YOLOFM: an improved fire and smoke object detection algorithm based on YOLOv5n.

To address the current difficulties in fire detection algorithms, including inadequate feature extraction, excessive computational complexity, limited deployment on devices with limited resources, missed detections, inaccurate detections, and low accuracy, we developed a highly accurate algorithm named YOLOFM. We utilized LabelImg software to manually label a dataset containing 18644 images, named FM-VOC Dataset18644. In addition, we constructed a FocalNext network, which utilized the FocalNextBlock module from the CFnet network. This improves the integration of multi-scale information and reduces model parameters. We also proposed QAHARep-FPN, an FPN network that integrates the structure of quantization awareness and hardware awareness. This design effectively reduces redundant calculations of the model. A brand-new compression decoupled head, named NADH, was also created to enhance the correlation between the decoupling head structure and the calculation logic of the loss function. Instead of using the CIoU loss for bounding box regression, we proposed a Focal-SIoU loss. This promotes the swift convergence of the network and enhances the precision of the regression. The experimental results showed that YOLOFM improved the baseline network's accuracy, recall, F1, mAP50, and mAP50-95 by 3.1%, 3.9%, 3.0%, 2.2%, and 7.9%, respectively. It achieves an equilibrium that combines performance and speed, resulting in a more dependable and accurate solution for detection jobs.

Weighted gene coexpression network analysis reveals negative regulation of hypertrophic cardiomyopathy by carboxylesterase 1 and cathepsin C.

Hypertrophic cardiomyopathy (HCM) is a primary cardiomyopathy characterized by hypertrophic cardiomyocytes. It is one of the leading causes of sudden death in adolescents. However, the molecular mechanism of HCM is not clear. In our study, ribonucleic acid (RNA) sequence data of myocardial tissue in HCM patients were extracted from the Gene Expression Omnibus (GEO) database (GSE130036) and analyzed by weighted gene coexpression network analysis (WGCNA). A total of 31 coexpression modules were identified. The coexpression black module significantly correlated with maximum left ventricular wall thickness (Maxi LVWT). We screened the differentially expressed mRNAs between normal tissues and HCM tissues using the dplyr and tidyr packages in R3.6.2. The genes in the black module and differentially expressed genes were further intersected. We found that the expression of carboxylesterase 1 (CES1) and cathepsin C (CTSC) was downregulated in HCM tissues and negatively correlated with Maxi LVWT. We further verified the expression of CES1 and CTSC was downregulated in HCM clinical blood and negatively correlated with Maxi LVWT. Finally, we demonstrated that overexpression of CTSC and CES1 could alleviate HCM in an HCM cell model. In summary, the study suggests that CES1 and CTSC negatively regulate the development of HCM and have potential as therapeutic and diagnostic targets for HCM.

KIAA1429 mediates epithelial mesenchymal transition in sorafenib-resistant hepatocellular carcinoma through m6A methylation modification.

BACKGROUND: Hepatocellular carcinoma (HCC) is a primary liver cancer with high mortality. The long-term use of sorafenib, a targeted drug for hepatocellular carcinoma, will lead to drug resistance, and patients are prone to cancer metastasis, the molecular mechanism of which is still unclear. METHODS: In our study, we constructed a sorafenib-resistant hepatocellular carcinoma cell line (HepG2/Sora) and validated the resistance in vivo and in vitro. Transwell assays confirmed the invasion and migration abilities of cells. Colorimetric assays confirmed that the level of m6A methylation modification in cells. RT-qPCR and Western blot assays confirmed that the expression levels of KIAA1429 in HepG2/Sora cells and tissues. The EMT related proteins were detected by Western blot assay. RESULTS: Transwell and Western blot assays confirmed that HepG2/Sora cells had higher invasion and migration abilities and showed EMT phenomena. Colorimetric assays confirmed that the level of m6A methylation modification was upregulated in HepG2/Sora cells. Transwell and Western blot assays confirmed that inhibiting m6A methylation in HepG2/Sora cells inhibited their invasion, migration ability and EMT phenomenon. RT-qPCR and Western blot assays confirmed that the expression levels of KIAA1429 in HepG2/Sora cells and tissues was increased. Silencing KIAA1429 in HepG2/Sora cells inhibited their invasion, migration ability and EMT phenomenon. Finally, we found that the medium supernatant of sorafenib-resistant HepG2/Sora cells induced vascular production of EA.hy926 cells, and silencing KIAA1429 inhibited this induction effect. CONCLUSION: We suggest that KIAA1429 promotes sorafenib-resistant hepatocellular carcinoma invasion, migration and EMT by mediating m6A methylation. KIAA1429 with its mediated m6A methylation may be a key factor for sorafenib-resistant patients prone to cancer cell metastasis.

