Recent development and future application of biodegradable ureteral stents.

Ureteral stenting is a common clinical procedure for the treatment of upper urinary tract disorders, including conditions such as urinary tract infections, tumors, stones, and inflammation. Maintaining normal renal function by preventing and treating ureteral obstruction is the primary goal of this procedure. However, the use of ureteral stents is associated with adverse effects, including surface crusting, bacterial adhesion, and lower urinary tract symptoms (LUTS) after implantation. Recognizing the need to reduce the complications associated with permanent ureteral stent placement, there is a growing interest among both physicians and patients in the use of biodegradable ureteral stents (BUS). The evolution of stent materials and the exploration of different stent coatings have given these devices different roles tailored to different clinical needs, including anticolithic, antibacterial, antitumor, antinociceptive, and others. This review examines recent advances in BUS within the last 5 years, providing an in-depth analysis of their characteristics and performance. In addition, we present prospective insights into the future applications of BUS in clinical settings.

Resveratrol Delays Diabetic Cardiomyopathy Fibrosis by Regulating Mitochondrial Autophagy.

Objective: To explore whether resveratrol can postpone the fibrosis associated with diabetic cardiomyopathy (DCM) by modulating the mitochondrial autophagy response through the AMPK/SIRT1-mediated IRE1α/PINK signaling pathway. Methods: A DCM mouse model was established using a high-sugar high-fat diet and streptozotocin. Resveratrol was administered to a subset of the DCM mouse models for comparison. Echocardiography, Masson staining, TNUEL assay, and transmission electron microscopy were employed to evaluate the cardiac status, myocardial fibrosis, myocardial cell apoptosis, and morphological changes of myocardial cells and their internal mitochondria in each group of mice. Western blot staining was performed on myocardial tissues to assess the protein expression levels of p-AMPK, SIRT1, SIRT3, p22, GP91, p-IRE1α, XBP1s PINK, Parkin, LC3I, and Beclin. Mouse myocardial cells were cultured in vitro and intervened with a high-sugar high-fat diet, resveratrol, and GSK690693 (an AMPK inhibitor) to observe the protein expression levels of p-AMPK, p22, XBP1s, and PINK in mouse myocardial cells in each group. Results: Results from echocardiography, Masson staining, TNUEL assay, and transmission electron microscopy showed that resveratrol administration alleviated cardiac damage, myocardial fibrosis, myocardial cell apoptosis, and mitochondrial autophagy in DCM mice. Resveratrol administration promoted the expression of phosphorylated AMP-activated protein kinase (p-AMPK), sirtuin 1 (SIRT1), and sirtuin 3 (SIRT3) in the myocardial tissue of mice, while lowering the elevated protein expression levels of p22 subunit (p22), guanine nucleotide-binding protein q polypeptide 1 (GP91), phosphorylated inositol-requiring enzyme 1 alpha (p-IRE1α), X-box binding protein 1 spliced form (XBP1s), PTEN-induced putative kinase 1 (PINK), Parkin, microtubule-associated proteins light chain 3 isoform I (LC3I), and Beclin (Bcl-2 interacting protein) caused by DCM. GSK690693 (an AMPK inhibitor) suppressed the expression of p-AMPK, SIRT1, and SIRT3 and enhanced the protein expression of p22, XBP1s, and PINK. Conclusion: Resveratrol postpones dilated cardiomyopathy fibrosis by regulating the mitochondrial autophagy response through the AMP-activated protein kinase (AMPK)/silent mating type information regulation 2 homolog 1 (SIRT1)-mediated inositol-requiring enzyme 1 alpha (IRE1α)/PTEN-induced putative kinase 1 (PINK) signaling pathway.

SIRT3 rs11246020 Polymorphism Associated Postprandial Triglyceride Dysmetabolism.

