Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Ovid Technologies (Wolters Kluwer Health)  (8)
  • Li, Min  (8)
Type of Medium
Publisher
  • Ovid Technologies (Wolters Kluwer Health)  (8)
Language
Years
  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Hepatology Communications Vol. 6, No. 10 ( 2022-10), p. 2914-2924
    In: Hepatology Communications, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 10 ( 2022-10), p. 2914-2924
    Abstract: It is interesting that high iron is an independent inducer or cofactor of hepatocellular carcinoma (HCC) while the amount of iron is decreased in the liver tumor tissues. Due to the previous findings that iron deficiency promoted HCC metastasis, it is of significance to identify the underlying mechanism of iron deficiency in HCC. The tumor iron content and expressions of iron‐metabolic molecules were observed in the primary liver cancers of rats and mice. The molecules that changed independently of iron were identified by comparing the expression profiles in the human HCC tissues and iron‐deprived HCC cells. The downstream effects of these molecules on regulating intracellular iron content were investigated in vitro and further validated in vivo . Both in primary liver cancers of rats and mice, we confirmed the decreased iron content in tumor tissues and the altered expressions of iron‐metabolic molecules, including transferrin receptor 1 (TfR1), six‐transmembrane epithelial antigen of prostate 3 (STEAP3), divalent metal transporter 1 (DMT1), SLC46A1, ferroportin, hepcidin, and ferritin. Among these, STEAP3, DMT1, and SLC46A1 were altered free of iron deficiency. However, only silence or overexpression of SLC46A1 controlled the intracellular iron content of HCC cells. The interventions of STEAP3 or DMT1 could not change the intracellular iron content. Lentivirus‐mediated regain of SLC46A1 expression restored the iron content in orthotopically implanted tumors, with correspondingly changes in the iron‐metabolic molecules as iron increasing. Conclusion : Taken together, these results suggest that the loss of SLC46A1 expression leads to iron deficiency in liver tumor tissues, which would be an effective target to manage iron homeostasis in HCC.
    Type of Medium: Online Resource
    ISSN: 2471-254X , 2471-254X
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2881134-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Medicine Vol. 102, No. 18 ( 2023-05-05), p. e33687-
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 18 ( 2023-05-05), p. e33687-
    Abstract: This study aimed to clarify the characteristics of intestinal microbiota in children with hand, foot, and mouth disease (HFMD) under 3 years old. Fresh feces were collected from 54 children with HFMD and 30 healthy children. All of them were 〈 3 years old. Sequencing of the 16S rDNA amplicons was performed. Between the 2 groups, the richness, diversity, and structure of the intestinal microbiota were analyzed by α-diversity and β-diversity. Linear discriminant analysis and LEfSe analyses were used to compare different bacterial classifications. The sex and age of the children in the 2 groups were not statistically significant ( P  = .92 and P  = .98, respectively). Compared to healthy children, the Shannon index, Ace index, and Chao index were lower in children with HFMD ( P  = .027, P  = .012, and P  = .012, respectively). Based on the weighted or unweighted UniFrac distance analysis, the structure of the intestinal microbiota in HFMD was also significantly changed ( P  = .002 and P   〈  .001, respectively). Linear discriminant analysis and LEfSe analysis showed that the changes of key bacteria were manifested as a decrease in Prevotella and Clostridium_XIVa (P   〈  .001 and P   〈  .001, respectively), while Escherichia and Bifidobacterium increased ( P  = .025 and P  = .001, respectively). Children with HFMD under 3 years of age have intestinal microbiota disorder and show a decrease in diversity and richness. The decrease in the abundance of Prevotella and Clostridium , which can produce short-chain fatty acids, is also one of the characteristics of the change. These results can offer a theoretical foundation for the pathogenesis and microecological treatment of HFMD in infants.
