Effects of preoperative inhaled budesonide combined with intravenous dexamethasone on postoperative sore throat in patients who underwent thyroidectomy: A randomized controlled trial.

BACKGROUND: This randomized controlled trial aimed to evaluate the efficacy of preoperative inhaled budesonide combined with intravenous dexamethasone on postoperative sore throat (POST) after general anesthesia in patients who underwent thyroidectomy. METHODS: Patients who underwent elective thyroidectomy were randomly divided into the intravenous dexamethasone group (group A) and budesonide inhalation combined with intravenous dexamethasone group (group B). All patients underwent general anesthesia. The incidence and severity of POST, hoarseness, and cough at 1, 6, 12, and 24 hours after surgery were evaluated and compared between the 2 groups. RESULTS: There were 48 and 49 patients in groups A and B, respectively. The incidence of POST was significantly lower at 6, 12, and 24 hours in group B than that in group A (P < .05). In addition, group B had a significantly lower incidence of coughing at 24 hours (P = .047). Compared with group A, the severity of POST was significantly lower at 6 (P = .027), 12 (P = .004), and 24 (P = .005) hours at rest, and at 6 (P = .002), 12 (P = .038), and 24 (P = .015) hours during swallowing in group B. The incidence and severity of hoarseness were comparable at each time-point between the 2 groups (P > .05). CONCLUSION: Preoperative inhaled budesonide combined with intravenous dexamethasone reduced the incidence and severity of POST at 6, 12, and 24 hours after extubation compared with intravenous dexamethasone alone in patients who underwent thyroidectomy. Additionally, this combination decreased the incidence of postoperative coughing at 24 hours.

Consolidation therapy with autologous stem cell transplantation after remission of induction chemotherapy prolongs the survival of patients with peripheral T-cell lymphoma.

Background: There was little evidence of autologous stem cell transplantation (ASCT) as consolidation therapy after remission of induction for patients with Peripheral T-cell lymphoma (PTCL). In this study, we conducted a comparative analysis of real-world survival outcomes between consolidation therapy and observation in patients with PTCL. Methods: A total of 92 patients with peripheral T-cell lymphoma (PTCL) who were admitted to the Department of Hematology, Huadong Hospital Affiliated with Fudan University from January 2013 to April 2019 were divided into two groups based on whether they were treated with high-dose therapy (HDT) followed by autologous hematopoietic stem cell transplantation (ASCT): ASCT as consolidation therapy (n=30) and observation (n=62). Clinical characteristics, treatment patterns, and survival outcomes were analyzed between the two groups. Univariate and Cox multivariate regression analyses were also performed to detect prognostic factors of survival. Results: With a median follow-up time of 41 months, the median overall survival (OS) of peripheral T-cell lymphoma patients treated with ASCT was not reached; the median progression-free survival (PFS) was 77.0 months, which was much higher than that of patients without ASCT (p<0.003 for OS, p=0.015 for PFS). Subgroup analysis found that patients with high risks benefited more from ASCT. Combination with hemophagocytic lymphohistiocytosis (HLH) (p<0.001), clinical stage more than III (p=0.014), IPI score above 3 (p=0.049), and bone marrow involvement (p=0.010) were the independent prognostic factors significantly associated with worse OS and PFS. Additionally, pegylated liposomal doxorubicin (PLD)-containing chemotherapy regimen could bring a higher overall response rate (ORR) and prolong the survival of patients with PTCL who underwent ASCT. Conclusion: ASCT may improve the long-term survival of patients with PTCL as consolidation therapy after achieving complete or partial remission of induction treatment, particularly for those with high risks. The chemotherapy regimen containing pegylated liposomal doxorubicin may induce deeper remission than traditional doxorubicin in PTCL. It is crucial to identify the specific groups most likely to benefit from upfront ASCT.

Machine learning-driven prognostic analysis of cuproptosis and disulfidptosis-related lncRNAs in clear cell renal cell carcinoma: a step towards precision oncology.