Purpose: Energy metabolism is regulated by SIRT3, no research has been done on the connection between lipid metabolism in the oral fat test and SIRT3 polymorphism. Thus, we conducted a case-control study to investigate the connection between postprandial lipid and SIRT3 polymorphism. Patients and Methods: 402 non-obese Chinese subjects were enrolled and their postprandial lipid response to oral fat tolerance test (OFTT) was observed to understand the relationship between rs11246020 gene and postprandial triglyceride metabolism. Results: In a binary logic regression model, a protective effect of the T allele of the rs11246020 SIRT3 for postprandial hypertriglyceridemia was shown (OR=0.417, 95% CI = 0.219-0.794, p=0.008). Compared to the CC genotype, individuals with the TT+CT variant of the rs11246020 SIRT3 gene demonstrated significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.04), postprandial plasma glucose (PPG) (p=0.037), fasting plasma glucose (FPG) (p=0.02), and 4-hour triglyceridemia (Tg) (p=0.032). Conclusion: The C allele of rs11246020 SIRT3 gene may be a risk factor to increased possibility of postprandial triglyceridemia after an oral fat test, which involved in the mechanism of glucose and insulin metabolism.

Dirhodium(II)/DPPM Catalyzed 1,2-Hydrosilylation of Conjugated Dienes with Tertiary Silanes.

A simple and efficient Rh2(OAc)4/DPPM (bis(diphenylphosphanyl)methane) catalyzed regioselective 1,2-anti-Markovnikov hydrosilylation of conjugated dienes with various tertiary silanes gave homoallylic silanes in acetonitrile, which tolerate broad functional groups. Control experiments proved that no π-allyl transition metal intermediates were involved in this 1,2-anti-Markovnikov hydrosilylation. Dirhodium hydride species was observed in hydrosilylation, suggesting that a direct insertion of the terminal double bond into a Rh-H bond is involved in this reaction.

Calorie restriction mimetic, resveratrol, attenuates hepatic ischemia and reperfusion injury through enhancing efferocytosis of macrophages via AMPK/STAT3/S1PR1 pathway.

Calorie restriction (CR) mimetic, resveratrol (RSV), has the capacity of promoting phagocytosis. However, its role in hepatic ischemia and reperfusion injury (HIRI) remains poorly understood. This study aimed to investigate the effect of RSV on alleviating HIRI and explore the underlying mechanisms. RSV was intraperitoneally injected in mice HIRI model, while RSV was co-incubated with culture medium for 24 h in RAW 264.7 cells and kupffer cells. Macrophage efferocytosis was assessed by immunostaining of PI and F4/80. The clearance of apoptotic neutrophils in the liver was determined by immunostaining of Ly6-G and cleaved-caspase-3. HE staining, Suzuki's score, serum levels of ALT, AST, TNF-α and IL-1ß were analyzed to evaluate HIRI. The efferocytosis inhibitor, Cytochalasin D, was utilized to investigate the effect of RSV on HIRI. Western blot was employed to measure the levels of AMPKα, phospho-AMPKα, STAT3, phospho-STAT3 and S1PR1. SiSTAT3 and inhibitors targeting AMPK, STAT3 and S1PR1, respectively, were used to confirm the involvement of AMPK/STAT3/S1PR1 pathway in RSV-mediated efferocytosis and HIRI. RSV facilitated the clearance of apoptotic neutrophils and attenuated HIRI, which was impeded by Cytochalasin D. RSV boosted macrophage efferocytosis by up-regulating the levels of phospho-AMPKα, phospho-STAT3 and S1PR1, which was reversed by AMPK, STAT3 and S1PR1 inhibitors, respectively. Inhibition of STAT3 suppressed RSV-induced clearance of apoptotic neutrophils and exacerbated HIRI. CR mimetic, RSV, alleviates HIRI by promoting macrophages efferocytosis through AMPK/STAT3/S1PR1 pathway, providing valuable insights into the mechanisms underlying the protective effects of CR on attenuating HIRI.

Genomic and epigenetic characterization of the arsenic-induced oncogenic microRNA-21.

