Annals of clinical and laboratory science最新文献

{"title":"Therapeutic and Mechanistic Effects of Granulocyte Colony Stimulating Factor and Neurotrophin Receptor on Cerebral Ischemia-Reperfusion Injury: An Experimental Pilot Study.","authors":"Qing Liu, Xiaoming Zhu, Xie Yan, Yang Hu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>To study the therapeutic effect and protective mechanism of granulocyte colony stimulating factor (G-CSF) and neurotrophin receptor (NTR) on cerebral ischemia-reperfusion injury.</p><p><strong>Methods: </strong>Rat models of permanent focal middle cerebral artery occlusion (MCAO) were constructed by using a modified suture method, and the rats were assigned into three groups such as treatment group (the rats were injected with mixed G-CSF and NTR once), sham operation group and PBS control group. The volume of the cerebral infarction was detected using Triphenyltetrazolium Chloride (TTC) staining method; the motor function in rats was evaluated; and qRT-PCR detection, double immunofluorescence histochemistry and immunohistochemistry were performed to observe various effects.</p><p><strong>Results: </strong>After G-CSF and NTR treatment, the infarct volume induced by MCAO in the treatment group was significantly lower than that in the PBS control group (<i>P</i><0.05). The motor function in the treatment group was significantly improved on day 7 and day 14 compared to the PBS control group (<i>P</i><0.05). The levels of MCP-1, TNF-<i>α</i>, TGF-β and IL-10 mRNA in the treatment group decreased by 22% compared with PBS control group, and the difference was statistically significant (<i>P</i><0.05). The Bcl-2 protein level in the treatment group was greater than that in the PBS control group, while the Bax level in the treatment group was lower than in the control group; and both the differences were statistically significant (<i>P</i><0.05). The number of BrdU + cells in the treatment group was significantly greater than that in the PBS control group (<i>P</i><0.05).</p><p><strong>Conclusion: </strong>G-CSF can promote the regeneration of neurons, promote the formation of new blood vessels, promote the reconstruction of neural network in rat MCAO models through anti apoptosis, anti-inflammation and mobilization of bone marrow hematopoietic cells to exert its powerful protective effect on neurons, and contribute to the repair of neural function and improvement of prognosis.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 4","pages":"474-482"},"PeriodicalIF":1.1,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ADAM15 in Fibroblasts: Improving the Matrix Remodeling by Blocking the Action of Transforming Growth Factor-β1.","authors":"Ye Li, Jiang Xue, Weiquan Zhang, Yongjie Wang, Wei Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>During the progression of chronic idiopathic pulmonary fibrosis (IPF), maladaptive tissue remodeling including excessive extracellular matrix (ECM) deposition occurs, which eventually leads to architectural distortion and loss of organ function in organ fibrosis. ADAM15, which is highly expressed in the developing lungs and kidneys, is a transmembrane-anchored multidomain protein belonging to the family of metalloproteinases. Compared to the extensive studies about functions of matrix metalloproteinases (MMPs), less are discussed about ADAM15, particularly in function and mechanism involving fibrogenesis. Our study aims to fill in this gap.</p><p><strong>Methods: </strong>We identified ADAM15 as a novel antifibrotic mediator in lung fibrosis. We found that ADAM15 has cross-talks with transforming growth factor-β1 (TGF-β1), which is the most potent profibrotic mediator. We provided molecular and translational evidence that knockdown of ADAM15 accelerated fibrogenic response induced by TGF-β1 and upregulation of ADAM15 rescued TGF-β1-induced myofibroblast activation in part.</p><p><strong>Results: </strong>Overexpression of ADAM15 ameliorates fibrotic changes and ADAM15 deficiency exacerbates changes from fibroblast to myofibroblast in NIH/3T3. Results were also presented and identified by the intuitive immunofluorescence staining.</p><p><strong>Conclusion: </strong>In this study, we uncover a new molecular mechanism of tissue fibrogenesis and identify ADAM15 as a potential therapeutic target in the treatment of fibrotic diseases.