Morphometric Study of Cerebral Arterioles in CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy(CADASIL) is the most common hereditary small vessel disease (SVD) leading to vascular dementia. The cause of the disease is mutations in NOTCH3 gene located at chromosome 19p13.1. The gene defect results in accumulation of granular osmiophilic material and extracellular domain of NOTCH3 at vascular smooth muscle cells (VSMCs) with subsequent degeneration of VSMCs. This arteriopathy leads to white matter (WM) rarefaction and multiple lacunar infarctions in both WM and deep grey matter (GM) visible in magnetic resonance imaging. This thesis is focused on the quantitative morphometric analysis of the stenosis and fibrosis in arterioles of the frontal cerebral WM, cortical GM and deep GM (lenticular nucleus (LN), i.e. putamen and globus pallidus). It was performed by assessing four indicators of arteriolar stenosis and fibrosis: (1) diameter of arteriolar lumen, (2) thickness of arteriolar wall, (3) external diameter of arterioles and (4) sclerotic index. These parameters were assessed (a) in 5 elderly CADASIL patients with the mean age of onset 47 years and of death 63 years, (b) in a 32-year-old young CADASIL patient with the first ischemic episode at the age of 29 years and (c) a very old CADASIL patient aged 95 years, who suffered the first stroke at the age of 71 years. These measurements were compared with age-matched controls without stroke, dementia, hypertension, and cerebral amyloid angiopathy. Morphometric analyses disclosed that in all age groups of CADASIL patients compared to corresponding controls there was significant narrowing of arteriolar lumen (stenosis) and fibrotic thickening of the walls (fibrosis) in the WM arterioles, although the significance of stenosis in the very old patient was marginal. In the LN arterioles there was only significant fibrosis without stenosis. These results suggest that the ischemic lesions and lacunar infarcts in the cerebral WM are mainly attributable to the stenosis of arterioles, whereas those in the LN are probably mainly due to hemodynamic changes of the cerebral blood flow. In conclusion: The SVD of CADASIL is characterized by narrowing of lumina and fibrotic thickening of walls predominantly in the cerebral WM arterioles. On the other hand, in the LN the ischemic lesions and lacunar infarcts are most probably hemodynamic due to impaired autoregulation caused by the rigidity of fibrotic arterioles. The pathological cerebral arteriolar alterations begin to develop already at a relatively young age but the onset may be delayed to a remarkably old age. This underlines the well known great variability in the clinical picture of CADASIL. The very late onset of CADASIL may cause its underdiagnosis, because the strokes are common in the elderly and are attributed to common risk factors.

Intellectual Property Protection in China in the Cases of Outsourcing and own Manufacturing

The intellectual property (IP) environment in China is still very immature. There are several problems in legal, political, economic, social-cultural, competitive and labor environment which have hindered IP legal enforcement. Under such circumstances, IP misappropriation is a major concern especially for foreign small and medium-sized enterprises (SMEs) doing business in China. These circumstances require foreign companies, no matter whether they are multinational corporations (MNCs) or SMEs and have own manufacturing in China or not, to take strong IP actions. Therefore, the purpose of this study is to discuss how IP can be protected in China in the case of outsourcing and in the case of own manufacturing. The comparison will consider the process of outsourcing and own manufacturing consisting two stages: preparation stage and operation stage. In order to clarify the conceptual arguments, two illustrative case studies were studied. The case data bases on two semi-structured interviews of the managing directors, field notes and archival data. The findings propose that attention in IP protection should be given to following issues: integrating IP strategy into the company’s business strategy, protecting the most critical knowledge, regarding IP steps as a whole in the protection mechanism and making IP strategy as proactive as possible. The major difference between outsourcing and own manufacturing in IP protection is in the operation stage. Besides, the findings also provide managerial advice on IP protection, e.g. foreign managers should be prepared for IP risks in China, they should establish an own IP protection mechanism which matches the company’s situation and they should consider IP protection as an on-going process.

