text:
Q: No attribute present I am quite new to python and I am getting an attribute error.
import FileHandeling as fh;
import os;

CounterFilePath = os.path.dirname(os.path.realpath(__file__))+"/counter.txt";
FilePath = os.path.dirname(os.path.realpath(__file__))+"/FileIO.txt";

class Employee:

    def createEmployee(self):
        numOfEmployees = int(input("Enter number of employees: "));
        empDetails = [];
        for i in range(numOfEmployees):
            empFName, empLName, empSalary,  empEmailId = raw_input("Enter employee first name: "), raw_input("Enter employee last name: "), raw_input("Enter employee salary: "), raw_input("Enter employee Email ID: ");
            string = str(i)+" "+empFName+" "+empLName+" "+empSalary+" "+empEmailId+"\n";
            empDetails.append(string);
        with open(FilePath,"a+") as fo:
            fo.seek(0);
            fh.createFile(fo,numOfEmployees,empDetails,CounterFilePath);

    def searchEmployee(self):
        choice = int(input("Press:\n1 to search by First Name\n2 to search by Last Name\n3 to search by Salary\n4 to search by Email ID\n"));
        print "Enter the",;
        if(choice == 1):
            print "First Name:",;
        elif(choice == 2):
            print "Last Name:",;
        elif(choice == 3):
            print "Salary:",;
        elif(choice == 4):
            print "Email ID:",;
        searchStr = raw_input();
        with open(FilePath,"r") as fo:
            string = fh.readFile(fo,searchStr,choice-1);
        while line in string:
            print line;

    def updateEmployee(self):
        print "Leave the entries empty if you dont want to update that entry.";
        lineNum = input("Enter the line number of the entry you want to update: ");
        with open(FilePath,"r") as fo:
            empFName, empLName, empSalary,  empEmailId = raw_input("Enter employee first name: "), raw_input("Enter employee last name: "), raw_input("Enter employee salary: "), raw_input("Enter employee Email ID: ");
            if(empFName == ""):
                record = fh.readFile(fo,lineNum-1,0);
                empDetails = record[0].split();
                empFName = empDetails[1];
            if(empLName == ""):
                record = fh.readFile(fo,lineNum-1,0);
                empDetails = record[0].split();
                empLName = empDetails[2];
            if(empSalary == ""):
                record = fh.readFile(fo,lineNum-1,0);
                empDetails = record[0].split();
                empSalary = empDetails[3];
            if(empEmailId == ""):
                record = fh.readFile(fo,lineNum-1,0);
                empDetails = record[0].split();
                empEmailId = empDetails[4];
            updateStr = str(lineNum-1)+" "+empFName+" "+empLName+" "+empSalary+" "+empEmailId+"\n";
            fh.updateRecord(fo,FilePath,updateStr,lineNum-1);

    def deleteEmployee(self):
        lineNum = input("Enter the line number of the entry you want to delete: ");
        with open(FilePath,"r") as fo:
            fh.deleteRecord(fo,FilePath,lineNum-1);

    def main(self):
        goOn = True;
        employee = Employee();
        while goOn:
            choice = input("Press:\n1 to enter a new employee\n2 to search employee\n3 to update employee\n4 to delete employee\n0 to exit\n");
            if(choice == 1):
                employee.createEmployee();
            elif(choice == 2):
                employee.searchEmployee();
            elif(choice == 3):
                employee.updateEmployee();
            elif(choice == 4):
                employee.deleteEmployee();
            elif(choice == 0):
                goOn = False;
            else:
                print "Wrong Choice!!!";

emp = Employee();
emp.main();

Here I am importing this class:
class FileHandeling:
    def createFile(fo,numOfRecords,data,counterFile):
        #Getting the value of counter
        frc = open(counterFile,"r");
        counter = int(frc.read());
        frc.close();

        #Taking input and writing to the file
        for i in range(counter,numOfRecords+counter):
            string = str(i)+data[i];
            fo.write(string);
            counter += 1;

        #Writing back to counter the updated value.
        fwc = open(counterFile,"w");
        fwc.write(str(counter)+"\n");
        fwc.close();

    def readFile(fo,searchStr,criteria):
        line = fo.readline();
        string = [];
        while line:
            entries = line.split();
            if(searchStr == entries[criteria]):
                string.append(line);
            line = fo.readline();
        return string;

    def printFile(fo):
        fo.seek(0);
        lines = fo.readlines();
        print "The File: "
        for line in lines:
            print line;

    def updateRecord(fo,fileLoc,updateStr,lineNum):

        #Replacing the given record with he updated record and writing back to file
        lines = fo.readlines();
        fwu = open(fileLoc, "w");
        lines[lineNum]= updateStr;
        for line in lines:
            fwu.write(line);
        fwu.close();

    def deleteRecord(fo,fileLoc,lineNum):
        #Deleting the record
        lines = fo.readlines();
        fwu = open(fileLoc, "w");
        lines.pop(lineNum);

        #Correcting the Employee Ids and Writing Back to File
        for line in lines:
            entry1, entry2, entry3, entry4, entry5 = line.split();
            entry1 = str(lines.index(line));
            line = entry1+" "+entry2+" "+entry3+" "+entry4+" "+entry5+"\n";
            fwu.write(line);
        fwu.close();

        #Reducing Counter value
        frc = open(counterFile,"r");
        counter = int(frc.read());
        frc.close();
        fwc = open(counterFile,"w");
        fwc.write(str(counter-1)+"\n");
        fwc.close();

In this code I am trying to replicate a database with the help of file but my code gives error saying that 'module' object has no attribute 'createFile'. I also tried creating packages and doing like in java but then it started saying that ImportError: No module named src.fileManipulation. they were just my folders in which I was working and wanted them as packages so I put an __init__.py in them and the tutorials said that this will help in making packages but that didn't happen and since both my files were in same directory I imported it directly but now it gives attribute error and I don't know what that means. Please Help.

A: I have executed the code in Python default IDLE after correcting some print statements. I am using Python3 so used print (" "). And the result was an endless loop of
Wrong Choice!!!
Press:
1 to enter a new employee
2 to search employee
3 to update employee
4 to delete employee
0 to exit

My kind requtest to you is to revise Python once again.


text:
Intimacy Coordinators and Vulnerability Consultants
Nathaniel Chua
Actor, Dancer
ACTRA
"Why fit in when you were born to stand out?"
Nathaniel is a 14-year-old versatile and gifted dancer with 10 years of dance training. For 8 years, Nathaniel competed in jazz, tap, hip hop, contemporary, lyrical, ballet and musical theatre. His natural ability and performance quality captivated many judges in Canada and the United States and has garnered him with many recognitions and titles. In 2018, he won the Junior Grand Champion title at the Canadian National Exhibition's Rising Star Talent competition and in 2016, he won Mini Male Best Dancer First Runner up at The Dance Awards in Las Vegas. He was also selected and won local titles such as Northern Movement's A-List Acrobat in 2014/2016, Face of Destiny Dance Competition 2018 and he was the Face of Fever in 2019.
Other accomplishments include winning several dance scholarships such as Jump Dance VIP Mini Male and Junior Winner from 2015 to 2019, Nuvo Breakout Artist Mini and Junior Male Winner from 2017 to 2019, 24 Seven Non-Stop Dancer Junior Male Winner from 2018 to 2020, Radix Core Performer Mini and Junior Male Winner from 2017 to 2018, New York City Dance Alliance Mini Male Outstanding Dancer Winner 2017, Hall of Fame Dance Junior All-Star Dancer 2017, and Dancer Palooza Beat Squad 2018. Throughout this journey, he trained under Travis Wall, Tessandra Chavez, Nick Lazzarini, Tyce Diorio, Mia Michaels, Teddy Forance, Misha Gabriel, Andrew Winghart, Stacey Tookey, Mandy Moore, Wade Robson, Phil Wright, Katy Spreadbury, Brook Pierotti, Francisco Gella, Jess Hendricks, Al Blackstone, Kirsten Russell, Randi & Hefa, Jaci Royal, Mark Meismer, Denise Wall, Lex Ishimoto, Martin Harvey and Blake McGrath.
Outside of his competitive life, he experienced a lot of performance opportunities. Nathaniel was extremely honoured to be selected by Justin Bieber's Choreographer Nick Demoura to dance alongside Justin in Minneapolis as one of the four 'children' during his 2016 World Purpose Tour in front of 15,000 concert fans. He also performed in many music videos as backup dancer for Mini Pop Kids from 2016 to 2020 which includes 24k Magic, Make It Pop, Happier, Who You Are, Truth Hurts, Me and Dance Monkey. Nathaniel made appearances in three commercials for Mini Pop Kids 15-16-17 Albums. He has also appeared on CHCH TV's Tiny Talent Time in 2019 performing his winning solo "Dance With Me" choreographed by Nick Lazzarini (Season One Winner of Fox reality show So You Think You Can Dance).
For the last two years, Nathaniel transitioned over to The National Ballet School of Canada's Professional Ballet Program, where he started to fine tune his technique and to dance with the utmost precision under the Artistic Director Mavis Staines. He performed in The Nutcracker at the Four Season's Centre for the Performing Arts with The National Ballet playing the roles of Rich Boy and Military Boy during the three-week run in the 2019 Christmas season.
Nathaniel will appear in the highly anticipated Netflix movie 13 The Musical starring Debra Messing, produced by Neil Meron (Chicago, Hairspray), written by Tony Award winner Robert Horn (Broadway's Tootsie the Musical, Teen Beach Movie), directed by Tamra Davis (Crossroads, High School Musical: The Series) and composed by three-time Tony Award Winner Jason Robert Brown (The Bridges of Madison County, Parade, Honeymoon in Vegas, 13 the Broadway production). He was selected by Choreographer Jamal Sims (Aladdin starring Will Smith, Disney Descendants 3, When the Beat Drops) to be a part of the male core dancer group Brett's Crew.
Nathaniel continues to expand his skill set by training in music, vocal and acting. In his spare time, Nathaniel likes to challenge himself and give back to our community by cycling across the Greater Toronto Area and raising funds for charity most notably Ride for Heart.
da Costa Talent was designed for a song and dance by 418QE

