Portal Hypertension & Cirrhosis
·
2024
·Vol. 3
·期 2
·86-95
·
IF 0
Kaibo Yang,Kunjin Wu,Zitong Lei,Tong Liu,Xing Zhang,Jing Li,Kun Yang,Qiuting Peng,Ting Lin,Chang Liu,Kai Qu
Aim Tumor budding (TB) has excellent prognostic value in many solid tumors, but there is little research on it in hepatocellular carcinoma (HCC). This study assessed the prognostic value of TB in patients with HCC who received hepatectomy. Methods This retrospective study included 210 patients with HCC who received curative hepatectomy at the First Affiliated Hospital of Xi'an Jiaotong University, between 2016 and 2018. TB was evaluated on hematoxylin- and eosin-stained slides according to the criteria established by the 2016 International Tumor Budding Consensus Conference. t -tests, Chi-squared tests, and rank-sum tests were used to correlate the extent of TB with clinicopathological parameters. Prognostic analysis was performed using Cox regression models and the Kaplan–Meier method. Results The positive detection rate of TB was 45.2% (95/210) in 210 patients with HCC. Patients positive for TB always exhibit lower tumor differentiation, higher hepatitis B virus DNA levels, and more severe liver fibrosis. Multivariate Cox analysis identified TB (hazard ratio [HR]: 2.232, 95% confidence interval [CI]: 1.479–3.368, p < 0.001) as an independent prognostic factor for patients' recurrence-free survival (RFS), similar to tumor size (HR: 1.070, 95% CI: 1.070–1.142, p = 0.042) and satellite nodule (HR: 2.266, 95% CI: 1.298–3.956, p = 0.004). Kaplan–Meier analysis also demonstrated that TB-positive patients had a significantly worse RFS. Interestingly, subgroup analysis revealed that among HCC patients with negative microvascular invasion (MVI), TB was also strongly associated with RFS (HR: 3.206, 95% CI: 1.667–6.168, p < 0.001). These findings suggest that TB may serve as a supplemental prognostic biomarker for HCC-negative MVI. Conclusions TB is an adverse prognostic biomarker for HCC, particularly in patients negative for MVI. TB evaluation should be considered in the postoperative pathological examination of HCC in clinical practice. Graphical This study assessed tumor budding (TB) in hepatocellular carcinoma patients. TB refers to the detachment of tumor cells from the primary tumor mass, infiltrating the adjacent matrix and forming separate clusters. It may represent two distinct pathological features compared to microvascular invasion, which involves the invasion of tumor cells into microvessels. ECM: extracellular matrix. Key points Significant findings of the study This single-center study found that tumor budding (TB) positivity was significantly associated with poor prognosis in patients with hepatocellular carcinoma (HCC). What this study adds TB could serve as a potential supplemental prognostic biomarker for HCC with negative microvascular invasion.
研究领域:
病理学
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肿瘤学
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外科学
✓ 已验证
DOI
CHEMICO-BIOLOGICAL INTERACTIONS
·
2024
·
IF 4.7
Shaofei Song,Hong Peng,Yuan Li,Tingting Zhao,Renjie Cao,Lei Zheng,Min Huang,Yiming Jiang
Liver regeneration after liver tumor resection or liver transplantation is crucial, the remaining liver frequently fails to regenerate in some patients. Oleanolic acid (OA), a pentacyclic triterpenoid compound which has been shown to protect against various liver diseases. However, the effect of OA on liver regeneration after partial hepatectomy (PHx) is still unclear. In this study, the results showed that OA (50 mg/kg, twice daily) treatment induced liver mass restoration and increased the liver-to-body weight ratio of mice following PHx. Meanwhile, OA promoted hepatocyte proliferation and increased the number of BrdU-, Ki67-and PCNA-positive cells. Furthermore, OA increased the nuclear accumulation of PXR and induced the expression of PXR downstream proteins such as CYP3A11, UGT1A1 and GSTM2 in mice, as well as in AML12 and HepRG cells. Luciferase reporter assay and nuclear localization of PXR further demonstrated the effect of OA on PXR activation in vitro . Molecular docking simulation showed that OA could interact with the PXR active sites. Moreover, OA inhibited the expression of FOXO1, RBL2 and CDKN1B, and increased the expression of PCNA, CCND1 and CCNE1 in vivo and in vitro . Silencing of Pxr further confirmed that OA-mediated upregulation of proliferation-related proteins depended on PXR. The current study illustrated that OA exhibited a significant promoting effect on liver regeneration following PHx, potentially through regulation of the PXR signaling pathway to accelerate liver recovery.
