Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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Query: EC:2.3.1.21 (
CPT
)
4,580
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In 1981 a double blind study was conducted at random with Ketotifen. Fifty children were chosen at random (40 males and 10 females) who had been diagnosed as suffering from extrinsic bronchial asthma and had not undergone any previous treatment either with sodium cromoglycate or with immunotherapy. In all cases the treatment lasted 12 weeks, with monthly controls, in some cases on a weekly basis, which measured the following parameters: Daily written control by the parents of the clinical evolution. Monthly clinical examination with cardiovascular control (Cardiac frequency, T A , etc.) respiratory examination with lung function study, auxomatric control (height, weight), etc. Monthly control of the additional medication received, specifying type of medication, dosage and length of time administered (bronchodilators, antihistamines, antibiotics, etc.). Monthly control of possible collateral and side effects: subjective symptoms: neurologic, digestive, dermatologic, psychic, neuro-vegetative, genito-urinary, cardiorespiratory, etc. Analytical control at the commencement and termination of treatment which consists of: a) complete blood cell count, b) platelets and c) hepatic function study (GOT,
CPT
and alkaline phosphatases). The results of the overall evaluation of the group of children submitted to treatment with active substances were as follows: In asthma 70.35% was VERY EFFECTIVE and EFFECTIVE and 29.61% SLIGHTLY or
NOT
EFFECTIVE. In dermorespiratory cases 57.13% was VERY EFFECTIVE or EFFECTIVE and 42.85% SLIGHTLY EFFECTIVE. In concomitant rhinitis 74.93% was VERY EFFECTIVE and EFFECTIVE and 25% SLIGHTLY EFFECTIVE.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Ketotifen in childhood asthma]. 666 Jan 72
A post 30,000 x g particulate fraction was isolated from rat heart. This mixed membrane fraction is enriched in a
carnitine palmitoyltransferase
which is sensitive to both malonyl-CoA and etomoxiryl-CoA at concentrations that inhibit the malonyl-CoA-sensitive
carnitine palmitoyltransferase
(
CPTo
/
CPT
-I) of intact mitochondria. Tritiated etomoxiryl-CoA labels two proteins with the same molecular weight as the labeled proteins from rat heart mitochondria. Malonyl-CoA-sensitive
carnitine palmitoyltransferase
in the particulate fraction is stable to freeze-thawing, and the activity is not latent. These data show that the
carnitine palmitoyltransferase
associated with this particle is
CPTo
/
CPT
-I. Positive Western blots were obtained, with the particle using anti-
CPTi
/
CPT
-II at a molecular weight identical with the CPT1/
CPT
-II purified from rat heart mitochondria. Catalytic activity was purified to near homogeneity in approximately 40% yield. The purified protein has a molecular weight identical with
CPTi
/
CPT
-II, it cross-reacts with antibody against
CPTi
/
CPT
-II, it is not inhibited by malonyl-CoA or etomoxiryl-CoA, and mass spectral analyses of the tryptic peptides give the same molecular masses as
CPTi
/
CPT
-II, and, when mixed with equal amounts of
CPTi
/
CPT
-II, one uniform spot is found by two-dimensional electrophoresis. These data indicate that the catalytic subunit of
CPTo
/
CPT
-I is the same as
CPTi
/
CPT
-II. The average inhibition of the
CPT
of frozen-thawed particles is 71% by 50 nM etomoxiryl-CoA and 62% by 50 nM malonyl-CoA. The inhibitor sensitivity, but not the catalytic activity, is lost by solubilization in 1% Triton X-114; removal of Triton X-114 using Extracti-Gel D restores etomoxiryl-CoA and malonyl-CoA sensitivity (both 50 nM) of
CPT
to an average of 77 and 48%, respectively. Consistent with previous reports, these results show that
CPTo
/
CPT
-I is
NOT
inactivated by detergents, rather detergents both desensitize it to malonyl-CoA and alter its Vmax. These data show the assumption that
CPTo
/
CPT
-I is inactivated by detergents is untenable.
...
PMID:Characterization of the malonyl-CoA-sensitive carnitine palmitoyltransferase (CPTo) of a rat heart mitochondrial particle. Evidence that the catalytic unit is CPTi. 813 45
Morgan Lorio, MD, FACS, Chair, ISASS Task Force on Coding & Reimbursement In 2011,
CPT
code 22551 was revised to combine or bundle
CPT
codes 63075 and 22554 when both procedures were performed at the same site/same surgical session. The add on code +22552 is used to report each additional interspace. 2014 heralded a downward pressure on this now prime target code (for non-coverage?) 22551 through an egregious insurer attempt to redefine cervical arthrodesis, effectively removing spine surgeon choice and altering best practice without clinical evidence. Currently, spine surgeons are equally split on the use of allograft versus cages for cervical arthrodesis. Structural allograft,
CPT
code 20931, is reported once per same surgical session, regardless of the number of allografts used.
CPT
code 22851 which is designated solely for cage use, has a higher reimbursement than structural allograft, and may be reported for each inner space. Hence, the rationale behind why some payers wrongly consider "spine cages
NOT
medically necessary for cervical fusion." A timely consensus paper summarizing spine surgeon purview on the logical progressive evolution of cervical interbody fusion for ISASS/IASP membership was strategically identified as an advocacy focus by the ISASS Task Force. ISASS appreciates the authors' charge with gratitude. This article has both teeth and transparent clinical real-world merit.
...
PMID:ISASS Policy Statement - cervical interbody. 2569 45