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Filename: drivers/Session_files_driver.php
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Filename: Session/Session.php
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File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
Line Number: 249
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 249
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
Severity: Warning
Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 249
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: models/Detail_model.php
Line Number: 71
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File: /var/www/html/application/models/Detail_model.php
Line: 71
Function: strpos
File: /var/www/html/application/controllers/Detail.php
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Function: insertAPISummary
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Function: require_once
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/helpers/my_audit_helper.php
Line: 8919
Function: str_replace
File: /var/www/html/application/controllers/Detail.php
Line: 255
Function: formatAIDetailSummary
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 256
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File: /var/www/html/application/controllers/Detail.php
Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Line: 259
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Function: require_once
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Filename: controllers/Detail.php
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Backtrace:
File: /var/www/html/application/controllers/Detail.php
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Function: require_once
Biodegradable coronary artery stents are sought-after alternatives to permanent stents. These devices are designed to degrade after the blood vessel heals, leaving behind a regenerated artery. The original generation of clinically available biodegradable stents required significantly thicker struts (∼150 μm) than nondegradable ones to ensure sufficient mechanical strength. However, these thicker struts proved to be a key contributor to the clinical failure of the stents. A current challenge lies in the fabrication of stents that possess both thin struts and adequate mechanical strength. In this contribution, we describe a method for the bottom-up, additive manufacturing of biodegradable composite stents with ultrathin fibers and superior mechanical properties compared to the base polymer. Specifically, we illustrate that melt electrowriting (MEW) can be used to 3D print composite structures with thin struts (60-80 μm) and a high degree of geometric complexity required for stenting applications. Additionally, this technology allows additive manufacture of personalized stents that are customized to a patient's unique anatomy and disease state. Furthermore, we illustrate that polycaprolactone-reduced graphene oxide nanocomposites have superior mechanical properties compared to original polycaprolactone without detriment to the material's cytocompatibility and that customizable stent-like structures can be fabricated from these materials with struts as thin as 60 μm, well below the target value for clinical use of 80 μm.
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http://dx.doi.org/10.1021/acsmacrolett.0c00644 | DOI Listing |
Front Cell Dev Biol
December 2024
Department of Biological Sciences, University of Notre Dame, Notre Dame, IN, United States.
Background And Objectives: Friedreich's Ataxia (FRDA) is a genetic disease that affects a variety of different tissues. The disease is caused by a mutation in the gene ( which is important for the synthesis of iron-sulfur clusters. The primary pathologies of FRDA are loss of motor control and cardiomyopathy.
View Article and Find Full Text PDFSheng Wu Gong Cheng Xue Bao
December 2024
National Center for Protein Sciences (Beijing), Academy of Military Medical Sciences, Beijing 100850, China.
Retinoic acid signaling pathway plays a role in regulating vertebrate development, cell differentiation, and homeostasis. As a key enzyme that catalyzes the oxidation of retinal to retinoic acid, aldehyde dehydrogenase 1 family member A2 (Aldh1a2) is involved in cardiac development, while whether it functions in heart diseases remains to be studied. In this study, we infected primary cardiomyocytes with adenovirus overexpressing (Ad-Aldh1a2) to explore the effects of overexpression on the biological function of cardiomyocytes.
View Article and Find Full Text PDFBMC Anesthesiol
December 2024
Department of Anesthesiology and Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330001, China.
Objective: This study aimed to observe the impact of Tthoracic paravertebral nerve blockade(TPVB) at left T7 level on the α7nAChR-dependent cholinergic anti-inflammatory pathway in patients undergoing thoracoscopic lobectomy.
Methods: Scheduled thoracoscopic lung surgery patients at the First Affiliated Hospital of Nanchang University from August to September 2023 were divided into two groups according to the surgical site. The experimental group underwent left T7 paravertebral nerve blockade (LTPVB group), while the control group underwent right T7 paravertebral nerve blockade (RTPVB group).
Mol Biol Rep
December 2024
Department of Internal Medicine II, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-ku, Hamamatsu, Shizuoka, 431-3192, Japan.
Background: Neprilysin (NEP) is a metalloprotease that has become a therapeutic target for the treatment of heart failure and hypertension. However, the significance of NEP in chronic liver diseases has rarely been investigated. In this study, we investigated the serum NEP levels in patients with chronic liver disease and their relationship with clinical parameters.
View Article and Find Full Text PDFBMJ Open Ophthalmol
December 2024
Ophthalmology, National Yang Ming Chiao Tung University - Yangming Campus, Taipei, Taiwan
Aim: There remain limited therapies to treat thyroid eye disease (TED) orbital fibrosis, highlighting the urgency to develop novel targets. Transforming growth factor-β1 (TGF-β1)-induced myofibroblast transdifferentiation from orbital fibroblasts are important pathogenetic factor of TED. Endoplasmic reticulum (ER) stress may play a role in TED pathogenesis since it has been linked to liver, kidney, heart and lung fibrotic remodelling.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!