Cuproptosis and disulfidptosis, recently discovered mechanisms of cell death, have demonstrated that differential expression of key genes and long non-coding RNAs (lncRNAs) profoundly influences tumor development and affects their drug sensitivity. Clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer, presently lacks research utilizing cuproptosis and disulfidptosis-related lncRNAs (CDRLRs) as prognostic markers. In this study, we analyzed RNA-seq data, clinical information, and mutation data from The Cancer Genome Atlas (TCGA) on ccRCC and cross-referenced it with known cuproptosis and disulfidptosis-related genes (CDRGs). Using the LASSO machine learning algorithm, we identified four CDRLRs-ACVR2B-AS1, AC095055.1, AL161782.1, and MANEA-DT-that are strongly associated with prognosis and used them to construct a prognostic risk model. To verify the model's reliability and validate these four CDRLRs as significant prognostic factors, we performed dataset grouping validation, followed by RT-qPCR and external database validation for differential expression and prognosis of CDRLRs in ccRCC. Gene function and pathway analysis were conducted using Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) for high- and low-risk groups. Additionally, we have analyzed the tumor mutation burden (TMB) and the immune microenvironment (TME), employing the oncoPredict and Immunophenoscore (IPS) algorithms to assess the sensitivity of diverse risk categories to targeted therapeutics and immunosuppressants. Our predominant objective is to refine prognostic predictions for patients with ccRCC and inform treatment decisions by conducting an exhaustive study on cuproptosis and disulfidptosis.

The TGFß2-Snail1-miRNATGFß2 Circuitry is Critical for the Development of Aggressive Functions in Breast Cancer.

There have been contradictory reports on the biological role of transforming growth factor-ßs (TGFßs) in breast cancer (BC), especially with regard to their ability to promote epithelial-mesenchymal transition (EMT). Here, we show that TGFß2 is preferentially expressed in mesenchymal-like BCs and maintains the EMT phenotype, correlating with cancer stem cell-like characteristics, growth, metastasis and chemo-resistance and predicting worse clinical outcomes. However, this is only true in ERα- BC. In ERα+ luminal-type BC, estrogen receptor interacts with p-Smads to block TGFß signalling. Furthermore, we also identify a microRNAs (miRNAs) signature (miRNAsTGFß2 ) that is weakened in TGFß2-overexpressing BC cells. We discover that TGFß2-Snail1 recruits enhancer of zeste homolog-2 to convert miRNAsTGFß2 promoters from an active to repressive chromatin configuration and then repress miRNAsTGFß2 transcription, forming a negative feedback loop. On the other hand, miRNAsTGFß2 overexpression reverses the mesenchymal-like traits in agreement with the inhibition of TGFß2-Snail1 signalling in BC cells. These findings clarify the roles of TGFß2 in BC and suggest novel therapeutic strategies based on the TGFß2-Snail1-miRNAsTGFß2 loop for a subset type of human BCs.

Exosomes-mediated drug delivery for the treatment of myocardial injury.

Cardiovascular disease has become a major cause of death worldwide. Myocardial injury (MI) caused by myocardial infarction, myocarditis, and drug overdose can lead to impaired cardiac function, culminating in serious consequences such as angina pectoris, arrhythmias, and heart failure. Exosomes exhibit high biocompatibility and target specificity, rendering them an important non-cellular therapy for improving MI. Exosomes are diminutive vesicles that encapsulate nucleic acids and proteins. Exosomes derived from cardiac stem cells themselves have therapeutic effects, and they can also serve as carriers to deliver therapeutic drugs to recipient cells, thereby exerting a therapeutic effect. The molecules within exosomes are encapsulated in a lipid bilayer, allowing them to stably exist in body fluids without being affected by nucleases. Therefore, the utilization of exosomes as drug delivery systems (DDS) for disease treatment has been extensively investigated and is currently undergoing clinical trials. This review summarizes the therapeutic effects of exosomes on MI and provides an overview of current research progress on their use as DDS in MI.

FOXD1 expression-based prognostic model for uveal melanoma.

FOXD1, a new member of the FOX transcription factor family, serves as a mediator and biomarker for cell reprogramming. But its contribution to prognosis of uveal melanoma (UVM) is unclear. This study demonstrated that FOXD1 might promote tumor growth and invasion, because FOXD1 expression was negatively correlated with overall survival, progression-free survival, and disease-specific survival in UVM patients. This conjecture was verified in cell culture with human uveal melanoma cell line (MUM2B) as model cells. Additionally, the biological mechanisms of FOXD1 based on FOXD1-related genomic spectrum, molecular pathways, tumor microenvironment, and drug treatment sensitivity were examined using The Cancer Genome Atlas (TCGA) database, aiming to reasonably explain why FOXD1 leads to poor prognosis of UVM. On these bases, a novel tumor prognostic model was established using the FOXD1-related immunomodulators TMEM173, TNFRSF4, TNFSF13, and ULBP1, which will enable the stratification of disease seriousness and clinical treatment for patients.

