Sobranie sochineniĭ.

t.1. Iskra Bozhʹi︠a︡. Tʹma. Manzhazha. Evreĭka. Volga.--t.2-3. Pugachevt︠︡sy.--t.4. Naĭdenysh. Samokrutka.--t.5. Na Moskvi︠e︡.--t.6. Peterburgskoe d︠ie︡ĭstvo.--t.7. Ataman Ust︠ia︡. Svadebnyĭ bunt.--t.8. Puteshestvenniki. Madonna. Chetvertoe izmi︠e︡renie.--t.9. Graf T︠ia︡tin Baltiĭskiĭ. Shirʹ i makh. Pozt nami︠e︡stnik.--t.10. Sluzhitelʹ Boga. Vi︠e︡dunʹi︠a︡.--t.11. Kudesnik. I︠a︡unkundze.--t.12. Samozvanka.--t.13. Brigadirckai︠a︡ vnuchka. Kruto︠ia︡rskai︠a︡. Donskie gishpan︠t︡sy.--t.14. Baryni-krestʹi︠a︡nki. Freĭlina Marĭi Leshchinskoĭ.--t.15. Dzhettatura. Pan krulʹ. Zaira.--t.16. Andaluzski︠ia︡ legendy. Los novios. Kamerʺ-i︠u︡ngfera. Filozof.--t.17. P︠ia︡toe koleso. Bylye gusary. Izbushka na kurʹikh nozhkakh. Senatskĭĭ sekretarʹ.--t.18-19. Nevi︠e︡sta fin de siècle. Melkie pazskazy.--t.20. Nozai︠a︡ Sandrilʹona.--t.21. Izlomannye li︠u︡di. Fran︠t︡suz. Rubikon.--t.22. Zkzotniki. Vahi︠a︡. Prestizh.--t.24. Las Españas.--t.25. Vladimĭrskĭe Monomakhi.--t.26. Nozvanet︠︡s. Podlozhnyĭ samoubiĭ︠t︡sa. Una niña. Pandurochka. Sa-e-ĭĭ Pa-ich. Mashkerad. V muromskikh li︠e︡sakh.--t.27. Zmi︠e︡ĭ-Gorynych.

Conversaciones de Cleandro y de Eudoxio sobre las Cartas al provincial /

Mode of access: Internet.

Biblia hebraica, secundum ultimam editionem Jos. Athiae, a Johanne Leusden denuo recognitam, recensita atque ad Masoram, et correctiores Bombergi, Stephani, Plantini, aliorumque editiones, exquisite adornata variisque notis illustrata ab Everardo van der Hooght.

Bound with Frey, J.S.C.F. Lexicon. Londini, 1814.

Katkov i ego vremi͡a︡.

Romanized.

Moskovskīĭ sbornik /

T͡Serkovʹ i gosudarstvo.--Novai͡a demokratīi͡a.--Velikai͡a lozhʹ nashego vremeni.--Sud prisi͡azhnykh.--Pechatʹ.--Narodnoe prosvi͡eshchenīe.--Gerbert Spenser o narodnom vospitanīi.--Zakon.--Boli͡ezni nashego vremeni.--Znanīe i di͡elo.--Vi͡era.--Idealy nevi͡erīi͡a.--Novai͡a vi͡era i novye braki.--Novoe khristīanstvo bez Khrista.--Dukhovnai͡a zhiznʹ.--T͡Serkovʹ.--Kharaktery.--Drevnīe klassicheskīe i͡azyki v shkoli͡e. S. Rachinskago.--Vlastʹ i nachalʹstvo.--Iz Karleĭli͡a.--Gladston ob osnovakh vi͡ery i nevi͡erīi͡a.--Di͡ela i dni.

Syllabus of dermal pathology.

Course 3; Rewritten and rev. by Robert Forbis, Elson B. Helwig and Hamilton Montgomery.

Die heilige Schrift : nach dem masoretischen Text neu übersetzt und erklärt, nebst einer Einleitung

von Dr. S. Bernfeld

Die heilige Schrift : nach dem masoretischen Text neu übersetzt und erklärt, nebst einer Einleitung

von Dr. S. Bernfeld

Salivary Gland and Tooth Abnormalities Massively Increase Caries Susceptibility in A Mouse Model of Cleft Lip/Palate

Thesis (Ph.D.)--University of Washington, 2016-04

Epidermal Growth Factor Gene (EGF) Polymorphism and Risk of Melanocytic Neoplasiay