As one of the first identified oncogenic microRNAs, the precise details concerning the transcriptional regulation and function of microRNA-21 (miR-21) are still not completely established. The miR-21 gene is situated on chromosome 17q23.2, positioned at the 3'-UTR of the gene that encodes vacuole membrane protein-1 (VMP1). In this current study, we presented evidence indicating that miR-21 possesses its own gene promoter, which can be found in the intron 10 of the VMP1 gene. Chromatin immunoprecipitation followed by global DNA sequencing (ChIP-seq) revealed the presence of a broad H3K4me3 peak spanning the entire gene body of the primary miR-21 and the existence of super-enhancer clusters in the close proximity to both the miR-21 gene promoter and the transcription termination site in arsenic (As3+)-induced cancer stem-like cells (CSCs) and human induced pluripotent stem cells (hiPSCs). In non-transformed human bronchial epithelial cells (BEAS-2B), As3+ treatment enhanced Nrf2 binding to both the host gene VMP1 of miR-21 and the miR-21 gene. Knockout of Nrf2 inhibited both the basal and As3+-induced expressions of miR-21. Furthermore, the As3+-enhanced Nrf2 peaks in ChIP-seq fully overlap with these super-enhancers enriched with H3K4me1 and H3K27ac in the miR-21 gene, suggesting that Nrf2 may coordinate with other transcription factors through the super-enhancers to regulate the expression of miR-21 in cellular response to As3+. These findings demonstrate the unique genetic and epigenetic characteristics of miR-21 and may provide insights into understanding the novel mechanisms linking environmental As3+ exposure and human cancers.

MLKL Protects Pulmonary Endothelial Cells in Acute Lung Injury.

The role of autophagy in pulmonary microvascular endothelial cells (PMVECs) is controversial in LPS-induced acute lung injury (ALI). Mixed lineage kinase domain-like pseudokinase (MLKL) has recently been reported to maintain cell survival by facilitating autophagic flux in response to starvation rather than its well-recognized role in necroptosis. Using a mouse PMVEC and LPS-induced ALI model, we showed that in PMVECs, MLKL was phosphorylated (p-MLKL) and autophagic flux was accelerated at the early stage of LPS stimulation (1-3 h), manifested by increases in concentrations of lipidated MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 ß; LC3-II), decreases in concentrations of SQSTM1/p62 (sequestosome 1), and fusion of the autophagosome and lysosome by pHluorin-mKate2-human LC3 assay, which were all reversed by either MLKL inhibitor or siRNA MLKL. In mice, the inhibition of MLKL increased vascular permeability and aggravated mouse ALI upon 3-hour LPS stimulation. The p-MLKL induced by short-term LPS formed multimers to facilitate the closure of the phagophore by HaloTag-LC3 autophagosome completion assay. The charged multivesicular body protein 2A (CHMP2A) is essential in the process of phagophore closure into the nascent autophagosome. In agreement with the p-MLKL change, CHMP2A concentrations markedly increased during 1-3-hour LPS stimulation. CHMP2A knockdown blocked autophagic flux upon LPS stimulation, whereas CHMP2A overexpression boosted autophagic flux and attenuated mouse ALI even in the presence of MLKL inhibitor. We propose that the activated MLKL induced by short-term LPS facilitates autophagic flux by accelerating the closure of the phagophore via CHMP2A, thus protecting PMVECs and alleviating LPS-induced ALI.

Recent advances in drug delivery systems based on natural and synthetic polymes for treating obesity.

Obesity stands as a pervasive global public health issue, posing a formidable threat to human well-being as its prevalence continues to surge year by year. Presently, pharmacological treatment remains the favored adjunct strategy for addressing obesity. However, conventional delivery methods suffer from low bioavailability and the potential for side effects, underscoring the pressing need for more efficient and targeted delivery approaches. Recent research has delved extensively into emerging drug delivery systems employing polymers as carriers, with numerous preclinical studies contributing to the growing body of knowledge. This review concentrates on the utilization of natural polymers as drug delivery systems for the treatment of obesity, encompassing recent advancements in both natural and synthetic polymers. The comprehensive exploration includes an analysis of the advantages and disadvantages associated with these polymer carriers. The examination of these characteristics provides valuable insights into potential future developments in the field of drug delivery for obesity treatment.

The G protein-coupled estrogen receptor of the trigeminal ganglion regulates acute and chronic itch in mice.