Erratum: CD151 promotes Colorectal Cancer progression by a crosstalk involving CEACAM6, LGR5 and Wnt signaling via TGFß1: Erratum.

[This corrects the article DOI: 10.7150/ijbs.53657.].

Secukinumab plays a synergistic role with starvation therapy in promoting autophagic cell death of hepatocellular carcinoma via inhibiting IL-17A-increased BCL2 level.

It is known that IL-17A inhibits autophagy of hepatocellular carcinoma (HCC) cells, thus contributing to the carcinogenesis of HCC. Starvation therapy can promote the autophagic death of HCC cells by blocking the nutrition supply. The purpose of this study was to explore whether the pharmacological antagonist of IL-17A, secukinumab, and starvation therapy have a synergistic effect on the autophagic cell death of HCC. Here, it could be observed that compared with serum-free condition, the combination of secukinumab and serum-free status better promoted autophagy (observed by LC3 conversion rate, p62 protein expression and the formation of autophagosomes), and more significantly inhibited the survival and function (observed by Trypan blue staining, CCK-8, Transwell, and scratch assays) in HCC HepG2 cells. Moreover, secukinumab significantly decreased BCL2 protein expression under serum-normal and serum-free conditions. However, both the addition of recombinant IL-17A and overexpression of BCL2 blocked the regulation of secukinumab on the survival and autophagy in HepG2 cells. Nude mice experiments demonstrated that compared to the lenvatinib-alone group, the combination group of lenvatinib and secukinumab better inhibited the in vivo tumorigenesis of HepG2 cells and enhanced autophagy in xenotumor tissues. Furthermore, secukinumab significantly decreased BCL2 protein expression in xenotumor tissues without or with lenvatinib application. In conclusion, the antagonism of IL-17A with secukinumab, due to the upregulation on BCL2-related autophagic cell death, can cooperate with starvation therapy in inhibiting HCC carcinogenesis. Our data suggested that secukinumab can become an effective adjuvant for the treatment of HCC.

Exploration of s new biomarker in osteosarcoma and association with clinical outcomes: TOP2A+ cancer associated fibroblasts.

BACKGROUND: Osteosarcoma (OS) is the leading malignant primary bone tumor in young adults and children and has a high mortality rate. Cancer-associated fibroblasts (CAFs) are major components of the tumor microenvironment, influencing cancer progression and metastasis. However, there is no systematic study on the role of CAF in OS. METHODS: We collected six OS patients' single-cell RNA sequencing data from the TISCH database, which was processed using the Seurat package. We selected gene sets from the well-known MSigDB database and resorted to the clusterprofiler package for gene set enrichment analysis (GSEA). The least absolute shrinkage and selection operator (LASSO) regression model was used for identification of the variables. Receiver operating characteristic and decision curve analyses were utilized for determining the efficacy of the monogram model. RESULTS: TOP2A+ CAFs was recognized as the carcinogenic CAFs subset, given its intense interaction with OS malignant cells and association with the critical cancer driver pathway. We intersected the differentially expressed genes of TOP2A+ CAFs with the prognostic genes selected from 88 OS samples. The acquired gene set was selected using the LASSO regression model and integrated with clinical factors to obtain a monogram model of high prognosis predicting power (area under the curve of 5 year survival at 0.883). Functional enrichment analysis revealed the detailed difference between two risk groups. CONCLUSION: We identified TOP2A+ CAFs as a subset of oncogenic CAFs in OS. Based on differentially expressed genes derived from TOP2A+ CAFs, combined with bulk transcriptome prognostic genes, we constructed a risk model that can efficiently predict OS prognosis. Collectively, our study may provide new insights for future studies to elucidate the role of CAF in OS.

