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The intermediate fluid thermoelectric generator (IFTEG) represents a novel approach to power generation, predicated upon the principles of gravity heat pipe technology. Its key advantages include high-power output and a compact module area. The generator’s performance, however, is influenced by the variable exhaust parameters typical of automobile operation, which presents a significant challenge in the design process. The present study establishes a mathematical model to optimize the design of the IFTEG. Our findings suggest that the optimal module area sees substantial growth with an increase in both the exhaust heat exchanger area and the exhaust flow rate. Interestingly, the optimal module area appears to demonstrate a low sensitivity to changes in exhaust temperature. To address the challenge of determining the optimal module area, this study introduces the concept of peak power deviation. This method posits that any deviation from the optimal module area results in an equivalent power deviation. For instance, with an exhaust heat exchanger area of 1.6 m2, the minimum peak power deviation is 27.5%, corresponding to a design module area of 0.124 m2. As such, the actual output power’s deviation from the maximum achievable output power will not exceed 27.5% for any given set of exhaust parameters. This study extends its findings to delineate the relationship between the optimal design module area and the exhaust heat exchanger area. These insights could serve as a useful guide for the design of future power generators.

Thermoelectric generator can directly convert thermal energy into electrical energy, and applying it to recover waste heat from automobile exhaust is conducive to energy saving. In this paper, a thermoelectric generation experimental system is built, the power output performance and channel power consumption of the flat-plate thermoelectric power generation system under different exhaust gas flow rates are experimentally studied. The results show that when the exhaust flow rate is 40 Nm3/h and the exhaust inlet temperature is 400 °C, the maximum output power of the system is 26.8 W, and the maximum net output power is about 23.3 W. In addition, the exhaust flow rate is changed from 10 Nm3/h to 40 Nm3/h, and the proportion of power consumption in the hot air channel is changed from 1.91% to 12.85%, which has increased by more than six times.

PurposeTo explain how the tumor microenvironment (TME) contributes to biological and clinical heterogeneity of colorectal cancer (CRC).MethodsUsing multi-omics analysis, single cell transcriptomic sequencing analysis and artificial intelligence-enabled spatial analysis of whole-slide images, we performed a comprehensive characterization of TME in colorectal cancer (CCCRC).ResultsCRC samples were classified into four CCCRC subtypes with distinct TME features, namely, C1 as the proliferative subtype with low immunogenicity; C2 as the immunosuppressed subtype with the terminally exhausted immune characteristics; C3 as the immune-excluded subtype with the distinct upregulation of stromal components and a lack of T cell infiltration in tumor core; and C4 as the immunomodulatory subtype with the remarkable upregulation of anti-tumor immune components. The four CCCRC subtypes had distinct histopathological and molecular characteristics, therapeutic efficacy, and prognosis. The C1 subtype was more sensitive to chemotherapy, the C2 and C3 subtypes were more sensitive to WNT pathway inhibitor SB216763 and Hedgehog pathway inhibitor vismodegib, and the C4 subtype was suitable for ICB treatment. Finally, we established a single-sample gene classifier for identifying the CCCRC subtypes.ConclusionsOur integrative analyses ultimately established a holistic framework to thoroughly dissect the TME of CRC, and the CCCRC classification system with high biological interpretability might facilitate biomarker discoveries and clinical treatment decisions in the future.

Data mining(DM) has been widely used in researching the auxiliary diagnosis of cancer. Circulating miRNAs are related to the occurrence and development of various cancer types. For this reason, they have the potential to be used as biomarkers for early tumor diagnosis. Previously, we found that SVM model combined with plasma miRNAs biomarkers could be a method for lung cancer prediction; However, it still has some limitations. So this study further enlarges the analysis to other DM techniques, and explores more accurate methods for auxiliary diagnosis of lung cancer. Univariate analysis showed the differences had statistical significance in the smoking, fever, chest tightness or pain, cough, bloody phlegm, haemoptysis, and 10 plasma miRNAs (miR-21, miR-20a, miR-210, miR-145, miR-126, miR-223, miR-197, miR-30a, miR-30d, and miR-25) between the lung cancer group and normal control group (P < 0.05); Logistic regression analysis showed that fever, chest pain or tightness, cough, miR-21, and miR-223 could be considered as indicators of the presence of cancer (P