Role of GADD45A in myocardial ischemia/reperfusion through mediation of the JNK/p38 MAPK and STAT3/VEGF pathways.

Rapid recovery of blocked coronary artery blood flow after myocardial infarction (MI) is the key to reducing the size of the infarcted area, improving clinical outcome and decreasing mortality. However, ischemia/reperfusion (I/R) injury has a complicated pathological mechanism and is an inevitable complication of coronary artery blood flow recovery. Growth arrest and DNA damage­inducible α (GADD45A) serves a vital role in myocardial injury induced by I/R. The present study aimed to explore the role and mechanisms of GADD45A in cardiac microvascular endothelial cells (CMEC)­I/R injury in vivo and in vitro. An I/R injury rat model and a hypoxia/reoxygenation (H/R) cellular model were established, and myocardial tissues were collected for GADD45A detection, 2,3,5­triphenyltetrazolium chloride staining, H&E staining, and dual staining of CD31 and TUNEL. Serum was also collected for the analysis of creatine kinase and lactate dehydrogenase in I/R rats following GADD45A silencing. Additionally, the protein expression levels of CD31, phosphorylated­endothelial nitric oxide synthase (p­eNOS), endothelin­1 (ET­1), JNK, p38 MAPK, STAT3 and VEGF were assessed by western blotting. The JNK and p38 MAPK activator, anisomycin, and the JAK2­STAT3 pathway inhibitor, AG490, were used to determine the involvement of JNK/p38 MAPK pathway and STAT3/VEGF pathway. GADD45A was highly expressed in I/R injury rat and cell models. GADD45A silencing reduced the ischemic area and improved myocardial pathological damage in vivo. Furthermore, the levels of CD31 and p­eNOS were increased, whereas ET­1 was decreased by GADD45A silencing in the I/R injury rats. Mechanistically, GADD45A silencing reduced JNK/p38 MAPK expression but activated STAT3/VEGF expression. GADD45A silencing inhibited H/R­induced viability reduction and apoptosis through MAPK signaling and suppressed angiogenesis via STAT3/VEGF in H/R­induced CMECs. Overall, GADD45A ameliorated apoptosis and functional injury of CMECs via the JNK/p38 MAPK and STAT3/VEGF pathways.

New prognostic factors and scoring system for patients with acute myeloid leukemia.

Acute myeloid leukemia (AML) is a malignant disease originating from myeloid hematopoietic stem or progenitor cells. It is important to identify molecules associated with the prognosis of AML and conduct an individual risk assessment for different patients. In the present study, the RNA expression profile of 132 patients with AML and 337 healthy individuals were downloaded from the University of California Santa Cruz Xena and the Genotype-Tissue Expression project databases. Differentially expressed mRNA (DEmRNA) transcripts between normal blood and AML blood were identified. Among these, prognosis-associated signature mRNA molecules were screened using univariate Cox and least absolute shrinkage and selection operator regression. A total of four genes, namely, family with sequence similarity 124 member B (FAM124B), 4-hydroxyphenylpyruvate dioxygenase-like protein (HPDL), myeloperoxidase (MPO) and purinergic receptor P2Y1 (P2RY1), were identified using multivariate Cox regression analysis and were used to construct a prognostic scoring system. Moreover, the expression levels of HPDL and MPO were higher in the samples with high immunity scores and estimate scores (sum of stromal score and immune score), compared with those with low scores. Reverse transcription-quantitative PCR and western blot analysis were used to confirm the upregulation of the four candidate genes in AML cell lines as well as in clinical AML samples. In summary, the present study identified a novel mRNA-based prognostic risk scoring system for patients with AML. The four genes used in this scoring system may also play an important role in AML.

