Are You Too Busy or Just Not Organised?
In my travels I have encountered business owners who don't seem to be able to keep a promise. Are you one of them?
In my travels I have encountered business owners who don't seem to be able to keep a promise.
A promise to return my call, send me that "important" document that you stated needs to be fixed today, pay me on time for work done, attend a scheduled meeting that you booked.
When you make a promise to another person that you will do something by this date/time and you don't think how that comes across.
Even worse – think what that person thinks about you if you fail to keep your promise more than once.
It really comes down to respect. If you promise to do something and you don't then the other person can only assume that you don't respect them enough to "follow through" on the promise.
Will I continue to do business with you if you keep breaking your promises? Of course not.
Will I bother to contact you when I get a great opportunity that is ideal for you? Of course not!
If you promise to do something make sure you do what you promised or if you don't show some respect and contact the person directly to apologize for breaking the promise.


text:
Q: Python - Append letters in alphabetical order based on specific variable to dataframe I would like to append a letter (in an alphabetical order)to my dataframe starting from a specific letter which I have stored in a variable.
Current dataframe:
col1
data1
data2
data3

Variable to assign (could be any letter of the alphabet)
variable ='D'

Desired output as dataframe
col1  | col2
data1 | E
data2 | F
data3 | G

I can assign ABCDE etc using the code below. For my case I have to assign it from a specific letter (e.g if letter B then next should be C etc

from string import ascii_uppercase as ABC
d = dict(zip(ABC[:len(df)], df.col1))

Desired output as dictionary
output = {'E': 'data1', 'F': 'data2', 'G': 'data3'}

Could someone guide me on the above?

A: Use ord to create start point for ascii code
start_ascii = ord(variable) + 1

Map using chr to the generated ord values
df['col2'] = list(map(chr, range(start_ascii, start_ascii + df.shape[0])))

Dataframe becomes
    col1 col2
0  data1    E
1  data2    F
2  data3    G

Convert to dictionary
dict(zip(df.col2, df.col1))

Output
{'E': 'data1', 'F': 'data2', 'G': 'data3'}

A: You can make use of the RangeIndex:
df["new"] = (df.index+ord(variable)+1).map(chr)

print (df.set_index("new")["col1"].to_dict())

{'E': 'data1', 'F': 'data2', 'G': 'data3'}

redpajama_set_name: RedPajamaStackExchange


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Our Misting Systems are a simple, inexpensive and appealing way to lower temperature by 10-12 °C outdoors and indoors without wetting.
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The Arctic Circle is the parallel of latitude that runs 66° 33' 39," or roughly 66.5°, north of the Equator. Approximately 15,000 kilometers (9,300 miles) to the south is the Antarctic Circle, of equal diameter to and parallel to the Arctic Circle as well as equally distant from the Equator. Together with the Equator and the tropics of Cancer and Capricorn, these five unseen circular lines comprise the major circles of latitude that mark maps of the Earth. All five are determined by the Earth's rotation on its axis and the Earth's tilt toward and away from the Sun in its orbit. The circle, though invisible and, in fact, moving, is a product of the same phenomenon that provides the world with four seasons and this largely austere part of the globe with an odd formula of light and darkness shared only by its polar opposite.
The Arctic Circle marks the southern extremity of the polar day of the summer solstice in June and the polar night of the winter solstice in December. Within the whole area of the Arctic Circle, the Sun is above the horizon for at least 24 continuous hours once per year, in conjunction with the Arctic's summer solstice, which is often referred to as the "midnight sun." Likewise, in conjunction with the Arctic's winter solstice, the Arctic sun will be below the horizon in the entire area for at least 24 continuous hours, which could just as easily be called the "noontime night." The darkness is often alleviated, though, by the awesome beauty of the Aurora Borealis, or "Northern Lights," which result from the interplay of the Earth's magnetic field and the solar wind. Points within the circle experience longer periods of continuous light and darkness depending on their proximity to the North Pole, where six months of sunlight alternate with a half-year of darkness.
Because of a slow wobble that the Earth has in its rotation over a period of more than 40,000 years, the Arctic Circle also moves slowly about, to the point that it is problematic to say exactly where it lies even one day to the next. Over a period of nearly 20 years, the Earth's tilt oscillates about 280 meters (924 feet), which causes the circle at present to be moving north at the rate of about 14 meters (46 feet) per year.
The Arctic Ocean lies wholly within the Arctic Circle. The ocean, the circle, and the region take their names from the Greek word arctus, meaning "bear," a reference to the Big and Little Bear constellations that can always be seen overhead on clear nights in the polar region.
Everything north of the Arctic Circle is properly known as the Arctic while the zone just to the south of the circle is the Northern Temperate Zone. The North Pole lies about 2,600 kilometers (1,600 miles) from the Arctic Circle. Because of the moderating influence of open water—even warm water escaping from under polar pack ice— the North Pole is often less cold than points on the circle.
The nation of Iceland barely grazes the Arctic Circle, with less than one km² of its territory lying north of it. The line crosses or passes south of just a few tiny islets.
Greenland is the only one of these countries with most of its area within the circle, though the vast majority of its population resides south of it.
In contrast to the area south of the Antarctic Circle, where there are virtually no permanent residents, the population of the total area north of the Arctic Circle is in the vicinity of two million. The majority (more than 60 percent) are in Russia, followed in order by Norway and Finland. The Arctic population of North America, including Greenland, comprises less than three percent of all people living within the circle. Murmansk in northwestern Russia is the circumpolar region's largest city.
The ethnic links among the indigenous people of the Arctic are not at all certain though they share some elements of their daily lifestyle, such as clothing, shelter, and weaponry. Linguistic connections haven't been found, and the different communities have historically been isolated from one another. The Inuit people (once called Eskimos) of Greenland, Canada, and Alaska have tenuous but slowly growing links with the native people of northern Siberia, such as the Nenet and Yakut.
The three Nordic nations have each built a railroad line extending north of the circle but connecting with their national capitals well to the south. In Norway's and Finland's case, the railways stretch a relatively short distance, but in Sweden's the track nearly reaches the nation's northern limits. In Russia there are two lines, one to Murmansk and the other farther east, yet west of the Ural Mountains. No rail lines have been built into the Arctic in North America. A proposed rail tunnel under the Bering Strait to Siberia would lie just south of the Arctic Circle.
The Nordic countries all have highway systems extending well into their Arctic territory, as does Russia in the Murmansk region. Canada's Dempster Highway, also referred to as Yukon Highway 5 and Northwest Territories Highway 8, is a highway that connects the Klondike Highway in Yukon, Canada to Inuvik, Northwest Territories on the Mackenzie River delta. During the winter months, the highway extends to Tuktoyaktuk, on the northern coast of Canada, using frozen portions of the Mackenzie River delta as an ice road also known as the Tuktoyaktuk Winter Road. The highway crosses the Peel River and the Mackenzie Rivers using a combination of seasonal ferry service and ice bridges. Canada has no such links into the Arctic sections of its Nunavut territories. The James Dalton Highway in Alaska reaches from Fairbanks, Alaska to the Arctic Ocean at the town of Deadhorse, Alaska along the North Slope. The town consists of facilities for the workers and companies that operate at the nearby Prudhoe Bay oil fields.
Though there is a growing interest in travel north of the Arctic Circle focusing particularly on the area's relatively non-endangered wildlife and endangered wildlife such as polar bears, tourism remains on a fairly low scale. Quick visits by adventurers to the North Pole are somewhat popular among those who seek to be able to claim they have been there.
Farming is difficult in the Arctic since much of the ground is tundra, though there are certain crops in prepared soil, such as cabbage, that grow large quickly in the continuous light of the midnight sun. Fishing and the land bound industries related to it are the dominant source of livelihood, along with hunting. The herding and care of reindeer are an enduring activity in the Lapland (or Sami) sections of Finland, Sweden, and Norway.
There are major, but not generally well known, rivers flowing north past the Arctic Circle into the Arctic Ocean. The Mackenzie River runs through the Northwest Territories and empties into the ocean a few hundred kilometers east of Alaska's northeast corner. The Ob, Yenisey, and Lena rivers of Siberia drain immense areas of northern Asia even as far south as Kazakhstan and Mongolia and meet the ocean in extensive estuaries and deltas that are frozen in winter.
Many islands and small archipelagoes are strewn about the Arctic. Besides Greenland, Earth's largest island, there are several others that are also among the world's biggest. They have such names as Canada's Baffin, Victoria, and Ellesmere islands; Norway's Spitsbergen; and Russia's Novaya Zemlya and Wrangel Island.
This page was last modified on 12 April 2016, at 15:37.