redpajama_set_name: RedPajamaCommonCrawl


text:
search filter All ContentAll JournalsJournal of Experimental Medicine
Article| May 07 2007
Cytomegalovirus exploits IL-10–mediated immune regulation in the salivary glands
Ian R. Humphreys,
Ian R. Humphreys
Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037
Carl de Trez,
Carl de Trez
April Kinkade,
April Kinkade
Chris A. Benedict,
Chris A. Benedict
Michael Croft,
Michael Croft
Carl F. Ware
CORRESPONDENCE Carl F. Ware: cware@liai.org OR Michael Croft: mick@liai.org
Abbreviations used: HCMV, human CMV; MCMV, mouse CMV; T reg, T regulatory.
Received: November 17 2006
Accepted: April 13 2007
The Rockefeller University Press
J Exp Med (2007) 204 (5): 1217–1225.
Ian R. Humphreys, Carl de Trez, April Kinkade, Chris A. Benedict, Michael Croft, Carl F. Ware; Cytomegalovirus exploits IL-10–mediated immune regulation in the salivary glands . J Exp Med 14 May 2007; 204 (5): 1217–1225. doi: https://doi.org/10.1084/jem.20062424
The salivary glands represent a major site of cytomegalovirus replication and transmission to other hosts. Despite control of viral infection by strong T cell responses in visceral organs cytomegalovirus replication continues in the salivary glands of mice, suggesting that the virus exploits the mucosal microenvironment. Here, we show that T cell immunity in the salivary glands is limited by the induction of CD4 T cells expressing the regulatory cytokine interleukin (IL)-10. Blockade of IL-10 receptor (IL-10R) with an antagonist antibody dramatically reduced viral load in the salivary glands, but not in the spleen. The mucosa-specific protection afforded by IL-10R blockade was associated with an increased accumulation of CD4 T cells expressing interferon γ, suggesting that IL-10R signaling limits effector T cell differentiation. Consistent with this, an agonist antibody targeting the tumor necrosis factor receptor superfamily member OX40 (TNFRSF4) enhanced effector T cell differentiation and increased the number of interferon γ–producing T cells, thus limiting virus replication in the salivary glands. Collectively, the results indicate that modulating effector T cell differentiation can counteract pathogen exploitation of the mucosa, thus limiting persistent virus replication and transmission.
Mucosal tissues serve as major sites of entry, replication, and exit for many pathogens. Indeed, herpesviruses often persist in and are shed from mucosal tissues for long periods of time despite strong adaptive immune responses in their host. Understanding how pathogens persist in mucosal tissue may assist the design of effective vaccination and immunotherapeutic strategies.
Human CMV (HCMV) is a β-herpesvirus that infects the majority of the world's population. Although this persistent/latent infection is asymptomatic in healthy individuals, HCMV causes multiorgan disease in the immunologically immature (e.g., congenital infection) and the immune-compromised population (e.g., AIDS patients and organ transplant recipients). Asymptomatic shedding in saliva is an important source of virus in natural transmission of HCMV (1–3), implying that virus replication in the salivary glands is pivotal for horizontal transmission. After systemic infection, mouse CMV (MCMV) initially replicates in visceral organs such as the spleen and liver, but virus production is limited by NK cell and adaptive cellular immunity within a week after infection. Despite strong cellular immunity, infectious virus is produced in the acinar glandular epithelial cells within the submaxillary salivary glands (4) and can be detected for several months after primary infection (4–6). Like all herpesvirus, MCMV establishes latency (5, 7), yet very little is known about how CMV persists within the salivary glands. CD4 T cells producing IFN-γ have been described to afford protection at this site (5, 8), but it is not clear if or how these cells are regulated. CMV can inhibit CD4 T cell activation by interfering with IFN-γ–induced MHC class II expression (9). Viral genes that interfere with antigen presentation to CD8 T cells influence virus replication in the salivary glands, suggesting mucosal CD8 T responses are also targeted (10). In BALB/c mice, NK cells and γδ T cells have also been detected within the salivary glands after MCMV infection (11), but their role in clearance is not known. As a target of persistent infection, the salivary glands are exposed to substantial antigenic burden without obvious pathology. Thus, it is likely that inflammatory immune cells at this site may be regulated differently than in other tissues. Potential mechanisms could include induction of T cell anergy or apoptosis (12). Immune responses may also be actively suppressed by regulatory T cells, such as naturally occurring CD4+CD25+ T regulatory (T reg) or T reg cells induced by antigen, which are defined by the expression of suppressive cytokines, including IL-10 or TGF-β (13, 14).
We now report that cellular immunity in the salivary glands to a persistent virus is regulated through an IL-10– dependent mechanism. We observed that persistent MCMV replication in the salivary glands was accompanied by the appearance of IL-10–expressing CD4 T cells specifically within this organ, but not elsewhere. Blockade of IL-10R signaling during infection dramatically decreased virus replication that correlated with increased accumulation of CD4 T cells expressing antiviral IFN-γ. Further, targeting CD4 T cell differentiation through activation of the TNFR family member OX40 (15) increased the ratio of CD4 T cells expressing IFN-γ compared with IL-10 in the salivary glands and reduced persistent replication of MCMV. Collectively, these data show that MCMV exploits the salivary gland environment favoring IL-10 expression by virus-induced CD4 T cells, thus enabling persistent virus replication and horizontal transmission to susceptible hosts.
IL-10–expressing CD4 T cells accumulate in the salivary glands as MCMV replicates
MCMV replication can be detected for 1–2 mo in the submaxillary salivary glands, but not in the spleen, after a primary infection in C57BL/6 (B6) mice (6). Persistent MCMV replication in the salivary glands induced the accumulation of CD4 and CD8 T cells, B cells, NK cells, and antigen-presenting cells (Fig. 1 A). Cytokine expression analysis of salivary gland–derived leukocytes revealed that T cells (primarily CD4 T cells) were the predominant source of low spontaneous expression of antiviral cytokine IFN-γ, which was amplified by ex vivo polyclonal stimulation (Fig. 1 B).
Interestingly, we observed a considerable accumulation in the salivary glands of CD4 T cells expressing the immunosuppressive cytokine IL-10 during persistent MCMV replication, although these cells were not detected in visceral sites such as the spleen or in the lymph nodes draining the salivary glands (Fig. 1, C and E). We found a low percentage of CD4 T cells making detectable IL-10 (0.5–1%) without ex vivo restimulation (Fig. 1 C), suggesting that the results derived from stimulation with CD3/CD28 represented an amplification of cytokine production by these cells. Further reinforcing the notion that this IL-10 production reflected a physiological event in vivo, we found strong expression of IL-10 in salivary gland extracts from infected but not naive mice (Fig. 1 D). Importantly, CD8 T cells and non–T cells did not express notable levels of IL-10, suggesting CD4 T cells were the predominant source of this cytokine (Fig. 1 C). IL-10–producing CD4 T cells did not co-express IL-4, IL-5, IL-13, or FoxP3, implying these cells were not conventional T helper (Th)2 cells or naturally occurring T reg cells (Fig. 1 E). Moreover, the accumulation of IL-10–expressing CD4 T cells accompanied MCMV replication in the salivary glands (Fig. 1 F), demonstrating these T cells were actively induced by the virus infection.
OX40 induces IFN-γ expression and limits persistent MCMV replication
IFN-γ–expressing CD4 T cells inhibit MCMV replication in the salivary glands (8). Although CD4+IFN-γ+ T cells were present (Fig. 1 B), the results suggested that IL-10– secreting cells might limit either antiviral activity of IFN-γ+ T cells or the IFN-γ itself. We hypothesized that shifting the ratio of CD4 T cells to favor IFN-γ production might limit virus replication. To accomplish this, we targeted the TNFR OX40 with an agonist antibody based on the ability of this receptor to enhance IFN-γ secretion (16, 17) and suppress IL-10 production by T cells (18, 19). OX40 was detected on CD4 but not CD8 T cells infiltrating the infected salivary glands (Fig. 2, A and B) and in draining lymph nodes (Fig. 2 B), indicating that ectopic targeting of OX40 with an agonist antibody was feasible. Mice treated with an agonist anti-OX40 antibody at the time of infection had no discernable effect on early (day 7 after infection) viral load in the salivary glands (Fig. 2 C). However, anti-OX40–treated mice had substantially reduced titers of replicating virus at 30 d after infection (Fig. 2 C). This was associated with increased infiltration of mononuclear cells compared with control mice (Fig. 2 D). Further analysis revealed that this cellular infiltrate consisted primarily of CD4 T cells (Fig. 2 E), and we found that the elevated CD4 response was critical for OX40-mediated inhibition of MCMV-persistent replication, as the protective effect was abolished in MHC class II–deficient mice (Fig. 2 F). In contrast, OX40 stimulation did not alter the accumulation of total or MCMV-specific CD8 T cells, or granzyme B–expressing CD8 T cells in the salivary glands (Fig. S1, A–C).
OX40 activation increased the percentage (Fig. 3, A and B) and total numbers (unpublished data) of CD4 T cells, but not CD8 T cells (Fig. S1 D), expressing IFN-γ. Moreover, anti-OX40 treatment also reduced the percentage of IL-10–expressing CD4 T cells (Fig. 3, C and D), altering the ratio of T cells expressing IFN-γ to IL-10 in the salivary glands (Fig. 3 E). This effect of OX40 activation was also reflected in a shift in the expression of IFN-γ and IL-10 in situ (Fig. 3 F). These data show that virus replication in the salivary glands is reduced when OX40 is activated, which is associated with an increased ratio of IFN-γ to IL-10–expressing CD4 T cells.
Blockade of IL-10R limits MCMV replication in the salivary glands
To determine whether the restricted virus replication and the increased ratio of IFN-γ to IL-10–secreting CD4 T cells involved IL-10, we used an antagonist IL-10R antibody (anti–IL-10R) to block signaling. Administration of this antibody enhanced the accumulation of total and IFN-γ–expressing CD4 T cells in the salivary glands (Fig. 4, A and B), but had no effect on the accumulation of CD8+ T cells or NK+CD3− cells expressing IFN-γ (Fig. S2 A). The accumulation of CD4+IL-10+ T cells was not a result of IL-10R signaling in this organ (Fig. 4, C and D). Importantly, virus replication was dramatically inhibited by blocking IL-10R, with no virus detectable in two treated mice (n = 3) after 30 d of infection (Fig. 5 A). Moreover, when anti–IL-10R treatment was started at 7 d after infection to coincide with the appearance of IL-10+ cells (Fig. 1 E), virus levels in salivary glands remained undetectable in five out of eight mice (Fig. 5 B). Collectively, these data highlight the salivary glands as sites of strong IL-10–dependent immune regulation and demonstrate that IL-10–producing CD4 T cells suppress antiviral effector CD4 T cells. The results demonstrate that modulation of the OX40 and IL-10 pathways can block virus replication in this important excretory organ.
The salivary glands are a site of IL-10–dependent immune regulation. We demonstrated that IL-10–producing CD4 T cells suppressed effector CD4 T cells in a model of persistent virus replication at this mucosal site. The results establish that the IL-10 immunoregulatory pathway enables MCMV to persistently replicate in this mucosal organ. Counteracting this viral strategy by modulation of either the costimulatory OX40 pathway with an agonist antibody or targeting the immunoregulatory IL-10 pathway with an antagonist antibody, limited persistent virus replication in the salivary glands, attenuating shedding of virus, thus potentially reducing transmission to susceptible hosts.
Sustained activation of the TNFR OX40 with an agonist antibody favored the differentiation and accumulation of CD4 T cells that produced IFN-γ in the salivary glands to counteract the inhibitory effects of the IL-10–dominated immune response. OX40 was expressed on antigen-activated CD4 T cells, which were readily detected in the spleen, salivary glands, and draining lymph nodes from MCMV-infected mice. T cells express OX40 for short periods of time after antigen activation; thus, virus reactive T cells were the mostly likely targets of the antibody, and therefore, treatment subsequently altered virus-specific cytokine expression. Activation of OX40 can favor generation of effector Th1 or Th2 cells (16, 17, 20, 21), which are distinguished by their expression of IFN-γ or IL-4, IL-5, and IL-13, respectively. OX40 stimulation during MCMV infection enhanced the accumulation of CD4 T cells coexpressing IFN-γ and the activation-associated isoform of CD43 (unpublished data), suggesting that OX40 signaling directly impacted the differentiation of antiviral Th1 primary effector cells.
CD4 T cells in the salivary glands were identified as the predominant source of IL-10, representing ∼80–90% of all IL-10–expressing cells. In contrast to peripheral chronic arenavirus infection (22, 23), MCMV replication in the salivary glands did not induce expression of IL-10 by CD11c+ dendritic cells (unpublished data). IL-10–expressing CD4 T cells did not co-express the Th2-associated cytokines IL-4, IL-5, or IL-13, nor did they express the transcription factor FoxP3, which is a marker of naturally occurring CD4+CD25+ T reg cells. Collectively, the data indicated these T cells were IL-10– producing T reg cells, which have been described to mediate peripheral tolerance (24, 25) and suppresses mucosal inflammation in the gut (26). Interestingly, recent studies have reported that conventional Th1 cells can express IL-10 during chronic parasitic infections (27, 28). Whether MCMV-induced IL-10–expressing CD4 T cells represent T regulatory 1 or Th1 cells, or a combination of both, is currently unknown. Regardless of the exact lineage of these cells, however, this current study is the first description of a role for IL-10– expressing CD4 T cells in the salivary glands.
