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Antoine Lin Hlne Sudour‐Bonnange Virginie Languillat‐Fouquet Herv Brisse Sabine Irtan Arnauld Verschuur Sabine Sarnacki Estelle Thbaud Aurore Coulomb‐L'Hermine Anne Notz‐Carrre Jean Michon Marie‐Dominique Tabone Ccile Boulanger Isabelle Pellier Claire Freycon Georges Audry Frdrique Dijoud Magali Morelle Christophe Bergeron Claudia Pasqualini 《Pediatric blood & cancer》2020,67(6)
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Calculation of cut‐off values based on the Autoimmune Bullous Skin Disorder Intensity Score (ABSIS) and Pemphigus Disease Area Index (PDAI) pemphigus scoring systems for defining moderate,significant and extensive types of pemphigus
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C. Boulard S. Duvert Lehembre C. Picard‐Dahan J.S. Kern G. Zambruno C. Feliciani B. Marinovic P. Vabres L. Borradori C. Prost‐Squarcioni B. Labeille M.A. Richard S. Ingen‐Housz‐Oro E. Houivet V.P. Werth D.F. Murrell M. Hertl J. Benichou P. Joly the International Pemphigus Study Group 《The British journal of dermatology》2016,175(1):142-149
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Nadge Sarrazin Estelle Chavret-Reculon Corinne Bachelin Mehdi Felfli Rafik Arab Sophie Gilardeau Elena Brazhnikova Elisabeth Dubus Lydia Yaha-Cherif Jean Lorenceau Serge Picaud Serge Rosolen Pierre Moissonnier Pierre Pouget Anne Baron-Van Evercooren 《Proceedings of the National Academy of Sciences of the United States of America》2022,119(10)
White matter disorders of the central nervous system (CNS), such as multiple sclerosis (MS), lead to failure of nerve conduction and long-lasting neurological disabilities affecting a variety of sensory and motor systems, including vision. While most disease-modifying therapies target the immune and inflammatory response, the promotion of remyelination has become a new therapeutic avenue to prevent neuronal degeneration and promote recovery. Most of these strategies have been developed in short-lived rodent models of demyelination, which spontaneously repair and do not reflect the size, organization, and biology of the human CNS. Thus, well-defined nonhuman primate models are required to efficiently advance therapeutic approaches for patients. Here, we followed the consequence of long-term toxin-induced demyelination of the macaque optic nerve on remyelination and axon preservation, as well as its impact on visual functions. Findings from oculomotor behavior, ophthalmic examination, electrophysiology, and retinal imaging indicate visual impairment involving the optic nerve and retina. These visual dysfunctions fully correlated at the anatomical level, with sustained optic nerve demyelination, axonal degeneration, and alterations of the inner retinal layers. This nonhuman primate model of chronic optic nerve demyelination associated with axonal degeneration and visual dysfunction, recapitulates several key features of MS lesions and should be instrumental in providing the missing link to translate emerging repair promyelinating/neuroprotective therapies to the clinic for myelin disorders, such as MS.White matter disorders are a large group of neurological diseases of various origins. Those affecting the central nervous system (CNS), such as multiple sclerosis (MS), lead to failure of nerve conduction, axon degeneration, and result in long-lasting neurological disabilities and tissue atrophy (1). The loss of myelin and healthy axons are believed to be responsible for irreversible damages, which affect a variety of sensory and motor systems, including vision. In MS, 70% of patients are affected with optic neuritis. It can manifest in an acute episode with decreased vision that can recover over several weeks in the majority of patients, while permanent visual symptoms persist in 40 to 60% of patients (2, 3). Chronic optic neuritis can lead to significant optic nerve atrophy and retinal alterations, affecting mainly the retinal inner layers, including the retinal nerve fiber and ganglion cell layers (4). Several visual assays, including visual fields (VF) (5), pupillary responses to luminance and color (pupillary light reflex, PLR) (6), electroretinograms (ERG) (7), optical coherence tomography (OCT) (4, 8), and visual evoked potential (VEP) (9–11) are routinely performed to assess noninvasively the anatomical and electrophysiological perturbations of visual functions in MS. While functional recovery was reported in some patients (9), the lack of anatomical–electrophysiological correlation has prevented to attribute directly these improvements to remyelination or other regenerative processes.Animal models of demyelination induced by toxins, such as lyso-phosphatidylcholine (LPC), are suitable for studying the mechanisms of demyelination/remyelination and developing approaches aimed at promoting CNS remyelination, as they show little inflammation and, therefore, provide means to assay directly the effect of a therapy on remyelination. However, most of these models are developed in short-lived rodents and spontaneously repair, thus lacking the long-lasting progressive degenerative disease context of MS. Besides, these models do not reflect the size or complex