Growth modulation of hepatocytes and rat liver epithelial cells (WB-F344) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

Modulation of DNA synthesis by 2,3,7,8-tetrachlorodi-benzo-p-dioxin(TCDD) was studied in primary cultures of hepatocytes and inrat liver epithelial cells (WB-F344) to develop models for studieson the interactions between the activated Ah receptor and cellulargrowth control. In hepatocytes TCDD either positively or negativelymodulated EGF-stimulated DNA synthesis. In the presence of ethlnylestradiol10^–12 M TCDD moderately increased EGF-stimulated DNA synthyesis(     

Hypotensive effect of the active fragment derived from factor XII is mediated by an activation of the plasma kallikrein-kinin system

Plasma protein fraction (PPF) contaminated by factor XII active fragment (XIIf) may cause hypotensive reactions when infused to patients. This study was planned to assess in conscious normotensive rats whether the blood pressure response to the factor XIIf is mediated by an activation of the plasma kallikrein-kinin system or by stimulation of prostaglandin synthesis. To test whether the factor XIIf-induced blood pressure fall is due partially to an enhanced generation of vasodilating prostaglandins, the blood pressure effect of XIIf (1 microgram i.v.) was investigated 15 min after treatment with indomethacin (5 mg i.v.), an inhibitor of cyclo-oxygenase. Factor XIIf reduced mean blood pressure similarly in indomethacin- and vehicle-treated rats (-23 +/- 4 mmHg, n = 5, and -23 +/- 5 mmHg, n = 4, respectively). Other rats received factor XIIf 15 min after depletion of circulating prekallikrein by the administration of dextran sulfate. Thirty minutes after a 0.25 mg i.v. dose of this agent, plasma prekallikrein activity averaged 0.12 +/- 0.015 mumol/min/ml (n = 6) as compared to 2.48 +/- 0.31 mumol/min/ml in control rats (n = 4, P less than .001). Factor XIIf decreased mean blood pressure by only 4 +/- 2 mm Hg in rats pretreated with dextran sulfate. Thus, it was possible to blunt the acute hypotensive effect of factor XIIf by depleting circulating prekallikrein, but not by inhibiting prostaglandin production. This strongly suggests that the blood pressure effects of factor XIIf is mediated by a stimulation of the plasma kallikrein-kinin system.     

Immunoreactivity of an antibody to a beta/A4 sequence with Alzheimer paired helical filaments and tau protein.

beta/A4, a peptide that forms the extracellular amyloid fibrils of Alzheimer senile plaques, has also been proposed to be a component of Alzheimer paired helical filaments (PHFs). We compared BR88, an antiserum to amino acids 1-12 of beta/A4, with BR126, an antiserum to the sequence SEKLDFKDRVQS in tau protein, since tau protein is the only confirmed component of PHFs. In enzyme-linked immunosorbent assays (ELISAs), both antibodies reacted with pronase-treated PHFs better after PHFs were treated with guanidine. tau protein shares no sequence homology with beta/A4. Nevertheless, BR88 cross-reacted with human recombinant tau isoforms by ELISA and Western blot analysis with potencies comparable to those for anti-tau antibodies. BR88 reacted with a beta/A4 peptide as well on a molar basis as with tau protein and showed some reactivity to the tubulin-binding region of tau protein. In conclusion, the beta/A4 antiserum BR88 cross-reacts with tau protein, possibly explaining its reactivity with PHFs.     

Lifetime diagnoses in patients with somatoform disorders: Which came first?

Thirty inpatients with somatoform disorders were examined with the structured clinical interview SCID for psychiatric lifetime diagnosis. In the present diagnoses, we found a concordance of 63% for somatoform and affective disorders and the lifetime comorbidity of both disorders was 87%. Additionally, patients with somatoform disorders frequently had a history of other psychiatric disorders (for example, anxiety disorders, 40%). For 73% of patients with somatoform disorders and a history of affective disorders, the onset of the somatoform disorder was prior to the onset of another psychiatric disorder. The time interval between the onsets of somatoform disorders and affective disorders was greater than 1 year for most patients; for 46% of the patients with a history of both disorders, the time interval between the two disorders was more than 5 years. The course of illness for somatoform and affective disorders was quite different; while affective disorders tended to episodic periods with interim remissions, the somatoform disorders usually showed long, chronic courses (mean duration of the current somatoform disorder was 11.9 years). Finally, the Symptom Check List SCL-90R demonstrated good discrimination between patients with affective and anxiety disorders. However, the SCL-90R failed to discriminate patients with somatoform disorders from affective- and anxiety-disordered subjects. Therefore, the development of other psychometric scales is necessary for the evaluation of patients with somatoform disorders.     

Hämatologische Störungen bei Intensivpatienten

This final issue of the series "Emergency and intensive care therapy for hematooncological diseases" reviews cytopenias in intensive care patients who do not offer any oncological or haematological problems in their medical history. Anaemia is a very common problem in the intensive care setting. We highlight aetiological aspects of anaemia in critically ill patients and discuss therapeutical options like substitution of blood and application of erythropoietin, respectively. The second paragraph focuses on leukocytopenia and agranulocytosis, their causation and therapy and among other things the application of G-CSF (Granulocyte colony-stimulating factor). Last but not least, we deal with thrombocytopenia, especially heparin-induced thrombocytopenia.     

Case Report: Corroboration of the lower extremity counterpart of the Poland sequence

Gluteal and lower extremity hypoplasia with ipsilateral toe brachysyndactyly were noted in a 23-year-old woman similarly affected to the only previously reported case of the lower extremity counterpart of Poland sequence. Since no neurological deficit was found, and electromyographic and nerve conduction studies in the affected limb were normal, we propose a vascular origin which would involve the external iliac artery supply analogous to the subclavian artery supply disruption in the upper extremity Poland sequence.