Today was "Take Your Dog to Work Day." My co-workers and I were really ecstatic that we got to bring our dogs. I just had to share with you this picture of my co-workers shih tzu "Maxwell". Doesn't he look so cute with his tie...very work appropriate I must add. To the right is my own doggy "Scrappy." I actually barricaded him in my cubicle with this baby gate. Did you take your dog to work today?
OMG!!! I am so sad I missed this. Who's idea was this anyway???
I wish I would have known about take your dog to work day ;(!!!


text:
package org.pentaho.di.core.database;

import static org.junit.Assert.assertArrayEquals;
import static org.junit.Assert.assertEquals;
import static org.junit.Assert.assertFalse;
import static org.junit.Assert.assertTrue;

import java.sql.ResultSet;

import org.junit.Before;
import org.junit.ClassRule;
import org.junit.Test;
import org.mockito.Mockito;
import org.mockito.invocation.InvocationOnMock;
import org.mockito.stubbing.Answer;
import org.pentaho.di.core.row.RowMetaInterface;
import org.pentaho.di.core.row.value.ValueMetaBigNumber;
import org.pentaho.di.core.row.value.ValueMetaBinary;
import org.pentaho.di.core.row.value.ValueMetaBoolean;
import org.pentaho.di.core.row.value.ValueMetaDate;
import org.pentaho.di.core.row.value.ValueMetaInteger;
import org.pentaho.di.core.row.value.ValueMetaInternetAddress;
import org.pentaho.di.core.row.value.ValueMetaNumber;
import org.pentaho.di.core.row.value.ValueMetaString;
import org.pentaho.di.core.row.value.ValueMetaTimestamp;
import org.pentaho.di.junit.rules.RestorePDIEnvironment;

public class MSSQLServerDatabaseMetaTest {
  MSSQLServerDatabaseMeta nativeMeta, odbcMeta;
  @ClassRule public static RestorePDIEnvironment env = new RestorePDIEnvironment();

  @Before
  public void setupOnce() throws Exception {
    nativeMeta = new MSSQLServerDatabaseMeta();
    nativeMeta.setAccessType( DatabaseMeta.TYPE_ACCESS_NATIVE );
    odbcMeta = new MSSQLServerDatabaseMeta();
    odbcMeta.setAccessType( DatabaseMeta.TYPE_ACCESS_ODBC );
  }

  @Test
  public void testSettings() throws Exception {
    assertFalse( nativeMeta.supportsCatalogs() );
    assertArrayEquals( new int[] { DatabaseMeta.TYPE_ACCESS_NATIVE, DatabaseMeta.TYPE_ACCESS_ODBC, DatabaseMeta.TYPE_ACCESS_JNDI },
        nativeMeta.getAccessTypeList() );
    assertEquals( 1433, nativeMeta.getDefaultDatabasePort() );
    assertEquals( -1, odbcMeta.getDefaultDatabasePort() );
    assertEquals( "net.sourceforge.jtds.jdbc.Driver", nativeMeta.getDriverClass() );
    assertEquals( "sun.jdbc.odbc.JdbcOdbcDriver", odbcMeta.getDriverClass() );

    assertEquals( "jdbc:jtds:sqlserver://FOO/WIBBLE", nativeMeta.getURL( "FOO", "", "WIBBLE" ) );
    assertEquals( "jdbc:jtds:sqlserver://FOO:BAR/WIBBLE", nativeMeta.getURL( "FOO", "BAR", "WIBBLE" ) );

    assertEquals( "jdbc:odbc:FOO", odbcMeta.getURL( null, null, "FOO" ) );
    assertEquals( "jdbc:odbc:FOO", odbcMeta.getURL( "xxxxxx", "zzzzzzz", "FOO" ) );

    odbcMeta.setUsingDoubleDecimalAsSchemaTableSeparator( true );
    assertEquals( "FOO..BAR", odbcMeta.getSchemaTableCombination( "FOO", "BAR" ) );

    assertEquals( "FOO.BAR", nativeMeta.getSchemaTableCombination( "FOO", "BAR" ) );
    assertFalse( nativeMeta.supportsBitmapIndex() );

    assertArrayEquals( new String[] {
      /*
       * Transact-SQL Reference: Reserved Keywords Includes future keywords: could be reserved in future releases of SQL
       * Server as new features are implemented. REMARK: When SET QUOTED_IDENTIFIER is ON (default), identifiers can be
       * delimited by double quotation marks, and literals must be delimited by single quotation marks. When SET
       * QUOTED_IDENTIFIER is OFF, identifiers cannot be quoted and must follow all Transact-SQL rules for identifiers.
       */
      "ABSOLUTE", "ACTION", "ADD", "ADMIN", "AFTER", "AGGREGATE", "ALIAS", "ALL", "ALLOCATE", "ALTER", "AND",
      "ANY", "ARE", "ARRAY", "AS", "ASC", "ASSERTION", "AT", "AUTHORIZATION", "BACKUP", "BEFORE", "BEGIN",
      "BETWEEN", "BINARY", "BIT", "BLOB", "BOOLEAN", "BOTH", "BREADTH", "BREAK", "BROWSE", "BULK", "BY", "CALL",
      "CASCADE", "CASCADED", "CASE", "CAST", "CATALOG", "CHAR", "CHARACTER", "CHECK", "CHECKPOINT", "CLASS",
      "CLOB", "CLOSE", "CLUSTERED", "COALESCE", "COLLATE", "COLLATION", "COLUMN", "COMMIT", "COMPLETION",
      "COMPUTE", "CONNECT", "CONNECTION", "CONSTRAINT", "CONSTRAINTS", "CONSTRUCTOR", "CONTAINS",
      "CONTAINSTABLE", "CONTINUE", "CONVERT", "CORRESPONDING", "CREATE", "CROSS", "CUBE", "CURRENT",
      "CURRENT_DATE", "CURRENT_PATH", "CURRENT_ROLE", "CURRENT_TIME", "CURRENT_TIMESTAMP", "CURRENT_USER",
      "CURSOR", "CYCLE", "DATA", "DATABASE", "DATE", "DAY", "DBCC", "DEALLOCATE", "DEC", "DECIMAL", "DECLARE",
      "DEFAULT", "DEFERRABLE", "DEFERRED", "DELETE", "DENY", "DEPTH", "DEREF", "DESC", "DESCRIBE", "DESCRIPTOR",
      "DESTROY", "DESTRUCTOR", "DETERMINISTIC", "DIAGNOSTICS", "DICTIONARY", "DISCONNECT", "DISK", "DISTINCT",
      "DISTRIBUTED", "DOMAIN", "DOUBLE", "DROP", "DUMMY", "DUMP", "DYNAMIC", "EACH", "ELSE", "END", "END-EXEC",
      "EQUALS", "ERRLVL", "ESCAPE", "EVERY", "EXCEPT", "EXCEPTION", "EXEC", "EXECUTE", "EXISTS", "EXIT",
      "EXTERNAL", "FALSE", "FETCH", "FILE", "FILLFACTOR", "FIRST", "FLOAT", "FOR", "FOREIGN", "FOUND", "FREE",
      "FREETEXT", "FREETEXTTABLE", "FROM", "FULL", "FUNCTION", "GENERAL", "GET", "GLOBAL", "GO", "GOTO",
      "GRANT", "GROUP", "GROUPING", "HAVING", "HOLDLOCK", "HOST", "HOUR", "IDENTITY", "IDENTITY_INSERT",
      "IDENTITYCOL", "IF", "IGNORE", "IMMEDIATE", "IN", "INDEX", "INDICATOR", "INITIALIZE", "INITIALLY",
      "INNER", "INOUT", "INPUT", "INSERT", "INT", "INTEGER", "INTERSECT", "INTERVAL", "INTO", "IS", "ISOLATION",
      "ITERATE", "JOIN", "KEY", "KILL", "LANGUAGE", "LARGE", "LAST", "LATERAL", "LEADING", "LEFT", "LESS",
      "LEVEL", "LIKE", "LIMIT", "LINENO", "LOAD", "LOCAL", "LOCALTIME", "LOCALTIMESTAMP", "LOCATOR", "MAP",
      "MATCH", "MINUTE", "MODIFIES", "MODIFY", "MODULE", "MONTH", "NAMES", "NATIONAL", "NATURAL", "NCHAR",
      "NCLOB", "NEW", "NEXT", "NO", "NOCHECK", "NONCLUSTERED", "NONE", "NOT", "NULL", "NULLIF", "NUMERIC",
      "OBJECT", "OF", "OFF", "OFFSETS", "OLD", "ON", "ONLY", "OPEN", "OPENDATASOURCE", "OPENQUERY",
      "OPENROWSET", "OPENXML", "OPERATION", "OPTION", "OR", "ORDER", "ORDINALITY", "OUT", "OUTER", "OUTPUT",
      "OVER", "PAD", "PARAMETER", "PARAMETERS", "PARTIAL", "PATH", "PERCENT", "PLAN", "POSTFIX", "PRECISION",
      "PREFIX", "PREORDER", "PREPARE", "PRESERVE", "PRIMARY", "PRINT", "PRIOR", "PRIVILEGES", "PROC",
      "PROCEDURE", "PUBLIC", "RAISERROR", "READ", "READS", "READTEXT", "REAL", "RECONFIGURE", "RECURSIVE",
      "REF", "REFERENCES", "REFERENCING", "RELATIVE", "REPLICATION", "RESTORE", "RESTRICT", "RESULT", "RETURN",
      "RETURNS", "REVOKE", "RIGHT", "ROLE", "ROLLBACK", "ROLLUP", "ROUTINE", "ROW", "ROWCOUNT", "ROWGUIDCOL",
      "ROWS", "RULE", "SAVE", "SAVEPOINT", "SCHEMA", "SCOPE", "SCROLL", "SEARCH", "SECOND", "SECTION", "SELECT",
      "SEQUENCE", "SESSION", "SESSION_USER", "SET", "SETS", "SETUSER", "SHUTDOWN", "SIZE", "SMALLINT", "SOME",
      "SPACE", "SPECIFIC", "SPECIFICTYPE", "SQL", "SQLEXCEPTION", "SQLSTATE", "SQLWARNING", "START", "STATE",
      "STATEMENT", "STATIC", "STATISTICS", "STRUCTURE", "SYSTEM_USER", "TABLE", "TEMPORARY", "TERMINATE",
      "TEXTSIZE", "THAN", "THEN", "TIME", "TIMESTAMP", "TIMEZONE_HOUR", "TIMEZONE_MINUTE", "TO", "TOP",
      "TRAILING", "TRAN", "TRANSACTION", "TRANSLATION", "TREAT", "TRIGGER", "TRUE", "TRUNCATE", "TSEQUAL",
      "UNDER", "UNION", "UNIQUE", "UNKNOWN", "UNNEST", "UPDATE", "UPDATETEXT", "USAGE", "USE", "USER", "USING",
      "VALUE", "VALUES", "VARCHAR", "VARIABLE", "VARYING", "VIEW", "WAITFOR", "WHEN", "WHENEVER", "WHERE",
      "WHILE", "WITH", "WITHOUT", "WORK", "WRITE", "WRITETEXT", "YEAR", "ZONE" }, nativeMeta.getReservedWords() );

    assertArrayEquals( new String[] { "jtds-1.2.5.jar" }, nativeMeta.getUsedLibraries() );
    assertEquals( "http://jtds.sourceforge.net/faq.html#urlFormat", nativeMeta.getExtraOptionsHelpText() );
    assertTrue( nativeMeta.supportsSchemas() );
    assertTrue( nativeMeta.supportsSequences() );
    assertTrue( nativeMeta.supportsSequenceNoMaxValueOption() );
    assertFalse( nativeMeta.useSafePoints() );
    assertTrue( nativeMeta.supportsErrorHandlingOnBatchUpdates() );
    assertEquals( 8000, nativeMeta.getMaxVARCHARLength() );
  }