Alternative splicing (AS) of pre-mRNAs is an essential process that regulates gene expression and functional diversity, yet the underlying regulatory mechanisms that control this process during cancer metastasis are not clear. Here, we uncovered that a long non-coding RNA (lncRNA), MIR99AHG, mediates regulation of AS to alter chromatin remodeler function and promote invadopodia formation in colorectal cancer (CRC). We found that MIR99AHG is highly expressed in metastatic CRC cells and patient tissue samples. In vitro and in vivo assays showed that MIR99AHG potently drove CRC cell motility, invasion, and metastasis. MIR99AHG bound to and stabilized the RNA splicing factor PTBP1, which cooperatively increased cassette exon inclusion of the chromatin remodeling gene SMARCA1. Mechanistically, MIR99AHG acted as an address label for PTBP1 to fine-tune its binding pattern on SMARCA1 pre-mRNA, thereby controlling the skipping-to-inclusion splicing switch of SMARCA1 and favouring the production of a long isoform (SMARCA1-L). Canonical SMARCA1 was found to suppress cell migration and invasiveness by inhibiting invadopodia formation, but SMARCA1-L was functionally inert. Clinicaldata revealed that MIR99AHG was positively correlated with PTBP1 and SMARCA1-L in human CRC specimens and predicted patient outcome. Furthermore, we showed that the crosstalk with cancer-associated fibroblasts triggers TGF-β/SAMD signalling in CRC cells and activates MIR99AHG expression. Our findings establish a novel mechanism for a lncRNA that interacts with PTBP1 to regulate AS process, providing a potential therapeutic target and predictive biomarker of CRC.

The incidence of lung cancer tends to be younger, and adenocarcinoma is the main histological type. Even patients with the same tumor type may have significant differences in clinical features, tumor microenvironment and genomic background at different ages. Immune checkpoint inhibitors (ICIs) have been shown to improve clinical outcomes in patients with lung adenocarcinoma (LUAD). However, differences in ICI efficacy between older and younger patients are unknown. Our study aimed to explore the relationship between age and immunotherapy in LUAD.In our study, 1313 resected LUAD patients in our hospital were divided into young (age ≤ 50) and old groups (age 50), and the clinical characteristic differences between them were analyzed. Of these, next-generation sequencing (NGS) was performed on the 311 cases. In addition, immune-related signatures of 508 LUAD patients were analyzed by TCGA RNA expression data. Then, we validated genomic and clinical information of 270 LUAD samples in the MSKCC cohort.ERBB2 and EGFR gene mutations were significantly different between the two groups, and the gene mutation number in the old group was significantly higher than that in the young group. In addition, immune-related signatures of LUAD patients were analyzed by TCGA RNA expression data, which indicated that the patients in the old group might have a better immune microenvironment. Then, we validated the MSKCC cohort and found that the TMB of the old group was significantly higher than that of the young group, and the OS of immunotherapy was longer in the old group.Our study was the first to analyze the differences in the genomic landscape and immune-related biomarkers between the young and old groups of LUAD patients and found that the old group had a better efficacy of immunotherapy, providing a reference for the study design and treatment of patients with LUAD.

Malignant progression such as bone metastasis, which is associated with pathologic fractures, pain and reduced survival frequently occurs in prostate cancer (PCa) patients at advanced stages. Accumulating evidence has supported that long non-coding RNAs (lncRNAs) participate in multiple biological processes. Nevertheless, the functions of most lncRNAs in PCa malignant progression remain largely unclear. Our current study is to elucidate the influence of lncRNA lncNAP1L6 on PCa malignant progression and uncover the possible regulatory mechanism. Firstly, RT-qPCR analysis was to detect lncNAP1L6 expression and suggested that lncNAP1L6 was markedly upregulated in PCa cells. Functional assays manifested that silencing of lncNAP1L6 hampered cell migration, invasion, and epithelial-mesenchymal transition (EMT) while overexpression of lncNAP1L6 exacerbated cell migration, invasion and EMT. In addition, mechanism assays were to determine the latent regulatory mechanism of lncNAP1L6. It turned out that METTL14/METTL3 complex mediated m6A methylation of NAP1L2 mRNA. Besides, lncNAP1L6 recruited HNRNPC to m6A-modified NAP1L2, leading to stabilization of NAP1L2 mRNA. Moreover, NAP1L6 interacted with YY1 to promote the transcription of MMP2 and MMP9 and activate MMP signaling pathway. In summary, lncNAP1L6 was identified as an oncogene in PCa, which revealed that lncNAP1L6 might be used as potential therapeutic target in PCa.

