Background To compare the clinical efficacy and safety of rituximab (RTX) monotherapy versus the combination of RTX and glucocorticoids (GC) in the treatment of primary membranous nephropathy (PMN). Methods This retrospective, single-center cohort study enrolled 128 patients diagnosed with PMN between January 2021 and November 2024. 51 patients received RTX monotherapy and 77 patients received RTX + GC therapy, who were all followed up for 12 months. Primary outcomes were defined as the complete remission and partial remission. Secondary outcomes included the changes in proteinuria, serum albumin, serum creatinine, eGFR and adverse events during the follow-up time. Results Within 12 months of follow-up time, the complete remission rates in RTX + GC and RTX groups were 55.84% and 43.14%, and the composite remission rates were 88.31% and 86.27%, respectively, which were no significant difference by Kaplan–Meier survival analysis. No statistically significant difference was observed in proteinuria, serum albumin, serum creatinine and eGFR between the two groups during the 12 months. Compared with RTX group, the RTX + GC group exhibited a significantly higher incidence of adverse events. Moreover, the results of the logistic regression identified RTX + GC as an independent risk factor and eGFR as an independent protective factor for infection. Conclusion Compared with RTX monotherapy, RTX + GC therapy did not significantly improve the clinical remission rate of patients with PMN, but was associated with a substantially increased risk of infections. These findings warrant validation in large-scale, prospective, randomized controlled trials in the future.

Defining next-generation immune therapeutics for the treatment of sepsis will involve biomarker-based therapeutic decision-making. Bone morphogenetic protein 9 (BMP9) is a cytokine in the transforming growth factor–β superfamily. Here, circulating BMP9 concentrations were quantified in two independent cohorts of patients with sepsis. Decreased concentrations of serum BMP9 were observed in the patients with sepsis at the time of admission as compared with healthy controls. Concentrations of BMP9 at the time of admission were also associated with 28-day mortality, because patients with sepsis at a higher risk of death had lower BMP9 concentrations. The mechanism driving the contribution of BMP9 to host immunity was further investigated using in vivo murine sepsis models and in vitro cell models. We found that BMP9 treatment improved outcome in mice with experimental sepsis. BMP9-treated mice exhibited increased macrophage influx into the peritoneal cavity and more efficient bacterial clearance than untreated mice. In vitro, BMP9 promoted macrophage recruitment, phagocytosis, and subsequent bacterial killing. We further found that deletion of the type 1 BMP receptor ALK1 in macrophages abolished BMP9-mediated protection against polymicrobial sepsis in vivo. Further experiments indicated that the regulation of macrophage activation by the BMP9-ALK1 axis was mainly mediated through the suppressor of mother against decapentaplegic 1/5 signaling pathway. Together, these results suggest that BMP9 can both serve as a biomarker for patient stratification with an independent prognostic value and be developed as a host-directed therapy for sepsis.

SASH1 (SAM and SH3 domain containing 1) has been increasingly reported as a tumor suppressor gene. However, there is limited research on the role of SASH1 in breast cancer. This manuscript aims to investigate the mechanism of SASH1 in the occurrence, development, and prognosis of breast cancer. Firstly, we obtained RNA-sequencing data of the tumors from the Genomic Data Commons data portal website, along with the corresponding clinical information of patients. Pan-cancer analysis was performed to analyze the expression of SASH1 across all tumors. Univariate Cox regression analysis was used to assess the correlation between SASH1 expression and the prognosis of breast cancer patients. Then, immunohistochemistry was utilized to evaluate the expression levels of SASH1, p-Akt, p-PI3K, and p-mTOR in breast cancer tissue. Finally, a cell assay was employed to analyze the impact of SASH1 on the proliferation and invasion of breast cancer cells (MDA-MB-231). The results revealed that SASH1 expression is decreased in BRCA, LUSC, LUAD, CESC, ESCA, and COAD. Meta-analysis also found that SASH1 is downregulated in most tumor tissues, and the expression level of SASH1 in breast cancer was significantly lower than that in the control group (OR = 0.14, 95% CI = 0.08-0.25; P < 0.001). Further experimental validation showed that SASH1 expression is significantly downregulated in breast cancer tissue (38.33%, 23/60), and the overexpression of SASH1 can inhibit the proliferation and invasion of breast cancer cells accompanied by the suppression of PI3K-Akt-mTOR signaling pathway. Additionally, SASH1 overexpression can improve OS and RFS of breast cancer patients.

