Microvascular research最新文献

{"title":"10× single-cell sequencing revealed cellular composition heterogeneity in cardiac myxoma with malignant glandular properties","authors":"Li Zhang ,&nbsp;Zhi-huang Qiu ,&nbsp;Xiaozhen Wei ,&nbsp;Mengge Yao ,&nbsp;Shao-kun Chen ,&nbsp;Jian He ,&nbsp;Jian-qiang Ye ,&nbsp;Yu-mei Li ,&nbsp;Liang-wan Chen","doi":"10.1016/j.mvr.2024.104697","DOIUrl":"10.1016/j.mvr.2024.104697","url":null,"abstract":"<div><p>Cardiac myxoma is the most common primary cardiac tumor in adults. The histogenesis and cellular composition of myxoma are still unclear. This study aims to reveal the role of myxoma cell components and their gene expression in tumor development. We obtained single living cells by enzymatic digestion of tissues from 4 cases of surgically resected cardiac myxoma. Of course, there was 1 case of glandular myxoma and 3 cases of nonglandular myxoma. Then, 10× single-cell sequencing was performed. We identified 12 types and 11 types of cell populations in glandular myxoma and nonglandular myxoma, respectively. Heterogeneous epithelial cells are the main components of glandular myxoma. The similarities and differences in T cells in both glandular and nonglandular myxoma were analyzed by KEGG and GO. The most important finding was that there was active communication between T cells and epithelial cells. These results clarify the possible tissue occurrence and heterogeneity of cardiac myxoma and provide a theoretical basis and guidance for clinical diagnosis and treatment.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104697"},"PeriodicalIF":3.1,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141156891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating miRNA-4701-3p as a predictive biomarker of cardiovascular disease which induces angiogenesis by inhibition of TOB2","authors":"Seung Min Lee ,&nbsp;Bo Hyun Yoon ,&nbsp;Jin Woo Lee ,&nbsp;I. Jin-Yong Jeong ,&nbsp;Inki Kim ,&nbsp;Chan-Gi Pack ,&nbsp;Young-Hak Kim ,&nbsp;Chang Hoon Ha","doi":"10.1016/j.mvr.2024.104698","DOIUrl":"10.1016/j.mvr.2024.104698","url":null,"abstract":"<div><p>Angiogenesis is mainly regulated by the delivery of VEGF-dependent signaling to cells. However, the angiogenesis mechanism regulated by VEGF-induced miRNA is still not understood. After VEGF treatment in HUVECs, we screened the changed miRNAs through small-RNA sequencing and found VEGF-induced miR-4701-3p. Furthermore, the GFP reporter gene was used to reveal that TOB2 expression was regulated by miR-4701-3p, and it was found that TOB2 and miR-4701-3p modulation could cause angiogenesis in an in-vitro angiogenic assay. Through the luciferase assay, it was confirmed that the activation of the angiogenic transcription factor MEF2 was regulated by the suppression and overexpression of TOB2 and miR-4701-3p. As a result, MEF2 downstream gene mRNAs that induce angiogenic function were regulated. We used the NCBI GEO datasets to reveal that the expression of TOB2 and MEF2 was significantly changed in cardiovascular disease. Finally, it was confirmed that the expression of circulating miR-4701-3p in the blood of myocardial infarction patients was remarkably increased. In patients with myocardial infarction, circulating miR-4701-3p was increased regardless of age, BMI, and sex, and showed high AUC levels in specificity and sensitivity analysis (AUROC) (AUC = 0.8451, 95 % CI 0.78–0.90). Our data showed TOB2-mediated modulation of MEF2 and its angiogenesis by VEGF-induced miR-4701-3p in vascular endothelial cells. In addition, through bioinformatics analysis using GEO data, changes in TOB2 and MEF2 were revealed in cardiovascular disease. We suggest that circulating miR-4701-3p has high potential as a biomarker for myocardial infarction.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"155 ","pages":"Article 104698"},"PeriodicalIF":3.1,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141156996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Activation of renal vascular smooth muscle TRPV4 channels by 5-hydroxytryptamine impairs kidney function in neonatal pigs” [Microvasc. Res. 148 (2023)104516]","authors":"Jeremiah M. Afolabi,&nbsp;Olugbenga S. Michael,&nbsp;Olufunke O. Falayi,&nbsp;Praghalathan Kanthakumar,&nbsp;Pratheesh D. Mankuzhy,&nbsp;Hitesh Soni,&nbsp;Adebowale Adebiyi","doi":"10.1016/j.mvr.2024.104696","DOIUrl":"https://doi.org/10.1016/j.mvr.2024.104696","url":null,"abstract":"","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104696"},"PeriodicalIF":3.1,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0026286224000451/pdfft?md5=d25045930139e2a146cd4ed7c11fb1cb&pid=1-s2.0-S0026286224000451-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141095528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of