IL-10 suppresses inflammatory immune responses by inhibiting the expression of proinflammatory cytokines and chemokines, and decreasing expression of MHC class II and costimulatory molecules by APC, which subsequently limits differentiation or expansion of CD4 T cell effector responses (29). The dramatic reduction in persistent virus replication after IL-10R blockade was associated with increased IFN-γ–producing Th1 cells in the salivary glands, implying that IL-10 might act directly on effector T cells in the local microenvironment. Alternatively, IL-10 may suppress T cells indirectly by down-regulating one or more functions associated with APC. A previous study showed that MCMV- induced IL-10 in APC suppressed MHC class II expression by macrophages in vitro (30). However, we observed no change in MHC class II expression by cells infiltrating the salivary glands after IL-10R blockade (Fig. S2, B and C), suggesting this explanation cannot account for the action of IL-10 in vivo. The strong effect of anti-OX40 treatment in promoting IFN-γ–secreting CD4 T cell accumulation in the salivary glands suggests that IL-10 may predominantly act to suppress expression of costimulatory ligands such as OX40L and/or production of antiviral cytokines by APC, either in the salivary glands, or in the case of dendritic cells, after migration to draining lymph nodes.
In this mouse model of persistent virus replication, we have identified two distinct approaches to counteracting immune regulation. Regardless of the mechanism of IL-10–mediated suppression, the efficacy of IL-10R blockade in preventing viral replication was remarkable. Furthermore, delaying treatment until a week after infection, after CD4 and CD8 primary responses were established, dramatically altered virus replication in the salivary glands, showing the importance of IL-10 during this late stage of the antiviral response.
Targeting OX40 was also efficacious perhaps because of the expression of OX40 on antigen-reactive T cells, altering cytokine expression. This conclusion is guarded because MCMV peptides presented by class II MHC have not yet been defined to directly visualize antigen-specific T cells. The blockade of persistent viral replication by OX40 activation was associated with the accumulation of IFN-γ–secreting CD4 T cells previously described to afford protection from MCMV replication in the salivary glands (5, 8). Furthermore, the protective effect of OX40 stimulation was accompanied by a strong alteration in the ratio of IFN-γ to IL-10–expressing CD4 T cells. In a tissue culture model, the presence of OX40L on dendritic cells inhibited IL-10 expression in human CD4 T cells differentiating under both Th1 and Th2 priming conditions (19), suggesting that OX40 may directly antagonize IL-10 expression. However, the transcription factor GATA-3, which is implicated in the transcriptional control of IL-10 expression (31), can also be induced by OX40 stimulation in an IL-4R–dependent manner (21). This latter result suggests that, in certain conditions, OX40 could enhance IL-10 expression. Indeed, although we found an altered ratio of IFN-γ to IL-10–expressing T cells after OX40 stimulation, the actual numbers of IL-10–producing CD4 T cells did not change significantly. Furthermore, the level of IL-10 expression by CD4+IL-10+ T cells, as indicated by mean fluorescent intensity, was also unaltered by OX40 stimulation (unpublished data). Thus, the action of OX40 most likely reflected a preferential increase of Th1 effector cell differentiation and/or accumulation of Th1 cells in the salivary glands independent of IL-10. This conclusion is consistent with data where OX40 was shown to promote Th1 cell accumulation at the site of infection with influenza (32, 33) and Cryptococcus neoformans (20). Moreover, OX40 signaling can directly induce IFN-γ secretion and promote Th1 differentiation in tissue culture (16, 17). Anti-OX40 treatment reduced the viral load in the salivary glands by 1–2 log10, whereas anti–IL-10R reduced titers by 3 log10. The difference between the two pathways may reflect the finding that the IL-10–expressing CD4 T cells were not eliminated by treatment with anti-OX40. The finding that neither treatment altered the numbers of CD4+IL-10+ T cells indicates the difference in efficacy in reducing virus replication represented a fundamental distinction between the OX40 and IL-10R signaling pathways.
The ratio of T cells expressing IFN-γ to IL-10 provides a useful marker of immune regulation in the salivary glands and perhaps at other mucosal sites. A shift to IFN-γ expression pattern is critical for effective clearance of chronic parasitic infections (34), and correspondingly IFN-γ is necessary for the control of chronic MCMV infection (35). Elevated IFN-γ expression in the salivary glands may reduce viral persistence by directly inhibiting virus replication (35–37) or activation of additional effector mechanisms, such as NK, γδ T cells, and macrophages in the salivary glands (11, 38–40). IFN-γ also promotes CD8 T cell responses; however, in the context of the salivary glands, CD8 T cells do not limit virus replication (5), and neither anti-OX40 nor anti–IL-10R treatment had any effect on virus-specific CD8 T cell numbers, IFN-γ expression, or granzyme B expression, suggesting a minimal role for CD8 T cells in the protective effect of either treatment.
Induction of CD4+IL-10+ T cells after MCMV infection may represent a mucosal tolerance mechanism used by the salivary glands that is exploited by MCMV. It is likely that MCMV takes an active role in the exploitation of the mucosal tissue. Interestingly, MCMV alters the microarchitecture of the spleen by selective depression of CCL21 chemokine mRNA expression, which alters T cell trafficking within the spleen (41). Mutations in the viral genes M155 (42), M35 (43), or M133 (44, 45) abrogate replication in the salivary glands, although the role of these genes in promoting IL-10–expressing T cells is not understood. Of significance is the presence of viral IL-10 orthologs in primate CMV (46, 47), Epstein-Barr virus (48), and equine herpesvirus 2 (49). Although MCMV does not encode an obvious IL-10 ortholog, the observation that MCMV utilizes an IL-10–dependent mechanism to persist in salivary glands suggests a strong selective pressure is driving the conservation of targeting the IL-10 pathway in herpesviridae. The results raise the intriguing possibility that the primary function of cmvIL-10 in vivo may be to mimic IL-10–expressing T reg cells to block the action of the effector T cells secreting IFN-γ, allowing persistent virus replication specifically at mucosal sites. Thus, viral IL-10 orthologs may represent important targets to limit persistent virus replication in mucosal tissues such as the salivary glands, which in turn may block transmission of virus to new hosts.
Mice.
Wild-type female C57BL/6 (B6) mice were purchased from The Jackson Laboratory, and MHC class II–deficient mice (50) were purchased from Taconic. All experiments were approved by institutional Animal Care and Use Committee.
Virus infections and antibody treatment
MCMV Smith (American Type Culture Collection) was prepared and titered as described previously (51). Mice were infected with 5 × 104 pfu MCMV by intraperitoneal route and, in some experiments, injected i.p. at the time of infection with 100 μg of either rat IgG (Chemicon) or anti-OX40 (clone OX86 [52]) purified by protein A affinity chromatography. In other experiments, mice were injected i.p. with 250 μg rat IgG1κ (clone R3-34; BD Biosciences) or anti-CD210 (anti–IL-10Rα clone 1B1.3a; BD Biosciences [53]).
Leukocyte isolation, intracellular cytokine staining, and flow cytometry
Salivary glands were surgically excised and tissue leukocytes were isolated as previously described (11). In brief, salivary glands, free of associated lymph nodes, were cut into small pieces and incubated in RPMI 1640 supplemented with 5 mM CaCl2, 5% fetal bovine serum, 1 mg/ml collagenase D (Roche Diagnostics), and 10 μg/ml DNase I (USB) at 37°C with mild agitation. After two consecutive incubations, dissociated cells and salivary gland tissue was passed through a 40-μm nylon cell strainer, and extruded cells were washed with PBS before analysis. The draining lymph nodes of the salivary glands were also excised, and cells were isolated by passage through a 40-μm nylon cell strainer.
Isolated leucocytes were then incubated at 5 × 106 cells/ml for 5 h at 37°C in the presence of 2 μg/ml brefeldin A (Sigma-Aldrich) and stimulated with or without 1 μg/ml anti-CD3 (clone 145–2C11) and 1 μg/ml anti-CD28 (clone 37.51; BD Biosciences), or 2 μg/ml of MCMV-derived peptides (Genemed Synthesis Inc.). The peptides used were the H-2Db–restricted M45-derived peptide HGIRNASFI and the H-2Kb–restricted peptides derived from the M38 (SSPPMFRVP), M57 (SCLEFWQRV), and M139 (TVYGFCLL) open reading frames, as previously described (54). Cells were then washed and incubated with Fc receptor blocking reagent and then stained with anti–CD8-PE-Cy7, anti–TCRβ-PE-cy5, and anti-CD4 antibody conjugated to FITC or APC-cy7 (BD Biosciences). Cells were then fixed with 4% formalin and permeabilized with saponin buffer (PBS, 2% FBS, 0.05% sodium azide, and 0.5% saponin) and stained with anti–IFN-γ-FITC or PE and, in some experiments, anti–IL-10-APC and PE-labeled anti–IL-5, anti–IL4, anti-FoxP3, or anti–IL-13 biotin (R&D Systems) followed by streptavidin-PE (BD Biosciences). In some experiments, unstimulated cells treated with brefeldin A were stained with anti-CD8 and anti–human granzyme B–PE (Catag/Invitrogen Life Technologies) or anti–NK1.1-APC and anti–IFN-γ. In other experiments, splenocytes were immediately stained with anti–MHC class II, anti-B220, anti-CD11c, anti–CD8-PE-cy7, anti–CD4-APC-cy7 (BD Biosciences), anti-F4/80 (eBioscience), and/or OX40-PE (Serotec). All cells were acquired on an LSR II flow cytometer (BD Bioscience).
Salivary glands were fixed in 10% formalin, paraffin-embedded, and 5-μm sections were stained with hematoxylin and eosin. Three sections from each gland were examined from four mice per group.
IFN-γ and IL-10 mRNA were assayed by quantitative RT-PCR using Stratagene Mx 4000 and SYBR green reagent (Bio-Rad Laboratories). Salivary glands from mock or MCMV-infected mice were snap frozen in liquid nitrogen before homogenization in TRIzol reagent (Invitrogen Life Technologies). Total cellular RNA was then isolated and quantified before performing DNase digestion and reverse transcription as described (55). The primer sequences for detection of mouse IFN-γ are GCCGTGGCAGTAACAGCC and AACGCTACACACTGCATCTGGG, and for IL-10 are CACTGCTATGCTGCCTTCTCT and TGTCTTCCCTGCTGTACTGT.
Online supplemental material
Fig. S1 shows time-course analysis of numbers of CD8 T cells (a), granzyme B expression by CD8 T cells (b), and accumulation of IFN-γ–expressing CD8 T cells (d), in the salivary glands of anti-OX40 or control IgG-treated mice. Panel c shows MCMV-specific CD8 T cell accumulation in the salivary glands at day 7 after infection in anti-OX40–treated or control IgG-treated mice.
Fig. S2 shows the numbers of CD8+/IFN-γ+ and NK+/CD3−/IFN-γ+ cells (a) and the percentage (b) and the mean fluorescent intensity (c) of MHC class II expression by leukocytes in the salivary glands of anti–IL-10R or control IgG-treated mice 14 d after infection.
The authors wish to thank Dr. Kirsten Schneider and Professor Brigitte Askonas for valuable discussions; Xiaohong Tang, Yan Fei Adams, and Antje Rhodes for excellent technical support; Dr. Ann Hill for MCMV peptide sequences recognized by CD8 T cells; and Dr. Tim Cheung for assistance with figure preparation.
This work was supported in part by National Institutes of Health (NIH) grants CA91837 and AI67341 (to M. Croft); NIH Predoctoral Fellowship T32 AI060536 (to A. Kinkade); and AI48073, AI057840, and R37AI33068 (to C.F. Ware). This is publication #793 from the La Jolla Institute for Allergy and Immunology.
The authors have no conflicting financial interests.
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Figure S1
OX40 ligation during MCMV infection does not enhance CD8 T cell responses in the salivary glands. (a, b and d) On days 0, 7, 14 and 30 post-infection, numbers of CD8 T cells (a), the proportion of granzyme B expressing CD8 T cells (b), and numbers of CD8+IFNγ+ T cells (following ex-vivo anti-CD3/CD28 stimulation) (d) in the salivary glands of IgG (black square) and anti-OX40 (white square) treated mice were measured. (c) After 7 days of infection, numbers of MCMV peptide specific CD8 T cells in the salivary glands were quantified by detection of IFNγ expression after restimulating in vitro with the respective peptide for 5 hr. Results are expressed as mean ± SD from 4 mice/group and represent two experiments.
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IL-10R blockade does not alter the accumulation of IFNγ expressing CD8 T cells and NK cells, or MHC class II expression by inflammatory infiltrate in the salivary glands. MCMV-infected mice were treated with or without anti-IL-10R antibody. After 14 days, IFNγ expressing CD8 T cells (after ex-vivo stimulation with anti-CD3/CD28) and NK+CD3- cells (unstimulated) were quantified (a). The proportion of MHC class II+ cells (b) and mean fluorescent intensity of MHC class II expression on gated class II+ cells (c) was also measured 14 days after infection. Results are expressed as mean ± SD from 4 mice/group and represent 2 experiments.
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IL-10–expressing CD4 T cells accumulate in the salivary glands during persistent MCMV infection. (A) 14 d after MCMV infection of mice, accumulation of CD4+CD3+, CD8+CD3+, B220+, NK+CD3−, F4/80+, and CD11c+ cells (A) were measured. (B and C) After 5 h with (white bars) or without (black bars) stimulation with anti-CD3/anti-CD28, IFN-γ (B), and IL-10 (C) expression by CD4+TCRβ+ and CD8+TCRβ+ cells and TCR-β− cells derived from the salivary glands was measured. (D) IL-10 expression in salivary gland extracts from naive and MCMV-infected mice 14 d after infection was measured by quantitative PCR and was normalized to 18S RNA. *, P < 0.05, with student's t test. All results are expressed as mean ± SD of three to four mice per group. (E) IL-10 expression by TCR-β+ cells in the salivary glands, draining lymph nodes, and spleen was analyzed by intracellular stain 5 h after stimulation with anti-CD3/anti-CD28 (top). Data are representative plots (n = 4) staining for CD4 versus IL-10 or isotype control on gated live lymphocytes. (bottom) Expression of IL-4, IL-5, IL-13, and FoxP3 (unshaded lines) compared with isotype control (shaded lines) by gated CD4+IL-10+ cells visualized 5 h after in vitro stimulation of salivary gland leukocytes 14 d after infection. Positive control for FoxP3 staining (dashed line) is CD4 T cells derived from spleens of naive mice. (F) On 0, 7, 14, and 30 d after infection, the number of CD4+IL-10+ cells (◯) and virus titers (•) in the salivary glands were measured. Results are expressed as mean ± SD of four mice per group, and all results are representative of three experiments.
