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Gardenia jasminoides fruits are extensively grown worldwide, with a large harvest, and its major medicinal ingredients are geniposide and crocins. Research on their accumulation and biosynthsis-related enzymes is rare. In this study, the accumulation of geniposide and crocin of G. jasminoides fruits at different developmental stages were clarified by HPLC. The highest cumulative amount of geniposide was 2.035% during the unripe-fruit period, and the highest content of crocin was 1.098% during the mature-fruit period. Furthermore, transcriptome sequencing was performed. A total of 50 unigenes encoding 4 key enzymes related in geniposide biosynthsis pathways were screened, and 41 unigenes encoding 7 key enzymes in the pathways of crocin were elucidated. It was found that the expression levels of differentially expressed genes of DN67890_c0_g1_i2-encoding GGPS, which is highly related to geniposide biosynthesis, and DN81253_c0_g1_i1-encoding lcyB, DN79477_c0_g1_i2-encoding lcyE, and DN84975_c1_g7_i11-encoding CCD, which are highly related to crocin biosynthesis, were consistent with the accumulation of geniposide and crocin content, respectively. The qRT-PCR results showed that the trends of relative expression were consistent with transcribed genes. This study provides insights for understanding the geniposide and crocin accumulation and biosynthsis during fruit development in G. jasminoides.

Purpose: This study aimed to describe the clinical response to five-step systematic therapy (FSST) in the management of plugged ducts and mastitis. FSST was a comprehensive milk stasis dredging treatment, which contained five steps to make the milk out of the plugged duct. Methods: This retrospective study included 922 breastfeeding women, 714 with plugged ducts, and 208 with mastitis who received FSST from June to September 2017. The breast pain score, swelling degree, and range of breast induration were recorded pre-FSST and post-FSST. Results: After a single FSST, pain score and swelling degree were significantly improved (both p

Tumor necrosis factor receptor 1 (TNFR1) associated death domain protein (TRADD) is a pivotal adaptor in TNF signaling pathway and plays an important role in apoptosis and immune regulation. The function of TRADD has been investigated extensively in mammals, however, the role of TRADD in ducks remains obscure. To reveal the function of duck TRADD (duTRADD) in the apoptosis and innate immune response, the TRADD homologue of mallard (Anas platyrhynchos) has been cloned and the function of duTRADD is investigated in this study. We conducted sequence analysis of the duTRADD, the open reading frame (ORF) region of duTRADD gene was 1065 bp, encoding 354 amino acids (aa), which shares similar functional domain to its mammalian counterpart. Tissue distribution profile of duTRADD in 7-day-old ducklings showed that the expression level of the gene was the highest in heart, followed by liver and brain. Accordingly, duck Tembusu virus (DTMUV) has been shown to decrease duTRADD expression, while overexpression of duTRADD inhibited DTMUV replication in a dose-dependent manner. Furthermore, duTRADD activated the transcriptional activity of caspase-3/8/9, the flow cytometry showed that duTRADD significantly induced apoptosis. However, duTRADD showed hardly any effect on the transcriptional activity of IFN-α/β and its downstream interferon-stimulated genes (ISGs). The current data support the conclusion that duTRADD is a novel pro-apoptotic protein with a critical role in defense against DTMUV invasion. These results lay the theoretical foundation for the development of new anti-DTMUV strategies.

Duck Tembusu virus (DTMUV) is an emerging pathogenic flavivirus that has caused enormous economic losses in Southeast Asia. However, the pathogenic mechanism and host's responses after DTMUV infection remain poorly understood. During this study, total mRNA sequencing (RNA-Seq) analysis was used to detect the global gene expression in DEFs at various time points after DTMUV infection. We identified 326 genes altered significantly at all time points, and these genes were dynamically enriched in multifarious biological processes, including apoptosis, innate immune response, DNA replication, cell cycle arrest and DNA repair. Next, the results showed that apoptosis was induced and the proportion of apoptosis increased with time, and pro-apoptotic molecules caspases were activated. The RNA-seq data analysis further revealed that most pro-apoptosis and anti-apoptosis genes were early continually responsive, and the genes involved in both intrinsic and extrinsic apoptotic pathways were initiated. Further, the considerably enriched immune-relevant pathways were involved in apoptosis process, and protein-protein interactions (PPIs) analysis showed that IL6, STAT1, TNFAIP3, CFLAR and PTGS2 may be key regulators of DEFs apoptosis. In conclusion, this study not only contributes to understanding the underlying mechanism of DEFs infection with DTMUV, but also provides new insights into targets screening for antiviral therapy.

