satzbu has asked for the wisdom of the Perl Monks concerning the following question:
dear monks i hav a code for convert a xml file as hash using XML::Simple but the hash output has changed the sequence of the XML tags pls tel me hw can i get the output without change the sequence
#!/usr/bin/perl use warnings; use strict; use Data::Dumper; use XML::Simple; my %xhash=(); my $file= $ARGV[0]; my $simple = XML::Simple->new(); my $xhash = $simple->XMLin($file); print Dumper($xhash); exit; open FH,"config.ini" or die $!; my $line; my %c_hash=(); my $c_hashRef = ''; my @tmpA = (); sub recur($); foreach $line (<FH>){ $line=~s/^(\s+)(.*)/$2/i; $line=~s/(.*?)(\s+)$/$2/i; chomp($line); if ($line ne ''){ $_=$line; $c_hashRef = ''; my @array = split(m/\|\|/, $line); print Dumper($c_hashRef); ($c_hashRef,@tmpA) = recur(\@array); } } print Dumper($c_hashRef); exit; sub recur($) { my $arrRef = $_[0]; my @procArr = @$arrRef; my $assign = ''; my %c_hash = (); my @tmpArr = @procArr; shift(@tmpArr); my $arr = $procArr[0]; if ($arr=~m/\[(.*)=(.*)\]/ig) { $assign = $1; my $tmpVal = ''; $tmpVal = $2; $tmpVal =~ s/\=(.*?)/$1/ig; $c_hash{$assign}{'repval'} = $tmpVal; ($c_hash{$assign}{'addval'},@tmpArr) = recur(\@tmpArr); $arr = shift(@tmpArr); if ($arr) { if ($arr=~m/\[(.*)=(.*)\]/ig) { my $key = $1; my $tmpVal = ''; $tmpVal = $2; $tmpVal =~ s/\=(.*?)/$1/ig; $c_hash{$key}{'repval'} = $tmpVal; ($c_hash{$key}{'addval'},@tmpArr) = recur(\@tmpArr +); $arr = shift(@tmpArr); } } } return (\%c_hash, @tmpArr); }
this is my output
$VAR1 = { 'chapter' => { 'subchap1' => { 'head1' => 'Prostaglandins', 'para' => [ { 'sub' => '2', 'content' => [ 'The p +rostaglandins are a group of biologically active derivatives of arach +idonic acid often referred to as eicosanoids for their basic 20-carbo +n atom structure. The two major pathways of eicosanoid metabolism are + the cyclooxygenase pathway, which yields the prostaglandins and thro +mboxanes, and the lipoxygenase pathway, which yields the leukotrienes +. A minor pathway termed epoxy-genase yields epoxides, which have rec +eived scant attention in the central nervous system (CNS). Arachidoni +c acid is synthesized on demand from dietary linoleic acid by either +a G protein-regulated phospholipase A', ' or d +iglyceride lipase activation (', '), an +d it yields a very broad array of bioactive metabolites, as shown in +', '. The + three major groups of arachidonic acid-derived metabolites are the p +rostaglandins, thromboxanes, and leukotrienes.' ], 'hotlink' => [ { 'xref' + => { + 'xref' => 'f012001', + 'xidtype' => 'figure' + }, 'conte +nt' => "Fig. 12\x{2013}1" }, { 'xref' + => { + 'xref' => 'f012002', + 'xidtype' => 'figure' + }, 'conte +nt' => "Figure 12\x{2013}2" } ] }, { 'c' => [ '\'', "\x{2014}", "\x{2014}" ], 'content' => [ 'Histo +rically, the earliest effect of prostaglandins arose with the recogni +tion in the 1930s that fresh semen could induce contraction of myomet +rial muscle, and the name arose from the factor', 's ant +icipated origin. As chemical detection methods improved in the 1950s, + two classes of prostaglandins were recognized', 'a PGE + class that was soluble in ether and a PGF class soluble in phosphate + buffer (', ' in S +wedish)', 'and o +ne of their sites of synthesis localized to seminal vesicles. Subsequ +ent work indicated that virtually every organ could manufacture prost +aglandins, and several distinct synthetic pathways were recognized. A + major advancement occurred when John Vane proposed that aspirin and +several other nonsteroidal anti-inflammatory drugs (NSAIDs) worked by + inhibiting the prostaglandin-synthesizing enzyme cyclooxygenase. Wor +k in the 1990s revealed that a second cyclooxygenase (COX-2) (and per +haps a third) was also present in the CNS. Since this enzyme was show +n to be induced by inflammatory cytokines, it immediately suggested a + separate target for relief of inflammatory pain, with the potential +for reduced symptoms from the gastrointestinal tract irritation typic +ally evoked by NSAIDs. COX-2 is also induced ', ' by t +he neurotransmitter GLU and inhibited by glucocorticoids. Unfortunate +ly, prolonged use of COX-2 inhibitors has untoward cardiovascular