Cardiovascular events and mortality in newly and chronically depressed persons > 70 years of age

The role of duration of depressed mood in the prediction of cardiovascular disease (CVD) requires further study, as it has been suggested that emerging depressive symptoms may be a better predictor than persistent depressive symptoms. This prospective cohort study of 3,701 men and women aged > 70 years uses 3 measurement occasions of depressive symptomatology (Center for Epidemiologic Studies-Depression Scale) during a 6-year period to distinguish persons who were newly (depressed at baseline but not at 3 and 6 years before baseline) and chronically depressed (depressed at baseline and at 3 or 6 years before baseline). Their risk of subsequent CVD events and all-cause mortality was compared with that of subjects who were never depressed during the 6-year period. Outcome events were based on death certificates and Medicare hospitalization records. During a median follow-up of 4.0 years, there were 732 deaths (46.2/1,000 person-years) and 933 new CVD events (64.7/1,000 person-years). In men, but not in women, newly depressed mood was associated with an increased risk of CVD mortality (relative risk 1.75, 95% confidence interval [CI] 1.00 to 3.05), new CVD events (relative risk 2.07, 95% CI 1.44 to 2.96), and new coronary heart disease events (relative risk 2.03, 95% CI 1.28 to 3.24) after adjustment for traditional CVD risk factors. The association between newly depressed mood and all-cause mortality was smaller (relative risk 1.40, 95% CI 0.95 to 2.07). Chronic depressed mood was not associated with new CVD events or all-cause mortality. Our findings suggest that newly depressed older men, but not women, were approximately twice as likely to have a CVD event than those who were never depressed. In men, recent onset of depressed mood is a better predictor of CVD than long-term depressed mood.     

Acute knee injuries: Part I. History and physical examination

A thorough history and physical examination are helpful in the diagnosis of meniscal damage, cruciate and collateral ligament sprains and patellar instability, the four major acute knee injuries. When performing a physical examination in a patient with a knee injury, the uninjured knee should always be assessed first and used for comparison. Examination includes passive and active range-of-motion testing, palpation of the joint line spaces, and a variety of maneuvers to evaluate knee stability. Valgus and varus testing provides assessment of the collateral ligaments. The Lachman and pivot shift tests are useful in the evaluation of the anterior cruciate ligament. The posterior drawer and tibial sag tests are used to evaluate the posterior cruciate ligament. The bounce test, McMurray's test and Apley's grind test can aid in the diagnosis of meniscal injury.     

Application of a mechanistic model of bovine milk protein synthesis to examine the use of isotope labeling methods

Two types of models of bovine milk protein synthesis were used to simulate collection and analysis of data from infusion experiments involving isotope-labeled amino acids (AA). Analytical solutions to a system of ordinary differential equations that describe isotope enrichment curves of each AA pool within the mammary gland were derived and are presented. Numerical solutions from a dynamic mechanistic model suggest that normal experimental procedures can affect the shape of enrichment curves and, therefore, results derived from them. Simulation results suggest that standard methods utilizing in vivo isotope kinetics may be of limited value to characterize the metabolism of the bovine mammary gland, especially AA metabolism and milk protein synthesis and secretion. The results clearly demonstrate the flexibility of such models for the testing of many hypotheses and possible experimental protocols.     

Glutamate-induced cytotoxicity in PC12 pheochromocytoma cells: role of oxidation of phospholipids, glutathione and protein sulfhydryls revealed by bcl-2 transfection

Incubation of mock-transfected PC12 rat pheochromocytoma cells (PC12) for 2 h with increasing concentrations of glutamate caused progressive loss of viability (e.g., 67% with 15 mM glutamate). In contrast, the viability of bcl-2-transfected cells (PC12/bcl-2) was unaffected by glutamate. Neither PC12 nor PC12/bcl-2 cells showed a significant incidence of apoptosis in response to glutamate. Conventional phospholipid analysis by high-performance TLC and phosphorous determination showed no significant changes in the phospholipid composition of either cell line incubated with 5 mM glutamate. The peroxyl radical initiator 2,2'-azobis(2,4-dimethylvaleronitrile) caused a pronounced loss of all major phospholipid classes in PC12 cells, but no loss of cell viability. No phospholipid peroxidation was detected in PC12/bcl-2 cells incubated with 相似文献   

Angiotensin II mediates systemic rebound hypertension after cessation of prostacyclin infusion in sheep

Prostacyclin (or epoprostenol), an arachidonic acid metabolite, is an effective treatment for patients with primary pulmonary hypertension. Interruption of chronic prostacyclin infusion can result in recurrent symptoms of dyspnea and fatigue. The etiology of this phenomenon is unknown. We hypothesized that sympathoadrenal activation could lead to increased vascular tone after abrupt termination of the infusion. To evaluate this effect, we monitored six chronically instrumented, awake sheep during and after infusion of prostacyclin. Prostacyclin decreased mean arterial pressure (MAP) by 14% and increased cardiac output by 33%. After the infusion ceased, MAP rebounded 23% above baseline, and cardiac output decreased by 28% from peak values within 10 min. We were unable to demonstrate an increase in norepinephrine levels after cessation of prostacyclin, nor did alpha-adrenergic blockade affect postinfusion hemodynamics. However, plasma renin activity increased >10-fold at peak infusion and remained elevated for up to 2 h after discontinuation of prostacyclin. Coinfusion of the angiotensin II-receptor antagonist L-158,809 resulted in complete abrogation of the postcessation rise in MAP. We conclude that renin-angiotensin system activation is primarily responsible for systemic hypertension occurring after abrupt cessation of prostacyclin infusion in sheep and that angiotensin II receptor blockade prevents this response. Our data do not support a role for sympathetic nervous system activation in the systemic pressor response after prostacyclin infusion.     