A common single nucleotide polymorphism (SNP) in the 5' untranslated region (5'UTR) of the epidermal growth factor (EGF) gene modulates the level of transcription of this gene and hence is associated with serum levels of EGF. This variant may be associated with melanoma risk, but conflicting findings have been reported. An Australian melanoma case-control sample was typed for the EGF+61A>G transversion (rs4444903). The sample comprised 753 melanoma cases from 738 families stratified by family history of melanoma and 2387 controls from 645 unselected twin families. Ancestry of the cases and controls was recorded, and the twins had undergone skin examination to assess total body nevus count, degree of freckling and pigmentation phenotype. SNP genotyping was carried out via primer extension followed by matrix-assisted laser desorption time of flight (MALDI-TOF) mass spectroscopy. The EGIF+61 SNP was not found to be significantly associated with melanoma status or with development of nevi or freckles. Among melanoma cases, however, G homozygotes had thicker tumors (p=0.05), in keeping with two previous studies. The EGF polymorphism does not appear to predispose to melanoma or nevus development, but its significant association with tumor thickness implies that it may be a useful marker of prognosis.

Interactive effects of MC1R and OCA2 on melanoma risk phenotypes

The relationships between MC1R gene variants and red hair, skin reflectance, degree of freckling and nevus count were investigated in 2331 adolescent twins, their sibs and parents in 645 twin families. Penetrance of each MC1R variant allele was consistent with an allelic model where effects were multiplicative for red hair but additive for skin reflectance. Of nine MC1R variant alleles assayed, four common alleles were strongly associated with red hair and fair skin (Asp84Glu, Arg151Cys, Arg160Trp and Asp294His), with a further three alleles having low penetrance (Val60Leu, Val92Met and Arg163Gln). These variants were separately combined for the purposes of this analysis and designated as strong 'R' (OR=63.3; 95% CI 31.9-139.6) and weak 'r ' (OR=5.1; 95% CI 2.5-11.3) red hair alleles. Red-haired individuals are predominantly seen in the R/R and R/r groups with 67.1 and 10.8%, respectively. To assess the interaction of the brown eye color gene OCA2 on the phenotypic effects of variant MC1R alleles we included eye color as a covariate, and also genotyped two OCA2 SNPs (Arg305Trp and Arg419Gln), which were confirmed as modifying eye color. MC1R genotype effects on constitutive skin color, freckling and mole count were modified by eye color, but not genotype for these two OCA2 SNPs. This is probably due to the association of these OCA2 SNPs with brown/green not blue eye color. Amongst individuals with a R/R genotype (but not R/r), those who also had brown eyes had a mole count twice that of those with blue eyes. This suggests that other OCA2 polymorphisms influence mole count and remain to be described.

Expression and localization of mutant p16 proteins in melanocytic lesions from familial melanoma patients

Little is known about the correlation between the loss of p16 expression and tumor progression in familial melanoma; no systematic study has been conducted on p16 expression in melanocytic tumors from patients carrying germline CDKN2A mutations. We analyzed 98 early primary lesions from familial patients, previously tested for germline CDKN2A status, by quantitative immunohistochemistry using 3 p16 antibodies. We found that p16 expression was inversely correlated with tumor progression and was significantly lower in melanomas,. including in situ lesions, than in nevi. Of other features analyzed, tumor thickness showed the most significant correlation with p16 levels. Lesions from mutation-negative patients displayed combined nuclear and cytoplasmic staining. However, some mutation-positive lesions (ie, G101W, 113insR, M53I, R24P, and 33ins24), including benign nevi, showed nuclear mislocalization, confirming previous studies suggesting that subcellular distribution indicates functional impairment of p16. (C) 2004 Elsevier Inc. All rights reserved.

The jigsaw sign. A reliable indicator of congenital aetiology in os odontoideum

There is evidence in the literature for both a congenital and a post-traumatic aetiology for os odontoideum. In no series published to date has CT been used to aid in the diagnosis. This is a prospective study of the history of trauma and presence of diagnostic features on CT of 18 consecutive cases with os odontoideum. Our objective was to derive clinically useful radiological features enabling accurate differentiation between congenital and post-traumatic aetiologies. A mid-sagittal CT reconstruction of the atlanto-dens joint was obtained. Hypertrophy of the anterior arch of the atlas was quantified by measurement of the arch-peg-area ratio. The presence of dysplastic features (a positive jigsaw sign) of the atlanto-axial joint were noted. These included narrowing of the cartilage space and interdigitation of the two joint surfaces. A history of a potential traumatic aetiology was only obtained in one of the 18 (6%) in our series. A significant elevation of the arch-peg ratio was found when comparing this series to 85 controls. And a positive jigsaw sign was observed in 75% of cases. These features were not seen in paediatric cases of atlanto-axial instability, including odontoid non-union. In conclusion, an elevated arch-peg ratio and the presence of a jigsaw sign are sensitive and specific diagnostic criteria for os odontoideum. This series supports a congenital aetiology for this condition.