Co-culture of chondrocytes and bone marrow mesenchymal stem cells in vitro enhances the expression of cartilaginous extracellular matrix components

Chondrocytes and bone marrow mesenchymal stem cells (BMSCs) are frequently used as seed cells in cartilage tissue engineering. In the present study, we determined if the co-culture of rabbit articular chondrocytes and BMSCs in vitro promotes the expression of cartilaginous extracellular matrix and, if so, what is the optimal ratio of the two cell types. Cultures of rabbit articular chondrocytes and BMSCs were expanded in vitro and then cultured individually or at a chondrocyte:BMSC ratio of 4:1, 2:1, 1:1, 1:2, 1:4 for 21 days and cultured in DMEM/F12. BMSCs were cultured in chondrogenic induction medium. Quantitative real-time RT-PCR and Western blot were used to evaluate gene expression. In the co-cultures, type II collagen and aggrecan expression increased on days 14 and 21. At the mRNA level, the expression of type II collagen and aggrecan on day 21 was much higher in the 4:1, 2:1, and 1:1 groups than in either the articular chondrocyte group or the induced BMSC group, and the best ratio of co-culture groups seems to be 2:1. Also on day 21, the expression of type II collagen and aggrecan proteins in the 2:1 group was much higher than in all other groups. The results demonstrate that the co-culture of rabbit chondrocytes and rabbit BMSCs at defined ratios can promote the expression of cartilaginous extracellular matrix. The optimal cell ratio appears to be 2:1 (chondrocytes:BMSCs). This approach has potential applications in cartilage tissue engineering since it provides a protocol for maintaining and promoting seed-cell differentiation and function.

Reference value of brachial-ankle pulse wave velocity for the eastern Chinese population and potential influencing factors

The present study was conducted to obtain reference values for brachial-ankle pulse wave velocity (baPWV) and to evaluate influencing factors of baPWV according to gender. Using automatic devices, baPWV was measured simultaneously in 2095 subjects. A total of 647 healthy subjects, none of whom presented atherosclerotic risk factors, were analyzed in the present study. Two different statistical methods were used to obtain reference values for baPWV according to subject gender and age. The association between baPWV value and gender, as well as other features, were analyzed. For male subjects, multiple stepwise analysis showed that age, systolic blood pressure (SBP), heart rate (HR), and plasma levels of triglycerides (TG) were independent predictors of baPWV. For female subjects, age, SBP, HR, and plasma levels of uric acid (UA) were independent predictors of baPWV. In male subjects, the upper limits of baPWV values were 1497.43/1425.00, 1518.67/1513.25, 1715.97/1726.50, 1925.20/1971.90, and 2310.18/2115.00 cm/s, obtained using two different statistical methods for the age ranges of 30-39, 40-49, 50-59, 60-69, and 70 and older, respectively. For females, the upper limits of baPWV values were 1426.70/1411.13, 1559.15/1498.95, 1733.50/1739.00, 1958.63/1973.78, and 2720.80/2577.00 cm/s for the age ranges of 30-39, 40-49, 50-59, 60-69, and 70 and older, respectively. Aging is the most important influencing factor for baPWV value and its effect is more prominent in females. The reference values of baPWV according to age and gender may be useful for the clinical diagnosis and preventive therapy of cardiovascular diseases.

Periodic mechanical stress activates MEK1/2-ERK1/2 mitogenic signals in rat chondrocytes through Src and PLCγ1

The mitogenic effects of periodic mechanical stress on chondrocytes have been studied extensively but the mechanisms whereby chondrocytes sense and respond to periodic mechanical stress remain a matter of debate. We explored the signal transduction pathways of chondrocyte proliferation and matrix synthesis under periodic mechanical stress. In particular, we sought to identify the role of the MEK1/2-ERK1/2 signaling pathway in chondrocyte proliferation and matrix synthesis following cyclic physiologic mechanical compression. Under periodic mechanical stress, both rat chondrocyte proliferation and matrix synthesis were significantly increased (P < 0.05) and were associated with increases in the phosphorylation of Src, PLCγ1, MEK1/2, and ERK1/2 (P < 0.05). Pretreatment with the MEK1/2-ERK1/2 selective inhibitor, PD98059, and shRNA targeted to ERK1/2 reduced periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis (P < 0.05), while the phosphorylation levels of Src-Tyr418 and PLCγ1-Tyr783 were not inhibited. Proliferation, matrix synthesis and phosphorylation of MEK1/2-Ser217/221 and ERK1/2-Thr202/Tyr204 were inhibited after pretreatment with the PLCγ1 inhibitor U73122 in chondrocytes in response to periodic mechanical stress (P < 0.05), while the phosphorylation site of Src-Tyr418 was not affected. Inhibition of Src activity with PP2 and shRNA targeted to Src abrogated chondrocyte proliferation and matrix synthesis (P < 0.05) and attenuated PLCγ1, MEK1/2 and ERK1/2 activation in chondrocytes subjected to periodic mechanical stress (P < 0.05). These findings suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis in part through the Src-PLCγ1-MEK1/2-ERK1/2 signaling pathway, which links these three important signaling molecules into a mitogenic cascade.

