Open medicine (Warsaw, Poland)最新文献_第3页

circ-LIMK1 regulates cisplatin resistance in lung adenocarcinoma by targeting miR-512-5p/HMGA1 axis. circ-LIMK1通过靶向miR-512-5p/HMGA1轴调控肺腺癌的顺铂耐药。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-10-07 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0542

Ya Li, Fangfang Li, Yaya Wang, Fangyu Song, Lin Qi, Qiang Hu

{"title":"circ-LIMK1 regulates cisplatin resistance in lung adenocarcinoma by targeting miR-512-5p/HMGA1 axis.","authors":"Ya Li, Fangfang Li, Yaya Wang, Fangyu Song, Lin Qi, Qiang Hu","doi":"10.1515/med-2022-0542","DOIUrl":"https://doi.org/10.1515/med-2022-0542","url":null,"abstract":"This study aimed to unveil the detailed role and new mechanism of circ-LIMK1 in lung adenocarcinoma. Real-time quantitative polymerase chain reaction was performed to analyze the expression of circ-LIMK1, miR-512-5p, and HMGA1. 3-(4,5)-Dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide assay was employed to test the half maximal inhibitory concentration of cisplatin (DDP). Western blot was used to measure the expression of HMGA1, multidrug resistance protein 1, mitochondrial 37S ribosomal protein, and vascular endothelial growth factor A. Colony formation assay, flow cytometry, transwell assay, and tube formation assay were performed to analyze cell functions. Animal models were established to assay the role of circ-LIMK1 in vivo. The expression of circ-LIMK1 was up-regulated in DDP-resistant tumor tissues and cells. Knockdown of circ-LIMK1 reduced DDP resistance, impaired cancer cell growth, migration, invasion, and angiogenesis. circ-LIMK1 targeted miR-512-5p, and HMGA1 was targeted by miR-512-5p. MiR-512-5p absence could restore the repressive effects of circ-LIMK1 knockdown on lung adenocarcinoma cell phenotypes. Overexpression of HMGA1 could restore the inhibitory effects of miR-512-5p enrichment on lung adenocarcinoma cell malignant phenotypes. Knockdown of circ-LIMK1 could reduce growth of DDP-resistant tumors in vivo. Collectively, circ-LIMK1 regulated DDP resistance in lung adenocarcinoma by targeting miR-512-5p/HMGA1 axis.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1568-1583"},"PeriodicalIF":2.1,"publicationDate":"2022-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9547352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40454605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

lncRNA FAM230B is highly expressed in colorectal cancer and suppresses the maturation of miR-1182 to increase cell proliferation. lncRNA FAM230B在结直肠癌中高表达，抑制miR-1182的成熟，增加细胞增殖。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-10-03 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0500

Ni Li, Chuane Zhou, Fan Yang

{"title":"lncRNA FAM230B is highly expressed in colorectal cancer and suppresses the maturation of miR-1182 to increase cell proliferation.","authors":"Ni Li, Chuane Zhou, Fan Yang","doi":"10.1515/med-2022-0500","DOIUrl":"https://doi.org/10.1515/med-2022-0500","url":null,"abstract":"Long non-coding RNA FAM230B and microRNA (miR-1182) have been characterized as critical players in cancer biology, while their roles in colorectal cancer (CRC) are unclear. We predicted that they could interact with each other and therefore explored the interaction between them in CRC. CRC and paired non-tumor tissue samples were collected from 60 CRC patients, and the expression of FAM230B and miR-1182 (premature and mature) in these samples was analyzed with RT-qPCR. The direct interaction between FAM230B and premature miR-1182 was analyzed with RNA-RNA pull-down assay, and the subcellular location of FAM230B was detected with subcellular fractionation assay. The interaction between FAM230B and miR-1182 was explored with overexpression assay, and their roles in regulating CRC cell proliferation, viability, and colony formation were assessed by BrdU assay, MTT assay, and colony formation assay, respectively. We found that FAM230B and premature miR-1182 were highly upregulated in CRC, while mature miR-1182 was downregulated in CRC. FAM230B was detected in both nucleus and cytoplasm, and it directly interacted with miR-1182. FAM230B overexpression increased the expression levels of premature miR-1182 but decreased the expression levels of mature miR-1182 in CRC cells. FAM230B promoted CRC cell proliferation, increased cell viability, accelerated colony formation, and suppressed the role of miR-1182 in inhibiting CRC cell proliferation. In conclusion, FAM230B is upregulated in CRC and it suppresses the maturation of miR-1182 to promote tumor growth.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1559-1567"},"PeriodicalIF":2.1,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9531775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40559233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Role of lncRNA MIAT/miR-361-3p/CCAR2 in prostate cancer cells. lncRNA MIAT/miR-361-3p/CCAR2在前列腺癌细胞中的作用

