Nd:YVO4/YVO4 cascaded Raman laser pumped dual-wavelength signal wave MgO:PPLN-OPO with wide range adjustable wavelength interval.

This article presents a dual-wavelength signal wave output system capable of generating a broad range of adjustable wavelength intervals. The setup involved the creation of a dual-wavelength cascaded Raman laser featuring composite cavities operating at 1176 nm and 1313 nm. Experimental investigations were carried out on an external cavity MgO:PPLN-OPO driven by the cascaded Raman laser. By setting the crystal polarization period to 27.6-34.4 µm and the temperature to 50-130°C, adjustable tunable output of dual-wavelength signal wave at 1176 nm-MgO:PPLN-OPO (1550-2294 nm) and 1313 nm-MgO:PPLN-OPO (1768-2189 nm) was achieved with a wavelength interval of 0-218 nm. Under the conditions of a period of 34.4 µm, temperature of 90°C, and an incident Raman power of 2.6 W, the highest conversion efficiency of Raman to dual-wavelength signal wave (2212, 2182 nm) was 34.2%. Furthermore, the maximum output power of dual-wavelength signal wave was recorded at 1.02 W with an incident Raman power of 3.33 W.

SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells.

Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, and cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxia, cytotoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene up-regulation is a common transcriptional stress response in RTECs to ischemia-, cisplatin-, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuroendocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia-, cisplatin-, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro Importantly, aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf up-regulation in RTECs is driven by the transcriptional regulator Sox9. These findings reveal a crucial downstream target of the Sox9-directed transcriptional program and identify Vgf as a stress-responsive protective gene in kidney tubular epithelial cells.

Kidney toxicity of the BRAF-kinase inhibitor vemurafenib is driven by off-target ferrochelatase inhibition.

A multitude of disease and therapy related factors drive the frequent development of kidney disorders in cancer patients. Along with chemotherapy, the newer targeted therapeutics can also cause kidney dysfunction through on and off-target mechanisms. Interestingly, among the small molecule inhibitors approved for the treatment of cancers that harbor BRAF-kinase activating mutations, vemurafenib can trigger tubular damage and acute kidney injury. BRAF is a proto-oncogene involved in cell growth. To investigate the underlying mechanisms, we developed cell culture and mouse models of vemurafenib kidney toxicity. At clinically relevant concentrations vemurafenib induces cell-death in transformed and primary mouse and human kidney tubular epithelial cells. In mice, two weeks of daily vemurafenib treatment causes moderate acute kidney injury with histopathological characteristics of kidney tubular epithelial cells injury. Importantly, kidney tubular epithelial cell-specific BRAF gene deletion did not influence kidney function under normal conditions or alter the severity of vemurafenib-associated kidney impairment. Instead, we found that inhibition of ferrochelatase, an enzyme involved in heme biosynthesis contributes to vemurafenib kidney toxicity. Ferrochelatase overexpression protected kidney tubular epithelial cells and conversely ferrochelatase knockdown increased the sensitivity to vemurafenib-induced kidney toxicity. Thus, our studies suggest that vemurafenib-associated kidney tubular epithelial cell dysfunction and kidney toxicity is BRAF-independent and caused, in part, by off-target ferrochelatase inhibition.

Involvement of the CDKL5-SOX9 signaling axis in rhabdomyolysis-associated acute kidney injury.