Characterization of tumour-infiltrating lymphocytes and apoptosis in colitis-associated neoplasia: comparison with sporadic colorectal cancer

The development of colorectal cancer is a major complication for patients with chronic idiopathic colitis. Colitis-associated tumours tend to occur at a younger age and be more aggressive than sporadic colorectal cancers. While we have previously associated the presence of tumour-infiltrating lymphocytes (TILs) and increased apoptosis in sporadic colorectal cancer with high-level microsatellite instability and improved prognosis, little is known of the relationship between these variables in colitis-associated colorectal cancer. The aim of this study was to correlate TILs and tumour cell apoptosis in colitis-associated neoplasms stratified according to microsatellite instability. Twenty tumour and 11 dysplastic samples resected from 21 patients with long-standing colitis were analysed for microsatellite instability at 10 microsatellite markers. TIL distribution (CD3, CD8) and function (granzyme B) were quantified by immunohistochemistry. Neoplastic cell apoptosis was assessed using the M30 CytoDEATH antibody. These findings were compared with 40 microsatellite stable (MSS) sporadic colorectal cancers previously evaluated for TILs and neoplastic apoptosis. Low-level microsatellite instability was found in 1/20 colitis-associated tumours. All other colitis-associated lesions were designated MSS. CD3(+) and CD8(+) TIL counts were significantly higher in colitis-associated lesions compared with NISS sporadic colorectal cancer (p < 0.0001, p = 0.001 respectively). Despite their higher TIL density, colitis-associated tumours were more likely to present late (Dukes' stage C or D) (P = 0.02). Functionally, colitis-associated TILs demonstrated significantly less granzyme B expression compared to sporadic cancers (p = 0.002). The level of tumour cell apoptosis was similar between the two groups (sporadic, 1.53%; colitis cancers, 1.45%). In conclusion, NISS colitis-associated tumours have a higher prevalence of CD3(+)/CD8(+) TILs but no associated increase in tumour cell killing by apoptosis. Unlike cytotoxic T cells in sporadic colorectal cancer, TILs do not appear to enhance the prognosis of colitis-associated colorectal cancer. This may be related to an impairment of granzyme B expression within these lesions. Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Liver fluke-associated and sporadic cholangiocarcinoma: an immunohistochemical study of bile duct, peribiliary gland and tumour cell phenotypes

Aim: To compare cell phenotypes displayed by cholangiocarcinomas and adjacent bile duct lesions in patients from an area endemic in liver-fluke infestation and those with sporadic cholangiocarcinoma. Methods: 65 fluke-associated and 47 sporadic cholangiocarcinomas and 6 normal livers were studied. Serial paraffin-wax sections were stained immunohistochemically with monoclonal antibodies characterising a Brunner or pyloric gland metaplasia cell phenotype (antigens D10 and 1F6), intestinal goblet cells (antigen 17NM), gastric foveolar apomucin (MUC5AC), a gastrointestinal epithelium cytokeratin (CK20) and the p53 protein. Results: 60% of the 112 cholangiocarcinomas expressed antigen D10, 68% MUC5AC, 33% antigen 17NM and 20% CK20; 37% showed overexpression of p53. When present together in a cholangiocarcinoma, cancer cells expressing D10 were distinct from those displaying 17NM or MUC5AC. Many more fluke-associated cholangiocarcinomas than sporadic cholangiocarcinomas displayed 17NM and p53 expression. Most cases of hyperplastic and dysplastic biliary epithelium expressed D10 strongly. Pyloric gland metaplasia and peribiliary glands displayed D10 and 1F6, with peribiliary gland hyperplasia more evident in the livers with fluke-associated cholangiocarcinoma; goblet cells in intestinal metaplasia stained for 17NM. No notable association of expression between any two antigens (including p53) was found in the cancers. Conclusions: Most cases of dysplastic biliary epithelium and cholangiocarcinoma display a Brunner or pyloric gland cell phenotype and a gastric foveolar cell phenotype. The expression of D10 in hyperplastic and dysplastic epithelium and in cholangiocarcinoma is consistent with a dysplasia-carcinoma sequence. Many more fluke-associated cholangiocarcinomas than sporadic cholangiocarcinoma display an intestinal goblet cell phenotype and overexpress p53, indicating differences in the aetiopathology of the cancers in the two groups of patients.