Abstract: Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine tumour with a poor prognosis. For decades, combination chemotherapy based on etoposide plus platinum (EP) constitutes the cornerstone of clinical treatment for SCLC. Although SCLC is highly sensitive to chemotherapy and radiotherapy, patients often develop resistance within a short period, leading to disease recurrence and progression. In recent years, immune checkpoint inhibitors targeting programmed death-1 (PD-1) and its ligand, when combined with chemotherapy, have significantly transformed the treatment landscape for SCLC, establishing a new standard for first-line therapeutic approaches. Numerous high-level clinical studies from global sources have extensively demonstrated that combined immunotherapy and chemotherapy can serve as a first-line treatment, providing significant overall survival (OS) benefits for patients with extensive-stage small cell lung cancer (ES-SCLC). However, challenges such as immunotherapy resistance, the lack of effective predictive biomarkers, and the management of immune-related adverse events persist in current research and clinical practice. This article aims to systematically review the current status and latest advances in first-line immunotherapy for ES-SCLC, focusing on the efficacy and safety of various immunotherapy combination regimens to provide guidance for clinical practice and future research.
Keywords: extensive-stage small cell lung cancer; first-line treatment; immune checkpoint inhibitor; immunotherapy; combination therapy
（Acta Laser Biology Sinica, 2026, 35(4): 289-297）

Abstract: As optical coherence tomography (OCT) is extended toward subcellular and deep-tissue target detection, stringent demands are imposed on light source performance. Characterized by ultra-broad spectral coverage, high spatial coherence, and exceptional temporal brightness, supercontinuum (SC) light sources are established as the core physical foundation for overcoming the axial resolution limits of traditional OCT and enabling ultra-high-speed scanning. Despite these optical advantages, the non-linear broadening process of SC generation inherently introduces high relative intensity noise (RIN). This degrades the signal-to-noise ratio and acts as a primary bottleneck for high-sensitivity imaging applications. Recently, researchers have mitigated this issue through structural innovations, such as all-normal dispersion (ANDi) architectures, and system-level optimizations like sub-pixel balanced detection. These improvements allow SC-OCT systems to operate much closer to the shot-noise limit, even at megahertz scanning rates. Consequently, the detection potential across specific spectral bands—including visible light, short-wave infrared, and mid-infrared—has been substantially expanded. This paper reviews the underlying physical mechanisms and recent architectural advancements in suppressing RIN for SC-OCT systems. Furthermore, we discuss its cross-band applications, ranging from the analysis of fundus microstructures and blood oxygen metabolism to deep-tissue imaging and the non-destructive testing of highly scattering materials, with the aim of providing a theoretical reference for medical diagnosis and non-destructive testing technologies in relevant fields.
Keywords: supercontinuum light source; optical coherence tomography; relative intensity noise; medical imaging; ophthalmic imaging
（Acta Laser Biology Sinica, 2026, 35(4): 298-309）

Abstract: Disordered glycolipid metabolism is the core pathological basis of metabolic diseases such as type 2 diabetes mellitus (T2DM) and obesity, and the epigenetic regulatory factor bromodomain-containing protein 4 (BRD4) plays a key role in this process. This article systematically reviews the molecular mechanisms by which BRD4 regulates glycolipid metabolism through epigenetic regulation, signaling pathway crosstalk, and organ-specific regulatory networks, as well as its pathological role and therapeutic potential in metabolic diseases.
Keywords: BRD4; glucose metabolism; lipid metabolism; epigenetic regulation; insulin signaling pathway
（Acta Laser Biology Sinica, 2026, 35(4): 310-318）

