RESUMEN
This paper focuses on the Gap Rock lighthouse, a legendary maritime infrastructure built 130 years ago in the Chinese territory and an early example of joint venture among the Qing Dynasty, the British Empire and the Hong Kong Colonial Government over a course of two decades. Based on 4 years of cross-territorial archival and field research as well as in-depth interviews with descendants of two key stakeholders, the origin of this lasting legacy on the sea is traced, followed by a detailed account of its challenging processes of planning, design and construction, and of the considerable damage to the compound by a severe typhoon in 1893. A qualitative analysis of the key contributing factors of the damage was conducted by taking into consideration the Island's unique topography and the historical records of territorial weather reports. A re-construction of the typhoon impact on the Lighthouse is presented to explain the possible mistakes in its siting and design that eventually caused the severe damage. This serves as a reminder of the significance of a thorough geographical investigation for any infrastructure for all construction professionals in the face of climatic change. This article is part of the theme issue 'Environmental loading of heritage structures'.
RESUMEN
We report the generation of transgenic mice designed to facilitate the study of vascular and nonvascular smooth muscle biology in vivo. The smooth muscle myosin heavy chain (smMHC) promoter was used to direct expression of a bicistronic transgene consisting of Cre recombinase and enhanced green fluorescent protein (eGFP) coding sequences. Animals expressing the transgene display strong fluorescence confined to vascular and nonvascular smooth muscle. Enzymatic dissociation of smooth muscle yields viable, fluorescent cells that can be studied as single cells or sorted by FACS for gene expression studies. smMHC/Cre/eGFP mice were crossed with ROSA26/lacZ reporter mice to determine Cre recombinase activity; Cre recombinase was expressed in all smooth muscles in adult mice, and there was an excellent overlap between expression of the recombinase and eGFP. Initial smooth muscle-specific expression of fluorescence and Cre recombinase was detected on embryonic day 12.5. These mice will be useful to define smooth muscle gene function in vivo in mice, for the study of gene function in single, live cells, and for the determination of gene expression in vascular and nonvascular smooth muscle.
Asunto(s)
Integrasas/genética , Músculo Liso/metabolismo , Proteínas Virales/genética , Animales , Animales Recién Nacidos , Embrión de Mamíferos/metabolismo , Femenino , Expresión Génica , Regulación del Desarrollo de la Expresión Génica , Genotipo , Proteínas Fluorescentes Verdes , Integrasas/metabolismo , Proteínas Luminiscentes/genética , Proteínas Luminiscentes/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Microscopía Fluorescente , Cadenas Pesadas de Miosina/genética , Regiones Promotoras Genéticas/genética , Proteínas Recombinantes de Fusión/genética , Proteínas Recombinantes de Fusión/metabolismo , Factores de Tiempo , Proteínas Virales/metabolismoRESUMEN
The protective effects of tetrandrine (Tet) on calcium paradox in isolated Langendorff's heart in rats were investigated. Tet was shown to reduce the release of lactate dehydrogenase (LDH) and protein from myocardial tissues and the loss of K+, Mg2+ and accumulation of Ca2+, Na+ in myocardial tissues during calcium paradox in a concentration-dependent manner. Decrease of Fe and Zn and increase of Cu in myocardial tissues were observed in calcium paradox and Tet 27 mumol/L was found to inhibit the decrease of Fe and Zn. In addition, Tet was also found to inhibit the decrease of Ca2+ and the increase of Na+ in myocardial tissues during calcium-free perfusion. These results indicate that Tet can protect the myocardium against calcium paradox by stabilizing cellular membrane and inhibiting the influx of Ca2+.
Asunto(s)
Alcaloides/farmacología , Bencilisoquinolinas , Bloqueadores de los Canales de Calcio/farmacología , Calcio/metabolismo , Animales , Femenino , Técnicas In Vitro , L-Lactato Deshidrogenasa/metabolismo , Masculino , Miocardio/metabolismo , Miocardio/ultraestructura , Ratas , Ratas Sprague-Dawley , Oligoelementos/metabolismo , Verapamilo/farmacologíaRESUMEN
Mf1 encodes a forkhead/winged helix transcription factor expressed in many embryonic tissues, including prechondrogenic mesenchyme, periocular mesenchyme, meninges, endothelial cells, and kidney. Homozygous null Mf1lacZ mice die at birth with hydrocephalus, eye defects, and multiple skeletal abnormalities identical to those of the classical mutant, congenital hydrocephalus. We show that congenital hydrocephalus involves a point mutation in Mf1, generating a truncated protein lacking the DNA-binding domain. Mesenchyme cells from Mf1lacZ embryos differentiate poorly into cartilage in micromass culture and do not respond to added BMP2 and TGFbeta1. The differentiation of arachnoid cells in the mutant meninges is also abnormal. The human Mf1 homolog FREAC3 is a candidate gene for ocular dysgenesis and glaucoma mapping to chromosome 6p25-pter, and deletions of this region are associated with multiple developmental disorders, including hydrocephaly and eye defects.