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Feb. 21), 1945. PATTEN 2,370,069
INFLATABLE BOAT Filed July 23, 1943 INVENTOR. Ffiffl F. P// fff/l ATTORNEY is out of the water.
Patented Feb. 20, 1945 INFLATABLE BOAT Fred F. Patten, Woonsocket, B. 1., assignor to United States Rubber Company, New York, N. Y.. a corporation of New Jersey Application July 23, 1943, Serial No. 495,819
7 Claim.
This invention relates to improved collamible boats and particularly to such boats having inflatable keels secured to the bottom of the boat.
Heretofore inflatable boats have been provided with keels constructed of fabric reinforced with rigid materials, such as struts of wood encased in pockets in the fabric. Keels of such prior construction do not provide the desired rigidity to the bottom of the boat because the reinforcing materials were made in sections and hinged together so that the keel could be folded. Furthermore, the rigid struts used in combination with the canvas presents a problem in collapsing and folding the boats into small packages, which may result in the tearing of the fabric and increasing the size of the folded boat.
The inflatable boat embodying the present invention is provided with an inflatable flexible keel, which is attached to the bottom of the boat. When the keel is deflated, it occupies a smaller space and is lighter than prior keels of the same effective size constructed of rigid materials. These advantageous characteristics facilitate the storage and transportation of the boat when it When the keel is inflated and is in the water, the inflated keel stiifens the boat, and thereby makes the boat easier to maneuver due to the decrease of the flow-resistance of the water against it and of any side slip of which there is a tendency to the latter when a sail and/or rudder is used. The inflatable keel also increases the buoyancy of the boat.
The foregoing and other objects of this invention will be more clearly understood by referring to the following description and accompanying drawing, in which:
Fig. i is a plan view of the boat embodying this invention;
Fig. 2 is a longitudinal side view of the boat shown in Fig. 1;
Fig. 3 is an enlarged cross-sectional view of the boat taken along line 3-3 of Fig. 1; and
Fig. d is an enlarged part of the view shown in Fig. 3.
Except as otherwise mentioned, the boat It illustrated in the drawings is made of flexible air impervious material, such as rubber or other air impervious synthetic coatings on canvas, and the parts are adhered together by the usual practice. The boat it is provided with a buoyant periphery ii comprising one or more inflatable tubular chambers it enclosed in walls or tubes it. A bottom it is secured to the buoyant periphcry 68 by cementing the bottom thereto in the manner.
As shown in the drawing, a tapering inflatable keel i5 is secured to the bottom H of the boat Ill. The keel I5 comprises an inflatable tube It which extends from the stem of the periphery II to the bow, and is cemented to the bottom ll of the boat along its longitudinal center line l1 (Fig. 1). The union between the bottom It and the tube I6 is reinforced by pairs of fabric hinges l8 extending longitudinally along each side of the tube It and having their wings I! and 20, respectively,
cemented to the bottom I4 and the tube It. Rig- I idity is imparted to the inflatable tube It and the union between the tube l8 and the bottom I! is further reinforced by a longitudinally extending fabric side stay 2|. The stay 2| embraces and is cemented to the tube It, and has its longitudinal edges 22 cemented to the bottom ll of the boat. The union of the edges 22 with the bottom I! is further reinforced by fabric hinges 23 having their wings cemented respectively to the bottom llandthestayfl.
Before applying the side stay 2| to the tube [6 a heavy longitudinal strip of fabric 24is cemented in a longitudinal told 25 in the side stay. The side stay 2| is then cemented to the tube. ll so that the fold 25 extends along the bottom of the tube l6 and forms a longitudinal fin 28 extending along the bottom of the keel, as shown in Fig. 2. The side stay 2| is provided with vent openings 21 on each side of the .tube It adjacent to th bottom ll so as to vent the spaces 28 between the tube and the stay. The purpose of venting this space is to prevent air from bein trapped in the spaces 28, so that the stay and the tube may be folded compactly. The vent openings 21 also admit water to the spaces 2%, which acts as a ballast.
Means is provided for inflating the tube it through a valve 29 which extends through the bottom IE or the boat and into the interior of the keel tube it. The valve is constructed so that the usual hand pump or CO2 bottle may be attached thereto for the purpose of inflating the tube through the bottom N of the boat It.
The remaining portion of the boat It may be of the usual construction, wherein the peripheral tube, or tubes l3 are made of fabric coated with natural rubber or other synthetic air impervious coating materials, and may be inflated through one or more valves similar to the valve 29. The boat is provided with an anchorage 30 in its bow 3| for securing a wooden mast 32 therein, to which a sail is adapted to be attached. The anchorage 30 comprises an upper fabric bracket 33 and a lower-socket 34, cemented respectively to the peripheral tube It and the bottom ll of the boat. A number of anchoring tabs 35 is cemented to the peripheral tube It for the purpose of bracing the sail mast 32 with guy ropes (not shown) secured to the mast 32 and the tabs 35. The usual oar locks 36 and rudder holder 31 are anchored to the tubes I3. The boat is also provided with inflatable canvas seats 38 which are anchored to the peripheral tubes I3 at each end.
The preferred form of this invention has been described more or less in detail herein. It will be understood that the details may be changed without departing from the spirit of the invention and the scope of the appended claims.
Having thus described my invention, what I claim and desire to protect by Letters Patent is:
1. An inflatable boat having a flat canvas bottom, 9. keel secured to the outside of said bottom, said keel comprising an inflatable fabric tube having its ends tapering from its intermediate portion and merging into the contour of the bottom portion of the boat at the ends thereof.
2. An inflatable canvas boat comprising an inflatable periphery, a flexible bottom secured to the inflatable periphery, an inflatable keel secured to the outside of said bottom, and means extending through said bottom and into said keel for inflating same.
3. An inflatable boat comprising an inflatable periphery, a flexible bottom secured to said perip'nery, an inflatable fabric keel including an inflatable tube extending longitudinally of said bottom and cemented thereto, a side stay embracing and cemented to said tube, and the edges of said side stay being secured to said bottom on each side of said tube.
4. An inflatable boat comprising an inflatable periphery, a flexible bottom secured to said periphery, an inflatable fabric keel comprising an inflatable fabric tube extending longitudinally of said bottom and cemented thereto, fabric hinges extending along each side of said tube and having one wing of each hinge cemented to said bottom and the other wing cemented to said tube, a side stay embracing and cemented to said tube, and the edges of said side stay being cemented to said bottom on each side of said tube.
5. An inflatable boat comprising a buoyant periphery, a flexible bottom secured to said periphery, an inflatable fabric keel secured to said bottom, said keel being reinforced by a longitudinal side stay embracing said keel and having its edges secured to said bottom on each side of said keel, and a fln extending along the bottom of said keel.
6. An inflatable collapsible boat comprising a buoyant periphery, a flexible bottom secured to said periphery. a keel including an inflatable tube secured to said bottom, said tube being reinforced by a side stay embracing said tube and having its edges secured to said bottom, a fin extending along the bottom of said tube and said fln comprising a longitudinal fold in said side stay.
7. An inflatable boat having a buoyant periphery, a. flexible bottom secured to said periphery, an inflatable keel extending longitudinally along the central portion of said bottom, said keel comprising an inflatable fabric tube secured to said bottom, a side stay for reinforcing said tube, said side stay being cemented to said tube and having its longitudinal edges cemented to the bottom of said boat on each side of said tube, and said side stay having openings formed therein adjacent to said bottom so as to vent the space between said side stay and said tube adjacent to said bottom.
