Association of dietary niacin intake with the prevalence and incidence of chronic obstructive pulmonary disease.

Evidence regarding the association between dietary niacin intake and chronic obstructive pulmonary disease (COPD) is limited. Our study investigates the relationship between dietary niacin intake and the prevalance and incidence of COPD in the adult population of the United States, using data from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2018. Data on niacin intake were extracted through dietary intake interviews. COPD diagnoses were based on lung function, medical history, and medication usage. We analyzed the association between niacin consumption and COPD using multiple logistic regression and restricted cubic spline models. The study included 7055 adult participants, divided into COPD (n = 243; 3.44%) and non-COPD (n = 6812; 96.56%) groups. Those with COPD had lower average niacin intake (21.39 ± 0.62 mg/day) compared to the non-COPD group (25.29 ± 0.23 mg/day, p < 0.001). In the adjusted multivariable model, the odds ratios (OR) and 95% confidence intervals (CI) for COPD in the highest versus lowest quartile of dietary niacin intake were 0.55 (0.33 to 0.89, P for trend = 0.009). Subgroup analysis, after adjustment for various variables, revealed no significant interaction effects. Dietary niacin intake was inversely associated with COPD prevalence in US adults. Participants with the highest dietary niacin intake demonstrated the lowest odds of COPD. The potential of dietary niacin supplementation as a strategy to mitigate COPD warrants further investigation.

Ferroelectric crystals with giant electro-optic property enabling ultracompact Q-switches.

Relaxor-lead titanate (PbTiO3) crystals, which exhibit extremely high piezoelectricity, are believed to possess high electro-optic (EO) coefficients. However, the optical transparency of relaxor-PbTiO3 crystals is severely reduced as a result of light scattering and reflection by domain walls, limiting electro-optic applications. Through synergistic design of a ferroelectric phase, crystal orientation, and poling technique, we successfully removed all light-scattering domain walls and achieved an extremely high transmittance of 99.6% in antireflection film-coated crystals, with an ultrahigh EO coefficient r33 of 900 picometers per volt (pm V-1), >30 times as high as that of conventionally used EO crystals. Using these crystals, we fabricated ultracompact EO Q-switches that require very low driving voltages, with superior performance to that of commercial Q-switches. Development of these materials is important for the portability and low driving voltage of EO devices.

Large-Area Piezoelectric Single Crystal Composites via 3-D-Printing-Assisted Dice-and-Insert Technology for Hydrophone Applications.

Compared with Pb(Zr,Ti)O3 (PZT) ceramics, piezoelectric ceramic composites (PCCs), and piezoelectric polyvinylidene fluoride (PVDF) polymer, piezoelectric single crystal composites (PSCCs) are thought to be the promising candidates for hydrophone applications because of their superior hydrostatic performance. However, due to the brittleness and small dimensions of single crystals, the preparation of large-area or conformal PSCCs is to be challenged. Herein, we prepared a large-area PSCC with dimensions of 50 mm × 50 mm × 5 mm using 3-D-printing-assisted dice-and-insert technology. The hydrostatic piezoelectric performances for PSCC were investigated using a quasi-static method. The hydrostatic figure-of-merit (HFOM) of PSCC is approximately [Formula: see text]/N, which is higher by 69.4% than that of PCC. Furthermore, PSCC shows advantages in the dielectric loss, frequency constant, electromechanical coupling coefficient, and hydrostatic pressure stability. The results suggest that PSCCs have great potential in substantially improving the sensitivity of hydrophones. In addition, 3-D-printing-assisted dice-and-insert technology breaks through the restriction of as-grown piezoelectric crystal size so as to make it possible for the applications where large-scale piezoelectric composites are required.

[A theoretical analysis of respiratory mechanics in mechanical ventilation].