  @Test
  public void testSQLStatements() {
    assertEquals( "SELECT TOP 1 * FROM FOO", nativeMeta.getSQLQueryFields( "FOO" ) );
    String lineSep = System.getProperty( "line.separator" );
    assertEquals( "SELECT top 0 * FROM FOO WITH (UPDLOCK, HOLDLOCK);"
      + lineSep + "SELECT top 0 * FROM BAR WITH (UPDLOCK, HOLDLOCK);" + lineSep,
      nativeMeta.getSQLLockTables(  new String[] { "FOO", "BAR" } ) );

    assertEquals( "ALTER TABLE FOO ADD BAR DATETIME",
        nativeMeta.getAddColumnStatement( "FOO", new ValueMetaDate( "BAR" ), "", false, "", false ) );
    assertEquals( "ALTER TABLE FOO ADD BAR DATETIME",
        nativeMeta.getAddColumnStatement( "FOO", new ValueMetaTimestamp( "BAR" ), "", false, "", false ) );

    assertEquals( "ALTER TABLE FOO DROP COLUMN BAR" + lineSep,
        nativeMeta.getDropColumnStatement( "FOO", new ValueMetaString( "BAR", 15, 0 ), "", false, "", true ) );

    assertEquals( "ALTER TABLE FOO ALTER COLUMN BAR VARCHAR(15)",
        nativeMeta.getModifyColumnStatement( "FOO", new ValueMetaString( "BAR", 15, 0 ), "", false, "", true ) );

    assertEquals( "ALTER TABLE FOO ALTER COLUMN BAR VARCHAR(100)",
        nativeMeta.getModifyColumnStatement( "FOO", new ValueMetaString( "BAR" ), "", false, "", true ) );

    odbcMeta.setSupportsBooleanDataType( true ); // some subclass of the MSSQL meta probably ...
    assertEquals( "ALTER TABLE FOO ADD BAR BIT",
        odbcMeta.getAddColumnStatement( "FOO", new ValueMetaBoolean( "BAR" ), "", false, "", false ) );
    odbcMeta.setSupportsBooleanDataType( false );

    assertEquals( "select o.name from sysobjects o, sysusers u where  xtype in ( 'FN', 'P' ) and o.uid = u.uid order by o.name",
        nativeMeta.getSQLListOfProcedures( "FOO" ) );

    assertEquals( "select name from sys.schemas", nativeMeta.getSQLListOfSchemas() );
    assertEquals( "insert into FOO(FOOVERSION) values (1)", nativeMeta.getSQLInsertAutoIncUnknownDimensionRow( "FOO", "FOOKEY", "FOOVERSION" ) );
    assertEquals( "SELECT NEXT VALUE FOR FOO", nativeMeta.getSQLNextSequenceValue( "FOO" ) );
    assertEquals( "SELECT current_value FROM sys.sequences WHERE name = 'FOO'", nativeMeta.getSQLCurrentSequenceValue( "FOO" ) );
    assertEquals( "SELECT 1 FROM sys.sequences WHERE name = 'FOO'", nativeMeta.getSQLSequenceExists( "FOO" ) );
    assertEquals( "SELECT name FROM sys.sequences", nativeMeta.getSQLListOfSequences() );
  }

  @Test
  public void testGetFieldDefinition( ) throws Exception {
    assertEquals( "CHAR(1)",
        nativeMeta.getFieldDefinition( new ValueMetaBoolean( "BAR" ), "", "", false, false, false ) );

    assertEquals( "BIGINT",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 10, 0 ), "", "", false, false, false ) );

    assertEquals( "BIGINT",
        nativeMeta.getFieldDefinition( new ValueMetaBigNumber( "BAR", 10, 0 ), "", "", false, false, false ) );

    assertEquals( "BIGINT",
        nativeMeta.getFieldDefinition( new ValueMetaInteger( "BAR", 10, 0 ), "", "", false, false, false ) );

    assertEquals( "INT",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 0, 0 ), "", "", false, false, false ) );

    assertEquals( "INT",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 5, 0 ), "", "", false, false, false ) );

    assertEquals( "DECIMAL(10,3)",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 10, 3 ), "", "", false, false, false ) );

    assertEquals( "DECIMAL(10,3)",
        nativeMeta.getFieldDefinition( new ValueMetaBigNumber( "BAR", 10, 3 ), "", "", false, false, false ) );

    assertEquals( "DECIMAL(21,4)",
        nativeMeta.getFieldDefinition( new ValueMetaBigNumber( "BAR", 21, 4 ), "", "", false, false, false ) );

    assertEquals( "TEXT",
        nativeMeta.getFieldDefinition( new ValueMetaString( "BAR", nativeMeta.getMaxVARCHARLength() + 2, 0 ), "", "", false, false, false ) );

    assertEquals( "VARCHAR(15)",
        nativeMeta.getFieldDefinition( new ValueMetaString( "BAR", 15, 0 ), "", "", false, false, false ) );

    assertEquals( "FLOAT(53)",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 10, -7 ), "", "", false, false, false ) ); // Bug here - invalid SQL

    assertEquals( "DECIMAL(22,7)",
        nativeMeta.getFieldDefinition( new ValueMetaBigNumber( "BAR", 22, 7 ), "", "", false, false, false ) );
    assertEquals( "FLOAT(53)",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", -10, 7 ), "", "", false, false, false ) );
    assertEquals( "DECIMAL(5,7)",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR", 5, 7 ), "", "", false, false, false ) );
    assertEquals( " UNKNOWN",
        nativeMeta.getFieldDefinition( new ValueMetaInternetAddress( "BAR" ), "", "", false, false, false ) );

    assertEquals( "BIGINT PRIMARY KEY IDENTITY(0,1)",
        nativeMeta.getFieldDefinition( new ValueMetaInteger( "BAR" ), "BAR", "", true, false, false ) );

    assertEquals( "BIGINT PRIMARY KEY",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR" ), "BAR", "", false, false, false ) );

    assertEquals( "BIGINT PRIMARY KEY IDENTITY(0,1)",
        nativeMeta.getFieldDefinition( new ValueMetaInteger( "BAR" ), "", "BAR", true, false, false ) );
    assertEquals( "BIGINT PRIMARY KEY",
        nativeMeta.getFieldDefinition( new ValueMetaNumber( "BAR" ), "", "BAR", false, false, false ) );
    assertEquals( "VARBINARY(MAX)",
        nativeMeta.getFieldDefinition( new ValueMetaBinary( ), "", "BAR", false, false, false ) );
    assertEquals( "VARBINARY(MAX)",
        nativeMeta.getFieldDefinition( new ValueMetaBinary( "BAR" ), "", "BAR", false, false, false ) );
  }

  private int rowCnt = 0;
  private String[] row1 = new String[] { "ROW1COL1", "ROW1COL2" };
  private String[] row2 = new String[] { "ROW2COL1", "ROW2COL2" };

  @Test
  public void testCheckIndexExists() throws Exception {
    String expectedSQL = "select i.name table_name, c.name column_name from     sysindexes i, sysindexkeys k, syscolumns c where    i.name = 'FOO' AND      i.id = k.id AND      i.id = c.id AND      k.colid = c.colid "; // yes, space at the end like in the dbmeta
    Database db = Mockito.mock(  Database.class );
    RowMetaInterface rm = Mockito.mock( RowMetaInterface.class );
    ResultSet rs = Mockito.mock( ResultSet.class );
    DatabaseMeta dm = Mockito.mock( DatabaseMeta.class );
    Mockito.when( dm.getQuotedSchemaTableCombination( "", "FOO" ) ).thenReturn( "FOO" );
    Mockito.when( rs.next() ).thenReturn( rowCnt < 2 );
    Mockito.when( db.openQuery( expectedSQL ) ).thenReturn( rs );
    Mockito.when( db.getReturnRowMeta() ).thenReturn( rm );
    Mockito.when( rm.getString( row1, "column_name", "" ) ).thenReturn( "ROW1COL2" );
    Mockito.when( rm.getString( row2, "column_name", "" ) ).thenReturn( "ROW2COL2" );
    Mockito.when( db.getRow( rs ) ).thenAnswer( new Answer<Object[]>() {
        @Override
        public Object[] answer( InvocationOnMock invocation ) throws Throwable {
          rowCnt++;
          if ( rowCnt == 1 ) {
            return row1;
          } else if ( rowCnt == 2 ) {
            return row2;
          } else {
            return null;
          }
        }
    } );
    Mockito.when(  db.getDatabaseMeta() ).thenReturn( dm );
    assertTrue( nativeMeta.checkIndexExists( db, "", "FOO", new String[] { "ROW1COL2", "ROW2COL2" } ) );
    assertFalse( nativeMeta.checkIndexExists( db, "", "FOO", new String[] { "ROW2COL2", "NOTTHERE" } ) );
    assertFalse( nativeMeta.checkIndexExists( db, "", "FOO", new String[] { "NOTTHERE", "ROW1COL2" } ) );

  }

}

redpajama_set_name: RedPajamaGithub


I don't know what part of this project is going to be easy/go smoothly...we should have braced ourselves for all that could go wrong based on our experience with the YEAR LONG journey (almost) trying to get these plans! We started last August and were promised completed plans then in October, twice in November, once in December, Every weekend in January, twice in February, on Wednesdays and Fridays in March, and then finally received them in April. I am surprised that Dana has not had a coronary....I really thought she would at any point from December on . So this has really put us behind the eight-ball on many different levels...It caused our estimates to be off from our contractor, pushed Dana and Sam out of their lease, Definitely (obviously) delayed construction, caused us to get a re-appraisal and delayed the closing until today!
While this is definitely one of those 20/20/hindsight situations...we at least have the plans now......and they are great!


text:
Monosporascus adenantherae är en svampart som först beskrevs av S.D. Patil & C. Ramesh, och fick sitt nu gällande namn av A. Pande 2008. Monosporascus adenantherae ingår i släktet Monosporascus, ordningen kolkärnsvampar, klassen Sordariomycetes, divisionen sporsäcksvampar och riket svampar.   Inga underarter finns listade i Catalogue of Life.