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Publications (58)333.59 Total impact
Article: The elevated preoperative neutrophil-to-lymphocyte ratio predicts poor prognosis in intrahepatic cholangiocarcinoma patients undergoing hepatectomy.[Show abstract] [Hide abstract]
ABSTRACT: A high preoperative peripheral blood neutrophil-to-lymphocyte ratio (NLR) has been reported to be a predictor of poor survival in patients with various cancers. The aim of this study was to evaluate the predictive significance of the NLR in patients undergoing hepatectomy for intrahepatic cholangiocarcinoma (ICC). From 2005 to 2011, 322 patients who underwent hepatectomy for ICC were enrolled in this retrospective study. Clinicopathological parameters, including NLR, were evaluated to identify predictors of overall and recurrence-free survival after hepatectomy. The best cutoff for NLR was 2.49, and 177 of 322 patients (54.9 %) had an NLR ≥ 2.49. The 5-year survival rate after hepatectomy was 51.1 % in patients with NLR < 2.49 and 24.8 % in those with NLR ≥ 2.49 (P = 0.0001). Univariate analyses revealed that NLR was significantly associated with recurrence-free survival (RFS) and overall survival (OS; both P < 0.05). Multivariable analyses revealed that elevated NLR independently predicted poorer OS (P = 0.003, hazard ratio [HR] = 1.600). In summary, our results indicate that elevated NLR is a promising independent predictor of poor survival after hepatectomy in patients with ICC.
Article: PKM2 promotes metastasis by recruiting myeloid-derived suppressor cells and indicates poor prognosis for hepatocellular carcinoma.[Show abstract] [Hide abstract]
ABSTRACT: Pyruvate kinase M2 (PKM2) is a member of the pyruvate kinase family. Recent work has defined the "non-metabolic" functions of PKM2. However, the role of PKM2 in HCC remains unclear. To investigate the role of PKM2 in tumor growth, invasion and the prognosis of hepatocellular carcinoma (HCC), PKM2 expression was measured in HCC cell lines and tissues using qRT-PCR, western blot, and immunofluorescence assays. In in vitro experiments, PKM2 was knocked down using a short hairpin RNA lentivirus vector, and tumor cell behavior and the downstream signaling pathways and chemokine were analyzed. For the analysis of in vivo tumor growth, intratumoral and peritumoral lymphocyte infiltration were examined in nude mice. The prognostic value of PKM2 was analyzed by immunohistochemistry in two cohorts including 721 HCC patients. Together, our data obtained from cell lines, tumorigenicity studies, and primary HCC samples illustrate an oncogenic role for PKM2 in tumors. Moreover, PKM2 may serve as a novel prognostic indicator for HCC patients after curative resection, targeted therapy aimed at PKM2 may represent an effective treatment approach for HCC.Oncotarget 12/2014; · 6.63 Impact Factor
Article: High Levels of Hepatitis B Surface Antigen are Associated with Poorer Survival and Early Recurrence of Hepatocellular Carcinoma in Patients with Low Hepatitis B Viral Loads[Show abstract] [Hide abstract]
ABSTRACT: Purpose Recurrence is a disastrous outcome in patients with hepatitis-related hepatocellular carcinoma (HCC) who have undergone curative resection, and little is known about whether high levels of hepatitis B surface antigen (HBsAg) increase the risk of HCC recurrence. Patients and Methods This retrospective study included 1,360 HBsAg-positive postoperative HCC patients with hepatitis B viral (HBV) DNA levels Results We demonstrated that 1,000 IU/mL, but not 10 or 100 IU/mL, was a meaningful cutoff level for significantly discriminating these patients into an HBsAgLow group and an HBsAgHigh group based on correlations between the HBsAg level and liver cirrhosis (p = 0.028), tumor size (p = 0.039), and hepatitis B e antigen level (p Low group were significantly higher than those of HCC patients in the HBsAgHigh group. Accordingly, the 5-year recurrence-free survival (RFS) rates of patients in the HBsAgLow group were markedly higher than those of HCC patients in the HBsAgHigh group. The HBsAg level was a prognostic indicator for OS (p = 0.014) and RFS (p = 0.01). Conclusion HBsAg level is correlated with more aggressive tumor behavior and serves as a prognostic indicator in patients with surgically resected HCC with low HBV load.Annals of Surgical Oncology 10/2014; 22(3). DOI:10.1245/s10434-014-4043-5 · 3.94 Impact Factor
Article: Activating Mutations in PTPN3 Promote Cholangiocarcinoma Cell Proliferation and Migration and Are Associated With Tumor Recurrence in Patients[Show abstract] [Hide abstract]
ABSTRACT: Background & Aims Pathogenesis of intrahepatic cholangiocarcinoma (ICC), the second-most common hepatic cancer, is a poorly understood and its incidence is increasing worldwide. We searched for mutations in human ICC tumor samples and investigated how they affect ICC cell function. Methods We performed whole-exome sequencing of 7 paired ICCs and their surrounding, non-tumor tissues to detect somatic alterations. We then screened 124 pairs of ICC and non-tumor samples for these mutations, including 7 exomes. We compared mutations in PTPN3 with tumor recurrence in 124 patients, and PTPN3 expression levels with recurrence in 322 patients (the combination of both in 86 patients). The functional effects of PTPN3 variations were determined by RNA interference and transgenic expression in cholangiocarcinoma cell lines (RBE, HCCC-9810, and Huh28). Results Based on exome sequencing, pathways that regulate protein phosphorylation were among the most frequently altered in ICC samples, and genes encoding protein tyrosine phosphatases (PTPs) were among the most frequently mutated. We identified mutations in 9 genes encoding PTPs in 4/7 ICC exomes. In the prevalence screen of 124 paired samples, 51.6% of ICCs contained somatic mutations in at least 1/9 PTP genes; 41.1% had mutations in PTPN3.Transgenic expression of PTPN3 in cell lines increased cell proliferation, colony formation, and migration. PTPN3L232R and PTPN3L384H, which were frequently detected in ICC samples, were found to be gain-of-function mutations; their expression in cell lines further increased cell proliferation, colony formation, and migration. ICC-associated variants of PTPN3 had altered phosphatase activity. Patients whose tumors contained activating mutations or higher levels of PTPN3 protein than non-tumor tissues had higher rates of disease recurrence than patients without. Conclusions Using whole-exome sequencing of ICC samples from patients, we found that more than 40% contain somatic mutations in PTPN3. Activating mutations in and high expression levels of PTPN3 were associated with tumor recurrence in patients.Gastroenterology 05/2014; 146(5). DOI:10.1053/j.gastro.2014.01.062 · 12.82 Impact Factor
Article: High expression of 5-hydroxymethylcytosine and isocitrate dehydrogenase 2 is associated with favorable prognosis after curative resection of hepatocellular carcinoma.[Show abstract] [Hide abstract]
ABSTRACT: The expression of 5-hydroxymethylcytosine (5-hmC) and isocitrate dehydrogenase 2 (IDH2) is frequently downregulated in numerous cancers. 5-hmC and IDH2 expression in hepatocellular carcinoma (HCC) has yet to be determined. The immunohistochemical expression of 5-hmC and IDH2 were analyzed in tissue microarrays containing samples from 646 patients who had undergone hepatectomy for histologically proven HCC. The prognostic value of 5-hmC and IDH2 were evaluated by Cox regression and Kaplan-Meier analyses. We discovered that low 5-hmC and IDH2 expression was associated with malignant behaviors. Low 5-hmC or IDH2 expression alone and combined 5-hmC and IDH2 expression were associated with lower overall survival (OS) rates and higher cumulative recurrence rates. Multivariate analysis indicated that 5-hmC or IDH2 and 5-hmC/IDH2 were independent prognostic indicators for OS and time to recurrence (TTR), which was confirmed in an independent validation cohort. 5-hmC and IDH2 correlate with less aggressive tumor behavior in HCC. When 5-hmC and IDH2 are considered together, they serve as a prognostic marker in patients with surgically resected HCCs.Journal of Experimental & Clinical Cancer Research 04/2014; 33(1):32. DOI:10.1186/1756-9966-33-32 · 3.27 Impact Factor