As a non-physiological way of ventilation, mechanical ventilation has a great effect on the respiratory mechanics. The biggest problem of artificial airway is that it brings extra airway resistance to the respiratory tract. For different parts of the lung, positive pressure ventilation could cause different mechanic states. We can find the formation and influencing factors of transpulmonary pressure, transchest wall pressure, trans-lung-chest pressure, trans-diaphragmatic pressure, trans-pulmonary-diaphragmatic pressure, intrapleural pressure, plateau pressure and driving pressure, by analyzing the mechanic state in a unit area of the chest or diaphragm position in the way of basic mechanics. It is obviously different in the pulmonary pressure gradient caused by inspiratory driving between in spontaneous breathing and in mechanical ventilation. The pressure is transmitted from the periphery to the center in spontaneous breathing in physiological state, playing a traction role for lung tissue. The pressure is transmitted from the center to the periphery in positive pressure ventilation without spontaneous breathing, playing a pushing role for lung tissue. It can be divided into two stages in positive pressure ventilation with spontaneous breathing. The first stage is from inspiratory trigger effort to trigger sensitivity. It is similar to spontaneous inspiration in physiological state. The pressure gradient in this stage is from the peripheral to center. But the period is very short. The second stage is the positive pressure ventilation progress after the trigger sensitivity. The pressure gradient is caused by the pulling of the patient's spontaneous inhalation and the pushing of the positive pressure ventilation of the ventilator. There is a certain complementarity in the distribution and transmission of pressure, especially for non-physiological positive pressure ventilation. Therefore, through these basic mechanical analysis, clinical medical staff can better understand the impact of mechanical ventilation on respiratory mechanics.

Frequency Dependence of Coercive Fields of [001]- and [011]-Poled Rhombohedral Pb(In1/2Nb1/2)O3-Pb(Mg1/3Nb2/3)O3-PbTiO3 Single Crystals.

Relaxor-PbTiO3 (PT-based) ferroelectric single crystals are important for many piezoelectric applications because of their outstanding performances. In order to expand their usage and avoid the failure during application, frequency dependence of coercive fields EC for [001]- and [011]-poled rhombohedral Pb(In1/2Nb1/2)O3-Pb(Mg1/3Nb2/3)O3-PbTiO3 (PIN-PMN-PT) single crystals was investigated from the frequency of 1 Hz to 300 kHz by using hysteresis loop measurement (frequency: from 1 Hz to 2 kHz) and a critical value method (frequency: from 5 to 300 kHz). The results showed that the coercive field EC , remnant polarization Pr , and saturation polarization Ps strongly depended on the crystal orientation and frequency. Compared with the [001]-poled crystals, the [011]-poled PIN-PMN-PT single crystals possessed higher EC , Pr , and Ps at the same testing frequencies. With increasing frequency from 1 Hz to 300 kHz, the coercive fields EC of the [001]- and [011]-poled PIN-PMN-PT single crystals increased from 4.0 and 4.8 kV/cm to 11.5 and 14.9 kV/cm, respectively. Moreover, the frequency dependence of the coercive fields was found to be consistent with the growth kinetics model, where the coercive fields EC were proportional to fß . This work benefits to the design of piezoelectric devices based on PIN-PMN-PT single crystals operated at high frequencies and high driving fields.

Correlations between EGFR gene polymorphisms and pleural metastasis of lung adenocarcinoma.