OX40 activation inhibits virus replication and enhances cellular infiltration in the salivary glands during MCMV infection. (A) OX40 expression by salivary gland–derived CD4+CD3+ (left) and CD8+CD3+ (right) cells 14 d after MCMV infection (unshaded line) compared with isotype-stained control (shaded line). (B) The percentage of OX40-expressing CD4+CD3+ T cells isolated from the salivary glands (•) and draining lymph nodes (○) 0, 7, 14, and 30 d after infection. (C) MCMV-infected mice were treated with IgG (black bars) or anti-OX40 (white bars), and after 7 and 30 d salivary glands were assayed for infectious virus (C). (D) Hematoxylin and eosin–stained salivary gland sections 14 d after infection from control Ig (left) and anti-OX40– (right) treated mice. Acinus (large black arrowhead), duct (white arrowhead), and glandular epithelial cells with an intranuclear inclusion indicative of virus cytopathic effect (small black arrowhead) are shown in the section from Ig-treated mice. Bars, 200 μm. (E) Numbers of CD4 T cells in the salivary glands of IgG (▪) and anti-OX40– (□) treated mice 0, 7, 14, and 30 d after infection. (F) Wild-type C57BL/6 and MHCII−/− mice were infected with MCMV and treated with IgG (black bars) or anti-OX40 (white bars), and 30 d later salivary glands were assayed for infectious virus. Data presented in B, C, E, and F represent mean ± SD of four mice per group, and all data is representative of three to five independent experiments. *, P < 0.05, with student's t test.
OX40 activation alters the ratio of IFN-γ to IL-10–expressing cells in the salivary glands during MCMV infection. B6 mice were infected with MCMV and treated with rat IgG or anti-OX40 at the time of infection. IFN-γ and IL-10 expression was measured in salivary gland–derived CD4 T cells from IgG and anti-OX40–treated mice at various times after MCMV infection, after ex vivo stimulation with anti-CD3 and anti-CD28. (A and C) Representative plots of IFN-γ (A) and IL-10 (C) expression by CD4 T cells from Ig (left) or anti-OX40– (right) treated mice 14 d after infection. (B and D) The percentage of CD4+ T cells expressing IFN-γ (B) or IL-10 (D) in the salivary glands of Ig and anti-OX40–treated mice over time. (E) Ratio of IFN-γ to IL-10–producing CD4 cells, calculated as the ratio of the percentages of IFN-γ–expressing CD4 cells to IL-10–expressing CD4 cells. All results are expressed as mean ± SD of four to seven mice per group over a 30-d time-course infection. (F) IFN-γ and IL-10 expression in salivary gland extracts measured by quantitative PCR and normalized to 18S RNA. Data are presented as a ratio of IFN-γ to IL-10 expression per mouse. All results represent two to three experiments. *, P < 0.05, with student's t test.
IL-10R blockade augments accumulation of IFN-γ– producing CD4 T cells in the salivary glands. C57BL/6 mice were infected with MCMV and treated with rat IgG or anti–IL-10R on days 0 and 7 after infection. Total CD4 T cells (A) and IFN-γ (A) and IL-10– (C) expressing CD4 T cells in the salivary glands of IgG (black bars) and anti–IL-10R– (white bars) treated mice were quantified 14 d after infection. Results are expressed as mean ± SD from three to four mice per group. *, P < 0.05, with student's t test. (B and D) Representative FACS plots of CD4 versus IFN-γ (B) or IL-10 (D). Quadrants were set using isotype control antibodies, and results represent four mice per group. All results are representative of three similar experiments.
Blockade of IL-10R signaling inhibits MCMV persistence. MCMV-infected mice were treated with IgG (•) or anti–IL-10R on days 0 and 7 (A) or 7 and 14 (B) after infection. After 30 d, salivary glands were assayed for infectious virus. Individual mice plus mean are shown. Results are representative of three similar experiments. Undetectable titers are expressed as an arbitrary value of 1 for display on a logarithmic scale.
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Lucy Anne-Holmes, heroine of the No More Page 3 campaign
Sarah Edmonds 21 January 2013
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Lucy Holmes has been spearheading the campaign to pressurise The Sun to drop the bare boobs from its Page 3. Sarah Edmonds speaks to Lucy about her inspiration and challenges
As I pick up the phone to call Lucy-Anne Holmes, founder of the No More Page 3 campaign to "drop the bare boobs from The Sun", I'm half expecting a no-nonsense, hard-line activist to pick up. So when Lucy answers in a soft, hushed voice, I am surprised until she explains she is babysitting for a friend's children who are asleep in the next room.
Political campaigning was never a career aspiration for Lucy; although, judging from the success of No More Page 3, she is better at it than she could have ever imagined. The petition has amassed 61,874 signatures since August and attracted considerable media attention – quite an achievement for a 35-year-old actress and writer from Brighton who has never been involved in a campaign before.
It all began when Lucy bought a copy of The Sun during the London Olympics and, after reading about Jessica Ennis' victories, turned to Page 3 to be confronted with a massive image of a topless young woman. The juxtaposition of a female athlete celebrating her medals with a Page 3 girl presenting her naked breasts was the turning point for Lucy. This was the moment her obsession with Page 3 began and she decided to follow in the footsteps of Clare Short by attempting to petition Dominic Mohan, editor of The Sun, to drop the boobs.
What will kids think when they see lots of pictures of men doing stuff and then this huge picture of a woman standing there in her knickers, showing her breasts
Lucy's break as a writer came when she started a blog detailing her disastrous love life; the blog landed her a book deal and she went on to write four novels. Lucy's novels – romantic comedies – spawned the No More Page 3 campaign, which is in many ways a personal crusade. She says: "I started writing quite openly about my messed up life. I was curious as to why I was lumping so much hate upon myself. I used to say 'I hate my bum and I hate my boobs'. If I ever did anything wrong I used to say 'God, I'm a twat'," Lucy laughs before continuing, "I thought: 'why am I doing this, why am I concentrating on this hate?'" Lucy uncovered the answer to these questions in her childhood. She grew up in a 'Sun' house and remembers her older brother and his friends ogling the bare breasted Page 3 girls at the same time as she, an 11-year-old girl, was developing. When her breasts made their arrival she couldn't help but feel her body had failed her. She didn't look like the girls on Page 3 – what man would want to look at her?
As I speak to Lucy, it is hard to imagine her as the self-deprecating, insecure woman she describes. She seems confident and not afraid to tell others what is important to her. Throughout our conversation, the passion she feels for the campaign seems to take over and she pauses momentarily to check she's making sense and isn't "wittering on" too much. It is clear the campaign is personally significant to Lucy, but she also feels concerned about the difficulties young women face growing up in a society where it is acceptable to publish naked breasts in a 'family-orientated' daily newspaper; "in a newspaper of all the places!" she says, still shocked at the notion. She continues, "What will kids think when they look through a family newspaper and see lots of pictures of men doing stuff – running the country – and then this huge picture of a woman standing there in her knickers, showing her breasts."
The campaign is less about the topless women themselves than the effects of Page 3: low self-esteem among young girls, eating disorders, the desire for plastic surgery and, most alarmingly, that young women appear to be accepting much higher levels of violence within relationships. For Lucy the campaign is about encouraging respect for women and inspiring girls to be more than just a "walking pair of tits".
With support comes criticism and Lucy has had her fair share. She is commonly told: "you've got shit tits" and "get a life"
Lucy doesn't have children but is extremely close to her family and friends; she speaks with admiration of her 20-year-old niece who helped her to start the campaign and describes with glee the moment a friend's three-year-old daughter stood on a chair to announce "I'm a feminist!" Lucy has also found strangers to be just as supportive as those close to her. The encouragement she has received is outstanding and she is both grateful and surprised by it, whether it is going out to spread the word and collect signatures or creating poems and songs, "There have been moments where I feel a bit tired and someone is attacking me, and then I read or hear something amazing and it's incredible." These messages of support obviously mean a lot to Lucy and when she recounts them to me the emotion is clear in her voice: "I had this email from this man saying: 'I'm sitting here with my seven month old daughter thinking about what an important job you're doing' and that made me well up… I'm getting a bit teary here."
With support comes criticism and Lucy has had her fair share. She is commonly told "you've got shit tits" and "get a life", which she says is weird not only because it sounds so juvenile, but because she actually really enjoys her life. It's probably this positivity that ensures Lucy doesn't let the insults worry or distract her; in fact she seems to have overcome the insecurities she felt as a teenager measuring her breasts against those she saw on Page 3. "When I look in the mirror it's just me," she says, "my body and face have taken me through life – I'm friends with them. So I find the criticism interesting but it doesn't really upset me."
The campaign is about being able to live in a world where sexual objectification of women is not the norm and newspapers value women for their minds
No More Page 3 has already attracted media attention from The Guardian, The Independent and The New York Times but Lucy recognises she still has a long way to go: "It's just a ripple and it needs to get bigger and bigger." I ask her how she envisions the campaign ending. Using her acting skills, she puts on her best Murdoch voice to say: "Murdoch could just pick up the phone and go: 'Come on, we are better than this…we've got a paper with enough going for it that we can lose the boobs and not affect sales…why don't we start showing that we respect women?'" Lucy has come so far in so short a time and is not going to give up easily on something that has become so important to her. She wants to shift the way society looks at women – to put an end to Dominic Mohan's Page 3 (which he described at the Leveson enquiry as a "celebration" of "youth", "freshness" and "natural beauty") and make the world a more respectful place for women.
No More Page 3 has not escaped criticism from commentators, some of whom see it as a white middle-class smear campaign against readers of The Sun, but the interesting thing about Lucy is that she is not a fierce political campaigner. Like Lucy's demeanour the campaign is sensitive. It's not about aggression or jealousy. It's about being able to live in a world where sexual objectification of women is not the norm and newspapers value women for their minds and the things they say and do, rather than how they look.
First image of a man standing in front of a wall and reading a newspaper uploaded by Flickr user Garry Knight. Photograph of Rupert Murdoch at the World Economic Forum 2009 obtained from Wikimedia Commons.
Sarah is a postgraduate journalism student living in South London. You can find her tweeting at @_SarahEd.
campaignPage 3sexual imagerysexualisation
Sarah Edmonds
Weekly round-up and open thread
Holly Combe 17 January 2022
Lissy Lovett 10 January 2022
4 February 2013 Elisa Log in to Reply
I think if I was a man to whom the Sun was marketed, I'd be quite offended at the idea that I would choose my news provider according to whether or not it also showed me bare boobs every day… Also Lucy Holmes rocks
4 March 2013 jillyc Log in to Reply
Hi, I am 53 and since the 70's I have felt so much like lucy. Back then you had pic's of women with there breast out, absolutely everywhere via… pubs; the work place; men reading the sun paper on buses; in cafes; park benches etc etc. I remember sitting on buses next to men with the sun news paper open on page 3 and feeling very uncomfortable, infact it was almost a daily event. I was just sixteen, how was a young girl ment to feel under the circumstances.
It wasn't that I minded or even now mind anyone looking at naked people, it's just there is a time and place. A man sitting next to a young girl on a bus looking at boobs, was and still is not the place and just plain wrong, particually as we know men are turned on by the visual.
Unfortuately back then if you past any comment against it, alot of men would resort to name calling; say something to belittle you; try to under mind your view or something similar, so you often just shut up and learnt to with it. It was the norm for men to have naked pic's around them, even when in the company of girls, teens and women.You could expect to walk into any work place back then and find a pic of a naked girl, even when women worked there to.
I use to wonder how men would handle it if they had to; sit next to women on a bus looking at willy pic's; walk into a garages, pubs, shops with willy pic's on a wall and deal with the constant in your face pic's that girl and women dealt with then and now on a daily basis. But they didn't have to and still don't because 'they had and have choice' and thats what use to and still does make me angry about page 3 and paper that show half naked women, for there suddenly there infront of you and through no choice of your own.
They are at eye level in shops which they shouldn't be and just recently I was sat in a cafe with my 9 year old grandaughter when a group of men walked in, sat down at a table and proceeded to open news papers with boobs and half naked women on. They gave no thought to the fact they were in the company of others and because it was the norm to them, it didn't even cross there minds there was a child present, and that is very sad. So Lucy keep up the fight because the end of page three has to happen, and it's only really there these days to get one over on femminist, after all it was brought about by 70's men with a similar mentality to that of jimmy saville; need I say more!
5 March 2013 anais Log in to Reply
Lucy Holmes is awesome! However, I was struck by the sentence, "…young women appear to be accepting much higher levels of violence within relationships." Much higher levels? Why should any level of violence be acceptable?