Källor

Kolkärnsvampar
adenantherae

redpajama_set_name: RedPajamaWikipedia


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text:
MRuby::Build.new do |conf|

  # Gets set by the VS command prompts.
  if ENV['VisualStudioVersion'] || ENV['VSINSTALLDIR']
    toolchain :visualcpp
  else
    toolchain :gcc
  end

  enable_debug

  # include the default GEMs
  conf.gembox 'default'

end

# Cross Compiling configuration for RX630
# http://gadget.renesas.com/
#
# Requires gnurx_v14.03
MRuby::CrossBuild.new("RX630") do |conf|
  toolchain :gcc

  # Linux
  BIN_PATH = "/usr/share/gnurx_v14.03_elf-1/bin"

  conf.cc do |cc|
    cc.command = "#{BIN_PATH}/rx-elf-gcc"
    cc.flags = "-Wall -g -O2 -flto -mcpu=rx600 -m64bit-doubles"
    cc.compile_options = "%{flags} -o %{outfile} -c %{infile}"

    #configuration for low memory environment
    cc.defines << %w(MRB_USE_FLOAT)
    cc.defines << %w(MRB_HEAP_PAGE_SIZE=64)
    cc.defines << %w(MRB_USE_IV_SEGLIST)
    cc.defines << %w(KHASH_DEFAULT_SIZE=8)
    cc.defines << %w(MRB_STR_BUF_MIN_SIZE=20)
    cc.defines << %w(MRB_GC_STRESS)
    cc.defines << %w(MRB_DISABLE_STDIO) #if you dont need stdio.
    #cc.defines << %w(POOL_PAGE_SIZE=1000) #effective only for use with mruby-eval
  end

  conf.cxx do |cxx|
    cxx.command = conf.cc.command.dup
    cxx.include_paths = conf.cc.include_paths.dup
    cxx.flags = conf.cc.flags.dup
    cxx.defines = conf.cc.defines.dup
    cxx.compile_options = conf.cc.compile_options.dup
  end

  conf.linker do |linker|
    linker.command="#{BIN_PATH}/rx-elf-ld"
  end

  conf.archiver do |archiver|
    archiver.command = "#{BIN_PATH}/rx-elf-ar"
    archiver.archive_options = 'rcs %{outfile} %{objs}'
  end

  #no executables
  conf.bins = []

  #do not build executable test
  conf.build_mrbtest_lib_only

  #disable C++ exception
  conf.disable_cxx_exception

  #gems from core
  conf.gem :core => "mruby-sprintf"
  conf.gem :core => "mruby-print"
  conf.gem :core => "mruby-math"
  conf.gem :core => "mruby-enum-ext"
  conf.gem :core => "mruby-numeric-ext"

  #light-weight regular expression
  #conf.gem :github => "masamitsu-murase/mruby-hs-regexp", :branch => "master"

  #Arduino API
  #conf.gem :github =>"kyab/mruby-arduino", :branch => "master"