    Type of Medium: Online Resource
    ISSN: 0025-7974
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2049818-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 3 ( 2021-01-22), p. e24352-
    Abstract: The effectiveness of anterior serratus plane block in postoperative analgesia of thoracic surgery is beginning to emerge. Currently, there are 2 methods of anterior serratus plane block: deep serratus plane block (DSPB) and superficial serratus plane block (SSPB). In clinical practice, there is no an unified view regarding the advantages and disadvantages between 2 methods. This study aimed to observe and compare the analgesic effects of 2 methods on patients undergoing thoracoscopic lobectomy, in order to provide some suggestions for anesthesiologists when they choose anterior serratus plane block to perform postoperative analgesia for patients. Patients were randomly divided into 3 groups (21 patients/group): The patients in groups S and D received 0.4 ml/kg of 0.375% ropivacaine for ultrasound-guided block after surgery. Postoperatively, flurbiprofen was used for rescue analgesia. Visual analog scale (VAS) pain scores were recorded at 6 hours, 12 hours, and 24 hours after surgery, and rescue analgesia, post-operative nausea, and vomiting were reported within 24 hours after surgery. At 6 hours, 12 hours, and 24 hours, the VAS scores and the rescue analgesia rates in groups S and D were significantly lower than those in group P (all P   〈  .001). With prolonging time, the VAS in group D was significantly increased by 0.11 per hour as compared with that of group P ( P   〈  .0001); VAS in group D was significantly increased by 0.12 per hour as compared with that of group S ( P   〈  .0001). Ultrasound-guided anterior serratus plane block can provide adequate analgesia for patients undergoing thoracoscopy lobectomy. SSPB can significantly improve VAS scores as compared to DSPB at 24 hours.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049818-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Medicine Vol. 97, No. 1 ( 2018-01), p. e9520-
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 1 ( 2018-01), p. e9520-
    Type of Medium: Online Resource
    ISSN: 0025-7974
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2049818-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    In: Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 65, No. 6 ( 2017-06), p. 1904-1919
    Abstract: Uncontrolled inflammatory response highlights the central theme of nonalcoholic steatohepatitis (NASH), a growing global pandemic. Hepatocytes and macrophages represent two major sources of hepatic inflammation during NASH pathogenesis, contributing to excessive synthesis of proinflammatory mediators. The epigenetic mechanism that accounts for the activation of hepatocytes and macrophages in this process remains obscure. Here, we report that compared to wild‐type littermates, mice with a deficiency in the histone H3K9 methyltransferase suppressor of variegation 39 homolog 2 (Suv39h2, knockout) exhibited a less severe form of NASH induced by feeding with a high‐fat, high‐carbohydrate diet. Pro‐NASH stimuli increased Suv39h2 expression in cell culture, in mice, and in human livers. In hepatocytes, Suv39h2 bound to the Sirt1 gene promoter and repressed Sirt1 transcription. Suv39h2 deficiency normalized Sirt1 expression, allowing nuclear factor kappa B/p65 to become hypoacetylated and thus dampening nuclear factor kappa B–dependent transcription of proinflammatory mediators. In macrophages, Suv39h2‐mediated repression of peroxisome proliferator–activated receptor gamma transcription favored a proinflammatory M1 phenotype over an anti‐inflammatory M2 phenotype, thereby elevating hepatic inflammation. Conclusion : Suv39h2 plays a pivotal role in the regulation of inflammatory response in hepatocytes and macrophages, contributing to NASH pathogenesis. (H epatology 2017;65:1904‐1919).
