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0% and 83.3%, respectively. The mOS and mPFS of patients with sensitive EGFR mutation were 24.8 months and 10.8 months, respectively, and RR and DCR were 75.0% and 100.0%, respectively. The mOS and mPFS of patients with unknown EGFR status were 35.6 months and 12.3 months, respectively, and RR and DCR were 53.3% and 86.7%, respectively. Treatment was well tolerated and no severe toxicities were observed. Common toxicities include rash in 15 patients (46.9%), diarrhea in 7 cases (21.9%) and oral ulcer in 1 case (3.1%).

Gefitinib was highly effective and well tolerated in lung adenocarcinoma patients with brain metastases, and could be recommended as a treatment choice for this population.

Gefitinib was highly effective and well tolerated in lung adenocarcinoma patients with brain metastases, and could be recommended as a treatment choice for this population.

It has been proven that peripherally inserted central catheter-related vein thrombosis is a unignorable complication which causes serious harm and economic burden to patients. We designed a study to analyze factors causing peripherally inserted central catheter (PICC)-related vein thrombosis, and find some nursing interventions to reduce the incidence of PICC-related vein thrombosis, and prolong the service time of peripherally inserted central catheters.

We designed a retrospective analysis. The study participants were 1,538 lung cancer patients who underwent PICCs placement between January 2010 and September 2013. And tried to determine age, gender, indwelling vein, platelet count, prothrombin time, fibrinogen associated with PICC-related vein thrombosis.

Of the 1,538 unique PICC placements, 38 patients developed PICC-related vein thrombosis, the incidence was 2.47%. The gender (OR=2.194, P=0.024), indwelling vein (OR=1.955, P=0.006), fibrinogen (OR=2.055, P=0.028) can significantly affect the occurrence of PICC-related vein thrombosis.

Patients' gender, indwelling vein, fibrinogen can affect the occurrence of PICC-related vein thrombosis. Assessing the patients' condition carefully, implementing individual nursing care can reduce the incidence of PICC-related vein thrombosis, and prolong the service time of PICCs.

Patients' gender, indwelling vein, fibrinogen can affect the occurrence of PICC-related vein thrombosis. Assessing the patients' condition carefully, implementing individual nursing care can reduce the incidence of PICC-related vein thrombosis, and prolong the service time of PICCs.

It has been proven that any changes of transforming growth factor β (TGF-β)-Smad signal transduction pathway will lead to abnormalities of signal transmission and the out of control during cell growth and differentiation, resulting in cancer development. The aim of this study is to investigate the prognostic values of TGF-β1, Smad2 and Smad4 in resected non-small cell lung cancer (NSCLC).

The expression of TGF-β1, Smad2, and Smad4 was evaluated by immunohistochemistry in 85 patients with NSCLC. The relationships among the expression of these proteins, clinicopathological factors, and prognosis were also analyzed.

TGF-β1 positive expression was significantly correlated with the late stage and lymph node involvement. No significant association existed between the expression of Smad2 and the clinicopathological characteristics. The lack of Smad4 expression was associated with the advanced tumor stage (P=0.014). Multivariate analysis indicated that lymph node involvement (P=0.001) was an independent prognostic factor in the 85 NSCLC patients. check details The positive expression levels of TGF-β1 (P=0.032) and N stage (P=0.028) were demonstrated to be independent risk factors for survival among 47 lung adenocarcinoma patients. Adenocarcinoma patients with TGF-β1 positive expression demonstrated an unfavorable survival outcome (P=0.0376).

TGF-β1 may be an independent predictor of survival in resected lung adenocarcinoma patients.
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TGF-β1 may be an independent predictor of survival in resected lung adenocarcinoma patients.
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Pulmonary sarcomatoid carcinoma is a rare histologic subtype of non-small cell lung cancer. The effective treatment for this disease has not well defined due to its extremely low morbidity. This study explores the clinicopathological characteristics and prognosis of 38 patients with PSC, so as to provide some clues for its diagnosis and treatment.

The study enrolled 38 patients with PSC that were diagnosed with histology or cytology in our hospital between January 2000 and December 2013. We retrospectively analyzed general clinical characteristics, smoking history, tumor size, TNM staging, pathology, immunohistochemistry, diagnostic method, treatment and prognosis. We used SPSS 19.0 statistical software and Kaplan-Meier method to analyze our data.

Patients in this study were aged from 26 to 76 years old (the median age was 57.5 years old). Among all of them, the male to female ratio was 41, and 81.6% of patients had smoking history. Cough and hemoptysis were the most common primary symptoms. The median target therapy may give new insight into treatment for PSC.
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Most small cell lung cancer (SCLC) patients relapse or progress and have low survival rate although they have significant response to initial chemotherapy and radiotherapy. This study intends to explore the factors affecting the relapse (or progression) of nonoperative SCLC and to explore the correlations between progression-free survival (PFS) and overall survival (OS).

Clinical data of 182 patients diagnosed with SCLC between January 2009 and December 2011 at Shanghai Chest Hospital has been reviewed and retrospectively analyzed. All of these patients accepted chemotherapy combined (or not combined) with radiotherapy, and relapsed or progressed after first-line therapy. Univariate Kaplan-Meier survival estimates as well as multivariate Cox regression survival analysis were used to locate the potential factors affecting PFS. The correlation between PFS and OS was analyzed via Bivariate Correlation Analysis method.

