Cement/Sulfur for Lithium-Sulfur Cells.

Lithium-sulfur batteries represent a promising class of next-generation rechargeable energy storage technologies, primarily because of their high-capacity sulfur cathode, reversible battery chemistry, low toxicity, and cost-effectiveness. However, they lack a tailored cell material and configuration for enhancing their high electrochemical utilization and stability. This study introduces a cross-disciplinary concept involving cost-efficient cement and sulfur to prepare a cement/sulfur energy storage material. Although cement has low conductivity and porosity, our findings demonstrate that its robust polysulfide adsorption capability is beneficial in the design of a cathode composite. The cathode composite attains enhanced cell fabrication parameters, featuring a high sulfur content and loading of 80 wt% and 6.4 mg cm-2, respectively. The resulting cell with the cement/sulfur cathode composite exhibits high active-material retention and utilization, resulting in a high charge storage capacity of 1189 mA∙h g-1, high rate performance across C/20 to C/3 rates, and an extended lifespan of 200 cycles. These attributes contribute to excellent cell performance values, demonstrating areal capacities ranging from 4.59 to 7.61 mA∙h cm-2, an energy density spanning 9.63 to 15.98 mW∙h cm-2, and gravimetric capacities between 573 and 951 mA∙h g-1 per electrode. Therefore, this study pioneers a new approach in lithium-sulfur battery research, opting for a nonporous material with robust polysulfide adsorption capabilities, namely cement. It effectively showcases the potential of the resulting cement/sulfur cathode composite to enhance fabrication feasibility, cell fabrication parameters, and cell performance values.

Back to the basics-risk factor identification of pediatric malignant lymphadenopathy proven by pathological studies.

PURPOSE: Lymphadenopathy (LAP) is a common problem in the pediatric patient. History, physical examinations (PE), ultrasounds, and blood tests were often obtained while studying such lesions. Malignancy should be highly suspected in certain conditions. This study evaluates the relationship between malignant LAP and risk factors for pediatric patients. MATERIALS AND METHODS: Medical records of matched patients are reviewed, and data are retrospectively collected. History, PE findings, laboratory data, ultrasound findings, and pathological findings were recorded and analyzed. The median values (interquartile range, IQR) were expressed for continuous variables, and the number of patients (percentage) for categorical variables. Comparisons between groups were performed using the Mann-Whitney U test and the chi-squared test. The significance was set as p value < 0.05. RESULTS: A total of 142 pediatric patients underwent a biopsy in our department for LAP from July 2004 to August 2021. Among them, 108 (76.1 %) patients had benign lesions, and 34 (23.9 %) had malignancies. Weight loss, fixed LAP, firm consistency, and serum lactate dehydrogenase (LDH) exceeding 240 U/L were more related to malignant LAP than other risk factors. Multiple regression analysis revealed two independent risk factors. The receiver operating characteristic curve regarding LDH level predicting malignancy revealed a sensitivity of 79.31 % and specificity of 36.51 % by applying the criterion as 230 U/L. CONCLUSIONS: For pediatric LAP, history-taking and physical examinations remained the most important approaches. Ultrasounds, serum LDH, and other laboratory studies may only provide clues. The cutoff level of LDH revealed low sensitivity and specificity for malignant LAP. With firm LAP, which is fixed, a biopsy for tissue proof should be performed.

Combination of FAK inhibitor and cytokine-induced killer cell therapy: An alternative therapeutic strategy for patients with triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is characterized by the loss of expression of several biomarkers, which limits treatment strategies for the disease. In recent years, immunotherapy has shown promising results in the treatment of various tumors. Emerging evidence demonstrated that TNBC is an immune-activated cancer, suggesting that immunotherapy could be a feasible treatment option for TNBC. Cytokine-induced killer (CIK) cell therapy is considered as a potential treatment for cancer treatment. However, it is still not approved as a standard treatment in the clinical setting. Our previous study demonstrated that focal adhesion kinase (FAK) plays important role in regulating the sensitivity of TNBC cells to CIK cells. In this study, we further verify the role of FAK in regulating the immune response in vivo. Our in vitro study indicated that knockdown of FAK in TNBC cells or treat with the FAK inhibitor followed by co-culture with CIK cells induced more cell death than CIK cells treatment only. RNA-seq analysis indicated that suppression of FAK could affect several immune-related gene expressions in TNBC cells that affects the immune response in the tumor microenvironment of TNBC cells. The combination of FAK inhibitor and CIK cells significantly suppressed tumor growth than the treatment of FAK inhibitor or CIK cells alone in vivo. Our findings provide new insights into the cytotoxic effect of CIK cell therapy in TNBC treatment and indicate that the combination of CIK cell therapy with FAK inhibitors may be an alternative therapeutic strategy for patients with TNBC.

