Functionalization of Doped ZnO through Solution Route Synthesis: A study Using Spectroscopy & Density of States

ZnO is one of the widely studied materials for multidimensional applications, viz. semiconductor material, catalysts, solid-state devices, etc. The primary functionalization is carried out by doping the required element (s) within the ZnO matrix, which can exist in either zinc blend or the wurtzite form. The present research reports synthesis of ZnO doped by Cr, Y, and Eu at two dopant concentrations. The synthesis technique is optimized using dual fuels during solution auto combustion synthesis. Detailed analysis of X-ray diffraction study reveals a comparative analysis of the peak area and FWHM magnitude. The influence of the doping element on the ZnO is studied in terms of UV and photoluminescence spectra. The highest bandgap of 3.08 eV is reported with Eu as the dopant within ZnO compared to Y, which shows lower bandgap energy of 2.44 eV. The density of states study of ZnO is found to be continuous with a significant nodal region within -3.4 to -2.4 eV. However, in the doped systems, irrespective of the dopant, nodal regions are more with specific band regions in the ZnO-Y/ZnO-Eu system. Irrespective of dopant type, doping within ZnO significantly influences the states in the conduction band.

Behind the pathology of macrophage-associated demyelination in inflammatory neuropathies: demyelinating Schwann cells

In inflammatory peripheral demyelinating disorders, demyelination represents segmental demyelination in which the myelin sheath of a myelinating Schwann cell (SC) is completely removed by macrophages or a partial myelin degeneration in the paranode occurring due to autoantibodies attacking the node/paranode. For the segmental demyelination from living myelin-forming SCs, macrophages infiltrate within the endoneurium and insinuate between myelin lamellae and the cytoplasm of SCs, and the myelin is then removed via phagocytosis. During the macrophage invasion into the SC cytoplasm from the node of Ranvier and internodal areas, the attacked SCs do not remain quiescent but transdifferentiate into inflammatory demyelinating SCs (iDSCs), which exhibit unique demyelination pathologies, such as myelin uncompaction from Schmidt-Lanterman incisures with myelin lamellae degeneration. The longitudinal extension of this self-myelin clearance process of iDSCs into the nodal region is associated with the degeneration of nodal microvilli and paranodal loops, which provides a potential locus for macrophage infiltration. In addition to the nodal intrusion, macrophages appear to be able to invade fenestrated internodal plasma membrane or the degenerated outer mesaxon of iDSC. These SC demyelination morphologies indicate that the SC reprogramming to iDSCs may be a prerequisite for macrophage-mediated inflammatory demyelination. In contrast, paranodal demyelination caused by autoantibodies to nodal/paranodal antigens does not result in iDSC-dependent macrophage infiltration and subsequent segmental demyelination. In the context of inflammatory demyelination, the novel perspective of iDSCs provides an important viewpoint to understand the pathophysiology of demyelinating peripheral neuropathies and establish diagnostic and therapeutic strategies.

Early clinicopathologic description of nodoparanodopathy in the 19th century

Nodoparanodopathy is a recent concept in the field of peripheral neuropathy, corresponding to peripheral nerve disorders stemming from an autoimmune attack directed and limited to the nodal region. This concept was identified using modern techniques of electrophysiology, immunology, and pathology (including electron microscopy). We present here what we believe to be the earlier well-documented case of nodoparanodopathy in the medical literature, based on an article written by Samuel Gilbert Webber (1838–1926) in 1884.

Autoimmune nodo-paranodopathies of peripheral nerve: the concept is gaining ground

Peripheral neuropathies are classified as primarily demyelinating or axonal. Microstructural alterations of the nodal region are the key to understand the pathophysiology of neuropathies with antibodies to gangliosides and the new category of nodo-paranodopathy has been proposed to better characterise these disorders and overcome some inadequacies of the dichotomous classification. Recently, the research in autoimmune neuropathies has been boosted by reports of patients carrying immunoglobulin G4 antibodies against paranodal axo–glial proteins with distinct phenotypes and showing loss of transverse bands, terminal myelin loop detachment, nodal widening and axonal loss. These patients have been classified up to now as chronic inflammatory demyelinating polyradiculoneuropathy but, in our opinion, better fit into the nodo-paranodopathy category because nerve injury is due to dismantling of the paranode, segmental de-remyelination is absent and the pathogenic mechanism is not inflammatory. Evidence from nerve conductions and electron microscopy studies in patients and mutant animal models can reconcile the apparent contrast between the electrophysiological ‘demyelinating’ features, explainable just by the paranodal involvement and the axonal pathology. These patients broaden the autoimmune nodo-paranodopathy category and re-emphasise the usage of the term that pointing to the site of nerve injury reminds specific pathophysiological mechanisms, reconciles contrasting electrophysiological and pathological findings, and avoids misdiagnosis and taxonomic confusion. In our opinion, the nodo-paranodopathy term more adequately classifies the peripheral nerve disorders due to an autoimmune attack directed and limited to the nodal region integrating the traditional classification of peripheral neuropathies.