Abstract: Contact-dependent inhibition plays an important role in bacterial competition and host colonization. However, its application in the control of fish bacterial pathogens and the underlying molecular mechanisms remain poorly understood. This study aimed to evaluate the contact-dependent inhibitory activity of Pseudomonas mosselii (P. mosselii) against Aeromonas veronii (A. veronii) and its protective effect on the host, as well as to preliminarily investigate the molecular basis of this antagonistic activity. Bacterial competition assays were performed to assess the contact-dependent inhibitory activity of P. mosselii against Escherichia coli (E. coli) and A. veronii. A zebrafish infection model was employed to evaluate the protective effect of P. mosselii against A. veronii infection. Furthermore, multiple mutants lacking different virulence secretion systems were constructed by using homologous recombination technology for analyzing the role of these secretion systems in contact-dependent inhibition. The results showed that P. mosselii exhibited significant contact-dependent inhibitory activity against both E. coli and A. veronii. In the zebrafish infection model, P. mosselii significantly increased host survival following A. veronii infection. When E. coli was used as the target strain, type VI secretion system (T6SS) played an important role in contact-dependent inhibition. In contrast, when A. veronii was used as the target strain, no significant difference in contact-dependent inhibitory activity was observed between the wild-type strain and mutants lacking type I～VI virulence secretion systems. This study provides an experimental basis for the development of a new strategy for controlling fish bacterial pathogens based on contact-dependent antibacterial activity.
Keywords: Pseudomonas mosselii; Aeromonas veronii; contact-dependent antibacterial activity; virulence secretion systems; gene knockout
（Acta Laser Biology Sinica, 2026, 35(4): 319-325）

Abstract: To evaluate the heterologous cross-neutralizing capacity of antisera induced by an inactivated EV-A71 vaccine (FY-23K-B strain) against common non-EV-A71 enteroviruses associated with hand-foot-mouth disease (HFMD), Wistar rats were immunized with the vaccine, and microneutralization assays were performed against 18 clinical enterovirus isolates, comprising one EV-A71 isolate and 17 non-EV-A71 isolates. P1-region phylogeny and sequence identity were analyzed, together with the local sequence conservation and structural localization of the EV-A71 VP1-derived linear epitope K1, which has previously been reported to be associated with enterovirus cross-neutralization. The antiserum showed a homologous neutralizing titer of 1 024 against EV-A71. Low-titer neutralizing activity was detected against eight heterologous enteroviruses, including CV-A6 of the EV-A species and CV-A9, CV-B4, ECHO6, ECHO11, ECHO14, ECHO30, and ECHO33 of the EV-B species. Among these, CV-A9 and ECHO14 showed relatively higher titers of 16 and 12, respectively, whereas no detectable neutralizing activity was observed against the remaining heterologous serotypes. Although most isolates with detectable cross-neutralization belonged to the EV-B species, neutralizing titers showed no clear correspondence with overall P1 sequence identity. The K1 epitope showed partial conservation in isolates with and without detectable cross-neutralization, suggesting that a single linear epitope is insufficient to determine the cross-neutralization phenotype. Overall, the inactivated EV-A71 vaccine elicited only limited, low-titer in vitro neutralizing activity against heterologous HFMD-associated pathogens, which may involve the coordinated conservation of multiple local antigenic epitopes and their spatial conformational accessibility. This study provides experimental evidence for understanding the heterologous cross-neutralizing characteristics and potential molecular basis of the inactivated EV-A71 vaccine, and may serve as a reference for future screening of broadly neutralizing epitopes and the design of multivalent HFMD vaccines.
Keywords: hand-foot-mouth disease; EV-A71; inactivated vaccine; cross-neutralization; enterovirus
（Acta Laser Biology Sinica, 2026, 35(4): 326-336）

Abstract: Tobacco root rot caused by Fusarium spp. is one of the most serious soil-borne diseases affecting tobacco production. In this study, a fungus HY31, which can antagonize seven Fusarium species, was isolated from the rhizosphere soil of tobacco plants infected with Fusarium root rot in Xiangxi Autonomous Prefecture, Hunan Province by using the plate-confrontation assay. It was identified as Trichoderma asperellum based on morphological characteristics and internal transcribed spacer (ITS) sequencing. Further studies showed that strain HY31 not only has the ability to solubilize potassium and both organic and inorganic phosphorus, but can also directly inhibit Fusarium mycelial growth, parasitize Fusarium mycelia, and indirectly activate the expression of tobacco defense genes. Pot experiments indicated that HY31 had a control efficacy of 61.53% against tobacco Fusarium root rot and also exhibited significant growth-promoting effects on tobacco plants. This study identified Trichoderma asperellum HY31 as a promising biocontrol agent for tobacco Fusarium root rot, providing an excellent candidate resource for the biological control of this disease.
Keywords: tobacco Fusarium root rot; Fusarium spp. ; Trichoderma asperellum; biological control; pot experiment
（Acta Laser Biology Sinica, 2026, 35(4): 337-346）