A multicenter study to compare the effectiveness of the inpatient post acute care program versus traditional rehabilitation for stroke survivors.

There is insufficient evidence to prove the effect of the Post-acute Care (PAC) program on post-stroke recovery. This study aimed to determine the effectiveness of the PAC versus traditional inpatient rehabilitation (non-PAC) for middle- and old-aged stroke survivors. This multicenter cohort study enrolled 334 stroke patients admitted for post-stroke rehabilitation. The outcome variables included the Barthel Index (BI), Functional Oral Intake Scale (FOIS), Mini Nutritional Assessment-Short Form (MNA-SF), EuroQoL-5D (EQ-5D), Lawton-Brody Instrumental Activities of Daily Living (ADL) Scale, and Mini-Mental State Examination (MMSE). The inverse-probability-of-treatment-weighting method was used to analyze the differences in outcomes between the PAC and non-PAC groups. The PAC group showed better improvements in BI, MNA-SF, EQ-5D, Instrumental ADL, and MMSE compared to the non-PAC group, with differences in effect sizes of 0.54 (95% confidence interval [CI] 0.38-0.71), 0.26 (95% CI 0.10-0.42), 0.50 (95% CI 0.33-0.66), 0.44 (95% CI 0.28-0.60) and 0.34 (95% CI 0.17-0.50), respectively. The PAC project showed more improvement in basic and instrumental ADL and status of swallowing, nutrition, and cognition than those of non-PAC, which had less length of stay restricted by the National Health Insurance. More studies are warranted to investigate the influence of hospital stay and duration from stroke onset on the PAC's effectiveness.

Artificial intelligence deep learning for 3D IC reliability prediction.

Three-dimensional integrated circuit (3D IC) technologies have been receiving much attention recently due to the near-ending of Moore's law of minimization in 2D IC. However, the reliability of 3D IC, which is greatly influenced by voids and failure in interconnects during the fabrication processes, typically requires slow testing and relies on human's judgement. Thus, the growing demand for 3D IC has generated considerable attention on the importance of reliability analysis and failure prediction. This research conducts 3D X-ray tomographic images combining with AI deep learning based on a convolutional neural network (CNN) for non-destructive analysis of solder interconnects. By training the AI machine using a reliable database of collected images, the AI can quickly detect and predict the interconnect operational faults of solder joints with an accuracy of up to 89.9% based on non-destructive 3D X-ray tomographic images. The important features which determine the "Good" or "Failure" condition for a reflowed microbump, such as area loss percentage at the middle cross-section, are also revealed.

The impact of age group in breast cancer survival outcome according to neoadjuvant treatment response: A matched case-control study.

This study aimed to investigate the effectiveness of neoadjuvant chemotherapy in patients with breast cancer in different age groups and evaluate the impact of age group on survival outcome according to different treatment responses. Data were retrospectively collected from the cancer registry database of Kaohsiung Medical University Hospital in Taiwan under an approved protocol. Overall, 96 elder patients (aged >50 years) and 96 younger controls (aged ≤50 years) who received neoadjuvant chemotherapy and breast surgical treatment were examined after 1:1 matching. Logistic regression analysis was used to investigate the effectiveness of treatment response in patients of different age groups. Additionally, the Kaplan-Meier estimator and log-rank test were performed to evaluate the effect of age group and treatment response on disease-free and overall survival (OS). Although no direct significant association was found between age group and treatment response, several significant results were found in treatment response stratification analysis. Among 16 pathological complete response (pCR) patients, elder patients showed significantly greater 5-year disease-free survival (DFS) than younger patients (DFS rate, 85.7% vs. 0%, p = 0.041). However, in 176 non-pCR patients, elder patients showed poor DFS compared to younger patients (DFS rate, 16.6% vs. 32.3%; log-rank test, p = 0.031). With limited sample size and study design, our study results demonstrate that patients aged >50 years who achieved pCR after neoadjuvant chemotherapy could obtain better survival outcome than younger patients. However, the younger patients showed no survival benefits regardless of pCR status.

FAK Regulates VEGFR2 Expression and Promotes Angiogenesis in Triple-Negative Breast Cancer.

