[Quality assurance through organizational measures].
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Anesthesiology↗
Biomedical subjects
B Stein
Publications and source records attributed to B Stein.
Personality status: changes through adolescence.
1. Forty-two percent of a nonclinical sample of urban 18 year olds displayed some degree of personality dysfunction. This rate of disturbance is similar to a previously reported rate for 13 year olds, but higher than the prevalence rate for 16 year olds. Thus, early and late adolescence seem to represent "at risk periods" for the genesis of character pathology. 2. In late adolescence, the form of this disturbance is as follows: 40% fall into a histrionic, borderline, narcissistic cluster, whereas nearly 30% demonstrate an atypical or mixed picture. This differs markedly from the distribution of dysfunction in earlier subphases. 3. Thirty-eight percent of the disturbed sample showed evidence of dysfunction at all three subphases (early, middle, and late), whereas 62% fluctuated in or out of disturbance at one subphase or another. 4. There was a notable lack of consistency with respect to type of personality dysfunction from both a group and individual perspective, except for paranoid, schizoid, and schizotypal disturbance. This particular cluster retained both group and individual stability from age 13 to 18. 5. Two trends were evident however: teenagers who initially presented as avoidant, dependent, compulsive, or passive-aggressive seemed to grow out of their dysfunction. By age 18, hardly any of the original subjects remained in this cluster, and most had become clear. Secondly, most of the adolescents identified as antisocial in early or middle adolescence migrated into the histrionic, narcissistic, borderline cluster in late adolescence. This latter group showed a steady increase throughout the time span studied, suggesting the importance of developmental factors.
Adolescent↗
[Clinical evaluation of testicular size in boys and adolescents].
On 596 healthy boys and adolescents from 4 to 17 years of age measurements of the length and the width of the left testis as well as of the thickness of scrotal skin were carried out by means of a caliper, and the testis volume was secondarily calculated. Age specific mean values (means) and their +/- 2 s-limits are listed. Nonlinear s-shaped regression lines of the three main parameters clearly underline that the greatest increase is to be found in the length of testis. Consequently, as an indicator for gonadal developmental disturbances instead of testis volume measuring of testis length is recommended for routine in the physical examination of inpatients and outpatients as well as for the screening of schoolboys and male teenagers.
Adolescent↗
[Clinical assessment of ear size in children and adolescents].
In 1271 children and adolescents of both sexes (596 boys and 675 girls) anthropometric measurements of the "physiognomic external ear length and ear width" were carried out by means of a caliper in order to make the clinical symptoms of macrotia and microtia, respectively, more objective than by clinical impression, only. In the mean ear lengths steadily and annually grow 0.66 mm in boys and 0.46 mm in girls, +/- 2s-border-lines based on a nonlinear regression model y = f(means +/- 2s) = a + b.ln x are calculated: For boys it is y + 2s = 47,9164 + 6,9539.ln x and y-2s = 36,7839 + 6,1172.ln x, respectively, for girls the regression equations are as follows: y + 2s = 49,1431 + 5,6002.ln x and y-2s = 41,3945 + 3,2266.ln x. The approximation of the regression model to the data observed is highly significant (alpha less than 0.0005). In contrast to the auricle length "physiognomic external ear width" is independent of age in both sexes, namely in boys means = 32.89 +/- 0.1176 mm and in girls means = 31.21 +/- 0.0876 mm. All sex differences are highly significant (alpha less than 0.0005).
Adolescent↗
Antithrombotic therapy in acute myocardial infarction: prevention of venous, left ventricular and coronary artery thromboembolism.