Sepsis shock was associated with worse mortality than common sepsis caused by disseminated infection. The present study had shown that repression of adaptive immunity was a characteristic of sepsis shock rather than sepsis, but the mechanism in which it exerted the adverse reaction was still need to be studied. In this study, we first employed weighted gene co-expression network analysis for acquiring the key modules with sepsis shock. Then, the differentially expressed genes and transcription factors were screened in the module for further function analysis, protein-protein interaction network building and long noncoding ribonucleic acid-micro ribonucleic acid-transcription factor network study. The study strengthened the concept that adaptive immune repression typically featured the sepsis shock concerning antigen presentation via major histocompatibility complex class II, T-cell activation and T-cell depletion. Among which T-cell depletion ranked as an overwhelming contributor to sepsis shock outcome. The transcription factor tumor protein P53, forkhead box protein O1 and GATA binding protein 3 served as the master regulator for the T-cell depletion process mainly through driving hematopoietic stem cells out of quiescence to unrestrained hematopoietic stem cell expansion with detrimental deoxyribonucleic acid damage, which greatly decreased hematopoietic stem cells long-term differentiation potential into T lymphocyte hierarchy. The study enlightened that manipulating the expression level of tumor protein P53, forkhead box protein O1 and GATA binding protein 3 to an optimized state will guarantee the T cell replenishment for fighting sepsis shock, which might support a potential efficient therapeutic way for sepsis shock treatment.

HCC is one of the most common malignant tumors. The life and health of humans are gravely threatened by HCC because of its hidden onset, high recurrence rate, poor therapeutic effect, and high mortality. It is essential to explore the particular pathological mechanisms of HCC in order to increase the rate of early diagnosis and enhance patient therapy outcomes. Recent research has demonstrated that SCUBE3 can influence HCC cell proliferation by regulating the TGFβ/PI3K/AKT/GSK3β pathway. The molecular regulatory network of HCC proliferation is improved by this research, which also offers a solid theoretical and experimental foundation for SCUBE3 as a potential new therapeutic target for HCC.

Background:The present study aimed to compare the safety and efficacy of minimally invasive hepatic resection (HR) and radiofrequency ablation (RFA) in the treatment of single small hepatocellular carcinoma via systematic review and meta-analysis.Methods:We conducted electronic literature searches of PubMed, Embase, and The Cochrane Library databases, A case-controlled trial comparing HR and RFA in the treatment of single small hepatocellular carcinoma published between 2010 and January 15, 2022 was searched and reported outcomes were overall survival, postoperative complications, intraoperative blood loss, duration of surgery, and recurrence. Literature met inclusion criteria were screened out, and the quality of the methodology used in the included literature was evaluated using the Newcastle-Ottawa Scale (NOS). Meta-analysis was performed using RevMan 5.4 software.Results:Eleven articles were included, including 2,001 patients, including 1,071 in the RFA group and 930 in the HR group. Offset risk assessment results are published offset. Meta-analysis showed that the overall survival rate at 1, 3, and 5 years in RFA group was higher than that in HR group, the difference between the two groups was statistically significant at 1 year [odds ratio (OR) =1.57, 95% confidence interval (CI): 1.14, 2.17, P=0.006], 3 years (OR =1.81, 95% CI: 1.42, 2.30, P<0.00001], and 5 years (OR =1.87, 95% CI: 1.47, 2.37, P<0.00001). The incidence of postoperative complications was significantly lower in the RFA group than in the human resources group [risk ratio (RR) =1.75, 95% CI: 1.02, 3.00, P=0.04], and length of hospital stay [standard mean difference (SMD) =2.92, 95% CI: 0.54, 5.30, P=0.02], operation time (SMD =2.87, 95% CI: 2.57, 3.16, P<0.00001) were shorter than those in HR group. However, the recurrence rate of RFA group was higher than that of HR group (OR =0.49, 95% CI: 0.36, 0.66, P<0.00001).Conclusions:RFA has the advantage of having more advantages and fewer complications in the treatment of small hepatocellular carcinoma. Minimal complications can occur for patients when achieving satisfactory treatment results. A new treatment option is available for clinicians in the treatment of small liver cancer.

