DOMAS: a data management software framework for advanced light sources.

In recent years, China's advanced light sources have entered a period of rapid construction and development. As modern X-ray detectors and data acquisition technologies advance, these facilities are expected to generate massive volumes of data annually, presenting significant challenges in data management and utilization. These challenges encompass data storage, metadata handling, data transfer and user data access. In response, the Data Organization Management Access Software (DOMAS) has been designed as a framework to address these issues. DOMAS encapsulates four fundamental modules of data management software, including metadata catalogue, metadata acquisition, data transfer and data service. For light source facilities, building a data management system only requires parameter configuration and minimal code development within DOMAS. This paper firstly discusses the development of advanced light sources in China and the associated demands and challenges in data management, prompting a reconsideration of data management software framework design. It then outlines the architecture of the framework, detailing its components and functions. Lastly, it highlights the application progress and effectiveness of DOMAS when deployed for the High Energy Photon Source (HEPS) and Beijing Synchrotron Radiation Facility (BSRF).

miRSNP rs188493331: A key player in genetic control of microRNA-induced pathway activation in hypertrophic scars and keloids.

BACKGROUND: Our study aims to delineate the miRSNP-microRNA-gene-pathway interactions in the context of hypertrophic scars (HS) and keloids. MATERIALS AND METHODS: We performed a computational biology study involving differential expression analysis to identify genes and their mRNAs in HS and keloid tissues compared to normal skin, identifying key hub genes and enriching their functional roles, comprehensively analyzing microRNA-target genes and related signaling pathways through bioinformatics, identifying MiRSNPs, and constructing a pathway-based network to illustrate miRSNP-miRNA-gene-signaling pathway interactions. RESULTS: Our results revealed a total of 429 hub genes, with a strong enrichment in signaling pathways related to proteoglycans in cancer, focal adhesion, TGF-ß, PI3K/Akt, and EGFR tyrosine kinase inhibitor resistance. Particularly noteworthy was the substantial crosstalk between the focal adhesion and PI3K/Akt signaling pathways, making them more susceptible to regulation by microRNAs. We also identified specific miRNAs, including miRNA-1279, miRNA-429, and miRNA-302e, which harbored multiple SNP loci, with miRSNPs rs188493331 and rs78979933 exerting control over a significant number of miRNA target genes. Furthermore, we observed that miRSNP rs188493331 shared a location with microRNA302e, microRNA202a-3p, and microRNA20b-5p, and these three microRNAs collectively targeted the gene LAMA3, which is integral to the focal adhesion signaling pathway. CONCLUSIONS: The study successfully unveils the complex interactions between miRSNPs, miRNAs, genes, and signaling pathways, shedding light on the genetic factors contributing to HS and keloid formation.

Fudan Zhongshan Plastic Surgery Forum.

ABSTRACT: The Fudan Zhongshan Plastic Surgery Forum along with the National Continuing Education Course is authorized and supported by the Shanghai Medical Association for Plastic and Reconstructive Surgery and the Fudan University. The annual conference this year along with the course focusing on the "Advances and New Techniques in Plastic Surgery" is successfully held at Zhongshan Hospital affiliated with Fudan University, on August 26-27, 2023 in Shanghai, China.

Surgical Management of Postoperative Nipple Necrosis After Inverted Nipple Correction: Experiences From a Series of 25 Cases.

INTRODUCTION: The inverted nipple is a condition that affects approximately 10% of women and can have negative cosmetic and psychological implications. Surgical correction is a common approach to address this concern; however, this method can lead to complications, such as nipple necrosis. As comprehensive guidelines are currently lacking for postoperative nipple necrosis management, this study reports our experience in the management of postoperative nipple necrosis following initial attempt at surgical management. METHODS: A retrospective chart review was conducted and included female patients who experienced postoperative nipple necrosis after inverted nipple correction between 2018 and 2021. Cases of recurrent nipple retraction following partial necrosis and cases of complete nipple necrosis were evaluated. Recurrent nipple retraction was managed using various inverted nipple correction techniques, while complete necrosis required a modified C-V flap for nipple reconstruction. RESULTS: A total of 25 patients with a total of 42 affected nipples were included. Thirteen cases (26 nipples) experienced recurrent nipple retraction following partial necrosis, while 12 cases (16 nipples) exhibited complete necrosis. No significant predictive variables for these complications were found. Notably, all patients achieved successful healing following single-stage surgical repair. At 6 months postoperation, the treated nipples exhibited satisfactory healing and appearance and an absence of infection or papillary necrosis. Seven reconstructed nipples showed a mean loss of projection (2.7 ± 0.98) compared with only 2 nipples in the inverted nipple correction group. CONCLUSIONS: Distinguishing between recurrent nipple retraction after partial necrosis and complete nipple necrosis is crucial and should be taken into consideration when managing patients following inverted nipple correction.