sid +e effects, leading to multiple litigious claims and diverting attenti +on from this once-promising therapeutic modification.' ], 'emphasis' => [ { 'cont +ent' => 'fosfat', 'styl +e' => 'it' }, { 'cont +ent' => 'in vitro', 'styl +e' => 'it' } ] }, { 'c' => [ "\x{3b3}", '[', ']', "\x{201c}", "\x{201d}" ], 'content' => [ "It is + well known that the eicosanoids, particularly the prostaglandin seri +es, play an important modulatory role in nervous tissue, but it has b +een difficult to write a lucid account of specifically how and where +they act. This is primarily due to the fact that they are not stored +in tissues, nervous or other, but synthesized on demand, particularly + in pathophysiological conditions. They act briefly (some with a half +-life of seconds) and at extremely low concentrations (10\x{2212}", ' M). +Although indomethacin is a good inhibitor of cyclooxygenase-1, blocki +ng the conversion of arachidonic acid to prostaglandins, there are fe +w specific inhibitors available to block lipoxygenase and epoxygenase +. Thus, although it had been postulated that the E series of prostagl +andins modulates noradrenergic release, blocks the convulsant activit +y of pentylenetetrazol, strychnine, and picrotoxin (possibly by incre +asing the level of ', '-amin +obutyric acid ', 'GABA' +, ' in t +he brain), and increases the level of cAMP in cortical and hypothalam +ic slices, these effects were noted ', ' with + the addition of substantial amounts of the prostaglandins. There was + very little evidence in intact animals to support these neuronal fin +dings. Since we skeptics all hold ', ' veri +tas', ' in h +igher regard, the physiological relevance of the effect was in doubt. +' ], 'emphasis' => [ { 'cont +ent' => 'in vitro', 'styl +e' => 'it' }, { 'cont +ent' => 'in vivo', 'styl +e' => 'it' } ], 'hotlink' => { 'xref' = +> { + 'xref' => 'r012010', + 'xidtype' => 'text' +}, 'sup' => + '10' } }, { 'sub' => '2', 'content' => [ 'Subse +quently, however, direct evidence has established arachidonic acid an +d lipoxygenases as second messengers. The cascade begins with the bin +ding of a neuroactive agent to its receptor. Then, according to findi +ngs from the Axelrod laboratory, the receptor is coupled to G protein +s, which may either activate or inhibit phospholipase A', ', alt +hough this has not been conclusively established for all neural tissu +es. The activated enzyme promotes the release of arachidonic acid, wh +ich will then act intracellularly as a second messenger. Arachidonic +acid and its metabolites can also leave the cell to act extracellular +ly as first messengers on neighboring cells. Eicosanoids have been sh +own to mediate the somatostatin-induced opening of an M channel in hi +ppocampal pyramidal cells and the release of VIP in mouse cerebral co +rtical slices. At the supracellular level, prostaglandins of the E se +ries have been held to be a mediator of fever and prostaglandins of t +he D series as regulators of sleep. It is thus becoming clear, despit +e enormous technological difficulties in assaying eicosanoids, that t +hese agents are major messengers.' ] }, 'Another exciting chapt +er of the arachidonic acid story has been told separately, namely the + endocannabinoids, which are described later in this chapter.' ] }, 'para' => { 'c' => [ "\x{201c}", "\x{201d}", "\x{201c}", "\x{201d}" ], 'content' => [ 'The previous chapters + were devoted to what we might now consider the ', 'classical', ' or perhaps ', 'conventional', ' neurotransmitters. B +y this, we mean those transmitters that are synthesized within the ne +uron (cell body or synaptic terminal) that releases them by activity- +dependent, Ca', '-dependent mechanisms + to act on discrete receptors largely, but not exclusively, on the ne +uron, smooth muscle, or gland cell opposite the nerve terminal. Howev +er, as the wheels of progress have turned, it seems that once again t +he more we learn about inter-cellular communication in the nervous sy +stem, the more complicated the situation becomes. The purine signals +discussed in ', ' provided an appetize +r by acting both pre- and postsynaptically, as do many of the other c +lassical