Anemia and frailty in the aging population: implications of dietary fiber intake (findings of the US NHANES from 2007-2018).

BACKGROUND: Frailty has long been seen as an indicator of reduced physical functions in the elderly, which may be caused by a variety of chronic illnesses or cancerous tumors. Dietary fiber was connected with anemia and frailty, whereas it was uncertain if dietary fiber consumption modifies the impact of anemia on frailty in elderly adults. METHODS: We performed a secondary analysis using older adults aged 60 years and over from the National Health and Nutrition Examination Survey (NHANES) 2007-2018 cycles. Dietary fiber intake was estimated using two 24-h dietary recalls. Participants were dichotomized as frail or non-frail based on a modified Fried physical frailty phenotype from previous NHANES studies. The weighted logistic regression was used to estimate the odds ratio (OR) and confidence interval (CI) for the associations between hemoglobin levels and frailty at high- and low-dietary fiber intake levels. RESULTS: A total of 9644 older adults were included in this study, and the weighted sample was 56,403,031, of whom 3,569,186 (6.3%) were deemed to be frail, and the remainder were deemed to be non-frail. Among the low dietary fiber intake group, higher hemoglobin was significantly associated with a lower risk of frailty (OR = 0.79, 95% CI: 0.71-0.87), and anemia was associated with an almost threefold elevated risk of frailty (OR = 3.24, 95% CI:1.98-5.29) in the fully adjusted model. However, this phenomenon was not observed in groups with high dietary fiber intake. In addition, L-shaped dose response relationship was found in the high dietary fiber intake group (P overall association < 0.001; P non-linear association = 0.076). Whereas the dose response relationship was not significant in the high dietary fiber intake group (P overall association 0.752; P non-linear association = 0.734). CONCLUSIONS: Frailty was positively associated with the severity of anemia in older adults with low, but not high, dietary fiber intake. Adequate fiber intake may be an innovative dietary strategy to reduce frailty in older adults.

LncRNA LINC00467 acted as an oncogene in esophageal squamous cell carcinoma by accelerating cell proliferation and preventing cell apoptosis via the miR-485-5p/DPAGT1 axis.

BACKGROUND AND AIM: Esophageal carcinoma has been regarded as one of the top 10 common malignancies globally. Esophageal squamous cell carcinoma (ESCC) is an important subtype of esophageal carcinoma with approximately 20% survival rate. Long noncoding RNAs were documented to regulate the occurrence or progression of several tumors. However, neither the biological role nor the molecular mechanism of LINC00467 has been explored. This research is aimed to investigating the regulatory mechanism of LINC00467 in ESCC. METHODS: In this study, a series of experiments including reverse transcription-quantitative polymerase chain reaction, Cell Counting Kit-8, luciferase reporter, western blot, and RNA immunoprecipitation were designed and conducted to explore the potential function and mechanism of LINC00467 in ESCC. RESULTS: According to experimental results, we found out upregulated LINC00467 improved cell proliferation, but hindered cell apoptosis. In mechanism, miR-485-5p was predicted, screened out, and validated to combine with LINC00467, which displayed lower expression in ESCC. Additionally, miR-485-5p negatively regulated and directly targeted DPAGT1. Rescue assays suggested that DPAGT1 amplification was able to recover the influence of LINC00467 deficiency on cell proliferation and apoptosis. Furthermore, knockdown of LINC00467 suppressed tumor growth in vivo. CONCLUSION: We proved that LINC00467 acted as an oncogene in ESCC by accelerating cell proliferation and preventing cell apoptosis via miR-485-5p/DPAGT1 axis. This may provide a potential diagnostic marker for ESCC treatment.

Rsf-1 Influences the Sensitivity of Non-Small Cell Lung Cancer to Paclitaxel by Regulating NF-κB Pathway and Its Downstream Proteins.