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"363-370"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of FAM114A1 Suppresses Hepatocellular Carcinoma by Targeting AKT1 Signaling.","authors":"Haifeng Zhang, Yu Zeng, Chihua Ye, Jianwu Cai, Xiao Hu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Hepatocellular carcinoma (HCC) poses a significant challenge owing to its aggressive nature and elevated mortality rates. Understanding the role of novel therapeutic targets is essential. Although linked to several diseases, the role of the family with sequence similarity 114 member A1 (FAM114A1) in HCC remains unclear.</p><p><strong>Methods: </strong>Utilizing UALCAN and GEPIA databases, the expression of FAM114A1 in HCC tissues was examined, alongside exploring its correlation with AKT1. FAM114A1 expression in HCC cells was assessed through qRT-PCR experiments. Following lentiviral transduction to suppress FAM114A1 expression in these cells, subsequent analyses involved MTT assays, scratch assays, Transwell analysis, and flow cytometry to investigate the impact of FAM114A1 depletion on cell proliferation, migration, apoptosis, and cell cycle dynamics. Furthermore, Western blot analysis assessed EMT-related proteins (Snail, MMP2, MMP9) and AKT1 expression. Overexpression of AKT1 in HCC cells was performed, and its effects on cell proliferation and migration were assessed using MTT assays and Transwell analysis.</p><p><strong>Results: </strong>Elevated FAM114A1 expression was observed in HCC tissues and cells. FAM114A1 suppression reduced cell proliferation and migration by modulating AKT1. FAM114A1 knockdown promoted apoptosis, arrested the cell cycle, and inhibited EMT.</p><p><strong>Conclusions: </strong>Overall, our study suggests that FAM114A1 plays a role in HCC cell proliferation and migration, involving the modulation of AKT1 expression. Furthermore, FAM114A1 impacts apoptosis, cell cycle, and EMT, contributing to HCC development. These findings highlight FAM114A1 as a potential novel therapeutic target for HCC treatment.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"378-387"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postpartum Glucose Monitoring in Pregnant Women with Gestational Diabetes Mellitus: A Dual Center Experience.","authors":"Ridwan B Ibrahim, Lily Olayinka, Anil K Chokkalla, Sridevi Devaraj","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Gestational diabetes mellitus (GDM) is known to be a predisposing factor in the development of type 2 diabetes mellitus in affected mothers and their offspring. Current guidelines recommend a two-hour postpartum glucose tolerance test (OGTT) in patients with a history of GDM. However, compliance rates for ordering and completion has been reported as suboptimal. The COVID-19 pandemic has had significant impact on healthcare systems, requiring the adaptation of novel strategies to manage patients. So far, there is a paucity of data on how this impacts compliance rates for the oral glucose tolerance test. We aimed to compare the compliance rate and impact of the pandemic on OGTT ordering and completion between a women's hospital and a community health center.</p><p><strong>Methods: </strong>A dual center retrospective cohort study was carried out to compare the compliance for ordering and completion of the two-hour postpartum OGTT in women diagnosed with GDM between a women's hospital and community health center two years pre-COVID-19 (2018-2019) and during the COVID-19 pandemic (2020-2021).</p><p><strong>Results: </strong>2569 pregnancies were included during these time periods. Prior to the pandemic, the test ordering compliance at the women hospital was 30.2% vs 79.3% for the community health center. During the pandemic, the test ordering compliance at the women's hospital dropped to 24.8%, while it remained steady at the community center (80.8%). Correspondingly, there was a drop in test completion compliance rate at both centers during the pandemic when compared to rate before the pandemic.</p><p><strong>Conclusion: </strong>Diagnosis of GDM increased during the pandemic, which may be attributed to factors like sedentary lifestyles, and restructuring of care models, among others. There was increased test ordering and test completion compliance at the community health center compared to the women's hospital, which can be attributed to routine follow-ups and other factors.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"331-334"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Communication:</i> High-Density Lipoprotein-Specific Phospholipid Efflux in Familial Hypercholesterolemia.","authors":"Masaki Sato, Masato Hamasaki, Edward B Neufeld, Alan T Remaley, Kazuhiko Kotani","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Familial hypercholesterolemia (FH) is characterized by elevated levels of low-density lipoprotein cholesterol (LDL-C) and cardiovascular disease (CVD). Although the role of LDL-C in FH has been studied, the contribution of high-density lipoproteins (HDL) to CVD in FH remains unknown. This study aimed at highlighting the role of HDL in FH.