Increased immunohistochemical expression of YKL-40 in the spleen of patients with portal hypertension

YKL-40 has been identified as a growth factor in connective tissue cells and also a migration factor in vascular smooth muscle cells. To a large extent, the increase of serum YKL-40 is attributed to liver fibrosis and asthma. However, the relationship of the expression and clinical/prognostic significance of YKL-40 to the splenomegaly of patients with portal hypertension is unclear. In the present study, the expression of YKL-40 was studied by immunohistochemistry in 48 splenomegaly tissue samples from patients with portal hypertension and in 14 normal spleen specimens. All specimens were quickly stored at -80°C after resection. Primary antibodies YKL-40 (1:150 dilution, rabbit polyclonal IgG) and MMP-9 (1:200 dilution, rabbit monoclonal IgG) and antirabbit immunoglobulins (HRP K4010) were used in this study. The relationship of clinicopathologic features with YKL-40 is presented. The expression of YKL-40 indicated by increased immunochemical reactivity was significantly up-regulated in splenomegaly tissues compared to normal spleen tissues. Overexpression of YKL-40 was found in 68.8% of splenomegaly tissues and was significantly associated with Child-Pugh classification (P = 0.000), free portal pressure (correlation coefficient = 0.499, P < 0.01) and spleen fibrosis (correlation coefficient = 0.857, P < 0.01). Further study showed a significant correlation between YKL-40 and MMP-9 (correlation coefficient = -0.839, P < 0.01), indicating that YKL-40 might be an accelerator of spleen tissue remodeling by inhibiting the expression of MMP-9. In conclusion, YKL-40 is an important factor involved in the remodeling of spleen tissue of portal hypertension patients and can be used as a therapeutic target for splenomegaly.

Gene transfer of Chlorella vulgaris n-3 fatty acid desaturase optimizes the fatty acid composition of human breast cancer cells

Chlorella vulgaris has the gene of n-3 fatty acid desaturase (CvFad3), which can synthesize the precursor of n-3 polyunsaturated fatty acids (PUFAs) or convert n-6 to n-3 PUFAs. The objective of the present study was to examine whether the CvFad3 gene from C. vulgaris can be functionally and efficiently expressed in human breast cancer cells and whether its expression can exert a significant effect on cell fatty acid composition. We inserted the CvFad3 gene into the plasmid pEGFP-C3 to construct the eukaryotic expression vector pEGFP-C3-n-3 and to express the n-3 Fad gene in human breast cancer cells (MCF-7 cells). Transfection of MCF-7 cells with the recombinant vector resulted in a high expression of n-3 fatty acid desaturase. Lipid analysis indicated that the ratio of n-6/n-3 PUFAs was decreased from 6:1 in the control cells to about 1:1 in the cells expressing the n-3 fatty acid desaturase. Accordingly, the CvFad3 gene significantly decreased the ratio of n-6/n-3 PUFAs of the MCF-7 cell membrane. The expression of the CvFad3 gene can decrease cell proliferation and promote cell apoptosis. This study demonstrates that the CvFad3 gene can dramatically balance the ratio of n-6/n-3 PUFAs and may provide an effective approach to the modification of the fatty acid composition of mammalian cells, also providing a basis for potential applications of its transfer in experimental and clinical settings.