Müller cells-derived exosomes in diabetic retinopathy","authors":"Mohamed S. Gad ,&nbsp;Nehal M. Elsherbiny ,&nbsp;Dalia R. El-Bassouny ,&nbsp;Nesreen M. Omar ,&nbsp;Safinaz M. Mahmoud ,&nbsp;Mohamed Al-Shabrawey ,&nbsp;Amany Tawfik","doi":"10.1016/j.mvr.2024.104695","DOIUrl":"10.1016/j.mvr.2024.104695","url":null,"abstract":"<div><p>Exosomes are nanosized vesicles that have been reported as cargo-delivering vehicles between cells. Müller cells play a crucial role in the pathogenesis of diabetic retinopathy (DR). Activated Müller cells in the diabetic retina mediate disruption of barrier integrity and neovascularization. Endothelial cells constitute the inner blood-retinal barrier (BRB). Herein, we aim to evaluate the effect of Müller cell-derived exosomes on endothelial cell viability and barrier function under normal and hyperglycemic conditions. Müller cell-derived exosomes were isolated and characterized using Western blotting, nanoparticle tracking, and electron microscopy. The uptake of Müller cells-derived exosomes by the human retinal endothelial cells (HRECs) was monitored by labeling exosomes with PKH67. Endothelial cell vitality after treatment by exosomes under normo- and hypoglycemic conditions was checked by MTT assay and Western blot for apoptotic proteins. The barrier function of HRECs was evaluated by analysis of ZO-1 and transcellular electrical resistance (TER) using ECIS. Additionally, intracellular Ca⁺² in HRECs was assessed by spectrofluorimetry. Analysis of the isolated exosomes showed a non-significant change in the number of exosomes isolated from both normal and hyperglycemic condition media, however, the average size of exosomes isolated from the hyperglycemic group showed a significant rise when compared to that of the normoglycemic group. Müller cells derived exosomes from hyperglycemic condition media markedly reduced HRECs cell count, increased caspase-3 and Annexin V, decreased ZO-1 levels and TER, and increased intracellular Ca⁺ when compared to other groups. However, treatment of HRECs under hyperglycemia with normo-glycemic Müller cells-derived exosomes significantly decreased cell death, preserved cellular integrity and barrier function, and reduced intracellular Ca⁺². Collectively, Müller cell-derived exosomes play a remarkable role in the pathological changes associated with hyperglycemia-induced inner barrier dysfunction in DR. Further in vivo research will help in understanding the role of exosomes as therapeutic targets and/or delivery systems for DR.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104695"},"PeriodicalIF":3.1,"publicationDate":"2024-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of angiopoietin-2 and Tie2: Organ specific effects of microvascular leakage and edema in mice","authors":"Anoek L.I. van Leeuwen ,&nbsp;Nicole A.M. Dekker ,&nbsp;Roselique Ibelings ,&nbsp;Anita M. Tuip-de Boer ,&nbsp;Matijs van Meurs ,&nbsp;Grietje Molema ,&nbsp;Charissa E. van den Brom","doi":"10.1016/j.mvr.2024.104694","DOIUrl":"10.1016/j.mvr.2024.104694","url":null,"abstract":"<div><h3>Introduction</h3><p>Critical illness is associated with organ failure, in which endothelial hyperpermeability and tissue edema play a major role. The endothelial angiopoietin/Tie2 system, a regulator of endothelial permeability, is dysbalanced during critical illness. Elevated circulating angiopoietin-2 and decreased Tie2 receptor levels are reported, but it remains unclear whether they cause edema independent of other critical illness-associated alterations. Therefore, we have studied the effect of angiopoietin-2 administration and/or reduced Tie2 expression on microvascular leakage and edema under normal conditions.</p></div><div><h3>Methods</h3><p>Transgenic male mice with partial deletion of Tie2 (heterozygous exon 9 deletion, Tie2^+/−) and wild-type controls (Tie2^+/+) received 24 or 72 pg/g angiopoietin-2 or PBS as control (<em>n</em> = 12 per group) intravenously. Microvascular leakage and edema were determined by Evans blue dye (EBD) extravasation and wet-to-dry weight ratio, respectively, in lungs and kidneys. Expression of molecules related to endothelial angiopoietin/Tie2 signaling were determined by ELISA and RT-qPCR.</p></div><div><h3>Results</h3><p>In Tie2^+/+ mice, angiopoietin-2 administration increased EBD extravasation (154 %, <em>p</em> &lt; 0.05) and wet-to-dry weight ratio (133 %, <em>p</em> &lt; 0.01) in lungs, but not in the kidney compared to PBS.