Article: HNRNPAB Induces Epithelial-Mesenchymal Transition and Promotes Metastasis of Hepatocellular Carcinoma by Transcriptionally Activating SNAIL[Show abstract] [Hide abstract]
ABSTRACT: Expression of heterogeneous nuclear ribonucleoprotein AB (hnRNPAB) has been reported to be dysregulated in tumors but its specific contributions to tumor formation and progression are not fully understood. Here, we demonstrate that hnRNPAB is overexpressed in highly metastatic cells and tumor tissues from hepatocellular carcinoma (HCC) patients with recurrence. We found that hnRNPAB overexpression promoted epithelial-mesenchymal transition (EMT) in a manner associated with HCC metastasis in vitro and in vivo. RNAi-mediated silencing of the EMT factor Snail attenuated hnRNPAB-enhanced cell invasion in vitro and lung metastasis in vivo. Mechanistically, HnRNPAB acted to transactivate Snail transcription, which in turn inhibited transcription of the pivotal Snail target gene E-cadherin. Overexpression of hnRNPAB in HCC samples correlated with higher Snail levels, shorter overall survival and higher tumor recurrence. HnRNPAB overexpression, alone or in combination with Snail, was found to be a significant independent risk factor for recurrence and survival after curative resection. In conclusion, our findings define hnRNPAB as an activator of EMT and metastasis in HCC that predicts poor clinical outcomes.Cancer Research 03/2014; 74(10). DOI:10.1158/0008-5472.CAN-13-2509 · 9.28 Impact Factor
Article: Quantitative assessment of the effect of glutathione S-transferase genes GSTM1 and GSTT1 on hepatocellular carcinoma risk.[Show abstract] [Hide abstract]
ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most serious health problems worldwide. As in many other diseases, environment and genetic factors are believed to be involved in the pathogenesis of HCC. Numerous epidemiologic investigations including case-control and cohort studies have suggested the association of glutathione S-transferase (GST) genetic polymorphisms and HCC risk. However, some studies have produced conflicting results. Therefore, we performed an updated meta-analysis to clarify this inconsistency and to establish a comprehensive picture of the association of the polymorphisms of GSTM1 and GSTT1 with HCC susceptibility. We searched PubMed, Embase, ISI Web of Science, and CNKI databases to identify eligible studies meeting the inclusion criteria up to August 30, 2013. Odds ratios (ORs) and 95 % confidence intervals (CIs) were used to assess the strength of association. Finally, there were a total of 33 studies with 4,232 cases and 6,601 controls included in this meta-analysis. In the pooled analysis, significantly increased HCC risks were found for null genotype of GSTM1 (OR = 1.31, 95 % CI = 1.07-1.61, P = 0.010, P heterogeneity < 10(-5)) and GSTT1 (OR = 1.47, 95 % CI = 1.25-1.74, P < 10(-5), P heterogeneity < 10(-5)). Potential sources of heterogeneity were explored by subgroup analysis based on ethnicity, sample size, and source of control. Significant results were found among East Asians and Indians when stratified by ethnicity, while no evidence of significant associations was observed among Caucasian and African populations. In the gene-gene interaction analysis, a statistically significant increased risk for HCC was detected for individuals with combined deletion mutations in both genes compared to those with wild genotypes (OR = 1.88, 95 % CI = 1.41-2.50, P < 10(-4), P heterogeneity = 0.004). The present meta-analysis demonstrated that the GSTM1 and GSTT1 null genotype may be associated with an increased risk of HCC and that individuals having the combination of both defective GST genotypes may be more susceptible to developing HCC.Tumor Biology 01/2014; DOI:10.1007/s13277-013-1524-2 · 2.84 Impact Factor
Article: CXCL5 contributes to tumour metastasis and recurrence of intrahepatic cholangiocarcinoma by recruiting infiltrative intratumoural neutrophils.[Show abstract] [Hide abstract]
ABSTRACT: CXCL5 is a member of the CXC-type chemokine family that may play a role in carcinogenesis and cancer progression. This study investigates the biological function and clinical significance of CXCL5 in intrahepatic cholangiocarcinoma (ICC). We demonstrated that CXCL5 was overexpressed in ICC cell lines and tumour samples compared with paired normal tissues. CXCL5 had a direct chemoattractant effect on neutrophils in vitro through PI3K-Akt and ERK1/2 signalling pathways. In animal studies, CXCL5 promoted tumour growth and metastasis without altering in vitro proliferative and invasive ability of ICC cells, and this effect was mediated by the recruitment of intratumoural infiltrative neutrophils by tumour-derived CXCL5. Immunohistochemical analysis of ICC samples showed that overexpression of CXCL5 correlated strongly with intratumoural neutrophil infiltration, shorter overall survival, and high tumour recurrence. Multivariate analysis revealed that CXCL5 overexpression alone, or combined with the presence of intratumoural neutrophils, was an independent prognostic indicator for ICC. In conclusion, our data showed that CXCL5 promotes ICC growth and metastasis by recruiting intratumoural neutrophils. CXCL5 alone or combined with intratumoural neutrophils is a novel prognostic predictor for ICC patients and a potential therapeutic target.Carcinogenesis 11/2013; DOI:10.1093/carcin/bgt397 · 5.27 Impact Factor
Article: Autophagy inhibition suppresses pulmonary metastasis of HCC in mice via impairing anoikis resistance and colonization of HCC cells[Show abstract] [Hide abstract]
ABSTRACT: Metastasis is one of the main causes of poor prognosis for hepatocellular carcinoma (HCC), which has been linked to cell-death resistance. Autophagy is an important survival mechanism under conditions of cell stress. We hypothesized that autophagy may play a role in HCC metastasis due to its prosurvival effect. Highly metastatic HCC cell lines with stable autophagy inhibition were established via lentivirus-mediated silencing of BECN1 and ATG5 genes. Mouse models of pulmonary metastasis were then developed using the cells with or without autophagy inhibition. The analysis of lung metastasis by histopathological examination and small animal imaging showed that autophagy inhibition significantly decreased the incidence of pulmonary metastases in vivo. Further invasion, migration, detachment, lung colonization, and epithelial-mesenchymal transition (EMT) assays indicated that autophagy inhibition did not affect cell invasiveness, migration or EMT but attenuated the anoikis-resistance and lung colonization of HCC cells. Investigation of the molecular mechanisms underlying showed that the autophagy-inhibition-mediated anoikis-resistance attenuation was associated with the regulation of apoptotic signaling. As autophagy inhibition was shown to be able to suppress HCC metastasis, an autophagy-based HCC tissue-specific target therapy system (AFP-Cre/LoxP-shRNA) was constructed. In vitro and in vivo analyses showed that the system was able to efficiently inhibit autophagy of HCC cells and tissue in a tissue-specific manner. Further in vivo metastasis assay showed that intratumoral administration of the system could significantly suppress lung metastasis. Together, our findings suggest that autophagy may be involved in HCC metastasis through facilitating anoikis resistance and lung colonization of HCC cells. Autophagy-based HCC tissue-specific target therapy may be a new strategy for the management of HCC metastasis.Autophagy 10/2013; 9(12). DOI:10.4161/auto.26398 · 11.42 Impact Factor