BACKGROUND/AIMS: The therapeutic efficacy of paclitaxel is hampered by chemotherapeutic resistance in non-small cell lung cancer (NSCLC). Rsf-1 enhanced paclitaxel resistance via nuclear factor-κB (NF-κB) in ovarian cancer cells and nasopharyngeal carcinoma. This study assessed the function of Rsf-1 in the modulation of the sensitivity of NSCLC to paclitaxel via the NF-κB pathway. METHODS: The mRNA and protein levels of the related genes were quantified by RT-PCR and Western blotting. Rsf-1 silencing was achieved with CRISPR/Cas9 gene editing. Cell cycle, migration and proliferation were tested with flow cytometry, transwell test and CCK8 test. Cell apoptosis was analyzed with flow cytometry and quantification of C-capase3. The parameters of the tumors were measured in H460 cell xenograft mice. RESULTS: Rsf-1 was highly expressed in H460 and H1299 cells. Rsf-1 knockout caused cell arrest at the G1 phase, increased cell apoptosis, and decreased migration and cell proliferation. Rsf-1 knockout increased the inhibition of cell proliferation, the reduction in cell migration and the augment in cell apoptosis in paclitaxel treated H460 and H1299 cells. Rsf-1 knockout further enhanced the paclitaxel-mediated decrease in the volume and weight of the tumors in H460 cell xenograft mice. Helenalin and Rsf-1 knockout decreased the protein levels of p-P65, BcL2, CFLAR, and XIAP; hSNF2H knockout decreased the protein level of NF-κB p-P65 without altering Rsf-1 and p65 protein levels, while Rsf-1 and hSNF2H double knockout decreased the level of NF-κB p-P65, in H1299 and H460 cells. CONCLUSION: These results demonstrate that Rsf-1 influences the sensitivity of NSCLC to paclitaxel via regulation of the NF-κB pathway and its downstream genes.

Design of double-notch UWB filter with upper stopband characteristics based on ACPW-DGS.

In this manuscript, a compact (size only 9.8mm*9.8mm) Ultra Wide Band (UWB) bandpass filter with a new structure is proposed, which can be used in the UWB wireless communication band authorized by the FCC. The top plane is composed of a pair of back-to-back microstrip lines, and the ground plane structure is based on an asymmetric coplanar waveguide-defect ground structure (ACPW-DGS). UWB is formed by the vertical electromagnetic coupling of the top plane and the ground plane. On this basis, split ring resonator (SRR) and C type resonator (CTR) are utilized to place double notch bands. A novel third order nested C-type resonator (TONCTR) is obtained by performing CTR, which can further optimize the upper stopband while ensuring double notch bands. The filter can be used for filtering within the UWB system, and it can also avoid the amateur radio band (9.2 -10.3GHz) and the X-band satellite link band (9.6-12.3GHz) on UWB communication systems. Finally, the measured results from the fabricated prototype are basically consistent with the simulation results.

Mortality from all-cause and cause-specific in the elderly: Joint implications of anemia and frailty.

BACKGROUND: Anemia is prevalent among older adults, and it contributes to the incidence of frailty. In turn, the frail elderly may be deficient in nutrients, including iron, vitamin B-12, and folate, that can be materials for human blood, as a result of their limited nutrient intake, resulting in anemia. Both anemia and frailty are associated with an increased risk of mortality in elderly adults. However, the combined influence of anemia and frailty on mortality is unclear. METHODS: Data obtained from NHANES 2007-2014 were analyzed in this study. Frailty status was determined using a modified Fried Phenotype, and anemia was defined according to the criteria set by the World Health Organization. Public-use Linked Mortality files until December 31, 2019 were available. The weighted Cox proportional hazard regression models were used to estimate separate effects and joint effects of frailty and anemia on all-cause and cause-specific mortality. RESULTS: This study analyzed 6,406 participants aged 60 years or older. Over a 13-year follow-up period, considering participants with no anemia and no frailty as reference, participants with both anemia and frailty had nearly fourfold the all-cause (HR (95% CI): 4.03 (2.95,5.52)), more than four-time the cardiovascular (HR (95% CI): 4.24(2.46,7.32)) mortality risk, and above five-time the non-CVD/non-cancer (HR (95% CI): 5.17 (3.58,7.46)) mortality risk. CONCLUSIONS: The study indicated that older adults who exhibit low levels of hemoglobin and frailty are at the greatest risk for all-cause, cardiovascular, cancer, and non-cancer/non-cardiovascular mortality, with the exception of cancer mortality, which was only increased by anemia.