Abstract: To investigate the effects of antioxidant stress of R-(+)-lipoic acid on apoptosis of nerve cells and on YAP/TAZ signaling pathway in brain tumor rats, fifty male SD rats were randomly divided into the Control group, the Model group, the R-(+)-lipoic acid group (RLA group), the N-acetyl-L-cysteine (NAC) group and the R-(+)-lipoic acid +NAC group (RLA+NAC group). All groups of C6 glioma model were established except the Control group. The RLA group was intraperitoneally injected with R-(+)-lipoic acid, the NAC group was intraperitoneally injected with NAC, the RLA+NAC group was intraperitoneally injected with both R-(+)-lipoic acid and NAC simultaneously, the Control group and the Model group were injected with the equal volume of normal saline. Each group was continuously intervened for 15 days. Tumor volume and tumor inhibition rate of rats in each group were recorded after the intervention. TUNEL fluorescence staining was used to detect the apoptosis of nerve cells in each group; malondialdehyde (MDA) was detected by the thiobarbiturate method; superoxide dismutase (SOD) was detected by the hydroxylamine method; total antioxidant capacity (TAC) was detected by the ferric reducing antioxidant power (FRAP) assay; the reduced glutathione (GSH) was detected by the microassay kit; the morphology of brain tissue was observed by hematoxylin and eosin (HE) staining; Western blot was used to detect the protein expression levels of Yes-associated protein (YAP), transcriptional co-activator with PDZ-binding motif (TAZ), large tumor suppressor kinase 1 (LATS1), cysteine-rich angiogenic inducer 61 (CYR61), and connective tissue growth factor (CTGF) in brain tissue. The study showed that compared with the Model group, the tumor volumes in all intervention groups (RLA group, NAC group, and RLA+NAC group) were significantly reduced (P<0.05), with the smallest tumor volume observed in the RLA+NAC group. Accordingly, the tumor inhibition rate of the RLA+NAC group was significantly higher than those of the RLA group and the NAC group (P<0.05), while there was no statistically significant difference between the RLA group and the NAC group (P>0.05). Histological observation revealed obvious neuronal apoptosis and abnormal tissue morphology in the Model group. In all intervention groups, neuronal apoptosis was reduced and tissue morphology was improved, with the most pronounced improvement observed in the RLA+NAC group. The results showed that compared with the Control group, the Model group and all intervention groups showed significantly increased contents of MDA, as well as protein expression levels of YAP, TAZ, CYR61, and CTGF (P<0.05), while the activities of SOD and TAC, the content of GSH, and the protein expression level of phosphorylated LATS1 (p-LATS1) were significantly decreased (P<0.05). Compared with the Model group, the aforementioned indicators in all intervention groups were reversed (P<0.05), with the RLA+NAC group exhibiting the most significant reversal effect (P<0.05). The RLA group and NAC group showed no significant differences in any of the aforementioned indicators (P>0.05). Under the conditions of this study, the antioxidant stress effect of R-(+)-lipoic acid is beneficial for alleviating excessive nerve cell apoptosis in rats with C6 glioma and regulating the YAP/TAZ-related pathway proteins.
Keywords: C6 glioma; R-(+)-lipoic acid; oxidative stress; Yes-associated protein; transcriptional co-activator with PDZ-binding motif
（Acta Laser Biology Sinica, 2026, 35(4): 361-368）