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FIA ETCR highlights its local CSR initiatives in support of Giving Tuesday
The FIA ETCR eTouring Car World Cup is showing its support of Giving Tuesday by highlighting its sustainability actions through the local associations wrought during the course of the inaugural FIA ETCR season.
Giving Tuesday (29/11/22) is designed to be a day to encourage people to do kind acts and celebrate generosity. Since 2012, this has been a global movement and pluralistic community with activities in every continent.
In 2022, FIA ETCR enjoyed a season full of action but also full of moments of sharing with local communities. FIA ETCR aims to have a positive local impact thanks to partnerships with local associations as part of its #TransitionInMotion sustainability programme.
FIA ETCR's CSR actions link to the United Nations Sustainable Development Goals (SDGs), which are 17 global goals established by the UN to achieve a more sustainable world for all by 2030.
FIA ETCR's local outreach in 2022
Food support to local communities
To avoid food waste, FIA ETCR redistributed food surplus to local associations. For example, in Pau, 174 meals were distributed thanks to two associations: Pau Charity for people in need and the Solidarity Grocery Store for Pau Students (ESEP).
When donating food surplus was not possible, Discovery Sports Events made donations of basic necessities and food items, such as in Budapest with the Hungarian Red Cross or in Madrid with the Food Bank.
(SDGs 2, 12)
Making the motorsport industry more inclusive
FIA ETCR raised awareness amongst the staff and teams thanks to Richard Morris and Sarah Moore from Racing Pride. In Zolder, the two drivers discussed with ETCR drivers how to fight against any kind of discrimination and how to be more inclusive in the motorsport industry, specifically regarding the LGBQT+ community. A video showing the importance of inclusion in the motorsport of tomorrow has been shared on social media. In addition to this, people from the local associations Regenbooghuis Limburg and OGWA had the opportunity to come on the circuit to experience FIA ETCR and to meet Racing Pride.
(SDG 10)
FIA ETCR worked on various projects with local schools and pupils ranging from children to university students.
Notably, in Vallelunga over 400 children attended the event and had a Q&A with the teams to discover electric racing and the Energy Station.
In Pau, FIA ETCR invited students from the ENSGTI, a specialized school in process engineering and energetics, and we discussed electric racing and potential improvements.
FIA ETCR has also highlighted the future of electric racing with the Formula Student teams.
In Sachsenring, the electric racing team from the Chemnitz University of Technology, TUC Racing, showed their racing car and exchanged information with the CUPRA EKS team. FIA ETCR also welcomed Formula Student teams from Politécnica and Comillas University in Jarama.
In full support of sport initiatives aiming at gathering people, students and expats from the Budapest Association for International Sport came on the Hungaroring circuit to discover the FIA ETCR new technologies.
(SDG 4)
FIA ETCR has partnered with a total of ten associations covering various sustainability topics and four universities.
Xavier Gavory, FIA ETCR, Series Director
With FIA ETCR we are trying to change perceptions of electric vehicles and show the world that electro mobility is part of the solutions that help us to live in a more sustainable way. We also know that to bring this message home we must work on a local level at every event and it has been educating and illuminating for us to do this at all out events in 2022. We really do examine every element of our existence as an entity to see how we can entertain and educate at every level. We are in full support of Giving Tuesday and hope we can help harness our fanbase, partners and competitors to support and encourage kind acts and celebrate generosity.