Article: Margin-Infiltrating CD20(+) BCells Display an Atypical Memory Phenotype and Correlate with Favorable Prognosis in Hepatocellular Carcinoma[Show abstract] [Hide abstract]
ABSTRACT: The role of infiltrating B cells in hepatocellular carcinoma (HCC) has been overlooked for many years. This study is aimed to delineate the distribution, prognostic value and functional status of B cells in human HCC. Immunohistochemistry was used to investigate the distribution and clinical significance of infiltrating CD20+ B cells in a series of 120 HCC patients. The results were further tested in an independent series of 200 HCC patients. The functional status of CD20+ B cells was determined by flow cytometry, immunofluorescence and in vitro co-culture assay. Infiltrating CD20+ B cells were predominantly concentrated in the tumor invasive margin, compared to the peri-tumor and intra-tumor areas. High density of margin infiltrating B cells (MIL-Bs) positively correlated with small tumor size, absence of vascular invasion and increased density of CD8+ T cells (P<0.05). Survival analyses revealed that increased MIL-Bs and their penetration through the tumor capsule were significantly associated with improved overall and recurrence-free survival, and were identified as independent prognosticators for HCC patients (P<0.05). Importantly, the results were further validated in another independent HCC cohort. Moreover, we found that MIL-Bs featured an atypical memory phenotype (IgD-IgG+CD27-CD38-), expressed surface markers characteristic of antigen-presenting cells, possessed tumor-killing potential by producing IFN-γ, IL-12p40, granzyme B, TRAIL, and acted in cooperation with CD8+ T cells. The profile of CD20+ B cells in situ is a new predictor of prognosis for HCC patients and provides a novel target for an optimal immunotherapy against this fatal malignancy.Clinical Cancer Research 09/2013; 19(21). DOI:10.1158/1078-0432.CCR-12-3497 · 8.19 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Autophagy is an important adaptive survival mechanism, which has been postulated to be involved in cancer metastasis. The purpose of this study was to investigate autophagy in metastasis of hepatocellular carcinoma (HCC). Immunohistochemical analysis of autophagic activity in metastatic and paired primary HCC tissues using LC3 as autophagosome marker was performed in samples from 216 HCC patients diagnosed with metastasis (including 158 intravascular, 42 intrabiliary, 8 lymph node, 4 bone and 4 lung metastases). Then a mouse model of pulmonary metastasis was established using a highly metastatic HCC cell line (HCCLM3). Autophagy in pulmonary metastases and paired primary tumors were analyzed by LC3 immunohistochemistry, transmission electron microscopy (TEM) and western blot analysis. Further, mouse model of pulmonary metastasis and in vitro cell migration, invasion and detachment models were established using a stable GFP-LC3-expressing HCCLM3 cell line (HCCLM3-GFP-LC3). Autophagic alterations during metastatic colonization, migration, invasion and detachment were determined by GFP-LC3 analysis and western blot analysis. LC3 immunohistochemistry of metastases and primary tumors from HCC patients revealed significantly higher LC3 expression in metastases than primary HCC, which suggested a higher level of autophagy in HCC metastases. Further immunohistochemical, TEM, western blot and in vivo GFP-LC3 analyses of lung metastases and primary tumors in mouse model of pulmonary metastasis confirmed that metastatic colonies displayed higher level of autophagy than primary tumors and the early metastatic colonies displayed highest level. The dynamic monitoring of autophagy in cell migration, invasion and detachment showed that autophagy did not significantly alter in those processes. Autophagy is activated in metastatic colonization but not in invasion, migration and detachment of HCC cells. Autophagy may play a role in HCC metastasis via promoting metastatic colonization of HCC cells.PLoS ONE 09/2013; 8(9):e74407. DOI:10.1371/journal.pone.0074407 · 3.53 Impact Factor
Article: αB-Crystallin complexes with 14-3-3ζ to induce epithelial-mesenchymal transition and resistance to sorafenib in hepatocellular carcinoma.[Show abstract] [Hide abstract]
ABSTRACT: The overall survival of patients with hepatocellular carcinoma (HCC) remains poor, and the molecular pathogenesis remains incompletely defined in HCC. Here, we report that increased expression of αB-Crystallin in human HCC predicts poor survival and disease recurrence after surgery. Multivariate analysis identifies αB-Crystallin expression as an independent predictor for postoperative recurrence and overall survival. We unveil that elevated expression of αB-Crystallin promotes HCC progression in vivo and in vitro. We demonstrate that αB-Crystallin overexpression fosters HCC progression by inducing epithelial-mesenchymal transition (EMT) in HCC cells through activation of the ERK cascade, which can counteract the effect of sorafenib. αB-Crystallin complexes with and elevates 14-3-3ζ protein, leading to up-regulation of ERK1/2 activity. Moreover, overexpression of αB-Crystallin in HCC cells induces EMT progression through an ERK1/2/Fra-1/slug signaling pathway. Clinically, our data reveal that overexpression of both αB-Crystallin and 14-3-3ζ correlates with the HCC poorest survival outcomes, and sorafenib response is impaired in patients with αB-Crystallin overexpression. Conclusions: These data suggest that the αB-Crystallin-14-3-3ζ complex acts synergistically to promote HCC progression by constitutively activating ERK signaling. This study reveals αB-Crystallin as a potential therapeutic target for HCC and a biomarker for predicting sorafenib treatment response. (HEPATOLOGY 2013.).Hepatology 06/2013; DOI:10.1002/hep.26255 · 11.19 Impact Factor
Article: Genetic Polymorphism of the Kinesin-Like Protein KIF1B Gene and the Risk of Hepatocellular Carcinoma[Show abstract] [Hide abstract]
ABSTRACT: BACKGROUND: Frequent deletions of the kinesin-like protein gene 1B (KIF1B) have been reported in neural tumors. Recently, a genome-wide association study revealed an association between polymorphisms in the KIF1B gene and the risk of hepatocellular carcinoma (HCC), and several case-control studies have further investigated this relationship. However, these studies have yielded controversial results. We therefore performed a meta-analysis to derive a more precise estimation of the association between the KIF1B gene polymorphisms and HCC risk. METHODOLOGYPRINCIPAL FINDING: PubMed, EMBASE, the ISI Web of Science and the CNKI databases were systematically searched to identify relevant studies. A total of 5 studies containing 13 cohorts with 5,773 cases and 6,404 controls were included. Odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were used to assess the strength of the associations. Subgroup analyses were conducted based on ethnicities, sample sizes and quality scores. Overall, the G allele at rs17401966 of the KIF1B gene was associated with a significantly decreased risk for HCC (OR = 0.81, 95%CI: 0.70-0.93; P = 0.003). Furthermore, subgroup analyses showed that the G allele at rs17401966 of the KIF1B gene significantly reduced the risk for HCC in Chinese cohorts (OR = 0.76, 95%CI: 0.64-0.90; P = 0.002), large-sample-size cohorts (OR = 0.80, 95%CI: 0.73-0.88, P<0.01) and high-quality cohorts (OR = 0.78, 95%CI: 0.71-0.87, P<0.01). However, no significant associations were found in small-sample-size cohorts, studies with low-quality scores and when excluding the cohorts from the study reporting the original discovery. CONCLUSIONSIGNIFICANCE: These findings demonstrate that the presence of the G allele at rs17401966 of the KIF1B gene may decrease the risk for HCC and suggest that KIF1B may play a critical role in the development of HCC. High-quality studies with larger sample sizes and different ethnic populations will be of great value to further confirm these findings.PLoS ONE 04/2013; 8(4):e62571. DOI:10.1371/journal.pone.0062571 · 3.53 Impact Factor
