2-Isopropyl-3-methyl­quinoxaline 1,4-dioxide

In the title compound, C12H14N2O2, the quinoxaline ring system and the C atoms of the methylene and methyl substituents lie on a mirror plane. The crystal packing is stabilized by weak π–π inter­actions [centroid–centroid distance = 3.680 (7) Å]

Electron Micrographs of the Nematocysts of Hydra

Seventeen different kinds of nematocysts have been described and classified by Weill (1930) on the basis of the characteristics of the discharged tube. Only four of these are known to be present on hydras, namely, volvents (desmonemes), streptoline glutinants (holotrichous isorhizas), stereoline glutinants (atrichous isorhizes), and penetrants (stenoteles). The discharged penetrant (fig. 1) consists of the capsule a, butt, which is composed of the shaft b, stylet c, spinneret d, and tube e. In the glutinants the tube is attached directly to the tube, and is either spiny (streptoline glutinant) or smooth (stereoline glutinant). In the resting nematocyst all the component parts are inverted and contained within the capsule

NETosis in Alzheimer's Disease

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive deterioration of cognitive functions. Its neuropathological features include amyloid-\u3b2 (A\u3b2) accumulation, the formation of neurofibrillary tangles, and the loss of neurons and synapses. Neuroinflammation is a well-established feature of AD pathogenesis, and a better understanding of its mechanisms could facilitate the development of new therapeutic approaches. Recent studies in transgenic mouse models of AD have shown that neutrophils adhere to blood vessels and migrate inside the parenchyma. Moreover, studies in human AD subjects have also shown that neutrophils adhere and spread inside brain vessels and invade the parenchyma, suggesting these cells play a role in AD pathogenesis. Indeed, neutrophil depletion and the therapeutic inhibition of neutrophil trafficking, achieved by blocking LFA-1 integrin in AD mouse models, significantly reduced memory loss and the neuropathological features of AD. We observed that neutrophils release neutrophil extracellular traps (NETs) inside blood vessels and in the parenchyma of AD mice, potentially harming the blood-brain barrier and neural cells. Furthermore, confocal microscopy confirmed the presence of NETs inside the cortical vessels and parenchyma of subjects with AD, providing more evidence that neutrophils and NETs play a role in AD-related tissue destruction. The discovery of NETs inside the AD brain suggests that these formations may exacerbate neuro-inflammatory processes, promoting vascular and parenchymal damage during AD. The inhibition of NET formation has achieved therapeutic benefits in several models of chronic inflammatory diseases, including autoimmune diseases affecting the brain. Therefore, the targeting of NETs may delay AD pathogenesis and offer a novel approach for the treatment of this increasingly prevalent disease

Histochemical Protein Markers of Monoamine Cell Bodies in Man

Neurons in brainstem and hypothalamus of postmortem, formaldehyde-fixed tissue of 25 healthy controls were studied with a double-staining procedure for the consecutive demonstration of Nissl material and of cytoplasmic spherical bodies, which are rich in basic proteins. The investigation established that the protein bodies are located in cells that correspond to the aminergic neurons demonstrable by histofluorescence. Protein bodies were also found in the neurons of the inferior olive, which are not as a rule included in the aminergic cell groups. The localization of protein bodies is perikaryal and dendritic and, thus, parallels the distribution of monoamines and monoaminesynthesizing enzymes reported in experimental animals. The invariable presence of protein bodies in all aminergic perikarya of control human brains and their absence from nonaminergic neurons permits us to consider them markers of monoamine neurons in man. © 1982 American Medical Association All rights reserved