研究领域:
药理学
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肝脏病学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2025
·
IF 12.5
Qiuxia Zheng,Jia Yao,Zongbin Sun,Rui Li,Yue Zhang,Pan Jiang,Ye Xie,Xiaojing Song,Hongfa Sun,Dan Zhu,Haixu Ni,Xun Li
Hepatectomy is the primary therapeutic intervention for liver disorders. Nonetheless, an increased risk of liver failure and postoperative mortality exists due to the rapid reduction in liver size after surgery. Human umbilical cord mesenchymal stem cell (hucMSC) exosomes (Exos) have been recognized in the promotion of liver regeneration. However, intravenous administration of Exos faces several challenges including poor targeting and rapid clearance. Herein, we employed CMCS/OHA/LA-loaded hucMSCs derived Exos (hydrogel-Exos) to address liver regeneration after hepatectomy. Release and uptake studies showed hydrogel-Exos enables localized release of Exos, prolonging their presence and concentration in liver tissue. Meanwhile, the hydrogel-Exos exhibited good characteristics in injectability, self-healing, biocompatibility, liver adhesion, swelling performance, postoperative hemostasis and minimization of peritoneal adhesions post-resection. Moreover, proliferation and scratch wound healing assays demonstrated the ability of hydrogel-Exos to promote liver cell proliferation and migration. During in vivo studies, the Exos-containing hydrogel was injected into the resected surface of a 70 % hepatectomy rat model. The result indicated Exos was released into the liver tissue through the hydrogel to promote angiogenesis and liver regeneration. Bioinformatics analysis revealed liver regeneration mechanisms involve cell cycle-related pathways. As such, hydrogel-encapsulated Exos appeared promising to be employed following hepatectomy.
研究领域:
医学
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生物材料学
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再生医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY
·
2024
·
IF 2.7
Guofang Bi,Fengting Liang,Ting Wu,Peng Wang,Xiaowen Jiang,Shuang Hu,Chenghua Wu,Wenhong Zhou,Jiayin Guo,Xiao Yang,Jian-hong Fang,Wenying Chen,Huichang Bi
Human pregnane X receptor (PXR) is critical for regulating the expression of key drug-metabolizing enzymes such as CYP3A and CYP2C. Our recent study revealed that treatment with rodent-specific PXR agonist pregnenolone-16α-carbonitrile (PCN) significantly induced hepatomegaly and promoted liver regeneration after two-thirds partial hepatectomy (PHx) in mice. However, it remains unclear whether PXR activation induces hepatomegaly and liver regeneration and simultaneously promotes metabolic function of the liver. Here, we investigated the metabolism activity of CYP1A2, CYP3A1/2 and CYP2C6/11 during PXR activation-induced liver enlargement and regeneration in rats after cocktail dosing of CYP probe drugs. For PCN-induced hepatomegaly, a notable increase in the metabolic activity of CYP3A1/2 and CYP2C6/11, as evidenced by the plasma exposure of probe substrates and the AUC ratios of the characteristic metabolites to its corresponding probe substrates. The metabolic activity of CYP1A2, CYP3A1/2 and CYP2C6/11 decreased significantly after PHx. However, PCN treatment obviously enhanced the metabolic activity of CYP2C6/11 and CYP3A1/2 in PHx rats. Furthermore, the protein expression levels of CYP3A1/2 and CYP2C6/11 in liver were up-regulated. Taken together, this study demonstrates that PXR activation not only induces hepatomegaly and liver regeneration in rats, but also promotes the protein expression and metabolic activity of the PXR downstream metabolizing enzymes such as CYP3A1/2 and CYP2C6/11 in the body.
