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.     

Inverse changes in erythroid cell volume and number regulate the hematocrit in newborn genetically hypertensive rats.

Erythrocytosis and microcytosis have been described in strains of genetically hypertensive rats and in essentially hypertensive humans. Published discussion of these phenomena has centered around their relationship to observed alterations in ionic transport and the pathogenesis of hypertension. In presenting data for another strain of spontaneously hypertensive rats in which these findings are exhibited, we note that erythroid cell size decreases concurrently with the increase in cell numbers so that the hematocrit and the mean corpuscular hemoglobin concentration remain constant. Data from the literature support the hypothesis that erythroid cell size is inversely proportional to cell count in a large number of species. Erythrocytosis, as it develops in the neonatal rat, is a consequence of the marked immaturity of this species at birth. Erythrocytosis in the spontaneously hypertensive rat is not due to a difference in the affinity of its hemoglobin for oxygen or to significant tissue anorexia. Microcytosis in the spontaneously hypertensive rat is the consequence of a continuation of the linear volume decrease with age of its erythroid cells seen in the normotensive animals and may be accounted for by the production of smaller cells with concomitant regulation of individual cell volume.     

A continuous striatal infusion of 6-hydroxydopamine produces a terminal axotomy and delayed behavioral effects

Rat models of Parkinson's disease typically employ a rapid nigral injection of 6-hydroxydopamine (6-OHDA) to produce a near-complete loss of nigrostriatal dopamine neurons, and thus model end stage disease. The present report describes the use of a continuous, low dose infusion of 6-OHDA into the striatum which produces a terminal axotomy of nigrostriatal dopamine neurons and protracted behavioral response. A solution of 6-OHDA in 0.4% ascorbate, delivered at 37°C from osmotic minipumps, was stable for 8 days as determined by its retained toxicity to a dopaminergic neuroblastoma cell line. The continuous infusion of 0.2 μg 6-OHDA per h did not affect the striatal uptake of [³H]GABA, [³H]choline, or [³H]glutamate but reduced [³H]dopamine uptake by 55% within 1.5 days after the start of the infusion. The striatal infusion of 6-OHDA produced a dose-dependent reduction of striatal dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA. An increase in amphetamine-induced ipsiversive rotations occurred within 1.5 days after the acute striatal injection of 20 μg or 30 μg of 6-OHDA but required 4 days to develop with the continuous 6-OHDA infusion. The topography of the lesion mapped by [³H]mazindol binding showed that, begining by 1.5 days, a diffuse depletion of terminals encompassed much of the striatum in the 30 μg acute injection group, whereas in the continuously infused rats, the lesion was apparent only by 4 days and was restricted to a smaller and more completely lesioned area. Unlike acutely lesioned animals, continuously infused rats revealed no obvious loss of dopamine neurons in the pars compacta by 5 weeks after 6-OHDA. The continuous striatal infusion of 6-OHDA can produce a topographically limited terminal axotomy of dopamine neurons and a protracted behavioral impairment.     

Vital Bleaching Agents and Oral Antiseptic: Effect on Anaerobic Bacteria

This in vitro study compared the antimicrobial effect of several at-home bleaching agents and an oral antiseptic against anaerobic bacteria that are commonly found in the oral cavity. Zones of inhibition produced by Rembrandt Lighten Bleaching Gel, Opalescence, and Peroxyl were measured and compared. All the materials produced zones of inhibition with the five bacteria used in the study.     

Computed extraocular muscle activity during blinks

The rotations and retractions of the eyeball due to co-contraction of the extraocular muscles are investigated using a model of the mechanics of the orbital plant. The hypothesis that the rotational movements are secondary to globe retraction is not supported.     