The innate immune system is the host’s first line of defense against the invasion of pathogens including flavivirus. The programmed cell death controlled by genes plays an irreplaceable role in resisting pathogen invasion and preventing pathogen infection. However, the inflammatory cell death, which can trigger the overflow of a large number of pro-inflammatory cytokines and cell contents, will initiate a severe inflammatory response. In this review, we summarized the current understanding of the innate immune response, inflammatory cell death pathway and cytokine secretion regulation during Dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus and other flavivirus infections. We also discussed the impact of these flavivirus and viral proteins on these biological processes. This not only provides a scientific basis for elucidating the pathogenesis of flavivirus, but also lays the foundation for the development of effective antiviral therapies.

Tigecycline has been used as one of the therapeutic choices for the treatment of infections caused by multidrug-resistant Klebsiella pneumoniae. However, the emergence of tigecycline heteroresistance has led to great challenges in treating these infections. The purpose of this study was to investigate whether tigecycline-heteroresistant K. pneumoniae (TGCHR-Kp) exists in clinical isolates, and to further characterize the underlying molecular mechanisms involved in the development of tigecycline-resistant subpopulations. Of the 268 tigecycline-susceptible clinical K. pneumoniae isolates, 69 isolates were selected as tigecycline-heteroresistant candidates in the preliminary heteroresistant phenotypic selection by a modified disk diffusion method, and only 21 strains were confirmed as TGCHR-Kp by the population analysis profile (PAP). Pulsed-field gel electrophoresis (PFGE) analysis demonstrated that all the parental TGCHR-Kp isolates were clonally unrelated, and colonies confirmed as the heteroresistant subpopulation showed no significant differences from their respective parental TGCHR-Kp isolates. Efflux pump inhibitors reversed the tigecycline susceptibility in heteroresistant subpopulations. Mutations in the ramR and soxR genes lead to upregulation of the ramA and soxS transcriptional regulators, which in turn induced overexpression of the AcrAB-TolC efflux pump genes in TGCHR-Kps-resistant subpopulations. Moreover, mutations of rpsJ were also found in resistant subpopulations, which suggested that the rpsJ mutation may also lead to tigecycline resistance. Time-kill assays showed that the efficacy of tigecycline against TGCHR-Kps was weakened, whereas the number of resistant subpopulations was enriched by the presence of tigecycline. Our findings imply that the presence of TGCHR-Kps in clinical strains causes severe challenges for tigecycline therapy in clinical practice.

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The changes of metabolite profiles in preterm birth have been demonstrated using newborn screening data. However, little is known about the holistic metabolic model in preterm neonates. The aim was to investigate the holistic metabolic model in preterm neonates. All metabolite values were obtained from a cohort data of routine newborn screening. A total of 261 758 newborns were recruited and randomly divided into a training subset and a testing subset. Using the training subset, 949 variates were considered to establish a logistic regression model for identifying preterm birth (80% accuracy in both the training and testing subsets. When identifying neonates ≤32 weeks from those >32 weeks, it had a robust performance with nearly 95% accuracy in both subsets. In summary, we have established an excellent metabolic model in preterm neonates. These findings could provide new insights for more efficient nutrient supplements and etiology of preterm birth.

Introduction: Plugged ducts and mastitis are common conditions in lactating women. Milk excretion and relief of local symptoms are equally important for the treatment of plugged ducts and mastitis.This study aimed to describe clinical response to 5-step systematic therapy (FSST) in the management of plugged ducts and mastitis. FSST was a comprehensive milk stasis dredging treatment, which contained five steps to make the milk out of the plugged duct. Materials and Methods: This retrospective study included 922 breastfeeding women, 714 with plugged ducts and 208 with mastitis who received FSST at the breast nursing outpatient department from June to September 2017. The breast pain score, swelling degree and range of breast induration were recorded pre-FSST and post-FSST. Results: After a single FSST, pain score and degree of swelling were significantly improved (both, p < 0.001) in all cases. After receiving FSST, the mean breast pain relief score was 1.7±0.7, while the mean swelling fade-away degree was 1.6±0.6. In subgroup analysis, pain score and degree of swelling were significantly improved (both, p < 0.001) in the plugged ducts group and the mastitis group. The score of pain relief in the plugged ducts group was less than that in the mastitis group (1.6±0.7 vs. 1.9±0.7, t=-5.301, p=0.000), while improvement of swelling fade-away was greater in the plugged ducts group than the mastitis group (1.7±0.6 vs. 1.5±0.6, t=3.488, p=0.001). The composition ratio of the changes in induration range between the two groups was statistically different (Pearsonχ2=137.865, p = 0.000), of which more obvious improvement in the plugged ducts group than the mastitis group (χ2=25.653, p = 0.000). Conclusion: FSST can relieve pain, reduce breast swelling and range of induration, and for plugged ducts or mastitis varied degree differently.