Acute kidney injury (AKI) is a common clinical syndrome associated with adverse short- and long-term sequelae. Renal tubular epithelial cell (RTEC) dysfunction and cell death are among the key pathological features of AKI. Diverse systemic and localized stress conditions such as sepsis, rhabdomyolysis, cardiac surgery, and nephrotoxic drugs can trigger RTEC dysfunction. Through an unbiased RNA inhibition screen, we recently identified cyclin-dependent kinase-like 5 (Cdkl5), also known as serine/threonine kinase-9, as a critical regulator of RTEC dysfunction associated with nephrotoxic and ischemia-associated AKI. In the present study, we examined the role of Cdkl5 in rhabdomyolysis-associated AKI. Using activation-specific antibodies and kinase assays, we found that Cdkl5 is activated in RTECs early during the development of rhabdomyolysis-associated AKI. Furthermore, we found that RTEC-specific Cdkl5 gene ablation mitigates rhabdomyolysis-associated renal impairment. In addition, the small-molecule kinase inhibitor AST-487 alleviated rhabdomyolysis-associated AKI in a Cdkl5-dependent manner. Mechanistically, we demonstrated that Cdkl5 phosphorylates the transcriptional regulator sex-determining region Y box 9 (Sox9) and suppresses its protective function under stress conditions. On the basis of these results, we propose that, by suppressing the protective Sox9-directed transcriptional program, Cdkl5 contributes to rhabdomyolysis-associated renal impairment. All together, the present study identified Cdkl5 as a critical stress-induced kinase that drives RTEC dysfunction and kidney injury linked with distinct etiologies.

Evolution of the Raman beam quality in a folded-coupled-cavity Nd:YVO4/YVO4 Raman laser.

An end-pumped actively $Q$Q-switched ${\rm Nd}\!:\!{{\rm YVO}_4}/{{\rm YVO}_4}$Nd:YVO4/YVO4 Raman laser with a folded coupled cavity is demonstrated to study the evolution of Raman beam quality. The theoretical mechanism of the beam cleanup effect of stimulated Raman scattering is analyzed. The beam quality ($M^2$M2) of the Raman beam and the fundamental beams before and after the Raman conversion are measured experimentally. The results show that with the incident pump power increasing, the ${M^2}$M2 of the fundamental beam increases from 1.85 to 3.08, while the ${M^2}$M2 of the Raman beam increases from 1.21 to 1.69. The beam quality of the Raman laser and its degradation are better than that of the fundamental laser.

High-performance second-Stokes generation of a Nd:YVO4/YVO4 Raman laser based on a folded coupled cavity.

We report an actively Q-switched Nd:YVO4/YVO4 intracavity Raman laser at second-Stokes wavelength of 1313.6 nm, which is capable of operating efficiently under pulse repetition frequency higher than 80 kHz. A folded coupled cavity is adopted to optimize the fundamental and the Stokes resonators individually and make full use of the high pump intensity on the Raman crystal. With relatively high output coupling of 82% at 1313 nm, the average output power of 5.16 W at 1313 nm is achieved under the incident pump power of 36.7 W. The cascaded Raman emission at both the first- and second-Stokes wavelength of 1176 and 1313 nm is investigated to discuss the optimization of the second-Stokes generation.

10.3-W actively Q-switched Nd:YVO4/YVO4 folded coupled-cavity Raman laser at 1176 nm.

We report herein an efficient actively Q-switched Nd:YVO4/YVO4 intracavity Raman laser operating at 1176 nm. Factors such as resonator geometry and pumping scheme are optimized to strengthen the power scalability and the conversion efficiency of the intracavity Raman laser. With a folded coupled cavity adopted to make full use of the high pump intensity on the Raman crystal, the first-order Stokes output of 10.32 W at 1176 nm is achieved under the incident pump power of 39 W and pulse repetition frequency of 160 kHz. The corresponding optical efficiency reaches 26.4%, and even higher efficiency of 27.8% is obtained at lower incident pump of 34.4 W.

Fine particulate matter air pollution and atherosclerosis: Mechanistic insights.