Optimal dimension of edge-lit light guide plate based on light conduction analysis.

Dimensions of the edge-lit light guide plate (LGP) have a non-negligible impact on its output performance based on a pre-determined micro-dot array. However, how the LGP's dimension affects the performance has not been systematically researched. In this paper, the dimension of the LGP is numerically established as a function to the light output performance, which can be divided into four successive procedures. Firstly, the micro-structural dot array is designed based on the calculated illuminance distribution of the LGP's bottom surface. Based on this, the light energy output can be derived by defining three key parameters, which are dot density, scatting coefficient, and collision loss coefficient. After that, the ray-tracing simulation is used to determine the above parameters. Finally, the optimal dimensions of the LGP can be obtained with a specific correlation function with the light energy output. The mathematical relation above is demonstrated via both simulation and experiment. Our approach provides a systematic design for balancing the efficiency and uniformity of backlight by combining the dot design and the dimensional optimization, which has important theoretical guiding significance for actual display application.

Numerical Analysis of Droplets from Multinozzle Inkjet Printing.

Multinozzle printing processing with the fabrication of a functional material film lays the foundation for the development of efficient scale production of a photoelectric device. However, a prominent challenge is how to realize the volume uniformity of the droplets. Here, a classical analysis method is introduced first by printing poly(3,4-ethylenedioxythiophene)/poly(styrenesulfonate) (PEDOT:PSS) to analyze the behavior of droplets. It relies on a variance calculation for the clarification of the law of implicit behavior of droplets in terms of digitizing. This method reveals the effect of printing parameters on the uniformity of the volume of droplets in multinozzle printing. Overall, by combining both ink formulations and printing parameter optimization, it is concluded that the minimum volume variance of nozzles with different numbers is less than 0.5% and the influence of various parameters in multinozzle printing is found to be ranked. The feasibility of this analysis method is presented and is of great significance to achieving a very stable, large-scale multinozzle printing device.

Effect of cigarette smoking on clinical outcomes of hospitalized Chinese male smokers with acute myocardial infarction.

BACKGROUND: Smoking is known to be a strong risk factor for premature atherosclerosis, acute myocardial infarction (AMI) and sudden cardiac death. According to a cross-sectional survey conducted in 2000 - 2001 in China, the prevalence of smoking among the Chinese men was 60.2%, the highest prevalence in the world. Up to date, the relationship between smoking and AMI in Chinese male smokers is still unclear. This study analyzed the baseline characteristics for male smokers hospitalized with AMI and investigated the effect of cigarette smoking on their clinical outcomes. METHODS: A total of 890 men aged 18 years or over with AMI were prospectively recruited from 1 January 2007 to 31 December 2009 from Shanxi Provincial People's Hospital. Patients were grouped into smokers and nonsmokers. The relationships between baseline characteristics and clinical outcomes were tested using either the chi-square test for trend for discrete variables or analysis of variance for continuous variables. RESULTS: Smokers accounted for 66.7% (594), more than twice of nonsmokers (296 (33.3%)), and were averaged 7 years younger ((56.61 ± 11.44) vs. (63.61 ± 11.62) years, P < 0.001). Smokers had the higher rate of TIMI flow grade 2 or 3 after thrombolytic therapy (42.4% vs. 24.5%, P = 0.002), 1 vessel disease (25.5% vs. 14.5%, P = 0.003) than nonsmokers. Smokers had better in-hospital outcome with lower in-hospital mortality rate than nonsmokers (6.2% vs. 10.8%, P = 0.023). CONCLUSIONS: Male smokers suffered from AMI in this study presented an average of 7 years earlier than nonsmokers and were more than twice as likely to have AMI as nonsmokers in China. Smoking appeared to result in earlier infarction, especially ST elevated myocardial infarction in otherwise healthier patients who are likely to survive.