Protein tyrosine phosphatase 1B regulates fibroblasts proliferation, motility and extracellular matrix synthesis via the MAPK/ERK signalling pathway in keloid.

Keloid is a fibroproliferative disorder resulting from trauma, characterized by abnormal activation of keloid fibroblasts and excessive deposition of extracellular matrix (ECM). It affects life quality of patients and lacks of effective therapeutic targets. Protein tyrosine phosphatase 1B (PTP1B) belongs to the protein tyrosine phosphatases and participates in many cellular processes such as metabolism, proliferation and motility. It has been reported that PTP1B negatively regulated diabetic wound healing and tumor progression. However, its effects in keloid remain unclear. Here, we aimed to evaluate the effects of PTP1B on keloid fibroblasts which play essential roles in keloids pathogenesis. Our results revealed that PTP1B expression was decreased both in keloid tissues and in keloid fibroblasts compared to healthy controls. Keloid fibroblasts (KFs) showed higher cell proliferation, motility, ECM production and ERK activity than normal fibroblasts (NFs). Overexpression of PTP1B in KFs and NFs inhibited cell proliferation, motility, ECM synthesis and the MAPK/ERK signalling pathway while knockdown of PTP1B showed converse effects. The rescue experiments with ERK inhibitor further verified that MAPK/ERK signalling pathway involved in PTP1B regulatory network. Taken together, our findings indicated that overexpression of PTP1B suppressed keloid fibroblasts bio-behaviours and promoted their phenotype switch to normal cells via inhibiting the MAPK/ERK signalling pathway, suggesting it may be a potential anti-keloid therapy.

The design of a data management system at HEPS.

According to the estimated data rates, it is predicted that 24 PB raw experimental data will be produced per month from 14 beamlines at the first stage of the High-Energy Photon Source (HEPS) in China, and the volume of experimental data will be even greater with the completion of over 90 beamlines at the second stage in the future. To make sure that the huge amount of data collected at HEPS is accurate, available and accessible, an effective data management system (DMS) is crucial for deploying the IT systems. In this article, a DMS is designed for HEPS which is responsible for automating the organization, transfer, storage, distribution and sharing of the data produced from experiments. First, the general situation of HEPS is introduced. Second, the architecture and data flow of the HEPS DMS are described from the perspective of facility users and IT, and the key techniques implemented in this system are introduced. Finally, the progress and the effect of the DMS deployed as a testbed at beamline 1W1A of the Beijing Synchrotron Radiation Facility are shown.

M2-polarized macrophages mediate wound healing by regulating connective tissue growth factor via AKT, ERK1/2, and STAT3 signaling pathways.

BACKGROUND: Timely and sufficient M1 recruitment and M2 polarization are necessary for fibrosis during wound healing. The mechanism of how M2 mediates wound healing is worth exploring. Abnormally up-regulated connective tissue growth factor (CTGF) influences multiple organ fibrosis, including cardiac, pulmonary, hepatic, renal, and cutaneous fibrosis. Previous studies reported that M2 contributed to hepatic and renal fibrosis by secreting CTGF. It is worth discussing if M2 regulates fibrosis through secreting CTGF in wound healing. METHODS AND RESULTS: We established the murine wound model and inhibited macrophages during proliferation phase with clodronate liposomes in vivo. Macrophages depletion led to down-regulation of wound healing rates, collagen deposition, as well as expression of collagen 1/3 and Ki67. M2 was induced by interleukin-4 (IL-4) and measured by flow cytometry in vitro. Secreted pro-fibrotic and anti-fibrotic factors were tested by enzyme-linked immunosorbent assay (ELISA). M2 was polarized, which producing more CTGF, transforming growth factor-beta1 (TGF-ß1), and IL-6, as well as less tumor necrosis factor-α (TNF-α) and IL-10. M2 CTGF gene was blocked using siCTGF. Effects of M2 on fibroblasts activities were detected by cell counting kit 8 (CCK8) and cellular wound healing assay. Expressions of related signaling pathway were assessed by western blotting. Blockade of CTGF in M2 deactivated fibroblasts proliferation and migration by regulating AKT, ERK1/2, and STAT3 pathway. Recombinant CTGF restored these effects. CONCLUSIONS: Our research, for the first time, indicated that M2 promoted wound healing by secreting CTGF, which further mediating proliferation and migration of fibroblasts via AKT, ERK1/2, and STAT3 pathway.

