Bacteria are one of the most common human pathogens, which not only seriously jeopardize human health and public health safety, but also bring about huge medical expenditures. Rapid and accurate bacterial detection is important for the treatment of bacterial infections. The spectral detection method can not only obtain the classification, content and functional status of bacteria promptly and in real time, but also has the advantages of simple operation and non-invasive, and has great potential in the field of bacterial detection. This paper describes the research and application of Raman spectroscopy, terahertz spectroscopy, visible and near-infrared light spectroscopy, fluorescence spectroscopy in bacterial detection, and the molecular mechanism of visible and near-infrared light spectroscopy, light targets, including bacterial retinal plasmids containing retinal chromophores, bacteriophytochromes with tetrapyrrole chromophores, photoactive proteins with p-coumarate chromophores, photo-oxidative stress structural domains with flavin-like mononucleotide chromophores, cryptochromes with flavin-adenine di-nucleotide chromophores. And blue-light sensing domains with flavin-adenine dinucleotides are described. Finally, optimization strategies for bacterial detection techniques are proposed with respect to the advantages and disadvantages of existing bacterial spectral detection techniques, hoping to provide help for the research of bacterial spectral detection.

Near-infrared (NIR) light-induced photothermal therapy (PTT) has become a new method for precise tumor treat-ment due to its non-invasive, low toxicity, and targeted treatment. Gold nanoparticles have become an ideal photothermal agents due to its unique surface plasmon resonance (SPR), efficient photothermal conversion efficiency, low biological toxicity and good photostability. High quality imaging technology is a reliable and powerful tool for achieving effective photothermal therapy, especially multimodal imaging technology, which has excellent performance compared to a single imaging method, providing the possibility for more comprehensive and accurate tumor imaging, thereby significantly improving the potential of non-invasive medical treatment. Owing to their rich 4f electronic structure, NIR light excited rare-earth doped upconversion nanoparticles (UCNPs) exhibit multifunctional properties such as magnetism, fluorescence, X-ray attenuation, and radiation, making them an important application prospect in multimodal imaging as contrast agents. Therefore, constructing NIR-induced Au NPs/UCNPs composite nanosystems for multimodal imaging-guided photothermal therapy is expected to become a newstrategy for cancer diagnosis and treatment. In this paper, we briefly introduced the optical properties of Au and UCNPs. In ad-dition, this paper reviewed the latest research progress of PTT research on NIR induced UCNPs Au (nanoshell, nanorod, nano-clusters) composite nano system under the guidance of visual fluorescence imaging. The future prospects for achieving integrat-ed diagnosis and treatment are presented, providing new ideas for its further research, development, and clinical application.

Phosphorylation, a widespread post-translational modification observed in eukaryotic cells, plays a crucial role in regulating various metabolic activities and cell signal transduction processes. In organisms, plant viral proteins have the ability to modulate the biological activity of proteins through phosphorylation and dephosphorylation modifications, thereby controlling the transmission of biological signals within cells. The phosphorylation-modified plant viral proteins actively participate in regu-lating viral infection, viral RNA synthesis, RNA silencing and host gene expression. In recent years, extensive research has been conducted to unravel the molecular mechanisms underlying the phosphorylation of plant virus proteins. This article provides an overview of phosphorylation modification sites, methods for identifying phosphorylation, and the biological functions of plant viral proteins, aiming to offer valuable insights into the role of phosphorylation in plant-virus interactions.

The damage effects and repair rules of pig skin tissue after different doses of 1 064 nm laser irradiation were ex-plored, so as to provide guidance for expanding the safe application of laser in clinical practice. This article used a fundamental mode fiber laser to output 1 064 nm continuous laser with different powers. Live pig skin was irradiated at multiple spots one time by using a grid-array method. The skin injury reaction was observed and its incidence was calculated immediately after la-ser irradiation from low to high doses. The weighted probit method was used to calculate the damage threshold ED50. The heal-ing and pathological changes after laser-induced skin injury were observed dynamically within 6 h and for 28 d after laser irra-diation. With the increase of irradiation dose, laser-induced skin injuries ranging from mild to severe appeared erythema, white spot and burnt spot in turn. When the dose was lower than 70.0 J/cm2, a reversible erythema predominantly occurred. When the dose was 192.2 J/cm2, a burnt spot predominantly occurred with an incidence of about 51.4 %. However, the incidence of burnt

