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Operating Systems Linux Perl program to print previous set of lines once a pattern is matched Post 302644495 by kaav06 on Tuesday 22nd of May 2012 02:54:19 AM
Old 05-22-2012
Hi Scrutinizer,

The expected output is given below:

Code:
*100710 CHOLINERGIC RECEPTOR, NICOTINIC, BETA POLYPEPTIDE 1; CHRNB1
;;CHRNB;;
ACETYLCHOLINE RECEPTOR, MUSCLE, BETA SUBUNIT; ACHRB
*FIELD* AV
.0001
MYASTHENIC SYNDROME, CONGENITAL, SLOW-CHANNEL
CHRNB1, VAL266MET
In a 19-year-old female with slow-channel congenital myasthenic syndrome
(601462), Engel et al. (1996) identified a heterozygous 796G-A
transition in exon 8 of the CHRNB1 gene, resulting in a val266-to-met
(V266M) substitution in a conserved residue in the M2 transmembrane
domain of the AChR-beta subunit. Functional expression studies showed
that the V266M mutation slowed the rate of AChR channel closure and
increased the apparent affinity for ACh. The mutation also caused
pathologic channel openings even in the absence of ACh, resulting in a
leaky channel. Cationic overload of the postsynaptic region caused an
endplate myopathy.
.0002
MYASTHENIC SYNDROME, CONGENITAL, SLOW-CHANNEL
CHRNB1, LEU263MET
In a 32-year-old male with slow-channel congenital myasthenic syndrome
(601462), Gomez et al. (1996) identified a heterozygous C-to-A
transversion in the CHRNB1 gene, resulting in a leu263-to-met (L263M)
substitution. Functional expression studies showed that the L263M
mutation interrupted the leucine ring of the AChR channel gate, causing
an 8-fold increase in channel open time and resulting in severe endplate
myopathy and extensive remodeling of the postsynaptic membrane. The
pronounced abnormalities in neuromuscular synaptic architecture and
function and the muscle fiber damage and weakness resulting from a
single point mutation were a dramatic example of a mutation having a
dominant gain of function and of hereditary excitotoxicity.
.0003
MYASTHENIC SYNDROME, CONGENITAL, ASSOCIATED WITH ACETYLCHOLINE RECEPTOR
DEFICIENCY
CHRNB1, 9-BP DEL, NT1276 
In 3 sibs with congenital myasthenia and AChR deficiency (608931),
Quiram et al. (1999) identified compound heterozygosity for 2 mutations
in the CHRNB1 gene. One mutation was a 9-bp deletion (1276del9) in exon
10, resulting in a deletion of 3 codons (426-428) in the long
cytoplasmic loop between the M3 and M4 domains of the protein. The
second mutation was a skipping of exon 8 (100710.0004), truncating the
beta subunit before its M1 transmembrane domain and abolishing surface
expression of pentameric AChR. By coexpressing the 3-codon deleted
subunit with combinations of wildtype subunits in HEK293 cells, Quiram
et al. (1999) demonstrated that the mutation impairs AChR assembly by
disrupting a specific interaction between the beta and delta (100720)
subunits. Studies with related deletion and missense mutations indicated
that secondary structure in this region of the beta subunit is crucial
for interaction with the delta subunit. The findings implied that the
mutated residues are positioned at the interface between beta and delta
subunits and demonstrated contribution of this local region of the long
cytoplasmic loop to AChR assembly.
.0004
MYASTHENIC SYNDROME, CONGENITAL, ASSOCIATED WITH ACETYLCHOLINE RECEPTOR
DEFICIENCY
CHRNB1, EX8DEL 
See 100710.0003 and Quiram et al. (1999).
*FIELD* SA
Beeson et al. (1989)
*FIELD* RF


Last edited by kaav06; 05-25-2012 at 05:19 AM..
 

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Bio::SeqEvolution::DNAPoint(3pm)			User Contributed Perl Documentation			  Bio::SeqEvolution::DNAPoint(3pm)

NAME
Bio::SeqEvolution::DNAPoint - evolve a sequence by point mutations SYNOPSIS
# $seq is a Bio::PrimarySeqI to mutate $evolve = Bio::SeqEvolution::Factory->new (-rate => 5, -seq => $seq, -identity => 50 ); $newseq = $evolve->next_seq; DESCRIPTION
Bio::SeqEvolution::DNAPoint implements the simplest evolution model: nucleotides change by point mutations, only. Transition/transversion rate of the change, rate(), can be set. The new sequences are named with the id of the reference sequence added with a running number. Placing a new sequence into a factory to be evolved resets that counter. It can also be called directly with reset_sequence_counter. The default sequence type returned is Bio::PrimarySeq. This can be changed to any Bio::PrimarySeqI compliant sequence class. Internally the probability of the change of one nucleotide is mapped to scale from 0 to 100. The probability of the transition occupies range from 0 to some value. The remaining range is divided equally among the two transversion nucleotides. A random number is then generated to pick up one change. Not that the default transition/transversion rate, 1:1, leads to observed transition/transversion ratio of 1:2 simply because there is only one transition nucleotide versus two transversion nucleotides. FEEDBACK
Mailing Lists User feedback is an integral part of the evolution of this and other Bioperl modules. Send your comments and suggestions preferably to the Bioperl mailing list. Your participation is much appreciated. bioperl-l@bioperl.org - General discussion http://bioperl.org/wiki/Mailing_lists - About the mailing lists Support Please direct usage questions or support issues to the mailing list: bioperl-l@bioperl.org rather than to the module maintainer directly. Many experienced and reponsive experts will be able look at the problem and quickly address it. Please include a thorough description of the problem with code and data examples if at all possible. Reporting Bugs Report bugs to the Bioperl bug tracking system to help us keep track of the bugs and their resolution. Bug reports can be submitted via the web: https://redmine.open-bio.org/projects/bioperl/ AUTHOR
Heikki Lehvaslaiho E<lt>heikki at bioperl dot orgE<gt> CONTRIBUTORS
Additional contributor's names and emails here APPENDIX
The rest of the documentation details each of the object methods. Internal methods are usually preceded with a _ seq Title : seq Usage : $obj->seq($newval) Function: Set the sequence object for the original sequence Returns : The sequence object Args : newvalue (optional) Setting this will reset mutation and generated mutation counters. set_mutated_seq Title : seq_mutated_seq Usage : $obj->set_mutated_seq($newval) Function: In case of mutating a sequence with multiple evolvers, this Returns : set_mutated_seq Args : newvalue (optional) rate Title : rate Usage : $obj->rate($newval) Function: Set the transition/transversion rate. Returns : value of rate Args : newvalue (optional) Transition/transversion ratio is an observed attribute of an sequence comparison. We are dealing here with the transition/transversion rate that we set for our model of sequence evolution. Note that we are using standard nucleotide alphabet and that there can there is only one transition versus two possible transversions. Rate 2 is needed to have an observed transition/transversion ratio of 1. next_seq Title : next_seq Usage : $obj->next_seq Function: Evolve the reference sequence to desired level Returns : A new sequence object mutated from the reference sequence Args : - mutate Title : mutate Usage : $obj->mutate Function: mutate the sequence at the given location according to the model Returns : true Args : integer, start location of the mutation, required argument Called from next_seq(). perl v5.14.2 2012-03-02 Bio::SeqEvolution::DNAPoint(3pm)
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