Duck Tembusu virus (DTMUV) has recently appeared in ducks in China and the key cellular determiners for DTMUV replication in host cells remain unknown. Autophagy is an evolutionarily conserved cellular process that has been reported to facilitate flavivirus replication. In this study, we utilized primary duck embryo fibroblast (DEF) as the cell model and found that DTMUV infection triggered LC3-II increase and polyubiquitin-binding protein sequestosome 1 (p62) decrease, confirming that complete autophagy occurred in DEF cells. The induction of autophagy by pharmacological treatment increased DTMUV replication in DEF cells, whereas the inhibition of autophagy with pharmacological treatments or RNA interference decreased DTMUV replication. Inhibiting autophagy enhanced the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-&kappa, B) and interferon regulatory factor 7 (IRF7) pathways and increased the p62 protein level in DTMUV-infected cells. We further found that the overexpression of p62 decreased DTMUV replication and inhibited the activation of the NF-&kappa, B and IRF7 pathways, and changes in the NF-&kappa, B and IRF7 pathways were consistent with the level of phosphorylated TANK-binding kinase 1 (p-TBK1). Opposite results were found in p62 knockdown cells. In summary, we found that autophagy-mediated p62 degradation acted as a new strategy for DTMUV to evade host innate immunity.

Duck tembusu virus (DTMUV) is a single-stranded, positive-polarity RNA flavivirus that has caused considerable economic losses in China in recent years. Innate immunity represents the first line of defense against invading pathogens and serves as an important role in resisting viral infections. In this study, we found that the infection of ducks by DTMUV triggers Toll-like receptors (TLRs) and (RIG-I)-like receptors (RLRs) signaling pathways and inducing abundant of pro-inflammatory factors and type I interferons (IFNs), in which melanoma differentiation-associated gene 5 (MDA5) and Toll-like receptor 3 (TLR3) play important immunity roles, they can inhibit the replication process of DTMUV via inducing type I IFNs. Moreover, we demonstrated that type I IFNs can inhibit the DTMUV replication process in a time- and dose-dependent manner. Exosomes are small membrane vesicles that have important roles in intercellular communication. MicroRNAs (miRNAs) are small non-coding RNAs that can modulate gene expression and are common substances in exosomes. In our experiment, we successfully isolated DEF cells derived exosome for the first time and explored its function. Firstly, we found the expression of miR-148a-5p is significantly decreased following DTMUV infect. Then we found miR-148a-5p can target TLR3 and down-regulate the expression of TLR3, serving as a negative factor in innate immunity. Unfortunately, we cannot find miRNAs with different expression changes that can target MDA5. Lastly, our experimental results showed that TLR3 was one of the causes of miR-148a-5p reduction, suggesting that the high level of TLR3 after DTMUV infect can both trigger innate immunity and suppress miR-148a-5p to resist DTMUV.

Tembusu virus (TMUV), a member of the genus flavivirus, primarily causes egg-drop syndrome in ducks and is associated with low disease mortality but high morbidity. The commercially available live vaccines for treating TMUV currently include the main WF100, HB, and FX2010-180P strains, and efficient treatment and/or preventative measures are still urgently needed. Capsid-targeted viral inactivation (CTVI) is a conceptually powerful new antiviral strategy that is based on two proteins from the capsid protein of a virus and a crucial effector molecule. The effector molecule can destroy the viral DNA/RNA or interfere with the proper folding of key viral proteins, while the capsid protein mainly plays a role in viral integration and assembly; the fusion proteins are incorporated into virions during packaging. This study aimed to explore the potential use of this strategy in duck TMUV. Our results revealed that these fusion proteins can be expressed in susceptible BHK21 cells without cytotoxicity and possess excellent Ca2+-dependent nuclease activity, and their expression is also detectable in DF-1 cells. Compared to those in the negative controls (BHK21 and BHK21/pcDNA3.1(+) cells), the numbers of viral RNA copies in TMUV-infected BHK21/Cap-SNase and BHK21/Cap-Linker-SNase cells were reduced by 48 h, and the effect of Cap-Linker-SNase was superior to that of Cap-SNase. As anticipated, these results suggest that these fusion proteins contribute to viral resistance to treatment. Thus, CTVI might be applicable for TMUV inhibition as a novel antiviral therapeutic candidate during viral infection.