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-28 eCollection Date: 2022-01-01 DOI: 10.1515/med-2021-0380

Tao Feng, Chunyu Song, Zhiyong Wu, Ke Zhao, Shenglan Ye

{"title":"Role of lncRNA MIAT/miR-361-3p/CCAR2 in prostate cancer cells.","authors":"Tao Feng, Chunyu Song, Zhiyong Wu, Ke Zhao, Shenglan Ye","doi":"10.1515/med-2021-0380","DOIUrl":"https://doi.org/10.1515/med-2021-0380","url":null,"abstract":"The study was aimed to investigate the role and mechanism of long non-coding RNAs (lncRNA) myocardial infarction-associated transcript (MIAT) in prostate cancer. The relationships between lncRNA MIAT and miR-361-3p, miR-361-3p and cell cycle and apoptosis regulator 2 (CCAR2) were predicted by StarBase and TargetScan, and verified by dual-luciferase reporter assay and RNA pull-down assay. Quantitative real-time PCR assay was performed to detect the mRNA expression of lncRNA MIAT, miR-361-3p, CCAR2, Bax, and Bcl-2 in the prostate cancer tissues or cells. The protein levels of CCAR2, Bax, and Bcl-2 were detected by Western blot analysis. The cell viability and apoptosis were detected by MTT assay and Flow cytometry analysis, respectively. lncRNA MIAT was upregulated, while miR-361 was downregulated in the prostate cancer tissues and Du145 cells. lncRNA MIAT negatively regulated miR-361-3p expression in Du145 cells. Downregulating lncRNA MIAT decreased the cell viability, induced the cell apoptosis, increased Bax expression, and decreased Bcl-2 expression in Du145 cells, while the effects were reversed by downregulating miR-361-3p or CCAR2 upregulation. Moreover, CCAR2 upregulation reversed the effects of miR-361-3p upregulation on Du145 cell viability and apoptosis. In conclusion, lncRNA MIAT participated in prostate cancer by regulating cell proliferation and apoptosis via miR-361-3p/CCAR2 axis.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1528-1537"},"PeriodicalIF":2.1,"publicationDate":"2022-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9520331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33513449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

The effect of dilution with glucose and prolonged injection time on dexamethasone-induced perineal irritation - A randomized controlled trial. 葡萄糖稀释和延长注射时间对地塞米松诱导的会阴部刺激的影响-一项随机对照试验。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-24 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0556

Yonghai Zhang, Hong Liang, Liwei Huang, Junwei Zheng, Yi Chen, Bin Li, Fan Yang, Jingfang Yu, Hanxiang Ma

{"title":"The effect of dilution with glucose and prolonged injection time on dexamethasone-induced perineal irritation - A randomized controlled trial.","authors":"Yonghai Zhang, Hong Liang, Liwei Huang, Junwei Zheng, Yi Chen, Bin Li, Fan Yang, Jingfang Yu, Hanxiang Ma","doi":"10.1515/med-2022-0556","DOIUrl":"https://doi.org/10.1515/med-2022-0556","url":null,"abstract":"Dexamethasone can be used to prevent nausea and vomiting after surgery, but there is concern that it may induced perineal irritation. The aim of this study was to investigate the attenuation effect of dilution and slow injection on dexamethasone-induced perineal irritation. In this prospective, randomized, double-blind study, a total of 400 patients were enrolled and allocated into four groups: Group I, receiving 2 mL dexamethasone (5 mg/mL), Group II, receiving 5 mL dexamethasone (2 mg/mL), Group III, receiving 10 mL dexamethasone (1 mg/mL), and Group IV receiving 20 mL dexamethasone (0.5 mg/mL). Dexamethasone was diluted with 5% glucose. The injection time of dexamethasone was less than 2 s in Group I, while it was 30 s in Groups II, III, and IV. The incidence, onset, duration, and severity of perineal irritation were recorded. The incidence of dexamethasone-induced perineal irritation was 49, 33, 17, and 15% in Groups I, II, III, and IV, respectively. Group IV had less severity than Group I in mild and moderate perineal irritation (P < 0.008). The onset and duration of perineal irritation of Groups II, III, and IV were significantly improved compared to Group I (P < 0.001). Dexamethasone-induced perineal irritation can be alleviated by dilution of dexamethasone to 0.5 mg/mL with 5% glucose combined with prolonged injection time of 30 s.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1509-1514"},"PeriodicalIF":2.1,"publicationDate":"2022-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9510821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33510426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

miR-146-5p restrains calcification of vascular smooth muscle cells by suppressing TRAF6. miR-146-5p通过抑制TRAF6抑制血管平滑肌细胞钙化。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-24 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0471