研究领域:
药理学
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肝病学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
·
2024
·Vol. 57
·期 4
·604
·
IF 3.3
Xuewei Li,Jinghui Feng,Haiqin Cheng,Ning Jin,Shanshan Jin,Zhizhen Liu,Jun Xu,Jun Xie
Liver fibrosis is a critical stage in the progression of various chronic liver diseases to cirrhosis and liver cancer. Early inhibition of liver fibrosis is crucial for the treatment of liver disease. Hepatectomy, a common treatment for liver-related diseases, promotes liver regeneration. However, in the context of liver fibrosis, liver regeneration is hindered. Many studies have shown that mesenchymal stem cells (MSCs) can promote liver regeneration after partial hepatectomy (PH). However, there are few reports on the impact of MSC therapy on liver regeneration post-PH in the context of hepatic fibrosis. The objective of this study is to examine the impact of MSCs on liver regeneration following PH in the fibrotic liver and uncover the related molecular mechanisms. This study reveals that MSC therapy significantly enhances liver function and mitigates liver inflammation after PH in the context of hepatic fibrosis. MSCs also significantly promote liver regeneration and alleviate liver fibrosis. In addition, this study identifies the role of MSCs in promoting liver regeneration and alleviating liver fibrosis via the activation of Wnt/β-catenin signaling. The combination of MSCs with hepatectomy may offer a novel approach for the treatment of liver fibrotic diseases.
研究领域:
医学
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细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
Genes & Genomics
·
2022
·Vol. 44
·期 8
·1017-1029
·
IF 2.164
Hou Fangxing,Li Xing,Wang Yanfeng,Xiao Xiangzuo
Background Liver regeneration is a highly orchestrated process concerning the modulation of various microRNAs (miRs). miR-183 was recently found to be involved in the process of liver regeneration, that miR-183 was remarkably up-regulated at 2–6 h after partial hepatectomy. Objective This study was aimed to explore the mechanism of miR-183 in on liver regeneration. Methods After partial hepatectomy (PH) or transfection, we measured the changes of miR-183 and programmed cell death protein 6 (PDCD6) levels in rats and the hepatocytes. The histopathology was observed with hematoxylin–eosin staining. The miR-183 mimic and inhibitor plasmids were intravenously injected into rats, and the liver weight/body weight ratio was calculated. The prediction of TargetScan and the validation of luciferase activity assay were employed to confirm the targeting relationship between miR-183 and PDCD6. The viability, apoptosis and cell cycle of transfected rat hepatocyte BRL-3A were determined via MTT and flow cytometry assays. Results MiR-183 expression showed a contrary tendency with that of PDCD6 during liver regeneration. Enhanced miR-183 in rats could notably increase liver/body weight ratio, while its inhibition did conversely. Overexpressed PDCD6, a target of miR-183, repressed the viability and cell cycle in hepatocytes, whereas its silence led to contrary results. Overexpressed miR-183 in BRL-3A cells enhanced cell viability and promoted the cell cycle yet suppressed apoptosis, whereas its inhibition showed contrary results, which were offset by PDCD6. Conclusions Collectively, miR-183 promoted liver regeneration via targeting PDCD6.
