syedzayyan/paper_mill_benchmark huggingface dataset:
Midazolam Suppresses Hepatocellular Carcinoma Cell Metastasis and Enhances Apoptosis by Elevating miR-217

Hepatocellular carcinoma (hcc) is a significant cause of human death in the world.Recently, it is found that midazolam can modulate mi rs to participate in hcc progression.This research project was designed to elucidate the impacts of midazolam and mi r-217 on hcc cell metastasis and apoptosis.Methods.Human hcc cell strains (hep3b and sk-hep-1) were selected and intervened by midazolam at different concentrations in our research.Mi r-217-inhibitor intervened in the two hcc cell strains to observe the alterations of cell migration, invasiveness, and apoptosis.The mi r-217 level in hcc cells was identified by reverse transcription-quantitative polymerase chain reaction (rt-q pcr).Results.As midazolam concentration was elevated, hep3b and sk-hep-1 viabilities were more obviously suppressed.The 10 μg/m l concentration was selected for analysis since hep3b and sk-hep-1 had an ic50 of 10.57 μg/m l and 9.35 μg/m, respectively.The q rt-pcr results showed the decreased of mi r-217 in hcc cells, which was enhanced notably by midazolam intervention.Compared with the blank group, the invasiveness and migration (transwell assay) of mi r-217-inhibitor-transfected hcc cells were distinctly enhanced and the apoptosis rate (flow cytometry) was noticeably reduced.Conclusion.Midazolam can upregulate mi r-217 in hcc cells, thus inhibiting hcc cell metastasis and apoptosis.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
MicroRNA-143-3p/TBX3 Axis Represses Malignant Cell Behaviors in Bladder Cancer

To offer new insight for bladder cancer therapy through researching the micro rna-143-3p/tbx3 axis.Methods.Differentially expressed micro rnas in bladder cancer were provided by databases to find micro rna that may regulate tbx3.Q rt-pcr was utilized to test levels of tbx3 m rna and micro rna-143-3p.Their binding was verified with a dual-luciferase method.Malignant cell behaviors were examined by cell functional experiments.Levels of tbx3 protein and proteins pertinent to epithelial-mesenchymal transition (emt) were tested by western blot.Results.Tbx3 was highly expressed in bladder cancer cells.Micro rna-143-3p presented the most conspicuously negative correlation with tbx3, and they had binding sites.Cell functional experiments proved that tbx3 facilitated bladder cancer cell functions and emt.Micro rna-143-3p was demonstrated to downregulate tbx3 expression.Rescue assay further illuminated that micro rna-143-3p repressed bladder cancer cell functions and emt through downregulating tbx3 expression.Conclusion.These data all indicated that tbx3 was modulated by micro rna-143-3p and acted as a cancer promoter gene in bladder cancer progression via affecting tumor proliferation, migration, invasion, and emt.Therefore, a micro rna-143-3p/tbx3 network might be an underlying target for bladder cancer.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
Mechanism of LncHOTAIR Regulating Proliferation, Apoptosis, and Autophagy of Lymphoma Cells through hsa-miR-6511b-5p/ATG7 Axis

To explore the role of lnc hotair in apoptosis and autophagy in lymphoma.Methods.The interaction between lnc hotair and mi r-6511b-5p, as well as between mi r-6511b-5p and atg7, was verified by a dual luciferase assay.Lnc hotair overexpression lentivirus was transducted and si atg7s were transfected into raji and bjab lymphoma cells, and the efficiency was verified by q pcr.Lymphocyte proliferation was detected by the cell counting kit-8 (cck8) test, and autophagy was detected by transmission electron microscopy.The protein expressions of ulk1, beclin1, atg7, lc3, bax, cleaved-caspase 3, and bcl-2 were detected using western blots.Results.There was a targeting relationship between lnc hotair and mi r-6511b-5p and between mi r-6511b-5p and atg7.Lnc hotair overexpression promoted the proliferation and autophagy of raji and bjab cells, significantly upregulated atg7, beclin1, ulk1, bcl-2, and lc3-ii/lc3-i levels, and downregulated bax and cleaved-caspase3 levels.Si atg7 significantly inhibited the proliferation and autophagy of raji and bjab cells and promoted their apoptosis.Conclusion.Lnc hotair/hsa-mi r-6511b-5p/atg7 could regulate the proliferation, apoptosis, and autophagy of raji and bjab lymphoma cells.