AIMS: Itch is an unpleasant sensation that severely impacts the patient's quality of life. Recent studies revealed that the G protein-coupled estrogen receptor (GPER) may play a crucial role in the regulation of pain and itch perception. However, the contribution of the GPER in primary sensory neurons to the regulation of itch perception remains elusive. This study aimed to investigate whether and how the GPER participates in the regulation of itch perception in the trigeminal ganglion (TG). METHODS AND RESULTS: Immunofluorescence staining results showed that GPER-positive (GPER+ ) neurons of the TG were activated in both acute and chronic itch. Behavioral data indicated that the chemogenetic activation of GPER+ neurons of the TG of Gper-Cre mice abrogated scratching behaviors evoked by acute and chronic itch. Conversely, the chemogenetic inhibition of GPER+ neurons resulted in increased itch responses. Furthermore, the GPER expression and function were both upregulated in the TG of the dry skin-induced chronic itch mouse model. Pharmacological inhibition of GPER (or Gper deficiency) markedly increased acute and chronic itch-related scratching behaviors in mouse. Calcium imaging assays further revealed that Gper deficiency in TG neurons led to a marked increase in the calcium responses evoked by agonists of the transient receptor potential ankyrin A1 (TRPA1) and transient receptor potential vanilloid V1 (TRPV1). CONCLUSION: Our findings demonstrated that the GPER of TG neurons is involved in the regulation of acute and chronic itch perception, by modulating the function of TRPA1 and TRPV1. This study provides new insights into peripheral itch sensory signal processing mechanisms and offers new targets for future clinical antipruritic therapy.

A bibliometric and visualized analysis of hepatic ischemia-reperfusion injury (HIRI) from 2002 to 2021.

Hepatic ischemia-reperfusion injury (HIRI) is a complex pathological phenomenon dominated by the innate immune system and involves a variety of immune cells. This condition frequently occurs during hepatectomy, liver transplantation or hemorrhagic shock. HIRI represents an important factor in the poor prognosis of patients after liver surgery. However, there is still a lack of effective intervention to reduce the incidence of HIRI. In this study, we aimed to describe the overall structure of scientific research on HIRI over the past 20 years and provide valuable information and guidelines for future researchers. Bibliometric analysis was used to comprehensively review developments in HIRI and changes in our understanding of HIRI over the past two decades. We identified a total of 4267 articles on HIRI that were published over the past 20 years of which basic research was predominant. Collaboration network analysis revealed that China, the University of California Los Angeles, and Ronald W Busuttil were the most influential country, institute, and scholar, respectively. Co-occurrence cluster analysis revealed that ischemic preconditioning, liver cirrhosis, hepatic I/R injury, autophagy, acute liver failure, oxygen, donation after circulatory death, Nlrp3, remote organ, and microdialysis were the top 10 clusters. Keyword burst detection indicated that autophagy, inflammation, and early allograft dysfunction represent the current research hotspots. In summary, this is the first bibliometric analysis of HIRI research. Our timely analysis of these hotpots and research trends may provide a framework for future researchers and further promote research on the key mechanisms and therapeutic measures in this field.

Advances in the Application of Photothermal Composite Scaffolds for Osteosarcoma Ablation and Bone Regeneration.

Photothermal therapy is a promising approach to cancer treatment. The energy generated by the photothermal effect can effectively inhibit the growth of cancer cells without harming normal tissues, while the right amount of heat can also promote cell proliferation and accelerate tissue regeneration. Various nanomaterials have recently been used as photothermal agents (PTAs). The photothermal composite scaffolds can be obtained by introducing PTAs into bone tissue engineering (BTE) scaffolds, which produces a photothermal effect that can be used to ablate bone cancer with subsequent further use of the scaffold as a support to repair the bone defects created by ablation of osteosarcoma. Osteosarcoma is the most common among primary bone malignancies. However, a review of the efficacy of different types of photothermal composite scaffolds in osteosarcoma is lacking. This article first introduces the common PTAs, BTE materials, and preparation methods and then systematically summarizes the development of photothermal composite scaffolds. It would provide a useful reference for the combination of tumor therapy and tissue engineering in bone tumor-related diseases and complex diseases. It will also be valuable for advancing the clinical applications of photothermal composite scaffolds.