Circular RNA circ_0020710 drives tumor progression and immune evasion by regulating the miR-370-3p/CXCL12 axis in melanoma.

BACKGROUND: Circular RNAs (circRNAs) have been reported to have critical regulatory roles in tumor biology. However, their contribution to melanoma remains largely unknown. METHODS: CircRNAs derived from oncogene CD151 were detected and verified by analyzing a large number of melanoma samples through quantitative real-time polymerase chain reaction (qRT-PCR). Melanoma cells were stably transfected with lentiviruses using circ_0020710 interference or overexpression plasmid, and then CCK-8, colony formation, wound healing, transwell invasion assays, and mouse xenograft models were employed to assess the potential role of circ_0020710. RNA immunoprecipitation, luciferase reporter assay and fluorescence in situ hybridization were used to evaluate the underlying mechanism of circ_0020710. RESULTS: Our findings indicated that circ_0020710 was generally overexpressed in melanoma tissues, and high level of circ_0020710 was positively correlated with malignant phenotype and poor prognosis of melanoma patients. Elevated circ_0020710 promoted melanoma cell proliferation, migration and invasion in vitro as well as tumor growth in vivo. Mechanistically, we found that high level of circ_0020710 could upregulate the CXCL12 expression via sponging miR-370-3p. CXCL12 downregulation could reverse the malignant behavior of melanoma cells conferred by circ_0020710 over expression. Moreover, we also found that elevated circ_0020710 was correlated with cytotoxic lymphocyte exhaustion, and a combination of AMD3100 (the CXCL12/CXCR4 axis inhibitor) and anti-PD-1 significantly attenuated tumor growth. CONCLUSIONS: Elevated circ_0020710 drives tumor progression via the miR-370-3p/CXCL12 axis, and circ_0020710 is a potential target for melanoma treatment.

Hsa-let-7b Suppresses Cell Proliferation by Targeting UHRF1 in Melanoma.

UHRF1 promotes melanoma progression by inducing cell proliferation, and is correlated with poor prognosis of melanoma patients. However, the regulation mechanism has not been fully elaborated. Here, we detected hsa-let-7b expression and its role in melanoma. Through Targetscan and miRanda predication, 30 overlapped miRNAs were found; further survival analysis revealed that hsa-let-7b was the only miRNA that affected the overall survival. Overexpressed hsa-let-7b could significantly inhibit the proliferation ability of A375 and A2058 cells, and this phenomenon was reversed after co-transfection with pLenti-UHRF1. In conclusion, hsa-let-7b regulates melanoma cells proliferation in vitro by targeting UHRF1.

Identification of key candidate genes and molecular pathways in white fat browning: an anti-obesity drug discovery based on computational biology.

BACKGROUND: Obesity-with its increased risk of obesity-associated metabolic diseases-has become one of the greatest public health epidemics of the twenty-first century in affluent countries. To date, there are no ideal drugs for treating obesity. Studies have shown that activation of brown adipose tissue (BAT) can promote energy consumption and inhibit obesity, which makes browning of white adipose tissue (WAT) a potential therapeutic target for obesity. Our objective was to identify genes and molecular pathways associated with WAT and the activation of BAT to WAT browning, by using publicly available data and computational tools; this knowledge might help in targeting relevant signaling pathways for treating obesity and other related metabolic diseases. RESULTS: In this study, we used text mining to find out genes related to brown fat and white fat browning. Combined with biological process and pathway analysis in GeneCodis and protein-protein interaction analysis by using STRING and Cytoscape, a list of high priority target genes was developed. The Human Protein Atlas was used to analyze protein expression. Candidate drugs were derived on the basis of the drug-gene interaction analysis of the final genes. Our study identified 18 genes representing 6 different pathways, targetable by a total of 33 drugs as possible drug treatments. The final list included 18 peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists, 4 beta 3 adrenoceptor (ß3-AR) agonists, 1 insulin sensitizer, 3 insulins, 6 lipase clearing factor stimulants and other drugs. CONCLUSIONS: Drug discovery using in silico text mining, pathway, and protein-protein interaction analysis tools may be a method of exploring drugs targeting the activation of brown fat or white fat browning, which provides a basis for the development of novel targeted therapies as potential treatments for obesity and related metabolic diseases.

