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We investigated the efficacy of a maxillary Jackson-Pratt (J-P) suction drain for preventing maxillary sinus hematoma and facial swelling after maxillary Le Fort I osteotomy (LF1).
We retrospectively evaluated 66 patients who underwent LF1 at a single institution. Of these, 41 had a J-P suction tube inserted in the mandible and maxilla (maxillary insertion), and 25 had a J-P drain inserted in the mandible only (no maxillary insertion). Facial CT was obtained before and 4 days after surgery. We compared mean midfacial swelling and maxillary sinus haziness by
test and examined correlations between bleeding amount and body mass index (BMI).
For the maxillary-insertion group, the ratio of total maxillary sinus volume to haziness (57.5 ± 24.2%) was significantly lower than in the group without maxillary drain insertion (65.5% ± 20.3;
= .043). This latter group, however, did not have a significantly greater midfacial soft tissue volume (7575 mm
) than the maxillary-insertion group (7250 mm
;
= .728). BMI did not correlate significantly with bleeding amount or facial swelling.
Suction drainage in the maxilla reduced maxillary sinus haziness after orthognathic surgery but did not significantly reduce midfacial swelling.
Suction drainage in the maxilla reduced maxillary sinus haziness after orthognathic surgery but did not significantly reduce midfacial swelling.[This corrects the article on p. 205 in vol. 9, PMID 32821732.].
Human adipose tissue-derived mesenchymal stem cells (ASCs) have been reported to promote angiogenesis and tissue repair. However, poor survival and engraftment efficiency of transplanted ASCs are the major bottlenecks for therapeutic application. Daporinad The present study aims to improve the therapeutic efficacy of ASCs for peripheral artery diseases.
Hydrogen peroxide (H
O
) was used to induce apoptotic cell death in ASCs. To measure apoptosis, we used flow cytometry-based apoptosis analysis and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. A murine hindlimb ischemia model was established to measure the ASC-mediated therapeutic angiogenesis and
survival ability of ASCs.
We identified that the inhibitor of lamin A-progerin binding, JH4, protects ASCs against H
O
-induced oxidative stress and apoptosis. Co-administration of ASCs with JH4 improved ASC-mediated blood reperfusion recovery and limb salvage compared to that of the control group in a mouse hind limb ischemia model. Immunofluorescence showed that JH4 treatment potentiated ASC-mediated vascular regeneration
reducing ASC apoptosis post transplantation.
JH4 exerts anti-apoptotic effects in ASCs in conditions of oxidative stress, and contributes to the repair of ischemic hind limb injury by improving cell survival.
JH4 exerts anti-apoptotic effects in ASCs in conditions of oxidative stress, and contributes to the repair of ischemic hind limb injury by improving cell survival.
Ischemic stroke and myocardial infarction are 2 of the leading causes of mortality. Both conditions are caused by arterial occlusion, resulting in ischemic necrosis of the cells in the cortex and heart. Long non-coding RNAs (lncRNAs) are a group of non-coding RNAs longer than 200 nucleotides without protein-coding potential. Thousands of lncRNAs have been identified but their involvement in ischemic stroke and myocardial infarction has not been studied extensively. Therefore, this study aimed to identify the role of lncRNAs, particularly those that are commonly altered in these two ischemic injuries.
We combined diverse RNA sequencing data obtained from public databases and performed extensive bioinformatics analyses to determine reliable lncRNAs commonly identified from these datasets. Using sequence analysis, we also detected the lncRNAs that may act as microRNA (miRNA) regulators.
We found several altered lncRNAs that were common in ischemic stroke and myocardial infarction models. Some of these lncRNAs, including zinc finger NFX1-type containing 1 antisense RNA 1 and small nucleolar RNA host gene 1, were previously reported to be involved in the pathogenesis of each of these models. Interestingly, several lncRNAs had binding sites for miRNAs that were previously reported to be involved in the hypoxic response, suggesting the possible role of these lncRNAs as regulators in ischemic responses.
The lncRNAs identified in this study will be useful in determining the regulatory networks in ischemic stroke and myocardial infarction and in identifying potential specific markers for each of these ischemic diseases.
The lncRNAs identified in this study will be useful in determining the regulatory networks in ischemic stroke and myocardial infarction and in identifying potential specific markers for each of these ischemic diseases.
The aim of this study was to analyze the available knowledge about the potential association between dyslipidemia and the severity of coronavirus disease 2019 (COVID-19) as reported in previous published systematic reviews.
In this umbrella review (an overview of systematic reviews), we investigated the association between dyslipidemia and COVID-19 severity. A systematic search was performed of 4 main electronic databases (MEDLINE, Embase, Scopus, and the Cochrane Library databases) from inception until August 2020. We evaluated the methodological quality of the included studies using the A MeaSurement Tool to Assess systematic Reviews (AMSTAR) 2 tool and used the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to assess the quality of evidence for the outcome. In addition, we evaluated the strengths and limitations of the evidence and the methodological quality of the available studies.
Out of 35 articles identified, 2 systematic reviews were included in the umbrella review. A total of 7,951 COVID-19-positive patients were included. According to the AMSTAR 2 criteria and GRADE system, the quality of the included studies was not high. A history of dyslipidemia is likely to be associated with the severity of COVID-19 infection, but the contrary is the case for cholesterol levels at hospitalization.
Although existing research on dyslipidemia and COVID-19 is limited, our findings suggest that dyslipidemia may play a role in the severity of COVID-19 infection. More adequately powered studies are needed.
PROSPERO Identifier CRD42020205979.
PROSPERO Identifier CRD42020205979.
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