BDNF promotes mouse follicular development and reverses ovarian aging by promoting cell proliferation.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) plays an important role in ovarian function including follicle development and oocyte maturation, and embryonic development. However, whether BDNF treatment can reimpose ovarian aging and impaired fertility remains elusive. In this study, we investigated the reproductive outcomes of BDNF treatment and potential mechanisms in aged mice. METHOD: "Aged" mice (35-37 weeks old, n = 68) were treated with recombinant human BDNF protein (rhBDNF, 1 µg/200 µL) through daily intraperitoneal (IP) injection for 10 days with/without ovulation induction. Reproductive age mice (8-10 weeks old, n = 28) were treated with ANA 12 (a selective BDNF receptor, TrkB antagonist) through daily IP injection for 5 days with/without ovulation induction. Ovarian function was assessed by ovarian weight, number of follicles, and sex hormone productions. Following induction of ovulation, the number of total oocytes or abnormal oocytes, and blastocyst formation were assessed. Reproductive functions of the mice were evaluated, including pregnancy rate, mating duration for conception, implantation sites, litter size, and weight of offspring. Finally, the molecular mechanism of the effects of BDNF on ovarian cell functions in mice were examined by Western blot and immunofluorescence. RESULTS: rhBDNF treatment increased the ovarian weight, number of follicles, number and quality of oocytes including increased blastocysts formation, blood estrogen levels, and pregnancy rate in 35-37-week-old mice. Conversely, BDNF receptor antagonist, ANA 12, treatment decreased the ovarian volume and number of antral follicles and increased the proportion of abnormal oocytes in 8-10-week-old mice. We further demonstrated that BDNF treatment promoted ovarian cell proliferation as well as activation of TrkB and cyclinD1-creb signalling. CONCLUSION: We demonstrated that ten consecutive days of daily IP injection of rhBDNF rescued ovarian function in aged mice. Our results further indicate that TrkB and cyclin D1-creb signaling may underlie the BDNF function in ovaries. Targeting BDNF-TrkB signaling is a potential novel therapeutic strategy to reverse ovarian aging.

Maintenance regimen of GM-CSF with rituximab and lenalidomide improves survival in high-risk B-cell lymphoma by modulating natural killer cells.

BACKGROUND: The treatment of high-risk B-cell lymphoma (BCL) remains a challenge, especially in the elderly. METHODS: A total of 83 patients (median age 65 years), who have achieved a complete response after induction therapy, were divided into two groups: R2 + GM-CSF regimen (lenalidomide, rituximab, granulocyte-macrophage colony-stimulating factor [GM-CSF]) as maintenance therapy (n = 39) and observation (n = 44). The efficacy of the R2 + GM-CSF regimen as maintenance in patient with high-risk BCL was analyzed and compared with observation. RESULTS: The number of natural killer cells in patients increased after R2 + GM-CSF regimen administration (0.131 × 109 /L vs. 0.061 × 109 /L, p = 0.0244). Patients receiving the R2 + GM-CSF regimen as maintenance therapy had longer remission (duration of response: 18.9 vs. 11.3 months, p = 0.001), and longer progression-free survival (not reached (NR) vs. 31.7 months, p = 0.037), and overall survival (OS) (NR vs. NR, p = 0.015). The R2 + GM-CSF regimen was safe and well tolerated. High international prognostic index score (p = 0.012), and high tumor burden (p = 0.005) appeared to be independent prognostic factors for worse PFS. CONCLUSIONS: The maintenance therapy of R2 + GM-CSF regimen may improve survival in high-risk BCL patients, which might be modulated by amplification of natural killer cells. The efficacy of the R2 + GM-CSF maintenance regimen has to be further validated in prospective random clinical trials.

The Role of a Deep Learning-Based Computer-Aided Diagnosis System and Elastography in Reducing Unnecessary Breast Lesion Biopsies.

OBJECTIVES: Ultrasound examination has inter-observer and intra-observer variability and a high false-positive rate. The aim of this study was to evaluate the value of the combined use of a deep learning-based computer-aided diagnosis (CAD) system and ultrasound elastography with conventional ultrasound (US) in increasing specificity and reducing unnecessary breast lesions biopsies. MATERIALS AND METHODS: Conventional US, CAD system, and strain elastography (SE) were retrospectively performed on 216 breast lesions before biopsy or surgery. The area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and biopsy rate were compared between conventional US and the combination of conventional US, SE, and CAD system. RESULTS: Of 216 lesions, 54 were malignant and 162 were benign. The addition of CAD system and SE to conventional US increased the AUC from 0.716 to 0.910 and specificity from 46.9% to 85.8% without a loss in sensitivity while 89.2% (66 of 74) of benign lesions in Breast Imaging Reporting and Data System (BI-RADS) category 4A lesions would avoid unnecessary biopsies. CONCLUSION: The addition of CAD system and SE to conventional US improved specificity and AUC without loss of sensitivity, and reduced unnecessary biopsies.