end


text:
Dec 15, 2002 Issue
Gluten-Sensitive Enteropathy (Celiac Disease): More Common Than You Think
DAVID A. NELSEN, JR., M.D., M.S., University of Arkansas for Medical Sciences, Little Rock, Arkansas
Am Fam Physician. 2002 Dec 15;66(12):2259-2266.
Patient Information Handout
Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia.
Although celiac disease was formally described late in the 19th century, treatment remained empiric until the middle of the 20th century when patients were noted to improve dramatically after wheat was removed from their diet. With the development of small-bowel biopsy techniques, the small intestine was identified as the target organ. Disease causality was established when the characteristic features of villous flattening, crypt hyperplasia, and increased intra-epithelial lymphocytes (Figure 1) were shown to normalize after the institution of a gluten-free diet.1
View/Print Figure
(Left) Photomicrograph of distal duodenal biopsy specimen in a patient with celiac disease. Note the characteristic features of crypt hyperplasia (CH), and increased intraepithelial lymphocytes (IEL). (Right) For comparison, a normal biopsy specimen is shown.
In the mid-1960s, an enteropathy strikingly similar to celiac disease was identified in patients with dermatitis herpetiformis. Subsequently, this skin disorder was shown to be a manifestation of gluten-sensitive enteropathy. In the mid-1960s, adult celiac disease was also noted to be associated with numerous neurologic disorders, including epilepsy, cerebral calcifications, and peripheral neuropathy.1
Recent population studies indicate that celiac disease is more common than was previously thought. Some patients with gluten-sensitive enteropathy have minimal or no symptoms and are unlikely to be referred to a gastroenterologist unless the disease is considered. Hence, family physicians need to be familiar with the diagnosis and management of gluten-sensitive enteropathy.
Jump to section +
Ingested protein does not normally provoke an immune response. This phenomenon is termed "oral tolerance." Patients who exhibit true allergy to an ingested protein (e.g., milk or soy protein) have a typical IgE-mediated response consisting of urticaria, angioedema, and bronchoreactivity.
The autoimmunity in gluten-sensitive enteropathy involves plasma cells that produce IgA and IgG; there is little or no IgE involvement. Current theory suggests that ingested α-gliadin (a component of the gluten protein) and related peptides bind with tissue transglutaminase (a ubiquitous intracellular enzyme) in enterocytes. The α-gliadin is rich in glutamine; transglutaminase deamidates glutamine residues, forming glutamic acid. Deamidation enhances the immunogenicity of α-gliadin by creating epitopes that are recognized as foreign by host cell–mediated immunity.2
Plasma cells produce IgA and IgG that are directed against a variety of antigens, including transglutaminase, endomysium, gliadin, and reticulin. Locally elaborated lymphokines attract inflammatory cells.3 This intense local inflammatory reaction produces the villous flattening characteristic of gluten-sensitive enteropathy. Malabsorption of micronutrients (e.g., vitamins and minerals) and macronutrients (e.g., protein, carbohydrate, fat) follows. Small-bowel involvement is most prominent proximally and may be "patchy," especially in patients with "silent" celiac disease (i.e., minimal or no symptoms) and those with dermatitis herpetiformis.
Approximately 95 percent of patients with celiac disease exhibit specific Human Leukocyte Antigen (HLA) class II alleles DQA1*0501 and DQB1*0201.4 Patients with type 1 diabetes, autoimmune thyroid disease,5 Sjögren's syndrome, primary biliary cirrhosis, Addison's disease, systemic lupus erythematosus, selective IgA deficiency, and alopecia areata may also exhibit similar genotypes and are at risk for gluten-sensitive enteropathy (Table 1). Because many persons have these genotypes and only a few develop gluten-sensitive enteropathy, investigators have hypothesized that other genes or cofactors may be involved.1
View/Print Table
Celiac Disease and Other Autoimmune Disorders*
Type 1 diabetes mellitus
Recurrent aphthous ulcerations
Vitiligo or alopecia areata
Autoimmune Addison's disease
Psoriasis†
*—Listed in descending order of clinical importance and prevalence.
†—Observed association.
Until recently, celiac disease was considered to be relatively uncommon. Previous U.S. figures suggested that it affected one in 6,000 persons.6 However, population studies published in the past four years suggest a much higher prevalence, particularly in persons of European ancestry.7 Studies conducted in Europe estimate the seroprevalence of celiac disease to be one case per 130 to 300 persons.8–10
In a recent U.S. study,11 investigators tested sera from 2,000 healthy Red Cross blood donors and found eight samples that were positive for antibodies associated with gluten-sensitive enteropathy (seven samples from white persons, one sample from a black person). The seroprevalence rate in this study (one case per 250 persons tested) is consistent with the rates in European studies.
The likelihood of having gluten-sensitive enteropathy increases to 10 to 20 percent in persons who have a first-degree relative with celiac disease.1 In addition, celiac disease is associated with other autoimmune syndromes. For example, as many as 7 percent of patients with type I diabetes also have gluten-sensitive enteropathy.12
Untreated gluten-sensitive enteropathy is associated with a range of symptoms13,14 (Table 2). The "classic" form typically presents in infancy and manifests as failure to thrive, diarrhea, abdominal distention, developmental delay, and, occasionally, severe malnutrition. Failure to diagnose the disorder may lead to a true medical emergency.
Symptoms of Celiac Disease and Possible Causes
Fatigue, malaise
Anemia, general immune system activation
Nutrient malabsorption
Diarrhea, abdominal pain
Accelerated gastrointestinal tract transit time, steatorrhea, malabsorption
Most commonly, iron deficiency; less commonly, vitamin B12 and/or folate deficiency
Aphthous oral ulcers, glossitis, stomatitis
Vitamin deficiency, "oral" celiac disease
Postulated cause: iron, folate, and/or zinc deficiency
Male impotence, decreased libido
Peripheral insensitivity to circulating testosterone
Immunologic attack on hair follicles
Dental enamel defects
Demineralization during tooth bud development in children
Delayed absorption of glucose
Gas, flatus, borborygmus
Secondary digestion of sugars by intestinal flora
Seizures, gluten ataxia, central nervous system symptoms
Increased affinity of celiac antibodies for brain vasculature
Beyond infancy, the symptoms of celiac disease tend to be less dramatic. Older children may present with constitutional short stature or dental enamel defects.
Women comprise approximately 75 percent of newly diagnosed adult celiac disease cases. Women also tend to have more clinically conspicuous disease.15 In adults of both sexes, gastrointestinal tract involvement may manifest as diarrhea, constipation, or other symptoms of malabsorption, such as bloating, flatus, or belching. Fatigue, depression, fibromyalgia-like symptoms, aphthous stomatitis, bone pain, dyspepsia, gastroesophageal reflux, and other nonspecific symptoms may be present and can make the diagnosis quite challenging.14 A number of other autoimmune syndromes have been associated with celiac disease (Table 1).
Fewer than 10 percent of adults with gluten-sensitive enteropathy present with dermatitis herpetiformis.16 This skin condition may be misdiagnosed as atypical psoriasis or nonspecific dermatitis.
The rash of dermatitis herpetiformis is intensely pruritic and typically occurs on the back, buttocks, knees, and elbows (Figure 2). Unexcoriated lesions (Figure 3) are remarkably like those of herpes simplex (thus, the term "herpetiformis"). Granular IgA deposition on immunofluorescence of a skin biopsy specimen is diagnostic (Figure 4).
Dermatitis herpetiformis, sometimes termed "celiac disease of the skin." Vesicular, crusted, intensely pruritic lesions develop on the back (top left and right), buttocks (lower left), and elbows (lower right). Secondary infection of the lesions is common.
Close-up view of dermatitis herpetiformis. Unexcoriated lesions are remarkably like those of herpes simplex (thus, the term "herpetiformis").
Photomicrograph of a skin biopsy specimen in a patient with dermatitis herpetiformis. Note the intense inflammatory infiltration at the dermoepidermal junction. Immunofluorescence demonstrated granular deposition of IgA (arrow).
Anemia is the most common laboratory manifestation of celiac disease13,14 (Table 3). One half of patients with newly diagnosed gluten-sensitive enteropathy are anemic. Iron is absorbed in the proximal small intestine, where celiac manifestations are most prominent; hence, iron malabsorption is common. In addition, occult blood loss related to intense small-bowel inflammation may occur in 50 percent of patients with gluten-sensitive enteropathy.17 Less commonly, vitamin B12 deficiency, folate deficiency, or both may be present.
Abnormal Laboratory Findings in Celiac Disease
Laboratory finding
Iron deficiency; vitamin B12 and/or folate deficiency
Elevated alkaline phosphatase level
Osteoporosis, osteomalacia
Elevated aspartate transaminase and alanine transaminase levels
Minimal elevation common in celiac disease; presumably autoimmune
Decreased albumin level
Elevated calcium level, decreased phosphate level
Vitamin D deficiency, secondary hyperparathyroidism
Thrombocytosis, leukocytosis
General inflammatory reaction
Decreased vitamin K absorption
Low high-density and low-density lipoprotein cholesterol levels
Decreased fat absorption, decreased hepatic lipoprotein production
SILENT CELIAC DISEASE
A number of investigators believe that clinically apparent gluten-sensitive enteropathy represents the "tip of the iceberg" of the overall disease burden.7 Patients who were detected in the seroprevalence studies8–11 were asymptomatic or oligosymptomatic (so-called "silent" celiac disease).
Family physicians should consider serologic testing in patients with the following: family history of celiac disease, personal history of thyroid disease or type I diabetes, irritable bowel syndrome, anemia (especially iron deficiency), chronic diarrhea, chronic fatigue, unexplained weight loss, short stature, epilepsy, infertility,18 or unexplained elevation of transaminase levels. Asymptomatic or oligosymptomatic patients are still at risk for complications of celiac disease.
When the diagnosis of gluten-sensitive enteropathy is suspected, serologic tests can identify many affected patients.19 (Figure 5). IgA antiendomysial antibody has been shown to be 85 to 100 percent sensitive and 96 to 100 percent specific for celiac disease. IgA antiendomysial antibody is measured using direct immunofluorescence of monkey esophagus or umbilical cord tissue processed with suspect serum.
Diagnosis of Celiac Disease
Algorithm for the diagnosis of celiac disease. (EGD = esophagogastroduodenoscopy)
IgG and IgA antigliadin antibodies are also useful in diagnosing celiac disease. The antibody directed against endomysium has recently been identified as identical to the antibody directed against (tissue) transglutaminase. An enzyme-linked immunosorbent assay has been developed to measure IgA antitransglutaminase; this test will generally replace the more tedious direct fluorescent antibody test for IgA antiendomysial antibody.20–22 In diagnosing celiac disease, antitransglutaminase antibody is considered to be approximately as sensitive and specific as antiendomysial antibody (Table 4).21,23-25
Serologic Tests for Celiac Disease
Antibody test
Sensitivity (%)
Specificity (%)
Time course
Cost*
IgA antiendomysial antibody
Antibody disappears within several months after institution of gluten-free diet.
$45 to 99
IgA antitransglutaminase antibody
Limited data; correlated with IgA antiendomysial antibody in studies
IgA antigliadin antibody
More persistent than IgA antiendomysial antibody; may persist for 6 months or longer
IgG antigliadin antibody
Most persistent; may be detectable up to 12 months after institution of gluten-free diet
False-positive tests reported in patients with Crohn's disease, wheat-protein allergy, and postdiarrhea states
*—Average of costs at three reference laboratories in the summer of 2001.
Information from references 21 through 23 and 25
The presence of IgA antiendomysial and antitransglutaminase antibodies correlates with intestinal damage. Tests for these antibodies are highly sensitive in patients with total and subtotal villous atrophy. IgA antiendomysial antibody testing has been reported to be 100 percent sensitive in patients with total villous atrophy. The combination of IgA antiendomysial antibody and IgG and IgA antigliadin antibodies detects 76 percent of patients with mucosal damage.
It is important to note that 2 to 3 percent of patients with gluten-sensitive enteropathy also have selective IgA deficiency. Because these patients may not produce the diagnostic IgA antibodies, a positive IgG antigliadin antibody test may be the only serologic evidence of the disease. If clinical suspicion is high, quantitative IgA measurements should be obtained in these patients.26 Endoscopy and biopsy should be strongly considered in patients with selective IgA deficiency.
Declining autoantibody titers correlate with resolution of the gastrointestinal lesion and may be used to document clinical improvement. In equivocal cases or when a patient has been on a gluten-free diet, a gluten challenge test may be used to provoke the gastrointestinal lesion and serologic response.
DISTAL DUODENAL BIOPSY