A novel noninvasive method to detect rejection after heart transplantation

Prompt and accurate detection of rejection prior to pathological changes after organ transplantation is vital for monitoring rejections. Although biopsy remains the current gold standard for rejection diagnosis, it is an invasive method and cannot be repeated daily. Thus, noninvasive monitoring methods are needed. In this study, by introducing an IL-2 neutralizing monoclonal antibody (IL-2 N-mAb) and immunosuppressants into the culture with the presence of specific stimulators and activated lymphocytes, an activated lymphocyte-specific assay (ALSA) system was established to detect the specific activated lymphocytes. This assay demonstrated that the suppression in the ALSA test was closely related to the existence of specific activated lymphocytes. The ALSA test was applied to 47 heart graft recipients and the proliferation of activated lymphocytes from all rejection recipients proven by endomyocardial biopsies was found to be inhibited by spleen cells from the corresponding donors, suggesting that this suppression could reflect the existence of activated lymphocytes against donor antigens, and thus the rejection of a heart graft. The sensitivity of the ALSA test in these 47 heart graft recipients was 100%; however, the specificity was only 37.5%. It was also demonstrated that IL-2 N-mAb was indispensible, and the proper culture time courses and concentrations of stimulators were essential for the ALSA test. This preliminary study with 47 grafts revealed that the ALSA test was a promising noninvasive tool, which could be used in vitro to assist with the diagnosis of rejection post-heart transplantation.

CHRNA5 polymorphism and susceptibility to lung cancer in a Chinese population

Polymorphisms in the nicotinic acetylcholine receptor subunit CHRNA5 gene have been associated with lung cancer positive susceptibility in European and American populations. In the present hospital-based, case-control study, we determined whether polymorphism in rs503464 of CHRNA5 is associated with lung cancer risk in Chinese individuals. A single nucleotide polymorphism in CHRNA5 rs503464, c.-166T>A (hereafter T>A), was identified using TaqMan-MGB probes with sequencing via PCR in 600 lung cancer cases and 600 healthy individuals. Genotype frequencies for rs503464 (T>A) were in Hardy-Weinberg equilibrium for the control population. However, genotype frequencies were significantly different between cases and controls (P < 0.05), while allele frequencies were not significantly different between groups. Compared to homozygous genotypes (TT or AA), the risk of lung cancer in those with the heterozygous genotype (TA) was significantly lower (OR = 0.611, 95%CI = 0.486-0.768, P = 0.001). Using genotype AA as a reference, the risk of lung cancer for those with genotype TA was increased 1.5 times (OR = 1.496, 95%CI = 1.120-1.997, P = 0.006). However, no difference in risk was observed between T allele carriers and A allele carriers (OR = 0.914, 95%CI = 0.779-1.073, P = 0.270). Stratification analysis showed that the protective effect of TA was more pronounced in those younger than 60 years, nonsmokers, or those without a family history of cancer, as well as in patients with adenocarcinoma or squamous cell carcinoma in clinical stages III or IV (P < 0.05). Therefore, the heterozygous genotype c.-166T>A at rs503464 of CHRNA5 may be associated with reduced risk of lung cancer, thus representing a susceptibility allele in Chinese individuals.

靜爭齋第八才子書. 花箋記Jing cheng zhai di ba cai zi shu — Hua jian ji.Le huitième roman de génie, le Hua jian ji (le Papier à fleurs), édition du pavillon Jing cheng.

Édition de Qing zi ; préface par Zhu Guang Zeng Shi shen (1713). Texte et notes.

繡像白圭全傳Xiu xiang bai gui quan zhuan.Histoire illustrée de la tablette blanche.

Par Cui Xiang chuan, de Bai ling ; le titre porte l'indication : édition du 10e romancier de génie par Ji Xiao lan. Ce dernier, postnom Yun, originaire de Xian, a vécu de 1724 à 1805. Préface de Qing chuan ju shi. Portraits des personnages. Édition de la salle Yong an.Livre préliminaire + 4 sections (16 hui).

今古奇觀Jin gu qi guan.Merveilles de l'antiquité et des temps modernes.