Comprehensive review of materials, applications, and future innovations in biodegradable esophageal stents.

Esophageal stricture (ES) results from benign and malignant conditions, such as uncontrolled gastroesophageal reflux disease (GERD) and esophageal neoplasms. Upper gastrointestinal endoscopy is the preferred diagnostic approach for ES and its underlying causes. Stent insertion using an endoscope is a prevalent method for alleviating or treating ES. Nevertheless, the widely used self-expandable metal stents (SEMS) and self-expandable plastic stents (SEPS) can result in complications such as migration and restenosis. Furthermore, they necessitate secondary extraction in cases of benign esophageal stricture (BES), rendering them unsatisfactory for clinical requirements. Over the past 3 decades, significant attention has been devoted to biodegradable materials, including synthetic polyester polymers and magnesium-based alloys, owing to their exceptional biocompatibility and biodegradability while addressing the challenges associated with recurring procedures after BES resolves. Novel esophageal stents have been developed and are undergoing experimental and clinical trials. Drug-eluting stents (DES) with drug-loading and drug-releasing capabilities are currently a research focal point, offering more efficient and precise ES treatments. Functional innovations have been investigated to optimize stent performance, including unidirectional drug-release and anti-migration features. Emerging manufacturing technologies such as three-dimensional (3D) printing and new biodegradable materials such as hydrogels have also contributed to the innovation of esophageal stents. The ultimate objective of the research and development of these materials is their clinical application in the treatment of ES and other benign conditions and the palliative treatment of malignant esophageal stricture (MES). This review aimed to offer a comprehensive overview of current biodegradable esophageal stent materials and their applications, highlight current research limitations and innovations, and offer insights into future development priorities and directions.

Functionalized TMC and ε-CL elastomers with shape memory and self-healing properties.

Introduction: Smart elastomers, which possess self-healing and shape memory capabilities, have immense potential in the field of biomedical applications. Polycarbonates and polyesters have gained widespread interest due to their remarkable biocompatibility over the last century. Nevertheless, the lack of functional versatility in conventional polyesters and polycarbonates means that they fall short of meeting the ever-evolving demands of the future. Methods: This paper introduced a new smart elastomer, named mPEG43-b-(PMBC-co-PCL)n, developed from polyester and polycarbonate blends, that possessed shape memory and self-heal capabilities via a physical crosslinking system. Results: The material demonstrated a significant tensile strength of 0.38 MPa and a tensile ratio of 1155.6%, highlighting its favorable mechanical properties. In addition, a conspicuous shape retrieval rate of 93% was showcased within 32.5 seconds at 37°C. Remarkably, the affected area could be repaired proficiently with no irritation experienced during 6h at room temperature, which was indicative of an admirable repair percentage of 87.6%. Furthermore, these features could be precisely modified by altering the proportion of MBC and ε-CL to suit individual constraints. Discussion: This innovative elastomer with exceptional shape memory and self-heal capabilities provides a solid basis and promising potential for the development of self-contracting intelligent surgical sutures in the biomedical field.

A 7-month-old girl with a suspected air embolism complication during a living-donor liver transplantation procedure: a case report.

Background: Pediatric liver transplantation is an important modality for treating biliary atresia. The overall survival rate of pediatric liver transplantation has significantly improved. The incidence of perioperative cardiac events was evaluated, and risk factors were also investigated in adult patients undergoing liver transplantation in previous studies. To the best of our knowledge, this is the first case of a cardiac event during a pediatric living-donor liver transplantation. Case summary: Our report describes the management of cardiac events during a liver transplantation in a 7-month-old girl. The ST segment began to increase to 3.0 mm immediately after reperfusion, with peak ST-segment elevation reaching 13.2 mm after 45 min. The procedure ended uneventfully after continuous symptomatic and etiological treatment. It was considered to be the occurrence of an acute air embolism complication during the procedure based on the electrocardiograph and biomarkers. An echocardiogram during follow-up showed a patent foramen ovale with a left-to-right shunt tract width of 2.7 mm. Discussion: Pediatric liver transplantation has become a state-of-the-art treatment for children with end-stage liver disease and can improve the quality of life to some extent. These children may be complicated with congenital heart disease, which increases the risk of surgery. Application of echocardiogram, close monitoring, and appropriate management may reduce the incidence of perioperative cardiac events.