532 nm laser photocoagulation is an established method to induce choroidal neovascularization (CNV) in rodents. 532 nm laser photocoagulation is an established method for inducing CNV in rodents. The aim of this study was to evaluate the degree of morphological variation of laser-induced CNV in vivo and in vitro over time so as to provide an observational met-ric for future CNV-related experiments. In this experiment, brown Norway rats were first laser-molded. Subsequently, in vivo fundus photography, optical coherence tomography (OCT), fundus fluorescence angiography (FFA) and indocyanine green an-giography (ICGA) were performed according to different time points, and finally histopathological examination was applied for in vitro validation.The results showed that CNV appeared at 7th day after photocoagulation, with the highest total incidence of CNV at 21th day. FFA showed typical disc-like strong fluorescence leakage, while ICGA displayed strong fluorescence at the periphery of the photocoagulation area and low fluorescence in the center with a wreath-like morphology. Subretinal CNV were formed 7th day after molding as seen under optical microscope. The central thickness of the CNV gradually increased from 7th to 21th day and remained relatively stable until 28th day. This suggests that the modeling approach utilizing 532 nm laser-induced BN rats with CNV exhibits a short duration and high success rate, rendering it applicable for preclinical experimental studies and providing insights for further research on the pathogenesis of CNV

Cuproptosis is a new programmed cell death pathway, which is initiated by the direct binding of copper to the fatty acyl tricarboxylic acid cycle proteins. Modulation of cuproptosis in tumor cells is a novel therapeutic approach. However, the potential role and clinical significance of cuproptosis-related long non-coding RNA (lncRNA) in hepatocellular carcinoma (HCC) remain unclear. In this study, a total of 994 cuproptosis-related lncRNA were identified by co-expression analysis of 19 cupro-ptosis-related genes based on the TCGA-LIHC dataset. LASSO regression and multivariate Cox regression analysis were used to screen out four prognostic lncRNA (TMCC1-AS1, AC009974.2, AL355574.1 and DDX11-AS1) related to copper mortality to construct a prognostic risk model, and the risk scores of all HCC patient samples were calculated. HCC patients were divided into high risk and low risk groups at a 1:1 ratio. Kaplan-Meier survival curve analysis showed that the overall survival rate (OS) of the high risk group was significantly lower than that of the low risk group. Regression analysis and ROC curve confirmed the prognostic value of the risk score. In addition, we analyzed the correlation between risk scores and pathway enrichment analysis, immune checkpoint genes, immune cell infiltration, anticancer drug sensitivity, and somatic gene mutations. The results of dif-ferential expression analysis showed that TMCC1-AS1, AC009974.2, AL355574.1 and DDX11-AS1 were all up-regulated in tumor tissues, which were verified by real-time fluorescent quantitative PCR (qRT-PCR) in tumor tissues and adjacent liver tis-sues collected from 8 patients with hepatocellular carcinoma undergoing radical surgery. This give histological evidence for this model. In conclusion, a risk model composed of four cuproptosis-related lncRNA was constructed, which was significantly relat-ed to the prognosis and immune infiltration environment of patients. This model has certain clinical application value in predict-ing the effects of immunotherapy and guiding the selection of chemotherapy drugs.

The programmed cell death protein 1 (PD-1)/ programmed cell death 1 ligand 1 (PD-L1) signaling pathway is mainly involved in negative immune regulation and plays a crucial role in the malignant development of many types of tumors. High expression of PD-L1 promotes HCC invasion and increases the risk of tumor recurrence. In addition, PD-L1 is often used as an immune checkpoint blockade target, mainly neutralized by monoclonal antibodies to trigger an anti-tumor immune re-sponse. Therefore, PD-L1 is one of the potential targets in HCC immunotherapy. This study mainly uses nano-scale function-alized graphene oxide (GO-PEI-PEG) to carry PD-L1 siRNA to explore the malignant biological effects on liver cancer cells. The results showed that after transfection of GO-PEI-PEG/PD-L1 siRNA into MHCC97H cells, the proliferation and migration of cells were inhibited, the cell cycle was arrested in the G1 phase, and the number of apoptotic cells increased. It was further found that the inhibitory effect of GO-PEI-PEG/PD-L1 siRNA on MHCC97H cells was achieved by blocking the activation of the AKT signaling pathway. These experimental results show that GO-PEI-PEG has excellent delivery performance, carriesPD-L1 siRNA to effectively interfere with PD-L1 expression, and then inhibits the malignant biological behavior of liver cancer cells, which provides a safer and more effective delivery strategy for the treatment of HCC.