To explore the molecular basis for a Chinese family affected with neurofibromatosis type I.Peripheral blood samples were collected from the proband and his parents. Potential mutations of NF1 gene were screened by PCR and Sanger sequencing. Pathogenicity of candidate mutations was analyzed using Polyphen-2 and Provean software.Two mutations of the NF1 gene, including c.702GA (synonymous mutation) and c.1733TG (missense mutation), were discovered in the proband. Neither mutation was found in his parents and 50 healthy controls. Bioinformatics analysis indicated that the c.1733TG mutation (p.Leu578Arg) was probably damaging. The affected codon L578 is highly conserved across various species.The c.1733TC mutation of the NF1 gene probably underlies the neurofibromatosis type I in this family.

Background The pathogenesis of allergic asthma is primarily characterized by abnormality in the immunoglobulin E (IgE) pathway, suggesting a possible role for follicular T-helper cells (Tfh) in the genesis of excessive IgE accumulation. The blood chemokine (C-X-C motif) receptor 5 (CXCR5)+CD4+ T cells, known as circulating Tfh, share common functional characteristics with Tfh cells from germinal centers. There are three subsets of circulating Tfh cells: Tfh1 (CXCR3+CC chemokine receptor [CCR] 6), Tfh2 (CXCR3CCR6) and Tfh17 (CXCR3CCR6+). However, data on circulating Tfh cell subsets distribution in patients with asthma are not available. Objective To investigate the circulating Tfh cell subsets distribution in patients with asthma and to assess the relationship between Tfh cell subsets distribution and the serum IgE level. Methods Thirty patients with severe allergic asthma and 30 age- and sex-matched healthy controls were enrolled in this study. The percentages and phenotypic assays of circulating Tfh cell subsets were assessed by flow cytometry. The total IgE levels were also measured. The correlation between the percentage of circulating Tfh cell subsets and the levels of serum total IgE was analyzed. Results Our results showed polarization of Tfh2 cells within circulating Tfh cell subsets in the patients with asthma. Phenotypic assays showed that activated Tfh2 subtypes displayed the features of Tfh cells, including invariably coexpressed programmed cell death 1 (PD-1), and inducible costimulator (ICOS). Furthermore, not only the frequency of Tfh2 cells but also the ratio (%Tfh2/%Tfh1) positively correlated with the total IgE level in the blood. Conclusion Results of our data described an altered circulating Tfh subset distribution, which implied that this cell subset might play an important role in the pathogenesis of asthma.

Duck Tembusu virus (DTMUV), an emerging infectious pathogen, has caused severe disease in ducks and huge economic losses to the poultry industry in China since 2009. Despite considerable advances in understanding the effects of microRNAs on host antiviral immune responses, it remains unclear how miRNAs regulate DTMUV replication in duck embryo fibroblast (DEF) cells. This study aims to clarify the role of host microRNA-148a-5p (miR-148a-5p) in regulating DTMUV replication by targeting SOCS1. First, we found that during DTMUV infection, the expression of miR-148a-5p in DEFs was downregulated in a time-dependent and dose-dependent manner, while the expression of SOCS1 was significantly upregulated. In addition, we found that when miR-148a-5p mimics were transfected into DEFs, viral RNA copies, viral E protein expression levels and viral titres, which represent viral replication and proliferation, were significantly downregulated, while the opposite result was observed when miR-148a-5p inhibitor was transfected into DEFs. Next, we found that SOCS1 was the target gene of miR-148a-5p through software analysis. Therefore, we further confirmed that SOCS1 was the target of miR-148a-5p and that miR-148a-5p could negatively regulate the expression of SOCS1 at the mRNA and protein levels. Furthermore, our results indicated that overexpression of SOCS1 promoted DTMUV replication, while knockdown of SOCS1 inhibited DTMUV replication. Finally, we found that in DTMUV-infected DEFs, the overexpression of SOCS1 inhibited the production of IFN-α and IFN-β, while knocking down SOCS1 produced the opposite result. This indicates that during DTMUV infection, the virus promotes the expression of SOCS1 by downregulating the expression of miR-148a-5p, while the upregulation of SOCS1 suppresses the production of type I interferon and promotes virus replication. Taken together, these findings provide new insights into virus-host interactions during DTMUV infection and provide potential new antiviral treatment strategies for DTMUV infection.

