Of all tissue heating techniques, RF-based technologies appear to be the most established and clinically proven. The design and specifications of the described vacuumassisted bipolar RF device fall within the range of the specifications currently prescribed for esthetic, nonablative RF systems.
Zinc maintains a diverse array of functions in the mammalian central nervous system as a key component of numerous enzymes, via its role in the activation of transcription factors, and as a neuroregulator, modulating neuronal receptors such as N-methyl-D-aspartate and gamma-aminobutyric acid. Zinc has a dark side, however, with massive influx of Zn(2+) to neurons considered to be a key factor in neuronal death secondary to ischemia and seizure. Several different putative zinc transporters, ZnT-1-4, have recently been identified and characterized. Among them, ZnT-1 has been suggested to play a key role in reducing cellular Zn(2+) toxicity. In the present study, we describe the regional and cellular distribution of ZnT-1 in the adult mouse brain using an antibody raised against the C-terminal domain of mouse ZnT-1. The distribution of ZnT-1 was compared to that of chelatable Zn(2+), visualized by means of neoTimm histochemistry or N-(6-methoxy-8-quinolyl)-p-toluene-sulfonamide (TSQ) histofluorescence. Extracts from various brain regions specifically stained a 60-kDa peptide corresponding to the expected molecular weight of ZnT-1. The expression of ZnT-1 was highest in the cerebral cortex and cerebellum, moderate in the hippocampus, hypothalamus, and olfactory bulb, and lowest in the striatum and septum. In brain sections, ZnT-1-immunoreactive neurons, in particular principle neurons, in the somatosensory cortex, hippocampus, and olfactory bulb, were closely related to synaptic Zn(2+). Robust ZnT-1 immunoreactivity was also observed in cerebellar Purkinje cells. Although the function of the protein in these cells is unclear, in the forebrain, ZnT-1 is strikingly present in cells and regions where significant Zn(2+) homeostasis is required. This finding suggests a protective role for neuronal ZnT-1 in the context of both normal and pathophysiological activity.
Recent evidence for the involvement of zinc in the formation of beta-amyloid plaques in the brain in Alzheimer's disease has led to the establishment of new therapeutic strategies for the degenerative disorder based on metal chelation. The present experiment was conducted on a membrane-permeable zinc chelator, clioquinol (CQ), that has shown potential in initial studies on a mouse model of Alzheimer's disease [1]. The degree of chelatable zinc in mice treated with CQ, delivered by two different routes, was measured using complementary protocols for identifying chelatable zinc: 6-methoxy-8-quinolyl- p-toluenesulfonamide (TSQ) histofluorescence, and selenite autometalography. Mice injected intraperitoneally with CQ showed a dramatic reduction in chelatable zinc in brain, testis, and pancreas. In contrast, mice given CQ orally showed no significant change in levels of chelatable zinc in these tissues. This suggests that CQ administered orally to patients with Alzheimer's disease should not significantly perturb chelatable zinc levels in key organs and may be used over long periods without adverse endocrinological and reproductive effects related to zinc deficiency. In contrast, CQ injected intraperitoneally may be used not only as a tool for investigating chelatable zinc pools but also in a clinical context. For example, injected CQ could be employed in situations requiring the rapid buffering of excessive chelatable zinc following ischemic episodes or brain trauma. Thus, our findings indicate that CQ has considerable potential as a versatile scientific and clinical tool used for selective modulation of zinc pools.
Background: Complete removal of some maxillary sinus pathologies may be challenging. We describe our experience in performing endoscopic inferior meatal antrostomy (EIMA) when approaching certain chronic maxillary sinus disease. Methods: Retrospectively reviewing charts of all patients whose surgery included EIMA between the years 2012 and 2015. EIMA was performed either after routine endoscopic middle meatal antrostomy (EMMA) failed to completely resect the lesion, or as the sole selected approach for specific maxillary pathologies. Results: A total of 56 patients were included in the study. Indications for EIMA included antrochoanal polyps (ACP), maxillary sinus chronic inflammatory disease, maxillary sinus pathology before sinus lift, and odontogenic maxillary sinusitis. In nearly one third of the patients, sinus surgery included only EIMA, of which, the majority were resection of ACP. Follow-up time ranged between 12 and 34 months (mean 14). Residual EIMA opening was variable in size. In the vast majority of our patients, the maxillary sinus cavities were cleared of disease. No major complications and no recirculation were observed in any of the patients. Conclusion: EIMA should be considered for various maxillary sinus pathologies. It provides better access to anteroinferior lesions of the maxillary sinus. EMMA is not mandatory for every maxillary sinus disease.
Parathyroidectomy success rate was similar in patients with primary HPT and MIBI-only or US-only positive localization studies compared to those with matched US/MIBI studies. The results support a clinical algorithm in which positive results from one imaging technique, either MIBI or US, are sufficient to refer a patient for parathyroid surgery.
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