Jing Yang, Xiaoman Zhou, Jingwei Lu, Meng Li

{"title":"miR-146-5p restrains calcification of vascular smooth muscle cells by suppressing TRAF6.","authors":"Jing Yang, Xiaoman Zhou, Jingwei Lu, Meng Li","doi":"10.1515/med-2022-0471","DOIUrl":"https://doi.org/10.1515/med-2022-0471","url":null,"abstract":"Vascular calcification is a prominent manifestation of advanced atherosclerosis. Tumor necrosis factor-receptor-associated factors (TRAFs) were reported to participate in atherosclerosis development. In this study, the role and mechanism of TRAF6 in vascular calcification were explored. To induce the vascular calcification, oxidized low-density lipoprotein (Ox-LDL) was applied to treat vascular smooth muscle cells (VSMCs). TRAF6 protein expression in VSMCs was assessed by western blotting. Osteogenic differentiation of VSMCs was assessed by alkaline phosphatase activity analysis. Mineral deposition in VSMCs was evaluated by von Kossa staining. VSMC proliferation, migration, apoptosis, inflammation, and reactive oxygen species (ROS) generation were detected using cell counting kit-8, Transwell, flow cytometry, reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), and dichlorodihydrofluorescein diacetate staining, respectively. Luciferase reporter assay was utilized to identify the binding relationship between miR-146-5p and TRAF6 in VSMCs. We found that Ox-LDL administration induced the calcification of VSMCs and elevated the TRAF6 level. TRAF6 knockdown restrained VSMC calcification, proliferation, migration, inflammation, and ROS generation caused by Ox-LDL. Mechanically, TRAF6 was targeted by miR-146-5p in VSMCs. Furthermore, TRAF6 overexpression offset the inhibitory effects of miR-146-5p upregulation on vascular calcification in VSMCs under the Ox-LDL condition. Overall, miR-146-5p restrains the calcification of VSMCs by suppressing TRAF6.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1515-1527"},"PeriodicalIF":2.1,"publicationDate":"2022-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9510824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33510425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Antisense lncRNA PCNA-AS1 promotes esophageal squamous cell carcinoma progression through the miR-2467-3p/PCNA axis. 反义lncRNA PCNA- as1通过miR-2467-3p/PCNA轴促进食管鳞状细胞癌的进展。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-20 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0552

Tao Hu, Yunfeng Niu, Jianfeng Fu, Zhiming Dong, Dongwei He, Junfeng Liu

{"title":"Antisense lncRNA PCNA-AS1 promotes esophageal squamous cell carcinoma progression through the miR-2467-3p/PCNA axis.","authors":"Tao Hu, Yunfeng Niu, Jianfeng Fu, Zhiming Dong, Dongwei He, Junfeng Liu","doi":"10.1515/med-2022-0552","DOIUrl":"https://doi.org/10.1515/med-2022-0552","url":null,"abstract":"Multiple studies have indicated that long non-coding RNAs are aberrantly expressed in cancers and are pivotal in developing various tumors. No studies have investigated the expression and function of long non-coding antisense RNA PCNA-AS1 in esophageal squamous cell carcinoma (ESCC). In this study, the expression of PCNA-AS1 was identified by qRT-PCR. Cell function assays were used to explore the potential effect of PCNA-AS1 on ESCC progression. A prediction website was utilized to discover the relationships among PCNA-AS1, miR-2467-3p and proliferating cell nuclear antigen (PCNA). Dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays were executed to verify the binding activity between PCNA-AS1, miR-2467-3p and PCNA. As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis. PCNA-AS1 overexpression strongly contributed to ESCC cell proliferation, invasion and migration. PCNA-AS1 and PCNA were positively correlated in ESCC. Bioinformatics analysis, RIP and luciferase reporter gene assays revealed that PCNA-AS1 could act as a competitive endogenous RNA to sponge miR-2467-3p, thus upregulating PCNA. In conclusion, the current outcome demonstrates that PCNA-AS1 may be a star molecule in the treatment of ESCC.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1483-1494"},"PeriodicalIF":2.1,"publicationDate":"2022-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33497865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Erratum to "Effect of femoral head necrosis cystic area on femoral head collapse and stress distribution in femoral head: A clinical and finite element study". “股骨头坏死囊区对股骨头塌陷和股骨头应力分布的影响:临床和有限元研究”的勘误。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-20 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0563

Tianye Lin, Zhaoming Zhang, Yuan Zhong, Wenting Song, Peng Yang, Ding Wang, Fan Yang, Qingwen Zhang, Qiushi Wei, Wei He

