Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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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)

This ad hoc committee report from the American Geriatrics Society proposes the prompt initiation of Medicare reimbursement for geriatric assessment (GA) services (also termed comprehensive geriatric assessment or geriatric evaluation and management services). Despite an extensive body of literature documenting the effectiveness of GA for improving health care outcomes in many settings for identifiable groups of frail elderly patients, no explicit Medicare reimbursement mechanisms currently exist to cover GA services provided by either hospital or physician. We believe that new physician reimbursement codes specific for geriatric assessment should be established in the Current Procedural Technology (CPT-4) manual and that reimbursement for GA should be specifically provided under Part B of Medicare. Further, we believe that hospital reimbursement within the Medicare prospective payment system should be modified to encourage GA during inpatient stays for appropriate patients. This paper summarizes the background for these recommendations. It defines the major content of GA at three levels of intensity--screening, intermediate, and comprehensive. It describes the major sites for conducting GA--hospital, office, home, nursing home. Finally, it proposes criteria for targeting patients most likely to benefit from GA.
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PMID:Medicare reimbursement for geriatric assessment: report of the American Geriatrics Society Ad Hoc Committee on Geriatrics Assessment. 188 68

Transcription of phosphoenolpyruvate carboxykinase (PEPCK) gene is induced in response to cyclic AMP (cAMP) or cAMP elevating hormones. The role of transcription factors (DNA binding proteins) in the induction process has been studied. Two nuclear proteins, apparent mol. wt of 53 and 30 kDa, have been shown to bind to the 5'-flanking DNA of PEPCK gene which contains hormonal responsive elements as well as TATA box. DNA binding activity of 53 kDa protein increases by 3.5 fold in cells treated with 8-(4-chlorophenylthio)-cAMP (8-CPT-cAMP). The increased binding activity may be due to the phosphorylation of this protein by an activated cAMP-dependent protein kinase (cA kinase) in treated cells. Based on this observation, a hypothesis that 53 kDa may be specific transcription factor for PEPCK and therefore, play a major role in the regulation of this gene is proposed.
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PMID:Identification of DNA binding proteins which may regulate phosphoenolpyruvate carboxykinase gene. 191 37

The effects of antiarrhythmic doses of lidocaine on efferent sympathetic outflow or sympathetic responses to autonomic stimuli in humans are unknown. In the present study, direct recordings of postganglionic muscle sympathetic nerve activity (MSNA), which modulates vascular tone, were obtained from the peroneal nerve of 22 healthy volunteers (aged 20 to 27 years). Baseline cardiac intervals (ECG), arterial pressure (radial artery), central venous pressure (CVP, jugular vein), forearm vascular resistance (FVR, Hg-in-Silastic plethysmography), and MSNA were identical in two randomized study groups (lidocaine [L], 1.5 mg/kg bolus, followed by 2 mg/min infusion, n = 12; and placebo [P] saline bolus and infusion, n = 10). Each underwent a cold pressor test (CPT, ice packs to foot for 90 seconds) and baroreceptor test (sequential boluses of 100 micrograms of sodium nitroprusside and 100 micrograms of phenylephrine). Five minutes after the bolus administration of L, plasma L levels were 3 micrograms/mL, which was associated with significant (P less than 0.05) increases in systolic and diastolic pressures (6.6 +/- 2.4 and 5.5 +/- 1.1 mm Hg). This elicited significant reflex decreases in MSNA (-3 +/- 1.1 bursts/100 cardiac cycles) and RR interval (-63 +/- 14 ms). The hypertension, tachycardia, forearm vasoconstriction, and MSNA increase in response to the CPT were significantly attenuated and the sympathoexcitatory response to baroreceptor unloading was blunted by L. These responses were not altered during the administration of P. In the steady-state L infusion period, plasma levels were subtherapeutic (1 microgram/mL) and were insufficient to consistently alter autonomic stress responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lidocaine attenuates efferent sympathetic responses to stress in humans. 193 48

Dietary administration of 0.05, 0.1, and 0.3% LY171883 to rats for 1 day caused a dose-related increase in hepatic triglycerides. When added to rat liver mitochondria in vitro, LY171883 caused competitive inhibition of carnitine palmitoyltransferase 1 (CPT-1), the rate-limiting enzyme for mitochondrial fatty acid oxidation. This effect appears to be involved in the lipid accumulation. The hepatic triglycerides in rats given 0.1% LY171883 increased progressively through 3 months of treatment. In contrast, hepatic triglycerides in high-dose rats returned to control levels by Day 3 and remained there throughout the study. The regression of the lipid corresponded with increases in hepatic peroxisomal beta-oxidation, mitochondrial beta-oxidation, and CPT-1 activity of up to 13-, 7-, and 3.2-fold, respectively. The 0.1% dose increased these parameters modestly compared to those of high-dose rats (2-, 3-, and 1.6-fold, respectively). Addition of LY171883 to mitochondria from rats given dietary treatment for 2 weeks inhibited CPT-I by the same percentage as in control mitochondria. In mid-dose rats, the induction of CPT-I was largely negated by LY171883 in vitro. Even with the inhibition, CPT-I activity in mitochondria from high-dose rats remained 2-fold higher than that in untreated controls. The data suggest that the induction of CPT-I in high-dose rats was sufficient to overcome the inhibitory action of LY171883. The increased oxidative capacity in peroxisomes and mitochondria led to the regression of the lipid in high-dose rats. The more modest increases in fatty acid oxidation in rats given 0.1% LY171883 were not sufficient to reverse the lipid accumulation.
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PMID:Changes in hepatic lipid metabolism associated with lipid accumulation and its reversal in rats given the peroxisome proliferator LY171883. 197 95