Journal: Evidence-Based Complementary and Alternative Medicine (2022)
Publication types: Research Article;
Meta-Analysis of the Efficacy and Safety of Olanzapine versus Clozapine when Treating Senile Dementia

To systematically assess the safety and efficacy of olanzapine versus clozapine when treating senile dementia and to provide evidence-based medicine basis for its promotion and use.Methods.Pub med, embase, science direct, cochrane library, china knowledge network database (cnki), china vip database, wanfang database, and china biomedical literature database (cbm) online database were searched for randomized controlled trials (rct) of olanzapine and clozapine when treating senile dementia.The retrieval time limit is from the establishment of the database to the present.The data were extracted independently by two researchers, and the bias risk of each contained literature was analyzed in accordance with the standard of cochrane handbook 5.3.Rev man 5.4 statistical software was used to analyze the collected data by meta-analysis.Results.Finally, 6 randomized controlled trial articles were included, with a total of 490 samples.Meta-analysis of clinical efficacy showed that the clinical efficacy was similar and there was no significant difference ( p &gt; 0.05 ).Two articles used alzheimer’s disease pathological behavior rating scale (behave-ad) to compare the pathological behavior of different stages after treatment.Statistical analysis showed that there was no significant difference between the total score of behave-ad and the scores of each factor in each week after treatment.The non-treatment adverse reaction scale (tess) of the study group and the control group was analyzed by meta-analysis.The tess score of the study group after treatment was significantly lower than that of the control group.The bprs scores of different stages after treatment were analyzed by meta-analysis, and there was no significant difference in the total score and factor scores of bprs in each week after treatment.Two clinical trials reported the incidence of neurological symptoms after treatment.Olanzapine and clozapine treatment can effectively reduce the risk of aging.There was no significant difference in the incidence of neurological symptoms in patients with dementia ( p &gt; 0.05 ).According to the analysis of meat products, the incidence of adverse reactions in the study group was significantly lower than that in the control group ( p &lt; 0.05 ).Conclusion.Olanzapine and clozapine have similar efficacy when treating mental and behavioral disorders in patients with senile dementia, in which olanzapine is more effective in improving the symptoms of patients with alzheimer’s disease (ad), with less adverse reactions and high safety, which is worth popularizing in clinical practice.However, more studies and follow-up with higher methodological quality and longer intervention time are needed to further verify.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Meta-Analysis;
Meta-Analysis of Contrast Enhanced Ultrasound in Judging Benign and Malignant Thyroid Tumors

In recent years, the incidence of thyroid cancer (tc) patients has gradually increased, and it ranks first among all endocrine tumors.Tc has no obvious characteristics at the initial stage of onset.Thyroid tumors (tt) have formed when they are discovered, and they are easy to see when they are diagnosed.The disease is confused, so it is necessary to rely on imaging methods for tumor diagnosis.Contrast-enhanced ultrasound (ceus), as the most commonly used imaging method in current clinical testing, is simple, safe, highly sensitive, can accurately display tumor conditions, and has high clinical value in the judgment of tc tumors.This article uses meta-analysis to select 63 published studies on ceus to determine benign and malignant (bam) tt to analyze and explore its clinical application value.This article understands the analysis of bam tt and its diagnostic methods, clarifies the diagnostic efficiency of ceus for tt, imaging methods, and imaging characteristics, and uses statistical analysis to analyze its heterogeneity.In this paper, the meta-analysis of ceus in judging bam tt is mainly based on references.The sensitivity, specificity, and difference of ceus in diagnosing bam tt are analyzed.Real-time elastography (rte) is the comparison experiment object, and ceus is used to compare the diagnostic efficiency, pathological results, and diagnostic efficiency of thyroid nodules in ceus mode.The results of the study show that the nodule with higher diagnostic sensitivity is the echo feature, with a sensitivity of 97.73%, followed by the halo feature, with a sensitivity of 86.36%.In terms of diagnostic specificity, the boundary feature is the most specific.The specificity is 89.47%.In the judgment of bam tumor nodules, the most obvious difference is the echo feature, which is as high as 14.09, followed by the acoustic halo feature, and the difference is 10.65.