Surgical myocardial revascularization

In conclusion, surgical myocardial revascularization has utilized diverse methods to increase blood flow to the starving myocardium. These methods initially used the microcirculation as the portal to reach myocytes until angiography showed that the obstructions were macrovascular. This resulted in a 30-year era of direct attack on the coronary blockages by coronary bypass. Surgical conduits unfortunately have longevity considerably less than that of native arteries and are limited in number. Alternative conduits, both biologic and prosthetic, have not yet proved to have the same clinical results as the ITA. More patients are living long enough to have the extensiveness of their disease exhaust conventional therapies. Newer therapy, restricted thus far to untreatables, revisits the microcirculation by making laser channels. These many innovative procedures have benefited hundreds of thousands of patients. They emerged from the probity and innovation of many individual surgeons.     

Systemic venous collateral development after the bidirectional cavopulmonary anastomosis. Prevalence and predictors

OBJECTIVES: To determine the prevalence of systemic venous collaterals after the bidirectional cavopulmonary anastomosis and the factors associated with their development. BACKGROUND: Systemic venous collaterals have been found after cavopulmonary anastomosis. Methods. Cardiac catheterization was performed in 103 patients before and after a bidirectional cavopulmonary anastomosis. RESULTS: After surgery, 51 venous collaterals were identified in 32 patients (31%). Collateral development was associated with an abnormal superior vena caval connection (56% incidence vs. 26% with a single right superior vena cava, p = 0.01) and postoperative factors including pulmonary artery distortion (53% incidence vs. 22% without distortion, p = 0.002); increased superior vena caval mean pressure (14 +/- 5 mm Hg versus 11 +/- 4 mm Hg with no collaterals, p = 0.0002); increased pulmonary artery mean pressure (13 +/- 4 mm Hg vs. 11 +/- 4 mm Hg with no collaterals, p = 0.02); lower right atrial mean pressure (5 +/- 2 mm Hg vs. 6 +/- 3 mm Hg with no collaterals, p = 0.04); and increased mean gradient between superior vena cava and right atrium (8 +/- 3 mm Hg vs. 5 +/- 4 mm Hg with no collaterals, p = 0.0002). Using multiple logistic regression, only this last factor was independently associated with collateral development with an odds ratio per 1 mm Hg of 1.33 (95% CI 1.12-1.58, p = 0.001) for their presence. CONCLUSIONS: Systemic venous collaterals occur frequently after a bidirectional cavopulmonary anastomosis and are found postoperatively when a significant pressure gradient occurs between cava and right atrium.     

Comparative analysis of breast cancer contamination in mobilized and nonmobilized hematopoietic grafts

We report a case of an 18-month-old female who presented with three supernumerary upper limbs of varying lengths on the right side. Each limb had a proximal, middle, and distal segment, and an intercalated elbow and wrist joint. A single digit was present in the superior limb, three digits in the middle limb, and two digits in the caudal-most limb. Right plagiocephaly, congenital torticollis, scoliosis involving the upper and mid thoracic region, and a hypoplastic right pectoralis major were the other abnormal features noted. Radiography showed two scapulae, humerus, a single forearm bone in each limb, and rudimentary metacarpals and phalanges. Limb duplication may rarely be encountered in parasitic conjoined twins. The role of mutagens, drugs, cellular contributions, and morphogens in the growth and differentiation of limbs has been studied in animals. It is rather difficult to deduce the time of action of the factors responsible for such a malformation.     

Structure-activity analysis of the interaction of curacin A, the potent colchicine site antimitotic agent, with tubulin and effects of analogs on the growth of MCF-7 breast cancer cells

Originally purified as a major lipid component of a strain of the cyanobacterium Lyngbya majuscula isolated in Cura?ao, curacin A is a potent inhibitor of cell growth and mitosis, binding rapidly and tightly at the colchicine site of tubulin. Because its molecular structure differs so greatly from that of colchicine and other colchicine site inhibitors, we prepared a series of curacin A analogs to determine the important structural features of the molecule. These modifications include reduction and E-to-Z transitions of the olefinic bonds in the 14-carbon side chain of the molecule; disruption of and configurational changes in the cyclopropyl moiety; disruption, oxidation, and configurational reversal in the thiazoline moiety; configurational reversal and substituent modifications at C13; and demethylation at C10. Inhibitory effects on tubulin assembly, the binding of colchicine to tubulin, and the growth of MCF-7 human breast carcinoma cells were examined. The most important portions of curacin A required for its interaction with tubulin seem to be the thiazoline ring and the side chain at least through C4, the portion of the side chain including the C9-C10 olefinic bond, and the C10 methyl group. Only two modifications totally eliminated the tubulin-drug interaction. The inactive compounds were a segment containing most of the side chain, including its two substituents, and analogs in which the methyl group at the C13 oxygen atom was replaced by a benzoate residue. Antiproliferative activity comparable with that observed with curacin A was only reproduced in compounds that were potent inhibitors of the binding of colchicine to tubulin. Molecular modeling and quantitative structure-activity relationship studies demonstrated that most active analogs overlapped extensively with curacin A but failed to provide an explanation for the apparent structural analogy between curacin A and colchicine.