transmitters. Nevertheless, through improved methods of subs +tance identification and detection of signal responsiveness, several +potent interneuronal signals have been recognized that are not stored + in vesicles, or even stored at all, but rather seem to be synthesize +d and released on demand to act more broadly than the immediate-relea +sing neuron terminals and to modify the effectiveness of the conventi +onal interneuronal signals.' ], 'hotlink' => [ { 'xref' => { 'xref' => 'r +012002', 'xidtype' => + 'text' }, 'sup' => { 'c' => '+', 'content' => +'2' } }, { 'xref' => { 'xref' => 'c +011', 'xidtype' => + 'text' }, 'content' => 'Chapter +11' } ] }, 'title' => '12 Other Interneuronal Signals', 'id' => 'c012', 'chapnum' => '12' } };
input xml file
<?xml version="1.0"?> <book> <chapter chapnum="12" id="c012"> <title>12 Other Interneuronal Signals</title> <para>The previous chapters were devoted to what we might now consider + the <c>“</c>classical<c>”</c> or perhaps <c>“</c>c +onventional<c>”</c> neurotransmitters. By this, we mean those t +ransmitters that are synthesized within the neuron (cell body or syna +ptic terminal) that releases them by activity-dependent, Ca<hotlink>< +xref xref="r012002" xidtype="text"/><sup>2<c>+</c></sup></hotlink>-de +pendent mechanisms to act on discrete receptors largely, but not excl +usively, on the neuron, smooth muscle, or gland cell opposite the ner +ve terminal. However, as the wheels of progress have turned, it seems + that once again the more we learn about inter-cellular communication + in the nervous system, the more complicated the situation becomes. T +he purine signals discussed in <hotlink><xref xref="c011" xidtype="te +xt"/>Chapter 11</hotlink> provided an appetizer by acting both pre- a +nd postsynaptically, as do many of the other classical transmitters. +Nevertheless, through improved methods of substance identification an +d detection of signal responsiveness, several potent interneuronal si +gnals have been recognized that are not stored in vesicles, or even s +tored at all, but rather seem to be synthesized and released on deman +d to act more broadly than the immediate-releasing neuron terminals a +nd to modify the effectiveness of the conventional interneuronal sign +als.</para> <subchap1><head1>Prostaglandins</head1> <para>The prostaglandins are a group of biologically active derivative +s of arachidonic acid often referred to as eicosanoids for their basi +c 20-carbon atom structure. The two major pathways of eicosanoid meta +bolism are the cyclooxygenase pathway, which yields the prostaglandin +s and thromboxanes, and the lipoxygenase pathway, which yields the le +ukotrienes. A minor pathway termed epoxy-genase yields epoxides, whic +h have received scant attention in the central nervous system (CNS). +Arachidonic acid is synthesized on demand from dietary linoleic acid +by either a G protein-regulated phospholipase A<sub>2</sub> or diglyc +eride lipase activation (<hotlink><xref xref="f012001" xidtype="figur +e"/>Fig. 12–1</hotlink>), and it yields a very broad array of b +ioactive metabolites, as shown in <hotlink><xref xref="f012002" xidty +pe="figure"/>Figure 12–2</hotlink>. The three major groups of a +rachidonic acid-derived metabolites are the prostaglandins, thromboxa +nes, and leukotrienes.</para> <para>Historically, the earliest effect of prostaglandins arose with t +he recognition in the 1930s that fresh semen could induce contraction + of myometrial muscle, and the name arose from the factor<c>'</c> +s anticipated origin. As chemical detection methods improved in the 1 +950s, two classes of prostaglandins were recognized<c>—</c>a PG +E class that was soluble in ether and a PGF class soluble in phosphat +e buffer (<emphasis style="it">fosfat</emphasis> in Swedish)<c>— +;</c>and one of their sites of synthesis localized to seminal vesicle +s. Subsequent work indicated that virtually every organ could manufac +ture prostaglandins, and several distinct synthetic pathways were rec +ognized. A major advancement occurred when John Vane proposed that as +pirin and several other nonsteroidal anti-inflammatory drugs (NSAIDs) + worked by inhibiting the prostaglandin-synthesizing