</p><p>Tie2^+/− mice had higher pulmonary (143 %, <em>p</em> &lt; 0.001), but not renal EBD extravasation, compared to wild-type control mice, whereas a more pronounced wet-to-dry weight ratio was observed in lungs (155 %, <em>p</em> &lt; 0.0001), in contrast to a minor higher wet-to-dry weight ratio in kidneys (106 %, <em>p</em> &lt; 0.05).</p><p>Angiopoietin-2 administration to Tie2^+/− mice did not further increase pulmonary EBD extravasation, pulmonary wet-to-dry weight ratio, or renal wet-to-dry weight ratio. Interestingly, angiopoietin-2 administration resulted in an increased renal EBD extravasation in Tie2^+/− mice compared to Tie2^+/− mice receiving PBS. Both angiopoietin-2 administration and partial deletion of Tie2 did not affect circulating angiopoietin-1, soluble Tie2, VEGF and NGAL as well as gene expression of angiopoietin-1, −2, Tie1, VE-PTP, ELF-1, Ets-1, KLF2, GATA3, MMP14, Runx1, VE-cadherin, VEGFα and NGAL, except for gene and protein expression of Tie2, which was decreased in Tie2^+/− mice compared to Tie2^+/+ mice.</p></div><div><h3>Conclusions</h3><p>In mice, the microvasculature of the lungs is more vulnerable to angiopoietin-2 and partial deletion of Tie2 compared to those in the kidneys with respect to microvascular leakage and edema.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104694"},"PeriodicalIF":3.1,"publicationDate":"2024-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0026286224000438/pdfft?md5=cc01ecd6c9bda53b12d6f6bb679b1e01&pid=1-s2.0-S0026286224000438-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial dysfunction and complement activation are independently associated with disease duration in patients with systemic vasculitis","authors":"Panagiotis Dolgyras ,&nbsp;Panagiota Anyfanti ,&nbsp;Antonios Lazaridis ,&nbsp;Eleni Gavriilaki ,&nbsp;Nikolaos Koletsos ,&nbsp;Areti Triantafyllou ,&nbsp;Nikolaidou Barbara ,&nbsp;Konstantinos Mastrogiannis ,&nbsp;Efi Yiannaki ,&nbsp;Anna Papakonstantinou ,&nbsp;Vasiliki Galanapoulou ,&nbsp;Stella Douma ,&nbsp;Eugenia Gkaliagkousi","doi":"10.1016/j.mvr.2024.104692","DOIUrl":"10.1016/j.mvr.2024.104692","url":null,"abstract":"<div><h3>Objectives</h3><p>Systemic vasculitis is a heterogenous group of autoimmune diseases characterized by enhanced cardiovascular mortality. Endothelial dysfunction is associated with accelerated vascular damage, representing a core pathophysiologic mechanism contributing to excess CV risk. Recent studies have also shown that complement activation holds significant role in the pathogenesis of Anti-Neutrophilic Cytoplasmic Autoantibody (ANCA) -associated vasculitis (AAV). Given the potential crosstalk between the endothelium and complement, we aimed to assess, for the first time simultaneously, easily accessible biomarkers of endothelial dysfunction and complement activation in SV.</p></div><div><h3>Methods</h3><p>We measured circulating endothelial microvesicles (EMVs) and soluble complement components representative of alternative, classical and terminal activation (C5b-9, C1q, Bb fragments, respectively) in a meticulously selected group of patients with systemic vasculitis, but without cardiovascular disease. Individuals free from systemic diseases, who were matched with patients for cardiovascular risk factors(hypertension, diabetes, smoking, dyslipidemia), comprised the control group.</p></div><div><h3>Results</h3><p>We studied 60 individuals (30 in each group). Patients with systemic vasculitis had elevated EMVs, higher levels of C5b-9 [536.4(463.4) vs 1200.94457.3), <em>p</em> = 0.003] and C1q [136.2(146.5 vs 204.2(232.9), <em>p</em> = 0.0129], compared to controls [232.0 (243.5) vs 139.3(52.1), <em>p</em> &lt; 0.001]. In multivariate analysis both EMVs and C5b-9 were independently associated with disease duration (<em>p</em> = 0.005 and <em>p</em> = 0.004 respectively), yet not with disease activity.</p></div><div><h3>Conclusion</h3><p>Patients with systemic vasculitis exhibit impaired endothelial function and complement activation, both assessed by easily accessible biomarkers, even in the absence of cardiovascular disease manifestations. EMVs and soluble complement components such as C5b-9 and C1q could be used as early biomarkers of endothelial dysfunction and complement activation, respectively, in clinical practice during the course of SV, yet their predictive value in terms of future cardiovascular disease warrants further verification in appropriately designed studies.