Journal: Computational and Mathematical Methods in Medicine (2021)
Publication types: Meta-Analysis;
Luteolin Inhibited the Self-Renewal and Altered the Polarization of Primary Alveolar Macrophages

Pure plant extract luteolin has been demonstrated to possess numerous biological and immunological effects.However, how luteolin affects mice alveolar macrophages’ self‐renewal and polarization closely related to inflammatory and immunomodulatory is still unknown.In our study, the transcriptomic analysis showed that several self‐renewal‐related pathways in luteolin‐pretreated alveolar macrophages were inhibited compared to the granulocyte‐macrophage colony‐stimulating factor (gm‐csf)‐treated group.Ki‐67 staining and ed u assay indicated that luteolin inhibited gm‐csf‐induced alveolar macrophage proliferation.Moreover, gm‐csf‐induced expressions of c‐myc and klf4 were significantly suppressed by luteolin at transcriptional and protein levels.Besides, we found that luteolin promoted m1 macrophage polarization induced by lps plus ifn‐ γ .At the same time, it inhibited m2 macrophage polarization induced by il‐4 in both alveolar and bone marrow‐derived macrophages by detecting macrophage polarization‐related gene expressions at m rna and protein levels.We found that luteolin inhibited self‐renewal and altered the polarization of primary alveolar macrophages.Taken together, our data will aid in a better understanding of the immunomodulatory effects of luteolin on the primary alveolar macrophages.

Journal: Contrast Media & Molecular Imaging (2022)
Publication types: Research Article;
Long Noncoding RNA LINC00857 Promotes Proliferation, Migration, and Invasion of Colorectal Cancer Cell through miR-1306/Vimentin Axis

Colorectal cancer is a commonly diagnosed cancer and the leading cause of cancer-related death which still increasing in many countries.The lack of biomarkers for early detection and clinic treatment results in high morbidity and mortality.The novel role of long noncoding rna linc00857 on cell proliferation migration and invasion was explored in this article.The expression level of linc00857 in colorectal cancer tissue samples and cells was determined notably higher than normal tissue samples and cells.Silence linc00857 can significantly inhibit colorectal cancer cell viability and metastasis in vitro.Moreover, linc00857 depletion caused cell accumulation in the g0/g1 phase.In addition, we recognized the novel linc00857–mi r-1306–vimentin axis and demonstrated it by dual-luciferase reporter assay.And this signaling axis could be considered as the target for colorectal cancer treatment.In conclusion, linc00857 can promote colorectal cancer progress by sponging mi r-1306 and upregulate vimentin to accelerate the epithelial-mesenchymal transition process.

Journal: Computational and Mathematical Methods in Medicine (2021)
Publication types: Research Article;
lncRNA NUTM2A-AS1 Targets the SRSF1/Trim37 Signaling Pathway to Promote the Proliferation and Invasion of Breast Cancer

Object.Proliferation and invasion are typical characteristics of breast cancer (bc) cells.Long noncoding rna nutm2a-as1 has been shown to be dysregulated in tumors.This research was to explore the effect of nutm2a-as1 on the proliferation and invasion of bc cell lines.Method.Using the tumor database (tcga) and analysis platform (gepia), nutm2a-as1 expression in breast cancer cases was compared with the normal cases.In addition, kaplan-meier curve of overall survival according to the various levels of nutm2a-as1 was assessed.Then, we constructed a knockdown plasmid of nutm2a-as1 and successfully reduced the expression function of nutm2a-as1 in bc cells.Results.We found nutm2a-as1 could promote the malignant phenotype of proliferation and invasion of bc.In terms of mechanism research, nutm2a-as1 was mainly located in the cytoplasm of bc cells, which indicated that nutm2a-as1 may achieve its function through transcriptional or posttranscriptional regulation pathways.While knocking down nutm2a-as1, we detected several major molecules of the trim family.The results showed that only trim37 m rna was significantly affected, and protein detection also showed that knockdown nutm2a-as1 expression could reduce the expression of trim37.The results of rip experiments suggested that nutm2a-as1 played a key role by combining with srsf1 and affecting the interaction between srsf1 and trim37 m rna.The stability test of m rna also confirmed that during the knockdown of nutm2a-as1, the m rna stability of trim37 decreased significantly, but this downward trend could be reversed by overexpressed srsf1.The above results suggested that nutm2a-as1 could maintain the stability and expression of trim37 through srsf1 pathway.The results of rescue experiment showed the overexpression of trim37, while knocking down nutm2a-as1 could reverse the decrease of proliferation and invasiveness of bc cells induced by nutm2a-as1 knockdown.Conclusion.Therefore, trim37 is seen as a necessary target for nutm2a-as1 to exert the biological function of bc.Additionally, nutm2a-as1 is to regulate the malignant phenotype of bc through nutm2a-as1/trim37 pathway.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-iκ/iB Pathway