Biodegradable polyester-based nano drug delivery system in cancer chemotherapy: a review of recent progress (2021-2023).

Cancer presents a formidable threat to human health, with the majority of cases currently lacking a complete cure. Frequently, chemotherapy drugs are required to impede its progression. However, these drugs frequently suffer from drawbacks such as poor selectivity, limited water solubility, low bioavailability, and a propensity for causing organ toxicity. Consequently, a concerted effort has been made to seek improved drug delivery systems. Nano-drug delivery systems based on biodegradable polyesters have emerged as a subject of widespread interest in this pursuit. Extensive research has demonstrated their potential for offering high bioavailability, effective encapsulation, controlled release, and minimal toxicity. Notably, poly (ε-caprolactone) (PCL), poly (lactic-co-glycolic acid) (PLGA), and polylactic acid (PLA) have gained prominence as the most widely utilized options as carriers of the nano drug delivery system. This paper comprehensively reviews recent research on these materials as nano-carriers for delivering chemotherapeutic drugs, summarizing their latest advancements, acknowledging their limitations, and forecasting future research directions.

Emerging trends and hotspots of the itch research: A bibliometric and visualized analysis.

AIMS: Itch, a common uncomfortable sensory experience, occurs frequently in inflammatory or allergic disorders. In recent years, with the discovery of itch-specific pathways in the peripheral and central nervous system, the association between immunology and neural pathways has gradually emerged as the main mechanism of itch. Although many studies have been conducted on itch, no bibliometric analysis study focusing on this topic has been conducted. This study aimed to explore the research hotspots and trends in the itch field from a bibliometric perspective. METHODS: Publications relevant to itch, published from 2003 to 2022, were retrieved from the Science Citation Index-Expanded of Web of Science Core Collection. Publications were critically reviewed and analyzed with CiteSpace software, Vosviewer, and the bibliometric online analysis platform. Visual maps were conducted in terms of annual production, collaborating countries or institutions, productive authors, core journals, co-cited references, and keyword bursts. RESULTS: 2395 articles on itch that met our criteria were identified and the quantity of publications has been increasing rapidly since 2012. The USA was the most influential country. University Hospital Münster was the institution with the most publications. Gil Yosipovitch was the most prolific author. Atopic dermatitis (AD), intradermal serotonin, chronic pruritus, mechanical itch, gastrin-releasing peptide, substance p, interleukin-31 receptor, histamine-induced itch, bile acid, scratching behavior, and h-4 receptor were the top 11 clusters in co-citation cluster analysis. Keyword burst analysis suggested that treatment, inflammation, and AD are current research hotspots. CONCLUSION: Global publications on itch research have increased steadily and rapidly over the past 20 years. Inflammation and AD are current research hotspots. The neuroimmunological and neuroinflammatory mechanisms of itch, as well as clinical assessment methods and therapeutic targets, will be novel research directions in the future. This study provides guidance for further itch research.

Correlation Between Fibrinogen/Albumin and Diabetic Peripheral Neuropathy.

