Tratados historicos, politicos, ethicos y religiosos de la monarchia de China : descripcion breue de aquel imperio y exemplos raros de emperadores y magistrados del : con narracion difusa de varios sucessos y cosas singulares de otros reynos ... : añadense los decretos pontificios y proposiciones calificadas en Roma para la mission Chinica ; y vna Bula de ... Clemente X en fauor de los missionarios/

El vol. II se publicó con tít.: "Controuersias antiguas y modernas de la mission de la gran China ...", según Quetif, J. (Fuente: Wellcome Library: This work was to consist of three volumes. The 2d vol, printed complete (?) Madrid 1679, is supposed to have been suppressed by the Spanish inquisition. A copy without t.-p., containing p. 1-668, is described in the Bibliotheca grenvilliana, p. 484. Another copy, in the same incomplete condition, quoted by Quaritch under no 61 of his Rough list no. 24, is now in the possession of H. Cordier. The 3d vol. was never published. cf. Cordier, Bibliotheca sinica, 2d ed., Paris, 1904; and Medina, Bibl. hisp. americana.)

Secretos raros de artes y oficios : obra útil a toda clase de personas /

Es el tomo 1.

Secretos raros de artes y oficios.

Mode of access: Internet.

Secretos raros de artes y oficios : Tomo X.

Mode of access: Internet.

Vidas de los padres del desierto de Dunas : en que se refieren exemplos raros y muchas antiguedades de varias prouincias, en particular de las de Flandes /

Mode of access: Internet.

Breviario medico y chyrurgico, de nuevos y raros secretos /

Mode of access: Internet.

Secretos raros de artes y oficios : Tomo XII.

Mode of access: Internet.

Documentos inéditos ó muy raros para la historia de México,

Vols. 6-36 edited by Genaro García.

El Decamerón español ó Colección de varios hechos históricos raros y divertidos /

Contiene: T. II: El negro Juan Latino o Cuidado con los maestros. Isaura ò Mi corto viaje. La pérfida o Enriqueta/Lucía. Ningun hombre quiere así ([4], 226, [1] p.)

Catálogo de libros raros y curiosos que se hallan de venta en la librería de Gabriel Sánchez ...

Mode of access: Internet.

Secretos raros de artes y oficios.

Mode of access: Internet.

Um caso pediátrico de tuberculose miliar: achados raros e evolução atípica

Introdução: A tuberculose miliar resulta da disseminação linfohematogénica do Mycobacterium tuberculosis, sendo uma manifestação grave da infeção. Caso clínico: Criança de 9 anos, género feminino, com his¬tória de febre prolongada. O diagnóstico de tuberculose miliar foi colocado após telerradiografia torácica com infiltrado reticu¬lonodular difuso bilateral, e corroborado pelo achado de tubér¬culos coroideus no olho direito e visualização de bacilos álcool¬ ¬ácido resistentes em amostra de suco gástrico. Detetaram¬-se tuberculomas cerebrais na ressonância magnética. Isolou¬se Mycobacterium tuberculosis multissensível em amostras de suco gástrico. Após mais de 40 dias de tratamento, persistia a febre e baciloscopia positiva. Foi excluída infeção pelo vírus da imunodeficiência humana. Não foram detetadas complicações. Posteriormente, a evolução clínica foi favorável. Discussão/Conclusão: A tuberculose mantém-¬se um diag¬nóstico relevante na criança com febre prolongada. A associa¬ção da imagem torácica, baciloscopias positivas e tubérculos coroideus foram fundamentais para a celeridade do diagnóstico e implementação do tratamento. Reforça¬-se a importância de manter elevado índice de suspeição para uma patologia que tem tratamento.

Con el Olaya Herrera, por que seremos tan raros, señor presidente

Fondo Margaritainés Restrepo

Molecular diagnosis of Huntington disease in Brazilian patients

Huntington disease (HD) is a progressive neurodegenerative disorder with autosomal dominant inheritance, characterized by choreiform movements and cognitive impairment. Onset of symptoms is around 40 years of age and progression to death occurs in approximately 10 to 15 years from the time of disease onset. HD is associated with an unstable CAG repeat expansion at the 5' and of the IT15 gene. We have genotyped the CAG repeat in the IT15 gene in 44 Brazilian individuals (42 patients and 2 unaffected family members) belonging to 34 unrelated families thought to segregate HD. We found one expanded CAG allele in 32 individuals (76%) belonging to 25 unrelated families. In these HD patients, expanded alleles varied from 43 to 73 CAG units and normal alleles varied from 18 to 26 CAGs. A significant negative correlation between age at onset of symptoms and size of the expanded CAG allele was found (r=0.6; p=0.0001); however, the size of the expanded CAG repeat could explain only about 40% of the variability in age at onset (r2=0.4). In addition, we genotyped 25 unrelated control individuals (total of 50 alleles) and found normal CAG repeats varying from 16 to 33 units. The percentage of heterozigocity of the normal allele in the control population was 88%. In conclusion, our results showed that not all patients with the HD phenotype carried the expansion at the IT15 gene. Furthermore, molecular diagnosis was possible in all individuals, since no alleles of intermediate size were found. Therefore, molecular confirmation of the clinical diagnosis in HD should be sought in all suspected patients, making it possible for adequate genetic counseling.

Six new cases confirm the clinical molecular profile of complete combined 17α-hydroxylase/ 17,20-lyase deficiency in Brazil

In 2004, Costa-Santos and cols. reported 24 patients from 19 Brazilian families with 17α-hydroxylase deficiency and showed that p.W406R and p.R362C corresponded to 50% and 32% of CYP17A1 mutant alleles, respectively. The present report describes clinical and molecular data of six patients from three inbred Brazilian families with 17α-hydroxlyse deficiency. All patients had hypogonadism, amenorrhea and hypertension at diagnosis. Two sisters were found to be 46,XY with both gonads palpable in the inguinal region. All patients presented hypergonadotrophic hypogonadism, with high levels of ACTH (> 104 ng/mL), suppressed plasmatic renin activity, low levels of potassium (< 2.8 mEq/L) and elevated progesterone levels (> 4.4 ng/mL). Three of them, including two sisters, were homozygous for p.W406R mutation and the other three (two sisters and one cousin) were homozygous for p.R362C. The finding of p.W406R and p.R362C in the CYP17A1 gene here reported in additional families, confirms them as the most frequent mutations causing complete combined 17α-hydroxylase/17,20-lyase deficiency in Brazilian patients.