Neuroimaging in Pineal Tumors

BACKGROUND AND PURPOSE: The authors report radiological findings in 11 tumors in the pineal region, which were histologically diagnosed as germinomas, pineocytomas pineoblastomas, ependymomas, teratomas, and astrocytomas. METHODS: Computed tomography (CT) was performed in seven patients and magnetic resonance imaging (MRI) was performed in all patients. RESULTS: CT showed a solid or solid/cystic mass with variable contrast enhancement. MRI showed a heterogeneous mass, with hypointense signal on T1 and iso/hyperintense signal on T2-weighted images (WI) and gadolinium enhancement. Extension to adjacent structures occurred in five patients and spread through the cerebral spinal fluid (CSF) in two. CONCLUSIONS: Pineal region tumors have no pathognomonic imaging pattern. MRI and CT are complementary in diagnosis and are important to determine localization, extension, and meningeal spread.     

Labial Adhesion with Acute Urinary Retention Secondary to Bartholin's Abscess

Labial adhesions are usually seen in early childhood or in the postmenopausal years, but this clinical entity is rarely seen in the reproductive years. We report a case of labial adhesion with acute urinary retention secondary to Bartholin's abscess in a reproductive‐aged woman with normal menstrual periods. We emphasize the possible occurrence of labial adhesion following Bartholin's abscess in the reproductive years with normal estrogen levels.     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.     

A humanised tissue‐engineered bone model allows species‐specific breast cancer‐related bone metastasis in vivo

Bone metastases frequently occur in the advanced stages of breast cancer. At this stage, the disease is deemed incurable. To date, the mechanisms of breast cancer‐related metastasis to bone are poorly understood. This may be attributed to the lack of appropriate animal models to investigate the complex cancer cell–bone interactions. In this study, two established tissue‐engineered bone constructs (TEBCs) were applied to a breast cancer‐related metastasis model. A cylindrical medical‐grade polycaprolactone‐tricalcium phosphate scaffold produced by fused deposition modelling (scaffold 1) was compared with a tubular calcium phosphate‐coated polycaprolactone scaffold fabricated by solution electrospinning (scaffold 2) for their potential to generate ectopic humanised bone in NOD/SCID mice. While scaffold 1 was found not suitable to generate a sufficient amount of ectopic bone tissue due to poor ectopic integration, scaffold 2 showed excellent integration into the host tissue, leading to bone formation. To mimic breast cancer cell colonisation to the bone, MDA‐MB‐231, SUM1315, and MDA‐MB‐231BO breast cancer cells were cultured in polyethylene glycol‐based hydrogels and implanted adjacent to the TEBCs. Histological analysis indicated that the breast cancer cells induced an osteoclastic reaction in the TEBCs, demonstrating analogies to breast cancer‐related bone metastasis seen in patients.     

Modulation of ornithine decarboxylase activity in Escherichia coli by positive and negative effectors.

Two effectors of ornithine decarboxylase (ODC; L-ornithine carboxy-lyase, EC 4.1.1.17) have been extracted from an ODC- (speC-) mutant, Escherichia coli MA 255. One of these is an ODC inhibitor (Mr 15,000 +/- 2000) that is labile to trypsin; its activity increases 20-fold in response to increased polyamine levels in the growth medium. It has additional characteristics similar to those of the ODC antizyme of eukaryote cells: it is a noncompetitive inhibitor of ODC; the complex formed between ODC and the ODC inhibitor can be dissociated with salt to provide active ODC and active ODC inhibitor; furthermore, this E. coli ODC inhibitor is inhibitory to eukaryote ODC. A thermostable nondialyzable factor that activates ODC in vitro has also been extracted from MA255; increased polyamine levels in the growth medium caused a 1.6-fold increase in the activity of this ODC activator. Effectors with comparable activities have also been identified in the parent ODC+ (speC+) strain MA197. The fluctuations of the intracellular levels of these two ODC effectors during the growth of E. coli MA255 have been related to the temporal changes of the activity of ODC in the parent ODC+ MA197 strain. The mode of interaction of these three macromolecules, as reflected in the changes of the activity of ODC, appears to be complex. The results suggest that ODC activity may be controlled post-translationally by macromolecules that act as positive and negative effectors and whose levels fluctuate in response to the concentration of the end products of the reaction.     

Captopril adjuvant therapy to beta-blockers and nitrates improves post-myocardial infarction left ventricular performance

A growing body of data support the beneficial effects of angiotensin-convertingenzyme inhibitors in the prevention of cardiac enlargement andimprovement of left ventricular function in patients with acutemyocardial infarction. However, very little information existsabout the direct effect of increased afterload on cardiac performancein these patients and the possible favourable effects of angiotensin-convertingenzyme inhibitors as adjunctive treatment to thrombolysis, beta-blockersand nitrates. We have, therefore, studied the effects of captoprilas adjuvant therapy to thrombolysis, beta-blockers and nitrates(standard therapy) on left ventricular performance in 77 consecutivepatients with uncomplicated Q-wave acute myocardial infarction,by the measurement of the pre-ejection period/left ventricularejection time ratio before and after (0·25–0·50mg) phenylephrine administration on the 4th and 30th post-infarctiondays. Patients were randomized on day 4 either to continue standardtherapy alone (group 1, 35 patients) or to receive oral captopriltherapy (12·5 mg t.i.d.) in addition to standard therapy(group 2, 42 patients) in a double-blind parallel study. Among the patients of group 1 there was a significant deteriorationof left ventricular function after phenylephrine administration.This was shown by an increase of pre-ejection period/left ventricularejection time ratio only in the subset of patients with ejectionfraction <40%, as measured by contrast ventriculography,on both the 4th and 30th post-infarction days changing from0·435±0·070 to 0·528±0·101,P<0·01 and from 0·404±0·098 to0·515±0·092, P<0·02, respectively.In contrast there were no significant changes in patients withejection fraction 40%. Among patients of group 2, phenylephrineadministration induced a significant increase, only on the 4thday, in pre-ejection period/left ventricular ejection time ratioonly in the subset of patients with ejection fraction <40%changing from 0·410±0·107 to 0·535±0·102,P<0·01. In the remaining patients with ejection fraction>40% there were no significant changes on either the 4thor 30th post-infarction days. Furthermore, a significant improvementwas observed after phenylephrine administration in the pre-ejectionperiod/left ventricular ejection time ratio between the 4thand 30th post-infarction days, which changed from 0·535±0·102on day 4 to 0·368± 0·052 on day 30 (P<0·004).Also, a four-way ANOVA detected a significant reduction of heartrate in patients with ejection fraction <40< from day4 to day 30. The results indicate that: (1) the response of pre-ejectionperiod/left ventricular ejection time ratio after increasingafterload may be a useful non-invasive method for the detectionof left ventricular dysfunction in myocardial infarction patients;and (2) captopril adjuvant therapy as compared to thrombolysis,beta-blockers and nitrates alone, after phenylephrine administration,improves the left ventricular performance response in asymptomaticQ-wave post-infarction patients and beneficially affects heartrate. This effect is most pronounced in patients with ejectionfraction 40% whereas those with ejection fraction 40% do notobtain clear benefit.