Triple-negative breast cancer (TNBC) remains a significant clinical challenge because of its high vascularity and metastatic and recurrent rates. Tumor angiogenesis is considered an important mediator in the regulation of tumor cell survival and metastasis in TNBC. Angiogenesis is induced by the binding of vascular endothelial growth factor to vascular endothelial growth factor receptor 2 (VEGFR2). Focal adhesion kinase (FAK) plays an important role in regulating various cell functions in normal and cancer cells. Previous studies have focused on investigating the function of endothelial FAK in tumor cell angiogenesis. However, the association between tumor FAK and VEGFR2 in tumor angiogenesis and the possible mechanisms of this remain unclear. In this study, we used a public database and human specimens to examine the association between FAK and VEGFR2. At the same time, we verified the association between FAK and VEGFR2 through several experimental methods, such as quantitative real-time polymerase chain reaction, Western blotting, and next-generation sequencing. In addition, we used the endothelial cell model, zebrafish, and xenograft animal models to investigate the role of FAK in TNBC angiogenesis. We found that FAK and VEGFR2 were positively correlated in patients with TNBC. VEGFR2 and several other angiogenesis-related genes were regulated by FAK. In addition, FAK regulated VEGFR2 and VEGF protein expression in TNBC cells. Functional assays showed that FAK knockdown inhibited endothelial tube formation and zebrafish angiogenesis. An animal model showed that FAK inhibitors could suppress tumor growth and tumor vascular formation. FAK promotes angiogenesis in TNBC cells by regulating VEGFR2 expression. Therefore, targeting FAK could be another antiangiogenic strategy for TNBC treatment.

Correction: Pan et al. Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer. Cancers 2020, 12, 94.

In the original article [...].

Utilizing NPWT improving skin graft taking in reconstruction for extended breast skin defects following mastectomy.

NPWT fulfill graft taking in complex breast wounds.

Comprehensive profiles and diagnostic value of menopausal-specific gut microbiota in premenopausal breast cancer.

In Western countries, breast cancer tends to occur in older postmenopausal women. However, in Asian countries, the proportion of younger premenopausal breast cancer patients is increasing. Increasing evidence suggests that the gut microbiota plays a critical role in breast cancer. However, studies on the gut microbiota in the context of breast cancer have mainly focused on postmenopausal breast cancer. Little is known about the gut microbiota in the context of premenopausal breast cancer. This study aimed to comprehensively explore the gut microbial profiles, diagnostic value, and functional pathways in premenopausal breast cancer patients. Here, we analyzed 267 breast cancer patients with different menopausal statuses and age-matched female controls. The α-diversity was significantly reduced in premenopausal breast cancer patients, and the ß-diversity differed significantly between breast cancer patients and controls. By performing multiple analyses and classification, 14 microbial markers were identified in the different menopausal statuses of breast cancer. Bacteroides fragilis was specifically found in young women of premenopausal statuses and Klebsiella pneumoniae in older women of postmenopausal statuses. In addition, menopausal-specific microbial markers could exhibit excellent discriminatory ability in distinguishing breast cancer patients from controls. Finally, the functional pathways differed between breast cancer patients and controls. Our findings provide the first evidence that the gut microbiota in premenopausal breast cancer patients differs from that in postmenopausal breast cancer patients and shed light on menopausal-specific microbial markers for diagnosis and investigation, ultimately providing a noninvasive approach for breast cancer detection and a novel strategy for preventing premenopausal breast cancer.

The CDK6-c-Jun-Sp1-MMP-2 axis as a biomarker and therapeutic target for triple-negative breast cancer.

Triple-negative breast cancer (TNBC) has high metastatic, drug-resistance, and recurrence rates, and is characterized by an angiogenic and fibrotic microenvironment that favors cancer malignancy. However, details of the mechanisms underlying malignancy are still largely unknown. Our mouse model indicated that knockdown of CDK6 inhibited lung metastasis significantly compared to parental cells. Immunohistochemical analyses revealed that the levels of collagen and the angiogenic marker matrix metalloproteinase (MMP)-2 were much lower in CDK6-deficient cells. To examine mechanisms in the CDK6-mediated phenotype of cancer cells, we studied its role in MMP-2 expression. CDK6 mediated the recruitment of transcription factors including c-Jun and Sp1 to the MMP2 promoter. Knockdown of CDK6 significantly suppressed the expression of MMP2 mRNA. Consistent with the in vitro data, the expression of CDK6 was positively correlated with the angiogenic and fibrotic tumor microenvironment in TNBC patient tissues as shown by MMP-2 and fibronectin staining, respectively. More importantly, after screening a small molecule library of 31 protein kinase inhibitors, we found that the Raf inhibitor sorafenib displayed the highest cytotoxicity in CDK6-depleted cells. These data indicate that CDK6 serves as an anti-microenvironment target and affects the drug response in retinoblastoma-proficient TNBC, suggesting that combining a CDK6 inhibitor and sorafenib leads to a synthetic effect that may represent a personalized therapeutic approach for patients with TNBC.

Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer.

