Objective : Lung cancer (LC) remains to be the most frequent cancer among male patients, nonsmall-cell lung cancer (NSCLC) is the most common type of LC. Here we aim to investigate the effect of Pro-b cell clonal enhancer factor (PBEF) on the growth of human NSCLC cells treated with hypoxia/reoxygenation (H/R). Methods : NSCLC A549 cells were divided into four groups: (1) control group; (2) model group; (3) model+ pCAGGS no-load control group; (4) model+ pCAGGS PBEF group. PCAGGS PBEF plasmid was constructed and transfected into the cells, and the expression of PBEF was detected by qPCR and WB, H/R model was constructed, western blot (WB) was used to detect the expressions of AQP1 and ENaC , and cell apoptosis was detected by flow cytometry. Results : Cell apoptosis ratio was higher in H/R model group than that of normal control group; there was no significant difference in apoptosis ratio between the model group and the no-load control group; while the apoptosis ratio in the overexpressed PBEF group was significantly higher than that of the no-load group. AQP1 and ENaC protein levels were significantly lower in the overexpressed PBEF group than the no-load group, while there was no significant difference among normal control group, the model group and the no-load group. Conclusion : Overexpression of PBEF promotes the apoptosis of H/R human NSCLC cells and inhibites the expression of AQP1 and ENaC proteins, indicating that PBEF may play potential adjuvant therapeutic role in the treatment of NSCLC.
To investigate the metastatic rate of segmental and/or sub-segmental lymph nodes and their roles in pathological staging after a major pulmonary resection.This prospective study recruited 90 cases of pulmonary resection performed at our department from February 2007 to February 2008. Hilar lymph nodes (No. 10), interlobar nodes (No. 11), lobar nodes (No. 12), segmental nodes (No. 13) and subsegmental nodes (No. 14) were resected and their clinic data analyzed.(1) The median number of total lymph nodes harvested, mediastinal nodes, nodes from No. 10-14 and nodes from No. 13-14 were 29 (11-50), 17 (6-35), 12 (2-26) and 4 (1-17) respectively. Lymph node metastatic rate from No.10, No. 11, No. 12, No. 13 + 14 were 12.2%, 6.7%, 23.3% and 38.9% respectively. (2) Forty-two cases of N0 and 27 cases of N1 were diagnosed in this group. The N1 subgroup included 12 cases of No. 13-14 metastasis solely and 15 cases of No. 10-12 and No. 13-14 metastasis simultaneously. If an analysis of No. 13-14 was omitted, the diagnostic accuracy of N0 could only reach 77.8% and 44.4% cases would be under-staged from N1. (3) In 33 cases of peripheral lung cancers smaller than 3 cm in diameter, 12.1% of metastatic lymph nodes from No.12-13 would be left in the original place if a segmental resection was performed. Similarly, 18.2% of metastatic lymph nodes could be neglected for wedge resection cases.Metastasis to segmental or subsegmental lymph nodes accounts for a large part of lung cancer patients. Therefore an analysis of these nodes can improve the accuracy of pathological staging. Secondly, limited pulmonary resection needs to follow a strict indication in consideration of the potential metastasis to segmental or subsegmental lymph nodes in peripheral small lung cancers.
With the continued development of RFID technology, a large number of RFID tags are being deployed having different protocols. Hence, a multiprotocol interrogator which can support all of these alternatives has become a design requirement for many systems. While multifunction capability may be implemented using a high performance DSP, CPU or FPGA, those solutions have a large area cost, so an innovative architecture is needed. Starting from an analysis of the algorithms in RFID systems, we propose a reconfigurable architecture for baseband processing to realize the various protocols in the ISO18000 standard. The structure has been specifically designed to support all of the functions needed, so that it performs very efficiently with low area cost. This design has been post-layout simulated with a clock frequency of up to 83 MHz, and the core area is 4 mm 2 in a UMC 0.18 mum CMOS process. Compared with other existing processors, the proposed architecture is much more efficient for this application area.
Objective
To explore the application value of the pathogen IgM antibody (IgM-Ab) and inflammatory indicators in the diagnosis of patients with respiratory tract infection (RTI).
Methods
We prospectively enrolled 1316 pateints with RTI from January to June 2016.Specimens from 557 patients were analyzed and compared the outcome of bacterial cuture and pathogen IgM-Ab detection of patients with bacterial infection (n=50), to those with viral(n=172), mycoplasma(n=112), virus-bacterial mixed infections (n=56), and with those of control group (n=180).
Results
Respiratory agents were detected in 936 (71.12%) of 1316 patients with RTI.A single agent was identified in 442 patients (47.22%), and multiple agents in 494 (52.78%). Positive bacterial culture results were obtained in 123 specimens (21.32%). Patients with virus-bacterial mixed infections had a significantly higher level of CRP than those with virus infection (Z=-3.070, P<0.05). We established that the mean level of PCT was statistically higher in patients with bacterial infection and those with virus-bacterial mixed infections than that in those with viral patients(Z=-5.512, -4.984, both P<0.05) and in those with mycoplasma infection(Z=-5.174, -5.654, both P<0.05). In patients with bacterial infection and those with virus-bacterial mixed infections, the positive rate of PCT were higher than that in patients with viral(χ2=30.286, 22.695, both P<0.05) and in those with mycoplasma infection (χ2=40.142, 31.156, both P<0.05). The area under receiver operating characteristic (ROC) curve was 0.751 for PCT, lager than that for CRP (P<0.05).
