Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of adenosine on impulse formation and conduction in the heart was studied in 20 dogs by the sinus node artery perfusion technique. Electrophysiologic studies were performed by using His electrograms and epicardial electrograms of the atria and left ventricle. This action potential was recorded in the hearts of 10 dogs. After adenosine administration, there first developed bradycardia, then sinus arrest. Instead of sinus rhythm, there appeared a junctional escape rhythm. Atrial extrasystoles could be also regularly detected. Impulse conduction slowed down in the AV node. Similar changes could be observed after local administration of verapamil. Adenosine decreased the resting membrane potential and the maximum rate of depolarisation in atrial tissue preparations. Experimental data support the assumption that slow Ca++ channels are involved in the bradycardiac effect of adenosine.
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PMID:The effect of adenosine on impulse formation and propagation in the heart. Electrophysiologic studies and clinical implications. 648 3

Aberrations of the APC gene, which plays an important role in the genesis of familial adenomatous polyposis and colorectal carcinoma, were investigated in 31 surgical specimens of primary breast carcinoma. These studies utilized the polymerase chain reaction followed by restriction-fragment-length polymorphism and single-strand-conformation polymorphism analyses combined with tumor cell enrichment by cell sorting. Loss of heterozygosity at the APC locus was detected in 8 (38%) of 21 informative cases, but only 2 (6%) of 31 tumors carried a mutated APC gene. Direct DNA sequencing analysis confirmed mutations at codon 1081 (AGC to ATC) resulting in an amino acid substitution of serine for isoleucine, and at codon 1096 (CAG to CAT) resulting in a substitution of glutamine for histidine. There were no significant correlations between the loss of heterozygosity or mutation at the APC locus and any clinicopathological characteristics. Our present observations suggest that the mutations of the APC gene may play an important role in the genesis of certain breast carcinomas, and that another tumor-suppressor gene, which is the true target of frequent loss of heterozygosity, may exist near the APC gene.
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PMID:Aberrations of the APC gene in primary breast carcinoma. 779 98

1. INTRODUCTION TO DEPARTMENTAL PACS. Full or partial Departmental PACS is generally taken to mean an image management system focused on serving the needs of a specific modality or modality application. It will provide a modality specific means of image acquisition, specialized redisplay of images, distribution, and local long term storage of images. A Departmental PACS can be considered in isolation or as a component in a distributed Radiology PACS which consists of one or more departmental work groups on a back bone, potentially with shared resources. 2. DEPARTMENTAL PACS Issues Implementation of a Departmental PACS requires an in-depth knowledge of departmental clinical practice and work flow in all affected areas in the department, including patient intake, image collection, data routing, retrieval of previous image data, reporting, and long term data management and storage. Optimization of modality specific image display systems requires significant involvement from representative physician users. System architectures and user interfaces must be flexible enough to support the span of variation in clinical practice encountered in the site. A departmental PACS should offer a variety of "open" communications interfaces, both local and wide area, recognizing that outreach efforts are often driven by specific imaging departments. Interfaces to other departmental PAC systems and other information systems must be considered in order to facilitate institutions developing "Best of Breed" PACS systems. As hospitals move toward the integrated electronic medical record, means need to exist for a client process launched from a physician desktop to acquire images and/or reports from a departmental system. At minimum, HIS/RIS interfaces need to be considered to minimize re-keying of data and reduce data entry errors. 3. DESIGN OBJECTIVES FOR ALI ULTRAPACS. The key objectives were to design a product which could function either as a free standing PACS or as a departmental subnet on a larger PACS backbone, one which could function in a local or mixed local and wide area environment and one which could provide a cost effective implementation based on currently available technologies. 4. IMPLEMENTATION STRATEGIES. In order to attain the product design objectives, ALI made the following critical implementation decisions: 1) to build the UltraPACS application as a suite of separable UNIX processes based on a message passing client server model; 2) to host the application and operating system on a Digital Equipment Corporation PC using an Intel microprocessor because of the competition and broad variety of suppliers in the PC arena; and 3) to use NEXTSTEP as the UNIX variant of choice because of NEXTSTEPUs strong object orientation, superb development tools, and the excellent integration between the Graphical User Interface level and the underlying operating system layers. 5. CONCLUSION. ALI is convinced that a departmental approach to PACS offers significant advantages over monolithic PACS in several key areas including: optimization for modality specific clinical practice and workflow, cost effectiveness, the potential for an institution to implement PACS in a stepwise fashion, starting with the department with the potential for the greatest savings, and the capability for an institution to build a "best of breed" solution for large scale PACS.
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PMID:Current developments in departmental PACS for ultrasound. 859 Dec 22

Prostate cancer is the most common cancer in aged men. Although ras and p53 gene mutations have been detected in some prostate cancers, the major genetic alterations involved in its carcinogenesis are not well understood. Mutation of the APC gene is responsible for colorectal tumors in which ras and p53 mutations are also often involved. Using PCR-SSCP analysis and sequencing, we examined 31 human primary prostate cancers (three cases at stage A, 10 at stage B, five at stage C and 13 at stage D) and four cases of lymph node metastasis from the stage D cases, for mutations in the APC gene. A mutation was detected in only one of the 35 samples (3%). This mutation, present in a primary stage B cancer, had a T to C transition in exon 15 at the first position of codon 956, resulting in substitution of histidine for tyrosine. This study clarified that APC gene mutations are not largely involved in the development of clinical prostate cancer.
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PMID:APC gene mutations in human prostate cancer. 860 98