Thioridazine, a phenothiazine drug, has a potential to induce tumor immunogenic cell death (ICD) and activate a tu-mor-specific immune response. In this study, we examined the ICD effect induced by Thioridazine and elucidated its underlying mechanisms using lung adenocarcinoma A549 and H1299 cells. Various concentrations of Thioridazine were employed to treat A549 and H1299 cells. The cell inhibition rate was determined using the methyl thiazol tetrazolium (MTT) assay, apoptosis rate was assessed by Flow Cytometry, extracellular ATP release was measured by using an ATP Assay Kit, and the presence of calre-ticulin (CRT) on the cell surface was evaluated via immunofluorescence. Furthermore, Western blot analysis was conducted to assess the expression levels of apoptosis-related proteins, including cleaved caspase 3, B-cell lymphoma-2 (Bcl-2), Bcl-2-asso-ciated X protein (Bax), and cytochrome C (Cyt C). Our findings revealed a significant, dose-dependent inhibition of A549 and H1299 cell proliferation and a marked increase in the apoptosis rate upon treatment with Thioridazine. Additionally, there was an elevation in extracellular ATP secretion and CRT expression on the cell surface, indicative of ICD occurrence. Consistently, the expression level of Bcl-2 decreased, while Bax, Cyt C, and cleaved caspase 3 were up-regulated that further indicate the in-duction apoptosis of tumor cell by Thiolidazine. Collectively, our results confirm that Thioridazine inhibits the proliferation of lung adenocarcinoma cells by inducing ICD through the mitochondrial stress signaling pathway.

To investigate the effects of anlotinib on proliferation and apoptosis of A549 cells based on phosphatidylinosi-tol 3-kinase (PI3K)/serine-threonine protein kinase (AKT) signaling pathway. A549 cells were divided into the control group, the experimental groups with different doses, the anlotinib group, the positive drug group, the inhibitor group and the activator group. The intervention time was 24 hours. The cell viability, cell morphology, the rate of proliferation, apoptosis and related protein expression levels were detected. The results showed that cell viability decreased after treatment with 20 μmol/L anlo-tinib. Compared with the control group, the cell growth of anlotinib group and positive drug group was inhibited, the cell prolif-eration rate, cysteinyl aspartate specific proteinase D1 (Cyclin D1) and the expression levels of p-PI3K and p-AKT decreased, and the number of apoptosis cells and the expression of cysteine aspartic protease-3 (Caspase-3) increased. The inhibitor en-hanced these changes, while the activator had the opposite trend to the inhibitor. These results of this study indicate that anlotinib can significantly inhibit the proliferation and promote apoptosis of A549 cells, and its mechanism might be related to the inhibi-tion of PI3K/AKT pathway signal transduction. The results of this study further illustrate the potential value of antilung cancer drugs and provide a new theoretical basis for the research and development of anti-lung cancer drugs.

To further explore the structure and function of the promoter and protein of human SIRT1 gene, our research used bioinformatic methods to analyze 5′-end promoter, promoter Motif, transcription factor binding sites, CpG island, single-nu-cleotide polymorphism, phylogenetic homology, physicochemical properties, hydrophilicity/hydrophobicity, secondary/tertiary structure, conserved domain, mutation site, N-glycosylation and phosphorylation sites, interacted proteins and biological func-tion. The number of promoters predicted by TSSW and Neural Network Promoter Prediction database was 3 and 2 respec-tively. There were 3 Motifs found in the promoter region by using MEME database. The CpG islands were clustered in the 1 600～2 200 bp, which were found by using EMBOSS, MethPrimer and CpG Finder database. PROMO and AliBaba2.1 da-tabase showed that there were 22 transcription factors in their promoter regions. And there were 6 transcription factors foundthat bind to the positive and negative chains by using JASPAR software. Besides, there were differences found in allele frequen-cies between different ethnic groups by using SNP Function Prediction database. Human SIRT1 gene is located at chromosome 10q21.3 and widely distributed in different tissues, which is a hydrophilic and unstable protein with a high conservation among different species. The domain is located at the 254～489 amino acid sequence, belonging to the SIR2 superfamily, mainly lo-cated in the nucleus and mitochondria. The secondary structure of the protein mainly contains α-helices and irregular coiling. Compared with AlphaFold2, the tertiary structure model constructed by SWISS-MODEL database was reliable. SIRT1 contained 106 mutation sites, 1 N-glycosylation and 61 phosphorylation sites, which interacted with EP300, TP53 and other proteins. It also participated in circadian rhythm process, steroid hormone response, and intracellular receptor signaling etc., which were as-sociated with longevity regulation pathway, AMPK signaling pathway, and FoxO signaling pathway etc. This study can provide a theoretical basis for further studying the effects on inflammatory reaction and other diseases of human SIRT1 gene.