BACKGROUND: Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous plaque in the arteries. Its etiology is very complicated and its risk factors primarily include genetic defects, smoking, hyperlipidemia, hypertension, lack of exercise, and infection. Recent studies suggest that fine particulate matter (PM2.5) air pollution may also contribute to the development of atherosclerosis. SCOPE OF REVIEW: The present review integrates current experimental evidence with mechanistic pathways whereby PM2.5 exposure can promote the development of atherosclerosis. MAJOR CONCLUSIONS: PM2.5-mediated enhancement of atherosclerosis is likely due to its pro-oxidant and pro-inflammatory effects, involving multiple organs, different cell types, and various molecular mediators. GENERAL SIGNIFICANCE: Studies about the effects of PM2.5inhalation on atherosclerosis may yield a better understanding of the link between air pollution and major cardiovascular diseases, and provide useful information for policy makers to determine acceptable levels of PM2.5 air quality. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.

Particulate Air pollution mediated effects on insulin resistance in mice are independent of CCR2.

BACKGROUND: Chronic exposure to fine ambient particulate matter (PM2.5) induces insulin resistance. CC-chemokine receptor 2 (CCR2) appears to be essential in diet-induced insulin resistance implicating an important role for systemic cellular inflammation in the process. We have previously suggested that CCR2 is important in PM2.5 exposure-mediated inflammation leading to insulin resistance under high fat diet situation. The present study assessed the importance of CCR2 in PM2.5 exposure-induced insulin resistance in the context of normal diet. METHODS AND RESULTS: C57BL/6 and CCR2-/- mice were subjected to exposure to concentrated ambient PM2.5 or filtered air for 6 months. In C57BL/6 mice, concentrated ambient PM2.5 exposure induced whole-body insulin resistance, macrophage infiltration into the adipose tissue, and upregulation of phosphoenolpyruvate carboxykinase (PEPCK) in the liver. While CCR2 deficiency reduced adipose macrophage content in the PM2.5-exposed animals, it did not improve systemic insulin resistance. This lack of improvement in insulin resistance was paralleled by increased hepatic expression of genes in PEPCK and inflammation. CONCLUSION: CCR2 deletion failed to attenuate PM2.5 exposure-induced insulin resistance in mice fed on normal diet. The present study indicates that PM2.5 may dysregulate glucose metabolism directly without exerting proinflammatory effects.

Exposure to concentrated ambient particulate matter induces reversible increase of heart weight in spontaneously hypertensive rats.

BACKGROUND: Exposure to ambient PM2.5 increases cardiovascular mortality and morbidity. To delineate the underlying biological mechanism, we investigated the time dependence of cardiovascular response to chronic exposure to concentrated ambient PM2.5 (CAP). METHODS: Spontaneously hypertensive rats (SHR) were exposed to CAP for 15 weeks, and blood pressure (BP), cardiac function and structure, and inflammations of lung, hypothalamus, and heart were measured at different time points. RESULTS: Chronic exposure to CAP significantly increased BP, and withdrawal from CAP exposure restored BP. Consistent with its BP effect, chronic exposure to CAP significantly decreased cardiac stroke volume and output in SHR, accompanied by increased heart weight and increased cardiac expression of hypertrophic markers ACTA1 and MYH7. Withdrawal from CAP exposure restored cardiac function, weight, and expression of hypertrophic markers, supporting the notion that cardiac dysfunction and hypertrophy is subsequent to hypertension. In agreement with the role of systemic inflammation in mediating the cardiovascular effects of CAP exposure, chronic exposure to CAP markedly increased expression of pro-inflammatory cytokines in lung, heart, and hypothalamus. However, withdrawal from exposure resolves inflammation in the heart and hypothalamus, but not in the lung, suggesting that CAP exposure-induced systemic inflammation may be independent of pulmonary inflammation. CONCLUSION: Chronic exposure to CAP induces reversible cardiac dysfunction and hypertrophy, which is likely to be subsequent to the elevation in BP and induction of systemic inflammation as evidenced by increased mRNA expression of pro-inflammatory cytokines in diverse tissues.

The role of oxidative stress in citreoviridin-induced DNA damage in human liver-derived HepG2 cells.

