186,597 research outputs found
Global beautyscapes. An innovation-centered netnography of Chinese skin care and cosmetics consumers
No full textThis chapter draws from a commercial netnography we conducted to explore Chinese cosmetics consumers’ changing notions of female beauty. Specifically, we were tasked with informing the new product development efforts of ArtCosmetics, an Italian B2B contract manufacturer operating in the global cosmetics market. We use the project to discuss how we used a team of researchers to collect, interpret, translate, and understand data about the central role of cultural codes of beauty in cosmetics tastes and routines. In response to the complexity involved in the project, we improvised a netnographic research design. As a result, our netnography with ArtCosmetics was a methodological and intellectual journey that challenged us in many ways: transnational and effective sampling, appropriately bricolaged research design, collecting and comprehending the nuance of foreign language and foreign culture data from new platforms, resolving heterogenous data, managing vast cultural complexity, and translating sophisticated ethnographic finding into pragmatic consumer, brand, and new product development insights. Today, Chinese notions of beauty and identity are firmly rooted in historical ethnic and national identities but are also fluidly global. Adapting netnography to this fluid transnational context allowed us to grasp a flow of beautyscapes, infoscapes, brandscapes, selfscapes, and usagescapes as shifting elements in a primordial process that oscillates between East and West, traditional and futuristic, and symbolic and functional
Experimental diabetic neuropathy: impairment of slow transport with changes in axon cross-sectional area.
No full textAnalysis of slow axonal transport in the sciatic and primary visual systems of rats with streptozotocin-induced diabetes of 4-6 weeks duration showed impairment of the transport of neurofilament subunits, tubulin, actin, and a 30- and a 60-kDa polypeptide in both systems. The degree of impairment was not uniform. Transport of polypeptide constituents of the slow component b, such as the 30- and 60-kDa polypeptides, appeared to be more severely affected than the transport of constituents of the slow component a, such as neurofilaments. Morphometric analysis of sciatic axons revealed a proximal increase and a distal decrease of axonal cross-sectional area. It is proposed that impairment of axoplasmic transport and changes of axonal size are related. Transport impairment results in a larger number of neurofilaments, microtubules, and other polypeptides in the proximal region of the axon, which increases in size, whereas fewer neurofilaments, microtubules, and other polypeptides reach the distal axons that show a size decrease. Such changes in axonal transport and area are likely to occur in other diabetic animal models and in human diabetes
Giant axonal neuropathy: acceleration of neurofilament transport in optic axons.
No full textGiant axonal neuropathies are a group of acquired and inherited human diseases morphologically characterized by accumulation of neurofilaments (NF) in enlargements of preterminal regions of central and peripheral axons. Slow axonal transport was studied in the optic systems of rats treated with 2,5-hexanedione, a toxic compound that produces an experimental model of giant axonal neuropathy. The transport rate of NF and of two other polypeptides of M(r) 64,000 and 62,000 were selectively increased. Other components of the slow axonal transport were not affected. Acceleration of labeled NF was also observed when 2,5-hexanedione was given after [35S]methionine administration. Morphometric analysis revealed that the number of NF and the axon size were decreased in regions of optic axons proximal to the enlargements. It is suggested that acceleration of NF transport leads to a longitudinal redistribution of NF: NF decrease proximally and increase distally, forming NF-containing enlargements. Evidence was obtained that polypeptides of M(r) 64,000 and 62,000 are cytoskeletal components related to intermediate filaments, normally migrating with the component a of the slow axonal transport. The 2,5-hexanedione axon may provide insight into the pathogenesis of inherited and acquired giant axonal neuropathies and offers a model to investigate the relationship between number of NF and axonal size in central axons
Alz 50 recognizes abnormal filaments in Alzheimer's disease and progressive supranuclear palsy.
No full textStatus spongiosus of rat central nervous system induced by actinomycin D
No full textThe effect on central myelin of Actinomycin D, an RNA--and, secondarily, a protein-synthesis inhibitor, has been studied by light and electron microscopy. The intracranial injection of this drug produced an extensive status spongiosus of the white matter in the cerebrum, cerebellum, brain stem and optic nerve within 48 h. The status spongiosus was due to vacuole formation within the myelin sheath and to enlargement of the extracellular space. Three types of vacuoles were observed: (a) the most common varieties formed between the inner tongue and the remainder of the myelin sheath; (b) a second variety formed by enlargement of the periaxonal space with separation of the axon from its myelin sheath, and (c) a less common type of vacuolization was due to splitting of the myelin lamellae at the interperiod line to form large intramyelinic vacuoles. Myelinic vacuoles were preceded by nuclear and cytoplasmic changes in oligodendrocytes, which included nucleolar segregation, disaggregation, and diminution in number of ribosomes. These changes were similar to those previously reported in a variety of cells exposed to Actinomycin D. It is suggested that myelin vacuoles result secondarily from the Actinomycin D inhibitory effect on oligodendroglial RNA--and protein-synthesis, rather than from a direct effect of this drug on the myelin sheath
Chemical neurotoxins accelerating axonal transport of neurofilaments.
No full textno abstract availabl
Variably Protease-Sensitive Prionopathy: a Novel Disease of the Prion Protein
No full textVariably protease-sensitive prionopathy (VPSPr) is a novel disease involving the prion protein (PrP) that has clinical similarities with non-Alzheimer's dementias especially frontotemporal dementia, diffuse Lewis body disease, and normal pressure hydrocephalus. VPSPr can be distinguished from sporadic Creutzfeldt-Jakob disease (sCJD) especially for the characteristics of the abnormal PrP. Furthermore, although VPSPr like sCJD affects patients with the three PrP genotypes as determined by the common methionine/valine polymorphism, the allelic prevalence is very different in the two diseases. These findings suggest that VPSPr is basically different from classical prion diseases such as sCJD being perhaps more akin to other neurodegenerative dementia
- …