Proliferation, growth, and differentiation of cells are strictly controlled by the signal system of epidermal growth factor receptor (EGFR). If any link of the EGFR signals system is interfered with or damaged, the proliferation, growth, and differentiation of cells would become uncontrolled. EGFR is overexpressed in a variety of malignant tumors, such as non-small-cell lung cancer, colorectal cancer and breast cancer. Results of the study have proved that EGFR overexpression is closely associated with mutations and variants of the EGFR genes, whose mutations and variants are associated with occurrence, metastasis, and prognosis of different types of tumors, including lung cancer. This study is aimed at investigating whether the polymorphisms of CA simple sequence repeat in intron 1 (CA-SSR1), -216G/T, and R497K in the EGFR are able to induce EGFR activation and whether overexpression is associated with pleural metastasis of lung adenocarcinoma. A total of 432 lung adenocarcinoma patients with pleural metastasis (metastasis group) and 424 patients with lung adenocarcinoma but without pleural metastasis (nonmetastasis group) were enrolled in this study. For all patients, the CA-SSR1 genotypes were determined by capillary electrophoresis, polymerase chain reaction amplification, and direct DNA sequencing, and the R497K and -216G/T genotypes were determined by polymerase chain reaction amplification and direct DNA sequencing. EGFR expression was evaluated by immunohistochemical staining in primary tumor tissues with different -216G/T, R497K, and CA-SSR1 genotypes. Our results showed significant differences between pleural metastasis and nonmetastasis groups in the genotype and allele distribution of -216G/T, R497K, and CA-SSR1 polymorphisms of the EGFR gene. The -216T allele, Arg allele, and shorter CA-SSR1 (<17) had significantly increased risks of pleural metastasis compared with the -216G allele, Lys allele, and longer CA-SSR1 (≥17), respectively. The expression of EGFR was higher in patients with genotypes of -216T/T or -216G/T, Arg/Arg or Arg/Lys, and shorter CA-SSR1 (<17) than that in patients with genotypes of -216G/G, Lys/Lys, and longer CA-SSR1 (≥17), respectively. These results indicate that -216G/T, R497K, and CA-SSR1 polymorphisms are associated with the risk of pleural metastasis of lung adenocarcinoma, which may be related to the overexpression of EGFR protein induced by -216G/T, R497K, and CA-SSR1 polymorphisms.

Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines.

BACKGROUND HDAC1 has been shown to be closely associated with the occurrence of tumors. We aimed to investigate the effects of siRNA-mediated HDAC1 knockdown on the biological behavior of esophageal carcinoma cell lines. MATERIAL AND METHODS HDAC1 expression in esophageal cancer cell lines TE-1, Eca109, and EC9706 was compared by Western blot analysis. These cells were transfected with siRNA-HDAC1 and cell proliferation was evaluated by MTT assay to select the optimum cell line for subsequent experiments. The effects of siRNA-HDAC1 on the migration and invasion of the selected cell line were assessed by transwell assay. The expression of cell cycle-related proteins cyclinD1, p21 and p27, and epithelial-mesenchymal transition (EMT)-related protein zonula occludens-1 (ZO-1), E-cadherin and vimentin was determined by Western blot analysis. RESULTS HDAC1 expression in TE-1, Eca109 and EC9706 cells was significantly higher compared with normal esophageal cell line HEEC (P<0.01). MTT assay, Western blot and RT-PCR analyses demonstrated that the inhibitory effects of siRNA on HDAC1 expression and cell viability in TE-1 cells were the highest among all cell lines, which was therefore used in subsequent experiments. After TE-1 cells were transfected with siRNA-HDAC1, their migration and invasion were significantly lower compared with the controls (P<0.01). CyclinD1 and vimentin expression was significantly lower compared with the controls (P<0.01), whereas the expression of p21, p27, ZO-1 and E-cadherin was significantly higher (P<0.01). CONCLUSIONS The siRNA-mediated HDAC1 knockdown significantly inhibited the proliferation, migration and invasion of TE-1 cells probably by regulating the expression of cell cycle- and EMT-related proteins.

-216G/T (rs712829), a functional variant of the EGFR promoter, is associated with the pleural metastasis of lung adenocarcinoma.