We hypothesize that citreoviridin (CIT) induces DNA damage in human liver-derived HepG2 cells through an oxidative stress mechanism and that N-acetyl-l-cysteine (NAC) protects against CIT-induced DNA damage in HepG2 cells. CIT-induced DNA damage in HepG2 cells was evaluated by alkaline single-cell gel electrophoresis assay. To elucidate the genotoxicity mechanisms, the level of oxidative DNA damage was tested by immunoperoxidase staining for 8-hydroxydeoxyguanosine (8-OHdG); the intracellular generation of reactive oxygen species (ROS) and reduced glutathione (GSH) were examined; mitochondrial membrane potential and lysosomal membranes' permeability were detected; furthermore, protective effects of NAC on CIT-induced ROS formation and CIT-induced DNA damage were evaluated in HepG2 cells. A significant dose-dependent increment in DNA migration was observed at tested concentrations (2.50-10.00 µM) of CIT. The levels of ROS, 8-OHdG formation were increased by CIT, and significant depletion of GSH in HepG2 cells was induced by CIT. Destabilization of lysosome and mitochondria was also observed in cells treated with CIT. In addition, NAC significantly decreased CIT-induced ROS formation and CIT-induced DNA damage in HepG2 cells. The data indicate that CIT induces DNA damage in HepG2 cells, most likely through oxidative stress mechanisms; that NAC protects against DNA damage induced by CIT in HepG2 cells; and that depolarization of mitochondria and lysosomal protease leakage may play a role in CIT-induced DNA damage in HepG2 cells.

IKK inhibition prevents PM2.5-exacerbated cardiac injury in mice with type 2 diabetes.

Epidemiological studies have found that individuals with diabetes mellitus (DM) display an increased susceptibility for adverse cardiovascular outcomes when exposed to air pollution. This study was conducted to explore the potential mechanism linking ambient fine particles (PM2.5) and heart injury in a Type 2 DM (T2DM) animal model. The KKay mouse, an animal model of T2DM, was exposed to concentrated ambient PM2.5 or filtered air for 8 weeks via a versatile aerosol exposure and concentrator system. Simultaneously, an inhibitor of IκB kinase-2 (IKK-â) (IMD-0354), which is a blocker of nuclear factor κB (NF-κB) nuclear translocation, was administrated by intracerebroventricular injection (ICV) to regulate the NF-êB pathway. The results showed that ambient PM2.5 induced the increase of, NF-êB, cyclooxygenase-2 (COX-2) and mitogen activated protein kinase (MAPK) expression in cardiac tissue, and that IMD-0354 could alleviate the inflammatory injury. The results suggested that the NF-êB pathway plays an important role in mediating the PM2.5-induced cardiovascular injury in the T2DM model. Inhibiting NFκB may be a therapeutic option in air-pollution-exacerbated cardiovascular injury in diabetes mellitus.

Exaggerated effects of particulate matter air pollution in genetic type II diabetes mellitus.

BACKGROUND: Prior experimental and epidemiologic data support a link between exposure to fine ambient particulate matter (<2.5 µm in aerodynamic diameter, PM2.5) and development of insulin resistance/Type II diabetes mellitus. This study was designed to investigate whether inhalational exposure of concentrated PM2.5 in a genetically susceptible animal model would result in abnormalities in energy metabolism and exacerbation of peripheral glycemic control. METHODS: KKay mice, which are susceptible to Type II DM, were assigned to either concentrated ambient PM2.5 or filtered air (FA) for 5-8 weeks via a whole body exposure system. Glucose tolerance, insulin sensitivity, oxygen consumption and heat production were evaluated. At euthanasia, blood, spleen and visceral adipose tissue were collected to measure inflammatory cells using flow cytometry. Standard immnunohistochemical methods, western blotting and quantitative PCR were used to assess targets of interest. RESULTS: PM2.5 exposure influenced energy metabolism including O2 consumption, CO2 production, respiratory exchange ratio and thermogenesis. These changes were accompanied by worsened insulin resistance, visceral adiposity and inflammation in spleen and visceral adipose depots. Plasma adiponectin were decreased in response to PM2.5 exposure while leptin levels increased. PM2.5 exposure resulted in a significant increase in expression of inflammatory genes and decreased UCP1 expression in brown adipose tissue and activated p38 and ERK pathways in the liver of the KKay mice. CONCLUSIONS: Concentrated ambient PM2.5 exposure impairs energy metabolism, concomitant with abnormalities in glucose homeostasis, increased inflammation in insulin responsive organs, brown adipose inflammation and results in imbalance in circulating leptin/adiponectin levels in a genetically susceptible diabetic model. These results provide additional insights into the mechanisms surrounding air pollution mediated susceptibility to Type II DM.