引用次数: 0

Retraction to "miR-519d downregulates LEP expression to inhibit preeclampsia development". 撤回到“miR-519d下调LEP表达抑制子痫前期发展”。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-19 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0562

Hairui Cai, Dongmei Li, Jun Wu, Chunbo Shi

引用次数: 0

TGF-β1 upregulates Sar1a expression and induces procollagen-I secretion in hypertrophic scarring fibroblasts. TGF-β1上调增生性瘢痕成纤维细胞Sar1a表达，诱导原胶原- i分泌。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-17 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0543

Keun Jae Ahn, Jun-Sub Kim

{"title":"TGF-β1 upregulates Sar1a expression and induces procollagen-I secretion in hypertrophic scarring fibroblasts.","authors":"Keun Jae Ahn, Jun-Sub Kim","doi":"10.1515/med-2022-0543","DOIUrl":"https://doi.org/10.1515/med-2022-0543","url":null,"abstract":"Hypertrophic scarring (HTS) is a common fibroproliferative disorder that typically follows thermal and other injuries involving the deep dermis. The underlying pathogenic mechanisms are regulated by transforming growth factor-β (TGF-β); however, the exact mechanisms in HTS have not been elucidated. We conducted this study to explore the cellular signaling mechanisms for expression of Sar1a, a coat protein complex II-associated small GTPase, in HTS fibroblasts (HTSF). We found that Sar1a was upregulated in HTSF as compared to that in normal fibroblasts. Furthermore, stimulation of TGF-β1 increased the expression of Sar1a in HTSF, and small interfering RNA for Sar1a suppressed procollagen-I (PC-I) secretion. Next we investigated the signaling mechanism from TGF-β1 to Sar1a expression and its association with PC-I secretion. In the presence of TGF-β-activated kinase 1 (TAK1), c-Jun N-terminal kinase, or p38 inhibitors, the effect of TGF-β1 on Sar1a expression and PC-I secretion significantly decreased; however, it had no effect on collagen-1A (Col-1A) expression. Further, the inhibitors of Smad3 or extracellular signal-regulated kinases inhibited TGF-β1-induced Col-1A expression but had no effect on PC-I secretion and Sar1a expression. Taken together, our results suggested that TGF-β1 induces Sar1a expression through TAK1 signaling and this signaling event regulates PC-I secretion in HTSF.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1473-1482"},"PeriodicalIF":2.1,"publicationDate":"2022-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9483117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40391424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lineage switch from lymphoma to myeloid neoplasms: First case series from a single institution. 从淋巴瘤到髓系肿瘤的谱系转换:来自单一机构的首例病例系列。

IF 2.1

Open medicine (Warsaw, Poland) Pub Date : 2022-09-08 eCollection Date: 2022-01-01 DOI: 10.1515/med-2022-0521

Wenjuan Yang, Shuangfeng Xie, Yiqing Li, Jieyu Wang, Jie Xiao, Kezhi Huang, Xiuju Wang, Yudan Wu, Liping Ma, Danian Nie

{"title":"Lineage switch from lymphoma to myeloid neoplasms: First case series from a single institution.","authors":"Wenjuan Yang, Shuangfeng Xie, Yiqing Li, Jieyu Wang, Jie Xiao, Kezhi Huang, Xiuju Wang, Yudan Wu, Liping Ma, Danian Nie","doi":"10.1515/med-2022-0521","DOIUrl":"https://doi.org/10.1515/med-2022-0521","url":null,"abstract":"Lymphoma relapse is very common in clinical work, but lineage switch at relapse is rare. Although some cases have reported acute lymphocytic leukemia (ALL) switch to acute myeloid leukemia (AML) or myeloid sarcoma upon relapse, phenotype switch seldom occurs in other types of lymphoma. Here we report six cases with lineage switch from lymphoma to myeloid neoplasms. In our cohort, three cases were mantle cell lymphoma (MCL), and the other three cases were T-cell lymphoblastic lymphoma (T-LBL), B-cell lymphoblastic lymphoma (B-LBL), and diffuse large B-cell lymphoma (DLBCL) at the initial diagnosis. When linage switch occurred, most cases were AML M5 phenotypes, and only one case was myelodysplastic syndrome (MDS) phenotype. 11q23/mixed-lineage leukemia (MLL) rearrangement was negative in all cases. Although intensive therapy and stem cell transplantation have been applied in most cases, the poor outcome cannot be reversed. Therefore, we found that lineage switch could occur not only from ALL to AML or vice versa, but also from MCL or DLBCL to AML. Moreover, the incidence of MLL rearrangement in lineage switch is lower in adult hematologic malignancies as compared with pediatric patients.","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1466-1472"},"PeriodicalIF":2.1,"publicationDate":"2022-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9462540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33468072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0