Background The small GTPase Ran is upregulated in multiple cancers and fundamental for cancer cell survival and progression, but its significance and molecular mechanisms in colorectal cancer (CRC) remain elusive. Methods Ran expression was detected in CRC cell lines and tumour tissues. In vitro and in vivo functional assays were performed to examine the effects of Ran on cell proliferation and metastasis. The pathways and effectors regulated by Ran were explored by an unbiased screening. Bioinformatics prediction and experimental validation were used to identify the miRNA regulator for Ran. Results Ran expression was frequently increased in metastatic CRC cells and tissues, especially in metastatic tissues. The upregulation of Ran correlated with poor CRC patient prognosis. Ran silencing reduced proliferation and metastasis of CRC cells both in vitro and in vivo. Ran regulated the expression of EGFR and activation of ERK and AKT signalling pathways. miR-802 was identified as an upstream regulator of Ran and miR-802 overexpression resulted in antiproliferative and antimetastatic activities. Conclusion Our study demonstrates the oncogenic roles and underlying mechanisms of Ran in CRC and the novel miR-802/Ran/EGFR regulatory axis may provide potential biomarkers for the treatment of CRC.

Background Metastasis leads to recurrence and death in colorectal cancer (CRC) patients; however, mechanisms underlying CRC metastasis, especially in its initial stages, remain largely unknown. In this study, we aim to identify long noncoding RNAs (lncRNAs) functionally involved in CRC metastasis initiation and their regulation that could lead to targeted therapeutics. Methods We performed whole transcriptome sequencing using CRC cell lines with divergent spontaneous metastatic properties. The biological roles and mechanisms of lncRNA MIR99AHG were characterized with a series of in vitro and in vivo models and molecular analyses. Results MIR99AHG was upregulated in CRC patients and associated with tumor stage and prognosis. MIR99AHG potently drove migration, invasion and metastasis in CRC cells, and these effects were dependent on its role in promoting invadopodia formation. MIR99AHG interacted with RNA splicing factor PTBP1, which cooperatively modulated alternative splicing of chromatin remodeling gene SMARCA1. Mechanistically, MIR99AHG acted as an address label for PTBP1 to direct its binding to the 5’ splice site of SMARCA1 intron 12, thereby facilitating inclusion of the alternative exon 13 to generate a long isoform (SMARCA1-L). The canonical SMARCA1 inhibited cell migration and invasion and suppressed a core set of genes involved in invadopodia, but the SMARCA1-L was functionally inert in metastasis suppression. Clinically, SMARCA1-L levels were positively correlated with MIR99AHG and PTBP1 in patients with metastatic CRC. Conclusions This study identified that invadopodia was regulated by a splicing switch of SMARCA1 due to the interaction between MIR99AHG and PTBP1, highlighting a novel regulatory mode mediated by lncRNA in alternative splicing of chromatin remodeler during CRC metastasis.

Background: DICER1 plays a significantly important role in short dsRNA-mediated post-transcriptional gene silencing that is deeply embedded in the network of cancer genes. Aberrant expression and mutation of DICER1 have been studied and reported to be closely associated with tumorigenesis and development, while lower levels of DICER1 mRNA or protein are associated with poorer prognosis in some cancers. However, there is little research about the effect and mechanism of mutated DICER1. Materials and Methods: In our study, DICER1 mutation in the TCGA database from the top 10 cancers were analyzed to explore the effect of DICER1 mutants in cancer prognosis and the possible potential mechanisms. Results: We found that DICER1 mutation was closely related to better clinical outcomes in pan-cancer and uterine corpus endometrial carcinoma (UCEC) treatment, which meant that DICER1 could be served as a prognosis factor for pan-cancer, especially UCEC. And mechanism research indicated that DICER1-mut facilitated antitumor immunity, which could be the potential mechanism for DICER1-mut prognosis value. Moreover, tumor microenvironment (TME) features and higher TMB of DICER1-mut manifested that DICER1 may be a potential biomarker of immunotherapy, which needed more clinical and basic research to validate.Conclusions: In summary, our finding suggested that DICER1 may be a potential prognostic biomarker and was associated with TME in UCEC. In addition, it might be a marker of immunotherapy.