Contient : I, livre 1三孝廉讓產立高名San xiao lian rang chan li gao ming.Les trois licenciés charitables qui acquièrent de la célébrité ; II, livre 2兩縣令競義婚孤女Liang xian ling jing yi hun gu nü.L'orpheline ; III, livre 3滕大尹鬼斷家私Teng da yin gui duan jia si.Le portrait de famille ; IV, livre 4裴晉公義還原配Pei jin gong yi huan yuan phei.Comment le mandarin Dan bi perdit et retrouva sa fiancée ; V, livre 5杜十娘怒沈百寶箱Du shi niang nu chen bai bao xiang.Du Shi niang, de colère, jette dans l'eau la cassette de bijoux ; VI, livre 6李謫仙醉草嚇蠻書Li zhe xian zui cao he man shu.Le poète Li Tai bai ; VII, livre 7賣油郎獨占花魁Mai you lang du zhan hua khoei.Le vendeur d'huile qui seul possède la reine de beauté ; VIII, livre 8灌園叟（alias 吏）晚逢仙女Guan yuan sou (alias li) wan feng xian nü.Les pivoines ; IX, livre 9轉運漢巧遇洞庭紅Zhuan yun han qiao yu dong ting hong.Le couli des transports, adroitement, reçoit la beauté du Dong ting ; X, livre 10看財奴刁買寃家主Kan cai nu diao mai yuan jia zhu.Richesse mal acquise (Comment le ciel donne et reprend les richesses) ; XI, livre 11吳保安棄家贖友Wu bao an qi jia shu you.Véritable amitié ; XII, livre 12羊角哀舍命全交Yang jue ai she ming quan jiao.Yang Jue ai fait le sacrifice do sa vie par dévouement pour un ami ; XIII, livre 13沈小霞相會出師表Shen xiao xia xiang hui chu shi biao.Shen Xiao xia rencontre et présente le modèle des maîtres ; XIV, livre 14宋金郎團圓破氊笠Song jin lang tuan yuan po zhan li.Les tendres époux ; XV, livre 15盧太學詩酒傲公侯Lu tai xue shi jiu ao gong hou.Lu tai xue, poète et ivre, brave les princes ; XVI, livre 16李汧公窮邸遇俠客Li qian gong qiong di yu xie ke.Li Qian gong, dans sa résidence misérable, traite un hôte magnanime ; XVII, livre 17蘇小妹三難新郎Su xiao mei san nan xin lang.La jeune Su trois fois maltraite un nouveau marié ; XVIII, livre 18劉元普雙生貴子Liu yuan pu shuang sheng gui zi.Liu Yuan pu obtient deux beaux enfants ; XIX, livre 19俞伯牙摔琴謝知音Yu bai ya choai qin xie zhi yin.Le luth brisé ; XX, livre 20莊子休鼓盆成大道Zhuang zi xiu gu phen cheng da dao.La matrone du pays de Song ; XXI, livre 21老門生三世報恩Lao men sheng san shi bao en.Le vieil élève montre sa reconnaissance à la troisième génération ; XXII, livre 22鈍秀才一朝交泰Dun xiu cai yi zhao jiao tai.Le bachelier obtus tout d'un coup exerce son influence formatrice ; XXIII, livre 23蔣興哥重會珍珠衫Jiang xing ge chong hui zheng zhu shan.Le négociant ruiné (La tunique de perles) ; XXIV, livre 24陳御史巧勘金釵鈿Chen yu shi qiao kan jin tchhai tian.Une cause célèbre ; XXV, livre 25徐老僕義憤成家Xu lao bu yi fen cheng jia.Un serviteur méritant ; XXVI, livre 26蔡小姐忍辱報讐Cai xiao jie ren ru bao chou .L'héroïsme de la piété filiale ; XXVII, livre 27錢秀才錯占鳳凰儔.Qian xiu cai tsho zhan feng huang chou .Mariage forcé ; XXVIII, livre 28喬太守亂㸃鴛鴦譜.Qiao tai shou luan dian yuan yang pu.Le préfet Qiao pointe à tort le registre des unions ; XXIX, livre 29懷私怨很僕告主Huai si yuan hen bu gao zhu.Le crime puni ; XXX, livre 30念親恩孝女藏兒Nian qin en xiao nü cang er.La calomnie démasquée ; XXXI, livre 31呂大郎還金完骨肉Lü da lang huan jin wan gu ru.Les trois frères ; XXXII, livre 32金玉奴棒打薄情郎.Jin yu nu bang da bai qing lang.Femme et mari ingrats ; XXXIII, livre 33唐解元玩世出奇.Tang jie yuan wan shi chu qi.Le mariage du licencié Tang (Tang le jie yuan) ; XXXIV, livre 34女秀才移花接木.Nü xiu cai yi hua jie mu.La bachelière du pays de Zhu ; XXXV, livre 35王喬鸞百年長恨.Wang qiao luan bai nian chang hen.Le ressentiment perpétuel de Wang Qiao luan ; XXXVI, livre 36十三郎五歲朝天.Shi san lang wu sui chao tian.Shi san lang pendant cinq ans se tourne vers le ciel ; XXXVII, livre 37崔俊臣巧合芙蓉屏.Cui jun chen qiao he fu yong ping.Paravent révélateur ; XXXVIII, livre 38趙縣君喬送黃柑子.Zhao xian jun qiao song huang gan zi.Chantage ; XXXIX, livre 39誇妙術丹容提金.Khoa miao shu dan yong ti jin.Les alchimistes ; XL, livre 40逞多財（alias 錢多） 白丁橫帶Cheng duo cai (qian duo) bai ding heng dai.Cupidité et dérèglement