The antithrombotic approach to patients with acute myocardial infarction in the prevention of venous, left ventricular and coronary artery thromboembolic events should be based on an understanding of pathogenesis and risk. Coronary thrombotic events involve conditions of high shear rate present in areas of vessel stenosis or disrupted atherosclerotic plaque, which lead to activation of both platelets and the coagulation system, and are best prevented by platelet inhibitors alone or in combination with an anticoagulant. However, thromboembolism that originates in the venous system or cardiac chambers is related to situations of blood stasis and low shear rate, which predominantly result in clotting activation and fibrin-thrombus formation and are best approached with anticoagulant therapy. For prevention of venous thrombosis and pulmonary embolism, early mobilization is essential and should be supplemented by low-dose heparin in patients at high risk, including the elderly and those with large infarcts, heart failure or previous thromboembolic events. For prevention of left ventricular mural thrombosis and systemic embolism, high-dose heparinization is indicated in patients with large infarcts, particularly in the anterior location and in those with heart failure. Subsequently, warfarin therapy should be considered for patients at high embolic risk, including those with echocardiographic evidence of mobile and protruding thrombi, severe left ventricular dysfunction or prior emboli. In patients with acute infarction, aspirin is recommended for preventing coronary reocclusion and reinfarction. Although anticoagulants may also be of benefit for this purpose, their use is still controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary Disease↗
Crime labs or the street for drug information?
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Data Collection↗
Tissue carcinoembryonic antigen levels in benign and malignant diseases of the breast.
The peroxidase-antiperoxidase histochemical method of staining for tissue carcinoembryonic antigen (CEA) was performed on 20 samples of malignant breast tissue, 20 samples of fibroadenomatous breast tissue, and 15 samples of breast tissue that variably contained minimal fibrosis (N = 7), ductal ectasia (N = 5), and sclerosing adenosis (N = 3; the fibrocystic changes of the breast). The intensity of staining was described to be either negative, weak, intermediate, or strong and was assigned a point value of 1, 2, 3, or 4, respectively. The following weighted average values of tissue CEA were obtained: carcinoma, 3.35 +/- 0.88; fibroadenomas, 2.85 +/- 0.67; fibrocystic changes, 2.13 +/- 0.52. Carcinomatous tissue is likely (55%) to display intense tissue staining, whereas fibrocystic disease (0%) or fibroadenoma (15%) are unlikely to exhibit such a reaction. The tissue CEA content between carcinoma and fibrocystic changes (P less than 0.01), carcinoma and fibroadenoma (P less than 0.01), and fibroadenoma and fibrocystic changes (P less than 0.05) are statistically significant.
Biomarkers, Tumor↗
Effects of adenosine analogues on contractile response and cAMP content in guinea-pig isolated ventricular myocytes.
In the present study the effects of adenosine analogues were investigated on cAMP content and contractile response in guinea-pig ventricular myocytes. The adenosine analogues (-)-N6-phenylisopropyladenosine (R-PIA), 5'-N-ethylcarboxamideadenosine (NECA) and (+)-N6-phenylisopropyladenosine (S-PIA) in the presence of 0.01 mumol/l isoprenaline reduced contractile response concentration-dependently. R-PIA and NECA were about equipotent (IC25: 0.01 mumol/l and 0.039 mumol/l respectively), while S-PIA was less potent (IC25: 0.6 mumol/l). Isoprenaline stimulated cAMP content was reduced by R-PIA (IC25: 0.004 mumol/l) and with lower potency by S-PIA (IC25: 0.15 mumol/l), but the extent of reduction of cAMP by R-PIA and S-PIA (to 55% and 64% respectively) was less than the reduction of contractile response (to 26% and 55% respectively). This suggests that the effects of R- and S-PIA on contractile response are only in part due to a reduction in cAMP content. In addition, NECA did not decrease cAMP content but decreased contractile response to the same extent as R-PIA. Similar results were obtained in the presence of the phosphodiesterase inhibitor Ro 20-1724. Time course studies revealed that the effects of R-PIA (1 mumol/l) on cAMP content and contractile response coincided reaching steady state after 5 min and remained stable thereafter. The effects of NECA (1 mumol/l) on contractility also reached steady state within 5 min, whereas it did not change cAMP content. It is concluded that the reduction of contractility by adenosine analogues in the presence of isoprenaline can only in part be explained by a reduction of cAMP content.(ABSTRACT TRUNCATED AT 250 WORDS)
3',5'-Cyclic-AMP Phosphodiesterases↗
Role of platelet inhibitor therapy in myocardial infarction.