[The C46359T polymorphism of DNMT3B promoter gene and pathogenesis of acute leukemia].

OBJECTIVE: To explore the relationship between the polymorphism of C46359T in DNMT3B promoter and the pathogenesis of acute leukemia (AL). METHODS: PCR-RFLP and DNA sequencing were used to analyze the genotypic polymorphism C46359T of promoter in genomic DNA of bone marrow cells/blood lymphocytes from 160 patients with AL and 240 normal controls. RESULTS: In people of the Hans in China, genotypic frequencies of 2.5% (CT), 97.5% (TT) and 0 (CC) were statistically significant (P < 0.001) comparing with the genotype frequencies of 41.8% (CT), 23.2% (TT) and 35.0% (CC) in Caucasian in USA. The genotypic frequency of CT heterozygote in 160 AL patients was 10.6%, significantly higher than that in the control subjects (2.5%, P < 0.001), indicating that the CT heterozygote might be a more frequent phenomenon in AL. Compared with TT homozygote, CT heterozygote had a 4.669-fold increased risk of acute leukemia (OR = 4.669; 95% confidence interval 1.700-14.747). It was suggested that CT heterozygote was relative to the pathogenesis of AL. CONCLUSIONS: Different distribution of genotypes in different races, the CT heterozygote was relative to the pathogenesis of AL.

[Methylation status of multidrug resistance (mdr1) gene and its correlation with expression of mdr1 gene in patients with hematologic malignancies].

To investigate the correlation between methylation and expression of multidrug resistance (mdr1) gene, restriction endonuclease HpaII combined with competitive PCR technique was used to quantitatively detect the methylation status of two CCGG sites located at -110 and -50 bp (region I and II) up to the transcription start site in mdr1 promoter in 54 AL and 9 MM patients. Semi-quantitative RT-PCR was used to detect the expression level of mdr1 gene. The results showed that inverse correlation between methylation rate of either region or total methylation rate and expression of mdr1 gene was observed. The correlation in the region I (r = -0.64) was closer than that in the region II (r = -0.4). High expression rate of mdr1 ascended significantly in low methylation group (n = 36) (P < 0.001). In comparison with chemotherapy sensitive group (n = 8), the methylation rate in refractory AL patients (n = 16) was lower (P = 0.05) in the region I, P < 0.05 in the region II and total regions. Comparing with the untreated patients (n = 36), the methylation rate in the region I and total methylation rate were lower in the patients with chemotherapy (n = 14) (P < 0.05). The methylation rate in the region II was also decreased after chemotherapy, however, no statistical significance was shown (P > 0.05). Increased mdr1 expression level accompanying with decreased methylation rate after chemotherapy was found, although no significant difference was shown (P = 0.06). It is concluded that the expression level of mdr1 gene was associated with the methylation status of CCGG in -110 and -50 bp upstream to the transcription start site, especially the -110 site. In both the patients treated with chemotherapy and the refractory patients, the methylation level of mdr1 gene decreased relatively. The rising expression of mdr1 gene after chemotherapy was associated with the decrease of methylation level.

[The expression of DNA methyltransferase DNMT1, 3A and 3B in acute leukemia and myelodysplastic syndrome].