Background The ratio of SpO 2 /FiO 2 to respiratory rate (ROX) index is commonly used to predict the failure of high-flow nasal cannula. However, its predictive power for noninvasive ventilation (NIV) failure is unclear. Methods This was a secondary analysis of a multicenter prospective observational study, intended to update risk scoring. Patients with de novo acute respiratory failure were enrolled, but hypercapnic patients were excluded. The ROX index was calculated before treatment and after 1–2, 12, and 24 h NIV. Differences in predictive power for NIV failure using the ROX index, PaO 2 /FiO 2 , and PaO 2 /FiO 2 /respiratory rate were tested. Results A total of 1286 patients with de novo acute respiratory failure were enrolled. Of these, 568 (44%) experienced NIV failure. Patients with NIV failure had a lower ROX index than those with NIV success. The rates of NIV failure were 92.3%, 70.5%, 55.3%, 41.1%, 35.1%, and 29.5% in patients with ROX index values calculated before NIV of ≤ 2, 2–4, 4–6, 6–8, 8–10, and > 10, respectively. Similar results were found when the ROX index was assessed after 1–2, 12, and 24 h NIV. The area under the receiver operating characteristics curve was 0.64 (95% CI 0.61–0.67) when the ROX index was used to predict NIV failure before NIV. It increased to 0.71 (95% CI 0.68–0.74), 0.74 (0.71–0.77), and 0.77 (0.74–0.80) after 1–2, 12, and 24 h NIV, respectively. The predictive power for NIV failure was similar for the ROX index and for the PaO 2 /FiO 2 . Likewise, no difference was found between the ROX index and the PaO 2 /FiO 2 /respiratory rate, except at the time point of 1–2 h NIV. Conclusions The ROX index has moderate predictive power for NIV failure in patients with de novo acute respiratory failure.

Background and Purpose: Breast cancer is one of the leading causes of death among women. RNA binding proteins (RBPs) play a vital role in the progression of many cancers. Functional investigation of RBPs may contribute to elucidating the mechanisms underlying tumor initiation, progression, and invasion, therefore providing novel insights into future diagnosis, treatment, and prognosis. Methods: We downloaded RNA sequencing data from the cancer genome atlas (TCGA) by UCSC Xena and identified relevant RBPs through an integrated bioinformatics analysis. We then analyzed biological processes of differentially expressed genes (DEGs) by DAVID, and established their interaction networks and performed pathway analysis through the STRING database to uncover potential biological effects of these RBPs. We also explored the relationship between these RBPs and the prognosis of breast cancer patients. Results: In the present study, we obtained 1092 breast tumor samples and 113 normal controls. After data analysis, we identified 90 upregulated and 115 downregulated RBPs in breast cancer. GO and KEGG pathway analysis indicated that these significantly changed genes were mainly involved in RNA processing, splicing, localization and RNA silencing, DNA transposition regulation and methylation, alkylation, mitochondrial gene expression, and transcription regulation. In addition, some RBPs were related to histone H3K27 methylation, estrogen response, inflammatory mediators, and translation regulation. Our study also identified five RBPs associated with breast cancer prognosis. Survival analysis found that overexpression of DCAF13, EZR, and MRPL13 showed worse survival, but overexpression of APOBEC3C and EIF4E3 showed better survival. Conclusion: In conclusion, we identified key RBPs of breast cancer through comprehensive bioinformatics analysis. These RBPs were involved in a variety of biological and molecular pathways in breast cancer. Furthermore, we identified five RBPs as a potential prognostic biomarker of breast cancer. Our study provided novel insights to understand breast cancer at a molecular level.