Distal duodenal biopsy is the gold standard for the diagnosis of celiac disease. Biopsy should be performed in most patients with suspected gluten-sensitive enteropathy. In determining the need for biopsy, family physicians should consult a gastroenterologist who is experienced in the diagnosis and management of celiac disease.1
Calcium and vitamin D malabsorption dramatically increases the risk of osteoporosis and osteomalacia in patients with gluten-sensitive enteropathy. Most patients with celiac disease have some degree of osteopenia or osteoporosis. Fortunately, calcium and vitamin D supplementation, coupled with a strict gluten-free diet, usually results in remineralization of the skeleton.27,28
Bone density should be assessed in all patients with newly diagnosed celiac disease. Postmenopausal women should be advised about the benefits of estrogen replacement. The use of antiresorptive agents (e.g., alendronate [Fosamax]) has not been extensively studied, but these drugs may be of benefit.
Cerebral calcifications and epilepsy have been associated with celiac disease29,30 and do not always resolve with the institution of a gluten-free diet. Peripheral neuropathy, postural instability, "gluten ataxia," and other vague neurologic complaints may be the sole manifestation of gluten-sensitive enteropathy.31 Autoantibodies associated with celiac disease have demonstrated a strong affinity for brain vasculature.32
REFRACTORY SPRUE
In patients with refractory sprue, gastrointestinal tract inflammation continues despite maintenance of a gluten-free diet. Dietary noncompliance is the most common reason for persistent inflammation; however, coexistent conditions such as hyperthyroidism and collagenous colitis should also be considered.
Patients who are truly refractory to dietary measures may have cryptic lymphoma of (bowel) intraepithelial lymphocytes. All diet-refractory patients should be evaluated by a gastroenterologist with expertise in the management of celiac disease. Corticosteroids and immunosuppressant drugs have been used to treat refractory sprue, but data on their effectiveness are sparse.
Intestinal strictures and bowel obstruction may develop in patients with refractory sprue or celiac disease that has been untreated over a long period.
LYMPHOMA AND BOWEL ADENOCARCINOMA
Enteropathy-associated T-cell lymphoma has been associated with untreated gluten-sensitive enteropathy and refractory sprue.33 Lymphoma may develop in patients with celiac disease who also have dermatitis herpetiformis.
Studies34,35 have shown that maintenance of a long-term gluten-free state reduces the risk of lymphoma to the level in the general population. Thus, it is imperative that patients with celiac disease (and dermatitis herpetiformis) maintain a gluten-free diet for the rest of their lives.
Patients with celiac disease are also at risk for the development of bowel adenocarcinoma in all sites. The risk is especially high in patients with a long period of disease preceding institution of a gluten-free diet.
Once the diagnosis of celiac disease has been made, patients should be evaluated for known manifestations and complications (Table 5). Iron deficiency should be treated with supplemental iron. Osteoporosis should be treated with calcium and vitamin D replacement. Depending on individual factors, patients with gluten-sensitive enteropathy may need to take a multivitamin, iron, calcium, magnesium, zinc, selenium, vitamin D, or other nutrients.
Laboratory Evaluation of Patients with Newly Diagnosed Celiac Disease
Complete blood cell count
Iron level, total iron-binding capacity determination, ferritin level*
Vitamin B12 and folate levels
Calcium and phosphate levels
Alkaline phosphatase level
Blood urea nitrogen and creatinine levels
Albumin and total serum protein levels
Aspartate transaminase and alanine transaminase levels
Dual energy x-ray absorptiometry (DEXA) of spine and hip
Serologic tests†
Quantitative IgA antiendomysial antibody or quantitative IgA antitransglutaminase
Quantitative IgA and IgG antigliadin antibodies
*—The ferritin level may be misleading: it may be elevated as an acute-phase reactant.
†—Serologic testing should be recommended for first-degree relatives of patients with newly diagnosed celiac disease.
The primary treatment for celiac disease is the removal of gluten and related proteins from the diet. Complete exclusion of dietary gluten generally results in rapid and complete healing of small-bowel inflammation. Advice from a registered dietitian is essential to outline an appropriate diet.
Gluten, a prolamine, is the primary protein in wheat. Hence, wheat and products containing wheat must be avoided. Barley and rye contain similar proteins and must also be avoided. Oats are a subject of controversy.36,37 Although oats themselves may be nontoxic in limited quantities, commercial oat products are measurably contaminated with wheat. Rice, corn, maize, flax, quinoa, tapioca, potato, amaranth, and other grain substitutes, such as nuts and beans, are safe.
There are many commercial gluten-free products, including breads, cookies, chips, and cereals, that can be used to fashion a rich and interesting diet. Meats, vegetables, fruit, and most dairy products are free of gluten, as long as they have not been contaminated during production.
A number of food manufacturers maintain lists of gluten-free products. These lists can be obtained from the manufacturers' Web sites or by telephone request. Information on gluten-free foods is also available from local or national support groups such as the Celiac Sprue Association. Selected resources are provided in Table 6.
Selected Resources
Celiac Sprue Association/United States of America, Inc.*
P.O. Box 31700, Omaha, NE 68131-0700
Web site:www.csaceliacs.org
E-mail address: celiacs@csaceliacs.org
Celiac Discussion List Archives
Web site:www.fastlane.net/homepages/thodge/archive.shtml
National Digestive Diseases Information Clearinghouse
Web site:www.niddk.nih.gov/health/digest/pubs/celiac/index.htm
Celiac Disease Resources for Medical Professionals†
Web site:www.uams.edu/celiac
*—The Celiac Sprue Association is a national organization that supports persons with celiac disease and related conditions.
†—David A. Nelsen, Jr., M.D., M.S., maintains a Web site with resources for primary care physicians to assist them in the care of patients with celiac disease.
show all author info
DAVID A. NELSEN, JR., M.D., M.S., is associate professor in the Department of Family and Community Medicine at the University of Arkansas for Medical Sciences, Little Rock, where he earned his medical degree and completed a family medicine residency. He completed a faculty development and clinical investigation fellowship at the University of Minnesota Medical School, Minneapolis, where he also earned a master's degree in family and community medicine. Dr. Nelsen has published and presented in the area of medical informatics and speech recognition. He serves on the technical panel of the American Academy of Family Physicians....
Address correspondence to David A. Nelsen Jr., M.D., M.S., University of Arkansas for Medical Sciences, Department of Family and Community Medicine, Mail Slot #530, 4301 W. Markham, Little Rock, AR 72205 (e-mail:nelsendavida@uams.edu). Reprints are not available from the author.
The author indicates that he does not have any conflicts of interest. Sources of funding: none reported.
Figure 1 provided by Laura Lamps, M.D., assistant professor of pathology, University of Arkansas for Medical Sciences (UAMS), Little Rock. Figure 4 provided by Bruce Smoller, M.D., professor of pathology and dermatology, UAMS.
1. Ciclitira PJ, King AL, Fraser JS. AGA technical review on celiac sprue. American Gastroenterological Association. Gastroenterology. 2001;120:1526–40....
2. Van De Wal Y, Kooy Y, Van Veelen P, Vader W, Koning F, Pena S. Coeliac disease: it takes three to tango! Gut. 2000;46:734–7.
3. Marsh MN. The natural history of gluten sensitivity: defining, refining and re-defining. QJM. 1995;88:9–13.
4. Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E. Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer. J Exp Med. 1989;169:345–50.
5. Collin P, Salmi J, Hallstrom O, Reunala T, Pasternack A. Autoim-mune thyroid disorders and coeliac disease. Eur J Endocrinol. 1994;130:137–40.
6. American Gastroenterological Association medical position statement: celiac sprue. Gastroenterology. 2001;120:1522–25.
7. Catassi C, Ratsch IM, Fabiani E, Rossini M, Bordicchia F, Candela F, et al. Coeliac disease in the year 2000: exploring the iceberg. Lancet. 1994;343:200–3.
8. Fasano A, Catassi C. Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology. 2001;120:636–51.
9. Hin H, Bird G, Fisher P, Mahy N, Jewell D. Coeliac disease in primary care: case finding study. BMJ. 1999;318:164–7.
10. Branski D, Troncone R. Celiac disease: a reappraisal. J Pediatr. 1998;133:181–7.
11. Not T, Horvath K, Hill ID, Partanen J, Hammed A, Magazzu G, et al. Celiac disease risk in the USA: high prevalence of antiendomysium antibodies in healthy blood donors. Scand J Gastroenterol. 1998;33:494–8.
12. Cronin CC, Shanahan F. Insulin-dependent diabetes mellitus and coeliac disease. Lancet. 1997;349:1096–7.
13. Iovino P, Ciacci C, Sabbatini F, Acioli DM, D'Argenio G, Mazzacca G. Esophageal impairment in adult celiac disease with steatorrhea. Am J Gastroenterol. 1998;93:1243–9.
14. Clemens PC. Coeliac disease in adults with atypical symptoms [Letter]. Lancet. 1996;347:1050.
15. Ciacci C, Cirillo M, Sollazzo R, Savino G, Sabbatini F, Mazzacca G. Gender and clinical presentation in adult celiac disease. Scand J Gastroenterol. 1995;30:1077–81.
16. Trier JS. Celiac sprue and refractory sprue. In: Feldman M, Fordtran JS, Sleisenger MH, Scharschmidt BF, eds. Sleisenger & Fordtran's Gastrointestinal and liver disease: pathophysiology, diagnosis, management. 6th ed. Philadelphia: Saunders, 1998:1557–73.
17. Fine KD. The prevalence of occult gastrointestinal bleeding in celiac sprue. N Engl J Med. 1996;334:1163–7.
18. Sher KS, Mayberry JF. Female fertility, obstetric and gynaecological history in coeliac disease. A case control study. Digestion. 1994;55:243–6.
19. Fotoulaki M, Nousia-Arvanitakis S, Augoustidou-Savvopoulou P, Kanakoudi-Tsakalides F, Zaramboukas T, Vlachonikolis J. Clinical application of immunological markers as monitoring tests in celiac disease. Dig Dis Sci. 1999;44:2133–8.
20. Troncone R, Maurano F, Rossi M, Micillo M, Greco L, Auricchio R, et al. IgA antibodies to tissue transglutaminase: an effective diagnostic test for celiac disease. J Pediatr. 1999;134:166–71.
21. Vitoria JC, Arrieta A, Arranz C, Ayesta A, Sojo A, Maruri N, et al. Antibodies to gliadin, endomysium, and tissue transglutaminase for the diagnosis of celiac disease. J Pediatr Gastroenterol Nutr. 1999;29:571–4.
22. Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken EO, et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med. 1997;3:797–801.
23. Biagi F, Ellis HJ, Yiannakou JY, Brusco G, Swift GL, Smith PM, et al. Tissue transglutaminase antibodies in celiac disease. Am J Gastroenterol. 1999;94:2187–92.
24. Russo PA, Chartrand L J, Seidman E. Comparative analysis of serologic screening tests for the initial diagnosis of celiac disease. Pediatrics. 1999;1041 pt 175–8.
25. Valdimarsson T, Franzen L, Grodzinsky E, Skogh T, Strom M. Is small bowel biopsy necessary in adults with suspected celiac disease and IgA anti-endomysium antibodies? 100% positive predictive value for celiac disease in adults. Dig Dis Sci. 1996;41:83–7.
26. Cataldo F, Marino V, Bottaro G, Greco P, Ventura A. Celiac disease and selective immunoglobulin A deficiency. J Pediatr. 1997;131:306–8.
27. Valdimarsson T, Lofman O, Toss G, Strom M. Reversal of osteopenia with diet in adult coeliac disease. Gut. 1996;38:322–7.
28. Sategna-Guidetti C, Grosso SB, Grosso S, Mengozzi G, Aimo G, Zaccaria T, et al. The effects of 1-year gluten withdrawal on bone mass, bone metabolism and nutritional status in newly-diagnosed adult coeliac disease patients. Aliment Pharmacol Ther. 2000;14:35–43.
29. Dickey W. Epilepsy, cerebral calcifications, and coeliac disease. Lancet. 1994;344:1585–6.
30. Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, Gibson A, Grunewald RA, Lobo AJ. Neuromuscular disorder as a presenting feature of coeliac disease. J Neurol Neurosurg Psychiatry. 1997;63:770–5.
31. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Davies-Jones GA, Gibson A, Jarratt JA, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet. 1998;352:1582–5.
32. Pratesi R, Gandolfi L, Friedman H, Farage L, de Castro CA, Catassi C. Serum IgA antibodies from patients with coeliac disease react strongly with human brain blood-vessel structures. Scand J Gastroenterol. 1998;33:817–21.
33. Pricolo VE, Mangi AA, Aswad B, Bland KI. Gastrointestinal malignancies in patients with celiac sprue. Am J Surg. 1998;176:344–7.
34. Lewis HM, Renaula TL, Garioch JJ, Leonard JN, Fry JS, Collin P, et al. Protective effect of gluten-free diet against development of lymphoma in dermatitis herpetiformis. Br J Dermatol. 1996;135:363–7.
35. Holmes GK, Prior P, Lane MR, Pope D, Allan RN. Malignancy in coeliac disease—effect of a gluten free diet. Gut. 1989;30:333–8.
36. Hoffenberg EJ, Haas J, Drescher A, Barnhurst R, Osberg I, Bao F, et al. A trial of oats in children with newly diagnosed celiac disease. J Pediatr. 2000;137:361–6.
37. Janatuinen EK, Pikkarainen PH, Kemppainen TA, Kosma VM, Jarvinen RM, Uusitupa MI, et al. A comparison of diets with and without oats in adults with celiac disease. N Engl J Med. 1995;333:1033–7.
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Home / Journals / afp / Vol. 66/No. 12(December 15, 2002) / Gluten-Sensitive Enteropathy (Celiac Disease): More Common than You Think