</p><p><strong>Methods: </strong>HDL-specific phospholipid efflux (HDL-SPE) assay was developed to predict CVD risk. HDL-SPE was examined in FH patients (n=30) and compared with age- and sex-matched non-FH controls (n=60).</p><p><strong>Results: </strong>FH patients had significantly lower HDL-SPE levels (0.90±0.12) than controls (1.12±0.10; <i>p</i><0.05), despite similar HDL-cholesterol levels in both groups (FH: 57.9±18.7 mg/dl; controls: 57.1±13.8 mg/dl). These differences remained significant after adjusting for confounders.</p><p><strong>Conclusions: </strong>These findings suggest there may be dysfunctionality of HDL in FH.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"419-422"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Timing of Histological Distal Villous Fetal Vascular Malperfusion in the Placenta: Clinical Significance and Placental Features.","authors":"Jerzy Stanek","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>This retrospective analysis compares the diagnostic value of placental large vessel (global, partial) and distal villous (complete, segmental) fetal vascular malperfusion (FVM), remote/established, recent and on-going.</p><p><strong>Methods: </strong>24 independent abnormal clinical and 46 placental phenotypes were retrospectively statistically analyzed among 1002 consecutive cases, mostly with congenital anomalies in which CD34 immunostaining was performed. Group A: 398 cases without distal FVM and none or up to two large vessels FVM lesions. Group B: 221 cases with distal villous FVM without clustered endothelial fragmentation by CD34 immunostain. Group C: 145 cases with clustered endothelial fragmentation by CD34 immunostain but no clustered sclerotic or mineralized distal villi. Group D: 163 cases with coexistence of distal villous lesions of Group B and Group C. Group E: 75 cases with three or four lesions of large vessel FVM, but no distal villous FVM lesions.</p><p><strong>Results: </strong>Established and/or remote FVM had clinical/placental associations similar to those of recent FVM, but on-going FVM was most commonly high grade and associated with preterm pregnancies, stillbirth, and fetal growth restriction. Large vessel FVM usually occurs in advanced third trimester pregnancies with fetal congenital anomalies, villitis of unknown etiology, and intervillous thrombi but no direct association with abnormal fetal condition.</p><p><strong>Conclusion: </strong>FVM was the most common pattern of placental injury in this material. Proximal FVM was more common than distal FVM, suggesting the sequence of occurrence and the likely umbilical cord compression etiology. CD34 immunostaining doubles the sensitivity of placental examination and frequently upgrades the FVM, making it an important adjunct to placental histology.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"289-298"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD8+CD60+T Cells and Disease Progression in Children Livingwith HIV.","authors":"Tamar A Smith-Norowitz, Haram Abdelmajid, Yecheskel S Gold, Stephan Kohlhoff","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>CD60 is a T cell marker expressed on blood lymphocytes. CD8+CD60+ T cells may play a role in inflammatory responses due to human immunodeficiency virus-1 (HIV-1). Our laboratory demonstrated that CD8+CD60+ T cells are higher in HIV positive compared with HIV negative subjects. The present study evaluated numbers of CD8+CD60+ in blood of HIV positive children at various stages of HIV-1 disease. The function of CD8+CD60+ T cells in HIV pathogenesis is unknown.</p><p><strong>Methods: </strong>CD8+CD60+ T cells were measured in blood of HIV positive (N=20) and HIV negative (N=10) children (flow cytometry). Children with HIV were classified into four clinical categories (N, A, B, C) based on symptoms/diagnoses related to HIV infection. Numbers of CD8+CD60+ T cells were compared in HIV positive versus HIV negative children (Wilcoxon signed rank test) and based on clinical categories.</p><p><strong>Results: </strong>CD8+CD60+ T cells were higher in HIV positive compared with HIV negative children (<i>P</i>=<0.0001). CD8+CD60+ T cells in blood of HIV positive children were highest in the C category; these cells were associated with disease progression (<i>P</i>=0.0158).</p><p><strong>Conclusion: </strong>CD8+CD60+ T cells were higher in HIV positive children and may be a marker for disease progression.