Simple Summary Colorectal cancer (CRC) is the third leading cause for cancer related death, in which metastasis exerts a pivotal role. Therefore, we aim to find out the possible mechanism underlying CRC metastasis. We found that the level of miR-125b was elevated in normal, primary CRC, and distant metastasis tissues stepwise, and high level miR-125b was positively correlated with lymph node metastasis and tumor differentiation. In vitro and in vivo assays showed miR-125b significantly promoted CRC migration and invasion. To elucidate the potential mechanism, cystic fibrosis transmembrane conductance regulator (CFTR) and cingulin (CGN) were defined as two target genes of miR-125b. On the one hand, miR-125b promoted epithelial-mesenchymal transition (EMT) and the production and secretion of urokinase plasminogen activator (uPA) by inhibiting CFTR; on the other hand, miR-125b activated Ras Homolog Family Member A (RhoA)/Rho Kinase (ROCK) signaling by repressing CGN. Therefore, we provided a potential biomarker for CRC prevention and treatment in the future. Abstract Metastasis contributes to the poor prognosis of colorectal cancer, the causative factor of which is not fully understood. Previously, we found that miR-125b (Accession number: MIMAT0000423) contributed to cetuximab resistance in colorectal cancer (CRC). In this study, we identified a novel mechanism by which miR-125b enhances metastasis by targeting cystic fibrosis transmembrane conductance regulator (CFTR) and the tight junction-associated adaptor cingulin (CGN) in CRC. We found that miR-125b expression was upregulated in primary CRC tumors and metastatic sites compared with adjacent normal tissues. Overexpression of miR-125b in CRC cells enhanced migration capacity, while knockdown of miR-125b decreased migration and invasion. RNA-sequencing (RNA-seq) and dual-luciferase reporter assays identified CFTR and CGN as the target genes of miR-125b, and the inhibitory impact of CFTR and CGN on metastasis was further verified both in vitro and in vivo. Moreover, we found that miR-125b facilitated the epithelial-mesenchymal transition (EMT) process and the expression and secretion of urokinase plasminogen activator (uPA) by targeting CFTR and enhanced the Ras Homolog Family Member A (RhoA)/Rho Kinase (ROCK) pathway activity by targeting CGN. Together, these findings suggest miR-125b as a key functional molecule in CRC and a promising biomarker for the diagnosis and treatment of CRC.

In order to improve the power generation performance of automobile exhaust thermoelectric generator, an intermediate fluid thermoelectric generator system is proposed in this work. In the proposed system, the waste exhaust heat is transferred through boiling and condensation of the intermediate fluid. Consequently, the separation between the exhaust channel and thermoelectric module induces a higher heat flux on the hot side of the module. A mathematical model is also established to analyze the power generation characteristics of the proposed system. Compared with the traditional thermoelectric generator system, for the same heat exchange area on the exhaust side, not only is the peak output power increased by 32.6%, but the optimal thermoelectric module area is also reduced by 73.8%. The generation capacity per unit area is 1162 W/m2 at peak output power, which is 5.12 times that of the traditional thermoelectric generator system.

Thermoelectric generators (TEGs) can effectively recover waste heat from the exhaust of automobiles and generate electricity. An intermediate-fluid TEG system is based on the vaporization and condensation of an intermediate medium, exhibiting high-efficiency thermoelectric conversion. In this study, a mathematical model of an intermediate-fluid TEG system is established, and the influences of cooling methods and condensed-boiling heat transfer performance in the cavity on the thermoelectric performance are analyzed. The results show that the new generator exhibits better characteristics than the traditional TEG system under both water-cooling and air-cooling methods. We not only improved the power output, but also reduced the optimal thermoelectric module area under the water-cooling method. Moreover, the condensation heat transfer coefficient in the cavity had a significant effect on the power performance of the proposed system. The boiling and condensation heat transfer coefficients should both remain greater than 5000 W/m2K for a high efficiency of the TEG. This work provides guidance for the design of new TEGs and high-efficiency utilization of exhaust.