Conclusion
PCT levels are superior predictors for the diagnosis of bacterial RTI.PCT values combined with IgM-Ab is a fair way to evaluate the etiologic agents at the time of suspicion of RTI.
Key words:
Respiratory tract infection; C-reactive protein; White blood cells counting; Prealbumin; Procalcitonin
Angiotensin II is an important mediator of CKD of diverse etiology. A common pathologic feature of CKD is glomerular fibrosis, a central mediator of which is the profibrotic cytokine TGF- β . The mechanisms underlying the induction of TGF- β and matrix by angiotensin II are not completely understood. Recent studies showed that overexpression of the transcription factor SREBP-1 induces glomerular sclerosis and that angiotensin II can activate SREBP-1 in tubular cells. We thus studied whether SREBP-1 is activated by angiotensin II and mediates angiotensin II–induced profibrogenic responses in primary rat mesangial cells. Treatment of cells with angiotensin II induced the upregulation and activation of SREBP-1. Angiotensin II–induced activation of SREBP-1 required signaling through the angiotensin II type I receptor and activation of PI3K/Akt in addition to the chaperone SCAP and protease S1P. Notably, angiotensin II-induced endoplasmic reticulum stress was identified as a key mediator of Akt-SREBP-1 activation, and inhibition of endoplasmic reticulum stress or SREBP-1 prevented angiotensin II–induced SREBP-1 binding to the TGF- β promoter, TGF- β upregulation, and downstream fibronectin upregulation. Endoplasmic reticulum stress alone, however, did not induce TGF- β upregulation despite activating SREBP-1. Although not required for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of the SREBP-1 cotranscription factor Sp1, which provided a required second signal for TGF- β upregulation. In vivo , endoplasmic reticulum stress and SREBP-1-dependent effects were induced in glomeruli of angiotensin II-infused mice, and administration of the SREBP inhibitor fatostatin prevented angiotensin II–induced TGF- β upregulation and matrix accumulation. SREBP-1 and endoplasmic reticulum stress thus provide potential novel therapeutic targets for the treatment of CKD.
To establish a classification model and serum proteomic patterns in non-small cell lung cancer (NSCLC) patients with lymph node metastasis by surface enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS).The relative contents of serum proteins of 84 NSCLC patients with different N stages (35 N0 cases, 19 N1 and 30 N2 respectively) were detected by CM10 chip and SELDI-TOF-MS; two decision trees were generated to distinguish lymph nodes metastasis (N0 versus N1 + N2) and mediastinal lymph nodes metastasis (N0 + N1 versus N2) respectively.The model in which 50 patients were randomly chosen differentiated patients with lymph nodes metastasis from N0 patients with a sensitivity of 96.3%(26/27) and a specificity of 95.7%(22/23) in the training set, a following blind test was taken. Subsequently, compared with 49 patients with lymph node metastasis (N1 + N2), 15 patients with total negative lymph nodes (including lobar, segmental and subsegmental nodes necessarily) were defined as "true" N0 and were chosen to form a better predictive model with a 77.6% (38/49) sensitivity and a 93.3% (14/15) specificity respectively. And 6682.0Da, together with other five proteins, had significant difference between two groups; the result of this model for distinguishing the mediastinal lymph nodes metastasis is more accurate than thoracic CT analyses by Alongi F and many other clinical centers. It had a sensitivity of 80.0% (24/30) and a specificity of 77.8% (42/54) respectively.SELDI-TOF-MS showed a potential value for predicting lymph nodes metastasis in NSCLC patients. And further studies are required to confirm the models and identify the related proteins.
V(D)J recombination is initiated by a specialized transposase consisting of the subunits RAG-1 and RAG-2. The susceptibility of gene segments to DNA cleavage by the V(D)J recombinase is correlated with epigenetic modifications characteristic of active chromatin, including trimethylation of histone H3 on lysine 4 (H3K4me3). Engagement of H3K4me3 by a plant homeodomain (PHD) in RAG-2 promotes recombination in vivo and stimulates DNA cleavage by RAG in vitro. We now show that H3K4me3 acts allosterically at the PHD finger to relieve autoinhibition imposed by a separate domain within RAG-2. Disruption of this autoinhibitory domain was associated with constitutive increases in recombination frequency, DNA cleavage activity, substrate binding affinity, and catalytic rate, thus mimicking the stimulatory effects of H3K4me3. Our observations support a model in which allosteric control of RAG is enforced by an autoinhibitory domain whose action is relieved by engagement of active chromatin.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