Purpose: To investigate the impact of Ramipril (RAM) on the expressions of insulin-like growth factor-1 (IGF-1) and renal mesangial matrix (RMM) in rats with diabetic nephropathy (DN). Methods: The Sprague Dawley rats were divided into normal control (NC) group (n = 12), DN group (n = 11), and DN+RAM group (n = 12). The ratio of renal weight to body weight (RBT), fasting blood glucose (FBG), HbA1c, 24-h urine protein (TPU), blood urea nitrogen (BUN), creatinine (Cr), renal pathological changes, the levels of IGF-1, fibronectin (FN), type IV collagen (Col-IV), and matrix metalloproteinases (MMP)-2 were compared among the groups. Results: Compared with NC group, the RBT, FBG, HbA1c, TPU, BUN, Cr, and RMM in DN group were significantly increased (P < 0.05), the IGF-1, FN, and Col-IV were significantly upregulated (P < 0.05), while MMP was significantly downregulated (P < 0.05). Compared with DN group, the indexes except for the FBG and HbA1c in DN+RAM group were significantly improved (P < 0.05), among which IGF-1 exhibited significant positive correlation with TPU(r=0.937), FN(r=0.896) and Col-IV(r=0.871), while significant negative correlation with MMP-2 (r=-0.826) (P<0.05). Conclusion: RAM may protect the kidneys by suppressing IGF-1 and mitigating the accumulation of RMM.

为了研究CTNNBIP1和ICMT基因共表达在膀胱尿路上皮癌中的作用及对患者预后的诊断价值,本研究选取癌症基因组图谱(TCGA)数据库中412例膀胱尿路上皮癌数据资料,利用cBioPortal数据库对膀胱尿路上皮癌CTNNBIP1基因、ICMT基因及其共表达基因作生存分析,将Pearson和Spearman相关系数均大于0.3的基因定义为中等程度以上共表达相关的基因.通过String数据库获取这些基因共表达的互作关系组.采用DAVID数据库、GO数据库、KEGG数据库分别对其进行信号通路和功能分析,生物学过程聚类分析,信号通路聚类分析.结果 显示:TCGA数据库中的膀胱尿路上皮癌患者CTNNBIP1和ICMT存在共表达(Pearson相关系数=0.46和Spearman相关系数=0.47).String数据库显示基因共表达有38组具有互作关系.KEGG数据库显示CTNNBIP1-ICMT基因共表达所富集的信号通路集中在细胞周期(P＜0.05).DAVID数据库分析其功能主要为调节细胞生长和有丝分裂、负性调控Wnt信号通路、蛋白激酶结合等.生存分析证实CTNNBIPI1和ICMT基因共表达与患者总生存率显著相关(p=0.002 72),CTNNBIPI1和ICMT共表达阳性患者的预后最差.由此得出结论:CTNNBIPl和ICMT在膀胱尿路上皮癌中存在共表达,对CTNNBIP1-ICMT基因共表达网络和生物信息学分析,可找到其在膀胱尿路上皮癌中的作用及信号通路,为深入研究膀胱尿路上皮癌的发病机制提供了理论基础,可提高膀胱尿路上皮癌患者的预后.

Abstract Purpose To investigate the impact of Ramipril (RAM) on the expressions of insulin-like growth factor-1 (IGF-1) and renal mesangial matrix (RMM) in rats with diabetic nephropathy (DN). Methods The Sprague Dawley rats were divided into normal control (NC) group (n = 12), DN group (n = 11), and DN+RAM group (n = 12). The ratio of renal weight to body weight (RBT), fasting blood glucose (FBG), HbA1c, 24-h urine protein (TPU), blood urea nitrogen (BUN), creatinine (Cr), renal pathological changes, the levels of IGF-1, fibronectin (FN), type IV collagen (Col-IV), and matrix metalloproteinases (MMP)-2 were compared among the groups. Results Compared with NC group, the RBT, FBG, HbA1c, TPU, BUN, Cr, and RMM in DN group were significantly increased (P < 0.05), the IGF-1, FN, and Col-IV were significantly upregulated (P < 0.05), while MMP was significantly downregulated (P < 0.05). Compared with DN group, the indexes except for the FBG and HbA1c in DN+RAM group were significantly improved (P < 0.05), among which IGF-1 exhibited significant positive correlation with TPU(r=0.937), FN(r=0.896) and Col-IV(r=0.871), while significant negative correlation with MMP-2 (r=-0.826) (P<0.05). Conclusion RAM may protect the kidneys by suppressing IGF-1 and mitigating the accumulation of RMM.