Numerous mutations and variants in the epidermal growth factor receptor (EGFR) gene have been demonstrated to be associated with the occurrence, metastasis and prognosis of various types of tumors, including lung cancer. Thus, the present study aimed to investigate whether -216G/T (rs712829), a functional polymorphism of the EGFR promoter that is able to induce EGFR activation and overexpression, is associated with the pleural metastasis of lung adenocarcinoma. The study subjects were comprised of 326 patients with primary lung adenocarcinoma and 312 matched cases with pleural metastasis. The -216G/T genotypes were determined in all subjects by PCR amplification and direct DNA sequencing, and EGFR expression was also evaluated by immunohistochemical staining in the primary tumor tissues with various -216G/T genotype backgrounds. The results showed that the frequencies of allele T and genotypes G/T and T/T in the pleural metastasis group were significantly higher compared with those in the non-metastasis group, with adjusted ORs of 1.46 (95% CI, 1.015-1.963) for G/T and 1.97 (95% CI, 1.051-3.152) for T/T. Furthermore, the expression of the EGFR protein was higher in the primary lung adenocarcinoma tissues with -216T/T and -216G/T compared with those with -216G/G (P<0.05). These results collectively indicate that the -216G/T polymorphism in the EGFR promoter is associated with the risk of the pleural metastasis of lung adenocarcinoma and that this effect may be associated with -216G/T-induced overexpression of the EGFR protein.

Prognostic nutritional index predicts outcomes of malignant pleural mesothelioma.

PURPOSE: Nutritional status has been associated with long-time outcomes in cancer patients. We investigated whether the prognostic nutritional index (PNI), an indicator of nutritional status, affects overall survival in patients with malignant pleural mesothelioma (MPM). METHODS: We enrolled 121 patients with histologically confirmed MPM, who had successfully undergone biopsy by medical thoracoscopy in this study. Demographic, clinical and laboratory data were collected retrospectively. The PNI was calculated as 10× serum albumin value (g/dl) + 0.005 × total lymphocyte count (per mm(3)) in peripheral blood. Univariate and multivariate analyses were used to identify prognostic factors. RESULTS: Mean pretreatment PNI was 44.6. PNI was significantly associated with age (P = 0.031), smoking habits (P = 0.039) and weight loss (P = 0.029). Survival analysis showed PNI to be an independent prognostic factor in MPM. Patients with lower PNIs (PNI < 44.6) had greater risk of death than those with higher PNIs (PNI ≥ 44.6; hazard ratio: 2.290; 95 % confidence interval: 1.415-3.706; P = 0.001). These analyses were adjusted for patient age, gender, smoking habits, dyspnea, chest pain, weight loss, primary site of tumor, histology, platinum-based systemic chemotherapy, hospital and stage. CONCLUSIONS: Pretreatment PNI is a novel independent prognostic factor in MPM.

Endostatin, an angiogenesis inhibitor, ameliorates bleomycin-induced pulmonary fibrosis in rats.

BACKGROUND: Recent evidence has demonstrated the role of angiogenesis in the pathogenesis of pulmonary fibrosis. Endostatin, a proteolytic fragment of collagen XVIII, is a potent inhibitor of angiogenesis. The aim of our study was to assess whether endostatin has beneficial effects on bleomycin (BLM)-induced pulmonary fibrosis in rats. METHODS: The rats were randomly divided into five experimental groups: (A) saline only, (B) BLM only, (C) BLM plus early endostatin treatment, (D) BLM plus late endostatin treatment, and (F) BLM plus whole-course endostatin treatment. We investigated the microvascular density (MVD), inflammatory response and alveolar epithelial cell apoptosis in rat lungs in each group at different phases of disease development. RESULTS: Early endostatin administration attenuated fibrotic changes in BLM-induced pulmonary fibrosis in rats. Endostatin treatment decreased MVD by inhibiting the expression of VEGF/VEGFR-2 (Flk-1) and the activation of extracellular signal-regulated protein kinase 1/2 (ERK1/2). Endostatin treatment also decreased the number of inflammatory cells infiltrating the bronchoalveolar lavage fluid during the early inflammatory phase of BLM-induced pulmonary fibrosis. In addition, the levels of tumour necrosis factor-α (TNF-α) and transforming growth factor ß1 (TGF-ß1) were reduced by endostatin treatment. Furthermore, endostatin decreased alveolar type II cell apoptosis and had an epithelium-protective effect. These might be the mechanism underlying the preventive effect of endostatin on pulmonary fibrosis. CONCLUSIONS: Our findings suggest that endostatin treatment inhibits the increased MVD, inflammation and alveolar epithelial cell apoptosis, consequently ameliorating BLM-induced pulmonary fibrosis in rats.