研究领域:
分子生物学
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肝病学
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细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Yanghao Li,Xu Yang,Tiantian Bao,Xiaojuan Sun,Xiang Li,Huilin Zhu,Bo Zhang,Tonghui Ma
Background The therapeutic efficacy of liver injuries heavily relies on the liver's remarkable regenerative capacity, necessitating the maintenance of glycose/lipids homeostasis and oxidative eustasis during the recovery process. Astragali Radix, an herbal tonic widely used in China and many other countries, is believed to have many positive effects, including immune stimulation, nourishing, antioxidant, liver protection, diuresis, anti-diabetes, anti-cancer and expectorant. Astragali Radix is widely integrated into hepatoprotective formulas as it is believed to facilitate liver regeneration. Nevertheless, the precise molecular pharmacological mechanisms underlying this hepatoprotective effect remain elusive. Purpose To investigate the improving effects of Astragali Radix on liver regeneration and the underlying mechanisms. Methods A mouse model of 70% partial hepatectomy (PHx) was employed to investigate the impact of Radix Astragali decoction (HQD) on liver regeneration. HQD was orally administered for 7 days before the PHx procedure and throughout the experiment. N-acetylcysteine (NAC) was used as a positive control for liver regeneration. Liver regeneration was assessed by evaluating the liver-to-body weight ratio (LW/BW) and the expression of representative cell proliferation marker proteins. Oxidative stress and glucose metabolism were analyzed using biochemical assays, Western blotting, dihydroethidium (DHE) fluorescence, and periodic acid-Schiff (PAS) staining methods. To understand the role of AQP9 as a potential molecular target of HQD in promoting liver regeneration, td-Tomato-tagged AQP9 transgenic mice (AQP9-RFP) were employed to determine the expression pattern of AQP9 protein. AQP9 knockout mice (AQP9 −/− ) were used to assess the specific targeting of AQP9 in the promotion of liver regeneration by HQD. Results HQD significantly upregulated hepatic AQP9 expression, alleviated liver injury and promoted liver regeneration in wild-type (AQP9 +/+ ) mice after 70% PHx. However, the beneficial impact of HQD on liver regeneration was absent in AQP9 gene knockout (AQP9 −/− ) mice. Moreover, HQD facilitated the uptake of glycerol by hepatocytes, enhanced gluconeogenesis, and concurrently reduced H 2 O 2 content and oxidative stress levels in AQP9 +/+ but not AQP9 −/− mouse livers. Additionally, main active substance of Radix Astragali, astragaloside IV (AS-IV) and cycloastragenol (CAG), demonstrated substantial upregulation of AQP9 expression and promoted liver regeneration in AQP9 +/+ but not AQP9 −/− mice. Conclusion This study is the first to demonstrate that Radix Astragali and its main active constituents (AS-IV and CAG) improve liver regeneration by upregulating the expression of AQP9 in hepatocytes to increase gluconeogenesis and reduce oxidative stress. The study revealed novel molecular pharmacological mechanisms of Radix Astragali and provided a promising therapeutic target of liver diseases.
研究领域:
药理学
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肝病学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Hu Chen,Minglei Teng,Qihui Hu,Xiaoliu Liang,Hui Liu,Zhenjie Li,Xing Gao,Yisheng Peng,Xiaoyong Wang,Syed Faheem Askari Rizvi,Yi Lv,Hongwei Cheng,Rui Tao,Gang Liu
Anatomical hepatectomy is a widely employed surgical technique due to its capacity to excise hepatic lesions and minimize risk variables associated with postoperative recurrence. However, preserving the anatomical and functional integrity of the liver remains a critical concern and a significant challenge in determining the boundaries of targeted liver segments. This study utilized a super-stable pure-nanomedicine formulation technology (SPFT) to synthesize methylene blue nanosheets (nanoMB) without external carrier, nanoMB did not alter the chemical composition of methylene blue (MB), it was purely a physical aggregation of molecules. The nanosize and morphology of nanoMB enhanced the internalization and retention in hepatocytes and liver tissues, addressing the limitations of unclear staining due to the rapid diffusion of MB during liver segment resection. The in vivo model of blue staining of liver segments in rats and rabbits confirmed that nanoMB can extend the staining duration of liver segments by over 3 h, whereas free MB continues for <1 min, thereby addressing the time constraints associated with liver resection. In subsequent human clinical trials, a single low-dose nanoMB injection was employed to mark hepatic segment boundaries during anatomical hepatectomy for hepatocellular carcinoma and hepatolithiasis. The boundaries continued to be distinct for over 30 min, effectively guiding the surgical resection. The postoperative liver function recovered to normal, with no complications or disease recurrence reported. In conclusion, carrier-free nanomedicine enhances hepatic visualization by improving cellular uptake and hepatic segment retention. This advancement facilitates precise surgery and establishes a new paradigm for translational research from bench to clinic.
