The Spreading of Christianity and the introduction of Modern Architecture in Shannxi, China (1840-1949): Christian churches and traditional Chinese architecture

La arquitectura china ha experimentado grandes cambios a lo largo de un extenso proceso histórico. El hito de mayor importancia es el que da paso al denominado Tiempo Moderno, periodo en el cual irrumpe por vez primera en China la arquitectura occidental, que comienza a tener una influencia muy activa y significativa sobre los rasgos y la identidad de la arquitectura tradicional china, hasta ese momento el único estilo o forma de hacer –muy diferente, en cuanto a su concepción y fisonomía, de los planteamientos occidentales- que había sobrevivido sin desvíos significativos, configurando un panorama milenario bastante homogéneo en los aspectos técnicos y artísticos en el desarrollo de esa arquitectura. Por un cúmulo de complejas razones, la mayor parte de la arquitectura china del periodo feudal -es decir el que forman todos los años anteriores a 1849- ha desaparecido. Sin embargo, desde la fecha indicada hasta la Revolución de 1949 (el denominado periodo semicolonial o semifeudal), sí se conservan muchas edificaciones, que fueron mejor construidas y mantenidas luego, destacando por su importancia en ese sentido las iglesias cristianas. Dichos templos representan cronológicamente, no sólo la primera irrupción de la arquitectura clásica occidental en China, sino el inicio de un proceso de modernización de la profundamente enraizada y, en buena medida, estancada arquitectura vernácula, combinando técnicas y estilos de ambos planteamientos, para dar como resultado originales edificaciones de un singular eclecticismo que caracterizarían buena parte de la arquitectura de dicha etapa semicolonial. En términos generales, últimamente se ha ido prestando cada vez más atención a esta arquitectura de los tiempos modernos, aunque las iglesias cristianas de la provincia de Shaanxi no han sido objeto de estudio específico, a pesar de que su tipología es muy representativa de las construcciones de esta clase en otras regiones del interior de China. La investigación que desarrolla la presente tesis doctoral sale al paso de esa deficiencia, abriendo puertas a la continuación del trabajo referido, extendido a otras zonas o arquitecturas, y, por extensión, a la profundización analítica de la hibridación arquitectónica y cultural entre China y Occidente. Sobre las bases de investigación documental, estudios de campo y dibujo, la tesis plantea un estudio aclaratorio de los rasgos y raíces de la arquitectura tradicional china, al que sigue otro histórico y tipológico de los templos cristianos en la provincia de Shaanxi, deteniéndose en sus características fundamentales, situación (uso) actual y estado de conservación. Se ha considerado imprescindible añadir al trabajo, como apéndice, un elaborado glosario conceptual ilustrado de términos básicos arquitectónicos y constructivos, en chino, inglés y español. ABSTRACT The Chinese architecture has gone through great changes during the long process of history. The tremendous changing period was the named Modern Times of China when, for the very first time, the western architecture was introduced into China and became to influence majorly on the traditional Chinese architecture. Before that, the traditional Chinese architecture which has its own, yet totally different system from the occidental architecture system was the only architectural style could be found in China. Although, due to many historical, conceptual and architectural characteristic reasons, large amount of the ancient Chinese architecture built in the feudal China was not preserved, there are a lot of buildings of semi-feudal China that was well constructed and conserved. The most important architectural type of the semi-feudal China is the Christian Churches. It was not only the first western architectural form that was brought into and well developed in China, but also was the beginner of the modernization process of Chinese architecture. Because of the deep root of the 2000-year traditional Chinese architecture, all the Christian Churches built in China during the semi-colonial society has a combined style of both the traditional Chinese architecture and the classic western churches. They are a priceless asset of the Chinese architectural history. Recently, more and more attention had been paid on the Chinese Modern Times architecture, however, the Christian Churches in Shaanxi Province, the province which has a unique history with the Christian, but less economically developed have never been researched yet. The Christian Churches of Shaanxi Province reflect the general feature of developing history of the Christian Churches of common inner-land regions in China. The research opens the door to further study on other Christian Churches and related buildings, and also for the further study on the Chinese-western architectural and culture communication. On the base of document research, field survey and mapping, in this thesis, an in-depth study had been done on the general history of the features and roots of the traditional Chinese architecture, the developing history of the Christian Churches of Shaanxi Province and the architectural types, examples, characteristics, present situation and conservation status. By comparing the Christian Churches of the cities in Shaanxi province to the Christian Churches in other more developed cities, and by comparing the Christian Churches in China to the classic western churches, the architectural combination feature of the Christian Churches in China are highlighted. The thesis is a fundamental research on which many further studies about the architectural developing history, characteristics and conservation of the Christian Churches in China could be done. It is considered essential to add to the work, as an appendix, an elaborate conceptual illustrated glossary of architectural and construction terms in Chinese, English and Spanish.