The univariate estimates showed that the TNM stage, liver metastasis or not, brain metastwithout brain metastasis.Ginsenosides are the main compounds with pharmacological activities in ginseng. Deglycosylated ginsenosides, which are more pharmacologically active than glycosylated ginsenosides, can be produced by the specific or nonspecific hydrolysis of the sugar moieties in glycosylated ginsenosides using glycosidases. The enzymes that hydrolyze specifically ginsenosides with different types can be classified according to the enzymatic activity on the positions, inner and outer residues and types of sugar moieties in ginsenosides. Glycosylated ginsenosides are also hydrolyzed to deglycosylated ginsenosides with different hydrolytic pathways by cell conversion or fermentation. The biochemical properties of glycosidases involved in ginsenoside hydrolysis - ginsenosidases - were newly arranged and reviewed in accordance with different types. link2 The combination of different-type ginsenosidases is suggested herein as an efficient tool to produce industrially important ginsenosides.Endoplasmic reticulum (ER) stress, defective autophagy and genomic instability in the central nervous system are often associated with severe developmental defects and neurodegeneration. Here, we reveal the role played by Rint1 in these different biological pathways to ensure normal development of the central nervous system and to prevent neurodegeneration. We found that inactivation of Rint1 in neuroprogenitors led to death at birth. Depletion of Rint1 caused genomic instability due to chromosome fusion in dividing cells. Furthermore, Rint1 deletion in developing brain promotes the disruption of ER and Cis/Trans Golgi homeostasis in neurons, followed by ER-stress increase. Interestingly, Rint1 deficiency was also associated with the inhibition of the autophagosome clearance. Altogether, our findings highlight the crucial roles of Rint1 in vivo in genomic stability maintenance, as well as in prevention of ER stress and autophagy.The tumor suppressor protein promyelocytic leukemia (PML) is a key regulator of inflammatory responses and tumorigenesis and functions through the assembly of subnuclear structures known as PML nuclear bodies (NBs). The inflammation-related cytokine tumor necrosis factor-α (TNFα) is known to induce PML protein accumulation and PML NB formation that mediate TNFα-induced cell death in cancer cells and inhibition of migration and capillary tube formation in endothelial cells (ECs). In this study, we uncover a novel mechanism of PML gene regulation in which the p38 MAPK and its downstream kinase MAP kinase-activated protein kinase 1 (MNK1) mediate TNFα-induced PML protein accumulation and PML NB formation. The mechanism includes the presence of an internal ribosome entry site (IRES) found within the well-conserved 100 nucleotides upstream of the PML initiation codon. The activity of the PML IRES is induced by TNFα in a manner that involves MNK1 activation. It is proposed that the p38-MNK1-PML network regulates TNFα-induced apoptosis in breast cancer cells and TNFα-mediated inhibition of migration and capillary tube formation in ECs.The vapor-liquid-solid (VLS) mechanism enables the bottom-up, or additive, growth of semiconductor nanowires. Here, we demonstrate a reverse process, whereby catalyst atoms are selectively removed from the eutectic catalyst droplet. This process, which is driven by the dicarbonyl precursor 2,3-butanedione, results in axial nanowire etching. Experiments as a function of substrate temperature, etchant flow rate, and nanowire diameter support a solid-liquid-vapor (SLV) mechanism. An etch model with reaction at the liquid-vapor interface as the rate-limiting step is consistent with our experiments. These results identify a new mechanism to in situ tune the concentration of semiconductor atoms in the catalyst droplet.

Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor-β super family of secreted factors. A recent study showed that reduced GDF11 blood levels with aging was associated with pathological cardiac hypertrophy (PCH) and restoring GDF11 to normal levels in old mice rescued PCH.

To determine whether and by what mechanism GDF11 rescues aging dependent PCH.

Twenty-four-month-old C57BL/6 mice were given a daily injection of either recombinant (r) GDF11 at 0.1 mg/kg or vehicle for 28 days. link3 rGDF11 bioactivity was confirmed in vitro. After treatment, rGDF11 levels were significantly increased, but there was no significant effect on either heart weight or body weight. Heart weight/body weight ratios of old mice were not different from 8- or 12-week-old animals, and the PCH marker atrial natriuretic peptide was not different in young versus old mice. Ejection fraction, internal ventricular dimension, and septal wall thickness were not significantly different between rGDF11 and vehicle-treated animals at baseline and remained unchanged at 1, 2, and 4 weeks of treatment. There was no difference in myocyte cross-sectional area rGDF11 versus vehicle-treated old animals. In vitro studies using phenylephrine-treated neonatal rat ventricular myocytes, to explore the putative antihypertrophic effects of GDF11, showed that GDF11 did not reduce neonatal rat ventricular myocytes hypertrophy, but instead induced hypertrophy.

Our studies show that there is no age-related PCH in disease-free 24-month-old C57BL/6 mice and that restoring GDF11 in old mice has no effect on cardiac structure or function.

Our studies show that there is no age-related PCH in disease-free 24-month-old C57BL/6 mice and that restoring GDF11 in old mice has no effect on cardiac structure or function.