今古奇觀Jin gu qi guan.Merveilles de l'antiquité et des temps modernes.

Contient : I, livre 1三孝廉讓產立高名San xiao lian rang chan li gao ming.Les trois licenciés charitables qui acquièrent de la célébrité ; II, livre 2兩縣令競義婚孤女Liang xian ling jing yi hun gu nü.L'orpheline ; III, livre 3滕大尹鬼斷家私Teng da yin gui duan jia si.Le portrait de famille ; IV, livre 4裴晉公義還原配Pei jin gong yi huan yuan phei.Comment le mandarin Dan bi perdit et retrouva sa fiancée ; V, livre 5杜十娘怒沈百寶箱Du shi niang nu chen bai bao xiang.Du Shi niang, de colère, jette dans l'eau la cassette de bijoux ; VI, livre 6李謫仙醉草嚇蠻書Li zhe xian zui cao he man shu.Le poète Li Tai bai ; VII, livre 7賣油郎獨占花魁Mai you lang du zhan hua khoei.Le vendeur d'huile qui seul possède la reine de beauté ; VIII, livre 8灌園叟（alias 吏）晚逢仙女Guan yuan sou (alias li) wan feng xian nü.Les pivoines ; IX, livre 9轉運漢巧遇洞庭紅Zhuan yun han qiao yu dong ting hong.Le couli des transports, adroitement, reçoit la beauté du Dong ting ; X, livre 10看財奴刁買寃家主Kan cai nu diao mai yuan jia zhu.Richesse mal acquise (Comment le ciel donne et reprend les richesses) ; XI, livre 11吳保安棄家贖友Wu bao an qi jia shu you.Véritable amitié ; XII, livre 12羊角哀舍命全交Yang jue ai she ming quan jiao.Yang Jue ai fait le sacrifice do sa vie par dévouement pour un ami ; XIII, livre 13沈小霞相會出師表Shen xiao xia xiang hui chu shi biao.Shen Xiao xia rencontre et présente le modèle des maîtres ; XIV, livre 14宋金郎團圓破氊笠Song jin lang tuan yuan po zhan li.Les tendres époux ; XV, livre 15盧太學詩酒傲公侯Lu tai xue shi jiu ao gong hou.Lu tai xue, poète et ivre, brave les princes ; XVI, livre 16李汧公窮邸遇俠客Li qian gong qiong di yu xie ke.Li Qian gong, dans sa résidence misérable, traite un hôte magnanime ; XVII, livre 17蘇小妹三難新郎Su xiao mei san nan xin lang.La jeune Su trois fois maltraite un nouveau marié ; XVIII, livre 18劉元普雙生貴子Liu yuan pu shuang sheng gui zi.Liu Yuan pu obtient deux beaux enfants ; XIX, livre 19俞伯牙摔琴謝知音Yu