Eur J Dent Educ. 2002;6 Suppl 3:162-6. 5.1 The demography of oral diseases, future challenges and the implications for dental education.
Zarkowski P, Gyenes M, Last K, Leous P, Clarkson J, McLoughlin J, Murtomaa H, Gibson J, Gugushe T, Edelstein B, Matthews R, Vervoorn M, Van Den Heuvel JL.
University of Detroit, USA.
This Section considered the immense challenges presented by the changing demography of populations (in particular, cross-boundary flow), changing oral and dental disease trends. It also considered the difficulties of gathering data on such information. It then considered how these challenges may affect the education of the dental team in the future. The Section considered the concept of the 'global village' as a representation of the changing world demography. We were at pains to recognize that our role was in considering both emerging and established market economies. In fact, a major part of the Section's activities concentrated on the development of the professional ethic of social responsibility - represented at the local, regional, national and international levels. We considered a finite group of oral and dental diseases, namely dental caries, periodontal diseases, oral cancer and cranio-facial disorders. In addition, we chose to comment on systemic diseases influenced by oral diseases, oral diseases influenced by systemic diseases and iatrogenic diseases (including prion disorders and cross-infection control issues). The Section recognized the profound difference between needs and demands in the provision of oral and dental health care. We considered the concept of best practices within our working remit and named these as: * the gathering of valid data on health trends; * uniformity in the measurement of disease and diagnostic parameters; * the identification of a core curriculum which best addresses an increased awareness of changing demography; and * a multidisciplinary approach to education and research in the context of global collaboration. The Section recognized the enormous potential for global networking with the explosion of information and communication technology. We investigated the requirements in converging towards higher global standards, while accepting and appreciating important regional and continental differences. To this end, the Section has put forward a number of important recommendations and realistic goals.
PMID:_12390274
J Neurosci. 2003 Jan 15;23(2):462-9. In vivo and in vitro neurotoxicity of the human prion protein (PrP) fragment P118-135 independently of PrP expression.
Chabry J, Ratsimanohatra C, Sponne I, Elena PP, Vincent JP, Pillot T.
Institut de Pharmacologie Moleculaire et Cellulaire, Unite Mixte de Recherche 6097, Centre National de la Recherche Scientifique, 06560 Valbonne, France. chabrpmc.cnrs.fr
We recently demonstrated that the 118-135 putative transmembrane domain of prion protein (PrP) exhibited membrane fusogenic properties and induced apoptotic neuronal cell death of rat cortical neurons, independently of its aggregation state. The aim of the present study was to analyze the in vivo neurotoxicity of the prion fragment P118-135 and to evaluate the potential role of the physiological isoform of PrP in the P118-135-induced cell death. Here, we demonstrate that the nonfibrillar P118-135 is cytotoxic to retinal neurons in vivo as monitored by intravitreal inoculation and recording of the electrical activity of retina and tissue examination. Moreover, knock-out PrP gene mice exhibit similar sensitivity to the nonfibrillar P118-135-induced cell death and electrical perturbations, strongly suggesting that cell death occurs independently of PrP expression. Interestingly, a variant nonfusogenic P118-135 peptide (termed P118-135theta) had no effects on in vivo neuronal viability, suggesting that the P118-135-induced cell death is mediated by its membrane destabilizing properties. These data have further been confirmed in vitro. We show that the fusogenic peptide P118-135 induces death of cultured neurons from both wild-type and knock-out PrP gene mice via an apoptotic-mediated pathway, involving early caspase activation and DNA fragmentation. Altogether these results emphasize the neurotoxicity of the fusogenic nonfibrillar PrP transmembrane domain and indicate that fibril formation and PrP expression are not obligatory requirements for neuronal cell death. The use of synthetic prion peptides could provide insights into the understanding of neuronal loss mechanisms that take place during the development of the various types of spongiform encephalopathies.
PMID:_12533606
Neurosci Lett. 2003 Jan 23;336(3):159-62. Copper-dependent generation of hydrogen peroxide from the toxic prion protein fragment PrP106-126.
Turnbull S, Tabner BJ, Brown DR, Allsop D.
Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK.
Oligomeric forms of many of the aggregating proteins associated with neurodegenerative diseases are toxic to cultured cells. We have shown recently that Abeta and alpha-synuclein can both induce the formation of hydroxyl radicals following incubation in solution, upon the addition of Fe(II). Thus, they appear to generate hydrogen peroxide, which is converted to hydroxyl radicals via the Fenton reaction. Here we show that the widely studied toxic peptide fragment of the prion protein, PrP106-126, has exactly the same property, but only in the presence of copper ions. Since the aggregation and toxicity of PrP106-126 have been reported to be critically dependent on copper binding, our data suggest that the published cytotoxic effects of this peptide could also be due to its ability to generate hydrogen peroxide.
PMID:_12505617
Brain. 2002 Nov;125(Pt 11):2558-66. Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology.
Tschampa HJ, Herms JW, Schulz-Schaeffer WJ, Maruschak B, Windl O, Jastrow U, Zerr I, Steinhoff BJ, Poser S, Kretzschmar HA.
Department of Neuropathology, Georg-August University, Goettingen, Germany.
The pathogenesis underlying the typical findings in Creutzfeldt-Jakob disease (CJD) such as periodic EEG changes or myoclonus is not fully understood. The thalamus possesses a high density of inhibitory neurones and serves as a crucial pacemaker of rhythmic EEG activity. As inhibitory neurones expressing parvalbumin (PV) are reduced in the cerebral cortex and hippocampus in sporadic CJD (sCJD), we studied the distribution and number of PV-immunoreactive neurones in sCJD thalami in order to determine whether damage to them could account for certain clinical findings. Immuno histochemical analysis was performed on the thalami from 21 sCJD patients and five controls. The number of PV+ neurones was counted in the thalamic nuclei and compared with clinical and molecular findings. In sCJD patients, PV+ neurones were significantly reduced in the ventrolateral posterior (VLp), ventrolateral anterior (VLa), anteroventral (AV), lateral dorsal (LD), mediodorsal (MD) and reticular (Re) thalamic nuclei (P < 0.05). The VLp was especially damaged in sCJD patients with homozygosity for methionine at codon 129 and scrapie prion protein (PrP(Sc)) type 1. Patients with typical EEG changes [periodic sharp wave complexes (PSWCs)] and myoclonus had a predominant loss of PV+ cells in the reticular thalamic nucleus. In conclusion, our data support the hypothesis that the damage to PV-immunoreactive neurones determines the generation of certain typical clinical features of CJD, i.e. PSWCs associated with myoclonus.
Hair loss is a problem of personal issues. Examining the factors of hair growth may
shed light on how hair loss might occur.
How long can hair grow before it stops growing eventually?
Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of
hair growth as well as hair loss.
The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.