Our previous study has demonstrated that 4-amino-2-trifluoromethyl-phenyl Retinate (ATPR) can induce human leukemia NB4 cells differentiation and G0/G1 phase arrest, but the underlying mechanism is still unclear. In this study, we used proteomics to screen differentially expressed protein profiles in NB4 cells before and after ATPR treatment in vitro. We analyzed the peptides digested from total cellular proteins by reverse phase LC-MS/MS and then performed label-free quantitative analysis. We found 27 significantly up-regulated proteins in the ATPR group compared to the control group. NCF1 was the most significantly changed protein. Immunoprecipitation and double immunofluorescent staining showed that EBP50 bind to NCF1. We further explored the potential molecular mechanism of EBP50/NCF1 complex in ATPR-induced differentiation and G0/G1 phase arrest. The results showed that ATPR remarkably reduced the expression of EBP50 in vivo and in vitro. Interestingly, the reduction of EBP50 contributed to ROS release by modulating the subcellular localization of NCF1. The reduction of EBP50 also contributed to G0/G1 phase arrest by inhibiting CyclinD1, CyclinA2 and CDK4, as well as promoting the differentiation of NB4 cells by increasing the expression of CD11b. Furthermore, we found that the overexpression of EBP50 restrained the effects of ATPR on differentiation and G0/G1 phase arrest in NB4 cells. These results suggest that ATPR-induced differentiation and G0/G1 phase arrest in acute promyelocytic leukemia (APL) by repressing EBP50/NCF1 complex to promote the production of ROS, and the results from in vivo experiments were consistent with those from in vitro studies. Therefore, our finding results suggest that EBP50 may be a new target for ATPR in the treatment of APL.

Bone morphogenetic protein 9 (BMP9) is a member of the BMP family, which is involved in the regulation of tumor biogenesis, development and metastasis. The present study aimed to investigate whether BMP9 inhibits the growth of MDA‑MB‑231 breast cancer cells via the phosphoinositide 3‑kinase (PI3K)/Akt signaling pathway. It was shown that the expression level of BMP9 was significantly decreased, while that of phosphorylated Akt (p‑Akt) was markedly increased in breast cancer tissues compared with these levels in the normal adjacent tissues. An adenovirus overexpressing BMP9 was used to infect the MDA‑MB‑231 cells. The expression level of p‑Akt in the MDA‑MB‑231/BMP9 group was shown to be significantly lower than that in the MDA‑MB‑231/green fluorescent protein (GFP) and MDA‑MB‑231 control groups. The expression levels of cyclins D1, B1 and E1, c‑Myc and matrix metalloproteinase 9 (MMP9) in the MDA‑MB‑231/BMP9 group were also reduced. The generation of a nude mouse xenograft tumor model revealed that the tumor volumes of the MDA‑MB‑231/BMP9 group (0.32±0.05 cm3) was significantly lower compared with that of the MDA‑MB‑231/GFP (1.10±0.05 cm3) and MDA‑MB‑231 (1.12±0.12 cm3) groups, and the expression level of p‑Akt protein in the MDA‑MB‑231/BMP9 group was significantly lower compared with that of the MDA‑MB‑231/GFP and MDA‑MB‑231 groups in the nude mouse xenograft model. Taken together, these results indicate that BMP9 inhibits the growth of MDA‑MB‑231 breast cancer cells by inhibiting the PI3K/Akt signaling pathway both in vivo and in vitro.

We previously reported that three point mutations in SASH 1 and mutated SASH 1 promote melanocyte migration in dyschromatosis universalis hereditaria ( DUH ) and a novel p53/ POMC /Gαs/ SASH 1 autoregulatory positive feedback loop is regulated by SASH 1 mutations to induce pathological hyperpigmentation phenotype. However, the underlying mechanism of molecular regulation to cause this hyperpigmentation disorder still remains unclear. In this study, we aimed to investigate the molecular mechanism undergirding hyperpigmentation in the dyschromatosis disorder. Our results revealed that SASH 1 binds with MAP 2K2 and is induced by p53‐ POMC ‐ MC 1R signal cascade to enhance the phosphorylation level of ERK 1/2 and CREB . Moreover, increase in phosphorylated ERK 1/2 and CREB levels and melanogenesis‐specific molecules is induced by mutated SASH 1 alleles. Together, our results suggest that a novel SASH 1/ MAP 2K2 crosstalk connects ERK 1/2/ CREB cascade with p53‐ POMC ‐ MC 1R cascade to cause hyperpigmentation phenotype of DUH .