Coronary artery fistula and lung adenocarcinoma: a case report and literature review.

Coronary artery fistula (CAF) is a rare condition, whilst lung cancer is one of the most common malignant tumors worldwide. We came cross an interesting case with both diseases. To the best of our knowledge, this is the first case report pertaining to a patient with a coexisting CAF and lung adenocarcinoma. The patient was a 67-year-old woman who was admitted to our hospital for evaluation of persistent cough. Through the examination she was diagnosed coronary artery fistula and lung adenocarcinoma. Both diseases were successfully treated in a single operation (artery ligation and pulmonary lobectomy). The post-operative period was uneventful. At 3-month follow-up, there were no signs of blood shunting or cancer recurrence. There is no standard guidelines to treat both diseases. We want to seek out a solution to the problem. In this patient, we successfully performed artery ligation and pulmonary lobectomy in a single operation without any complications. We believe the treatment of patients with CAFs should be individualized. But, there is still a lot of shortcomings in our research. First of all, we have no enough cases to support our approach. What's more, the long-term effects of the operation are not certain. Last but not least, we have no proof in genetics with both diseases.

Crosstalk between endothelial cell-specific calpain inhibition and the endothelial-mesenchymal transition via the HSP90/Akt signaling pathway.

HYPOTHESIS: The role of non-cardiomyocytes in cardiac remodeling and fibrosis has not been totally understood until now. This study investigated if endothelial cell (EC)-specific calpain participates in myocardial endothelial injury via the endothelial- mesenchymal transition (EndMT) and in cardiac fibroblasts during cell proliferation, thereby contributing to cardiac fibrosis eventually. METHODS: in vitro cultured mouse cardiac ECs were induced with transforming growth factor (TGF)-ß1 (10 ng/ml) and calpain inhibitor III (20 µM) or Akt inhibitor (LY294002, 20 µM). Isolated cardiac fibroblasts were induced by TGF-ß1 and an HSP90 inhibitor (17AAG, 20 µM), and EndMT were analysed. Capn4-knockout (KO) specific to ECs of mice was generated. We induced the pathological process mimicking cardiac hypertrophy and fibrosis in both Capn4-KO mice and their wild-type littermates. The histological analysis was used to measure cardiomyocyte size and collagen contained in the heart. The immunofluorescence analysis was performed to demonstrate that the ECs went through the EndMT, transforming mesenchymal cells into fibroblasts and myofibroblasts. RESULTS: Capn4 deletion specific to ECs abrogated activity of both calpain 1 and calpain 2 in ECs, lowered the volume of cardiac collagen and cardiomyocytes size, and ameliorated myocardial dysfunction in the isoproterenol-treated cardiac fibrosis model. An ex vivo analysis of cardiomyocytes by Evans Blue staining revealed that isoproterenol increased cell death compared with the control, and Capn4-KO alleviated this result. Inhibiting calpain in cultured cardiac microvascular endothelial cells (MCECs) reversed the EndMT process, which was induced by TGF-ß1. Overexpression of calpastatin decreased the pathological EndMT process, showing that the cultured MCECs have more mesenchymal markers, such as α-smooth muscle actin (SMA), and fewer endothelial markers, such as VE-cadherin. Activating calpain elevated phosphorylated Akt in mice cultured ECs, and inhibiting calpain decreased phosphorylated Akt. Upregulation of phosphorylated Akt by calpain promoted the EndMT, whereas inhibiting calpain switched on the protective mechanism during the EndMT via the heat shock protein (HSP)90/Akt signaling way in cultured ECs. CONCLUSIONS: This study demonstrated a vital role of calpain in ECs for inducing myocardiocyte hypertrophy, cell death and the EndMT via the HSP90/Akt signaling pathway, thereby promoting cardiac fibrosis. The results indicate that inhibiting ECs calpain is a novel therapeutic target to retard cardiac fibrosis and has positive effects on heart failure.

The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression.