e14523 Background: ACVR2A (activin A receptor type 2A) encodes a receptor that mediates the functions of activins, and it contains two polyadenine (A8) microsatellite loci, which are located in exon 3 and exon 10. Recent studies have shown that ACVR2A mutant was associated with microsatellite instability-high (MSI-H) and high tumor mutational burden(TMB-H) in gastrointestinal cancers. However, this association remains unclear in other solid tumors. Methods: We retrospectively analyzed the ACVR2A mutations from comprehensive 539-gene profiling of 10434 Chinese patients with pan-cancer. Somatic mutations in tumor tissue were assessed. We screened out ACVR2A mutations, calculated the mutation frequency, TMB in different types of cancer. Results: ACVR2A mutants were detected in 340 (2.9%) samples. The top 5 frequently cancers were colorectal cancer (98, 28.8%), lung carcinoma (68, 20%), hepatocellular carcinoma (64, 18.8%), gastric cancer (48, 14.1%) and biliary tract cancers (19, 5.6%). And 12.7% were other cancers (e.g., pancreatic cancer, small bowel adenocarcinoma, brain cancer). ACVR2A variants included truncation (50%), splicing site variant (9.0%), and other mutant types(41.1%). Truncation was the most common type, recurring in a few hot spots (K437Rfs*5/ K437Rfs*19, D96Tfs*54/ D96Rfs*4, V433del, R438Efs*19). The TMB in ACVR2A mutation group was significantly higher than that in ACVR2A wild-type group (p < 0.001). In addition, TMB ≥10 muts/Mb was seen in 76.7% tumors with ACVR2A truncation or splicing site mutant(INACT) and 20.6% tumors with other mutant types(VUS)(p = 0.002). The median TMB of INACT group and VUS group was 35.46 muts/Mb (0.74-344.12) and 6.62 muts/Mb(0.5-598.53), respectively. Conclusions: We analyzed the distribution of ACVR2A mutants in Chinese patients with solid tumors. Our data shows that ACVR2A truncation or splice site mutant type is significantly associated with TMB-H, and this may be potential molecular marker of immunotherapy.

4025 Background: B7-H6, also known as NCR3LG1, is a promising molecule in B7 family and a ligand of natural killer (NK) -cell-activating receptor NKp30. B7-H6 can bind NKp30 and induce NK activation and cytokine secretion to exert anti-tumor effects. Studies have reported that the B7-H6 expression is significantly correlated with post-operative prognosis and distant metastasis status in patients with cancer. In patients with gastric cancer, B7-H6 high expression is significantly associated with longer OS. However, the effects of B7-H6 on immunotherapy and immune microenvironment are unknown. Herein, we used the data from TCGA database of gastric cancer to analyze the influence of B7-H6 expression on immune microenvironment. Methods: The gene expression profile and clinical data in gastric cancer were extracted from TCGA database ( http://cancergenome.nih.gov ). According to the previous reported article, 15 was chosen as the cutoff value for the expression of B7-H6, and the expression of B7-H6 is divided into two groups, high group (B7-H6 expression＞15) and low group (B7-H6 expression≤15). Kaplan-Meier analysis was used to verify the influence of B7-H6 expression on OS prognosis. “Cell Type Identification by Estimating Relative Subsets of RNA Transcripts” (CIBERSORT) algorithm was used to analyze the proportion of immune-related cells in the two groups. “Estimation of STromal and Immune cells in Malignant Tumours using Expression data” (ESTIMATE) algorithm was used to analyze stromal and immune scores in the two groups. The differences of immune-related signatures between the two groups were calculated according to previous reports. Results: Kaplan-Meier survival analysis showed that high group was significantly associated with longer overall survival (p value = 0.016), which was consistent with previous reports. The result of CIBERSORT algorithm showed that the proportion of activation immune correlation CD8(+) T cells and NK active cells was significantly higher in low group than in high group (p＜0.05). Meanwhile, the proportion of immune suppressive correlation CD4 resting memory T cell was significantly lower in low group than in high group (p＜0.05). The result of ESTIMATE algorithm showed that the stromal score, immune score, and ESTIMATE score in low group were significantly higher than in high group (p＜0.01). The immune-related signatures, including immune signature, expanded immune signature, TLS signature, myeloid cell chemotaxis, tertiary lymphoid structure, were significantly higher in low group than in high group (p＜0.05). Conclusions: The low B7-H6 expression was correlated with better immune microenvironment. The effect of B7-H6 expression on immunotherapy needs to be further explored.