p53‐Transcriptional‐regulated proteins interact with a large number of other signal transduction pathways in the cell, and a number of positive and negative autoregulatory feedback loops act upon the p53 response. P53 directly controls the POMC /α‐ MSH productions induced by ultraviolet ( UV ) and is associated with UV ‐independent pathological pigmentation. When identifying the causative gene of dyschromatosis universalis hereditaria ( DUH ), we found three mutations encoding amino acid substitutions in the gene SAM and SH 3 domain containing 1 ( SASH 1), and SASH 1 was associated with guanine nucleotide‐binding protein subunit‐alpha isoforms short (Gαs). However, the pathological gene and pathological mechanism of DUH remain unknown for about 90 years. We demonstrate that SASH 1 is physiologically induced by p53 upon UV stimulation and SASH and p53 is reciprocally induced at physiological and pathophysiological conditions. SASH 1 is regulated by a novel p53/ POMC /α‐ MSH /Gαs/ SASH 1 cascade to mediate melanogenesis. A novel p53/ POMC /Gαs/ SASH 1 autoregulatory positive feedback loop is regulated by SASH 1 mutations to induce pathological hyperpigmentation phenotype. Our study demonstrates that a novel p53/ POMC /Gαs/ SASH 1 autoregulatory positive feedback loop is regulated by SASH 1 mutations to induce pathological hyperpigmentation phenotype.

This paper presents the development of a low-cost integrated control system for aerial survey based on pan-tilt and multi-sensor data fusion. The design of aerial vehicle route planning, pan-tilt mechanical structure and attitude estimation are discussed in detail. A route planning file containing flight paths and automatic exposure points is firstly derived by the route plan software to control the whole aerial photography task. As for the most challenging task, accurate attitude estimation, a custom Kalman filtering hardware module based on FPGA is introduced. The introduced module invokes the build-in multipliers of FPGA to achieve Kalman filtering hardware implementation, which leads to a rapid attitude estimation. After that mechanical structure of a specialized pan-tilt is designed and fabricated to adjust the camera attitude to the vertical direction of the ground plane. The practice aerial survey is also conducted to evaluate the accuracy and performance of designed control system. Our studies indicates that with the designed control system, it would be feasible to configure an aerial survey system while cooperate with professional aerial camera or some other civil cameras, which will make it easier to focusing on evaluation of aerial survey concepts and approaches.

An enhanced anti-apoptotic capacity of tumor cells plays an important role in the process of breakpoint cluster region/Abelson tyrosine kinase gene (BCR/ABL)-independent imatinib resistance. We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis. However, the mechanism by which BEX1 executes its pro-apoptotic function remains unknown. We identified B-cell lymphoma 2 (BCL-2) as a BEX1-interacting protein using a yeast two-hybrid screen. The interaction between BEX1 and BCL-2 was subsequently confirmed by co-immunoprecipitation assays. Like BCL-2, BEX1 was localized to the mitochondria. The region between 33K and 64Q on BEX1 is important for its localization to the mitochondria and its ability to interact with BCL-2. Additionally, we found that this region is essential for BEX1-regulated imatinib-induced apoptosis. Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers. Our results revealed an interaction between BEX1 and BCL-2 and a novel mechanism of imatinib resistance mediated by the BEX1/BCL-2 pathway.

Objective To design a temperature control system for glass-polydimethylsiloxane(PDMS) perfusion cell culture chips to replace the traditional cell culture incubator.This system has a better integration with cell infusion culture devices and facilitates continuous observation under a microscope in the process of cell culture.Methods In this system,the transparent indium tin oxide(ITO) coated conductive glass was used as a heating element,a Pt100 sensor was used as temperature sensor,and a closed loop temperature control system was constructed with a PID controller.A glass-PDMS cell culture chip was fabricated using micro-wires molding technology.The temperature field distribution on the ITO heating element surface was verified by infrared thermal imaging experiments.Space temperature field distribution in the cell culture chip on this ITO heating element was checked through numerical simulation.Results and Conclusion The designed temperature control system had a simple structure and a good accuracy of 0.2℃.A uniform space temperature field distribution could be obtained on the heating element surface and in the cell culture chip culture cavity.Human lung cancer cells A549 perfusion culture experiments show that this designed system not only provides a fine temperature environment for cell culture,but is applicable to dynamic characterization of biological behavior of cells.