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104692"},"PeriodicalIF":3.1,"publicationDate":"2024-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140853445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incorporation of immunotherapies and nanomedicine to better normalize angiogenesis-based cancer treatment","authors":"Saade Abdalkareem Jasim ,&nbsp;Irina M. Farber ,&nbsp;Sara Abdalrazzaq M. Noraldeen ,&nbsp;Pooja Bansal ,&nbsp;Hashem O. Alsaab ,&nbsp;Bekhzod Abdullaev ,&nbsp;Adnan Taan Alkhafaji ,&nbsp;Ahmed Hussien Alawadi ,&nbsp;Hamza Fadhel Hamzah ,&nbsp;Bahira Abdulrazzaq Mohammed","doi":"10.1016/j.mvr.2024.104691","DOIUrl":"https://doi.org/10.1016/j.mvr.2024.104691","url":null,"abstract":"<div><p>Neoadjuvant targeting of tumor angiogenesis has been developed and approved for the treatment of malignant tumors. However, vascular disruption leads to tumor hypoxia, which exacerbates the treatment process and causes drug resistance. In addition, successful delivery of therapeutic agents and efficacy of radiotherapy require normal vascular networks and sufficient oxygen, which complete tumor vasculopathy hinders their efficacy. In view of this controversy, an optimal dose of FDA-approved anti-angiogenic agents and combination with other therapies, such as immunotherapy and the use of nanocarrier-mediated targeted therapy, could improve therapeutic regimens, reduce the need for administration of high doses of chemotherapeutic agents and subsequently reduce side effects. Here, we review the mechanism of anti-angiogenic agents, highlight the challenges of existing therapies, and present how the combination of immunotherapies and nanomedicine could improve angiogenesis-based tumor treatment.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104691"},"PeriodicalIF":3.1,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140844018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between nailfold videocapillaroscopic findings and cardiovascular risk factors","authors":"Eva Álvarez Andrés ,&nbsp;Eugenio de Miguel ,&nbsp;María Jesús García de Yébenes ,&nbsp;Loreto Carmona ,&nbsp;Cristina Gómez Miranda ,&nbsp;Paz Collado Ramos ,&nbsp;Paloma García de la Peña Lefebvre","doi":"10.1016/j.mvr.2024.104693","DOIUrl":"10.1016/j.mvr.2024.104693","url":null,"abstract":"<div><h3>Background</h3><p>Nailfold Videocapillaroscopy (NVC) is a valuable tool in the differential diagnosis of Raynaud's phenomenon (RP), present in certain Rheumatic diseases (RD). Knowing that many people have cardiovascular risk factors (CVRF), the main objective was to demonstrate that CVRF and carotid plaques produce NVC alterations.</p></div><div><h3>Methods</h3><p>Cross-sectional unicentric study carried out from 2020 to 2023. Four groups were formed: subjects with RD and RP, participants with RD without RP, subjects with RP without RD and finally participants without RP or RD (study group). Each subject exhibiting CVRF presented only a single risk factor. The variables collected were: sociodemographic, CVRF (diabetes, tobacco, alcohol (ALC), obesity (OBE), dyslipidemia and arterial hypertension (AH)), diseases, RP, treatments, tortuosities and NVC alterations (ramified capillaries, enlarged capillaries, giant capillaries, haemorrhages and density loss) and carotid ultrasound (CU).</p></div><div><h3>Results</h3><p>402 subjects were included (76 % women, mean age 51 ± 16 years), 67 % had CVRF, 50 % RP and 38 % RD. Tortuosities were present in 100 % of CVRF participants. A statistically significant association was found between the presence of CVRF and all the NVC alterations: ramified capillaries (OR = 95.6), enlarged capillaries (OR = 59.2), giant capillaries (OR = 8.32), haemorrhages (OR = 17.6) and density loss (OR = 14.4). In particular, an association was found between giant capillaries with AH (<em>p</em> = 0,008) and OBE (p 〈0,001), and haemorrhages and density loss with ALC and OBE (<em>p</em> &lt; 0,001). On the other hand, 40 subjects presented CU plaques (9.9 %), associated with enlarged capillaries (OR = 8.08), haemorrhages (OR = 4.04) and ramified capillaries (OR = 3.01). The pathological intima-media thickness was also associated with haemorrhages (OR = 3.14).</p></div><div><h3>Conclusions</h3><p>There is a clear association between CVRF and ultrasound atherosclerotic findings in carotid with NVC alterations. These findings are of special interest for a correct NVC interpretation and to avoid false positives in the diagnosis of primary and secondary RP.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104693"},"PeriodicalIF":3.