Time-motion analysis on Chinese male field hockey players

The aim of the study was to evaluate the match work-rate of Chinese field hockey players by analyzing the distance covered at different intensities pooled by specific positions during different periods of matches. Thirty-eight players from twenty-four male field hockey matches at the 11th Chinese National Games were filmed and analyzed.

Time-motion analysis on Chinese male field hockey players

The aim of the study was to evaluate the match work-rate of Chinese field hockey players by analyzing the distance covered at different intensities pooled by specific positions during different periods of matches. Thirty-eight players from twenty-four male field hockey matches at the 11th Chinese National Games were filmed and analyzed.mas

Control of phosphatidylserine biosynthesis through phosphatidylserine-mediated inhibition of phosphatidylserine synthase I in Chinese hamster ovary cells

Phosphatidylserine (PtdSer) synthesis in Chinese hamster ovary (CHO) cells occurs through the exchange of l-serine with the base moiety of phosphatidylcholine or phosphatidylethanolamine. The synthesis is depressed on the addition of PtdSer to the culture medium. A CHO cell mutant named mutant 29, whose PtdSer biosynthesis is highly resistant to this depression by exogenous PtdSer, has been isolated from CHO-K1 cells. In the present study, the PtdSer-resistant PtdSer biosynthesis in the mutant was traced to a point mutation in the PtdSer synthase I gene, pssA, resulting in the replacement of Arg-95 of the synthase by lysine. Introduction of the mutant pssA cDNA, but not the wild-type pssA cDNA, into CHO-K1 cells induced the PtdSer-resistant PtdSer biosynthesis. In a cell-free system, the serine base-exchange activity of the wild-type pssA-transfected cells was inhibited by PtdSer, but that of the mutant pssA-transfected cells was resistant to the inhibition. Like the mutant 29 cells, the mutant pssA-transfected cells grown without exogenous PtdSer exhibited an ≈2-fold increase in the cellular PtdSer level compared with that in CHO-K1 cells, although the wild-type pssA-transfected cells did not exhibit such a significant increase. These results indicated that the inhibition of PtdSer synthase I by PtdSer is essential for the maintenance of a normal PtdSer level in CHO-K1 cells and that Arg-95 of the synthase is a crucial residue for the inhibition.

Isolation of a Chinese hamster ovary cell mutant defective in intramitochondrial transport of phosphatidylserine

A CHO-K1 cell mutant with a specific decrease in cellular phosphatidylethanolamine (PE) level was isolated as a variant resistant to Ro09–0198, a PE-directed antibiotic peptide. The mutant was defective in the phosphatidylserine (PS) decarboxylation pathway for PE formation, in which PS produced in the endoplasmic reticulum is transported to mitochondria and then decarboxylated by an inner mitochondrial membrane enzyme, PS decarboxylase. Neither PS formation nor PS decarboxylase activity was reduced in the mutant, implying that the mutant is defective in some step of PS transport. The transport processes of phospholipids between the outer and inner mitochondrial membrane were analyzed by use of isolated mitochondria and two fluorescence-labeled phospholipid analogs, 1-palmitoyl-2-{N-[6(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]caproyl}-PS (C6-NBD-PS) and C6-NBD-phosphatidylcholine (C6-NBD-PC). On incubation with the CHO-K1 mitochondria, C6-NBD-PS was readily decarboxylated to C6-NBD-PE, suggesting that the PS analog was partitioned into the outer leaflet of mitochondria and then translocated to the inner mitochondrial membrane. The rate of decarboxylation of C6-NBD-PS in the mutant mitochondria was reduced to ≈40% of that in the CHO-K1 mitochondria. The quantity of phospholipid analogs translocated from the outer leaflet of mitochondria into inner mitochondrial membranes was further examined by selective extraction of the analogs from the outer leaflet of mitochondria. In the mutant mitochondria, the translocation of C6-NBD-PS was significantly reduced, whereas the translocation of C6-NBD-PC was not affected. These results indicate that the mutant is defective in PS transport between the outer and inner mitochondrial membrane and provide genetic evidence for the existence of a specific mechanism for intramitochondrial transport of PS.