Sodium cholate was used as an anionic detergent to discriminate the two components of liver overt carnitine palmitoyltransferase (CPT1); namely a catalytic entity and a regulatory component that bound malonyl-CoA. Cholate solubilized approx. 40% of the malonyl-CoA binding entity from mitochondrial outer membranes without appreciable solubilization of CPT1 activity. Cholate did not interfere with binding of [14C]malonyl-CoA to outer membranes or to crude total mitochondrial membrane fractions. By contrast, the non-ionic detergent Tween-20 was ineffective in solubilizing the malonyl-CoA binding entity and also substantially interfered with the binding of [14C]malonyl-CoA. Both detergents appeared to cause total disengagement of the malonyl-CoA binding entity from the catalytic entity of CPT1 only when some inner membrane material was present. 'Reconstitution' experiments were performed in which a malonyl-CoA sensitivity conferring factor in cholate extracts from outer membranes was associated with CPT derived from inner membranes (CPT2). The IC50 for inhibition of CPT2 by malonyl-CoA in this artificial system was similar to that observed with CPT1 in situ in outer membranes. Extracts containing malonyl-CoA sensitivity conferring factor derived from outer membranes of fed or 48 h fasted rats were associated with CPT2 derived from fed rats. The outer membrane extracts from fasted animals conferred a lower maximum responsiveness to malonyl-CoA, but appeared to have a higher affinity for CPT2 than the extracts from fed rats. These results suggest that physiological state can alter the intrinsic properties of the malonyl-CoA sensitivity confering factor.
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PMID:Cholate separates the catalytic and malonyl-CoA-binding components of carnitine palmitoyltransferase from liver outer mitochondrial membranes. 203 50

Rats were fed for 35 days a high-fat diet containing either 36% of total calories as ethanol (ethanol group) or an isocaloric amount of carbohydrate (control group). Then, mitochondria were isolated from the periportal and the perivenous zone of the liver in order to study the acinar heterogeneity of the effects of prolonged ethanol administration upon the properties of carnitine palmitoyltransferase I (CPT-I) and its membrane environment. Chronic ethanol ingestion selectively decreased CPT-I activity in periportal hepatocytes but equally increased enzyme sensitivity to malonyl-CoA and enzyme energy of activation in the two zones of the liver. In control animals, mitochondrial membrane showed higher fluidity and lower degree of saturation of phospholipid fatty acyl moieties in periportal than in perivenous hepatocytes. Prolonged ethanol feeding (i) decreased mitochondrial membrane fluidity; (ii) increased the proportion of palmitic acid and decreased that of arachidonic acid in mitochondrial phosphatidylcholine and phosphatidylethanolamine, whereas it drastically reduced the content of linoleic acid and concomitantly increased that of saturated and monoenoic fatty acids in cardiolipin; (iii) suppressed the disordering effects of the addition of ethanol to mitochondrial suspensions. All these ethanol-induced alterations of membrane fluidity and fatty acyl composition were not significantly different between periportal and perivenous mitochondria. In conclusion, chronic ethanol feeding changes the activity of CPT-I in a zone-selective manner but modifies both the regulatory properties of the enzyme and the properties of its lipid environment in a non-zone-selective manner. Hence factors in addition to the properties of the mitochondrial membrane seem to be involved in the ethanol-induced alterations of the CPT-I enzyme.
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PMID:Properties of the mitochondrial membrane and carnitine palmitoyltransferase in the periportal and the perivenous zone of the liver. Effects of chronic ethanol feeding. 203 48