GSDMD deficiency ameliorates hyperoxia-induced BPD and ROP in neonatal mice.

Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are among the most common morbidities affecting extremely premature infants who receive oxygen therapy. Many clinical studies indicate that BPD is associated with advanced ROP. However, the mechanistic link between hyperoxia, BPD, and ROP remains to be explored. Gasdermin D (GSDMD) is a key executor of inflammasome-induced pyroptosis and inflammation. Inhibition of GSDMD has been shown to attenuate hyperoxia-induced BPD and brain injury in neonatal mice. The objective of this study was to further define the mechanistic roles of GSDMD in the pathogenesis of hyperoxia-induced BPD and ROP in mouse models. Here we show that global GSDMD knockout (GSDMD-KO) protects against hyperoxia-induced BPD by reducing macrophage infiltration, improving alveolarization and vascular development, and decreasing cell death. In addition, GSDMD deficiency prevented hyperoxia-induced ROP by reducing vasoobliteration and neovascularization, improving thinning of multiple retinal tissue layers, and decreasing microglial activation. RNA sequencing analyses of lungs and retinas showed that similar genes, including those from inflammatory, cell death, tissue remodeling, and tissue and vascular developmental signaling pathways, were induced by hyperoxia and impacted by GSDMD-KO in both models. These data highlight the importance of GSDMD in the pathogenesis of BPD and ROP and suggest that targeting GSDMD may be beneficial in preventing and treating BPD and ROP in premature infants.

Protective role of PERK-eIF2α-ATF4 pathway in chronic renal failure induced injury of rat hippocampal neurons.

PURPOSE: Chronic renal failure (CRF) is associated with impairment of hippocampal neurons. This study investigated the effect of PERK-eIF2α-ATF4 pathway in CRF. METHODS: Rat CRF model was established and rat hippocampal neurons were separated. Xanthine Oxidase method, fluorescence spectrophotometry and flow cytometry were applied to detect superoxide dismutase (SOD) content, reactive oxygen species (ROS) level and apoptosis in hippocampal neurons, respectively. The levels of phosphorylated (p)-PERK, phosphorylated (p)-eIF2α, CHOP, Bax, C-Caspase-3 and Bcl-2 in rats were measured using Western blot. Then, the neurotoxicity of serum from CRF rats was assessed in rat hippocampal neurons after treatment with rat CRF serum and transfection with or without PERK overexpression or knockdown plasmid. RESULTS: SOD activity was reduced, while ROS level and apoptosis rate were increased in hippocampal tissues of CRF rats. PERK-eIF2α-ATF4 and apoptosis pathways were activated in CRF rats. Cells treated with serum from CRF rats showed increases in apoptosis rate and LDH and ROS levels, and decreases in cell viability and SOD activity. However, overexpressed PERK could reverse the cytotoxic effect of serum from CRF rats. PERK overexpression could enhance the activation of PERK-eIF2α-ATF4 pathway in hippocampal neurons induced by serum from CRF rats. Furthermore, PERK overexpression could alleviate the increases in CHOP, Bax, C-Caspase-3 expressions and the reduction of Bcl-2 expression in hippocampal neurons induced by serum from CRF rats. CONCLUSION: PERK-eIF2α-ATF4 pathway induced by increased endoplasmic reticulum stress may alleviate CRF-induced hippocampal neuronal damage.

c-Myc Drives inflammation of the maternal-fetal interface, and neonatal lung remodeling induced by intra-amniotic inflammation.