enzyme cyclooxyg +enase. Work in the 1990s revealed that a second cyclooxygenase (COX-2 +) (and perhaps a third) was also present in the CNS. Since this enzym +e was shown to be induced by inflammatory cytokines, it immediately s +uggested a separate target for relief of inflammatory pain, with the +potential for reduced symptoms from the gastrointestinal tract irrita +tion typically evoked by NSAIDs. COX-2 is also induced <emphasis styl +e="it">in vitro</emphasis> by the neurotransmitter GLU and inhibited +by glucocorticoids. Unfortunately, prolonged use of COX-2 inhibitors +has untoward cardiovascular side effects, leading to multiple litigio +us claims and diverting attention from this once-promising therapeuti +c modification.</para> <para>It is well known that the eicosanoids, particularly the prostagl +andin series, play an important modulatory role in nervous tissue, bu +t it has been difficult to write a lucid account of specifically how +and where they act. This is primarily due to the fact that they are n +ot stored in tissues, nervous or other, but synthesized on demand, pa +rticularly in pathophysiological conditions. They act briefly (some w +ith a half-life of seconds) and at extremely low concentrations (10&# +8722;<hotlink><xref xref="r012010" xidtype="text"/><sup>10</sup></hot +link> M). Although indomethacin is a good inhibitor of cyclooxygenase +-1, blocking the conversion of arachidonic acid to prostaglandins, th +ere are few specific inhibitors available to block lipoxygenase and e +poxygenase. Thus, although it had been postulated that the E series o +f prostaglandins modulates noradrenergic release, blocks the convulsa +nt activity of pentylenetetrazol, strychnine, and picrotoxin (possibl +y by increasing the level of <c>γ</c>-aminobutyric acid <c>[</c> +GABA<c>]</c> in the brain), and increases the level of cAMP in cortic +al and hypothalamic slices, these effects were noted <emphasis style= +"it">in vitro</emphasis> with the addition of substantial amounts of +the prostaglandins. There was very little evidence in intact animals +to support these neuronal findings. Since we skeptics all hold <c> +220;</c><emphasis style="it">in vivo</emphasis> veritas<c>”</c> + in higher regard, the physiological relevance of the effect was in d +oubt.</para> <para>Subsequently, however, direct evidence has established arachidon +ic acid and lipoxygenases as second messengers. The cascade begins wi +th the binding of a neuroactive agent to its receptor. Then, accordin +g to findings from the Axelrod laboratory, the receptor is coupled to + G proteins, which may either activate or inhibit phospholipase A<sub +>2</sub>, although this has not been conclusively established for all + neural tissues. The activated enzyme promotes the release of arachid +onic acid, which will then act intracellularly as a second messenger. + Arachidonic acid and its metabolites can also leave the cell to act +extracellularly as first messengers on neighboring cells. Eicosanoids + have been shown to mediate the somatostatin-induced opening of an M +channel in hippocampal pyramidal cells and the release of VIP in mous +e cerebral cortical slices. At the supracellular level, prostaglandin +s of the E series have been held to be a mediator of fever and prosta +glandins of the D series as regulators of sleep. It is thus becoming +clear, despite enormous technological difficulties in assaying eicosa +noids, that these agents are major messengers.</para> <para>Another exciting chapter of the arachidonic acid story has been +told separately, namely the endocannabinoids, which are described lat +er in this chapter.</para></subchap1> </chapter> </book>
here the tags are changed their places i want as the sequence output hash how can i get please help me to guide
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Re: hash sequence error
by CountZero (Bishop) on Jun 15, 2010 at 06:09 UTC | |
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Re: hash sequence error
by CountZero (Bishop) on Jun 21, 2010 at 06:49 UTC | |
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Re: hash sequence error
by CountZero (Bishop) on Jun 23, 2010 at 15:50 UTC |