Mammalian interferon-induced protein with tetratricopeptide repeats family proteins (IFITs) play important roles in host innate immune response to viruses. Recently, studies have shown that IFIT from poultry also plays a crucial part in antiviral function. This study first reports the regulation of duck Tembusu virus (DTMUV) replication by IFIT5 and the effect of duck IFIT5 (duIFIT5) on the innate immune response after DTMUV infection. Firstly, duIFIT5 was obviously increased in duck embryo fibroblast cells (DEFs) infected with DTMUV. Compared to the negative control, we found that in the duIFIT5-overexpressing group, the DTMUV titer at 24 h post infection (hpi) was significantly reduced, but the viral titer was strikingly increased at 48 hpi. Moreover, overexpression of duIFIT5 could significantly inhibit IFN-β transcription and IFN-β promoter activation at indicated time points after DTMUV infection. Further, in DTMUV-infected or poly(I:C)-stimulated DEFs, overexpression of duIFIT5 also significantly inhibited the activation of NF-κB and IRF7 promoters, as well as the activation of downstream IFN induced the interferon-stimulated response element (ISRE) promoter. Meanwhile, the transcription level of antiviral protein Mx, but not OASL, was obviously decreased at various time points. The opposite results were obtained by knockdown of duIFIT5 in DTMUV-infected or poly(I:C)-stimulated DEFs. Compared to the negative control, knockdown of duIFIT5 promoted DTMUV titer and DTMUV envelope (E) protein expression at 24 hpi, but DTMUV titer and E protein expression was markedly decreased at 48 hpi. Additionally, the promoters of IFN-β, NF-κB, IRF7 and ISRE were significantly activated in the duIFIT5 knockdown group. Collectively, duIFIT5 differentially regulates DTMUV replication and inhibits virus-triggered innate immune response.

Human cytomegalovirus (HCMV) is a well-studied β-herpesvirus virus, which adopts a variety of strategies to evade immune surveillance. It has been reported that in HCMV-infected cells, classical major histocompatibility (MHC) class I molecules are down-regulated, but the MHC class Ib molecule human leukocyte antigen (HLA)-E is normally expressed or even overexpressed on the cell surface. HLA-E has been first described to interact with CD94/NKG2 receptors expressed mainly on the surface of natural killer (NK) cells, thus confining its role to the regulation of NK-cell function. The engagement of CD94/NKG2A with HLA-E, with a signal peptide of the HCMV glycoprotein UL40, usually induces inhibitory signals. However, HLA-E also serves as a ligand for the TCR expressed by αβCD8(+) T cells. Recognition of peptides presented by HLA-E may result in CD8(+) effector T-cell activation. These findings will help to understand more on both pathogenic and protective roles of HLA-E in HCMV infection. In this review, we discussed recent studies about the roles of HLA-E in HCMV infection.

Prefabricated house as a form of housing industrialization mode not only can improve the efficiency, but also has the advantage of the comprehensive cost reduction, energy saving, environmental protection, promote the development of the construction industry. Firstly, the article introduces status of housing industrialization development at home and abroad and a comparison of the prefabricated housing system and the traditional construction technology is made in terms of cost construction and construction process. Then, the comparison of direct cost is made for 100 m2 of walls between precast concrete wall panel and the cast-in-site wall by using the method of fixed set of price. Moreover, sensitivity analysis is done. As a result, the use of prefabricated housing system on a large scale is recommended for prefabricated house developments in Chinese Mainland.