Stephanie Hudson, 74, 769 McDermott Ave., Melbourne, died Wednesday. Born in Providence, R.I., she moved to Melbourne from Hialeah in 1962. She was a homemaker. Survivors: sons, Ralph and Eugene, both of Melbourne, John, Pembrook Pines, James, Westville; daughter, Mrs. Opal Clark, Hollywood; 15 grandchildren; and three great-grandchildren. Brownlie and Maxwell Funeral Home, Melbourne.


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Arsenal told to pay £44m to complete transfer of Serie A duo
June 5, 2019 June 5, 2019 - by admin - Leave a Comment
Arsenal have been busy in the transfer window as the club are looking to strengthen after a decent debut season for manager Unai Emery.
It is believed that the Spanish tactician is keen to make a sensational transfer for Sampdoria stars Dennis Praet and Joachim Anderson.
The Mirror claims that the Gunners have seen an opening bid of £37 million rejected by the Italian side.
Dennis Praet and Joachim Anderson are considered key members of the first team and Sampdoria have demanded a fee of £44 million for both players.
Emery has identified the defensive and midfield as two positions that need new faces this summer.
Praet and Anderson fits the bill as young players that can bring instant impact to the team and are versatile enough to play different positions.
Anderson is considered one of the best defenders in the Italian League and would be an upgrade to Shkodran Mustafi while Praet would be a good replacement for Juventus-bound Aaron Ramsey.
Italian giants AC Milan are also said to be interested in the players but the failure to qualify for the Champions League could thwart their plans.
This looks like a good deal for the Premier League outfit, £44 million is a decent price for both players.