Article: Alpha-Fetoprotein Promoter-Driven Cre/LoxP-Switched RNA Interference for Hepatocellular Carcinoma Tissue-Specific Target Therapy.[Show abstract] [Hide abstract]
ABSTRACT: BACKGROUD: RNA interference (RNAi) has recently emerged as a potential treatment modality for hepatocellular carcinoma (HCC) therapy, but the lack of cellular targets and sustained efficacy limits its application. The purpose of this study is to develop an HCC tissue-specific RNAi system and investigate its possibility for HCC treatment. Two different HCC-specific RNAi systems in which therapeutic miRNA or shRNA against target gene (Beclin 1) was directly or indirectly driven by alpha-fetoprotein promoter (AFP-miRNA and AFP-Cre/LoxP-shRNA) were constructed. Human HCC cell lines (HepG2, Hep3B and HCCLM3) and non-HCC cell lines (L-02, Hela and SW1116) were infected with the systems. The effectiveness and tissue-specificity of the systems were examined by Q-PCR and western blot analysis. The efficacy of the systems was further tested in mouse model of HCC by intravenous or intratumoral administration. The feasibility of the system for HCC treatment was evaluated by applying the system as adjuvant therapy to enhance sorafenib treatment. An AFP-Cre/LoxP-shRNA system targeting Atg5 gene (AFP-Cre/LoxP-shRNA-Atg5) was constructed and its efficacy in sensitizing HCC cells (MHCC97L/PLC) to sorafenib treatment was examined by apoptosis assay and tumorigenesis assay . The AFP-miRNA system could silence target gene (Beclin 1) but required a high titer which was lethal to target cells. The AFP-Cre/LoxP-shRNA system could efficiently knockdown target gene while maintain high HCC specificity. Intratumoral injection of the AFP-Cre/LoxP-shRNA system could efficiently silence target gene (Beclin 1) while intravenous administration could not. The AFP-Cre/LoxP-shRNA system target Atg5 gene could significantly sensitize MHCC97L/PLC cells to sorafenib-induced apoptosis and tumor growth suppression . An efficient HCC tissue-specific RNAi system (AFP-Cre/LoxP-shRNA) was successfully established. The system provides a usable tool for HCC-specific RNAi therapy, which may serve as a new treatment modality for HCC.PLoS ONE 02/2013; 8(2):e53072. DOI:10.1371/journal.pone.0053072 · 3.53 Impact Factor
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ABSTRACT: Hepatocellular carcinoma (HCC) is considered to be a fatal disease because of its late diagnosis, underlying liver disease, and refractoriness to systemic treatments. Biomarkers with high sensitivity and specificity that are minimally invasive, reproducible, and easily available have important clinical utility for early diagnosis, prognostication, and pharmacodynamics evaluation. Until now, most of the circulating HCC biomarkers used in clinical practice were protein molecules. However, these biomarkers often had low sensitivity and specificity. In the past decade, circulating cell-free nucleic acids (cfNAs) have been extensively studied. We review the studies that evaluated cfNAs as circulating HCC biomarkers and discuss recent advances with regard to their diagnostic and prognostic significance.Seminars in Oncology 08/2012; 39(4):440-8. DOI:10.1053/j.seminoncol.2012.05.013 · 3.94 Impact Factor
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ABSTRACT: Autophagy is a lysosomal degradation pathway that can degrade bulk cytoplasm and superfluous or damaged organelles, such as mitochondria, to maintain cellular homeostasis. It is now known that dysregulation of autophagy can cause pathogenesis of numerous human diseases. Here, we discuss the critical roles that autophagy plays in the pathogenesis of liver diseases such as non-alcoholic and alcoholic fatty liver, drug-induced liver injury, protein aggregate-related liver diseases, viral hepatitis, fibrosis, aging and liver cancer. In particular, we discuss the emerging therapeutic potential by pharmacological modulation of autophagy for these liver diseases.Pharmacological Research 07/2012; 66(6). DOI:10.1016/j.phrs.2012.07.003 · 3.98 Impact Factor
Article: Overexpression of HnRNP A1 promotes tumor invasion through regulating CD44v6 and indicates poor prognosis for hepatocellular carcinoma[Show abstract] [Hide abstract]
ABSTRACT: Heterogeneous ribonucleoprotein (hnRNP) A1 is a member of the A/B subfamily of ubiquitously expressed hnRNPs, which have a wide variety of functions in gene expression and signal transduction. To investigate the biological function and clinical significance of hnRNP A1 in hepatocellular carcinoma (HCC), we measured hnRNP A1 expression in four HCC cell lines and two independent cohorts of HCC patients. We found that hnRNP A1 was overexpressed in the highly metastatic HCC cell lines and in tumor tissues of patients with recurrent HCC. Knockdown of hnRNP A1 in highly metastatic HCC cells caused a significant decrease in cell invasion, while upregulation of hnRNP A1 in poorly metastatic HCC cells led to a significant increase in their invasive capacity. We found that this effect may occur through the regulation of CD44v6 expression by hnRNP A1 in HCC cells. Both quantitative reverse transcription-polymerase chain reaction (qRT-RCR) and immunohistochemistry revealed that hnRNP A1 was upregulated in HCC tissues and coincided with overexpression of CD44v6. HCC patients with high hnRNP A1 tended to have higher levels of CD44v6, shorter overall survival (OS) and higher rates of tumor recurrence. Multivariate analyses revealed that hnRNP A1 alone or in combination with CD44v6 were independent prognostic indicators for OS and time to recurrence and have potential as therapeutic targets. In conclusion, overexpression of hnRNP A1 promotes HCC invasion by regulating the level of CD44v6 and indicates a poor prognosis for HCC patients after curative resection.International Journal of Cancer 07/2012; 132(5). DOI:10.1002/ijc.27742 · 6.20 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Epigenetic changes refer to stable alterations in gene expression with no underlying modifications in the genetic sequence itself. It has become clear that not only gene variations but also epigenetic modifications may contribute to varied diseases, including cancer. This review will provide an overview of how epigenetic factors, including genomic DNA methylation, histone modifications, and miRNA regulation, contribute to hepatocellular carcinoma (HCC) dissemination, invasion, and metastasis. Additionally, the reversal of dysregulated epigenetic changes has emerged as a potential strategy for the treatment of HCC, and we will summarize the latest epigenetic therapies for HCC.Chinese medical journal 07/2012; 125(13):2349-60. · 1.02 Impact Factor
Article: Serum DKK1 as a protein biomarker for the diagnosis of hepatocellular carcinoma: a large-scale, multicentre study.[Show abstract] [Hide abstract]
ABSTRACT: Hepatocellular carcinoma (HCC) is prevalent worldwide and improvements in timely and effective diagnosis are needed. We assessed whether measurement of Dickkopf-1 (DKK1) in serum could improve diagnostic accuracy for HCC. We analysed data for patients with HCC, chronic hepatitis B virus (HBV) infection, liver cirrhosis, and healthy controls, recruited from two Chinese centres between December, 2008, and July, 2009. A validation cohort matched for age and sex was recruited from another centre in China between July, 2010, and June, 2011. DKK1 was measured in serum by ELISA by independent researchers who had no access to patients' clinical information. We used receiver operating characteristics (ROC) to calculate diagnostic accuracy. We assessed serum DKK1 in 831 participants: 424 with HCC, 98 with chronic HBV infection, 96 with cirrhosis, and 213 healthy controls. The validation cohort comprised 453 participants: 209 with HCC, 73 with chronic HBV infection, 72 with cirrhosis, and 99 healthy controls. Levels of DKK1 in serum were significantly higher in patients with HCC than in all controls. ROC curves showed the optimum diagnostic cutoff was 2·153 ng/mL (area under curve [AUC] 0·848 [95% CI 0·820-0·875], sensitivity 69·1%, and specificity 90·6% in the test cohort; 0·862 [0·825-0·899], 71·3%, and 87·2% in the validation cohort). Similar results were noted for early-stage HCC (0·865 [0·835-0·895], 70·9%, and 90·5% in the test cohort; 0·896 [0·846-0·947], 73·8%, and 87·2% in the validation cohort). Furthermore, DKK1 maintained diagnostic accuracy for patients with HCC who were α-fetoprotein (AFP) negative (0·841 [0·801-0·882], 70·4%, and 90·0% in the test cohort; 0·869 [0·815-0·923], 66·7%, and 87·2% in the validation cohort), including for patients with early-stage HCC (0·870 [0·829-0·911], 73·1%, and 90·0% in the test cohort; 0·893 [0·804-0·983], 72·2%, and 87·2% in the validation cohort), compared with all controls. Raised concentrations of DKK1 in serum could differentiate HCC from chronic HBV infection and cirrhosis (0·834 [0·798-0·871], 69·1%, and 84·7% in the test cohort; 0·873 [0·832-0·913], 71·3%, and 90·6% in the validation cohort). Moreover, measurement of DKK1 and AFP together improved diagnostic accuracy for HCC versus all controls compared with either test alone (0·889 [0·866-0·913], 73·3%, and 93·4% in the test cohort; 0·888 [0·856-0·920], 78·5%, and 87·2% in the validation cohort). DKK1 could complement measurement of AFP in the diagnosis of HCC and improve identification of patients with AFP-negative HCC and distinguish HCC from non-malignant chronic liver diseases. National Key Basic Research Programme of China, National Key Sci-Tech Special Projects of Infectious Diseases, National Natural Science Foundation of China, Research Fund for the Doctoral Programme of Higher Education of China.The Lancet Oncology 06/2012; 13(8):817-26. DOI:10.1016/S1470-2045(12)70233-4 · 25.12 Impact Factor
Article: CXCR6 Upregulation Contributes to a Proinflammatory Tumor Microenvironment That Drives Metastasis and Poor Patient Outcomes in Hepatocellular Carcinoma[Show abstract] [Hide abstract]
ABSTRACT: CXC chemokines and their cognate receptors have been implicated widely in cancer pathogenesis. In this study, we report a critical causal relationship between CXCR6 expression and tumorigenesis in the setting of human hepatocellular carcinoma (HCC). Among the CXC chemokine receptors, only CXCR6 was detected in all the hepatoma cell lines studied. Moreover, in HCC tissue, CXCR6 expression was significantly higher than in noncancerous liver tissues. Reduction of CXCR6 or its ligand CXCL16 in cancer cells reduced cell invasion in vitro and tumor growth, angiogenesis, and metastases in vivo. Importantly, loss of CXCR6 led to reduced Gr-1+ neutrophil infiltration and decreased neoangiogenesis in hepatoma xenografts via inhibition of proinflammatory cytokine production. Clinically, high expression of CXCR6 was an independent predictor of increased recurrence and poor survival in HCCs. Human HCC samples expressing high levels of CXCR6 also contained an increased number of CD66b+ neutrophils and microvessels, and the combination of CXCR6 and neutrophils was a superior predictor of recurrence and survival than either marker used alone. Together, our findings suggest that elevated expression of CXCR6 promotes HCC invasiveness and a protumor inflammatory environment and is associated with poor patient outcome. These results support the concept that inhibition of the CXCR6-CXCL16 pathway may improve prognosis after HCC treatment.Cancer Research 06/2012; 72(14):3546-56. DOI:10.1158/0008-5472.CAN-11-4032 · 9.28 Impact Factor
Top Journals
- PLoS ONE (6)
- Clinical Cancer Research (5)
- Hepatology (4)
- Cancer Research (3)
- Autophagy (3)
Fudan University
Shanghai, Shanghai Shi, China
- Institutes of Biomedical Sciences
Moffitt Cancer CenterTampa, Florida, United States
Zhongshan UniversityShanghai, Shanghai Shi, China


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Youth Grants 2015
Westmeath Community Development -LCDP Youth Grants 2015
WCD are pleased to announce their Youth grants scheme for 2015
Applications are invited from youth groups/organisations who are working with young people aged 10-25 in either Athlone/Mullingar RAPID areas or other designated rural disadvantaged areas in Westmeath covered by the LCDP.
Eligible activities that groups can apply for are:
- Development of facilities where young people can meet in informal relaxed settings. These could include Youth cafes and drop in centres.-Can include equipment and materials which must be NEW.
- Educational activities/ Arts and music workshops/After school projects contributing to life long learning
- Support for Comhairle Na Og as a mechanism for linking into the views, opinions and ideas of young people in Co Westmeath.
- Once off events will be considered, providing they are new initiatives and have a focus on reducing poverty and social exclusion.
Grant monies available are between €1,000- €2,500 per project:
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Brainerd City Council: City attorney to retire
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If you insist on putting a label on me, I prefer Granite Stater
To The Daily Sun,
As a candidate for state representative, I expect to have people debate and discuss the issues, even when we disagree. It's quite unfortunate that people who don't even know me would try to disparage me through the use of meaningless labels and fear-mongering. But if you must use a label, I prefer Granite Stater.
Most folks around here consider themselves to be independent-minded politically. In New Hampshire, more people are registered to vote as independent/unaffiliated than either Republican or Democrat. So readers of this newspaper do not respond well to name-calling and scare tactics. Labels such as "tea party" and "right wing" have all but lost any significance for most people.
For my part, I prefer to speak about guiding principles, such as a preference for government that protects people's rights. Or one that lives within its means, by reducing spending on unnecessary bureaucracy. Or a state Legislature that honors constituents and taxpayers by adhering to the Constitution and promoting private charity, property rights, and the concept of personal responsibility.
My wife, Marie, and I, along with our two Labs, Lola and Raven, moved to New Hampshire from New Jersey (can you blame me?) after visiting and exploring the state for a number of years to make sure we were making the right decision. Our state is a destination for people who appreciate and understand the benefits of freedom. More than 60 percent of New Hampshire residents were born outside the state. Twenty-five percent moved here from Massachusetts. Unlike those who want to change it by passing ever-more restrictions on our freedoms, I simply want to help protect the "Live Free or Die" tradition and keep New Hampshire awesome.
As a member of the Central New Hampshire Amateur Radio Club I've enjoyed meeting many of our neighbors while volunteering at public service and charity events like the Laconia Sled Dog Derby, Meredith Book-It! Road Race and the upcoming Meredith Bay Trick or Trot 5K, and by organizing regular litter pick-up outings along Route 3 in Belmont from the Mosquito Bridge to the Laconia town line.
Leadership should be by example, not by trying to knock down those with whom you disagree politically. If elected to the state House, I'll do my best to follow the above principles and to represent your interests in Concord. Thank you in advance for your vote on Nov. 4.
Glen Aldrich
Candidate for State Representative – Gilford and Meredith
Last Updated on Wednesday, 22 October 2014 11:31
Hits: 215
Scott Brown whining about negative ads is pot calling kettle black
To The Daily Sun,
Most of us shop around, for the best buy on a car, a TV, and other big purchases. Scott Brown shopped around for a state. He packed his carpetbag, drove to New Hampshire, and is trying to buy a U.S. Senate seat. He's doing this by relying on at least $8 million from outside interests and by dishonestly pretending to be someone he isn't.
His record shows that Scott Brown is an empty-headed kept boy who does the bidding of whoever is paying him. First were Wall Street banks, on whose behalf he helped water down new bank regulations and held a bill hostage until he was able to give them a $19 billion exemption. After its passage he continued to try to weaken the law's consumer protections. In return, Brown received more campaign contributions from financial institutions than any other candidate in 2012.
He is also an errand boy for the oil industry, supporting loopholes and $24 billion in tax subsidies for corporations that are already among the most profitable in the world. In 2012 he said with a straight face that "oil companies don't get subsidies... I'm positive," even though they do and he voted to protect them.
After the voters of Massachusetts turned him out of office he received over $1 million in stock for joining the board of directors and lending his name to a shady firm that was attempting to attract investors. This business was a beauty supply company that claimed to be an arms manufacturer. In reality it had no factories, no products, no trademarks, no revenue and was run by executives who had been sued for securities fraud. It wasn't even listed in the building that it claimed as its address. After this came to light, Brown was forced to resign from the board.
Now, as a candidate in New Hampshire. he is giving us a compost pile worth of cliché's, double talk, and claims contradicted by his own actions and votes.
Running in New Hampshire he opposes "magnets" for illegal immigrants "like in-state tuition for illegals," despite having voted for in-state tuition for undocumented students when he was in the Massachusetts Senate.
He suddenly imagines himself to be an expert on national security, but he's only grandstanding. First he misrepresents his military experience. Now Brown is emphasizing border security, apparently thinking we are about to be overrun by Ebola-infected terrorists from Mexico. Yet when he was in the U.S. Senate he skipped all of his committee and subcommittee hearings on border security. He also opposed a bipartisan immigration reform bill supported by Sen. Ayotte as well as Sen. Shaheen which included increased border security.
He wants us to believe he will protect women's health care. The evidence says the opposite. The facts are that he co-sponsored a Senate amendment to give employers the right to deny birth-control coverage — as well as any kind of healthcare coverage — to women. He also co-sponsored and voted for legislation in Massachusetts to create roadblocks for a woman's right to choose — a bill supported by anti-choice groups, who also endorsed Brown when he ran for re-election. Quite simply, those organizations do not endorse someone who is pro-choice.
He claims he favors more jobs, with "decent pay" and "annual raises." But he voted for tax breaks for companies to send jobs overseas, He received over $250,000 to serve on the board of directors of a company that sends jobs abroad, then tried to claim that he didn't know that the firm was doing this, despite the fact that he signed legal documents for the SEC endorsing its outsourcing strategy. Brown also voted multiple times against extending unemployment benefits, opposes raising the minimum wage and has voted against equal pay for women.
In Massachusetts he said that climate change was real and partly man-made. In New Hampshire he said that man-made climate change isn't proven. Then a few days ago, he said it is. Whiplash and flip-flop. And for someone who claims to support education he voted to cut Pell Grants to college students and to cut Head Start for pre-schoolers.
Now he is whining that Sen. Shaheen runs negative ads. This is Scott Pot calling the kettle black. Has anyone seen any ads of his that aren't purely attacks on Jeanne Shaheen? Bonus points if you've seen any Brown ad that presents specific policies or programs that he will support. He said only that he would save the government money by going after "waste, fraud, and abuse," which is the lazy cliché used for years by candidates who have no idea what to do.
Brown knows little about, and cares little about, New Hampshire The only thing Scott Brown cares about is Scott Brown. His history shows that he is motivated by two things: His own career advancement, and his bank balance. He will say anything to try to get himself elected. His campaign has consisted of distortions, convenient memory lapses, and hypocrisies. At best he's confused, at worst dishonest. Scott Brown can be summed up in one phrase: "Empty Head, Empty Suit."
Ed Allard
Last Updated on Wednesday, 22 October 2014 11:26
Hits: 139
Lisa DiMartino has all the qualities I look for in a public servant
To The Daily Sun,
The most basic character qualities I look for in candidates for public office are honesty, integrity, and the ability to treat all people with respect and dignity, including those with whom they have differences of opinion. The absence of any of the three is a sign that the quality will be absent in public life, and will not get my support.
Following closely on my search for these qualities in elected officials are two other requirements: the demonstrated ability to think critically and to interact with political opponents in a manner that finds solutions to public problems.
A person who thinks critically starts with an open mind by genuinely listening to all views that constituents want to have considered. Listening and open-mindedness are lifelong skills most people must work to develop and perfect. Those lacking the skill are busy thinking what to say when they get the chance, then are engaged in pouring their own biases on the other person.
Critical thinking involves more than just listening. It centers on engaging in the evaluation of alternative points of view, doing true research, and working out conclusions about solving a problem. Many people bypass this step and substitute a process of arriving at a conclusion by drawing only on their own biases. This results in largely discarding research and the views of others. Often they also eliminate the listening step. So many letters to the editor do exactly this, with an air of being authentic. Wow!
Solutions, to the contrary, requires finding common ground in an environment of the pet views of those in the conversation, and doing true research to find what has happened in the past and suggested for the future. I do not want candidates who only support my views because I know there are even better solutions available to those who listen, do their homework, and find common ground. The very essence of democracy requires elected officials to listen, find better answers, and not to be blinded by their own biases or bought by high bidders. And today our democracy is being beaten to death by those professing to love her.
Further, I want my elected officials, after engaging in critical thinking and allowing common ground to emerge, to vote their own unbiased position and to allow the solution to be tried in real life. All solutions will not be proven good in real time and can be improved in the future. Even then, I will honor a candidate who is a critical thinker but can admit s/he would not vote that way again. That is proof of critical thinking and does not deserve punishment.
It is apparent, in our county, state and nation that many elected officials do not know how to govern.
If in our families we are wedded to unproven biases and we keep poking each other in the nose, the family will break down. Our political system majors in fielding unproven philosophies and in poking the opposition in the nose or worse. The truth is that both sides have caring and intelligent people who deserve respect from each other — and energies focused on finding the common ground and acting out solutions that can be changed in the future if not successful.
These, then, are the qualities I look for in elected officials. I am a registered independent voter and look to both parties for this kind of candidate: Honest, with integrity, and respect for all people, including those in opposition parties. I honor critical thinking and the focus on finding common ground, and not punishing nor demonizing those who hold different views than my own.