This study has monitored junctional and nonjunctional resistance, [Ca2+]i and [H+]i, and the effects of various drugs in crayfish septate axons exposed to neutral anesthetics. The uncoupling efficiency of heptanol and halothane is significantly potentiated by caffeine and theophylline. The modest uncoupling effects of isoflurane, described here for the first time, are also enhanced by caffeine. Heptanol causes a decrease in [Ca2+]i and [H+]i both in the presence and absence of either caffeine or theophylline. A similar but transient effect on [Ca2+]i is observed with halothane. 4-Aminopyridine strongly inhibits the uncoupling effects of heptanol. The observed decrease in [Ca2+]i with heptanol and halothane and negative results obtained with different [Ca2+]o, (Ca2+)-channel blockers (nisoldipine and Cd2+) and ryanodine speak against a Ca2+ participation. Negative results obtained with 3-isobutyl-1-methylxanthine, forskolin, CPT-cAMP, 8Br-cGMP, adenosine, phorbol ester and H7, superfused in the presence and absence of caffeine and/or heptanol, indicate that neither the heptanol effects nor their potentiation by caffeine are mediated by cyclic nucleotides, adenosine receptors and kinase C. The data suggest a direct effect of anesthetics, possibly involving both polar and hydrophobic interactions with channel proteins. Xanthines and 4-aminopyridine may participate by influencing polar interactions. The potentiating effect of xanthines on cell-to-cell uncoupling by anesthetics may provide some clues on the nature of cardiac arrhythmias in patients treated with theophylline during halothane anesthesia.
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PMID:Effects of the anesthetics heptanol, halothane and isoflurane on gap junction conductance in crayfish septate axons: a calcium- and hydrogen-independent phenomenon potentiated by caffeine and theophylline, and inhibited by 4-aminopyridine. 205 74

The main alterations of carnitine metabolism are mentioned synthetically in order to point up the heterogeneity of clinical, biohumoral, instrumental and enzymatic pictures deriving from the deficiency of carnitine-palmitoyl-transferase. We describe a case with a slight deficiency of CPT, showing a typical symptomatology, but with some peculiarities, such as the absence of myoglobinuria and, in particular way, the presence of haemolysis caused by a long fasting, that doesn't find an easy interpretation. On the basis of some experimental dates described in literature, we may suppose that the red blood cells might be somewhat affected by the consequence of the metabolical deficiency (change). The case is mentioned also in order to focus the attention on the possibility of diagnosing this disease since childhood, before the symptoms deriving as a consequence from the enzymatic deficiency are completely clear. And this in order to allow an early dietetic and therapeutic treatment.
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PMID:[Changes in carnitine metabolism. A case report about probable partial deficiency of muscle carnitine palmitoyltransferase]. 207 7

Since December 1985, we have performed 38 transplantations: cardiac (CT) n: 31, cardiopulmonary (CPT) n: 1, or bipulmonary (BPT) n: 6. There were 31 male and 7 female patients, aged 7 to 62, mean 46. In the cardiac group, the cardiomyopathy was primitive in 13, ischemic in 16, valvular in 2. Five patients had undergone one or more previous operations. Three patients had a biventricular assist device (1,6 and 7 days before transplant) for acute cardiac failure. The indication of CPT or BPT was pulmonary artery hypertension (1), silicosis (1), cystic fibrosis (4). There were 4 post-operative deaths in the CT group (12.9%); failure of graft, low cardiac output, pulmonary artery hypertension by multiple pulmonary thrombosis, and 2 deaths in the CPT and BPT groups (28%). The mean post-operative hospital stay was one month. All patients with CT were treated by an initial maintenance bitherapy protocol (cyclosporine, steroids) and observed by myocardial biopsies and echocardiograms. In 40 per cent of the patients, Azathioprine was subsequently added. The patients had 2.1 rejection episode/patient/year, either spontaneously reversed of treated medically. There were two late deaths (2 and 7 months) by refractory rejection. 78 per cent of the patients were alive one year after transplant. All survivors have recovered a normal life, some of them with full-time work.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Heart and heart-lung transplantation. 3 years' experience in Timone CHU (Marseilles 1985-1988)]. 210 56

In vitro EDTA-induced platelet aggregation is a fairly rare event but can have serious clinical consequences producing pseudothrombocytopenia and pseudoleukocytosis. Sixteen specimens with previously recognized EDTA-induced platelet aggregation were collected in a new anticoagulant-antiaggregant mixture containing trisodium citrate 17 mmol/l, pyridoxal 5'-phosphate 11.3 mmol/l and Tris 24.76 mmol/l (CPT mixture) and analyzed at various times after venepuncture with four hematological instruments: Coulter Counter S-Plus STKR, Technicon H6000, Technicon H1 and Ortho ELT-8. In CPT-anticoagulated specimens the signals and instrumental flags of platelet clumping were absent, and the platelet number correlated very well with a microscopic count from a finger stick drawn into Unopette. The complete blood count was very similar in "normal" hematological specimens either collected in K3. EDTA or in CPT, although Technicon H1 and Ortho3 ELT-8 required a suitable calibration for MCV and hematocrit in the latter mixture. Mean platelet volume was stable for up to 24 h only in CPT-collected specimens, if it was measured on a Coulter Counter S-Plus STKR. In routine hematological practice CPT can be an alternative anticoagulant to K3. EDTA, most suitable for automated complete blood count and useful in avoiding EDTA-induced platelet clumping.
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PMID:EDTA-induced platelet aggregation can be avoided by a new anticoagulant also suitable for automated complete blood count. 211 Sep 27


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