    Type of Medium: Online Resource
    ISSN: 0270-9139 , 1527-3350
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1472120-X
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    In: Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 74, No. 6 ( 2021-12), p. 3037-3055
    Abstract: Insulin receptor (IR) transduces cell surface signal through phosphoinositide 3‐kinase (PI3K)–AKT pathways or translocates to the nucleus and binds to the promoters to regulate genes associated with insulin actions, including de novo lipogenesis (DNL). Chronic activation of IR signaling drives malignant transformation, but the underlying mechanisms remain poorly defined. Down‐regulation of fructose‐1,6‐bisphosphate aldolase (ALDO) B in hepatocellular carcinoma (HCC) is correlated with poor prognosis. We aim to study whether and how ALDOB is involved in IR signaling in HCC. Approach and Results Global or liver‐specific ALDOB knockout (L‐ALDOB −/− ) mice were used in N‐diethylnitrosamine (DEN)–induced HCC models, whereas restoration of ALDOB expression was achieved in L‐ALDOB −/− mice by adeno‐associated virus (AAV). 13 C 6 ‐glucose was employed in metabolic flux analysis to track the de novo fatty acid synthesis from glucose, and nontargeted lipidomics and targeted fatty acid analysis using mass spectrometry were performed. We found that ALDOB physically interacts with IR and attenuates IR signaling through down‐regulating PI3K–AKT pathways and suppressing IR nuclear translocation. ALDOB depletion or disruption of IR/ALDOB interaction in ALDOB mutants promotes DNL and tumorigenesis, which is significantly attenuated with ALDOB restoration in L‐ALDOB −/− mice. Notably, attenuated IR/ALDOB interaction in ALDOB‐R46A mutant exhibits more significant tumorigenesis than releasing ALDOB/AKT interaction in ALDOB‐R43A, whereas knockdown IR sufficiently diminishes tumor‐promoting effects in both mutants. Furthermore, inhibiting phosphorylated AKT or fatty acid synthase significantly attenuates HCC in L‐ALDOB −/− mice. Consistently, ALDOB down‐regulation is correlated with up‐regulation of IR signaling and DNL in human HCC tumor tissues. Conclusions Our study reports a mechanism by which loss of ALDOB activates IR signaling primarily through releasing IR/ALDOB interaction to promote DNL and HCC, highlighting a potential therapeutic strategy in HCC.
    Type of Medium: Online Resource
    ISSN: 0270-9139 , 1527-3350
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1472120-X
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Medicine Vol. 98, No. 27 ( 2019-07), p. e16321-
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 27 ( 2019-07), p. e16321-
    Abstract: Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction that can be triggered by anticholinergic agents. Patient concerns: We present a 4-year-old female patient who was admitted to the outpatient clinic. She complained of drooped eyelids, which first appeared 2 days after taking a 200 mg dose of pyrantel pamoate. Past medical history is negative. Diagnoses and treatment: She was hospitalized with a diagnosis of ocular type MG, and pyridostigmine (40 mg/day) treatment was started. Outcomes: The patient recovered, and subsequently, the treatment dose was tapered. Conclusion: Pyrantel is an antihelminthic that acts as an agonist of nicotinic acetylcholine receptors (AChRs) of nematodes and exerts its therapeutic effects by depolarizing their muscle membranes. Consequently, there may be an association between pyrantel pamoate and MG.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2049818-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    In: Pancreas, Ovid Technologies (Wolters Kluwer Health), Vol. 50, No. 4 ( 2021-4), p. 617-624
    Abstract: As one of the most aggressive human tumors, pancreatic cancer (PC) is accompanied by poor treatment and prognosis. Although emerging evidence has highlighted the importance of long noncoding RNAs in multiple cancers, the specific regulatory roles mostly remain obscure. Our aim was to disclose the role of CERS6 antisense RNA 1 (CERS6-AS1) in PC. Methods Quantitative real-time polymerase chain reaction analysis was used to examine the expression of CERS6-AS1 in PC cell lines. Western blot analysis was used to assess the protein levels of high-mobility group AT-hook 1 (HMGA1). Colony formation, 5-ethynyl-20-deoxyuridine, transwell, and wound healing assays were performed to detect the functions of CERS6-AS1 on PC development. In addition, RNA pull-down, RNA immunoprecipitation, and luciferase reporter assays were implemented to delve into the regulatory mechanism of CERS6-AS1 in PC. Results CERS6-AS1 was significantly upregulated in PC. CERS6-AS1 silence obviously inhibited cell proliferation and migration in PC. Furthermore, CERS6-AS1 sponged microRNA-15a-5p (miR-15a-5p) and microRNA-6838-5p (miR-6838-5p) to regulate HMGA1. Moreover, rescue assays verified that CERS6-AS1 was involved in cell proliferation and migration in PC via targeting miR-15a-5p/miR-6838-5p/HMGA1 axis. Conclusions CERS6-AS1 enhanced HMGA1 expression to contribute to the progression of PC by sequestering miR-15a-5p and miR-6838-5p.
    Type of Medium: Online Resource
    ISSN: 1536-4828 , 0885-3177
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2053902-2
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages