text:
namespace WinAPI
{
  HINSTANCE Application::hinstance = 0;

  Application::Application(HINSTANCE hinstance, DWORD dwICC)
  {
    Application::hinstance = hinstance;

    INITCOMMONCONTROLSEX iccex;
    iccex.dwSize = sizeof(INITCOMMONCONTROLSEX);
    iccex.dwICC = dwICC;
    VERIFY(InitCommonControlsEx(&iccex));
  }

  void Application::setModule(HMODULE hmodule)
  {
    Application::hinstance = hmodule;
  }

  UINT Application::run()
  {
    MSG msg;
    while (GetMessage(&msg, NULL, 0, 0))
    {
      //if (!TranslateAccelerator(msg.hwnd, hAccelTable, &msg))
      {
        TranslateMessage(&msg);
        DispatchMessage(&msg);
      }
    }
    return (UINT) msg.wParam;
  }

  void Application::quit(UINT exitCode) {PostQuitMessage(exitCode);}

  bool Shell::getFolderPath(INT folder, LPTSTR path, UINT size)
  {
    if(size < MAX_PATH)
    {
      TCHAR maxPath[MAX_PATH];
      if(SHGetFolderPath(0, folder, 0, SHGFP_TYPE_CURRENT, maxPath) == S_FALSE)
        return false;
      _tcscpy_s(path, size, maxPath);
      return true;
    }
    else if(SHGetFolderPath(0, folder, 0, SHGFP_TYPE_CURRENT, path) == S_FALSE)
        return false;
    return true;
  }

  bool Shell::createLink(LPCTSTR file, LPCTSTR link, LPCTSTR description, LPCTSTR workingDir)
  {
      bool success = false;

#ifdef UNICODE
      LPCTSTR wsFile = file;
      LPCTSTR wsLink = link;
      LPCTSTR wsDescription = description;
      LPCTSTR wsWorkingDir = workingDir;
#else
      WCHAR wsFile[MAX_PATH];
      WCHAR wsLink[MAX_PATH];
      WCHAR wsDescription[MAX_PATH];
      WCHAR wsWorkingDir[MAX_PATH];
      MultiByteToWideChar(CP_ACP, 0, file, -1, wsFile, MAX_PATH);
      MultiByteToWideChar(CP_ACP, 0, link, -1, wsLink, MAX_PATH);
      MultiByteToWideChar(CP_ACP, 0, description, -1, wsDescription, MAX_PATH);
      MultiByteToWideChar(CP_ACP, 0, workingDir, -1, wsWorkingDir, MAX_PATH);
#endif

      // Get a pointer to the IShellLink interface. It is assumed that CoInitialize
      // has already been called.
      IShellLink* psl;
      HRESULT hres = CoCreateInstance(CLSID_ShellLink, NULL, CLSCTX_INPROC_SERVER, IID_IShellLink, (LPVOID*)&psl);
      if (SUCCEEDED(hres))
      {
          // Set the path to the shortcut target and add the description.
          psl->SetPath(wsFile);
          psl->SetDescription(wsDescription);
          psl->SetWorkingDirectory(wsWorkingDir);

          // Query IShellLink for the IPersistFile interface, used for saving the
          // shortcut in persistent storage.
          IPersistFile* ppf;
          hres = psl->QueryInterface(IID_IPersistFile, (LPVOID*)&ppf);

          if (SUCCEEDED(hres))
          {
              // Add code here to check return value from MultiByteWideChar
              // for success.

              // Save the link by calling IPersistFile::Save.
              hres = ppf->Save(wsLink, TRUE);
              if (SUCCEEDED(hres))
                success = true;
              ppf->Release();
          }
          psl->Release();
      }
      return success;
  }

  HINSTANCE Shell::execute(HWND hwnd, LPCTSTR lpOperation, LPCTSTR lpFile, LPCTSTR lpParameters,
      LPCTSTR lpDirectory, INT nShowCmd)
  {
    return ShellExecute(hwnd, lpOperation, lpFile, lpParameters, lpDirectory, nShowCmd);
  }

  String::String(UINT stringId)
  {
#ifdef UNICODE
    data = 0;
    buffer = 0;
    LoadString(Application::getInstance(), stringId, (LPTSTR)&data, 0);
#else
    data = 0;
    buffer = 0;
    LPCWSTR wdata;
    LoadStringW(Application::getInstance(), stringId, (LPTSTR)&wdata, 0);
    if(wdata)
    {
      int len = wstrlen(wdata);
      data = buffer = new TCHAR[len];
      WideCharToMultiByte(
#error TODO
    }
#endif
  }

  String::~String()
  {
    if(buffer)
      delete[] buffer;
  }

  Icon::Icon(LPCTSTR icon) : hicon(LoadIcon(NULL, icon)) {}
  Icon::Icon(UINT iconId) : hicon(LoadIcon(Application::getInstance(), MAKEINTRESOURCE(iconId))) {}
  Icon::Icon(HINSTANCE hinst, UINT iconId) : hicon(LoadIcon(hinst, MAKEINTRESOURCE(iconId))) {}

  Cursor::Cursor(LPCTSTR cursor) : hcursor(LoadCursor(NULL, cursor)) {}
  Cursor::Cursor(UINT cursorId) : hcursor(LoadCursor(Application::getInstance(), MAKEINTRESOURCE(cursorId))) {}
  Cursor::Cursor(HINSTANCE hinst, UINT cursorId) : hcursor(LoadCursor(hinst, MAKEINTRESOURCE(cursorId))) {}

  Menu::Menu(UINT menuId) : hmenu(LoadMenu(WinAPI::Application::getInstance(), MAKEINTRESOURCE(menuId))) {}
  Menu::~Menu()
  {
    if(hmenu)
      DestroyMenu(hmenu);
  }

  Window::~Window()
  {
    if(hwnd)
      DestroyWindow(hwnd);
  }

  bool Window::create(LPCTSTR className, UINT windowClassStyle,
      HWND hwndParent, HICON icon, HICON smallIcon,
      HCURSOR cursor, LPCTSTR windowName, UINT exStyle, UINT style)
  {
    if(hwnd)
      return false; // already created

    struct WndProc
    {
      static LRESULT CALLBACK wndProcInit(HWND hwnd, UINT message, WPARAM wParam, LPARAM lParam)
      {
        if(message == WM_CREATE)
        {
          LPCREATESTRUCT cs = (LPCREATESTRUCT) lParam;
          Window* wnd = (Window*) cs->lpCreateParams;
          wnd->hwnd = hwnd;
          SetWindowLongPtr(hwnd, GWLP_USERDATA, (LONG_PTR) wnd);
          SetWindowLongPtr(hwnd, GWLP_WNDPROC, (LONG_PTR) wndProc);
          return wnd->onMessage(message, wParam, lParam);
        }
        return DefWindowProc(hwnd, message, wParam, lParam);
      }
      static LRESULT CALLBACK wndProc(HWND hwnd, UINT message, WPARAM wParam, LPARAM lParam)
      {
        Window* wnd = (Window*) GetWindowLongPtr(hwnd, GWLP_USERDATA);
        return wnd->onMessage(message, wParam, lParam);
      }
    };

    // register window class
    HINSTANCE hinst = Application::getInstance();
    {
      WNDCLASSEX wcex;
      wcex.cbSize = sizeof(WNDCLASSEX);
      wcex.style = windowClassStyle; //CS_HREDRAW | CS_VREDRAW;
      wcex.lpfnWndProc = WndProc::wndProcInit;
      wcex.cbClsExtra = 0;
      wcex.cbWndExtra = 0;
      wcex.hInstance = hinst;
      wcex.hIcon = icon;
      wcex.hCursor = cursor;
      wcex.hbrBackground = 0; //(HBRUSH)(COLOR_WINDOW+1);
      wcex.lpszMenuName = 0; //MAKEINTRESOURCE(IDC_BDOCK);
      wcex.lpszClassName = className;
      wcex.hIconSm = smallIcon;
      RegisterClassEx(&wcex);
    }

    // create window
    hwnd = CreateWindowEx(exStyle, className, windowName, style, 0, 0, 0, 0, hwndParent, NULL, hinst, this);
    if(!hwnd)
      return false;

    return true;
  }

  LRESULT Window::onMessage(UINT message, WPARAM wParam, LPARAM lParam)
  {
    switch(message)
    {
    case WM_CONTEXTMENU:
      if(onContextMenu(GET_X_LPARAM(lParam), GET_Y_LPARAM(lParam)))
        return 0;
      break;
    case WM_COMMAND:
      if(onCommand(LOWORD(wParam), (HWND) lParam))
        return 0;
    }
    return DefWindowProc(hwnd, message, wParam, lParam);
  }

  bool Window::setTheme(LPCTSTR pszSubAppName, LPCTSTR pszSubIdList) {return SetWindowTheme(hwnd, pszSubAppName, pszSubIdList) == S_OK;}
  bool Window::isVisible() {return IsWindowVisible(hwnd) == TRUE;}
  bool Window::show(INT nCmdShow) {return ShowWindow(hwnd, nCmdShow) == TRUE;}
  bool Window::move(INT X, INT Y, INT nWidth, INT nHeight, bool bRepaint) {return MoveWindow(hwnd, X, Y, nWidth, nHeight, bRepaint) == TRUE;}
  bool Window::registerShellHookWindow() {return RegisterShellHookWindow(hwnd) == TRUE;}
  bool Window::deregisterShellHookWindow() {return DeregisterShellHookWindow(hwnd) == TRUE;}
  bool Window::setTimer(UINT_PTR nIDEvent, UINT uElapse, TIMERPROC lpTimerFunc) {return SetTimer(hwnd, nIDEvent, uElapse, lpTimerFunc) == TRUE;}
  bool Window::killTimer(UINT_PTR nIDEvent) {return KillTimer(hwnd, nIDEvent) == TRUE;}
  LRESULT Window::sendMessage(UINT msg, WPARAM wParam, LPARAM lParam) {return SendMessage(hwnd, msg, wParam, lParam);}
  bool Window::postMessage(UINT msg, WPARAM wParam, LPARAM lParam) {return PostMessage(hwnd, msg, wParam, lParam) == TRUE;}

  Dialog::~Dialog()
  {
    if(hwnd)
    {
      end(IDCANCEL);
      hwnd = 0;
    }
  }

  bool Dialog::create(UINT ressourceId, HWND hwndParent)
  {
    if(hwnd)
      return 0; // already created

    struct DlgProc
    {
      static INT_PTR CALLBACK dlgProcInit(HWND hDlg, UINT message, WPARAM wParam, LPARAM lParam)
      {
        if(message == WM_INITDIALOG)
        {
          Dialog* dlg = (Dialog*) lParam;
          dlg->hwnd = hDlg;
          SetWindowLongPtr(hDlg, DWLP_USER, (LONG_PTR) dlg);
          SetWindowLongPtr(hDlg, DWLP_DLGPROC, (LONG_PTR) dlgProc);
          if(dlg->onDlgMessage(message, wParam, lParam))
            return (INT_PTR)TRUE;
        }
        return (INT_PTR)FALSE;
      }
      static INT_PTR CALLBACK dlgProc(HWND hDlg, UINT message, WPARAM wParam, LPARAM lParam)
      {
        Dialog* dlg = (Dialog*) GetWindowLongPtr(hDlg, DWLP_USER);
        if(dlg->onDlgMessage(message, wParam, lParam))
          return (INT_PTR)TRUE;
        return (INT_PTR)FALSE;
      }
    };

    HWND hwnd = CreateDialogParam(Application::getInstance(), MAKEINTRESOURCE(ressourceId), hwndParent, DlgProc::dlgProcInit, (LPARAM)this);
    return hwnd != NULL;
  }

  UINT Dialog::show(UINT ressourceId, HWND hwndParent)
  {
    if(hwnd)
      return 0; // already created

    struct DlgProc
    {
      static INT_PTR CALLBACK dlgProcInit(HWND hDlg, UINT message, WPARAM wParam, LPARAM lParam)
      {
        if(message == WM_INITDIALOG)
        {
          Dialog* dlg = (Dialog*) lParam;
          dlg->hwnd = hDlg;
          SetWindowLongPtr(hDlg, DWLP_USER, (LONG_PTR) dlg);
          SetWindowLongPtr(hDlg, DWLP_DLGPROC, (LONG_PTR) dlgProc);
          if(dlg->onDlgMessage(message, wParam, lParam))
            return (INT_PTR)TRUE;
        }
        return (INT_PTR)FALSE;
      }
      static INT_PTR CALLBACK dlgProc(HWND hDlg, UINT message, WPARAM wParam, LPARAM lParam)
      {
        Dialog* dlg = (Dialog*) GetWindowLongPtr(hDlg, DWLP_USER);
        if(dlg->onDlgMessage(message, wParam, lParam))
          return (INT_PTR)TRUE;
        return (INT_PTR)FALSE;
      }
    };

    UINT result = (UINT) DialogBoxParam(Application::getInstance(), MAKEINTRESOURCE(ressourceId), hwndParent, DlgProc::dlgProcInit, (LPARAM)this);
    hwnd = 0;
    return result;
  }

  bool Dialog::end(UINT result)
  {
    return EndDialog(hwnd, result) != FALSE;
  }

  bool Dialog::onDlgMessage(UINT message, WPARAM wParam, LPARAM lParam)
  {
    switch(message)
    {
    case WM_INITDIALOG: return onInitDialog();
    case WM_COMMAND: return onCommand(LOWORD(wParam), (HWND) lParam);
    }
    return false;
  }

  bool Dialog::onInitDialog()
  {
    return true;
  }

  bool Dialog::onCommand(UINT command, HWND source)
  {
    if(command == IDOK || command == IDCANCEL)
    {
      end(command);
      return true;
    }
    return false;
  }

  bool Control::initialize(Window& parent, UINT id)
  {
    if(hwnd)
      return false;
    hwnd = GetDlgItem(parent, id);
    return hwnd != NULL;
  }

  bool Button::setCheck(INT check)
  {
    Button_SetCheck(hwnd, check);
    return true;
  }

  INT Button::getCheck()
  {
    return Button_GetCheck(hwnd);
  }

  ImageList::~ImageList()
  {
    if(himagelist)
      ImageList_Destroy(himagelist);
  }

  bool ImageList::create(INT cx, INT cy, UINT flags, INT cInitial, INT cGrow)
  {
    if(himagelist)
      return false;
    himagelist = ImageList_Create(cx, cy, flags, cInitial, cGrow);
    return himagelist != NULL;
  }

  INT ImageList::add(HICON icon)
  {
    return ImageList_AddIcon(himagelist, icon);
  }

  bool ListView::setImageList(HIMAGELIST imageList, INT iImageList)
  {
    ListView_SetImageList(hwnd, imageList, iImageList);
    return true;
  }

  INT ListView::addItem(LVITEM& item)
  {
    item.iItem = ListView_GetItemCount(hwnd);
    return ListView_InsertItem(hwnd, &item);
  }

  bool TreeView::setImageList(HIMAGELIST imageList, INT iImageList)
  {
    TreeView_SetImageList(hwnd, imageList, iImageList);
    return true;
  }

  HTREEITEM TreeView::insertItem(TVINSERTSTRUCT& item)
  {
    return TreeView_InsertItem(hwnd, &item);
    return 0;
  }

} // namespace

redpajama_set_name: RedPajamaGithub


text:
This was a unique group, bringing together an unusual combination
Posted on January 30, 2017 by her26451
This was a unique group, bringing together an unusual combination of domestic and international partners, committed to social innovation with a clear goal of developing a safe and effective vaccine
that would reach the populations that most needed it at an affordable price. In 2003, BBIL Bharat convened the various partners to discuss the clinical development plan for the 116E and I321 vaccine lots. Trials conducted in 2005 showed that E7080 clinical trial while both of them were safe, 116E provided significantly better immune response to the vaccine [5]. The development was then taken forward to late phase II and then phase III with the 116E candidate, under the leadership of Nita Bhandari at the Society for Applied Studies, a non-governmental organization formed of researchers formerly at AIIMS, committed to child health research. The partners then expanded to include researchers
Quizartinib at the KEM hospital and Research Centre, Pune and the Christian Medical College, Vellore to carry out the phase III clinical trial for efficacy that required recruitment of 6800 infants and their follow up for a period of two years, and the Translational Health Science and Technology Institute, Delhi to analyze all the clinical samples. The clinical trial was carried out to the highest international standards, with remarkably low loss to follow up, a critical determinant of trial quality. In addition, the intensive monitoring and follow up of participants and provision of access to medical care these and referrals resulted in lower than expected numbers of deaths at all three sites, pointing to the attention paid to participant safety in the trial. Despite the early treatment and referrals, the data indicate that
116E based vaccine (now known as Rotavac) provided a level of protection (56% during the first year) comparable to other licensed rotavirus vaccines in developing countries [6] which did not drop significantly in the second year of life [7]. The sharing of the costs of development between several partners played a crucial role in the ability to limit the price of the vaccine to just $1 per dose. BBIL invested in a highly efficient manufacturing process and innovative product development efforts, which also contribute to keeping the costs low. This joint, very collaborative, effort has been a new paradigm for innovation in strategy and process and has resulted in the availability of safe and effective product for Indian and other developing country markets. The deployment of this product now requires further partnerships—in consideration of the introduction of the vaccine into the public health system and in continued safety surveillance.
A transparent strain was used in accordance with the recommendati
A transparent strain was used in accordance with the recommendations from the Pneumococcal Vaccine Animal Model Consensus Group and with previous studies on the appropriateness and effectiveness of transparent strains in the animal colonization model [15] and [25]. A total of 80 commercially acquired Swiss-Webster adult females (ND4), 6–8 week old (20–25 g), were used in each experiment. They were housed under standard conditions (25 °C, relative humidity ∼40%; pathogen-free)
with food and water available, ad libitum in filter-top cages. Mice were allowed to acclimate for a week prior to immunization. Mouse immunization and challenge protocol were approved by the Animal Care and Use RG7204 research buy Committee (CDC, Atlanta, GA), which holds an accreditation from the American Association
for the Accreditation of Laboratory Animal Care. Prevnar™ (PCV7) was obtained from Wyeth-Lederle, Pearl River, NY. rPsaA was the kind gift of Sanofi Aventis (Swiftwater, PA). In keeping with previously established regimens for rPsaA [18] and PCV7 [26], a schedule of 3-doses was used for rPsaA and PCV7 in combination and for individual immunizations. Inoculations were given at 2-week intervals. One microgram of PCV7 was administered subcutaneously at each Paclitaxel purchase interval. rPsaA suspended in PBS with 6.3 mg/ml aluminum phosphate adjuvant was subcutaneously administered at 100 μg per dose initially and followed with 50 μg boosters. For combination immunizations (PCV7 + rPsaA), PCV7 and rPsaA were given as two separate inoculations. Mice which were unimmunized, immunized with aluminum phosphate adjuvant in PBS, and immunized with either rPsaA (in PBS plus aluminum phosphate adjuvant) or PCV7
alone served as controls. Sera were collected prior to immunizations, a week after the last dose, and 3–5 days after intranasal challenge. These collections were evaluated Sclareol for Immunoglobulin G (IgG) levels by using enzyme-linked immunosorbent assays (ELISA) and for functional antibody by using an opsonophagocytic assay. Antigen-specific IgG levels were measured with ELISA. For the measurement of PsaA antibodies, an anti-PsaA ELISA described for human sera was followed with minor modifications [27]. A highly specific mouse monoclonal antibody, 8G12G11B10 (8G12), produced against native PsaA, served as the reference serum with a stock concentration of 8 mg/ml [28]. Pooled sera from mice immunized with two doses of 100 μg PsaA was used as the quality control and a goat anti-mouse horse peroxidase conjugate (Biorad Laboratories, Richmond, CA) was used for the enzyme-conjugate. IgG antibodies specific to Pnc capsular polysaccharide (Ps) for serotypes 4, 14, or 19A were measured in the ELISA platform as described previously [26]. Pnc Ps used to coat ImmulonII plates (Dynex, Chantilly, VA) were purchased from ATCC (Manassas, VA). A heterologous Ps, serotype 22F, was added for absorption of cross-reactive antibodies [29] and [30].
The challenge is that several studies have shown more than 30% of
The challenge is that several studies have shown more than 30% of women with pelvic floor dysfunction are not able to contract the pelvic floor muscles correctly even after thorough individual teaching and feedback (Benvenuti et al 1987, Bump et al 1991, Bø et al 1988). The most common errors
are to bear down or to use hip adductor, gluteal, or abdominal muscles instead of the pelvic floor find more muscles (Bump et al 1991, Bø et al 1988). Group training of pelvic floor muscles has been shown in several randomised controlled trials to be effective, but these programs included individual instruction and feedback of the contraction (Bø et al 1990, Bø et al 1999, Mørkved and Bø 1997, Mørkved et al 2003). It is not yet known whether it is possible to teach HA-1077 order women participating in a general group-based exercise class to contract the pelvic floor muscles. Culligan et al (2010) concluded, on the basis of their finding that Pilates training produced similar strength gains to pelvic floor muscle
training, that their results may 'lead to widespread use of Pilates-based exercise programs to treat and prevent pelvic floor dysfunction'. In our opinion that conclusion is premature because no randomised trials have demonstrated benefical effects of Pilates exercise on clinically important outcomes (continence) in a sample of incontinent women. Indeed, observational data suggest that this is not the case: a study on group fitness instructors showed that the prevalence of incontinence was the same amongst female yoga and Pilates instructors as in the general population, suggesting that the exercises did not provide a beneficial effect (Bø et al 2011). The suggestion of an association or causal link between breathing, posture, and pelvic floor muscle dysfunction should
be tested in case-control or cohort studies with blinded assessors. A large cross-sectional study found associations between incontinence, Sodium butyrate low back pain, and respiratory disease (Smith et al 2006), but it is quite possible the associations were confounded, so that while participants had multiple complaints at the same time the conditions were not causally related. Cross-sectional studies usually provide weak evidence of causality. There are two contradictory hypotheses on the effect of general exercise on the pelvic floor, previously described by Bø (2004). One hypothesis holds that general exercise makes pelvic floor muscles co-contract, and thus strengthens pelvic floor muscles and prevents stress urinary incontinence. The other hypothesis is that repetitive or heavy impact on the pelvic floor, such as is caused by heavy lifting or marathon running, may fatigue, stretch, and weaken the muscles.
5% NP-40, 0 2 mM EDTA, 2 mM EGTA, 10% glycerol) [28] and immunopr
5% NP-40, 0.2 mM EDTA, 2 mM EGTA, 10% glycerol) [28] and immunoprecipitated with anti-RSV-F antibody. The IP products were resolved on a 10% SDS-PAGE gel and visualized using a Typhoon 9700 Phosphorimager (GE Healthcare Life Sciences, Piscataway, NJ, USA). To examine RSV-G protein expression, rPIV5-RSV-G-infected MDBK cells and RSV A2-infected A549 cells were lysed with WCEB. The lysates were processed and resolved by SDS-PAGE as described before. The proteins were transferred onto a polyvinylidene difluoride (PVDF) membrane and detected using mouse anti-RSV-G antibody (1:2000 dilution) as previously described [14]. 6-Well
plates of Vero cells were infected with rPIV5-RSV-F, rPIV5-RSV-G, or PIV5 at a MOI = 5 or 0.01. 100 μL samples of supernatant were collected at 0, 24, 48, 72, 96, and 120 h post-infection. Virus was quantified by plaque assay as described in Chen et al. [14]. All animal www.selleckchem.com/products/Perifosine.html experiments
were performed according to the protocols approved PF-01367338 mw by the Institutional Animal Care and Use Committee at the University of Georgia. Six-to-eight week-old female BALB/c mice (Harlan Laboratories, Indianapolis, IN, USA) were anesthetized by intraperitoneal injection of 200 μL of 2, 2, 2-tribromoethanol in tert-amyl alcohol (Avertin). Immunization was performed by intranasal administration of 106 PFU of rPIV5-RSV-F, rPIV5-RSV-G, or RSV A2 in a 50 μL volume. Negative controls were treated intranasally with 50 μL of PBS. Three weeks post-immunization, blood was collected via the tail vein for serological analysis. Four weeks post-immunization, all mice were challenged intranasally with 106 PFU of RSV A2 in a 50 μL volume. Four days later, lungs were collected from 5 mice per group to assess viral burden. The Phosphoprotein phosphatase lungs of the other 5 mice in each group were perfused with 10% formalin solution
and sent for histology. To detect neutralizing antibody titers, mice were immunized as described above and terminally bled 4 weeks post-immunization. RSV-F and RSV-G-specific serum antibody titers were measured by ELISA. Immulon® 2HB 96-well microtiter plates were coated with 100 μL of purified RSV-F or G protein at 1 μg/mL in PBS [21] and incubated overnight at 4 °C. Two-fold serial dilutions of serum were made in blocking buffer (5% nonfat dry milk, 0.5% BSA in wash buffer; KPL, Inc., Gaithersburg, MD, USA). 100 μL of each dilution was transferred to the plates and incubated for one hour at room temperature. After aspirating the samples, the plates were washed three times with wash buffer. Secondary antibody was diluted 1:1000 [alkaline phosphatase-labeled goat anti-mouse IgG (KPL, Inc.) or horseradish-peroxidase-labeled goat anti-IgG1 or IgG2a (SouthernBiotech, Birmingham, AL, USA)] in blocking buffer. 100 μL of diluted secondary antibody was added to each well, and the plates were incubated for one hour at room temperature.
5) Mice immunized with NLA + ArtinM or ArtinM alone presented th
5). Mice immunized with NLA + ArtinM or ArtinM alone presented the highest scores of morbidity (Fig. 5A) and the most pronounced body weight losses (Fig. 5B) in relation to other groups (P < 0.05). In contrast, NLA + JAC and NLA groups showed the lowest scores of morbidity ( Fig. 5A) (P < 0.05), with Anti-cancer Compound Library chemical structure no significant weight changes. JAC and PBS groups also showed no significant weight changes and morbidity scores. Regarding the survival curves ( Fig. 5C), the highest survival rate (86%) was observed for NLA + ArtinM group, whereas the PBS control group had the lowest survival (41%) (P < 0.05). Mice immunized with NLA + JAC, NLA, ArtinM or JAC presented intermediate survival rates (50–62%) ( Fig.
5C). Brain parasite burden after Nc-1 challenge determined by real-time PCR (Fig. 6A) was lower in mice immunized with NLA + ArtinM and ArtinM alone than in NLA + JAC and PBS groups (P < 0.05), whereas NLA and JAC groups showed similar parasite burden with no significant difference
in relation to NLA + JAC and PBS groups. Brain tissue parasitism was also evaluated by immunohistochemical assay Kinase Inhibitor Library ( Fig. 6B) and showed similar results to PCR data, with a lower parasitism in mice immunized with NLA + ArtinM and ArtinM, in addition to NLA alone, when compared to NLA + JAC, PBS and JAC groups (P < 0.05), which showed similar tissue parasitism among them. Representative photomicrographs of antigen-immunized groups and PBS group
after challenge are shown in Fig. 6C, with strongly stained free parasites or within parasitophorous vacuoles. Concerning the brain inflammation (Fig. 7A), mice immunized with NLA + ArtinM and ArtinM alone showed the highest inflammation scores in relation to all other groups (P < 0.05), whereas NLA + JAC and JAC groups presented the lowest inflammation scores (P < 0.05). The brain histopathological changes included lesions characterized by mononucleated cell infiltrates in the parenchyma, glial nodules, vascular cuffing by lymphocytes and focal mononucleated cell infiltrates in the meninges ( Fig. 7B). Control of neosporosis in cattle involves three main options: Isotretinoin (i) a yet hypothetical treatment with a parasiticide drug; (ii) a test-and-cull approach, where infected animals are identified and eliminated from the herd; and (iii) a vaccination strategy. From these options, economic analyses suggest that vaccination might be the most cost-effective approach in controlling neosporosis [17]. Previous studies have investigated live [19], gamma-irradiated [21] tachyzoites, or live tachyzoites attenuated through high passage in cell culture [18] as candidate antigens in immunization procedures. Other studies have approached immunization against N. caninum using recombinant proteins, such as NcSRS2 and NcSAG1 [23] and [27], NcSAG4 and NcGRA7 [34], GRA1, GRA2 and MIC10 [25], among others.
In turn this permits evaluation of the implemented intervention/s
In turn this permits evaluation of the implemented intervention/s to be better informed by the use of theory-driven
approaches (Connell and Kubisch, 1998 and Pawson and Tilley, 2009). The validity of considering www.selleckchem.com/products/MDV3100.html intervention components separately (as was done in the FG discussions) could be challenged, given that the effects of a complex intervention may be greater than the sum of its parts. However, the exploratory and prioritisation processes that the participants were guided through enabled them implicitly to consider individual components and the synergies between them in their local contexts. This further contributed to the development of a theoretical understanding of the change RG7204 price pathways interventions were likely to invoke. Researchers may argue that the prioritised intervention components ultimately included in the intervention programme could have varied depending
on factors such as the mix of FG participants or the professionals recruited. This is a frequent challenge to those working with qualitative techniques. However our analysis showed thematic concordance across groups and given our breadth of sampling we believe the prioritised outcomes are transferable within comparable communities. The information on local context gained from the groups, together with the existing resource review, was crucial in the detailed planning of programme components. The processes undertaken have led to the development of an intervention founded within existing research evidence, but also taking into account the local context. The intervention development balanced pragmatism with theory driven approaches. The result is a childhood obesity
prevention programme that is tailored to UK South Asian communities, but one which could be transferred and tailored to other settings. Emergent data from similar intervention development research that we have undertaken in Iran, Qatar and China supports this approach (Al-Muraikhi, 2012, Li, 2013 and Mohammadpour-Ahranjani, 2011). Data gained from stakeholders in these settings has shown too that the contexts that contribute to the development of childhood obesity are broadly similar, suggesting that prevention programmes could be transferred from one setting to another. However, this research has also highlighted that there are specific contextual differences that are critical to identify and understand in order to successfully tailor obesity prevention programmes to the different settings. The authors have no competing interests to declare. The Birmingham healthy Eating, Active lifestyle for Children Study (BEACHeS) is funded by the National Prevention Research Initiative (NPRI, http://www.mrc.ac.
Table 2 summarises the relationships between the distance covered
Table 2 summarises the relationships between the distance covered during the 6-minute walk test and various clinical characteristics of the participants. In the multivariate analysis, shorter distances on the 6-minute walk test were found in participants with advanced age, heart failure of ischaemic aetiology,
and advanced heart failure (advanced NYHA class, lower LVEF, lower eGFR and higher uric acid). The mean follow-up period for all participants was 931 days (SD 474, median 990, range 6 to 1774). The 1-year and 3-year mortality rates were 16% and 44%, respectively. The participants who died had higher NYHA classifications and lower LVEF, eGFR, BMI, and haemoglobin. The participants who died also had higher levels of NT-proBNP, hsCRP and UA, as presented in Table 1. During the 1-year and 3-year follow-up, 54% and 69% participants Talazoparib solubility dmso were urgently admitted to hospital for cardiovascular reasons or died. The proportionality assumption and the assumption of a log-linear relationship between the potential predictors and the hazard function were fulfilled for all tested variables. The 1-year prediction models are presented in Tables 3 and 4. The 3-year prediction models are presented in Tables 5 and 6. The following variables showed a significant
association with a higher 1-year risk of cardiovascular death, and of check details death or hospitalisation, in the single predictor (ie, univariate) Cox proportional Tryptophan synthase hazards models: high NYHA class, low LVEF, high NT-proBNP, high hsCRP, low haemoglobin, low eGFR, high uric acid, and low 6-minute walk test distance (all p < 0.05), as presented in Tables 3
and 4. Interestingly, exactly the same factors were related to an increase in the composite outcome of 3-year cardiovascular death or hospitalisation in this group of participants with chronic heart failure, as presented in Table 6. On multivariate analysis, high plasma NT-proBNP and low 6-minute walk test distance were strong predictors of the 1-year risk of death, as presented in Table 3. More events occurred for the composite outcome 'death or hospitalisation' than for death alone. Therefore, the multivariate models permitted the inclusion of more predictors: age, NYHA class, LVEF, diabetes mellitus, hypertension, NT-proBNP, hs-CRP, haemoglobin, eGFR, uric acid, and distance covered in the 6-minute walk test. (The 6-minute walk test distance was included as a continuous variable, analysing the effect of a 10 m increase, and dichotomously, as ≤ 468 m vs > 468 m.) Only high level of uric acid, a low 6-minute walk test distance, and high plasma NT-proBNP remained as significant predictors of an increase in the composite outcome of 1-year cardiovascular death or hospitalisation, as presented in Table 4. In the 3-year analysis, only a low 6-minute walk test distance, high plasma NT-proBNP and a high uric acid remained independent predictors of the 3-year risk of death and death or hospitalisation.
The reason for this relapse is related to the poor targeting abil
The reason for this relapse is related to the poor targeting ability of the antiretroviral agent to the latent sites of infection. The two main objectives of the antiretroviral therapy are virological control and restoration of immunity.
Once these two objectives are achieved, it is possible selleck inhibitor to delay the progression of the disease, minimize opportunistic infections, malignancies and prolong the survival of the patient. Currently the five different classes of antiretroviral drugs available are Nucleoside Reverse Transcriptase Inhibitors (NRTI's), Nucleotide Reverse Transcriptase Inhibitors (NtRTI), Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI), Protease Inhibitors (PIs), and more recently, fusion and integrase inhibitors. NRTI's are among the first agents to be used for the treatment of HIV/AIDS. These agents inhibit the reverse transcriptase enzyme responsible for the conversion of viral RNA to DNA within the host cell.
These agents require intracellular metabolism to their triphosphate form, before activation. The approved NRTI's include zidovudine, didanosine, zalcitabine, stavudine, lamivudine, abacavir and most recently, emtricitabine.2 Furthermore several antiretroviral drugs suffer from low bioavailability due to extensive first-pass effects and gastrointestinal degradation. In addition, for most drugs the half-life is short, thus necessitating frequent administration
crotamiton of doses thereby decreasing patient compliance and increasing side effects due to peak-trough fluctuations. Stavudine Selleck GDC0449 is the FDA-approved drug for clinical use for the treatment of HIV infection, AIDS and AIDS-related conditions either alone or in combination with other antiviral agents. Stavudine, a nucleoside analog of thymidine, is phosphorylated using cellular kinases to the active metabolite stavudine triphosphate. Stavudine triphosphate inhibits the activity of HIV 1 reverse transcriptase by competing with the natural substrate thymidine triphosphate and by causing DNA chain termination following its incorporation into viral DNA. Stavudine triphosphate inhibits cellular DNA polymerases β and γ and markedly reduces the synthesis of mitochondrial DNA. Stavudine is typically administered orally as a capsule and an oral solution. The drug has a very short half-life (1.00 h) thus necessitating frequent administration to maintain constant therapeutic drug levels. However patients receiving stavudine develop neuropathy and lactic acidosis. The side effects of stavudine are dose-dependent and a reduction of the total administered dose reduces the severity of the toxicity.3 One of the suitable methods to overcome these problems could be association with biodegradable polymeric carriers such as nanoparticles.
Syndrome Eisenmenger Inclut tous les défets intra et extracardiaq
Syndrome Eisenmenger Inclut tous les défets intra et extracardiaques Selleckchem Dasatinib qui se manifestent au départ par un shunt systémique-pulmonaire et qui progressent entraînant une élévation des résistances vasculaires pulmonaires (RVP) et l'inversion du shunt (pulmonaire-systémique) ou un shunt bidirectionnel ; les patients ont dans la plupart des cas une cyanose, une polyglobulie et une atteinte multi-organe. Shunts gauches – droits • Corrigeables Incluent les défets modérés à larges : les RVP sont augmentées de façon légère à modérée, le shunt systémique-pulmonaire est toujours prévalent et la cyanose est absente Hypertension artérielle
pulmonaire associée à une découverte fortuite de cardiopathie congénitale Élévation importante des RVP dans un contexte de défets cardiaques minimes, qui n'explique pas ce niveau très important des RVP ; le tableau clinique est similaire à l'HTAP idiopathique. La fermeture de ces défets est contre-indiquée. Hypertension artérielle pulmonaire post-opératoire La cardiopathie congénitale a été corrigée chirurgicalement, mais l'HTAP soit persiste dans le post-opératoire immédiat soit va réapparaitre des mois ou des années après la chirurgie.
Le phénotype clinique est souvent grave. Depuis 2008, l'HTAP associée à une schistosomiase fait partie du groupe screening assay 1 des HTP. La schistosomiase touche 200 millions de personnes au niveau mondial, dont 10 % vont développer la forme hépatosplénique [27] and [28]. Parmi les patients avec atteinte hépatosplénique, 5 % vont avoir une HTAP qui devient MTMR9 par conséquence la forme d'HTAP la plus courante au monde [27] and [28]. Le mécanisme est multifactoriel, impliquant l'hypertension porto-pulmonaire, l'inflammation locale due aux œufs de schistosoma et l'obstruction mécanique par les œufs. Le résultat se traduit par des modifications histologiques artérielles pulmonaires à type de lésions plexiformes, similaires à ceux de l'HTAPi [27]. La mortalité de l'HTAP associée à la schistosomiase peut atteindre 15 % à 3 ans, mais les traitements
spécifiques de l'HTAP semblent améliorer le pronostic [28]. La maladie veino-oclusive (MVO) et l'hémangiomatose capillaire pulmonaire (HCP) sont des pathologies rares et graves. Sur le plan histologique, la MVO et l'HCP sont caractérisées, en proportions différentes, par une prolifération intimale au niveau des veines septales associée à une dilatation et une prolifération des capillaires pulmonaires [29]. Comme la preuve anatomopathologique est difficile à obtenir chez les patients avec une HTP, une approche non invasive incluant la tomodensitométrie thoracique, la fonction respiratoire, les paramètres gazométriques et le lavage broncho-alvéolaire est fiable dans la pratique courante pour affirmer le diagnostic [29] (tableau II).
The participants had centralisation, which is a feature of reduci
The participants had centralisation, which is a feature of reducible Derangement Syndrome. In the study, MDT was compared to a rehabilitation program including infrared irradiation, massage and exercises for the neck and shoulder. The outcome measures included pain intensity at the head, neck, shoulders, upper extremities, and overall. Pain intensity on a scale of 0 to 100 favoured MDT, with mean differences (95% CI) of 28 (17 to 39) at the head, 29 (20 to 38) at the
neck, 31 (21 to 41) at the shoulders, 40 (31 to 48) at the upper extremities, and 40 (32 to 48) overall. Except at the head, these confidence intervals had lower limits that were higher learn more than 20 on a scale of 0 to 100. A recent systematic review40 concluded that centralisation
was generally a good prognostic factor and a treatment-effect modifier. The present review included studies of any participants with neck pain, not specific subgroups such as those with centralisation. The estimate of the effect of MDT may therefore have been influenced by the inclusion of less-responsive subgroups such as irreducible Derangement Syndrome, Dysfunction Syndrome, Posture Syndrome and Other. Among people with neck pain, the prevalence of irreducible Derangement Syndrome, Dysfunction Syndrome, Posture this website Syndrome and Other is 0.9%, 8.1%, 2.7% and 7.2%, respectively.41 In particular, it may be difficult for non-Diploma MDT therapists to guide patients in the irreducible Derangement Syndrome and Other subgroups appropriately because the treatment for these subgroups requires a biopsychosocial approach, which is introduced in the Diploma MDT education program, rather than a simple-mechanical approach, which is introduced in the general MDT
workshops. This present review accepted all measures of disability. The Neck Disability Index42 was used by two trials: the Northwick Park Neck Pain Questionnaire43 by one trial, and the 15-item Copenhagen Neck Functional Disability Scale44 by the other trial. These questionnaires are spine-specific questionnaires and therefore may not accurately reflect the most troublesome construct for each patient. The Neck Disability Index and Vasopressin Receptor the Copenhagen Neck Functional Disability Scale have lower responsiveness than the Patient Specific Functional Scale45 in people with chronic whiplash-associated disorders.46 The Neck Disability Index was also inferior to the Patient Specific Functional Scale in people with cervical radiculopathy in terms of test-retest reliability, construct validity, and responsiveness.47 Therefore, it may be appropriate for future research to include a patient-centered questionnaire for the assessment of disability and functional performance, as well as a spine-specific disability measure.

redpajama_set_name: RedPajamaCommonCrawl


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Isolation Increases Risk of High Blood Pressure, Especially For Women
Joni Sweet
Joni Sweet is an experienced health and wellness writer who balances science with self-care.
Researchers have found a connection between social isolation and increased risk of hypertension, especially among women.
Social isolation and loneliness have also been tied to higher rates of early death, anxiety, depression, and suicide.
Connecting with loved ones virtually can help maintain your physical and mental health while stuck at home during the pandemic.
Staying at home and avoiding close contact with others are critical ways to curb the spread of COVID-19. But while following guidelines is an important part of protecting public health at large, social isolation can have a negative impact on the health of individuals—especially women.
A recent study from Canada has found that women who are single and socially isolated face a higher likelihood of having high blood pressure. Interestingly, marital status and social participation didn't have much effect on hypertension rates in men. The most important important variable for men was living situation: men who lived with other people were much more likely to have high blood pressure than men who lived alone.
The findings could provide insight into how people of different genders may fare over the long term as we head into a winter of lockdowns.
Humans are social creatures. Even though the relationship between isolation and high blood pressure varied slightly among men and women, a well-established body of research shows that loneliness can be harmful to everyone's physical and mental health.
Stay-at-home guidance has made it difficult—but not impossible—to maintain our social lives. As we head into a winter of quarantine, embracing virtual gatherings with loved ones can make a positive impact on your wellbeing.
Social Isolation and Heart Health
In a study published in the Journal of Hypertension, researchers from British Columbia looked at data from the Canadian Longitudinal Study on Aging on 28,238 adults between 45 and 85 years old.
The study asked participants about their marital status, living arrangements, social network size, and participation in social activities. It also collected information on which participants had hypertension, which was defined as 140/90 mmHg, or more than 130/80 mmHg in participants who had diabetes.
The data showed that single women tended to have a higher risk of hypertension than married women. More specifically, the risk was 28% higher for single women, 21% higher for divorced women, and 33% higher for widowed women compared with their married counterparts.
Tips for Coping With Coronavirus If You Live Alone
Researchers also found a strong association in rates of high blood pressure in women based on their social networks, which included work colleagues, close friends, relatives, children, siblings, and neighbors. Women with the smallest social networks (85 people or less) were 15% more likely to have hypertension compared with participants who had the largest social groups (220 people or more).
Women who participated in little to no social activities, like family gatherings, clubs, or sports, within the last year were up to 30% more likely to have hypertension.
Petros Levounis, MD
We know that when we're together with other people, we're happier, we're healthier, and now we have hard evidence that our heart is working better.
— Petros Levounis, MD
"We know that when we're together with other people, we're happier, we're healthier, and now we have hard evidence that our heart is working better," says Petros Levounis, MD, professor and chair of the psychiatry department at the Rutgers New Jersey Medical School and chief of service at University Hospital.
Things were a little different among men, though. Men who lived with other people were 15% more likely to have hypertension than those who lived alone (co-living had no significant effect on women). Like women, men who were single, divorced, or widowed also had increased risk of high blood pressure, but the association was much weaker. The impact of social participation was also much smaller for men. Finally, the size of a man's social network didn't have a significant effect on his risk of hypertension.
Understanding Gender Differences
The overall findings of this study echo earlier research, which has found that older adults who have partners and are more socially active tend of have lower rates of hypertension. According to the Centers for Disease Control and Prevention (CDC), social isolation also comes with higher risk of early death that rivals the mortality risk of smoking, obesity, and lack of exercise.
However, the gender-based differences in this research (particularly in regard to lower rates of hypertension among men who live alone) have not been seen in two other studies on the subject.
The authors think that the effect may be the result of many lone-living older men residing in senior housing communities that offer opportunities to interact with others and access information on health. They also suspect that the lower rates of hypertension seen in married people may be the result of "different social and economic expectations" that come with being in a partnership in Canada.
More research is needed to determine exactly why the effects of social isolation and hypertension differed between men and women, says Leonard Pianko, MD, cardiologist at Aventura Cardiovascular Center in Florida.
"My hypothesis is that women have a different response to loneliness than men because they produce more epinephrine from the adrenal gland, and that produces hormones and neurotransmitters that elevate blood pressure," he explains.
Isolation and Mental Health
Social isolation not only makes an impact on cardiovascular health—it has ripple effects on our psychological and emotional well-being too.
In a 2017 review of 40 other studies on the public health consequences of social isolation, researchers found that loneliness was associated with poor mental health outcomes. Loneliness has also been found to increase a person's risk for suicide, depression, and anxiety.
Given the negative health effects of isolation, Dr. Pianko hopes that questions about a patient's social life will become a routine part of health screenings.
"Doctors should be asking, 'Who's at home with you? What social contacts are you having?' This is a real thing and it's often overlooked," he says.
The rising rates of COVID-19 infections mean that we may be in for at least a few more months of staying home and limiting our contact with others. That's why it's more important than ever to get creative and find other ways to connect with friends, family, and colleagues to maintain your health and fend off feelings of loneliness.
"Don't write off the virtual gatherings," says Dr. Levounis. "Virtual parties and dating and connections of all sorts may not be on par with the real thing, but something is better than nothing."
Ways to Feel Less Lonely During the Coronavirus Pandemic
Hosseini Z, Veenstra G, Khan NA, Conklin AI. Social connections and hypertension in women and men: a population-based cross-sectional study of the Canadian Longitudinal Study on Aging. J Hypertens. 2020. doi:10.1097/HJH.0000000000002688
Kamiya Y, Whelan B, Timonen V, Kenny RA. The differential impact of subjective and objective aspects of social engagement on cardiovascular risk factors. BMC Geriatrics. 2010;10(1):81. doi:10.1186/1471-2318-10-81
Centers for Disease Control and Prevention. Loneliness and social isolation linked to serious health conditions. Updated November 4, 2020.
Ramezankhani A, Azizi F, Hadaegh F. Associations of marital status with diabetes, hypertension, cardiovascular disease and all-cause mortality: A long term follow-up study. PLoS ONE. 2019;14(4):e0215593. doi:10.1371/journal.pone.0215593
Leigh-Hunt N, Bagguley D, Bash K, et al. An overview of systematic reviews on the public health consequences of social isolation and loneliness. Public Health. 2017;152:157-171. doi:10.1016/j.puhe.2017.07.035
Adverse Childhood Experiences Linked to Justice System Contact
Why More Men Are Taking Their Own Lives
Medically reviewed by Daniel B. Block, MD
Women With PTSD and Depression Face Increased Early Mortality Risk
Further COVID Lockdowns Could Trigger PTSD Symptoms
See If Zyban or Wellbutrin Can Cause High Blood Pressure?
Are There Gender Differences in Suicide and Suicidal Behaviors?
Medically reviewed by Carly Snyder, MD
What Is Toxic Masculinity?
Discrimination Can Lead to Increased Risk of Hypertension
How Bad Relationships Affect Your Health
By Mark Stibich, PhD
How the "Widowhood Effect" Puts Widows at Risk After a Spouse's Death
Social Distancing Has Led to Touch Deprivation: Here's What to Do
How Many People Are Alcoholics in the United States?
Is Depression Really More Common in Women?
Is Drinking a Cause of Domestic Abuse?
How Are Stress and Stroke Risk Linked?
By Elizabeth Scott, MS


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Fantasy Draft Day Pick or Pass: Top 12 Tight Ends by ADP
Draft Strategy, Player Rankings August 15, 2009 Jacob2 Comments
After going through the "pick or pass" of the average draft positions for running backs and wide receivers, we come to the next position on many draft boards, tight end.
While there's a top tier of elite options, the tight end position is pretty deep this year. Players that didn't even make this list could be valuable starters by season's end, but here we'll just review the top 12 picks at tight end according to average draft position.
These ADP values were taken from Fantasy Football Calculator and were current as of August 13, 2009.
Pick or Pass: Top 12 Tight Ends as Drafted in Mock Drafts
1. Jason Witten, Dallas Cowboys – ADP: 4.05 – PICK
As a favorite target of Tony Romo, Witten will get plenty of love this season. He's likely to lead the team in receptions, and that makes him in a class of his own when it comes to tight ends this year. Witten is a pick, and you'll have to burn an early one if you want him on your team.
2. Antonio Gates, San Diego Chargers – ADP: 4.12 – PASS
Many would write off last season as the result of a nagging injury and expect Gates to return to form in 2009, but I think the 2008 season showed us a little something more. Philip Rivers has more targets than just Gates in the Chargers offense now, and Vincent Jackson might be the top target on this team for the future. While he's still one talented tight end, I'd worry about taking Gates this high and expecting him to produce like the Gates of old. I'd much rather wait a bit for a tight end with less risk. I'll pass.
3. Tony Gonzalez, Atlanta Falcons – ADP: 5.04 – PICK
While Gates is questionable, Gonzalez remains steady among the elite tight ends. He's no longer in Kansas City, but Atlanta should utilize him in plenty of passing situations and has christened him as the new "hot route" for Matt Ryan. Don't expect him to be more productive than he was last season — that was likely a career year for Tony G. — but a few touchdowns below that level should be possible. He's a good pick.
4. Dallas Clark, Indianapolis Colts – ADP: 5.10 – PICK
Despite an injury this offseason, Clark's stock has been on the rise lately. As I mentioned in our wide receiver pick or pass, Clark could benefit more than Anthony Gonzalez from Marvin Harrison's departure. He should excel as the second look in this offense and is likely to see the ball coming his way as much as he has in past seasons or more. As a late fifth- or sixth-round pick, you could do worse than taking your tight end a bit early and picking Clark.
5. Greg Olsen, Chicago Bears – ADP: 6.06 – PICK
Unfortunately for those of you drafting later this month, you won't have the benefit of snagging Olsen while his value was still on the rise. With Cutler in town and reports out of training camp that Olsen is already his shiny new toy, Greg Olsen is projected to finish the year as a top-five tight end. As such, he's now being drafted as one, so don't expect a bargain. If you can get him in the late sixth round, that's still pretty good. Any later than that, and you're picking him at a steal of a price. He's a pick.
6. Kellen Winslow, Tampa Bay Buccaneers – ADP: 7.05 – PASS
Kellen Winslow would normally be among the elite tight ends, but his move to the Bucs has hurt his value. While the Bucs expect to use him quite a bit in two-tight-end sets, Tampa Bay is not the play-from-behind, passing offense that Winslow thrived in while in Cleveland. They will rule the field with their defense and two- to three-headed running attack. Even more damaging, Jerramy Stevens will still line up at tight end and has the talent to take some opportunities away from Winslow. Winslow could get some looks in the red zone, but Tampa Bay's talk about spreading the ball around and an unnamed quarterback make him unworthy of a selection before the eighth round. There's better value to be had, and I'll pass.
7. Chris Cooley, Washington Redskins – ADP: 7.11 – PICK
Cooley's one-touchdown season last year was a bit of a fluke. Santana Moss received a lot of attention early in the year, and the Redskins punched it in on the ground throughout the majority of the season. While they looked a little lackluster in their first preseason game this year, the Redskins' offense should still look to Cooley when they need a play, and I'd expect him to return to form this season. Cooley is a solid tight end pick, and he's likely to still be available in the eighth round.
8. Owen Daniels, Houston Texans – ADP: 8.03 – PICK
As a Texan, Daniels carries the hype that the Houston team and fans create every season — the hype that convinces us all that they could be the next explosive offense to hit fantasy football. In truth, they showed they could be a force in 2008. Andre Johnson's always been elite when healthy, and Kevin Walter is on his way to being a known name. Owen Daniels was a blessing at tight end last season for those who snagged him late, and he should continue to be a solid option this year. Much like Witten, he's a primary target when the Texans need a play, and he has the upside to rise higher than this draft stock. Don't be afraid to take him with your pick in the eighth round.
9. John Carlson, Seattle Seahawks – ADP: 9.09 – PICK
Carlson may lose some touches to the newcomer T.J. Houshmandzadeh but he's developing into one of the elite tight ends in the game. Don't expect him to take a big step from his rookie totals in just his second season, but I wouldn't be disappointed if he added a few touchdowns to his 627 yards and five touchdowns from last year. As a late-round tight end selection, Carlson is dependable enough to target in your draft if you'd rather stockpile depth at other positions with your early picks. Carlson is a solid pick.
10. Jeremy Shockey, New Orleans Saints – ADP: 11.04 – PASS
Despite his brutal playing style and his reputation as a playmaker with the Giants, Shockey hasn't done much for the Saints since his trade. Fantasy football is very much about what a player has done for you lately, and Shockey's not earning any street cred. Brees throws the ball more than most, but Shockey was never healthy enough or useful enough to warrant a significant number of passes. He's still carrying this ADP value simply because he's a known name, but I'd much rather have a tight end who has proven their worth in the offense they run — Zach Miller comes to mind. Avoid falling for the name game and pass on Shockey.
11. Heath Miller, Pittsburgh Steelers – ADP: 12.08 – PICK
The Steelers don't give Miller many chances to leave his blocking duties at the line, but Miller can catch the ball very well when called upon. He seemed to be on the rise for several seasons until he had a setback last year. I'm afraid he may have already peaked, but it's hard to complain about a guy that you can draft in the 12th round. I don't love Miller because he lacks upside, but he's solid enough to be worth the pick.
12. Tony Scheffler, Denver Broncos – ADP: 12.12 – PICK
I was a big Scheffler fan when Jay Cutler was in town, but without his great quarterback, I'm not sure where Scheffler lands with this new offense. There were rumors that he would be traded early this offseason, followed by rumors that he was touted by coaches as one of the best pass-catching tight ends in the NFL. I side with the coaches on that one, but he might not be able to show it unless Kyle Orton makes a point of getting him the ball. Scheffler will still share time with Daniel Graham, the better blocker and a former Patriot, which limits Scheffler's value, but it does not limit it enough to prevent me from taking a chance on him in the 12th round. Expect to see what he's worth this preseason. If he looks like he's getting involved, he's worth this pick.
While we only covered the top-12 tight ends in this "pick or pass" feature, there are plenty more out there to be had in your fantasy drafts. The tight end position should be fairly deep this season, and guys like Visanthe Shiancoe or Zach Miller might be all you need to win your championship.
As always, the comments are yours. If you have questions about tight ends or comments on our rankings or passes, you know what to do.
2009 draft, ADP, Antonio Gates, average draft position, Chris Cooley, Dallas Clark, draft prep, fantasy football draft, Greg Olsen, Heath Miller, Jason Witten, Jeremy Shockey, Jerramy Stevens, John Carlson, Kellen Winslow, Owen Daniels, pick or pass, Player Rankings, stud, TE, tight end, Tony Gonzalez, Tony Scheffler, Visanthe Shiancoe, Zach Miller
NFL Divisional Championships: Hot Hands and Cold Shoulders
Start or Sit January 17, 2009 Jacob1 Comment
Once again, this weekend, we get a game that could very literally end with a final score of 3-0 and a game that could have a combined score of more than 70 points. Welcome the AFC and NFC championship games.
When I logged into the site to get geared up for this weekend, I got an extra treat. You want to know what the top search term of late leading people to Fantasy Football Fools is?
Booty. That's right. I have a sneaking suspicion why that is, but it still doesn't make it any less funny.
So with booty said, let's get down to booty, er, business.
If you're setting your salary cap playoff rosters this week, you're probably locked in with them until the Super Bowl. There's two ways to go here. You can either pick a collection of players from both teams that you expect to do well enough in this round and in the Super Bowl or you can suck it up and only pick players from the two teams you see making it all the way.
I'll admit, I have the fear in me about being bold and only choosing players from my Super Bowl pick teams, but I'm so going there.
Philadelphia Eagles at Arizona Cardinals
I don't know what to think of the Arizona Cardinals. Many analysts predicted they would match the Falcons in the Wild Card round after their strong final game of the season, but I doubted them when they went into Carolina. I thought their possession of a running game was just an oversight by the Falcons defense and that the defensive plays made the Wild Card round were fluky.
In Carolina, Arizona showed us that they have a defense that will make plays on the ball. Their secondary was outstanding. They complimented it with a little bit of a running game again, thanks to Edgerrin James and Tim Hightower, despite being able to get the ball into Larry Fitzgerald's hands even if he was covered by a flock of Canadian geese — the kind that brings down planes.
Despite their success, it's hard not to keep betting on their demise…they are the Buzzsaw after all.
Of course, there's no overwhelming favorite on the other side of the field. The Eagles are practically the same team, only in the NFC East. The Eagles started off looking like one of the best in the division before they sank to the bottom of the barrel after a ferociously embarrassing tie with the Cincinnati Bengals when Donovan McNabb didn't even know that ties were possible.
Thanks to the failings of many a team standing in their way, the Eagles got hot at the right moment and went on a streak to get into the playoffs. Donovan McNabb has looked great, and Brian Westbrook has been required to do only light lifting. The formula has been working to perfection.
On Thanksgiving, the Eagles began their winning streak against the Cardinals. Arizona was clobbered by the combined scoring power of Brian Westbrook and Donovan McNabb, but since that game, Brian Westbrook has virtually and literally disappeared from the field.
If the Eagles are going to win this one, the offense is going to need a big game from Brian Westbrook. Otherwise, it's very possible that McNabb gets Delhomme-d and leaves his team fighting on the wrong side of a turnover battle if Arizona's suddenly-dominant secondary shows up again.
I'm going with the Cardinals here. They're at home with a newfound spirit in the playoffs. Maybe that's crazy. Maybe I just don't really want to see an all Pennsylvania Super Bowl, or maybe I hate part of myself. Maybe I just want an offensive team to get in the Super Bowl. Whatever the reason, I'm on the Buzzsaw bandwagon.
At least we know their going to put up some fantasy points this week.
Hot Hands: Kurt Warner, Larry Fitzgerald, Donovan McNabb, Brian Westbrook (Q), David Akers
Bubble Boys: Tim Hightower, Anquan Boldin (Q), Neil Rackers, Arizona D/ST, Eagles D/ST, Brent Celek
Cold Shoulders: DeSean Jackson, Kevin Curtis, Jason Avant, L.J. Smith, Edgerrin James
Baltimore Ravens at Pittsburgh Steelers
Personally, I am not a fan of this matchup.
Watching these two teams slam into each other repeatedly for four hours with minimal points on the board just leaves me feeling unsatisfied — especially as a fantasy football fan. The team that makes the most mistakes is going to lose this one, and since I called it twice before, I have to continue my trend of calling on Joe Flacco's rookie shortcomings to suddenly rise to the forefront.
If the Steelers can successfully take Derrick Mason out of this game, Flacco will become pretty ineffective. Without Flacco, the Ravens have LeRon McClain, who is already a little banged up, and some guy we used to know the name of named Willis McGahee. Sure, they could put something together with that running back committee. They even have Ray Rice, too, but not against the Steelers defense.
Ben Roethlisberger may be concussed, but maybe he plays better when he sees two or three of every receiver. His long ball and a healthy Willie Parker helped the Steelers run right over the Chargers last week, and it'll help them put up enough of a fight against the Ravens.
If you're looking for a kicker, I like Jeff Reed in this game. I know that the Cardinals and the Eagles are playing in a more offensively friendly matchup, but Jeff Reed is probably going to be one of the only players scoring points this Sunday night. You might as well get a piece of the action.
Hot Hands: Ben Roethlisberger, Santonio Holmes, Jeff Reed, Matt Stover, Steelers D/ST, Ravens D/ST
Bubble Boys: Willie Parker, Hines Ward, LeRon McClain, Joe Flacco, Todd Heap, Derrick Mason
Cold Shoulders: Ray Rice, Willis McGahee, Heath Miller, Mark Clayton
Lineup Calls
I don't know about you guys, but I'm going to go all-in with the Cardinals and Steelers on my roster this weekend. At least if Larry Fitzgerald and Kurt Warner end up sitting out the Super Bowl, I will know that I tried and failed brilliantly.
Sure, I could throw Brian Westbrook on my roster as a safety valve and capitalize if the Eagles were to make it into the Super Bowl, but where's the fun in that? Besides, no matter what running back gets to the Super Bowl from the NFC, they're not going to do much against the Baltimore Ravens or the Pittsburgh Steelers.
So this weekend, I'm a Buzzsaw-lovin' Arizona Cardinals fan. Maybe they'll make it to their first Super Bowl, and that's a story that might even spare us the press on T.O. and Brett Favre for a few days.
Anquan Boldin, Ben Roethlisberger, Brent Celek, Brian Westbrook, championship, David Akers, Derrick Mason, DeSean Jackson, Donovan McNabb, Edgerrin James, Heath Miller, Hines Ward, Jason Avant, Jeff Reed, Joe Flacco, Kevin Curtis, Kurt Warner, L.J. Smith, Larry Fitzgerald, LeRon McClain, Mark Clayton, Matt Stover, Neil Rackers, NFL, playoffs, postseason, Ray Rice, Santonio Holmes, Tim Hightower, Todd Heap, Willie Parker, Willis McGahee
Divisional Playoffs, Part 2: Hot Hands and Cold Shoulders
Start or Sit January 11, 2009 JacobLeave a comment
So the Cardinals have game — and a run game at that. Of course, who really needs a balanced attack when Larry Fitzgerald can do whatever he wants on the field and you benefit from more than five turnovers?
Looks like the Buzzsaw is bound for the next round, so who will get you there in the fantasy playoffs?
San Diego Chargers at Pittsburgh Steelers
The Chargers come into Pittsburgh after finishing strong and knocking the Indianapolis Colts off in overtime with the legs of Darren Sproles, but the Steel Curtain closes this attack. Without LaDainian Tomlinson, I don't see Sproles being able to carry the Chargers far against the Pittsburgh defense, and Philip Rivers cannot do it all with Troy Polamalu covering the field.
The Steelers offense is weakened with a concussed Ben Roethlisberger, but they can still pound the ball with Willie Parker and Mewelde Moore. The Chargers will make more mistakes, and the Steelers have enough to capitalize on them. Even though San Diego has been nice to opposing quarterbacks all season, it's hard to put faith in the arm of a guy who got taken off in a stretcher just weeks ago. I'll stick with the run game.
Try as he might, Rivers shouldn't be able to take this one, but he can certainly try with Vincent Jackson and some help from Sproles.
Hot Hands: Willie Parker, Philip Rivers, Vincent Jackson, Darren Sproles
Bubble Boys: Mewelde Moore, Ben Roethlisberger, Santonio Holmes, Hines Ward, Antonio Gates, Nate Kaeding
Cold Shoulders: Heath Miller, LaDainian Tomlinson
Philadelphia Eagles at New York Giants
The Eagles, much like the Chargers, had it all fall into their lap at the end of the season. They're hot right now, and it's hard to like the Giants more than the Eagles with the Giants cold finish to the regular season.
Despite the return of Brandon Jacobs, the Giants are likely to have a hard time running the ball against this Eagles squad, and the momentum is in the Eagles' favor. The Giants will miss having Plaxico Burress as a playmaker. They either lose this game or take it in a nail-biter.
Calling it for Philadelphia, I like Brent Celek as a sleeper tight end. L.J. Smith is only going to see limited action, and Celek gets the start. For those of you trying to budget your roster for this week, Celek is a nice 'buy low' to go big at other positions.
Hot Hands: Donovan McNabb, Brian Westbrook, Brent Celek, Brandon Jacobs, David Akers
Bubble Boys: Eli Manning, Kevin Boss, Domenik Hixon, Ahmad Bradshaw, Derrick Ward
Cold Shoulders: L.J. Smith, Amani Toomer
Ahmad Bradshaw, Amani Toomer, Antonio Gates, Ben Roethlisberger, Brandon Jacobs, Brent Celek, Brian Westbrook, Darren Sproles, David Akers, Derrick Ward, Domenik Hixon, Donovan McNabb, Eli Manning, Heath Miller, Hines Ward, Kevin Boss, L.J. Smith, LaDainian Tomlinson, Larry Fitzgerald, Mewelde Moore, Nate Kaeding, Philip Rivers, playoffs, Santonio Holmes, Start or Sit, Vincent Jackson, Willie Parker
Q&A QB: How to Draft First Overall in Nine-Team Division
Draft Strategy August 20, 2008 JacobLeave a comment
Q&A QB is a new head-smacking, hard-hitting, name-taking question and answer series where Jacob assists readers and his Twitter followers in perfecting their draft strategy and winning their league. This post is the first run at it. Let Jacob know what you think in the comments, and if you'd like to be featured in a future Q&A QB post, send Jacob an email or tweet him, whatever that means.
This week in Q&A QB, we'll take a look at several questions and a walkthrough for how to draft with the first overall pick in a nine-team division.
QUESTION: I have the first pick in the draft, and there are nine teams in a point-only division. What would your team look like?
Basically, you luck out with LaDainian Tomlinson then load up on wide receivers that score a lot and a top quarterback. Once you have found your top players in each category, snag a productive second running back and another receiver.
I suggest using this draft strategy: L.T., WR, WR, RB or QB, RB or QB, WR. Flesh out your roster from there.
After taking L.T. in the first, hopefully you will still be able to pick two out of Marshawn Lynch, Reggie Wayne, Terrell Owens and Braylon Edwards for your second and third round back-to-back picks. Lynch is hard to pass up if he is there, but he is more a yardage guy than a touchdown machine. Of course, one can always hope for change.
FOLLOW-UP QUESTION: I'm obviously going L.T. first, and since it's a nine-team league, my next pick will be the 18th overall pick.
With the second and third round back-to-back picks, I was thinking Braylon Edwards then, if available, one of the top-10 QBs. Hoping Romo will slip and fall that far, but I'm doubting it. So most likely it will be Drew Brees or Matt Hasselbeck. That way, I at least have a top tier in each position and fill in from there.
On my next picks, I'm thinking players like Santonio Holmes will slip to me and maybe someone like LenDale White. What are your suggestions?
I'd target Braylon Edwards if you can get him in the second round. If not, take one of the top-10 WRs if there is still one on the board.
In your third round, I think you could go WR or QB. If Romo is still on the board, definitely take him. Brees is probably worth taking as well.
If a top WR like Andre Johnson, Larry Fitzgerald or T.J. Houshmandzadeh is still on the board, I might pass on Brees and take another WR hoping that an elite QB will fall to you.
I definitely would not use your third round pick on Hasselbeck. I'm avoiding him this season, and I don't think he's worth a high pick this year. His WRs are all banged up and the new RBBC could reduce Hasselbeck's throwing attempts.
In the fourth round, I would look at the QB situation and decide what you want to do. There may still be one or two elite QBs here. This pick is close to where Ben Roethlisberger is being taken, but I think it's a little high for him.
If you are worried you are going to miss out on all the top QBs, take one here with one of your picks in the fourth and fifth rounds. Otherwise, you could wait longer.
Here's the strategy with waiting:
You could push your luck and hope that Derek Anderson falls to you in the sixth round. I think he's got about as good a chance as Big Ben of being a strong QB this year. With just nine teams, you'll only be about 54 picks in by the sixth round and just across the 60 pick mark when your pick comes up.
In standard scoring, that's where Anderson, Hasselbeck (if you like him) and Jay Cutler are all going. You could take two of those guys back-to-back in the sixth and seventh rounds to have a strong QB tandem that could trade off every week.
Note: This advice was given before Anderson's concussion against the Giants, but I still think he can be counted on this season.
It's really up to you how you want to play the QB, but don't reach for anyone. Brett Favre, Aaron Rodgers and Jake Delhomme also make good backup QBs that you can probably get in the eighth round with just nine teams. Just depends on how many teams are in need of a QB by the time the sixth round rolls around.
Back to the fourth round, if you decide to pass on a QB there or have taken one already in the third round, you should look at Michael Turner, Edgerrin James, Thomas Jones or LenDale White here. All of them are 1) strong workhorse RBs that will get the majority of carries for their team and 2) not going to lose TD touches.
Turner and Edge are both going to get plenty of carries as their young QBs develop. Jones will have the running lanes open because of Favre. White gets so many chances to run the ball that gravity forces him to produce. If any of them are available, spend a pick on them and then another WR like Plaxico Burress, Torry Holt, Roy Williams or maybe Brandon Marshall if you don't mind his two- or three-game suspension.
I like all of those guys better than Santonio Holmes. I have some concern that Big Ben is not going to throw the TDs as much this year, and when he does throw them, I think Holmes loses catches to Heath Miller and Hines Ward.
From there on out, look for value picks that get a lot of touches and targets in their offense.
Stick with guys that have huge upsides and little risk, and you should improve a lot this year. With a nine-man league, there will probably be plenty of waiver wire grabs to save your team by the middle of the season as well.
2008 draft, Aaron Rodgers, Andre Johnson, Ben Roethlisberger, Brandon Marshall, Braylon Edwards, Brett Favre, Derek Anderson, Drew Brees, Edgerrin James, fantasy football draft, fantasy football draft strategy, Heath Miller, Hines Ward, Jake Delhomme, Jay Cutler, LaDainian Tomlinson, Larry Fitzgerald, LenDale White, Marshawn Lynch, Matt Hasselbeck, Michael Turner, Plaxico Burress, Q&A, QB, quarterback, Reggie Wayne, Roy Williams, Santonio Holmes, T.J. Houshmandzadeh, Terrell Owens, Thomas Jones, Tony Romo, Torry Holt, wide receiver, WR
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Any idea what's the make and the model of that yellow car?
The cast includes Nicholas Hoult, Felicity Jones, Anthony Hopkins and Ben Kingsley.
There's no release date yet.
Update – According to fellow movie fan Glenn, the car is a Jaguar F-Type S Coupe.