Triple-negative breast cancer (TNBC) is a special subtype of breast cancer in which several common diagnostic biomarkers are lost. Due to the loss of expression of receptors, treatment options for TNBC are limited. Therefore, finding safe and effective treatments for patients with TNBC is a major objective for clinicians. Previous studies suggested that cytokine-induced killer (CIK) cells may be beneficial for patients with a variety of tumor types. However, CIK therapy is not effective for all patients. In this study, we found that focal adhesion kinase (FAK), a non-receptor protein tyrosine kinase that regulates several cellular functions in different cells, has the potential to regulate tumor cells sensitized to CIK cells. Knockdown of FAK expression in TNBC cells or the treatment of TNBC cells with a FAK inhibitor followed by coculture with CIK cells increases death of TNBC cells, suggesting that FAK plays important roles in sensitizing tumor cells to CIK cells. This phenomenon could be regulated by a FAK-programmed death-ligand 1 (PD-L1)-related mechanism. Overall, our findings provide new insights into the cytotoxic effect of CIK cell therapy in TNBC treatment, and show that CIK cell therapy combined with FAK inhibitors may be a novel therapeutic strategy for patients with TNBC.

Inhaled fluticasone and salmeterol suppress eosinophilic airway inflammation in chronic obstructive pulmonary disease: relations with lung function and bronchodilator reversibility.

The aim of this study was to determine whether combined inhaled corticosteroids and long-acting beta(2) agonists can suppress eosinophilic inflammation in chronic dostructive plumonary disease (COPD) and to investigate the association between the level of eosinophilia and the degree of bronchodilator reversibility. Sixty-two patients with stable COPD (forced expiratory volume in 1 [FEV(1)] of 30%-70% predicted before bronchodilation) were enrolled from our outpatient clinic. Patients received inhaled fluticasone (100 microg)/salmeterol (50 microg) twice daily for two months. Lung function measurements, bronchodilator tests, and sputum induction were performed. The number of inflammatory cells and mediators, including interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and eosinophilic cationic protein (ECP), were measured. Treatment with inhaled fluticasone and salmeterol significantly suppressed eosinophilic inflammation in COPD patients with sputum eosinophilia (mean 8.9% +/- 2.0% vs. 1.6% +/- 0.5%, p = 0.003), but insignificant differences in FEV(1) and FVC between patients with and without eosinophilia suggested that suppression of eosinophilic inflammation had no effect on FEV(1) or FVC. Reduction in the percentage of eosinophils was significantly correlated with decreased levels of ECP (r = 0.48, p < 0.001). Levels of neutrophils, IL-8, and TNF-alpha were not affected. Sputum eosinophilia was not related to the degree of bronchodilator reversibility. The degree of bronchodilator reversibility did not predict the increase in FEV(1) and FVC after treatment with inhaled corticosteroids/long-acting beta(2) agonists. Suppression of eosinophilic inflammation and bronchodilator responsiveness indices were not correlated with clinical outcomes in COPD patients treated with inhaled corticosteroids/long-acting beta(2) agonists.

Additive benefits of tiotropium in COPD patients treated with long-acting beta agonists and corticosteroids.

OBJECTIVE AND BACKGROUND: The addition of an alternative class of long-acting bronchodilator is recommended for COPD patients who do not respond satisfactorily to monotherapy. The aim of this study was to investigate the additive benefit of tiotropium in severe COPD and to establish whether the improvement in lung function in these patients can be predicted from their acute bronchodilator response to ipratropium or salbutamol. METHODOLOGY: Forty-six patients with severe COPD treated with inhaled long-acting beta(2) agonists and corticosteroids (LABA/CS) were enrolled. Their prebronchodilator FEV(1) was less than 50% of the predicted value. Tiotropium (18 microg, once daily) was added via a dry-powder inhaler device. After a month of treatment, tiotropium was stopped but their previous medication was continued. Patients were reassessed a month later. Acute bronchodilator response to ipratropium and salbutamol was assessed prior to tiotropium treatment. Pulmonary function and health status were evaluated. RESULTS: Adding tiotropium significantly improved FVC, FEV(1) and inspiratory capacity (IC). The increase in FVC was significantly associated with an increase in IC (r = 0.36, P = 0.019) and a decrease in residual volume (r =-0.56, P < 0.001). Total scores of St. George Respiratory Questionnaire scores were significantly improved after adding tiotropium treatment (P < 0.001). After tiotropium withdrawal, FVC, FEV(1) and IC decreased markedly. Bronchodilator response to ipratropium did not predict the tiotropium-mediated improvement in FEV(1) or FVC. CONCLUSIONS: Adding tiotropium to inhaled LABA/CS can yield clinical benefits in lung function and improved quality of life in COPD patients, as both drugs act through separate yet complementary pathways to maintain airway calibre.