Aldehyde dehydrogenase-positive melanoma stem cells in tumorigenesis, drug resistance and anti-neoplastic immunotherapy.

Cancer stem cells (CSCs), a rare subset of cancer cells, are well known for their self-renewing capacity. CSCs play a critical role in therapeutic failure and are responsible for poor prognosis in leukemia and various solid tumors. However, it is still unclear how CSCs initiate carcinogenesis and evade the immune response. In humans, the melanoma initiating cells (MICs) are recognized as the CSCs in melanomas, and were verified to possess CSC potentials. The enzymatic system, aldehyde dehydrogenase (ALDH) is considered to be a specific marker for CSCs in several tumors. The expression of ALDH in MICs may be closely correlated with phenotypic heterogeneity, melanoma-genesis, metastasis, and drug resistance. The ALDH+ CSCs/MICs not only serve as an indicator for therapeutic efficacy, but have also become a target for the treat of melanoma. In this review, we initially introduce the multiple capacities of MICs in melanoma. Then, we summarize in vivo and in vitro studies that illustrate the relationship between ALDH and MICs. Furthermore, understanding of chemotherapy resistance in melanoma relies on ALDH+ MICs. Finally, we review studies that focus on melanoma immunotherapies, rendering ALDH a potential marker to evaluate the efficacy of anti-neoplastic therapies or an adjuvant anti-melanoma target.

Alda-1, an Aldehyde Dehydrogenase 2 Agonist, Improves Cutaneous Wound Healing by Activating Epidermal Keratinocytes via Akt/GSK-3ß/ß-Catenin Pathway.

BACKGROUND: The cutaneous wound healing process mainly comprises re-epithelialization, fibrosis, and neovascularization. Impaired wound healing is common but tricky in plastic surgery. Aldehyde dehydrogenase 2 (ALDH2), the most effective subset of the ALDH enzyme family, is known to exert a major role in detoxification of aldehydes. Activation of ALDH2 by Alda-1 (a specific agonist) has been found to protect against cardiovascular diseases. However, no research has paid attention to the potential of ALDH2 activation in regulating wound healing. The previous studies suggested a high expression of ALDH2 in normal skin tissue. The aim of this study was to investigate if Alda-1 may ameliorate wound healing. METHODS: A full-thickness excisional wound model was established in vivo. Adult male C57BL/6 mice were randomly divided into DMSO and Alda-1 groups. Mice received an intraperitoneal injection of DMSO or 10 mg/mL Alda-1 (10 mg/kg body weight, dissolved in DMSO) for 7 days. The wound healing rate was measured at 0, 3, 5, and 7 days. Distribution of ALDH2 in wound tissue was showed. ALDH2 enzymatic activity was examined at 3, 5, and 7 days. The elongation of epithelial tongue was detected by hematoxylin-eosin staining, and collagen deposition was analyzed by Masson's trichrome staining at 7 days. Expressions of alpha-smooth muscle actin (alpha-SMA), transforming growth factor beta (TGF-beta), CD31, collagen 1, collagen 3, and elastin were stained by immunohistochemistry at 5 and 7 days. The HaCaT cell line was applied in vitro. Proliferation and migration were tested using CCK8 and wound healing assay separately. The level of TGF-ß was examined by ELISA. Protein levels of the Akt/glycogen synthase kinase-3 beta (GSK-3 beta)/beta-catenin pathway were determined by western blotting. RESULTS: Alda-1 accelerated wound healing rates. ALDH2 activity in wound sites was restored. Alda-1 promoted the length of the epithelial tongue, collagen deposition, as well as expressions of alpha-SMA, TGF-beta, collagen 1/3, elastin, but did not affect CD31. Proliferation, migration, and TGF-ß secretion were promoted by Alda-1 and deregulated by CVT-10216 (an ALDH2 inhibitor). Protein variations of the Akt/GSK-3ß/ß-catenin pathway were found to accord with ALDH2 changes. CONCLUSIONS: Alda-1, an ALDH2 agonist, improves cutaneous wound healing in a full-thickness excisional wound model. Alda-1 activates proliferation, migration, and TGF-ß secretion of HaCaT (epidermal keratinocytes) by regulating the Akt/GSK-3ß/ß-catenin pathway. NO LEVEL ASSIGNED: This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

HDAC6 interacts with PTPN1 to enhance melanoma cells progression.