研究领域:
纳米医学
·
肝脏外科
·
转化医学
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生物医学工程
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肿瘤外科学
✓ 已验证
产品关联
DOI
高影响因子
International Journal of Nanomedicine
·
2024
·
IF 6.6
Xiangdong Gongye,Peng Xia,Tianyin Ma,Yibo Chai,Zhang Chen,Yimin Zhu,Chengming Qu,Jie Liu,Wing Wa Guo,Minghe Zhang,Yingyi Liu,Ming Tian,Yufeng Yuan
Background The liver’s regenerative capacity allows it to repair itself after injury. Extracellular vesicles and particles (EVPs) in the liver’s interstitial space are crucial for signal transduction, metabolism, and immune regulation. Understanding the role and mechanism of liver-derived EVPs in regeneration is significant, particularly after partial hepatectomy, where the mechanisms remain unclear.Methods A 70% hepatectomy model was established in mice, and EVPs were isolated and characterized using electron microscopy, nanocharacterization, and Western blot analysis. Combined metabolomic and transcriptomic analyses revealed β-sitosterol enrichment in EVPs and activation of the Hedgehog signaling pathway during regeneration. The role of β-sitosterol in EVPs on the Hedgehog pathway and its targets were identified using qRT-PCR, Western blot analysis. The regulation of carnitine synthesis by this pathway was determined using a dual luciferase assay. The effect of a β-sitosterol diet on liver regeneration was verified in mice.Results After 70% hepatectomy, the liver successfully regenerated without liver failure or death. At 24 hours post-surgery, tissue staining showed transient regeneration-associated steatosis (TRAS), with increased Ki67 positivity at 48 hours. EVPs displayed a spherical lipid bilayer structure with particle sizes of 70–130 nm. CD9, CD63, and CD81 in liver-derived EVPs were confirmed. Transcriptomic and metabolomic analyses showed EVPs supplementation significantly promoted carnitine synthesis and fatty acid oxidation. Tissue staining confirmed accelerated TRAS resolution and enhanced liver regeneration with EVP supplementation. Mass spectrometry identified β-sitosterol in EVPs, which binds to Smo protein, activating the Hedgehog pathway. This led to the nuclear transport of Gli3, stimulating Setd5 transcription and inducing carnitine synthesis, thereby accelerating fatty acid oxidation. Mice with increased β-sitosterol intake showed faster TRAS resolution and liver regeneration compared to controls.Conclusion Liver-derived EVPs promote regeneration after partial hepatectomy. β-sitosterol from EVPs accelerates fatty acid oxidation and promotes liver regeneration by activating Hedgehog signaling pathway.
研究领域:
肝病学
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分子生物学
·
再生医学
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代谢组学
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转录组学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
·
2025
·
IF 3.3
Hong-Yu Li,Wei-Lan Zeng,Yi-Wen Ye,Xin Chen,Ming-Ming Zhang,Yi-Si Chen,Cui-Ting Liu,Zhun-Qiang Zhong,Jing Li,Yan Wang
Glia maturation factor-β (Gmfb), an actin filament debrancher, was initially identified in brain and recently linked to liver diseases. To investigate the role of hepatocyte Gmfb (hep-Gmfb) in liver reparative regeneration, hepatocyte-specific gmfb knockout (HepGKO) and overexpression (HepGOE) zebrafish strains were constructed. Both transgenic and wild-type (WT) zebrafish underwent partial hepatectomy (PHX) or were fed high fat, high cholesterol diets to model metabolism-associated steatotic liver disease (MASLD). Under physiological conditions, the HepGKO, HepGOE, and WT fish displayed similar survival, gross appearance, and liver histology. Following PHX, WT liver gmfb levels positively correlated with cell proliferation and proinflammatory cytokine levels. HepGOE showed enhanced regeneration and reduced liver steatosis compared to WT, while HepGKO exhibited opposite effects. In MASLD, WT liver gmfb increased with disease progression. HepGKO experienced worsening liver enlargement, steatosis, ballooning, inflammation, and endoplasmic reticulum stress, while HepGOE showed improvements. HepGOE liver had the highest cell proliferation, but all three groups showed similar levels of cell apoptosis. Moreover, elevated proinflammatory cytokines were observed across MASLD groups, being the highest in HepGKO and lowest in HepGOE. However, stat3 activation was the lowest in HepGKO and highest in HepGOE, while jnk and mapk/erk activation was consistent across the MASLD groups. In il6-treated primary hepatocytes, gmfb abundance influenced stat3 activation, and hep-gmfb abundance significantly affected actin filaments distribution in hepatocytes both in vivo and vitro. Conclusions: Hep-Gmfb boosts regenerative processes by enhancing hepatocyte proliferation, alleviating fatty liver histological abnormalities, and modulating the Il6/Stat3 signaling, potentially through remodeling of actin-filament network within hepatocytes.