Aneuploidy correlated 100% with chemical transformation of Chinese hamster cells

Aneuploidy or chromosome imbalance is the most massive genetic abnormality of cancer cells. It used to be considered the cause of cancer when it was discovered more than 100 years ago. Since the discovery of the gene, the aneuploidy hypothesis has lost ground to the hypothesis that mutation of cellular genes causes cancer. According to this hypothesis, cancers are diploid and aneuploidy is secondary or nonessential. Here we reexamine the aneuploidy hypothesis in view of the fact that nearly all solid cancers are aneuploid, that many carcinogens are nongenotoxic, and that mutated genes from cancer cells do not transform diploid human or animal cells. By regrouping the gene pool—as in speciation—aneuploidy inevitably will alter many genetic programs. This genetic revolution can explain the numerous unique properties of cancer cells, such as invasiveness, dedifferentiation, distinct morphology, and specific surface antigens, much better than gene mutation, which is limited by the conservation of the existing chromosome structure. To determine whether aneuploidy is a cause or a consequence of transformation, we have analyzed the chromosomes of Chinese hamster embryo (CHE) cells transformed in vitro. This system allows (i) detection of transformation within 2 months and thus about 5 months sooner than carcinogenesis and (ii) the generation of many more transformants per cost than carcinogenesis. To minimize mutation of cellular genes, we have used nongenotoxic carcinogens. It was found that 44 out of 44 colonies of CHE cells transformed by benz[a]pyrene, methylcholanthrene, dimethylbenzanthracene, and colcemid, or spontaneously were between 50 and 100% aneuploid. Thus, aneuploidy originated with transformation. Two of two chemically transformed colonies tested were tumorigenic 2 months after inoculation into hamsters. The cells of transformed colonies were heterogeneous in chromosome number, consistent with the hypothesis that aneuploidy can perpetually destabilize the chromosome number because it unbalances the elements of the mitotic apparatus. Considering that all 44 transformed colonies analyzed were aneuploid, and the early association between aneuploidy, transformation, and tumorigenicity, we conclude that aneuploidy is the cause rather than a consequence of transformation.

Streptogramin- and tetracycline-responsive dual regulated expression of p27Kip1 sense and antisense enables positive and negative growth control of Chinese hamster ovary cells

We constructed a dual regulated expression vector cassette (pDuoRex) whereby two heterologous genes can be independently regulated via streptogramin- and tetracycline-responsive promoters. Two different constructs containing growth-promoting and growth-inhibiting genes were stably transfected in recombinant Chinese hamster ovary (CHO) cells that express the streptogramin- and tetracycline-dependent transactivators in a dicistronic configuration. An optimally balanced heterologous growth control scenario was achieved by reciprocal expression of the growth-inhibiting human cyclin-dependent kinase inhibitor p27Kip1 in sense (p27Kip1S) and antisense (p27Kip1AS) orientation. Exclusive expression of p27Kip1S resulted in complete G1-phase-specific growth arrest, while expression of only p27Kip1AS showed significantly increased proliferation compared to control cultures (both antibiotics present), presumably by decreasing host cell p27Kip1 expression. In a second system, a derivative of pDuoRex encoding streptogramin-responsive expression of the growth-promoting SV40 small T antigen (sT) and tetracycline-regulated expression of p27Kip1 was stably transfected into CHO cells. Expression of sT alone resulted in an increase in cell proliferation, but the expression of p27Kip1 failed to provide the expected G1-specific growth arrest despite having demonstrated expression of the protein. This illustrates the difficulty in balancing the complex pathways underlying cell proliferation control through the expression of two functionally distinct genes involved in those pathways, and how a single-gene sense/antisense approach using pDuoRex can overcome this barrier to complete metabolic engineering control.

High-level production of recombinant human lysosomal acid alpha-glucosidase in Chinese hamster ovary cells which targets to heart muscle and corrects glycogen accumulation in fibroblasts from patients with Pompe disease.