Abstract: To investigate the immunomodulatory effect of icariin on asthmatic young mice and its related mechanism, an asthma model was established by ovalbumin sensitization combined with aerosol challenge in this study. The young mice were randomly divided into the control group (Con group), model group (Mod group), low-dose icariin group (Low-Ica group), high-dose icariin group (High-Ica group), and high-dose icariin + Janus kinase 2 (JAK2) activator coumermycin A1 (CA1) group (High-Ica+CA1 group), with 12 mice in each group. Airway reactivity and enhanced pause (Penh) value were detected by a pulmonary function detector. Morphological changes in lung tissue were observed by hematoxylin and eosin (HE) staining. Serum levels of immunoglobulin E (IgE), interleukin-4 (IL-4), IL-17, and interferon-γ (IFN-γ) were measured by enzyme-linked immunosorbent assay. The apoptosis level of eosinophil (EOS) in bronchoalveolar lavage fluid was detected by flow cytometry. The protein expression levels of JAK2, signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 (p-STAT3) in lung tissue were detected by Western blot (WB). The results showed that compared with the Con group, the Penh value increased (P<0.05), lung tissue injury was aggravated, and the levels of IgE, IL-4, IL-17, and the protein expression levels of JAK2 and p-STAT3 increased (P<0.05), while the level of IFN-γ and the apoptosis percentage of EOS decreased (P<0.05) in the Mod group; compared with the Mod group, the Penh value decreased (P<0.05), lung tissue injury was alleviated, and the levels of IgE, IL-4, IL-17, and the protein expression levels of JAK2 and p-STAT3 decreased (P<0.05), while the level of IFN-γ and the apoptosis percentage of EOS increased (P<0.05) in the Low-Ica group and High-Ica group; the JAK2 activator was found to reverse the aforementioned changes in the High-Ica group. The study indicates that icariin can alleviate lung tissue injury in asthmatic young mice, and its mechanism may be related to the inhibition of the JAK2/STAT3 signaling pathway, promotion of EOS apoptosis, and regulation of T helper 1 cell (Th1)/Th2 and Th17 immune imbalance.
Keywords: icariin; asthma; immunomodulation; Janus kinase 2; signal transducer and activator of transcription 3
（Acta Laser Biology Sinica, 2026, 35(4): 369-375）

Abstract: This study aims to investigate the therapeutic effects of Ginkgo biloba extract (GBE) on Sprague-Dawley rats (Rattus norvegicus) with cerebral infarction (CI) and its potential mechanisms. A CI rat model of multiple arterial occlusion was established by injecting fluorescent micropheres via the external carotid artery. The rats with successful model induction were randomly divided into a CI group, a butylphthalide (NBP) group, a low-dose Ginkgo biloba extract (GBE-L) group, a high-dose Ginkgo biloba extract (GBE-H) group, and a GBE-H plus sirtuin 7 (SIRT7) inhibitor 97491 (SIRT7i) group, with 20 rats in each group. An additional 20 healthy rats were selected as the Control group. Following treatment, neurological impairment scores were assessed across all rat groups. 2, 3, 5-triphenyltetrazolium chloride (TTC) staining was employed to quantify cerebral infarct volume. Haematoxylin and eosin (HE) staining was used to examine pathological changes in brain tissue. Enzyme-linked immunosorbent assay (ELISA) kits were utilized to measure levels of vascular endothelial growth factor (VEGF), angiopoietin (Ang), and platelet-derived growth factor (PDGF) in brain tissue. Immunofluorescence was used to detect cluster of differentiation 31 (CD31) positive expression in the cortical area of rat cerebral ischemia. Western blot (WB) analysis was used to measure the expression levels of proteins associated with the SIRT7/vascular endothelial growth factor A (VEGFA) pathway in brain tissue. The results showed that, compared with the Control group, rats in the CI group exhibited worsened pathological damage in brain tissue, significantly increased neurological impairment scores and cerebral infarct area (P<0.05), and markedly reduced levels of VEGF, Ang, PDGF, CD31-positive expression, as well as SIRT7, VEGFA, and VEGF2R protein expression level (P<0.05). Compared with the CI group, the NBP, GBE-L, and GBE-H groups exhibited significantly improved pathological damage in rat brain tissue, markedly reduced neurological impairment scores, and decreased cerebral infarct area (P<0.05). Levels of VEGF, Ang, PDGF, CD31-positive expression, SIRT7, VEGFA, and VEGF2R protein expression level were markedly elevated (P<0.05), with the GBE-H group demonstrating the most pronounced effects. SIRT7i partially reversed the pro-angiogenic effects of GBE in CI rats (P<0.05). Therefore, GBE can improve angiogenesis-related responses after CI in rats and alleviate brain tissue damage, which may be related to the activation of the SIRT7/VEGFA signaling pathway.
Keywords: Ginkgo biloba extract; cerebral infarction; sirtuin 7/vascular endothelial growth factor A signaling pathway; angiogenesis; neurological function
（Acta Laser Biology Sinica, 2026, 35(4): 376-384）