The presence of point mutation G-->A of nucleotide 1691 of Factor V gene (Leiden mutation) is responsible for the resistance of factor Va to activated protein C (APC-resistance) and is associated with an increased risk for thrombosis. Herein, we reported on a case of 20 year male with a two years history of recurrent, extensive deep vein thrombosis. His family history showed grand-mother from mother side, who died from thromboembolic disease many years ago. His laboratory investigation reveals abnormal results of APC-resistance test (R = 1.80) and normalized APC-resistance test sensitivity ratio (0.57). Moreover, on the basis of a sequence specific primer polymerase chain reaction (SSP-PCR) a heterozygous from (G/A at 1691 position) of Leiden mutation was found. Family study showed two between 8 others asymptomatic persons with abnormal results of APC-resistance test and heterozygous genotype.
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PMID:[Point mutation G-->A nucleotide 1691 factor V gene as a cause of developing thrombotic complications in a family with plasma resistance to activated protein C]. 884 15

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

Bovine and human protein C show high homology in the amino acids of their GLA domains (amino-terminal 44 residues), despite the about 10-fold higher membrane affinity of the human protein. A proposed membrane contact site and mechanism suggested that this difference was largely due to the presence of proline at position 10 of bovine protein C versus histidine at position 10 of human protein C [McDonald, J.F., Shah, A.M., Schwalbe, R.A., Kisiel, W., Dahlback, B., and Nelsestuen, G.L. (1997) Biochemistry, 36, 5120-5127]. This study examined the impact of replacing proline-10 in bovine protein C with histidine, and the reverse change in human protein C. In both cases, the protein containing proline-10 showed lower membrane affinity, about 10-fold lower for bovine protein C and 5-fold lower for human protein C. As expected, activated human protein C (hAPC) containing proline at position 10 showed 2.4-3.5-fold lower activity than wild type hAPC, depending on the assay used. Most interesting was that bovine APC containing histidine-10 displayed up to 15-fold higher activity than wild type bAPC. This demonstrated the ability to improve both membrane contact and activity by mutation. This general strategy should be applicable to other vitamin K-dependent proteins, providing opportunities to study function as well as to produce proteins that may find use as promoters and inhibitors of blood coagulation in pathological states.
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PMID:Enhancing the activity of protein C by mutagenesis to improve the membrane-binding site: studies related to proline-10. 944 Aug 75

This article is based on the author's presentations to the New York State Governor's Health Care Advisory Board's Task Force on the President's Health Care Plan, November 22, 1993, and to a hearing of the New York State Attorney General on the experience of consumers with health insurers and health maintenance organizations, September 20, 1993. His comments deal with the effects of the Clinton health care reform proposal and other forms of managed care on those most in need of care. Particularly interesting are his suggestions for protecting the rights of health care consumers.
Health PAC Bull 1993
PMID:Managed care as health care rationing. 1017 30

Pituitary adenylate cyclase-activating peptide (PACAP) type 1 (PAC(1)) and common PACAP/vasoactive intestinal peptide (VIP) type 1 and 2 (VPAC(1) and VPAC(2), respectively) receptors were detected in the human lung by RT-PCR. The proteins were identified by immunoblotting at 72, 67, and 68 kDa, respectively. One class of PACAP receptors was defined from (125)I-labeled PACAP-27 binding experiments (dissociation constant = 5.2 nM; maximum binding capacity = 5.2 pmol/mg protein) with a specificity: PACAP-27 approximately VIP > helodermin approximately peptide histidine-methionine (PHM) >> secretin. Two classes of VIP receptors were established with (125)I-VIP (dissociation constants of 5.4 and 197 nM) with a specificity: VIP approximately helodermin approximately PACAP-27 >> PHM >> secretin. PACAP-27 and VIP were equipotent on adenylyl cyclase stimulation (EC(50) = 1.6 nM), whereas other peptides showed lower potency (helodermin > PHM >> secretin). PACAP/VIP antagonists supported that PACAP-27 acts in the human lung through either specific receptors or common PACAP/VIP receptors. The present results are the first demonstration of the presence of PAC(1) receptors and extend our knowledge of common PACAP/VIP receptors in the human lung.
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PMID:Expression, pharmacological, and functional evidence for PACAP/VIP receptors in human lung. 1040 29

The Schizosaccharomyces pombe stress-activated Sty1p/Spc1p mitogen-activated protein (MAP) kinase regulates gene expression through the Atf1p and Pap1p transcription factors, homologs of human ATF2 and c-Jun, respectively. Mcs4p, a response regulator protein, acts upstream of Sty1p by binding the Wak1p/Wis4p MAP kinase kinase kinase. We show that phosphorylation of Mcs4p on a conserved aspartic acid residue is required for activation of Sty1p only in response to peroxide stress. Mcs4p acts in a conserved phospho-relay system initiated by two PAS/PAC domain-containing histidine kinases, Mak2p and Mak3p. In the absence of Mak2p or Mak3p, Sty1p fails to phosphorylate the Atf1p transcription factor or induce Atf1p-dependent gene expression. As a consequence, cells lacking Mak2p and Mak3p are sensitive to peroxide attack in the absence of Prr1p, a distinct response regulator protein that functions in association with Pap1p. The Mak1p histidine kinase, which also contains PAS/PAC repeats, does not regulate Sty1p or Atf1p but is partially required for Pap1p- and Prr1p-dependent transcription. We conclude that the transcriptional response to free radical attack is initiated by at least two distinct phospho-relay pathways in fission yeast.
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PMID:Peroxide sensors for the fission yeast stress-activated mitogen-activated protein kinase pathway. 1117 24


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