For this reason, I will vote for Lisa DiMartino. She demonstrates all the qualities I seek, and has proven herself in a very unfortunate political battle in Belknap County. She is intelligent, does her homework, and wants to find alternate solutions to community problems. She wants to engage in respectful dialogue with fellow officials to find even better solutions than she started with. She offers herself for re-election genuinely dedicated to public service. What a prize!
We need dozens more elected officials with the qualities Lisa lives out. Thus I am scanning the other candidates in our district to decide who else to vote for. And finally, I urge all voters in Belknap County to elect the candidates with these qualities who can solve our county's very severe problems. This requires all of us to reach beyond our own political biases and party loyalties. I cannot possibly vote a straight-party ticket because I find candidates best qualified on both sides. Please think critically and please vote.
Miller C. Lovett
Last Updated on Wednesday, 22 October 2014 10:08
Hits: 89
George Hurt will bring leadership and fresh ideas to legislature
To The Daily Sun,
In this time of economic hardship. The November election is a critical time for both the county and state. Because of the redistricting two years ago Gilford is now combined with Meredith.
This leads me to the real point of this letter. As a citizen and voter of Gilford, I am pleased there is a credible candidate from Gilford who is running for one of the four seats to represent us in Concord and at the county level as well. George Hurt, a resident of Gilford for over 30 years and a local business man, is the candidate whom I believe will represent all of us when it comes to budget matters and protecting our constitutional freedoms.
I have known George for 15 years and I have known him to be a very honest man that cares about not just our town, but also the future of our state and nation. He enlightens me on some issues that I may not have known about. I cannot think of a time when we did not discuss politics and current events. I always come away from these discussions feeling like we need more people like George in our government. He really cares and he has great ideas.
I know for certain, he is opposed to any broad-base tax and any attempt to abridge our Second Amendment rights. I also know, because of his strong business background. He is focused on legislation that will start the process of creating jobs through a less regulated business environment and a tax-friendly climate.
I find his thinking well-grounded and reasonable, which I cannot say for our current Democrat representative from Gilford.
George will bring leadership and fresh ideas to the legislative process and I am looking forward to Nov. 4 when I can cast my vote for a hard-working and honest individual that will protect the economic future of our families and communities.
Jean M. Ferreira
Last Updated on Wednesday, 22 October 2014 09:49
Hits: 93
Seeking publicc's help in making WRHS's 75th Anniversary special
To The Daily Sun,
The Winnisquam Regional High School History Club is a place where you can spread your patriotic excitement and contribute ideas freely within the school community. History Club is where important projects are created to better the school community through the use of educational activities. This year is one of the most important as we celebrate the 75th anniversary of Winnisquam Regional High School.
The school was dedicated on Jan. 24, 1940, so our club is focusing on this anniversary over the current school year. Students and advisers generated the idea to take a videoed tour of the school and interview community members who were former students or teachers to get their reflections on what the school used to be like and demonstrate how it has changed. The club plans to do other related projects throughout the year related to this anniversary celebration.
Aine Foley & Sydni Chapman
Class of 2017 & WRHS History Club members
Denise Lessard
Social Studies Teacher/History Club Advisor
Last Updated on Wednesday, 22 October 2014 09:46
Hits: 79


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Friday, February 18, 2011 - 12:00 PM Source: SportsFanAuthor: Steve Lavell
Those with even a cursory interest in the NBA would be aware of the exploits of 21-year-old Blake Griffin, who has taken the league by storm in his rookie season.
The fact that Griffin, the No.1 pick in the 2009 NBA Draft, spent his first year on the LA Clippers roster recovering from a broken kneecap has only heightened his arrival.
He's posting numbers (22.6 points and 12.6 rebounds per game) to match the premier power forwards, while his 47 points against Indiana last month remains the equal second-highest score for any player in 2010-11.
Inevitably, when Griffin comes out of contract at the end of next season, rival teams will come for him, and come hard.
At this rate, expect a tug of war similar to the one that sent LeBron James spiralling to Miami after seven seasons at Cleveland.
But we say Griffin should be a Clipper for life (or until he's 30 at least). Here's why.
1. He's been loyal until now, so why change?
Born and bred in Oklahoma City, Griffin emerged from high school as one of the best young players in the country. Despite offers to join high-profile basketball colleges including Duke, North Carolina, Michigan State and Kansas, he followed older brother Taylor to the University of Oklahoma. Griffin led the Sooners to the Sweet 16 in his second year there, and was named the Naismith College Player of the Year. The prestigious John R. Wooden Award was among the other achievements that spurred his nomination for the draft, despite two more years' college eligibility.
2. He should be the best player in Clippers history by the time he's 23
This says as much about Griffin as it does his franchise, which has made the playoffs just seven times since it entered the NBA as the Buffalo Braves in 1970. Bob McAdoo set the early standard as the league's rookie of the year (1972-73) and MVP (1974-75). From the true Clippers era (1984 onwards), throw a blanket over Danny Manning, Elton Brand and Corey Maggette – with Charles Smith at a stretch – for who Griffin is up against. Wow. The Clippers can also count Hall of Famers Adrian Dantley and Bill Walton among their alumni, but their best 'ball was played elsewhere.
3. He could stick it to the Lakers, and from within Los Angeles
So much for a cross-town rivalry; since 1984 the star-studded Lakers have won more championships (eight) than the Clippers have made playoffs. Such has been the on-court gulf between the teams that the Clippers bucked a 12-season trend when finishing higher than the Lakers in 2004-05. The teams share the Staples Center, into which 19,905 patrons crammed last month to see the less-fancied Clippers win a fiery contest 99-92. Griffin finished with 18 points and 15 rebounds. With master coach Phil Jackson expected to retire at the end of this season, will the Lakers stay big brother? Courtesy of Griffin's attack on the basket, the Clippers' game is already better to watch.
4. Fans from other clubs will love him even more
There's little grey area with the Lakers: their success (power, attitude, etc) has made them loved and loathed. Inoffensive and unthreatening, the Clippers have probably had campaigns that barely stirred their own supporters. Griffin has put the team back on the map, and will hit the NBA All-Star Game on February 20 as the first rookie since 2003. (Expect a bigger buzz when he competes in the slam dunk contest a day earlier.) As much as every fan would want Griffin at their club, there's more respect to be had if he sticks with the rebuilding Clippers, and gives the finger to the rest.
5. He should look at Kobe, not LeBron
They're the two best players in the game, but LeBron James' ego-driven switch to Miami (cue The Decision) killed his standing in Cleveland, whose Cavaliers could almost pass as the Clippers of the Midwest. He alienated many others when determining that the Heat would deliver his championship ring that the Cavs failed to in their NBA Finals encounter with San Antonio in 2007. Sure, Bryant has been blessed with timing – he's won five championships with the Lakers – but he's one of few franchise players in a competition where old-school allegiances are rare. And it hasn't been all smooth sailing for him. When Bryant retires with a seat next to Magic Johnson, James could be at his third team.
6. He should want the rivalry with Kevin Durant
Another NBA phenomenon, 22-year-old Durant is on track to claim his second straight league scoring title. In his fourth season, Durant plays anywhere from shooting guard to power forward for the Oklahoma City Thunder, the team in Griffin's hometown. The Thunder face years of pampering to keep Durant, who could be the biggest name in the competition by 2013. Think what Durant-Griffin epics could mean for the Thunder and Clippers: Jordan v Isiah, Olajuwon v Ewing, Magic v Bird ... you get the drift.
The views in this article are those of the author and not necessarily those of BigPond Sport.
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