bai ya choai qin xie zhi yin.Le luth brisé ; XX, livre 20莊子休鼓盆成大道Zhuang zi xiu gu phen cheng da dao.La matrone du pays de Song ; XXI, livre 21老門生三世報恩Lao men sheng san shi bao en.Le vieil élève montre sa reconnaissance à la troisième génération ; XXII, livre 22鈍秀才一朝交泰Dun xiu cai yi zhao jiao tai.Le bachelier obtus tout d'un coup exerce son influence formatrice ; XXIII, livre 23蔣興哥重會珍珠衫Jiang xing ge chong hui zheng zhu shan.Le négociant ruiné (La tunique de perles) ; XXIV, livre 24陳御史巧勘金釵鈿Chen yu shi qiao kan jin tchhai tian.Une cause célèbre ; XXV, livre 25徐老僕義憤成家Xu lao bu yi fen cheng jia.Un serviteur méritant ; XXVI, livre 26蔡小姐忍辱報讐Cai xiao jie ren ru bao chou .L'héroïsme de la piété filiale ; XXVII, livre 27錢秀才錯占鳳凰儔.Qian xiu cai tsho zhan feng huang chou .Mariage forcé ; XXVIII, livre 28喬太守亂㸃鴛鴦譜.Qiao tai shou luan dian yuan yang pu.Le préfet Qiao pointe à tort le registre des unions ; XXIX, livre 29懷私怨很僕告主Huai si yuan hen bu gao zhu.Le crime puni ; XXX, livre 30念親恩孝女藏兒Nian qin en xiao nü cang er.La calomnie démasquée ; XXXI, livre 31呂大郎還金完骨肉Lü da lang huan jin wan gu ru.Les trois frères ; XXXII, livre 32金玉奴棒打薄情郎.Jin yu nu bang da bai qing lang.Femme et mari ingrats ; XXXIII, livre 33唐解元玩世出奇.Tang jie yuan wan shi chu qi.Le mariage du licencié Tang (Tang le jie yuan) ; XXXIV, livre 34女秀才移花接木.Nü xiu cai yi hua jie mu.La bachelière du pays de Zhu ; XXXV, livre 35王喬鸞百年長恨.Wang qiao luan bai nian chang hen.Le ressentiment perpétuel de Wang Qiao luan ; XXXVI, livre 36十三郎五歲朝天.Shi san lang wu sui chao tian.Shi san lang pendant cinq ans se tourne vers le ciel ; XXXVII, livre 37崔俊臣巧合芙蓉屏.Cui jun chen qiao he fu yong ping.Paravent révélateur ; XXXVIII, livre 38趙縣君喬送黃柑子.Zhao xian jun qiao song huang gan zi.Chantage ; XXXIX, livre 39誇妙術丹容提金.Khoa miao shu dan yong ti jin.Les alchimistes ; XL, livre 40逞多財（alias 錢多） 白丁橫帶Cheng duo cai (qian duo) bai ding heng dai.Cupidité et dérèglement