Atherosclerotic plaque disruption is the predominant pathogenetic mechanism underlying the acute coronary syndromes. Plaque rupture leads to the exposure of collagen and vessel media, resulting in platelet and clotting activation, and occlusive thrombus formation. While drugs that interfere with platelet activation and function have been available for years, more powerful agents with novel mechanisms of action are being developed. Of the available platelet inhibitor drugs, only aspirin, sulfinpyrazone, and dipyridamole have undergone extensive clinical testing in patients with cardiovascular disease. More recently ticlopidine, a new and potent platelet inhibitor, has been successfully tested in patients with coronary and vascular disease. In acute myocardial infarction, aspirin significantly reduces cardiovascular mortality and reinfarction. Furthermore, the combination of aspirin and a thrombolytic agent produces maximal benefit. A role for heparin in the prevention of early mortality and reinfarction is emerging. This drug is effective for the prevention of left ventricular thrombosis in patients with anterior myocardial infarction. In the secondary prevention of reinfarction and cardiovascular mortality, available data support the use of a platelet inhibitor. Trials have shown that aspirin is as effective alone as in combination with dipyridamole, and is probably more effective than sulfinpyrazone. Long-term anticoagulant therapy also appears to be beneficial, but is associated with a high cost, need for extensive monitoring, and potential for hemorrhagic side effects. The role of aspirin in primary prevention is controversial. It may be indicated for patients at high risk for coronary disease in whom the benefit of therapy may outweigh the potential risk of cerebral bleeding. Coronary atherosclerotic plaque rupture, associated with thrombus formation, is fundamental to the development of acute myocardial infarction. Based on this concept, the role of antithrombotic therapy for the prevention or treatment of ischemic events in patients with coronary artery disease has stimulated enormous interest among clinicians and basic investigators. In this review we will examine: a) the pathogenesis of coronary thrombosis, b) the pharmacology of platelet-inhibitor agents, and c) their role in the management of patients with acute myocardial infarction and in primary and secondary prevention of cardiovascular disease. Platelets interact with both the coagulation and fibrinolytic systems in the pathogenesis of thrombosis.(ABSTRACT TRUNCATED AT 400 WORDS)
Aspirin↗
Synergistic effect of tumor necrosis factor-alpha and interferon-gamma on collagen synthesis of human skin fibroblasts in vitro.
The effect of tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) on collagen metabolism by human diploid fibroblasts in confluent monolayer culture was examined. Recombinant TNF alpha reduced collagen mRNA levels 2-fold and stimulated collagenase mRNA levels 5-fold, while recombinant IFN gamma affected only collagen mRNA levels. The combination of TNF alpha (10 ng/ml) and IFN gamma (100 ng/ml) resulted in a much stronger (about 30-fold) reduction of collagen mRNA levels indicating that the two cytokines act synergistically. In contrast no such synergism was observed with respect to collagenase mRNA levels. The effect of TNF alpha and IFN gamma on collagen metabolism reported here indicates a complex interaction of different cytokines in the control of tissue remodeling that occurs during inflammation, repair, or atrophy.
Adult↗
Platelet inhibitor agents in cardiovascular disease: an update.