We donated an astonishing £52,328 to school in 2017/18 following liaison with Stephen Locke (Bursar) and Shirley Park (from the Development Office).
In October we donated £12,500 which bought 54 much-needed chairs and nine tables for the refectory, a host of online subscriptions and the much enjoyed UKMT challenges entry fees for our brilliant mathematicians, planners for every student in the school and a wee top up of £57 towards a special art gun we bought last summer.
We then heard that the Humanities departments were in dire need of some simple but effective support. We spent a total of £1,314.96 on books for History, digital text books for Politics, revision webinars for Geography and yoga mats for the PTE department.
Our phenomenally successful Spring Fair in March raised all the funds (plus some!) needed to support our cherished performing arts departments, Music and Drama. First off when we heard there were no music chairs available for left-handed students we immediately purchased six of them for £174.95. We were then able to purchase a beautiful piano for £3,400, 15 electronic keyboards and Sibelius licenses for £3,520, and then a lighting desk and snazzy lights for Performing Arts at a cost of £2,918.
A wonderful example of school and the PA working brilliantly together was when Mr Locke heard that there was a spotless second-hand mini-bus on sale at a local primary school. We knew School needed another but hadn't dared think we could afford it but at a great price of £3,500 we pounced and within weeks it was ours, sporting our logo, and on the road ferrying students here, there and everywhere.
Our biggest contribution this year has been an astonishing £25,000 towards the new Sixth Form Block. Whilst a government grant covered the actual build, there was no financial support for IT, furniture, books, supplies etc. When the building was officially opened at the end of 2018, the Parents' Association input was apparent to all on the ground floor where we have bought furniture and IT.
My Maths Subscriptions - £1,269, Maths Challenge Entries £624 Not surprisingly in the least, Maths remains a highly subscribed subject at Pate's and, like every other department, has limited resources. The PA have recently contributed to essential online study subscriptions and competition entry fees for this department. Student Council Requests - £2,240 We are always keen to support the Student Council and regularly ask them what they feel, as representatives of all our children, is needed. This year they suggested a new bike rack for the increasing number of students cycling to school, and four outdoor picnic benches for outside the sixth form area. These are all now in place. We eagerly await their next shopping list.
To cope with a growing number of remote users and to maintain a smooth and reliable user experience for staff, students and parents, an additional server unit was deemed necessary. The PA committed its main fund raising event, the Spring Fair, to generate this considerable sum. We cracked it! On top of this we donated £1,915 for much needed licenses.
The refit provided for 33 new workstations in Room E106. The new computers are faster, smaller, more energy-efficient and easier to manage with much more capacity for modern programmes and multimedia.
A good number of the old P.E mats were no longer fit for purpose. We were happy to support the purchase of a new set of high-quality mats for the P.E Department and see the old ones sent down for use in the shooting range.
Each new Y7 student is given a book they have chosen from a list. The Book Buzz scheme then provides the school with two sets of these books for the library.
Every Pate's student uses their daily planners throughout the year to log their homework and assignments. As part of Making £nds Meet this valuable resource will now continue.
As well as replacing and developing the fiction/non-fiction collection, the Library budget pays for a range of print books and magazines as well as online resources (available on Plato and accessible from home) to support students in both their academic studies and reading for pleasure. The library budget also covers: Daily Newspapers, Author visits, Requests to the British Library for articles/books and School Library Association membership.
2015/2016 School Planners for every student to log their homework and assignments.
This went towards new wireless spotlights for the Tech Crew to safely enhance productions and presentations in the hall. We particularly wanted to help buy these as the students had raised £560 themselves by producing and selling CDs and DVD's of school performances.
£1,575 was spent on a UV Light Box. This is being used by students studying photography. We have also donated £1,473 to buy 5 Panasonic cameras, 1 tripod, 2 tablets and a spotlight. These can be used by all year groups and will allow digital photography to flourish at Pate's.
In November £10,000, specifically from the 100 Club profits, was donated to help the Annual Fund with some of its targets. Intelligent lighting was bought for the Hall which has already transformed school productions and assemblies. Remaining funds were towards a much-needed new minibus.
As part of the Annual Fund 2013 -14, the school was successful with a bid made to the Wolfson Foundation to enable the refurbishment and extension of one of the phyics labs. The very generous grant of £40,000 itself was not quite enough to enable to works to be carried out so it was with great delight that we stepped in to help at short notice, by donating a further £10,000. Further details are available here.
Business Studies and Economics and the PE Department use the new Tatam block of classrooms which opened in September 2013. We are pleased to announce the donation of £8000 to fund a set of 20 iPads together with storage and charging trolley, TV screens and wifi points for use in the new facility.
This donation has gone towards a portable sound system, atheletics vests and weights for the fitness room.
T he school has made huge strides in recent years in upgrading the IT structure, but there is more to do and, as with all IT, some of the equipment now needs to be replaced again. In Easter 2012 the Parent's Association took great pleasure in donating £25,000 to fund the full cost of refurbishment of one of the IT classrooms. This ensures the technology continues to be fast and current, thus enhancing the education experience for all pupils across many subjects. The revamped classroom opened during the Summer Term 2012.
The PA was delighted to contribute £900 to enable the purchase of a new printing press by the Art Department, bringing the total in the school to three. It significantly improves the printing facilities as large scale items can now be printed. In addition queuing times are reduced for pupils.
From Summer 2012 many Pate's students will benefit from ten new Flip Cams and memory cards costing £900, funded with your donations. The school already had three similar cameras which were used daily. The flip camera is simple to use and the film is easy to transfer to the computer. Students use them when working with the charity committee and when preparing assemblies. They are also used in lessons, filming assessments or practical work in areas as diverse as science and languages.
The new Pate's minibus arrived in Spring 2011, funded entirely by a £14,000 donation from the Parents' Association. This is a great asset and it will serve our school for many years to come. The purchase of the minibus was As a result this new minibus now has the opportunity to benefit every child in the school.
In 2011 the school has recently replaced its tired and ageing piano with a fantastic new one. The old piano was over 100 years old and served many talented pupils and staff well over the years. The music department ran a hugely successful campaign to raise funds for the £23,000 new piano and the PA were delighted to be able to give a donation of approximately £14,000 towards the cost of the new instrument. As a result, the music department were able to obtain a better model and much more quickly than had been anticipated. Once again your support has made a difference and will go on to benefit Pate's students for many, many years to come.


Mr. Viens was born in Connecticut in 1964 and moved to Okeechobee when he was in ninth grade. He graduated from Okeechobee High School in 1982 and was the first of his group of about 20 friends, "the military pack," to join the army.
His mother was dead set against it, he said, because his grandfather had been killed at Normandy, but he didn't tell her the recruiter was coming and when he showed up, he explained what they were offering, and she couldn't refuse. Mr. Viens had scored pretty well on the tests, he said, and they offered him two years in Germany, his choice of just about any job he wanted, $25,000 for college and a signing bonus. In addition, he would have joined the following year anyway, so his mother finally gave in and signed so he could join even though he was only 17 years old.
Because of his test scores and the fact that he brought two friends with him, he went in one rank higher than he would have. He went to Germany immediately following his "one-station" unit training in Fort Knox. He was trained as a reconnaissance scout. He explained, they were considered part of the tank community but they did the reconnaissance for the tanks. They traveled 20 miles ahead of the lead unit. He joked, "We used to tease them that we were just there to find their sleeping places and to make sure no one attacked them while they slept." He liked being out in front of everyone and especially enjoyed doing what he called some "super cool secret" missions.
One of his favorite memories was the transition from the old vehicles to the new Bradley Fighting Vehicles, which he said were named after Gen. Omar Bradley. He said when they had motorcycles or dune buggies, they carried them inside and when they were ready to use them, they dropped a hatch on the back and just drove them out. They were much quieter than a tank, he explained.
When he left Germany, he went to Texas for three years. He had applied for ROTC training or recruiting but was hoping to get ROTC training. He ended up with recruiting, though. He said it wasn't bad. He had four months of training, which was basically teaching him how to be a salesman. He was a recruiter in a mall for three years, and he said it was not a bad duty, but the only day off you ever got was Christmas.
After that, he was sent to Fort Riley in Kansas where he was back to recon scouting and, soon after, he was sent to Iraq for Desert Storm. He said he was there for six months, but the conflict lasted only four days.
When he left the U.S. to head to Iraq, his wife was eight months pregnant, and she gave birth to their son Zack on the day of the cease-fire, but it took a month for them to find him to tell him the baby had arrived. He didn't get to see the baby until he was 5 months old, and that helped Scott make the decision to end his career in the Army, although he did remain in the reserves until retiring after 25 years in the service. The birth of baby Zack and the fact that Mr. Viens was deployed during his birth was featured on the front page of the Okeechobee News in February 1992.
When he and his family returned to Okeechobee, he went to college to become a teacher and taught elementary school for 13 years. He was a dean for three years and is now a behavioral interventionalist for all 10 Okeechobee schools. He explained, he "puts out the fires." He helps anywhere he can with children with behavior issues.
He is married to Tammy, who works as a surgery scheduler at Raulerson Memorial Hospital, and has three children — Brianne, his oldest; Zack, the baby who was born while he was deployed and who is now in dental school; and Jason, who is on active duty in the Air Force and is an interpreter of Middle Eastern languages. He has two stepchildren — Chad and Brenda Ellerbee, 11 grandchildren and one on the way.
In his spare time, he has worked as an auxiliary sheriff's deputy for the last nine years. He is a member of a band in which he sings. They play classic rock, he says, mostly over on the coast. He is a Mason. He said he became a Mason because they promote making you a better man. He is the county trainer for youth mental health first aid — suicide prevention, and finally, his family has Disney World passes.
Special to the Lake Okeechobee News This is an Avenger Weapon System. Scott Viens sat in the turret so he could shoot down planes.
Special to the Lake Okeechobee News A very young Scott Viens stands in front of a Bradley Fighting Vehicle.
Special to the Lake Okeechobee News Scott Viens is pictured upon arrival in Iraq during Dessert Storm.
Special to the Lake Okeechobee News Scott Viens is shown guarding the oil fields which Saddam Hussein had blown up to keep the U.S. from getting the oil.
Special to the Lake Okeechobee News Scott Viens is standing in front of the Fiori Barracks in West Germany in 1982. He was just barely over 18 and was totally unprepared for the extreme cold.
Special to the Lake Okeechobee News Scott Viens is on his way home after Desert Storm. They were all a little dusty but cleaned up so they could kiss the governor.
Special to the Lake Okeechobee News Scott Viens proudly carries the flag during this march. They marched 25 miles a day for four days and marched 700 miles in preparation for the event.
Special to the Lake Okeechobee News This picture was taken inside the Bradley vehicle at the training center. Scott Viens is in the front.
Special to the Lake Okeechobee News This is the photo from Scott Viens' basic training yearbook from Fort Knox, Ky. in 1982.
Special to the Lake Okeechobee News For several years, Scott Viens was a guest speaker at Everglades Elementary School's Veteran's Day ceremony.
Special to the Lake Okeechobee News Veteran Scott Viens is pictured with his wife Tammy.