今古奇觀Jin gu qi guan.Merveilles de l'antiquité et des temps modernes.

Contient : I, livre 1三孝廉讓產立高名San xiao lian rang chan li gao ming.Les trois licenciés charitables qui acquièrent de la célébrité ; II, livre 2兩縣令競義婚孤女Liang xian ling jing yi hun gu nü.L'orpheline ; III, livre 3滕大尹鬼斷家私Teng da yin gui duan jia si.Le portrait de famille ; IV, livre 4裴晉公義還原配Pei jin gong yi huan yuan phei.Comment le mandarin Dan bi perdit et retrouva sa fiancée ; V, livre 5杜十娘怒沈百寶箱Du shi niang nu chen bai bao xiang.Du Shi niang, de colère, jette dans l'eau la cassette de bijoux ; VI, livre 6李謫仙醉草嚇蠻書Li zhe xian zui cao he man shu.Le poète Li Tai bai ; VII, livre 7賣油郎獨占花魁Mai you lang du zhan hua khoei.Le vendeur d'huile qui seul possède la reine de beauté ; VIII, livre 8灌園叟（alias 吏）晚逢仙女Guan yuan sou (alias li) wan feng xian nü.Les pivoines ; IX, livre 9轉運漢巧遇洞庭紅Zhuan yun han qiao yu dong ting hong.Le couli des transports, adroitement, reçoit la beauté du Dong ting ; X, livre 10看財奴刁買寃家主Kan cai nu diao mai yuan jia zhu.Richesse mal acquise (Comment le ciel donne et reprend les richesses) ; XI, livre 11吳保安棄家贖友Wu bao an qi jia shu you.Véritable amitié ; XII, livre 12羊角哀舍命全交Yang jue ai she ming quan jiao.Yang Jue ai fait le sacrifice do sa vie par dévouement pour un ami ; XIII, livre 13沈小霞相會出師表Shen xiao xia xiang hui chu shi biao.Shen Xiao xia rencontre et présente le modèle des maîtres ; XIV, livre 14宋金郎團圓破氊笠Song jin lang tuan yuan po zhan li.Les tendres époux ; XV, livre 15盧太學詩酒傲公侯Lu tai xue shi jiu ao gong hou.Lu tai xue, poète et ivre, brave les princes ; XVI, livre 16李汧公窮邸遇俠客Li qian gong qiong di yu xie ke.Li Qian gong, dans sa résidence misérable, traite un hôte magnanime ; XVII, livre 17蘇小妹三難新郎Su xiao mei san nan xin lang.La jeune Su trois fois maltraite un nouveau marié ; XVIII, livre 18劉元普雙生貴子Liu yuan pu shuang sheng gui zi.Liu Yuan pu obtient deux beaux enfants ; XIX, livre 19俞伯牙摔琴謝知音Yu bai ya choai qin xie zhi yin.Le luth brisé ; XX, livre 20莊子休鼓盆成大道Zhuang zi xiu gu phen cheng da dao.La matrone du pays de Song ; XXI, livre 21老門生三世報恩Lao men sheng san shi bao en.Le vieil élève montre sa reconnaissance à la troisième génération ; XXII, livre 22鈍秀才一朝交泰Dun xiu cai yi zhao jiao tai.Le bachelier obtus tout d'un coup exerce son influence formatrice ; XXIII, livre 23蔣興哥重會珍珠衫Jiang xing ge chong hui zheng zhu shan.Le négociant ruiné (La tunique de perles) ; XXIV, livre 24陳御史巧勘金釵鈿Chen yu shi qiao kan jin tchhai tian.Une cause célèbre ; XXV, livre 25徐老僕義憤成家Xu lao bu yi fen cheng jia.Un serviteur méritant ; XXVI, livre 26蔡小姐忍辱報讐Cai xiao jie ren ru bao chou .L'héroïsme de la piété filiale ; XXVII, livre 27錢秀才錯占鳳凰儔.Qian xiu cai tsho zhan feng huang chou .Mariage forcé ; XXVIII, livre 28喬太守亂㸃鴛鴦譜.Qiao tai shou luan dian yuan yang pu.Le préfet Qiao pointe à tort le registre des unions ; XXIX, livre 29懷私怨很僕告主Huai si yuan hen bu gao zhu.Le crime puni ; XXX, livre 30念親恩孝女藏兒Nian qin en xiao nü cang er.La calomnie démasquée ; XXXI, livre 31呂大郎還金完骨肉Lü da lang huan jin wan gu ru.Les trois frères ; XXXII, livre 32金玉奴棒打薄情郎.Jin yu nu bang da bai qing lang.Femme et mari ingrats ; XXXIII, livre 33唐解元玩世出奇.Tang jie yuan wan shi chu qi.Le mariage du licencié Tang (Tang le jie yuan) ; XXXIV, livre 34女秀才移花接木.Nü xiu cai yi hua jie mu.La bachelière du pays de Zhu ; XXXV, livre 35王喬鸞百年長恨.Wang qiao luan bai nian chang hen.Le ressentiment perpétuel de Wang Qiao luan ; XXXVI, livre 36十三郎五歲朝天.Shi san lang wu sui chao tian.Shi san lang pendant cinq ans se tourne vers le ciel ; XXXVII, livre 37崔俊臣巧合芙蓉屏.Cui jun chen qiao he fu yong ping.Paravent révélateur ; XXXVIII, livre 38趙縣君喬送黃柑子.Zhao xian jun qiao song huang gan zi.Chantage ; XXXIX, livre 39誇妙術丹容提金.Khoa miao shu dan yong ti jin.Les alchimistes ; XL, livre 40逞多財（alias 錢多） 白丁橫帶Cheng duo cai (qian duo) bai ding heng dai.Cupidité et dérèglement