Neonatal damage to the rat's infraorbital nerve upregulates both galanin and neuropeptide Y in individual vibrissae-related primary afferent axons

Previous studies in adult animals have suggested that the peptides galanin and neuropeptide Y (NPY) may be upregulated in the same primary afferent neurons after peripheral axotomy. The present study was undertaken to determine whether such upregulation occurred in vibrissae-related primary afferent neurons and their axons after damage to the infraorbital nerve [ION; the trigeminal (V) branch that innervates the vibrissae follicles]. Double-labelling experiments demonstrated that approximately 75% of axotomized V ganglion cells and the central arbors of vibrissae-related primary afferents expressed both galanin and NPY after perinatal, but not adult, nerve damage. However, additional experiments demonstrated that the sensitive periods for lesion-induced upregulation of the two peptides and the period over which they were expressed after neonatal ION transection differed substantially. Staining for both peptides was increased after ION damage on P-0 through P-14, but only galanin staining was increased in vibrissae-related primary afferents after lesions on P-21. Galanin expression was elevated in vibrissae-related primary afferents in rats killed 3,8, and 15 days after neonatal ION transection, while increased NPY was observed at only the middle time point. The lesion-induced increases in galanin and NPY in vibrissae-related ION primary afferents suggest that these peptides may modulate central V reorganization after such damage.     

Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial.

Industrial workers exposed to the organochlorine pesticide, chlordecone (Kepone), had signs of toxicity in several organs. The extent of toxicity was proportional to the levels of this chemical in the tissues. In 22 patients, chlordecone was eliminated slowly from blood (half time of 165 +/- 27 days--mean +/- S.E.M.) and fat (half time of 125 days, with a range of 97 to 177), chiefly in the stool. Output of chlordecone in bile was 10 to 20 times greater than in stool, suggesting that chlordecone is reabsorbed in the "ntestine. Cholestyramine, an anion-exchange resin that binds chlordecone, increased its fecal excretion by seven times. In a five-month trial, cholestyramine significantly accelerated elimination of chlordecone from blood, with a half life of 80 +/- 4 days (S.E.M.) (P less than 0.005) and fat (half life of 64 days, with a range of 52 to 85) (P less than 0.05). Cholestyramine offers a practical means for detoxification of persons exposed to chlordecone and possibly to other lipophilic toxins.     

Self-expanding oesophageal metal stents for the palliation of dysphagia due to extrinsic compression

The role of self-expanding metallic stents is well established in the palliation of oesophageal stenosis and dysphagia due to primary oesophageal malignancy. However, their role in palliation of dysphagia due to external compressive mediastinal malignancies is not well established. The purpose of this study was to assess the efficacy of self-expanding metallic stents in the palliation of dysphagia due to extrinsic oesophageal compression by mediastinal malignancy. Between January 1995 and January 1998, 21 patients with oesophageal compression due to malignant mediastinal tumours underwent oesophageal stent placement for palliation of dysphagia. Complete data were available in 17 patients (10 men and 7 women). The mean age was 63.5 years (range 46–89 years). A total of 19 stents were placed successfully. The dysphagia grade prior to and after oesophageal stent placement was assessed and the complications documented. Of the 17 patients, 16 reported an improvement in dysphagia. The mean dysphagia score improved from 3.1 prior to treatment to 1.3 after treatment. In 1 patient the stent slipped during placement and another stent was placed satisfactorily. Early complications (within 48 h) in the form of mild to moderate retrosternal chest pain occurred in 5 patients. This was treated symptomatically. Late complications (after 48 h) in the form of bolus impaction occurred in 2 patients. This was successfully treated with oesophagoscopy and removal of bolus. In 2 patients the stent was overgrown by tumour and in one of these an additional stent was placed. In 1 patient incomplete closure of a tracheo-oesophageal fistula was observed. There was no procedure- or stent-related mortality. The mean survival time of this group was 2.1 months. Self-expanding metallic stents can be safely and effectively used in the palliation of dysphagia due to external mediastinal malignancies. Received: 21 October 1998; Revised: 1 February 1999; Accepted: 4 February 1999