研究领域:
分子生物学
·
细胞生物学
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肝脏病学
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发育生物学
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遗传学
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信号转导
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病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACS Nano
·
2024
·
IF 15.8
Meng Sun,Min Li,Min Hu,Yueyun Fan,Yanhong Liu,Jian Sun,Jinfeng Zhang
Acute liver failure (ALF) is a serious global disease characterized by rapid onset and high mortality. Currently, the clinical treatment of ALF faces considerable hurdles due to limited medication options and the scarcity of liver transplants. Despite biomacromolecules such as hepatocyte growth factor (HGF) and glutathione (GSH) having been applied for ALF symptom relief in the clinic, they still face substantial challenges including poor stability, difficulty in acting on intracellular targets, and inadequate therapeutic outcome. In this work, by taking advantage of the innate targeting and regenerative capabilities of mesenchymal stem cells (MSCs), we harnessed MSC-derived exosomes as natural bioactive carriers for the simultaneous delivery of HGF and GSH, forming a fully bioactive nanodrug termed HG@Exo. Impressively, the HG@Exo demonstrated potent therapeutic effects against both carbon tetrachloride (CCl4)- and extreme hepatectomy-induced ALF through multiple mechanisms, including regulation of oxidative stress, reduction of inflammation, and promotion of hepatocyte regeneration, which were facilitated by its inflammation-targeting to damaged liver tissues. Furthermore, an FDA-approved near-infrared fluorescent dye, indocyanine green (ICG), has been incorporated into the exosomes (HGI@Exo) to endow them with real-time in vivo tracking capability, which showed favorable liver accumulation of the HGI@Exo in both CCl4- and surgery-induced ALF animal models, providing crucial insights into their biodistribution and therapeutic efficacy. Overall, the presented fully bioactive nanodrugs with targeting and theranostic abilities hold significant promise for potentiating the therapeutic efficacy of biomacromolecules for the improved treatment of ALF and other inflammatory diseases.
研究领域:
药理学
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纳米医学
·
干细胞治疗
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肝脏疾病
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2022
·
IF 8.025
Xiangyu Wei,Chunyan Cui,Chuanchuan Fan,Tengling Wu,Yuan Li,Xiaoping Zhang,Kuan Wang,Yudi Pang,Puqing Yao,Jianhai Yang
Hemostasis and prevention of postoperative adhesions after hepatectomy are still challenges. In this work, we chose chitosan, a competitive candidate hemostatic material, as the backbone, and konjac glucomannan as the functional moieties, to form an injectable hydrogel. The hydrogel was prepared by the Schiff base reaction of dodecyl-modified N -carboxyethyl chitosan (DCEC) and oxidized konjac glucomannan (OKGM), which could effectively prevent bleeding and postoperative adhesions. The resultant hydrogel possessed self-healing and tissue adhesive capability, and combined the unique bioactivities of two polysaccharides: DCEC endowed the hydrogel with excellent antibacterial and hemostatic ability by the electrostatic and hydrophobic interactions between the cell membrane and amine/dodecyl groups, and OKGM imparted hydrogel anti-inflammatory action by activating macrophages. Moreover, the notable hemostatic efficacy of the hydrogel was confirmed in a rat hepatectomy model. The hydrogel could prevent postoperative adhesions and down-regulate the inflammatory factor TNF-α and the pro-fibrotic factor TGF-β 1 in situ, which might be caused by the combination of the barrier function of hydrogel and instinct bioactivities of DCEC and OKGM. Thus, this multifunctional injectable hydrogel is potentially valuable for preventing bleeding and postoperative adhesions after hepatectomy.
研究领域:
生物材料
·
生物医学工程
·
外科手术
·
药剂学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）