms, signs, disease history, lesion position and pathophysiology linked to different genders in patients with PE have rarely been evaluated. One hundred and forty-nine PE patients (73 males and 76 females) were sequentially recruited to this study over the last five years whilst attending our Emergency Department. Data relating to the symptoms, signs, disease history, biochemical testing, cardiac electrophysiology, imaging detection, treatment and outcome were collected and the gender differences were analyzed. We found that embolisms occurred significantly more frequently in the right lung (89.7%) than in the left lung (42.6%). The presence of dyspnea, the number of patients presenting with tumors, the number of patients with chronic pulmonary disease, those with emboli in the right pulmonary artery and emboli in the right lung, as well as the average systolic and diastolic blood pressure were: 78.1%, 15.1%, 31.5%, 32.9%, 94.5%, 129.9+20.0 and 75.0+11.2 in the male patients and 59.2%, 1.3%, 14.5%, 17.1%, 69.7%, 125.1+14.6 and 69.3+11.0 in the female patients. These indicators were found to be significantly higher in male patients. In contrast, the rate of V1-V4 T-wave inversion and level of D-dimer in the blood were significantly lower in males than in females. No significant difference was observed in the remaining observational indicators. Gender differences regarding the symptoms, signs, disease history, lesion position and pathophysiology exist in patients with PE and should be considered in clinical practice.

Our previous work showed that geniposide affected glucose-stimulated insulin secretion (GSIS) via regulating glucose uptake and metabolism in pancreatic β cells; however, the molecular mechanisms remain largely unknown. Substantial evidence suggests that activation of 5'-AMP-activated protein kinase (AMPK) plays a central role in GSIS. Here, we aim to determine the role of AMPK on geniposide-regulated GSIS in rat pancreatic INS-1 cells. The results demonstrated that 6-[4-(2-piperidin-1-yletoxy)-phenyl]-3-pyridin-4-yl-pyrazolo[1,5-α] pyrimidine (Compound C; an AMPK inhibitor) significantly attenuated the effects of geniposide on glucose uptake, energy metabolism, and insulin secretion in INS-1 cells. We also observed that geniposide induced phosphorylation of acetyl-CoA carboxylase (ACC), a marker of AMPK activity, in a time-dependent manner in INS-1 cells; however, in the presence of Compound C, the influence of geniposide on ACC phosphorylation was obviously inhibited. Furthermore, the knockdown of AMPK protein with AMPK siRNA treatment decreased the effects of geniposide on glucose uptake, adenosine triphosphate production, and GSIS. All these data indicate that AMPK plays an essential role in geniposide-regulated GSIS in pancreatic β cells.

The vascular endothelium is a modulator of a variety of biological systems and plays important structural and functional roles in vascular homeostasis. Normal endothelium is antithrombogenic and yet promotes platelet aggregation and coagulation if injured. Moreover, endothelial damage can cause vasospasm, intimal hyperplasia, and arteriosclerotic acceleration. Endothelial injury is harmful even in the absence of disruption of its monolayer integrity.1 However, research in clinical settings has been hindered by the inaccessibility of vascular endothelium in both healthy subjects and patients, owing to the paucity of non invasive methods and specific endothelial markers. Circulating endothelial cells (CEC), released from vascular endothelial cell to peripheral blood, can directly reflect the severity of endothelial damage. Thus far CEC is the only specific direct indicator of vascular injury in vivo. 2ABSTRACT: Background and Purpose: Vascular endothelial cell (VEC) injury represents a major initiating step in the process of atherosclerosis, which may lead to cerebral infarction. "Circulating endothelial cell" (CEC) is an index of ongoing endothelial injury, while intimal-medial thickness (IMT) detected by sounography was used to evaluate the severity of atherosclerosis. However, to our knowledge, there is no study that investigated the relationship of these two determinations. Our study was designed to address correlate CEC with IMT. Methods and Results: The study population consisted of 30 patients with acute cerebral infarction (ACI) and 30 ageand sex-matched volunteers as controls. The CEC counts were determined using Hladovec's method. All subjects underwent a 2-dimensional ultrasound examination of both carotid arteries to measure IMT. CEC counts in ACI group were significantly increased compared with control group (4.88±2.14 cells /0.9μl vs 2.73±1.95/0.9μl, P<0.01); IMT in ACI patients was also significantly thicker compared with volunteers (2.72±1.07 mm vs 1.73±0.99 mm, P<0.01). There was positive correlation between CEC counts and maximal carotid artery IMT in both groups (r=0.522, P<0.01 in ACI patients and r=0.395, P<0.05 in healthy volunteers). Conclusions: Circulating endothelial cell counts can directly reflect the vascular injury. CEC counts parallel IMT. The CEC may be an independent predictor of cerebral infarction.RÉSUMÉ: Cellules endothéliales circulantes comme marqueurs potentiels de l'athérosclérose. Contexte et objectif : Une lésion des cellules endothéliales vasculaires constitue une étape majeure initiant le processus de l'athérosclérose et pouvant mener à l'infarctus cérébral. La cellule endothéliale circulante (CEC) est un témoin de la lésion endothéliale active alors que l'épaisseur intima-média (ÉIM) évaluée par ultrasonographie a été utilisée pour déterminer la sévérité de l'athérosclérose. Cependant, à notre connaissance, aucune étude n'a examiné la relation entre ces deux mesures. Le but de notre étude était d'analyser la relation entre la CEC et l'ÉIM. Méthodes et résultats : La pop...

Background: A bibliometric analysis was performed to reveal the current status of investigations in infectious diseases in patients with liver transplantation (LT) and to prioritize future research needs. Methods:The present study comprehensively retrieved publications relevant to infectious diseases in LT recipients published between 2010 and 2020. The search was conducted on the Web of Science (WoS) database. A bibliometric analysis was conducted through machine learning and visualization tools, including VOSviewer, Bibliographic Item Co-Occurrence Matrix Builder, and Graphical Clustering Toolkit. Research hotspots and trends in the field were assessed, while the contributions and collaborations of countries, institutions, and authors were documented.Results: A total of 691 publications were analyzed. Research output sharply increased in 2015, with a fast drop afterward. "Liver transplantation" was the most frequent keyword, with strong links to "hepatitis C virus" and "infection". Study areas included risk factors of infectious diseases in LT recipients, pathogens causing post-transplantation infections, antibacterial therapy and prophylaxis for peritransplant infection complications, living donor LT, and pediatric LT. The efficacy and safety of direct-acting antivirals (DAAs) for hepatitis C virus (HCV) infection among liver transplant recipients has attracted recent research interest.Didier Samuel was the most productive author, while Xavier Forns was the top-cited author. Shanghai Jiao Tong University was the most productive contributor, and Gilead Sciences was the most cited organization.Moreover, the USA was the greatest contributor. Gastroenterology was the most cited journal, while Liver Transplantation was the most prolific journal.Conclusions: This bibliometric analysis will better understand the research status of infectious complications in LT recipients and forecast future research trends. Priority should be given to identifying risk factors for peritransplantation infections and effective treatments against infectious complications in the coming years.

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