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A Xennial's Perspective on the use of Social Media Apps in the Workplace
kbarrett October 17, 2017
Sdo omaBgle TAsmlackAppB
© (Brian G Peters, Medium.com. Retrieved from Medium on October 17, 2017)
Born in 1981, I am an in-betweener, or a Xennial; I am able to identify with members of both Gen X and Gen Y. As a Xennial, I have the unique experience of living in both realities of the X's and Y's – the advantage is that I have lived, experienced and functioned in a world without internet and instant communication. I understand the need for the occasional digital detox, and often miss life without a smart phone. Additionally, I have the advantage that I belong to one of the first generations to be taught "computers" in school. As a result, I am comfortable working on a computer.
In this blog post, I will examine the link between Slack, a social media and collaboration tool used in businesses, and higher levels of performance in the workplace.
© David Ko, screenshot. Retrieved from Slack on October 17th 2017.
Slack.com is a social app that describes itself as a place "where work happens". Slack is used in the work place to collaborate on projects, communicate with coworkers from different departments, and coalesce with contacts from different organizations altogether. Charley Locke says the app "has become the social network where we spend our workdays."
Since I do not have any personal experience using Slack, I wrote to David Ko, an active user and proponent of Slack. In order to gain more insight into the user experience of social media apps in the workplace, I asked David the following questions.
David Ko is a Gen Y.
How were you introduced to the app? Did you join right away?
Introduced by co-worker and new manager. Yes, joined right away.
Are 100% of employees signed up and participating?
Almost. I would say about 95%.
Do you use Slack on your phone and desktop? Do most of your coworkers use it on their phone?
All that participated use at least the desktop version. I would say about half of them have it on their phone.
Besides Slack, on which social platforms are you active?
Facebook, Twitter.
Can you briefly explain the customization aspect of the app?
The app is fully customizable, and lends towards developers to create their own apps. Slack can interface existing applications geared towards office automation, such as bug-tracking systems like Jira.
Explain how it makes your job faster than life pre-Slack.
Unlike Microsoft Lync, it (1) buffers messages for users when they are offline, (2) has a subscription service so that you can receive only the relevant messages, (3) office automation tools can publish results directly into Slack, (4) it's a simple tool to use, (5) embeds graphics and videos, and (6) geared towards fun.
Do you feel like it has improved your day to day work life? Made it more enjoyable
Would you miss your friends/experience on Slack if you were change employers?
Have you observed any generational differences when it comes to app usage? I suspect younger employees are on it more frequently and thus more active on it.
Everyone in the office uses it, regardless of age. But yes, I tend to see the younger ones more active on it.
What star rating would you give Slack?
I would give it 4.5/5
© Slack introduction screen, screenshot. Retrieved from Google Play store application on October 17, 2017 at 1:51 PM
I foresee this app having great success and continuing its momentum as daily users have steadily increased since the day it went live (in Aug 2013). Most recent stats reveal that the daily usage has risen to 6 million users (as of September 12th 2017).
From my observations, the adoption of the Slack's software makes great business sense for corporations. Clearly Slack contributes positively to the day-to-day work life experience for the employees. Online reviews in the app store are overwhelmingly positive.
According to statistics from the Google Play app store, Slack has recorded five million downloads and scores a 4.4 (out of 5) rating, which is impressive.
It remains to be seen how these platforms will evolve over the decades. How all-encompassing will the world of communication via social media be for my child? As the mother of a Gen TBD, I am ever aware of the alarming statistics that come from the study of children's exposure to devices (ipads, smart phones, computers etc). It has been demonstrated that the over use of devices has a negative impact on the mental health of children.
Ironically, addiction to devices may be of benefit to businesses. It makes sense for companies to adopt this type of social software. Overwhelmingly, those who embrace social media in the workplace report loving the experience. Humans are naturally drawn to the instant gratification of the pop ups; I can relate to the urge to look at my phone when I hear a notification. Could employees who enjoy using work-related social applications be unknowingly led down a path of enslavement to their jobs?
This subject leaves me with many questions. How effectively do these apps contribute to the retention of employees? What will my Gen TBD child's future work-life balance look like?
Organization: https://www.sylvania.com/en-us/Pages/default.aspx
Name of Organization Contact: David Ko, Senior Software Engineer
Authored by: Kimberly Barrett
Insight into the Xennial Generation
Over-use of ipads, iphones and smart screens hurting kids
https://play.google.com/store/apps/details?id=com.Slack
https://www.theatlantic.com/national/archive/2014/03/here-is-when-each-generation-begins-and-ends-according-to-facts/359589/
#Addiction, #casestudy, #employeeengagement, #Future, #GenX, #GenY, #RelationshipBuilding, #socialmedia, #Tool, #worklife, #Xennial, apps, Blog, channels, communication, engagement, slack, Software


Some Russians crowed over the investigation not finding collusion by the Trump campaign. But the report's focus on election interference tempered hopes for better relations.
A senior Russian lawmaker said on Monday it was unlikely there would be a sudden change in relations with Washington after the conclusion of a U.S. investigation into collusion between Donald Trump and Russia in the 2016 presidential election, RIA news agency reported.


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Upcoming Pertinent Changes to Member Web Portal
Magellan is implementing pertinent changes to our web portals and web-based applications and tools. Members who desire to check their eligibility, third-party liability, and pharmacy claims, will be able to register on the updated web portal for secure access to this information. Check back here for additional details regarding the date of implementation and registration process of the new and improved web portal.
Pertinent Changes to Provider Web Portal
Effective 11/23/2022, Magellan implemented Okta with multifactor authentication for our provider web-based applications accessed via the web portal. Current users of Web Claims Submission (WCS) and WebRA (now known as MRxPay) will need to complete a short migration process to verify their access credentials and move all existing application permissions to the new Okta platform. Please review the migration step-by-step job aid. ***Important to Note: Once the steps are taken to migrate your User ID to Okta-based credentials for WCS and MRxPay, providers should continue to log in to the secure web portal with their previous credentials - the new credentials will only be utilized after logging in to the secure portal and if accessing WCS or MRxPay.***
If a new pharmacy provider would like to register for WCS and/or MRxPay, they can still do so by clicking the Register link to access our User Administration Console (UAC). An MRxPay Job Aid has also been created for your reference. Please access the job aid to learn about the MRxPay navigation and functionality.
Upcoming Pertinent Changes to Provider Web Portal
In the coming months, Magellan will implement pertinent changes to our web portals and web-based applications and tools. A new look and feel for the web pages and tools, such as Find a Pharmacy and Drug Lookup, will be observed. While the look may be changing, the functionality of these tools will remain the same.
Emergency Drug Coverage Reminder
This is a reminder to pharmacies regarding the federal statute that required Medicaid programs to provide payment for dispensing of at least a 72-hour supply for any drugs requiring prior authorizations if prior authorization cannot be obtained outside of Medicaid business hours. View the provider notice for more information.
New Hampshire Fee-for-Service Medicaid recently updated the preferred drug list. It is effective 09/01/2022. View the PDL.
Diabetic Supply Program
New Hampshire Fee-for-Service Medicaid recently updated the preferred diabetic supply list. It is effective 10/01/2022. View the preferred diabetic supply list.
New Hampshire Fee-for-Service Medicaid will be having a Drug Utilization Review Board meeting on December 13, 2022 with the public session beginning at 2pm via Zoom Webinar or in the Brown Building Cafeteria. Please view the agenda. Register for the Zoom Webinar.
Pharmacy Program Changes
Effective 04/14/2022, pharmacy claims for At-Home Over-The-Counter COVID-19 Test Kits are covered under Medicare benefit for dual eligible members. For details see the provider notice.
Effective 01/21/2022, pharmacy claims for At-Home Over-The-Counter COVID-19 Test Kits will be reimbursed at Point of Sale. For details see the provider notice.
PERM - Payment Error Rate Measurement
The PERM Audit is designed to measure improper payments in the Medicaid and CHIP programs, as required by the Improper Payments Information Act (IPIA) of 2002 (amended in 2010 by the Improper Payments Elimination and Recovery Improvement Act or IPERA, and the Improper Payments Elimination and Recovery Improvement Act of 2012 IPERIA). The improper payment rates are based on reviews of the Fee-for-Service (FFS), managed care, and eligibility components of Medicaid and CHIP in the year under review.
Beginning in April 2022, the Center for Medicare and Medicaid Services (CMS) will be starting the New Hampshire PERM review of NH Medicaid claims and provider enrollment.
Providers will be receiving medical document request from the CMS PERM contractor, NCI Information System, Inc. starting in April 2022. Providers must submit the requested information by the due date noted on the request. Please note that it will be the responsibility of the billing provider identified on the claim to ensure that all supporting medical records, from the provider who rendered a Medicaid covered service for which the claim payment under review was requested, is submitted in a timely manner.
Morphine Equivalent Dose Calculator
The Morphine Equivalent Dose Calculator calculates the dosage of common opioids as equivalent to 1mg of Morphine.
The calculator is courtesy of the Washington State Agency Medical Directors' Group.
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UCLA's Adam Plutko said when he heads to the mound tonight for Game 1 of the finals against Mississippi State, he'll just worry about himself and believe that somehow, some way his teammates will come through.
UCLA has backed its outstanding pitching in Omaha by committing a total of one error in wins over LSU, N.C. State and North Carolina.
The Bruins carry a nine-game winning streak into the finals. They're 19-4 since May 1 and came to the CWS off the momentum created by sweeping No. 5 national seed Cal State Fullerton in super regionals.