OBJECTIVE: To explore the relationship between methyltransferases and the pathogenesis of acute leukemia (AL) and the leukemic transformation of myelodysplastic syndromes (MDS). METHODS: Semi-quantitative RT-PCR method was used to detect the mRNA expression level of DNMT1, 3A and 3B in bone marrow cells from 75 patients with AL or MDS. RESULTS: There was no significant difference in mRNA expression level of DNMTs between a low-risk MDS group (n = 21) and a normal group. However, increased expression level of DNMT1, 3A and 3B was found in 47.6%, 47.6% and 42.9% of the patients in the low-risk group, respectively, if the upper limit of 80% of the normal controls was considered as the critical level. In high-risk MDS (n = 13), a more proportion of the cases with increased expression level of DNMTs were found, that was 53.8%, 76.9% and 92.3% respectively, and only expression level of DNMT3B was significantly higher than that in the low-risk MDS group (P < 0.01). In the AL group (n = 41) expression level of all the three subtypes was coordinately higher than that in the MDS group (P < 0.01), companying with a more frequency of 92.7%, 97.6% and 100%. Comparing with the AML group, a significantly increased expression level of DNMT1 (P < 0.01) with the same level of DNMT 3A and 3B was interestingly observed in the ALL group. CONCLUSIONS: It is possible that up-regulated DNMTs contribute to the pathogenesis of AL and the leukemic transformation of MDS, and DNMT3B might be the most important enzyme among the three subtypes.

[Experimental study on TCRbeta idiotypic antigenic determinants DNA vaccine to induce anti-lymphoma antibodies].

OBJECTIVE: To investigate the anti-human CEM lymphoma cell activities induced by TCR idiotypic DNA vaccine containing different antigen determinants in BALB/c mice. METHODS: The specific rearranged gene fragment encoding TCRVbeta region of CEM cell line was obtained by RT-PCR technique. The PCR product was cloned into eukaryocytic expression vector pcDNA3, which was used as DNA vaccine and template for PCR amplifying different antigen determinant. Gene fragments encoding different antigen determinant were amplified and cloned into pcDNA3, separately. The experimental mice were immunized by intramuscular injection of the DNA vaccines. The specific anti-idiotype antibodies were detected by indirect immunofluorescence assay. RESULTS: TCRbetaV of CEM cell line contains five antigen determinants. Specific anti-idiotype antibody was detected in all of the six mice immunized with DNA vaccine containing all the five determinants (the highest titer was 1:480). Although the antibody could also be detected in four of the six mice immunized with DNA vaccine containing four of the five antigen determinants, the antibody titer was lower (the highest titer was 1:80). DNA vaccine containing two of the five determinants could not induce the specific antibody. CONCLUSION: The idiotypic DNA vaccine containing the whole TCRbetaV five antigen determinants could induce the specific anti-lymphoma idiotypic antibody in BALB/c mice.

[The Experimental Study on the TCR Idiotypic DNA Vaccine to Induce Antitumor Immune Response to Lymphocytic Malignancy]

This study was undertaken to investigate the anti-lymphocytic malignacy immunologic effects induced by TCR idiotypic DNA vaccine on BALB/c mice. CEM lymphoma cell line and BALB/c mice were used as models. The rearrangement gene fragment coding TCR Vbeta region of CEM cell line was obtained by RT-PCR technique. The PCR product was cloned into the eukaryocytic expression vector pcDNA3 to be used as DNA vaccine. The experimental animals were immunized by intramuscular injection with DNA vaccine. The specific anti-idiotypic antibody was detected by indirect immunofluorescence assay. The specific anti-idiotypic cellular immunity was detected by CTL activity assay using MTT method. The results showed that specific anti-idiotypic antibody in the immunized mice sera could be found since four weeks after immunization and came to the peak of titer on the sixth week. Using IL-6 as immunological adjuvant could significantly increase the antibody titers. It was concluded that the TCR idiotypic DNA vaccine could induce effectively the specific anti-lymphoma idiotypic antibody in BALB/c mice. Using IL-6 as immunological adjuvant could significantly increase the antibody titers induced by idiotipic DNA vaccine.