Histone deacetylase 6 (HDAC6) plays an important role in oncogenic transformation and cancer metastasis. Our previous study has demonstrated that HDAC6 was highly expressed in melanoma cells, and contributed to the proliferation and metastasis of melanoma cells. However, the underlying mechanism of HDAC6 in melanoma metastasis and progression remains largely unclear. In this study, we reported that HDAC6 directly interacted with Tyrosine-protein phosphatase non-receptor type 1 (PTPN1) by performing co-immunoprecipitation (Co-IP) combined with liquid chromatography tandem mass spectrometry (LC-MS/MS). HDAC6 increased the protein level of PTPN1 independent of histone modifying activity. In addition, PTPN1 promoted proliferation, colony formation and migration while decreased apoptosis of melanoma cells through activating extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, we found that matrix metallopeptidase 9 (MMP9) was increased by HDAC6/PTPN1/ERK1/2 axis, which might serve as a mechanism for melanoma invasion and metastasis. In conclusion, HDAC6 might enhance aggressive melanoma cells progression via interacting with PTPN1, which was independent of its histone modifying activity.

Knockdown of the KINDLIN-2 Gene and Reduced Expression of Kindlin-2 Affects Vascular Permeability in Angiogenesis in a Mouse Model of Wound Healing.

BACKGROUND Angiogenesis is an important component of wound healing and tissue repair. Kindlin-2 is an integrin-associated protein, encoded by the KINDLIN-2 gene, which has been shown to affect cell adhesion and migration of cells, including endothelial cells. The aim of this study was to use a mouse model of wound healing to evaluate the effects of expression of KINDLIN-2 on angiogenesis in wound healing in vivo. MATERIAL AND METHODS Thirty-six male C57BL/6 mice were studied in an established model that used a wound created on the back. Mice were divided randomly into three groups: the normal group (n=12) received injections of normal (0.9%) saline; the KINDLIN-2(-) group (n=12) received injections of adeno-associated virus with small interfering (si)RNA targeting the KINDLIN-2 gene (AAV-KINDLIN-2-siRNA); and the control (group (n=12) received injections of adeno-associated virus containing a scrambled RNA sequence (AAV-control-RNA). Wound healing was analyzed by biochemical examination of the exudates and histology. Evans blue dye was injected into the caudal vein of each mouse, two weeks after wound healing to assess neovascular permeability. RESULTS Wound healing was significantly delayed in the KINDLIN-2 gene knockdown mice (AAV-KINDLIN-2-siRNA) compared with that of the normal group and the control group, and neovascular permeability was increased. In the AAV-KINDLIN-2-siRNA group, blood vessels were shorter and thinner compared with the normal group and the control group. CONCLUSIONS In a mouse model of wound healing, KINDLIN-2 gene knockdown inhibited wound healing, and increased neovascular permeability in vivo.

Perioperative Glucocorticoid Treatment of Soft Tissue Reconstruction in Patients on Long-term Steroid Therapy: The Experience of 6 Cases Using Reversed Posterior Interosseous Flap for Hand Neoplasm Surgery.

INTRODUCTION: Long-term steroid therapy is associated with increased postoperative morbidity. Whether to use a stress dose of glucocorticoids (GCs) in surgical patients remains controversial. In the present study, we reported our experience in perioperative GC treatment of 6 patients on long-term steroid therapy for autoimmune diseases undergoing hand reconstruction using reversed interosseous flap. METHODS: The reversed interosseous flap reconstructions were performed after local extended resection of hand neoplasms. The patients were all diagnosed with autoimmune diseases and were undergoing long-term steroid therapy. Stress dose of GCs was not given in any case, and all the patients either remained on their baseline maintenance dose or decreased the dose until the morning of the operation day. Hypotension, water-electrolyte imbalance, hypoglycemia, and other symptoms of adrenal insufficiency were carefully assessed. Appearances of flap complications were recorded. RESULTS: None of the patients developed hypotension or other symptomatic adrenal insufficiency. Flap infection, venous congestion, or complete or partial loss of flap was not observed in any patient. Effusion underneath the flap was developed in only 1 case and was solved by proper drainage. CONCLUSIONS: It is safe, reliable, and versatile to use reversed interosseous flap to repair hand defects in patients on long-term steroid therapy. A stress dose of GCs might not be necessary in this procedure and other equally moderate soft tissue reconstructive surgeries.

Both HDAC5 and HDAC6 are required for the proliferation and metastasis of melanoma cells.