Platelets interact with the coagulation and fibrinolytic systems in the maintenance of hemostasis. However, these physiologic mechanisms may become pathologic, requiring prevention and treatment. In this review, the following clinical developments are analyzed: 1) the role of platelets in thrombogenesis; 2) the pharmacology of platelet inhibitory agents; and, most important, 3) the results of recent randomized trials of platelet inhibitor agents in different cardiovascular disorders. Aspirin reduces mortality and infarction rates in unstable angina and significantly decreases vascular mortality in acute myocardial infarction. Platelet inhibitors decrease mortality and recurrent cardiovascular events in the chronic phase after myocardial infarction. They also decrease vein graft occlusion rates after coronary bypass surgery. Although platelet inhibitors are beneficial in preventing acute vessel occlusion during coronary angioplasty, they are ineffective in preventing chronic restenosis. Antiplatelet agents, combined with warfarin, reduce thromboembolic events in patients with a mechanical prosthesis. Platelet inhibitors are also effective in secondary prevention of vascular events in patients with cerebrovascular disease. Finally, the use of aspirin for primary prevention of cardiovascular disease is still evolving, particularly in individuals at high risk. In conclusion, platelet inhibitors are effective in patients with a variety of cardiovascular disorders. The best studied, most inexpensive and least toxic agent is aspirin at a daily dose of 160 to 325 mg. Studies using new platelet inhibitor agents with different mechanisms of action are currently underway.
Aspirin↗
Differentiation of endocrine cells in chick allantoic epithelium combined with pancreatic mesenchyme.
Allantoic endoderm of 3-day chick embryos was combined with pancreatic mesenchyme of 5-day embryos and cultured as chorio-allantoic grafts for a total of 14 days. Recombinations of endoderm and mesenchyme of the pancreas and of the allantois served as controls. The usual types of endocrine cells differentiated in the pancreatic controls, none in the allantoic controls. In experimental grafts simple columnar epithelium with goblet cells and a sucrase-positive brush border developed; a few insulin cells and endocrine cells typical of the intestine differentiated. Hence allantoic endoderm has endocrine potentiality not realised in vivo, where its own mesenchyme may be inhibitory.
Allantois↗
Basal and isoprenaline-stimulated cAMP content in failing versus nonfailing human cardiac preparations.
We measured force of contraction and cAMP content in human isolated electrically driven right ventricular trabeculae carneae with and without the addition of isoprenaline (0.2 microM). Basal cAMP content was approximately 200% higher in preparations from nonfailing hearts than from hearts with end-stage myocardial failure. Isoprenaline was less effective in increasing force of contraction in failing (by approximately 100%) than in nonfailing cardiac preparations (by approximately 500%). With isoprenaline, cAMP content was approximately 50% lower in failing than in nonfailing preparations. We conclude that the reduced increase in force of contraction of failing human cardiac preparations with isoprenaline added may be causally related to an inadequately increased cAMP content.
Cyclic AMP↗
UV-induced transcription from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat and UV-induced secretion of an extracellular factor that induces HIV-1 transcription in nonirradiated cells.
UV irradiation, but not visible sunlight, induces the transcription of human immunodeficiency virus type 1 (HIV-1). Chimeric constructs carrying all or parts of the HIV-1 long terminal repeat linked to an indicator gene were transfected into HeLa cells or murine and human T-cell lines, and their response to irradiation was tested. The cis-acting element conferring UV responsiveness is identical to the sequence binding transcription factor NF kappa B. UV irradiation enhances NF kappa B binding activity as assayed by gel retardation experiments. Interestingly, the requirement for UV irradiation can be replaced by cocultivation of transfected cells with UV-irradiated nontransfected (HIV-1-negative) cells. A UV-induced extracellular protein factor is detected in the culture medium conditioned by UV-treated cells. The factor is produced upon UV irradiation by several murine and human cell lines, including HeLa, Molt-4, and Jurkat, and acts on several cells. These data suggest that the UV response of keratinocytes in human skin can be magnified and spread to deeper layers that are more shielded, including the Langerhans cells, and that this indirect UV response may contribute to the activation of HIV-1 in humans.
Cell Line↗
Infection with the intracellular protozoan parasite Theileria parva induces constitutively high levels of NF-kappa B in bovine T lymphocytes.