Background: Intra-amniotic inflammation (IAI) is associated with increased risk of preterm birth and bronchopulmonary dysplasia (BPD), but the mechanisms by which IAI leads to preterm birth and BPD are poorly understood, and there are no effective therapies for preterm birth and BPD. The transcription factor c-Myc regulates various biological processes like cell growth, apoptosis, and inflammation. We hypothesized that c-Myc modulates inflammation at the maternal-fetal interface, and neonatal lung remodeling. The objectives of our study were 1) to determine the kinetics of c-Myc in the placenta, fetal membranes and neonatal lungs exposed to IAI, and 2) to determine the role of c-Myc in modulating inflammation at the maternal-fetal interface, and neonatal lung remodeling induced by IAI. Methods: Pregnant Sprague-Dawley rats were randomized into three groups: 1) Intra-amniotic saline injections only (control), 2) Intra-amniotic lipopolysaccharide (LPS) injections only, and 3) Intra-amniotic LPS injections with c-Myc inhibitor 10058-F4. c-Myc expression, markers of inflammation, angiogenesis, immunohistochemistry, and transcriptomic analyses were performed on placenta and fetal membranes, and neonatal lungs to determine kinetics of c-Myc expression in response to IAI, and effects of prenatal systemic c-Myc inhibition on lung remodeling at postnatal day 14. Results: c-Myc was upregulated in the placenta, fetal membranes, and neonatal lungs exposed to IAI. IAI caused neutrophil infiltration and neutrophil extracellular trap (NET) formation in the placenta and fetal membranes, and neonatal lung remodeling with pulmonary hypertension consistent with a BPD phenotype. Prenatal inhibition of c-Myc with 10058-F4 in IAI decreased neutrophil infiltration and NET formation, and improved neonatal lung remodeling induced by LPS, with improved alveolarization, increased angiogenesis, and decreased pulmonary vascular remodeling. Discussion: In a rat model of IAI, c-Myc regulates neutrophil recruitment and NET formation in the placenta and fetal membranes. c-Myc also participates in neonatal lung remodeling induced by IAI. Further studies are needed to investigate c-Myc as a potential therapeutic target for IAI and IAI-associated BPD.

Clinical use and adjustment of ultrasound elastography for breast lesions followed WFUMB guidelines and recommendations in the real world.

Objective: This study aimed to explore the value of strain elastography (SE) and shear wave elastography (SWE) following the World Federation of Ultrasound in Medicine and Biology (WFUMB) guidelines and recommendations in the real world in distinguishing benign and malignant breast lesions and reducing biopsy of BI-RADS (Breast Imaging Reporting and Data System) 4a lesions. Methods: This prospective study included 274 breast lesions. The elastography score (ES) by the Tsukuba score, the strain ratio (SR) for SE, and Emax for SWE of the lesion(A) and the regions(A') included the lesion and the margin (0.5-5 mm) surrounding the lesion were measured. The sensitivity, specificity, and AUC were calculated and compared by the cutoff values recommended by WFUMB guidelines. Results: When scores of 1 to 3 were classified as probably benign by WFUMB recommendation, the ES was significantly higher in malignant lesions compared to benign lesions (p < 0.05) in all lesions. For the cohort by size >20 mm, the sensitivity was 100%, and the specificity was 45.5%. ES had the highest AUC: 0.79(95% CI 0.72-0.86) with a sensitivity of 96.2%, and a specificity of 61.8% for the cohort by size ≤20 mm. For the Emax-A'-S2.5mm, when the high stiffness would be considered with Emax above 80 kPa in SWE, the malignant lesions were diagnosed with a sensitivity of 95.8%, a specificity of 43.3% for all lesions, a sensitivity of 88.5% for lesions with size ≤20 mm, and sensitivity of 100.0% for lesions with size >20 mm. In 84 lesions of BI-RADS category 4a, if category 4a lesions with ES of 1-3 points or Emax-A'-S2.5 less than 80 kPa could be downgraded to category 3, 52 (61.9%) lesions could be no biopsy, including two malignancies. If category 4a lesions with ES of 1-3 points and Emax-A'-S2.5 less than 80kPa could be downgraded to category 3, 23 (27.4%) lesions could be no biopsy, with no malignancy. Conclusions: The elastography score for SE and Emax-A' for SWE after our modification were beneficial in the diagnosis of breast cancer. The combination of SWE and SE could effectively reduce the biopsy rate of BI-RADS category 4a lesions.

Predictors of impaired effectiveness of carbon nanoparticle-based central lymph node tracing in patients who underwent surgery for papillary thyroid cancer: A retrospective cohort study.