BACKGROUND: Histone deacetylase (HDAC) inhibitors are widely used in clinical investigation as novel drug targets. For example, panobinostat and vorinostat have been used to treat patients with melanoma. However, HDAC inhibitors are small-molecule compounds without a specific target, and their mechanism of action is unclear. Therefore, it is necessary to investigate which HDACs are required for the proliferation and metastasis of melanoma cells. METHODS: We used overexpression and knocking down lentivirus to clarify the influence of HDAC5 and HDAC6 in melanoma development. Also, we introduced stable HDAC5 or HDAC6 knockdown cells into null mice and found that the knockdown cells were unable to form solid tumors. Finally, we tested HDAC5 and HDAC6 expression and sub-location in clinical melanoma tissues and tumor adjacent tissues. RESULTS: In this study, and found that HDAC5 and HDAC6 were highly expressed in melanoma cells but exhibited low expression levels in normal skin cells. Furthermore, we knocked down HDAC5 or HDAC6 in A375 cells and demonstrated that both HDAC5 and HDAC6 contributed to the proliferation and metastasis of melanoma cells. CONCLUSIONS: This study demonstrated both HDAC5 and HDAC6 were required for melanoma cell proliferation and metastasis through different signaling pathways.

Pedicle muscle flap transposition for chronic empyema with persistent bronchopleural fistula: experience of a single clinical center in China.

PURPOSE: The management of chronic empyema with persistent bronchopleural fistula (BPF) is a major challenge for surgeons. We report our experience of performing pedicle muscle flap transposition for chronic empyema with BPF in a clinical center in China. METHODS: The subjects of this study were 13 patients with postoperative chronic empyema and persistent BPF. The surgical procedure performed was chosen according to the degree of infection in the empyema cavity. Patients with mild contamination underwent one-stage cavity decortication with flap transposition, whereas patients with severe infection underwent two-stage surgery including open-window thoracostomy and pedicle muscle flap transposition. RESULTS: Five patients underwent one-stage surgery, followed by an uneventful postoperative course in all except one. The other eight patients underwent two-stage surgery. The fistulas closed spontaneously during the course of dressings and six of these eight patients underwent second-stage surgery uneventfully. A bronchopleurocutaneous sinus developed in the wounds of the other two patients. CONCLUSIONS: Pedicle muscle flap transposition is a viable option for chronic empyema with BPF; however, surgical procedures should be selected according to the degree of contamination. For two-stage surgery, obliteration of the cavity should be considered, preferably after closure of the fistula.

A retrospective study on a hospital-based cleft care center in Shanghai.

OBJECTIVE: The objective of this investigation was to describe the characteristics of the current cleft treatment situation in a hospital-based cleft center in Shanghai and provide references to clinical diagnosis, treatment, and nursing. METHODS: A total of 1584 patients from the Center for Cleft Lip and Palate, Department of Oral and Cranio-Maxillofacial Science, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine during June 2006 to February 2008 were analyzed retrospectively. Data regarding sex, native place, type of cleft, cleft side, accompanied malformations, family history, and age at surgery were analyzed in detail. Length of stay after surgery, the primary operation fee, and some other hospitalized information were also investigated. RESULTS: From 1584 patients(1590 operations; 6 patients had 6 operations), there were 939 male and 645 female patients (M:F = 1.46:1). The number of Shanghai local patients is 249 (15.72%), whereas the other 1335 patients were from out of Shanghai. Approximately 15% of the patients had certain family history. The age at operating varied from 2 months to 36 years; the mean value was 6.95 years. The postoperation hospital stay varied from 1 day to 15 days; the mean value was 5.54 days. The primary operation fee was 235 to 673 USD depending on the different surgical procedures. The number of cleft types or other malformation, which had not been treated in the statistics varied from zero to 3; the mean value was 0.4375. The cleft morphology was classified as follows: cleft lip, 591 cases (37.31%); cleft palate, 651 cases (41.10%); alveolar cleft, 144 cases (9.10%); facial traverse cleft, 27 cases (1.70%); velopharyngeal insufficiency, 105 cases (6.63%); velocardiofacial syndrome, 57 cases (3.60%); and Pierre Robin sequence, 15 cases (0.95%). In all the classifications, left was more than right (L:R = 2.10:1). CONCLUSION: As a busy hospital-based cleft care center, most of the patients are from out of Shanghai. The current multidisciplinary protocol for cleft care in such specialist cleft center is cost-effective. There may be a tendency that the patients with cleft palate are more than the patients with cleft lips in recent years, which may due to the popularization of prenatal examination in China.