Wellshire is a subdivision located at the intersection of E Yale Ave & S St Paul St in Denver, CO. The Wellshire Golf Course is a major attraction located just a short drive from Wellshire. Children and pets can enjoy Three Pond Park which is located near by this subdivision.
See what your home is worth With an Instant Home Valuation Online. Want advice on selling your house? We provide a free staging consultation, pre-listing prep plan, and a Wellshire real estate market analysis. Call us at 303-325-5690 to learn more.
New to the Area? Call our Wellshire real estate agent at 303-325-5690 to schedule your tour of Homes in Denver CO.


Wren likes to sprint through fields, chasing birds, gophers and all sorts of critters. Sometimes, Wren loses track of her humans in the tall grass. Good thing Wren wears a Hattie Tag. Hattie brings you home.
Hattie Rex Pet ID Tags are personalized by you and handmade by our three talented metalsmiths/dog tag artists in our downtown Bozeman, Montana studio, and retail store.
We make these unique dog tags for pets by hand from start to finish. We start with thick sheets of metal, including copper, brass, aluminum, nickel silver, and sterling silver. We cut the metal pieces of each handcrafted dog tag using a disc cutter, a pancake die with a hydraulic press, or by hand using a jeweler's saw. We remove any metal burrs or rough edges with a belt sander. We'll do the final polish later, but we sand it down first to make sure we have an even, flat surface for the next step.
This step is our favorite because it's where the piece of metal becomes your dog's tag! We place the metal pieces on a steel bench block and use an antique hammer to hand-stamp your dog's name and phone number (and any other information you like) on the dog tag. The hand-stamping process is what differentiates our handmade dog tag method from machined dog tags or engraved dog name tags. Every letter and number is stamped individually by hand, creating a unique, one-of-a-kind artisan dog name tag. The spacing of the letters is artistically executed, ensuring that your handmade dog tag isn't mistaken for a robot-produced dog name tag.
The dog tags go through a round of polishing in a tumbler. After tumbling, we darken the tags to add contrast before they go through a final polishing by hand. For our traditional hanging dog tags, we attach a USA-made, heavy-duty, zinc-plated stainless steel split ring to attach to your dog's collar. This makes our mixed metal dog id tags durable and safe to ensure that your dog tag art will last for years to come.
Our custom pet id tags make great gifts for dog lovers or anyone who needs a dog gift. Shopping for someone who has everything? A gift for their dog is always a hit. Our dog tags are available in sizes extra small to extra large, so we have tags for every dog breed and cat tags, too! If you're not sure which dog tag to get, we offer gift cards, too. It's the perfect gift when it has to be special.
Dog or cat id tags can save your dog's life if she ever runs away. Every year, thousands of dogs are lost from their owners. When they are found, how do they communicate their phone number and address without a dog ID tag? Wearing a tag --any tag -- is the quickest and easiest way for your dog's finder to help your dog come home when she is lost. Whether you choose to buy a machine tag engraved dog tag, or write your dog's phone number on her collar with a Sharpie, or treat yourself to a high-quality, handmade metal dog tag like ours, it's imperative that your dog wears a pet name tag that includes a phone number.
While microchipping is a very common dog id method, the dog microchip requires that the finder take the dog to a veterinarian or animal shelter to scan the chip to retrieve the information. Although we all hope that anyone who finds a dog would take this step, there is no guarantee that someone would take the time to do this, or would have the time to do it quickly. Just think, every minute that it takes someone to drop everything and run your lost dog to the humane society is a minute that you are worried and scared because your dog is missing! Save yourself the heartache and make sure your dog is wearing an identification tag.


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Q: System.NullReferenceException when attempting to nullify Listbox.DataContext - windows phone I have spend the good part of today trying to work out why I am getting this exception. I have a Listbox that is bound to a List in my application. Here is the code:
XAML:
    <ListBox x:Name="SavePanel"
                     ItemsSource="{Binding}"
                     Background="{StaticResource PhoneBackgroundBrush}" Visibility="Visible" SelectionChanged="SavePanel_SelectionChanged" >
                <ListBox.ItemTemplate>
                    <DataTemplate>
                        <TextBlock Margin="20,5,5,5" Text="{Binding}" FontSize="43"></TextBlock>
                    </DataTemplate>
                </ListBox.ItemTemplate>
    </ListBox>

C#:
List<string> saveNames;

public SaveProject()
{

    InitializeComponent();

    populateList();

    SavePanel.DataContext = saveNames;
}

private void populateList()
{
    if (settings.Contains("saveNames")) //if there are previous saves, pull the names from localstorage
    {
        string test = settings["saveNames"] as string;
        string[] tempArray = test.Split(',');
        totalSaves = tempArray.Length;
        saveNames.Clear(); // clear list
        for (int i = 0; i < totalSaves; i++)
        {
            saveNames.Add(tempArray[i]); // populate list
        }
    }
}

Just a quick explanation of "populateList": if "saveNames" exists in localstorage (a list of names separated by commas) the function will split it into an array and then add each name to the List, which in turn goes into the ListBox. This works fine.
I also have no problems displaying, adding, or deleting items from the list. The problem is updating it in the ListBox;  want to delete an item from the List "saveNames", and then update the ListBox with the new values. I currently have a button on the application bar that is supposed to do this. I've removed all other code from the event and narrowed it down to simply attempting to nullify the ListBox, and then add the data context again without making any changes; I figured this will work and I can move up from there to find out where I am going wrong in my code. So here is the code for the application bar event now:
private void DeleteProject_Click(object sender, EventArgs e)
{

    SavePanel.DataContext = null;
    SavePanel.DataContext = saveNames;

}

I run my code, everything works until I hit the "delete" button. VS breaks and I get:
A first chance exception of type 'System.NullReferenceException'

This has me stumped; Im not even making changes to the List! It's clear the exception is because of the SavePanel.DataContext = null line. I just have no clue what I am doing wrong here.
Any help would be greatly appreciated!
private void SavePanel_SelectionChanged(object sender, SelectionChangedEventArgs e)
{

    var lb = (sender as ListBox);
    theFileName = lb.SelectedItem.ToString();

    // repopulate appbar to show delete and save buttons
    for (int i = ApplicationBar.Buttons.Count - 1; i >= 0; i--)
    {
        ApplicationBar.Buttons.RemoveAt(i);
    }

    if (totalSaves < 10)
    {
        ApplicationBarIconButton button1 = new ApplicationBarIconButton();
        button1.IconUri = new Uri("/Assets/Icons/add.png", UriKind.Relative);
        button1.Text = "Add";
        ApplicationBar.Buttons.Add(button1);
        button1.Click += new EventHandler(AddProject_Click);
    }

    ApplicationBarIconButton button2 = new ApplicationBarIconButton();
    button2.IconUri = new Uri("/Assets/Icons/delete.png", UriKind.Relative);
    button2.Text = "Delete";
    ApplicationBar.Buttons.Add(button2);
    button2.Click += new EventHandler(DeleteProject_Click);

    ApplicationBarIconButton button3 = new ApplicationBarIconButton();
    button3.IconUri = new Uri("/Assets/Icons/save.png", UriKind.Relative);
    button3.Text = "Save";
    ApplicationBar.Buttons.Add(button3);
    button3.Click += new EventHandler(SaveProject_Click);
}

The selectionchanged handler is just to store the value in a string called "theFileName"; There is also some manipulation of the appbar buttons here.

A: Your problem is, if you select an item in your list box, then click delete button. SelectionChanged event will be fired right after the line
SavePanel.DataContext = null;

This happen because your SavePanel selected index has change to -1 when you clear the Datacontext and rise the event. This cause NullReferenceException. There're several ways to bypass this. One suggestion is check SavePanel.DataContext in SelectionChanged event. Add this code at the start of the event
if(SavePanel.DataContext == null)
   return; //if save panel data context is null then do nothing

redpajama_set_name: RedPajamaStackExchange


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'Rings' Pushed Back From October To February By Paramount
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rings online - http://ringsonlinemovie.com. After having several release date delays, Paramount is finally bringing its long-awaited horror sequel Rings to theatres next month. The film is directed by F. Javier Gutierrez (Before the Drop) from a screenplay by Jacob Estes (Suggest Creek), David Loucka (Home at the End of the Avenue) and Akiva Goldsman (I, Robot). While Paramount dropped a creepy new preview last week, another one has since made its cheerful way online (along with a new poster) that will without a doubt send chills down your back as more footage for the upcoming picture is revealed. It functions as a final episode in this horror franchise, plus it features the original cast of A. Michael Baldwin, Reggie Bannister, Bill Thornbury, Kathy Lester, and Angus Scrimm. Audiences will have the capacity to determine if the next episode, Rings, can meet the original on February 3, 20 17. Moviegoers will see in Rings movie the girl needs to save her boy friend at any price.
Directed by F. Javier Gutierrez, Rings is the newest entry in the horror franchise, reports Movie Web The cast of the film also includes Vincent D'Onofrio, Bonnie Morgan, Aimee Teegarden and Johnny Galecki. A video in the marketing staff of the approaching third instalment of horror franchise the minute everyone has been captured by The Ring dreads: a horror-movie visiting li Fe in front of us.
The 3rd entry features a brand new cast that contains Vincent D'Onofrio, A-Lex Roe, Johnny Galecki, Aimee Teegarden, Bonnie Morgan and Matilda Lutz. Rings doesn't appear bad enough to eliminate you (despite what the poster appears to suggest ), but it also doesn't look like anything specific. The plot centers on a video tape which will end up in the viewer a week later, being killed. Rings is an up and coming 20 17 American strong mental blood and gore movie coordinated by F. Javier Gutiérrez, produced by Laurie MacDonald and Walter Parkes, and composed by David Loucka, Jacob Estes and Akiva Goldsman.
Paramount released the very first trailer back making fans wait a year to get a second look at this sequel that was sure to be frightening. See today's front and back pages, download the paper, buy back problems and utilize the historic Daily Express newspaper archive. With the entrance of a preview that is new as well as this poster, it seems that this date may finally be set in stone for Samara's return. One of the common criticisms of Lord of the Rings and The Hobbit is that the heroes are virtually all guys. Take a gander at the poster, as we wait for the new trailer to drop after this week, while we wait to determine if Rings can provide this franchise back to its former box office glory. The film releases on February 3. Watch the newest trailer above as well as the original one below. It's the first picture that was an American re make of a horror movie classic.
Among the most iconic moments in horror during the past number of decades is definitely the second when Samara comes out from the television set in the original picture. Rings stars Bonnie Morgan, Alex Roe, Johnny Galecki, Aimee Teegarden, Matilda Lutz and Vincent D'Onofrio.
rings online
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Congrats!! A lovely lovely line! Will you be in the May 2019 group?
That's funny! I'm surprised they didn't test for pregnancy first!
I'm due 22nd of may! So close!
Congratulations again and try to not stress to much... it's very easy to get anxious during early pregnancy, enjoy it!
Congrats I got my BFP at 12dpo.
Were trying for baby #3 since late 2015. Started on vitex and iron coq10 last cycle had a chemical. Now this. Nervous though we had two miscarriages last year. Just need to stay relaxed.
Thanks so much for getting back to me! Yes I think being happy not just physically but mentally is so important, and something I probably need to work on myself. It is hard when you are the one who is trying to make everyone else happy. At the end (and start) of the day I just have no energy cause i'm so burnt out. I have tried and failed at so many fitness / diet plans because I just don't enjoy it. Here's to finding what works :) i'm glad you have been able to make positive changes, with the latest positive being the most special!
Congratulations what a wonderful story. A happy and healthy 9 months ahead!


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Q: Changing symbology orientation in QGIS I have a project based on data from a water company, but the arrow heads are all pointing in the wrong direction to indicate the direction of flow.
Basically I need to turn all the SYMBOLROTA values to negatives. How can I change all the values of a set of features to become minus - it might be a search function of a script or something?
Better than that would be to be able to change the type of rotation (like you can do in AutoCAD) to be anti-clockwise rather than clockwise. I haven't been able to find out how to do that but that would be the easiest?

A: We worked it out - in the attributes table there's a Field Calculator where you can do various calculations based on the data.
We selected all the data points and then opened the Field Calculator and updated the existing field (tickbox near top right) and applied the simple calc  "SYMBOLROTA" * -1 which just multiplies all the values in the SYMBOLROTA column and puts the answers back in the SYMBOLROTA column replacing the original values.