BACKGROUND: Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are approved for patients with recurrent non-small cell lung cancer (NSCLC). However, the efficacy of EGFR-TKIs in NSCLC therapy is limited by primary and acquired resistance. Recent studies have revealed that long non-coding RNAs (LncRNA) may be involved in EGFR-TKI resistance. Therefore, a better understanding of the interactive mechanisms underlying LncRNA-mediated EGFR-TKIs resistance may help us to improve clinical response rates. METHOD: To investigate the expression of growth arrest-specific 5 (GAS5) in lung adenocarcinoma, we performed real-time reverse-transcriptase polymerase chain reaction. The correlation between GAS5 expression levels and the samples' clinicopathological features was also analyzed. Primary resistance to EGFR-TKIs was identified in the human lung adenocarcinoma cell line A549. Plasmid vectors were used to overexpress GAS5 in A549 cells. MTT (3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide) colony formation assays and EdU (5-ethynyl-2'-deoxyuridine) assays were used to assess cell proliferation, and flow-cytometric analysis was used to evaluate the apoptosis rate. The expression levels of our target proteins, namely, EGFR, p-EGFR, ERK, p-ERK, Akt, p-Akt, IGF-1R (insulin-like growth factor 1 receptor), and p-IGF-1R, were analyzed by western blotting. A549 cells transfected with pcDNA-GAS5 were injected into nude mice. The transplanted mice were treated with gefitinib to study the effect of GAS5 on the resistance to EGFR-TKIs in vivo. RESULTS: Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. Furthermore, lower GAS5 expression levels were associated with larger tumor sizes, poor tumor differentiation, and advanced pathological stages. However, GAS5 was almost equally expressed between benign tumors compared with the adjacent normal tissues. GAS5 was also overexpressed in EGFR-TKI sensitive cell lines compared with the resistant cell line. Using MTT, EdU incorporation, and colony formation assays, we showed that GAS5-expressing A549 cells displayed an elevated level of cell death. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. CONCLUSIONS: Collectively, our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib, which could be reversed by overexpressing GAS5.

Evaluation of video-assisted thoracoscopic surgery for pulmonary metastases: a meta-analysis.

BACKGROUND: To evaluate the evidence comparing video-assisted thoracic surgery (VATS) and open thoracotomy in the treatment of metastatic lung cancer using meta-analytical techniques. METHODS: A literature search was undertaken until July 2013 to identify the comparative studies evaluating disease-free survival rates and survival rates. The pooled odds ratios (OR) and the 95% confidence intervals (95% CI) were calculated with the fixed or random effect models. RESULTS: Six retrospective studies were included in our meta-analysis. These studies included a total of 546 patients: 235 patients were treated with VATS, and 311 patients were treated with open thoracotomy. The VATS and the thoracotomy did not demonstrate a significant difference in the 1-,3-,5-year survival rates and the 1-year disease-free survival rate. There were significant statistical differences between the 3-year disease free survival rate (p = 0.04), which favored open thoracotomy. CONCLUSIONS: The VATS approach is a safe and feasible treatment in terms of the survival rate for metastatic lung cancer compared with the thoracotomy. The 3-year disease-free survival rate in the VATS group is inferior to that of open thoracotomy. The VATS approach could not completely replace open thoracotomy.

Facile synthesis of hierarchical core-shell Fe3O4@MgAl-LDH@Au as magnetically recyclable catalysts for catalytic oxidation of alcohols.

A novel core-shell structural Fe(3)O(4)@MgAl-LDH@Au nanocatalyst was simply synthesized via supporting Au nanoparticles on the MgAl-LDH surface of Fe(3)O(4)@MgAl-LDH nanospheres. The catalyst exhibited excellent activity for the oxidation of 1-phenylethanol, and can be effectively recovered by using an external magnetic field.

Bird's-eye view on gastric cancer research of the past 25 years.

This paper provides a bird's-eye view of our 25-year research work on gastric cancer, including both exploration of pathogenesis and preclinical or clinical applications of diagnosis and treatment. Although there have been achievements and reasons for applause, there are, nonetheless, more failings and teachings. Some problems that we experienced 25 years ago are still problems we have to face today. We are absolutely not singing the same old tune. Looking back makes us wiser and our way smoother. Although it is a long and arduous way to further study gastric cancer, we are willing to devote ourselves to it.