redpajama_set_name: RedPajamaCommonCrawl


The reality of an amazing summer came to a head today around 11 a.m. yesterday.
And yes, a day earlier than announced by the middle school our daughter will attend next month, her first class schedule was available.
Life as I knew it for the last seven years is changing. Our daily routine, support network, and drop off/pick up schedule will all change.
And change doesn't always happen the way you want it to.
Moms across the community are realizing that they too need help with making sure their children are well taken care of when it comes to their safety in getting to/from schoo each day.
It reminds us that all are not as fortunate as others who have neither flexible work schedules nor the extra funds to pay for before/after school care.
But if we lean on one another we can hopefully take a little stress out of our already stressful lives.
But will you? You need a Parent Possee and here's how you can create one.
I encourage you to create a network of support to help ease your stress and vice versa.
Don't be afraid to ask for help. We all want to be Wonder Woman, and we are in many ways, but sometimes it's okay to lean on others.
I gave up trying to do it all. I can't and I won't act like I can. I'll drive myself crazy.
While I don't have blood relatives within an hour of my home, my local family has helped me tremendously.
Now, ask yourself who can you ask to help you? Let's make some calls and start recruiting your Parent Possee today.


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DP Training allows its students, graduates and staff to share their training experiences. Get a glimpse of what they feel by checking this.
DP Training Pty Ltd (Deb Goodeve) has been at all times, professional and prompt in replying to any enquiries, prior to starting my course and during, which left me in no doubt that I had selected the correct Training Provider.
My dealings and furthering of my career with DP Training Pty Ltd, was fulfilling and beyond my expectations. I would not hesitate to do future courses through DP Training and would highly recommend this Provider.


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What's right about America?
Dear Reader, thank you for allowing me to share my thoughts on the anniversary of a powerful day in our nation's history. Being raised by parents who came through the Great Depression and World War II, on the victor's side, meant being raised to be a patriot. Sadly, sometimes, I feel like a stranger in my own country. But mostly, I look for and see hope for America all around me; I see what's right about America.
The "Star-Spangled Banner" sung at ballgames does it to me. Seeing young adults holding hands and praying at "See You at the Pole" in front of their schools does it. Hearing the Pledge of Allegiance echo in school hallways always does it to me. My red, white and blue heart nearly bursts with pride when I see or hear the heartbeat of our nation.
What's right about America is driving to work in the pre-dawn hours and seeing the long line of headlights behind me. People going to work because it's the right thing to do. What's right about America is that most people still have a say in the work they do, based on their interests, their education, their personal needs, not the stoic needs of an unfeeling government.
What's right about America is knowing that even if I find some content offensive on social media, there are men and women who are willing to give the "last full measure of devotion" (Abraham Lincoln) in order to protect our right to freedom of speech.
There's so much right about America that sometimes we forget that we are blessed to live in the greatest nation in the world. We're a country of many colors, faiths, and flaws, but when push comes to shove, we're "one nation under God" (Francis Bellamy).
What's right about America isn't rock stars, or flashy cars. It isn't outrageously paid athletes or actors. What's right about America is rights and opportunities and motivation to follow your own dreams, not a path chosen and forced upon you.
What's right about America is that we're still working on equality and equity. We haven't given up because we're trying to remember each child is a blessing and a promise. What's right about America is that we're still moving forward to make sure each child has the opportunity to dream and strive toward that dream.
There's so much more that's right about America. I wonder what would happen if we focused more on what's right about America, and a little less on what's wrong. What's right about America is that we're not perfect, but we're not giving up. We'll never be a perfect nation, but we may be the best one this side of heaven.
9/11 changed many lives forever. My prayer for our country is that the willing and unwilling sacrifices made that day will not be vain. Perhaps our rallying cry should "Remember the Towers!", not for what we lost, but for what we have.


Dirt or stains on the carpet is annoying, but it turns out the handling is not as difficult as imagined. The important thing to note is different stains, different ways of handling it. Apart from that, you may need to hire the astonish carpet cleaner if your carpet is dirty and you don't have the time to wash it by yourself.
The first step, absorb the stain with a wet white cloth, absorb as much as possible. Then mix & frac12; a cup of salt with 1 liter of clean water. Use a sponge to clean the affected area.
After that, dry it by wiping it with a wet white cloth (not too much water). If it's still dirty, mix two teaspoons of non-alkaline detergent with & frac12; liters of clean water, then clean it. After that, dry it using a wet white cloth.
Because most carpets are made of natural materials, to remove these stains you can use a nail polish remover, which is nail polish remover or can use eye drops. After a few minutes, clean the stain with a dry white cloth.
Remove as many stains as possible using a tablespoon, a dull knife, or a bread knife. Then, put tissue paper (to absorb dirt) in the area with stains and gently press it using a warm iron, do it repeatedly until the greasy stain is not visible on the paper.
After that, mix two tablespoons of non-alkaline detergent with two tablespoons of white vinegar and 0.5 liters of warm water, then enter the affected area into the solution. After that wash with warm water. Dry the entire area stained with a hair-dryer (low setting) and let the carpet be exposed to sunlight (if possible).
Clean the stain by gently rubbing it. Absorb the stain with a wet white cloth. Do it several times.
Mix a cup of non-alkaline detergent with four glasses of warm water. Dip a white cloth, then squeeze it and rub it in the dirty part. Do it several times.
After feeling clean, dry it with a wet white cloth (not too wet).


Paris Saint-Germain laboured to a 2-1 victory over Orleans in the Coupe de la Ligue.
Paris Saint-Germain scraped into the Coupe de la Ligue quarter-finals thanks to a late goal from Moussa Diaby that secured a laboured 2-1 victory over Orleans.
In their first domestic cup outing of the season, PSG, winners of the last five Coupe de la Ligue trophies, rarely got out of first gear on Tuesday, and were almost punished when Joseph Lopy hauled Ligue 2 side Orleans level in the 69th minute.
Edinson Cavani's moment of quality had separated the sides at the interval, with fine goalkeeping from Thomas Renault denying Cavani and Kylian Mbappe – making his final appearance as a teenager after replacing the injured Angel Di Maria – at bay after the restart.
But it was another teenager who would settle the contest, as Diaby breezed through weak Orleans defending to book PSG's place in the last eight.
Eric Maxim Choupo-Moting almost made the most of a rare start inside two minutes, but his strike was kept out by Renault.
Cavani, however, showed no such profligacy four minutes before half-time, lofting home a superb first-time finish after latching onto Di Maria's dinked throughball.
PSG's goalscorer could have put the game to bed in the 48th minute, only for Renault's trailing leg to prevent Cavani's close-range effort doubling the visitors' advantage before Orleans' goalkeeper made an equally impressive stop to deny Mbappe.
And Orleans took full advantage of their keeper's good work – Lopy arrowing a strike into the bottom-right corner after Christopher Nkunku had squandered possession.
Orleans' hopes of an upset were quashed with nine minutes remaining, though, as Diaby made the most of poor defending to settle the tie in PSG's favour.
Mbappe had Orleans' goal at his mercy in stoppage time but Gauthier Pinaud somehow pulled off an incredible block on the line to prevent the youngster adding further gloss after Renault had come up for a set-piece.
The domestic cups will likely present Thomas Tuchel with the best opportunity to rotate his hugely talented squad but, even with just a few of their stars missing, PSG lacked the intensity and cutting edge that has seen them cruise clear at the top of Ligue 1. Orleans stayed in the game, and PSG's defensive vulnerabilities almost came back to bite them.
With Cavani and Mbappe both on the field, it was 19-year-old Diaby who took matters into his own hands, driving through Orleans' defence before slotting beyond Renault.
Tuchel handed youngster Nkunku a chance to impress, but the winger failed to take it and made a poor performance worse by conceding possession in the build up to Orleans' equaliser. Compounding his miserable evening, his replacement Diaby showed PSG just what they had been missing.
Orleans travel to Beziers in their next Ligue 2 outing, while PSG round off 2018 by hosting Nantes in Ligue 1 on Saturday.


