Über eine seltene Komplikation der eitrigen Mastoiditis. Syndrom der Bulbuskompression infolge osteomyelitischer Zerstörung des Atlas

Ohne Zusammenfassung     

Anisakiasis as a cause of acute appendicitis and rheumatologic picture: the first case in medical literature

We report a case of acute abdomen due to appendicular lumen occlusion by anisakis larvae. This is the first case of human anisakiasis known in Spain, and the first case of acute appendicitis, in the medical World literature, produced by this nemathode. The association of myalgias and arthralgias stands out, being in this aspect the second case found the in medical litterature.     

Comparative analyses of the neurodegeneration induced by the non-competitive NMDA-receptor-antagonist drug MK801 in mice and rats

Non-competitive NMDA-receptor-antagonist drugs such as dizocilpine (MK801) induce behavioral changes and neurotoxicity that have made an impact in different fields of neuroscience. New approaches in research use transgenic mice to elucidate cellular mechanisms and circuits involved in the effects of these drugs. However, the neurodegeneration induced by these drugs has been extensively studied in rats, but the data in mice is limited. Therefore it is important to characterize if the neurotoxic pattern in mice corresponds to that of rats.A comparative analysis of the neurodegeneration induced by MK801 (10 mg/kg) between Wistar rats, and CD-1, CF-1, and C57BL/6-129/Sv mice of both sexes, at different survival times (15, 24, 32, 48, 56 and 72 h) was analysed with the amino-cupric-silver and fluoro-jade B techniques. To compare different administration patterns, groups of mice received subchronic treatments with different doses (final doses of 20 and 40 mg/kg).Results showed that mice treated with MK801 presented different neurotoxic profiles, such as excitotoxic-like cell death in the retrosplenial cortex, terminal degeneration in CA1 and apoptotic-like degeneration in the olfactory bulb. Unlike rats, mice subjected to the same treatment failed to show neurodegeneration in corticolimbic areas such as piriform cortex and dentate gyrus. The amount of degeneration was lower in mice, and the subchronic administration of MK801 did not change the neurotoxic pattern. Additionally, mice lacked the sexually dimorphic response to MK801 toxicity observed in rats. Altogether these results indicate important species dissimilarities. Neurotoxicological studies aimed to explore pathways and mechanisms of MK801 toxicity should consider these differences when using mice as rodent models.     

Glutamate activates PP125FAK through AMPA/kainate receptors in Bergmann glia

Glial glutamate receptors are likely to play a role in plasticity, learning, and memory and in a number of neuropathologies. An enhanced glutamate‐dependent tyrosine phosphorylation has been detected in such processes. Using primary cultures of chick Bergmann glia cells and chick cerebellar slices, we addressed whether glial glutamate receptors can activate the nonreceptor tyrosine kinase pp125 focal adhesion kinase (pp125^FAK). A dose‐ and time‐dependent tyrosine phosphorylation of pp125^FAK was found in both preparations upon glutamate treatment. This effect was mediated through α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoaxazolepropionate (AMPA)/kainate (KA) receptors, as shown by its inhibition by the specific antagonists 2,3‐dioxo‐6‐nitro‐1,2,3,4‐tetrahydrobenzo[f]quinoxaline‐7‐ sulfonamide (NBQX) and 6,7‐dinitroquinoxaline‐2,3‐dione (DNQX) and the lack of effect of metabotropic agonists. FAK tyrosine phosphorylation was dependent on phosphatidylinositol 3‐kinase activity. As expected, an increase in pp125^FAK catalytic activity was found upon glutamate treatment. Immunprecipitation experiments demonstrated that FAK associates with ionotropic glutamate receptors. Taken together, these results suggest a role for glial glutamate receptors in cytoskeletal rearrengments and focal adhesion contact formation and provide new insight into the signaling transactions elicited by this neurotransmitter in glial cells. J. Neurosci. Res. 66:723–729, 2001. © 2001 Wiley‐Liss, Inc.     

Clinical evaluation of a new collagen matrix (Mucograft® prototype) to enhance the width of keratinized tissue in patients with fixed prosthetic restorations: a randomized prospective clinical trial

Aim: The aim of this study was to test a new collagen matrix (CM) aimed to increase keratinized gingiva/mucosa when compared with the free connective tissue graft (CTG).
Material and Methods: This randomized longitudinal parallel controlled clinical trial studied 20 patients with at least one location with minimal keratinized tissue (1 mm).
Main Outcome Measure: The 6-month width of keratinized tissue. As secondary outcomes, the aesthetic outlook, the maintenance of periodontal health and the patient morbidity were assessed pre-operatively at 1, 3 and 6 months.
Results: At 6 months, the CTG attained a mean width of keratinized tissue of 2.6 (0.9) mm, while the CM was 2.5 (0.9) mm, these differences being insignificant. In both groups, there was a marked contraction (60% and 67%, respectively) although the periodontal parameters were not affected. The CM group had a significantly lower patient morbidity (pain and medication intake) as well as reduced surgery time.
Conclusions: These results prove that this new CM was as effective and predictable as the CTG for attaining a band of keratinized tissue, but its use was associated with a significantly lower patient morbidity.     

Predictive value of nigrostriatal dysfunction in isolated tremor: A clinical and SPECT study

The overlap among tremor disorders is wide and complex because essential tremor patients may present resting tremor coexisting with postural tremor, while postural may coexist with resting tremor in Parkinson's disease. We investigated dopamine transporter binding in 61 subjects presenting with isolated atypical tremors defined as unilateral either postural, resting, or mixed (i.e. resting and postural) tremor, without rigidity or bradykinesia, by means of 123I‐FPCIT SPECT imaging at baseline. Patients were followed‐up clinically for 28.4 ± 7.2 months. Twenty‐five patients with baseline normal SPECT continued to present only tremor at follow‐up. Among 36 patients with abnormal SPECT, 23 (64%) developed PD, while the remaining 13 continued to present only tremor at follow‐up. The value of 123I‐FPCIT SPECT in predicting the evolution to PD was very high in a way independent from the first clinical presentation of tremor (Rest tremor, P = 0.015; Mixed tremor, P = 0.015; Postural tremor, P = 0.039; chi‐square test). Our data suggest that the clinical presentation of isolated tremors is insufficient to allow a precise early‐stage diagnosis, whereas the detection of presynaptic nigrostriatal dopaminergic dysfunction could lead to diagnosis of atypical tremor disorders at a very early stage. We suggest this disorder to be labeled as “isolated tremor with dopaminergic presynaptic dysfunction.” © 2008 Movement Disorder Society