Infantile Pompe disease is a fatal genetic muscle disorder caused by a deficiency of acid alpha-glucosidase, a glycogen-degrading lysosomal enzyme. We constructed a plasmid containing a 5'-shortened human acid alpha-glucosidase cDNA driven by the cytomegalovirus promoter, as well as the aminoglycoside phosphotransferase and dihydrofolate reductase genes. Following transfection in dihydrofolate reductase-deficient Chinese hamster ovary cells, selection with Geneticin, and amplification with methotrexate, a cell line producing high levels of the alpha-glucosidase was established. In 48 hr, the cells cultured in Iscove's medium with 5 mM butyrate secreted 110-kDa precursor enzyme that accumulated to 91 micrograms.ml-1 in the medium (activity, > 22.6 mumol.hr-1.ml-1). This enzyme has a pH optimum similar to that of the mature form, but a lower Vmax and Km for 4-methylumbelliferyl-alpha-D-glucoside. It is efficiently taken up by fibroblasts from Pompe patients, restoring normal levels of acid alpha-glucosidase and glycogen. The uptake is blocked by mannose 6-phosphate. Following intravenous injection, high enzyme levels are seen in heart and liver. An efficient production system now exists for recombinant human acid alpha-glucosidase targeted to heart and capable of correcting fibroblasts from patients with Pompe disease.

Influence of alkyltransferase activity and chromosomal locus on mutational hotspots in Chinese hamster ovary cells.

High-density mutational spectra have been established for exon 3 of the gene encoding adenine phosphoribosyltransferase (APRT) of the Chinese hamster ovary (CHO) cell line derivative D422 and closely related and/or modified lines by using the mutagen ethyl methanesulfonate (EMS). The total number of selectable sites (GC-->AT transitions yielding a selectable APRT- phenotype) was estimated at 31 based on our own accumulated data base of 136 sequenced exon 3 mutations and on literature reports. D422 and two other APRT hemizygous lines each yielded very similar spectra and showed two populations of mutable sites: (i) 24 "baseline" sites that followed the Poisson distribution and therefore were equally susceptible to mutation and (ii) two hotspots, one comprising a cluster at nucleotides 1293-1309 and the other at nucleotide 1365. Collectively, the latter sites were about 10-fold more frequently mutated than the others. CHO cells are mer- as they lack the repair enzyme O6-methylguanidine methyltransferase (EC 2.1.1.63). In modified repair-proficient CHO cells, the distribution of mutations among all of the 31 sites was random, with only 3 of the 19 GC-->AT transitions in the above hotspots. To determine whether the distribution was locus-dependent, two independent lines carrying single copies of transfected APRT genes were generated from a derivative of D422 carrying a deletion in the endogenous APRT gene. Nucleotides 1293-1309 were again no longer preferentially mutated, but the site at nucleotide 1365 was still a hotspot. We conclude that mutational spectra in mer- cells are at least in part locus dependent and that some sequences are particularly susceptible to EMS mutagenesis and perhaps also to methyltransferase repair.

Differential toxicity of mitomycin C and porfiromycin to aerobic and hypoxic Chinese hamster ovary cells overexpressing human NADPH:cytochrome c (P-450) reductase.

Purified NADPH:cytochrome c (P-450) reductase (FpT; NADPH-ferrihemoprotein oxidoreductase, EC 1.6.2.4) can reductively activate mitomycin antibiotics through a one-electron reduction to species that alkylate DNA. To assess the involvement of FpT in the intracellular activation of the mitomycins, transfectants overexpressing a human FpT cDNA were established from a Chinese hamster ovary cell line deficient in dihydrofolate reductase (CHO-K1/dhfr-). The parental cell line was equisensitive to the cytotoxic action of mitomycin C under oxygenated and hypoxic conditions. In contrast, porfiromycin was considerably less cytotoxic to wild-type parental cells than was mitomycin C in air and markedly more cytotoxic under hypoxia. Two FpT-transfected clones were selected that expressed 19- and 27-fold more FpT activity than the parental line. Levels of other oxidoreductases implicated in the activation of the mitomycins were unchanged. Significant increases in sensitivity to mitomycin C and porfiromycin in the two FpT-transfected clones were seen under both oxygenated and hypoxic conditions, with the increases in toxicity being greater under hypoxia than in air. These findings demonstrate that FpT can bioreductively activate the mitomycins in living cells and implicate FpT in the differential aerobic/hypoxic toxicity of the mitomycins.