Overexpression of Numb suppresses tumor cell growth and enhances sensitivity to cisplatin in epithelioid malignant pleural mesothelioma.

Malignant pleural mesothelioma (MPM) is a highly aggressive and conventional treatment-resistant tumor with a dismal prognosis. Among the three histological subtypes of MPM, the epithelioid is the most common type. Numb is considered as a tumor suppressor playing a critical role in controlling asymmetric cell division, maintenance of stem cell compartments, ubiquitination of specific substrates and regulating Notch-, Hedgehog- and TP53-activated pathways. The present study was designed to analyze the role of Numb in epithelioid MPM. We investigated the expression of Numb in 39 epithelioid MPM and 22 normal pleural tissues by immunohistochemistry. Furthermore, we overexpressed Numb in NCI-H2452, an epithelioid human MPM cell line, and investigated the effect of Numb overexpression on the proliferation, apoptosis and sensitivity to cisplatin in cells. The expression of Numb was significantly lower in MPM compared to the control group and Numb had an inverse correlation with the ki-67 labeling index. Loss of Numb expression was associated with poor prognosis in epithelioid MPM. Overexpression of Numb in NCI-H2452 cells significantly inhibited proliferation, promoted apoptosis and enhanced sensitivity to cisplatin. Moreover, Numb overexpression activated caspase-9 and caspase-3 through release of cytochrome c as well as downregulation of XIAP and survivin. We speculate that cytochrome c/caspase signaling is a possible mechanism through which Numb enhances the apoptosis of NCI-H2452 cells. These results suggest that Numb may be involved in epithelioid MPM development, and its upregulation may confer sensitivity to cisplatin, suggesting potential therapeutic options for MPM.

EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy.

The aim of the present study was to evaluate the therapeutic effects and adverse reactions of Tarceva treatment for malignant pleural effusion (MPE) caused by metastatic lung adenocarcinomas. One hundred and twenty-eight patients who failed first-line chemotherapy drug treatment were divided into a mutation and a non-mutation group according to the presence or absence of epidermal growth factor receptor (EGFR) mutations. Each patient received closed drainage combined with simple negative pressure suction after thoracoscopic talc poudrage pleurodesis and oral Tarceva treatment. Short-term and long-term clinical therapeutic effects of Tarceva were evaluated. The EGFR mutation rate in pleural metastatic tissues of lung adenocarcinoma acquired through video-assisted thoracoscopic surgery was higher compared to that in surgical resection specimens, plasma specimens and pleural effusion specimens compared to previously reported results. There were significant statistical differences in the average extubation time (p<0.01), drainage volume of pleural effusion (p<0.05), Karnofsky score and formation of encapsulated pleural effusion 4 weeks after surgery (p<0.05) between these two groups. The number of patients with mild pleural hypertrophy in the mutation group was significantly higher compared to the non-mutation group (p<0.01), while the number of patients with severe pleural hypertrophy was significantly reduced (p<0.05). There was significant statistical discrepancy between these two groups in terms of improvement of peripheral blood carcinoembryonic antigen and tissue polypeptide antigen after 4 weeks of therapy. The complete remission rate and the efficacy rate were higher in the mutation group compared to that in the non-mutation group (p<0.05). There was a longer overall survival time after Tarceva treatment in patients with EGFR mutations than those without EGFR mutation. EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy. Detection of EGFR mutations may determine the responsiveness of malignant pleural effusion to Tarceva treatment.