Purpose: This study aimed to examine the correlation between fibrinogen/albumin (FAR) and diabetic peripheral neuropathy (DPN). Patients and Methods: A total of 342 patients were included and categorized into either the DPN group or the Non-DPN (NDPN) group based on their DPN status. The FAR index was determined by calculating the ratio of fibrinogen (FIB) to serum albumin (ALB), multiplied by 100. The participants were then divided into a High-FAR group and a Low-FAR group using the median FAR value as the threshold. Neurophysiological data were collected from the participants, which included motor conduction velocity (MCV) and sensory conduction velocity (SCV). Results: The DPN group displayed higher FAR levels [(DPN vs NDPN:6.72 (5.89,7.74) vs 5.94±1.14], in addition to slower SCV and MCV data compared to the NDPN group. The high FAR group had a higher prevalence of DPN (78.9% vs 55.6%) (P<0.05). There was a negative correlation between FAR and NCV, including bilateral median nerve SCV, left ulnar nerve SCV, bilateral median nerve MCV, bilateral common peroneal nerve MCV, bilateral tibial nerve MCV, and left ulnar nerve MCV. FAR was revealed to be an independent risk factor for the development of DPN in patients and demonstrated a greater predictive value for DPN development in Type 2 diabetes mellitus (T2DM) compared with FIB, HbA1c. Conclusion: The results suggest that monitoring FAR levels in patients with T2DM could identify those at higher risk for developing DPN, making the FAR index a valuable predictor of DPN development. Furthermore, since FAR has an inverse relationship with NCV, it stands to reason that high FAR levels may indicate nerve damage and slower conduction velocities. Thus, managing FAR could prove beneficial in both preventing and delaying the onset of DPN in T2DM patients.

In vitro enzymatic degradation of the PTMC/cross-linked PEGDA blends.

Introduction: Poly(1,3-trimethylene carbonate) (PTMC) is a flexible amorphous polymer with good degradability and biocompatibility. The degradation of PTMC is critical for its application as a degradable polymer, more convenient and easy-to-control cross-linking strategies for preparing PTMC are required. Methods: The blends of poly(trimethylene carbonate) (PTMC) and cross-linked poly(ethylene glycol) diacrylate (PEGDA) were prepared by mixing photoactive PEGDA and PTMC and subsequently photopolymerizing the mixture with uv light. The physical properties and in vitro enzymatic degradation of the resultant PTMC/cross-linked PEGDA blends were investigated. Results: The results showed that the gel fraction of PTMC/cross-linked PEGDA blends increased while the swelling degree decreased with the content of PEGDA dosage. The results of in vitro enzymatic degradation confirmed that the degradation of PTMC/cross-linked PEGDA blends in the lipase solution occurred under the surface erosion mechanism, and the introduction of the uv cross-linked PEGDA significantly improved the resistance to lipase erosion of PTMC; the higher the cross-linking degree, the lower the mass loss. Discussion: The results indicated that the blends/cross-linking via PEGDA is a simple and effective strategy to tailor the degradation rate of PTMC.

Serum Soluble Vascular Endothelial Growth Factor Receptor 1 as a Potential Biomarker of Hepatopulmonary Syndrome.

Background and Aims: The results of basic research implicate the vascular endothelial growth factor (VEGF) family as a potential target of hepatopulmonary syndrome (HPS). However, the negative results of anti-angiogenetic therapy in clinical studies have highlighted the need for markers for HPS. Therefore, we aimed to determine whether VEGF family members and their receptors can be potential biomarkers for HPS through clinical and experimental studies. Methods: Clinically, patients with chronic liver disease from two medical centers were enrolled and examined for HPS. Patients were divided into HPS, intrapulmonary vascular dilation [positive contrast-enhanced echocardiography (CEE) and normal oxygenation] and CEE-negative groups. Baseline information and perioperative clinical data were compared between HPS and non-HPS patients. Serum levels of VEGF family members and their receptors were measured. In parallel, HPS rats were established by common bile duct ligation. Liver, lung and serum samples were collected for the evaluation of pathophysiologic changes, as well as the expression levels of the above factors. Results: In HPS rats, all VEGF family members and their receptors underwent significant changes; however, only soluble VEGFR1 (sFlt-1) and the sFlt-1/ placental growth factor (PLGF) ratio were changed in almost the same manner as those in HPS patients. Furthermore, through feature selection and internal and external validation, sFlt-1 and the sFlt-1/PLGF ratio were identified as the most important variables to distinguish HPS from non-HPS patients. Conclusions: Our results from animal and human studies indicate that sFlt-1 and the sFlt-1/PLGF ratio in serum are potential markers for HPS.