e20544 Background: Lung adenocarcinomas (LUAD) is the most common histological subtype of lung cancers. Immunotherapies (ICIs) have been confirmed to improve the clinical outcomes of LUAD patients. Efficacies of ICIs are considered strongly associated with tumor immune microenvironments (TIME). Age-related immune dysfunction might induce difference on the efficacy of ICIs between younger and older patients. However, the potential effect of age on TIME remains little known and controversial. Herein, we aimed to analysis the association between age and TIME based on The Cancer Genome Atlas (TCGA) database. Methods: We screened out 582 LUAD patients with complete information, whose tumors underwent next-generation sequencing (NGS) detection in TCGA. All patients were divided into two groups according to age, the younger group (age < 50-year old) and the older group (age≥50-year old). The differences of immune-related signatures between the two groups were calculated according to previous reports. We also analyzed the differences in immune-related signature between different clinical stages. P-values were calculated via the T.Test. Results: In total 582 patients with LUAD in our study, 115 (19.76%) patients in younger group and 467 (80.24%) patients in older group were found. Many immune-related signatures were found significantly higher in older group than in younger group, including cytolytic activity (CYT) (p = 0.0352), expanded immune signature (p = 0.0065), T cell inflamed gene expression profile (GEP) (p = 0.0048), IFN-γ-related response genes (p = 0.0346), immune signature (p = 0.0022), immunosuppression (p = 0.0065), major histocompatibility complex class I (MHC class I) (p = 0.0319), T-cell survival (p = 0.0235), tertiary lymphoid structures (TLS) signature (p = 0.0001) and total_TILs_scores (p = 0.0020). In addition, tertiary lymphoid structure (p = 0.0355) and TLS_signature (p = 0.0243) were found significantly difference in different clinical staging, which decreased as the staging get later. On the contrary, cell cycle score (p = 0.0001) increased as the staging get later. Conclusions: Our study evaluated the impact of age and clinical stage on the TIME in patients with LUAD using a threshold of 50 years old for the first time. We founded that LUAD patients in older group had better TIME than in younger group and some immune-related signatures were significantly related with clinical staging.

Use of an efficient cooling system is critical from the performance viewpoint of solar thermoelectric generation (STEG) systems. This study proposes the use of spray cooling as an effective technique for use in applications involving STEG systems. A mathematical model has been established to analyze STEG systems from the perspective of net generating efficiency and output power. Results demonstrate that compared to water-cooling, use of the spray-cooling technique results in enhanced generating efficiency, especially under high concentration ratios, owing to inherent advantages, such as high heat transfer performance, low power consumption, and no contact resistance. At a concentration ratio of roughly 200, the net generating efficiency when using spray cooling was observed to be 31.3% higher compared to that achieved when using water cooling. Under conditions of fixed module parameters and structure, there exist optimum values of the spray flow rate and concentration ratio that result in maximization of the net generating efficiency of STEG systems. This maximum efficiency of 13.203% occurs at a concentration ratio of 165 and corresponding flow rate of 0.35 L·min−1, at ZT = 1. Additionally, the net generating efficiency can be further enhanced by reducing the temperature of cooling water. The structural parameter γ is proposed to characterize the geometry of the thermoelectric module. As observed, there exists an optimum value of γ as well that tends to maximize the net generating efficiency of the system. Moreover, this optimum value of γ gradually increases with increase in concentration ratio. Results also demonstrate that optimum values of the spray flow rate and concentration ratio follow an approximately linear increase with increase in the ZT value of STEG modules.

Thermoelectric generation technology, which is used to recover the waste heat of wet flue gas, is studied by establishing a mathematical model to analyze the generation characteristics of wet and dry flue gas. The effects of flue gas parameters are analyzed and discussed. The results show that differently from dry flue gas, when condensation occurs in wet flue gas, it not only releases a large amount of latent heat, but also increases the heat transfer coefficient between the flue gas and the module, and an increase in module area creates an inflection point in the output power curve for wet flue gas. Moreover, the maximum output power of wet flue gas is significantly larger than that of dry flue gas. The maximum output power and corresponding module area are clearly observed to increase as the gas flux increases, but the extreme value of generating efficiency decreases slightly. Specifically, as flue gas temperature increases, the maximum output power increases, whereas the optimal module area required remains unchanged beyond a certain temperature. In addition, an increase in the flue gas temperature has a greater impact on the performance of sensible heat. When the water vapor content decreases to a certain value, the maximum output power can be obtained without condensation. Therefore, there exists a critical water vapor content that can directly determine whether the latent heat of condensation can be recovered. This critical value increases as the flue gas temperature increases. Furthermore, increasing the flux ratio of cooling water and flue gas can also effectively reduce this critical value.

To promote steam condensation with high concentration of non-condensable gas, vapor mixture with 45–95% CO2 is adopted to experimentally investigate the effects of extended surface and surface gold plating on the heat-transfer enhancement. The results show that a gold-plated stainless vertical surface does not exhibit superior performance under the influence of less condensate and slower update frequency of the drops. A V-shaped fluted surface can enhance heat transfer under CO2 concentrations of 85% and 95%, but no further enhancement is shown after the gold-plating treatment on the surface. Although droplets formed at both the inclined surfaces and bottom of the groove, the disturbance of the droplet movement on the gas boundary layer is much weaker due to the lower heat flux. Both experimental results indicate that a proper increase in the fin spacing and height can improve the heat-transfer process on both untreated and gold-plated fluted surfaces.