To explore the effect of long noncoding rna h19 (lnc rna h19) on brain injury in rats following experimental intracerebral hemorrhage (ich).Methods.Rat ich model was established with type iv collagenase.The neurological function scores were evaluated, and the water content in brain tissue was measured.The nerve injury indexes, inflammatory factors, and oxidative stress indexes were also measured.Moreover, the expression of lnc rna h19 was determined by q rt-pcr, and western blot detected nf-κb pathway-related protein expression.Results.Compared with the sham group, the neurological function scores, the water content in brain tissue, and levels of injury indicators myelin basic protein (mbp), s-100b, and neuron-specific enolase (nse) in the ich rats were significantly increased.Meanwhile, the levels of tnf-α, il-6, il-1β, ros, and mda were significantly increased, but the levels of sod were significantly decreased.In addition, the expression of lnc rna h19 in the brain tissue in the ich group was significantly higher than that in the sham group.After further interference with lnc rna h19 expression (sh-h19 group), the levels of all the above indicators were reversed and the neurological damage was improved.Western blot results showed that the expression of nf-κbp65 and ikkβ was significantly higher, and iκbα expression was lower in the perivascular hematoma tissue in the ich group compared with the sham group.Compared with the sh-nc group, nf-κbp65 and ikkβ expression were significantly lower and iκbα was significantly higher in the sh-h19 group.Conclusion.Lnc rna h19 exacerbated brain injury in rats with ich by promoting neurological impairment, brain edema, and releasing inflammatory responses and oxidative stress.This may be related to the activation of nf-κb signaling pathway.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
LncRNA GAS5 Interacts with MicroRNA-10b to Inhibit Cell Proliferation and Migration and Induces Apoptosis in Colorectal Cancer

The purpose of this study was to study the effects of the gas5/micro rna-10b (mi r-10b) axis on proliferation, migration, and apoptosis of colorectal cancer (crc).Methods.The expression levels of gas5 and mi r-10b in crc tissues and cells were detected by quantitative real-time polymerase chain reaction (q rt-pcr).Wound healing experiment was used to detect the effects of gas5 and mi r-10b on the migration of crc cells.The luciferase reporter gene experiment was used to verify mi rna targets.Immunohistochemical assay was used to detect the expression of proteins related to metastasis and apoptosis in tumor tissues.Results.The expression of gas5 was downregulated in crc tissues and cell lines.The overexpression of gas5 can inhibit cell proliferation and progression, induce apoptosis in vitro, and inhibit the growth of crc tumor in vivo.In contrast, the expression of mi r-10b, a downstream target of gas5, was increased in crc tissues and cells.Suppression of the mi r-10b gene can inhibit proliferation and metastasis and cause apoptosis of crc cells.In addition, luciferase reports show that gas5 inhibits the progression of crc cells by binding to mi r-10b.Rescue experiments showed that overexpressed mi r-10b could reverse gas5-mediated antitumor effect on crc cells in vivo and in vitro.Conclusions.Lnc rna gas5 interacts with mi r-10b to inhibit cell proliferation and migration and induces apoptosis in colorectal cancer.Gas5 and mi r-10b could become potential therapeutic targets for crc.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma

Long noncoding rnas (lnc rnas) stand as indispensable regulators of initiation and development in melanoma (melanoma).However, the action molecular mechanisms linked to melanoma remain unclear.In the current study, the findings revealed that agap2-as1 was considerably greater in melanoma than in healthy tissues and that the level of agap2-as1 in cancer tissue was significantly linked to the cancerous tnm stage of patients.Individuals with high agap2-as1 had a considerably shorter survival duration than patients with low agap2-as1, regardless of progression-free survival or overall survival.Functionally, downregulating the expression of agap2-as1 can inhibit the growth of melanocytes.Compared with the control group, agap2-as1 knockdown increased erastin-mediated iron death in melanoma cells.However, iron death inhibitor fersint-1 restored this effect, while erastin induced melanoma cell death.Besides, intracellular iron and fe2+ levels increased after agap2-as1 knockdown in melanoma cells treated with erastin compared with the si-nc group.In addition, agap2-as1 silencing resulted in a significant decrease in glutathione (gsh) content in erastin-treated melanoma cells.The mechanistic results suggest agap2-as1 increases slc7a11 m rna stability through the igf2bp2 pathway.In this investigation, we discovered new activities for agap2-as1 and firstly discovered its mechanistic basis in ferroptosis and melanoma formation that might help in the search for potential therapy options in melanoma.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression

Oral squamous cell carcinoma (oscc) has increasingly become a worldwide health concern, and its survival rate has not been much improved partially due to a deficiency of precise molecular markers.Dysregulation of linc01116, a long noncoding rna sequence, has been observed in several types of cancer.However, the role played by linc01116 in oscc has not yet been fully elaborated.This study explored how linc01116 was involved in the regulation of oscc progression by analyzing expressions of linc01116 in oscc patients.The findings demonstrated upregulation of linc01116 in oscc tissues as opposed to regular oral mucosa, and overexpression of linc01116 was correlated with advanced tumor status.Linc01116 knockdown using sh rna markedly reduced the oscc cell invasion and migration in vitro.Moreover, the expression of linc01116 was negatively correlated with that of micro rna-9-5p (mi r-9).Luciferase reporter and loss-of-function assays demonstrated that linc01116 functioned as a competing endogenous rna (ce rna) that could effectively sponge mi r-9, thus regulating the derepression of matrix metalloproteinase 1 (mmp1).Furthermore, we confirmed that linc01116 knockdown did not affect the expression of mmp1 messenger rna (m rna).Collectively, it is demonstrated in this study that overexpression of linc01116 can promote the oscc progression.The linc01116–mi r-9-mmp1 axis provides a novel insight into the oscc pathogenesis and offers potential therapeutic targets against oscc.

Journal: Computational and Mathematical Methods in Medicine (2022)
Publication types: Research Article;
LAG3 and PD1 Regulate CD8+ T Cell in Diffuse Large B-cell Lymphoma Patients

Diffuse large b-cell lymphoma (dlbcl) is a clinically and genetically heterogeneous lymphoid malignancy.The unsatisfactory outcome for refractory patients has prompted efforts to explore new therapeutic approaches for dlbcl.However, the mechanisms involved in treatment associated with immune checkpoints remain unclear.This study is aimed at investigating the potential roles of programmed cell death protein 1 (pd1) and lymphocyte activation gene 3 (lag3) in cd8+ t cells for treatment in dlbcl.Methods.Utilizing flow cytometry, we examined the content of t cells, the levels of cytokines, and the expression of pd1 and lag3 in patients with dlbcl as well as in healthy controls.Levels of cytokines in cd8+ t cells from dlbcl patients before and after treatment were compared by blocking of pd1 and lag3 in magnetic bead-sorted cd8+ t cells.Results.We found that the proportion of cd4+ t cells and cd8+ t cells was increased in dlbcl patients after treatment.The levels of cytokines trended toward those of healthy controls in treatment.Pd1 (+), lag3 (+), or pd1 (+) lag3 (+) were all expressed in lower amounts in cd4+ t cells and cd8+ t cells after treatment than in untreated dlbcl patients.In addition, blockade of pd1 and lag3 in sorted cd8+ t cells markedly inhibited cytokine production in response to treatment.Conclusion.Pd1 and lag3 in cd8+ t cells may be important targets of therapy and play therapeutic role in patients with dlbcl.

Journal: Computational and Mathematical Methods in Medicine (2021)
Publication types: Research Article;