organization of the human primate CNS (12). They do not inform on the biology of primate cells, which differs from rodents (13, 14), nor on the security, toxicity, and long-term efficacy of cell- or compound-based promyelinating/neuroprotective therapies. Thus, experiments in long-lived nonhuman primates appear an essential step toward clinical trials.While promoting remyelination may prevent axon degeneration, only a few promyelination strategies have been translated to the clinic (15,16). One of the roadblocks is the absence of studies addressing the clinical benefit of promyelination approaches that could be applied to the clinic (17). A positive correlation between changes in VEP parameters and the degree of demyelination/remyelination was established in rodents (18–21), cats (22), and dogs (23), and exploited successfully to follow promyelination therapies in rodents (24, 25). OCT has been used to identify loss of optic nerve and retinal damages in animal models of myelin disorders as well (23, 26). While used seldomly in nonhuman primates (27), none of these clinical assays were exploited to monitor the impact of optic nerve demyelination in nonhuman primates.We previously demonstrated that LPC injection in the macaque optic nerve induced demyelination with fair axon preservation but little remyelination up to 2 mo post demyelination (28). Taking advantage of the fact that nonhuman primates are long-lived and are able to perform several tasks awake, as do humans, we questioned whether this model could be used to follow the consequence of long-term demyelination on axon preservation, and whether multimodal noninvasive assays, such as VF, VEP, OCT, and PLR could be instrumental to follow/predict the functional and anatomical outcome of optic nerve demyelination. Using multidisciplinary approaches, we provide compelling evidence that LPC-induced demyelination of the macaque optic nerve leads to modified VF, VEP, PLR, and altered inner retinal layers, but preserved photoreceptors based on OCT and ERG. These clinical and functional anomalies were correlated at the histological level with failed remyelination and progressive optic nerve axon loss, followed by neuronal and fiber loss of the inner retinal layers. The postmortem validation of OCT, VEP, and PLR as pertinent markers of optic nerve demyelination/degeneration could further help the translation of therapeutic strategies toward the clinic for myelin diseases associated with long-term demyelination of the optic nerve. 相似文献
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Audrey?Pettifor Amanda?Selin F.?Xavier?Gómez-Olivé Molly?Rosenberg Ryan?G.?Wagner Wonderful?Mabuza James?P.?Hughes Chirayath?Suchindran Estelle?Piwowar-Manning Jing?Wang Rhian?Twine Tamu?Daniel Philip?Andrew Oliver?Laeyendecker Yaw?Agyei Stephen?Tollman Kathleen?Kahn The HPTN protocol team 《AIDS and behavior》2016,20(9):1863-1882
Young women in South Africa are at high risk for HIV infection. Cash transfers offer promise to reduce HIV risk. We present the design and baseline results from HPTN 068, a phase III, individually randomized trial to assess the effect of a conditional cash transfer on HIV acquisition among South African young women. A total of 2533 young women were randomized to receive a monthly cash transfer conditional on school attendance or to a control group. A number of individual-, partner-, household- and school-level factors were associated with HIV and HSV-2 infection. After adjusting for age, all levels were associated with an increased odds of HIV infection with partner-level factors conveying the strongest association (aOR 3.05 95 % CI 1.84–5.06). Interventions like cash transfers that address structural factors such as schooling and poverty have the potential to reduce HIV risk in young women in South Africa. 相似文献
49.
Estelle Mounier-Geyssant Jean-François Barthélemy Lory Mouchot Christophe Paris Denis Zmirou-Navier 《BMC public health》2007,7(1):311
Background
This study describes exposure levels of bakery and pastry apprentices to flour dust, a known risk factor of occupational asthma. 相似文献50.
Antianaerobic activity of moxifloxacin compared with that of ofloxacin,ciprofloxacin, clindamycin,metronidazole and beta-lactams 总被引:4,自引:0,他引:4
Behra-Miellet J Dubreuil L Jumas-Bilak E 《International journal of antimicrobial agents》2002,20(5):366-374
Minimal inhibitory concentrations of moxifloxacin were compared with those of ofloxacin, ciprofloxacin, clindamycin, metronidazole and six beta-lactams for 159 anaerobes isolated from human clinical samples. Unlike other fluoroquinolones, moxifloxacin demonstrated high activity against the 76 strains of the Bacteroides fragilis group as the minimal inhibitory concentration(50) was 0.5 mg/l. Porphyromonas, Prevotella, Fusobacterium and Gram-positive anaerobic cocci were inhibited by 1 mg/l or less of moxifloxacin. It inhibited 93.7, 94.9 and 98% of the 159 strains investigated at concentrations of 1, 2 and 4 mg/l, respectively. Moxifloxacin was more potent than ofloxacin and ciprofloxacin against Gram-positive rods and anaerobic cocci. Its broad anaerobic spectrum in vitro is promising for the treatment of intra-abdominal and respiratory infections. 相似文献