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"326-330"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Information About The Association of Clinical Scientists.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"425"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanism of SIRT3 Regulating SRV2-Mediated Mitochondrial Fission of Fibroblasts to Inhibit Myocardial Fibrosis after Acute Myocardial Infarction.","authors":"Jia Zhou, Yuanyuan Chen, Qiang Li, Guodong Wang, Gao Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Cardiac dysfunction can result from excessive fibrosis in cardiac fibroblasts (CFs) following an acute myocardial infarction (AMI). SIRT3 has been shown to be associated with numerous cardiovascular diseases. This study aimed to investigate the mechanism by which SIRT3 influences myocardial fibrosis following AMI.</p><p><strong>Methods: </strong>An AMI model was established in rats and echocardiography was used to assess cardiac systolic function. Triphenyl tetrazolium chloride (TTC) and H&E staining were employed to observe the myocardial histopathological status. Masson trichrome staining was used to detect fibrosis, and the changes in expression of fibrosis-related proteins were detected by Western Blot (WB). In this study, we utilized in vitro cell models stimulated by Ang II to investigate the underlying mechanisms. We employed Transwell and CCK-8 assays to detect the function of CFs. Additionally, we used transmission electron microscopy (TEM) to observe the structural morphology of mitochondria, whereas WB was performed to quantify fibrosis-associated proteins and to assay the changes in SIRT3, SRV2, and Drp1.</p><p><strong>Results: </strong>We observed a significant decrease in the expression of SIRT3 and an increase in mitochondrial fragmentation in rats with AMI. Additionally, we observed upregulation of fibrosis-associated signature proteins and collagen proteins expression. Through the use of vitro Ang II stimulation we observed a downregulation of SIRT3 expression, an increase in mitochondrial fragmentation, and an increase in the proliferation and migration of CFs. Opposite effects were observed when SIRT3 was overexpressed. Additive mitochondrial division agonists were found to stimulate the proliferation and migration of CFs, however, SIRT3 expression was unchanged. Interference with SRV2 and SIRT3 revealed that SIRT3 effectively prevented the expression of SRV2/Drp1, resulting in the inhibition of mitochondrial division and the suppression of CFs proliferative migration.</p><p><strong>Conclusion: </strong>In summary, SIRT3 can suppress myocardial fibrosis after acute myocardial infarction by regulating SRV2/Drp1-mediated mitochondrial division.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"335-346"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analytical and Clinical Validation of an Automated Microfluidic Interleukin-6 Immunoassay.","authors":"Jianbo Yang, Mustafa A Barbhuiya, Christopher Hamilton, Kimberly Robyak, Yusheng Zhu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>We validated an automated microfluidic interleukin-6 (IL-6) immunoassay on the Ella platform for clinical use.</p><p><strong>Methods: </strong>The assay was validated for precision, lower limit of quantification, analytical measurement range, accuracy, specificity, interference of biotin, tocilizumab, GP130, IL-6R<i>α</i>, hemolysis, icterus, and lipemia, and establishing the reference value. The clinical performance was evaluated in 96 COVID-19 patients.</p><p><strong>Results: </strong>The within-run and between-run coefficient of variations (CV) ranged 1.8%-4.8%. This assay has an analytical measurement range (AMR) 0.7-2652 pg/ml. There was a moderate correlation between Ella IL-6 assay (y) and a Luminex Quantitative Multiplex Bead Assay in a reference lab (x): y=8.561x-475.38, R=0.5047, SEE=1592.8 pg/mL, N=48). Measurement of IL-6 in plasma samples from 45 healthy adults showed the upper limit of reference of 5.0 pg/mL. 95.83% (95% CI: 89.67%-98.85%) of COVID-19 patients had IL-6 >5.0 pg/mL. This assay is resistant to the interference from hemoglobin up to 1,144 mg/dL, triglyceride 1,699 mg/dL, bilirubin 35 mg/dL, biotin 1000 ng/mL, tocilizumab 240 μg/mL, IL-11 50,000 pg/mL, GP130 50,000 pg/mL, and IL-6R<i>α</i> 1,000 pg/mL.</p><p><strong>Conclusions: </strong>The IL-6 assay on the Ella platform is robust with minimum manual operation. The analytical and clinical performance characteristics meet the clinical needs.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 3","pages":"388-393"},"PeriodicalIF":1.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}