Interleukin (IL)-27 is a novel member of the IL-6/IL-12 family of cytokines with a broad range of pro- and anti-inflammatory properties. Recently, accumulating evidence has shown that IL-27 can play either a pathogenic or a protective role in animal models of inflammatory arthritis, depending upon the model and underlying pathogenic mechanisms. As to human system, elevated expression of IL-27 has clearly been detected in the synovial membranes and fluid from patients with rheumatoid arthritis (RA). Moreover, stimulation of IL-27 receptor with IL-27 of fibroblast-like synoviocytes from RA had a suppressive effect on the production of proinflammatory cytokines in vitro. All these findings suggest that IL-27 may have promise as a potential therapeutic target for RA. In this review, we will discuss the biological features of IL-27 and summarize recent advances on both pathogenic and protective roles of IL-27 in RA.

This paper reviews the policy risks existing in the process of developing commodity houses in Mainland China. Policy risks have been identified, and their effects on the implementation of a property project across various stages have been analyzed. The study provides useful references for professionals, in particular those overseas property investors, to identify proper risk management strategies for mitigating the effects of policy risks to their property business in the Chinese market.

Various industrialized housing technologies were introduced to developing countries in the early 1950–1970s, volumetric (i.e. box), panelized units and tunnel-form are typical examples. These technologies lead to improvements in housing production, such as high turnover, improved productivity of both machines and labour, quick assembly and better quality of industrialized products. However, there are limitations for these technologies such as high production costs, application of heavy and large components, lack of standardization in design, and lack of consideration given to the local environment in choosing materials. Owing to the surging demands for housing, industrialization seems to be an inevitable trend in housing construction particularly for those densely populated cities like Chongqing. Thus, this paper aims to evaluate different innovative systems and determine the most suitable system(s) for the construction of industrialized housing in China, by using Chongqing as a case study. Six innovative housing systems have been considered in this study. These systems have been successfully adopted in major cities in the Chinese Mainland, using prefabrication of standardized components, which provide valuable reference to the undertaking of this study. An analytical hierarchy process (AHP) was adopted as a tool to determine the preferences of Chongqing practitioners in relation to the use of selected innovative housing systems. The finding has highlighted a practical and logical approach to identify the most appropriate industrialized housing system to be adopted in densely populated cities such as Chongqing, as well as promoting the implementation of industrialized housing system in other major cities in China.

The housing industrialization process could reduce the amount of site work associated with production and thereby accelerate the on-site construction process. This implies that design should be coordinated and integrated to ensure easy and proper fixture. The key features of housing industrialization are standardization of housing design. The design plan for industrialized housing development in Chongqing should accommodate the small-middle components in key areas of a housing unit. Such units include staircase, partition wall, facades and floor slabs. Classification of housing component systems is first given, and an alternative design plan for producing housing components is presented. The investigation includes the major housing parameters such as most preferable type of housing, appropriate number of storeys, and room height. Attention is drawn to the importance of the inter-relations between design and supply chain and coordination between designer and producer. Keywords—housing industrialization; housing components; design plan I. INTRODUCTION Housing industrialization is defined as the use of on- and off-site construction methods, which utilize principles associated with factory production to prefabricate components, elements or modules, when fixed in position, will form part of a completed building. The housing industrialization process could reduce the amount of site work associated with production and thereby accelerate the on-site construction process. This implies that design should be coordinated and integrated to ensure easy and proper fixture, utilizing a "right first time" philosophy. The key features of housing industrialization are standardization of housing design (1). The previous findings (2) show that the characteristics for the most suitable housing systems for application in Chongqing have to be small-middle, simple, cost effective, lightweight and easy to handle. This design plan must be able to incorporate the conventional construction methods into the production process for producing industrialized housing components, including small-middle component systems and partial prefabrication. The production process should involve minimal capital and the use of local materials, require small-middle and affordable equipment or machinery, and demand simple skill specialization.

Housing industrialization is defined in this study as the use of construction methods, both on and off site that utilize principles associated with factory production to prefabricate components, elements or modules that when fixed in position form part of the completed building. Housing industrialization is oriented with housing market demand and supported by science and technological advancement, based on systemized building systems and housing components. The key features of housing industrialization are standardization of housing design; industrialization as well as socialization of housing production and management. This paper aims to focuses on the design of housing for the city Chongqing which include the alternative design methods of energy-saving, ecological design methods; the factors having major impacts on buildings; local climate condition; and the use of local materials. Technology and measure of energy-saving and the application of appropriate materials and equipment need to be considered at the planning and design stages are also covered.