Carbon nanoparticles (CNs) are used in papillary thyroid cancer (PTC) surgery to facilitate central lymph node dissection (CLND) and protect the parathyroid glands (PGs). However, some cases develop hypoparathyroidism after using CNs. This cohort study was undertaken to explore the predictors of the reduced effectiveness of CNs. Data on patients with PTC who underwent surgery wherein CNs were used during CLND were reviewed retrospectively. Patients who did not develop hypoparathyroidism and developed hypoparathyroidism were classified into Group A and B, respectively. Demographic and clinical characteristics were compared between the 2 groups. Univariate and multivariate logistic regression analysis were performed on related variables. The receiver operating characteristic curve was used to evaluate the predictors of the binary logistic model and the cutoff value of each predictor was obtained. A total of 265 patients were included. Compared with Group A, the patients in Group B had a higher body mass index (BMI) (P = .003), were more frequently associated with Hashimoto thyroiditis (HT) (P = .001), and tumors were larger in size (P = .026). Multivariate logistic regression analyses were performed on these variables and showed that HT (P = .001) and tumor size (P = .001) predicted the impaired role of CNs. CNs are not always useful in protecting PG function in patients who undergo CLND for PTC. In patients with coexisting HT (blood thyroid peroxidase antibody [TPOAb] level higher than 44.0 IU/mL or blood anti-thyroglobulin antibody [ATG] level higher than 125.0 IU/mL) or a tumor size exceeding 1.1 cm in diameter, the protective role of CNs may be impaired.

[Effect of modified Danggui Shaoyao Powder on SOCS3/TLR4 signaling pathway in rats with chronic atrophic gastritis].

This study aims to investigate the effect of modified Danggui Shaoyao Powder on the suppressor of cytokine signaling 3(SOCS3)/Toll-like receptor 4(TLR4) signaling pathway in gastric tissue of rats with chronic atrophic gastritis(CAG).Sixty SPF-grade SD rats were randomly assigned into the normal group, model group, Moluo Pills group, and high-, medium-, and low-dose groups of modified Danggui Shaoyao Powder.The rats in other groups except the normal group were treated with N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) to establish the CAG model.After 12 weeks of modeling, the rats in each group were administrated with corresponding drugs by gavage for 8 weeks.After the last administration, the histopathological changes of rat gastric mucosa were observed via hematoxylin-eosin(HE) staining.The serum levels of IL-6, TNF-α, and CRP were determined by enzyme-linked immunosorbent assay(ELISA).The mRNA levels of SOCS3 and TLR4 were determined by real-time PCR.The protein levels of SOCS3, TLR4, JAK2, p-JAK2, STAT3, and p-STAT3 in rat gastric tissue were measured by Western blot.Immunohistochemical method was employed to determine the protein levels of NF-κB, MyD88, NLRP3, Bcl-2, Bax, and Bad in rat gastric tissue.The results showed that modified Danggui Shaoyao Powder alleviated gastric mucosal atrophy of rats, significantly lowered the levels of IL-6, TNF-α, and CRP in rat serum, up-regulated the mRNA level of SOCS3, and down-regulated the mRNA level of TLR4 in rat gastric tissue.Furthermore, modified Danggui Shaoyao Powder up-regulated the protein level of SOCS3, down-regulated the protein levels of TLR4, p-JAK2, p-STAT3, NF-κB, MyD88, NLRP3, Bax, and Bad, and promoted the expression of Bcl-2 protein.Therefore, modified Danggui Shaoyao Powder may mitigate the gastric mucosal atrophy of rats by regulating the SOCS3/TLR4 signaling pathway.

Establishment of prognostic model for postoperative patients with metaplastic breast cancer: Based on a retrospective large data analysis and Chinese multicenter study.

Purpose: Models for predicting postoperative overall survival of patients with metaplastic breast cancer have not yet been discovered. The purpose of this study is to establish a model for predicting postoperative overall survival of metaplastic breast cancer patients. Methods: Patients in the Surveillance, Epidemiology, and End Results database diagnosed with MBC from 2010 to 2015 were selected and randomized into a SEER training cohort and an internal validation cohort. We identified independent prognostic factors after MBC surgery based on multivariate Cox regression analysis to construct nomograms. The discriminative and predictive power of the nomogram was assessed using Harrell's consistency index (C-index) and calibration plots. The decision curve analysis (DCA) was used to evaluate the clinical usefulness of the model. We verify the performance of the prediction model with a Chinese multi-center data set. Results: Multifactorial analysis showed that age at diagnosis, T stage, N stage, M stage, tumor size, radiotherapy, and chemotherapy were important prognostic factors affecting OS. The C-index of nomogram was higher than the eighth edition of the AJCC TNM grading system in the SEER training set and validation set. The calibration chart showed that the survival rate predicted by the nomogram is close to the actual survival rate. It has also been verified in the SEER internal verification set and the Chinese multi-center data set. Conclusion: The prognostic model can accurately predict the post-surgical OS rate of patients with MBC and can provide a reference for doctors and patients to establish treatment plans.