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0026286224000426/pdfft?md5=66707598627c44a0e87911a5f233f2f7&pid=1-s2.0-S0026286224000426-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140861969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Digital thermography complements Laser Speckle Contrast Imaging for the diagnosis of quantified severe mesenteric traction syndrome — A prospective cohort study","authors":"August A. Olsen ,&nbsp;Stefan Burgdorf ,&nbsp;Dennis Richard Bigler ,&nbsp;Mette Siemsen ,&nbsp;Eske K. Aasvang ,&nbsp;Jens P. Goetze ,&nbsp;Morten Bo Søndergaard Svendsen ,&nbsp;Lars Bo Svendsen ,&nbsp;Michael Patrick Achiam","doi":"10.1016/j.mvr.2024.104690","DOIUrl":"https://doi.org/10.1016/j.mvr.2024.104690","url":null,"abstract":"<div><h3>Introduction</h3><p>The diagnosis of severe mesenteric traction syndrome (MTS) is based on assessing the developed degree of facial flushing. Only one validated objective diagnostic method, Laser Speckle Contrast Imaging (LSCI), exists. However, this method is sensitive to distance, motion, and angulation. Digital thermography is known to correlate well with LSCI without the same limitations, but has never been tested in relation to MTS. This study aimed to examine the thermographic changes during the development of severe MTS and to calculate a cut-off value for identifying severe MTS.</p></div><div><h3>Methods</h3><p>A prospective cohort study was performed on patients planned for open esophagectomy and pancreatic surgery from March 2021 to April 2022. All patients underwent continuous measurement on their forehead using LSCI and digital thermography during the first hour of surgery. The validated LSCI cut-off value was used to grade the severity of MTS. Blood samples and hemodynamics were collected at predefined time points.</p></div><div><h3>Results</h3><p>Fifty-seven patients were included. Patients developing severe MTS had increased facial skin temperature 15 min (<em>p</em> = 0.002) and 30 min into surgery (<em>p</em> &lt; 0.001). A cut-off value for identifying severe MTS using thermography was identified (35.55 °C, <em>p</em> &lt; 0.001). Patients identified as developing severe MTS using this cut-off value had a higher level of prostacyclin (<em>p</em> = 0.001) and lower systemic vascular resistance (<em>p</em> &lt; 0.001) 15 min into surgery, as compared with patients not developing severe MTS.</p></div><div><h3>Conclusion</h3><p>This study shows that digital thermography may complement LSCI in the objective identification of severe MTS.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104690"},"PeriodicalIF":3.1,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0026286224000396/pdfft?md5=2292610ef9de5d3ae07e00cce551254c&pid=1-s2.0-S0026286224000396-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140649322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term efficacy of liposomal nanocarriers of preassembled glycocalyx in restoring cerebral endothelial glycocalyx in sepsis","authors":"Shinya Ishiko ,&nbsp;An Huang ,&nbsp;Dong Sun","doi":"10.1016/j.mvr.2024.104684","DOIUrl":"10.1016/j.mvr.2024.104684","url":null,"abstract":"<div><p>The endothelial glycocalyx (EG) undergoes early degradation in sepsis. Our recent work introduced a novel therapeutic approach involving liposomal nanocarriers of preassembled glycocalyx (LNPG) to restore EG in lipopolysaccharide (LPS)-induced sepsis model of mice. While short-term effects were promising, this study focuses on the long-term impact of LNPG on mouse cerebral microcirculation. Utilizing cranial window, we assessed the stability of vascular density (VD) and perfused boundary region (PBR), an index of EG thickness, over a five-day period in normal control mice. In septic groups (LPS, LPS + 1-dose LNPG, and LPS + 2-dose LNPG), the exposure of mice to LPS significantly reduced VD and increased PBR within 3 h. Without LNPG treatment, PBR returned to the normal control level by endogenous processes at 48 h, associated with the recovery of VD to the baseline level at 72 h. However, mice receiving LNPG treatment significantly reduced the increment of PBR at 3 h. The therapeutic effect of 1-dose LNPG persisted for 6 h while the 2-dose LNPG treatment further reduced PBR and significantly increased VD at 12 h compared to LPS group. This study provides valuable insights into the potential therapeutic benefits of LNPG in mitigating EG degradation in sepsis.</p></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"154 ","pages":"Article 104684"},"PeriodicalIF":3.1,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140781025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}