The intracellular protozoan parasite Theileria parva causes a lymphoproliferative disease of T cells in cattle and uncontrolled lymphocyte proliferation in culture. We have identified and characterized in infected cells the transcriptional activator, NF-kappa B, whose recognition motifs have been identified in several gene enhancers important for lymphocyte-specific gene expression. NF-kappa B is normally constitutively activated in nuclear extracts derived from B cells and can be induced in T cells and nonlymphoid cells by phorbol esters. Theileria-infected lymphocytes contained constitutively high levels of activated NF-kappa B in nuclear fractions and inactive NF-kappa B in cytoplasmic fractions. The inactive cytoplasmic precursor could be activated by treatment of extracts with deoxycholate, which was shown previously to dissociate NF-kappa B from an inhibitor, I kappa B. Treatment of lymphocyte extracts with 3 mM GTP stimulated NF-kappa B binding to its recognition motif in vitro, thereby distinguishing it from a related nuclear factor, H2-TF1. Selective killing of the parasite, which left the host cells intact, resulted in a rapid loss of NF-kappa B from the nuclear fractions and a slower loss from the cytoplasmic fractions. In parasitized cells, NF-kappa B could not be further stimulated by treatment with 12-O-tetradecanoylphorbol-13-acetate whereas in cells treated to remove the parasite, this compound stimulated elevated levels of NF-kappa B. We propose that high levels of activated NF-kappa B are maintained by the presence of the parasite in infected T cells. Similarly, we propose that the high levels of inactive cytoplasmic precursor are a result of increased synthesis due to the presence of the parasite.
Animals↗
UV-induced DNA damage is an intermediate step in UV-induced expression of human immunodeficiency virus type 1, collagenase, c-fos, and metallothionein.
UV irradiation of human and murine cells enhances the transcription of several genes. Here we report on the primary target of relevant UV absorption, on pathways leading to gene activation, and on the elements receiving the UV-induced signal in the human immunodeficiency virus type 1 (HIV-1) long terminal repeat, in the gene coding for collagenase, and in the cellular oncogene fos. In order to induce the expression of genes. UV radiation needs to be absorbed by DNA and to cause DNA damage of the kind that cannot be repaired by cells from patients with xeroderma pigmentosum group A. UV-induced activation of the three genes is mediated by the major enhancer elements (located between nucleotide positions -105 and -79 of HIV-1, between positions -72 and -65 of the collagenase gene, and between positions -320 and -299 of fos). These elements share no apparent sequence motif and bind different trans-acting proteins; a member of the NF kappa B family binds to the HIV-1 enhancer, the heterodimer of Jun and Fos (AP-1) binds to the collagenase enhancer, and the serum response factors p67 and p62 bind to fos. DNA-binding activities of the factors recognizing the HIV-1 and collagenase enhancers are augmented in extracts from UV-treated cells. The increase in activity is due to posttranslational modification. While AP-1 resides in the nucleus and must be modulated there, NF kappa B is activated in the cytoplasm, indicating the existence of a cytoplasmic signal transduction pathway triggered by UV-induced DNA damage. In addition to activation, new synthesis of AP-1 is induced by UV radiation.
Adult↗
Antithrombotic therapy in cardiac disease. An emerging approach based on pathogenesis and risk.
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Angioplasty, Balloon, Coronary↗
Personality dysfunction in depressed adolescents.
The personality characteristics of 35 consecutively assessed adolescents who met the DSM-III criteria for a current depressive disorder were assessed using independent structured interviews and paper and pencil measures. Sixty-five percent of the sample met the criteria for an Axis II personality disorder. The single most common diagnosis was borderline personality disorder (30%). Depressed adolescents with a concurrent personality disorder were less self-confident, displayed more neuroticism, and were emotionally reliant on others. They also demonstrated greater cognitive distortion. Teenagers who present with a depressive disorder warrant a comprehensive personality assessment. The combination of affective and personality disorder in such patients is associated with attitudes and interpersonal problems which should be therapeutically addressed in addition to symptomatic treatment of the depressed mood. Clinicians should be aware that depressed adolescents with personality disorder may be more likely to make a suicide attempt.
Adolescent↗