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Q: Add component stylesheet to Jasmine test in Angular 2 I'm running my unit tests and seeing the actual application page below the results. It'd be nice if it had the styling applied to it, as the images etc go massive and it's not worth looking at.
Here is my setup code:
    describe('ResultImageComponent', () => {
       let fixture: ComponentFixture<UserAttributesCardComponent>;
       let component: UserAttributesCardComponent;
       let element: HTMLElement;
       let result: Result;
       let page: Page;

       beforeAll(() => {
          TestBed.resetTestEnvironment();
          TestBed.initTestEnvironment(BrowserDynamicTestingModule,
             platformBrowserDynamicTesting());
       });

       beforeEach(async(() => {
          TestBed.configureTestingModule({
             declarations: [UserAttributesCardComponent],
          }).compileComponents();
       }));

       beforeEach(async(() => {
          fixture = TestBed.createComponent(UserAttributesCardComponent);
          component = fixture.componentInstance;
          createComponent();
       }));

       function createComponent() {
          page = new Page();
          component.user = new UserService().getBen();
          fixture.detectChanges();
          return fixture.whenStable().then(() => {
             fixture.detectChanges();
             page.addPageElements();
          });
       }

The component under test has an external template which is being loaded fine but it also has an external style sheet which isn't loading.
Can this be done while configuring the test bed?

A: In the karma.conf.js file you can add an array of files to the config object.
files: [
    "../path/to/file.css"
],


Dentistry is an art as well as a science; dental crowns offer a perfect example of this. A dental crown or cap is a covering that fits over a damaged, decayed or unattractive tooth. It can even replace a tooth entirely as part of dental bridgework.
There are other materials besides porcelain that we can use to make dental crowns, depending on what qualities are most important. For durability, cast gold can't be beat. However, this is not always the most aesthetic choice ó especially towards the front of the mouth. Other possibilities include porcelain-fused-to-metal crowns (PFM), which have a metal interior for strength and a porcelain exterior for a more natural appearance, and all-porcelain crowns with zirconia, representing the strongest ceramic. We would be happy to discuss the pros and cons of these various options with you.
Crowns and bridgework require the same conscientious care as your natural teeth. Be sure to brush and floss between all of your teeth restored and natural every day to reduce the buildup of dental plaque. When you have crowns, it is even more important to maintain your regular schedule of cleanings at the dental office. Avoid using your teeth as tools (to open packages, for example). If you have a grinding habit, wearing a night guard would be a good idea to protect your teeth and your investment.


In the winter of 2014-2015, a group approached our church, Amazing Grace Baptist Church, about a youth camp property that they owned, but were unable to continue to maintain. After much prayer and consideration, we moved forward in accepting the property. Our desire is for this property to become a place for young people and families to come to meet with the Lord and deepen their relationship with Him.
The visions and excitement of future camps and special events was put on hold with the enormity of the task before us. The property, though used for many years as a summer camp, was in need of a lot of work. Our church, along with our sister churches in the area, caught the vision for this property. People of the churches here spent several months working hard, cleaning up, clearing land, and tearing down buildings. It has been a blessing to see God's people have a mind to work!
On October 9th, 2015 the camp was renamed and dedicated to the Lord for His use and His glory! It has been so exciting to see what God has already done.
In the summer of 2016, with limited facilities, El Bethel Bible Camp is opened for first group of young people. Since that time, we have been able to have two more youth camps, and two camps for the deaf. Several souls have already been saved and many decisions have been made for the Lord.
We continue to push toward the goal of having a fully functional camp property that will minister to the needs of the young people in our churches and in our area. We are using the property as much as possible in its current condition, but there is much work to be done. We are committed to the task to make this camp a place that will minister to many and preserve the testimony of the Lord for generations to come.


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History Club Honour Former Lord's Mayor
Home / News / School News / History Club Honour Former Lord's Mayor
January 7, 2020 May 28, 2019
The History Club were invited to city hall last Friday. This was for a ceremony that was to honour all the former Lord's Mayor of Cork that were also past pupils of the school. The boys selected a Lord Mayor each and introduced them and list their accomplishments before presenting them with a scroll acknowledging their achiements. During the ceremony the boys received high praise from both the former Lord's Mayor and the current Lord Major as well as the President of the PPU Mr Barry Hill who thanked them for their excellent work. The History Club Head Mr. Ryan was also in attendance and noted how the boys represented the school in a fantastic manner as usual! The North Monastery currently holds the record as the secondary school to have produced the most Lord's Mayor!
History Club return from Western Front
€5,000 Scholarship for History Club


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Idiostolidae  — семейство полужесткокрылых из подотряда клопов. 3 рода и 4 вида.

Распространение
Представители встречаются только в Южном полушарии (Австралия и Южная Америка).

Описание
Длина около 1 см. Форма тела вытянуто-овальная. Усики и лабиум состоят из 4 сегментов. Брюшко покрыто многочисленными трихоботриями, которые расположены на III—VII стернитах. Все абдоминальные дыхальца вентральные. Сперматеки отсутствуют. Вид Idiostolus  insularis ассоциирован с растениями рода Нотофагус (Nothofagus, Букоцветные).
Филогенетический анализ (Henry, 1997) показал родство Idiostolidae с австралийским эндемичным семейством Henicocoridae, с которым они были выделены в надсемейство Idiostoloidea, образующего монофилетическую группу.

Idiostolus Berg, 1883
Idiostolus  insularis — Аргентина и Чили
Monteithocoris Woodward, 1968
Monteithocoris hirsutus Woodward, 1968 — Тасмания
Trisecus Bergroth, 1895
Trisecus armatus Woodward, 1968 — Новый Южный Уэльс
Trisecus pictus Bergroth, 1895 — Тасмания, Новый Южный Уэльс, Тасмания

Примечания

Литература

 Schaefer, C. W. 1966. The morphology and higher systematics of the Idiostolinae (Hemiptera: Lygaeidae). Annals of the Entomological Society of America 59: 602—613.
 Schaefer, C. W. & Wilcox, D. 1969. Notes on the morphology, taxonomy, and distribution of the Idiostolidae (Hemiptera-Heteroptera). Annals of the Entomological Society of America 62: 485—502.

Pentatomomorpha
Семейства насекомых


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Home / Atlantic League / Independent Baseball / Long Island Ducks / Ducks Not Out Of It...Yet
Ducks Not Out Of It...Yet
As bad as the Long Island Ducks have played through their first 15 games, they are not completely out of the race for the first half championship. Currently, the Ducks sit five games behind the Liberty Division leading Bridgeport Bluefish.
The Ducks have had their fair share of problems early in the 2013 season. Most notably is an anemic offense which is batting .224. The Ducks don't have a player in the top thirty in league batting average. Ramon Castro is thirty-third on the list with a .256 average.
One glaring offensive stat is that the Ducks have drawn the least amount of walks in the Atlantic League with 34, which could be contributed to over aggressiveness in trying to jump start the offense. If the Ducks are going to right the ship they'll need to start taking more pitches, and waiting for a pitch to hit. Also, the Ducks have many former major league players who are looking to get the call back to the big leagues and they may swinging for the fences to increase their personal stats. The Ducks are second in the Atlantic League with 15 home runs.
Danny Perales is tied for the team lead with 3 home runs this season.
The Ducks pitching has also been dismal, posting a 5.37 ERA so far this season. It's hard to win games when your pitchers are giving up over 5 runs a game.
The Ducks will finish up the last game of a three game set with the York Revolution today, and then travel up the road to face the Lancaster Barnstormers for a four game series next week.
Atlantic League Independent Baseball Long Island Ducks


The Mirte van Wijngaarden Spring/Summer 2015 collection was presented during Mercedes-Benz Fashion Week Amsterdam. The designer's work is "characterized by the use of masculine elements that are translated in a new and groundbreaking way."
Mirte's models resembled modern Vikings and donned ensembles made up of layered fabrics and dramatically draped details. The guys took to the runway stage in draped coats, drop crotch trousers and layered vest looks that were paired with top-knot hair and metallic comsetics that were reminiscent of war paint.
In addition to her complex constructions, the Mirte van Wijngaarden Spring/Summer 2015 collection features the use of experimental textures and materials. Her collections capture movement and are designed with both aesthetics and comfort in mind.


Colombia Photo Expeditions philosophy is based in environmentally friendly and sustainable tourism. Our aim is to ensure that the travel development in Colombia takes a sustainable path.
Colombia Photo Expeditions promotes partnerships with local businesses in the destinations we travel rather using big international companies. This also means that the people you meet on the ground are locals who know their area better than anyone, and can take you deep into their home country or region.
Colombia Photo Expeditions has pledged to donate a percentage of our annual profit to conservation efforts in Colombia, along with supporting local photographers in our projects.
We also aim to source local products and services as part of our daily office procedures.


Bay Estate and Letting Agents approached us to design and build a new website to showcase their impressive range of high quality self catering apartments they have available in Swansea. They also needed a full admin suite to enable staff to maintain the website and also manage any back office fucntionality.
We built a custom web application a custom Microsoft.NET application on the Azure platform that firstly focused on the public facing website to showcase apartments, then worked with the Bay Team to build the back office features needed to support the application. We took an agile approach to delivery working with Bay Team to establish a backlog of requirements, mock up and prototype a few ideas, before getting small increments delivered into production on a regular basis.


I want to submit a novel manuscript to a small press in the US and their guidelines say "indented, not tabbed."
What's the difference? Usually I just hit the tab key once. Should I be doing something else?
I have Word Starter 2010, and I can't see any distinction between "indent" and "tab."
How do I make sure I'm indenting and not tabbing? If I'm tabbing, how do I change it to indent?
This is an excellent question, and I'm sure the cause of much confusion among word-processing novices. There is in fact a distinction between tabbing and indenting—or rather, it might be more accurate to say that tabbing is only one way to indent a paragraph. I will try to explain a method for indenting paragraphs that makes your document more portable* and easier for your publisher to use.
Back in the Stone Age, when we still used typewriters, there were two ways to indent a paragraph. You could hit the space bar five times at the start of your first line, or you could set up a tab stop half an inch in from your left margin and just hit the tab key once. "Tab" is short for "tabular," because tab stops were useful for helping a typist arrange figures in tables.
Click the manuscript page below to see William Shunn's original guide to formatting your short story or novel the way professionals do.
Copyright © 1995-2015 by William Shunn.