Central IKKß inhibition prevents air pollution mediated peripheral inflammation and exaggeration of type II diabetes.

BACKGROUND: Prior experimental and epidemiologic data support a link between exposure to fine ambient particulate matter (<2.5 µm in aerodynamic diameter, PM2.5) and development of insulin resistance/Type II diabetes mellitus (Type II DM). We investigated the role of hypothalamic inflammation in PM2.5-mediated diabetes development. METHODS: KKay mice, a genetically susceptible model of Type II DM, were assigned to either concentrated PM2.5 or filtered air (FA) for 4-8 weeks via a versatile aerosol concentrator and exposure system, or administered intra-cerebroventricular with either IKKß inhibitor (IMD-0354) or TNFα antibody (infliximab) for 4-5 weeks simultaneously with PM2.5 exposure. Glucose tolerance, insulin sensitivity, oxygen consumption and heat production were evaluated. At euthanasia, blood, spleen, visceral adipose tissue and hypothalamus were collected to measure inflammatory cells using flow cytometry. Standard immunohistochemical methods and quantitative PCR were used to assess targets of interest. RESULTS: PM2.5 exposure led to hyperglycemia and insulin resistance, which was accompanied by increased hypothalamic IL-6, TNFα, and IKKß mRNA expression and microglial/astrocyte reactivity. Targeting the NFκB pathway with intra-cerebroventricular administration of an IKKß inhibitor [IMD-0354, n = 8 for each group)], but not TNFα blockade with infliximab [(n = 6 for each group], improved glucose tolerance, insulin sensitivity, rectified energy homeostasis (O2 consumption, CO2 production, respiratory exchange ratio and heat generation) and reduced peripheral inflammation in response to PM2.5. CONCLUSIONS: Central inhibition of IKKß prevents PM2.5 mediated peripheral inflammation and exaggeration of type II diabetes. These results provide novel insights into how air pollution may mediate susceptibility to insulin resistance and Type II DM.

In need of each other: the moderator of task interdependence between LMX variability and justice.

AIM: This study examined how leader-member exchange differentiation could affect nurses' perception of organisational justice as well as the moderating effect of task interdependence on this link. BACKGROUND: Teams are essential to the health-care industry. However, the perception of injustice may lead to a high level of nurse turnover. METHOD: Data was collected from 187 nurses distributed in eight units in a mid-western hospital in the USA. Hierarchical linear modeling was used to analyze the cross-level interaction of leader-member exchange variability and task interdependence on individual-level perceptions of justice. RESULTS: Leader-member exchange variability was significantly related to distributive justice and interactional justice but not significantly related to procedural justice. The interaction term was significantly related to interpersonal justice, but not to procedural justice or distributive justice. CONCLUSION: This study showed that if leaders demonstrated a variation in treatment of different subordinates, nurses could perceive this as unfair regarding distribution and interaction; when the group was highly task interdependent, this kind of perception of 'unfairness,' particularly regarding interpersonal treatment, became even more salient. IMPLICATIONS FOR NURSING MANAGEMENT: Preferential and inconsistent treatment by them within the work group could introduce nurses' perceptions of unfair treatment. It is of crucial importance to provide training for supervisors on how to display relatively consistent behaviour towards nurses, particularly when the teams are highly task interdependent.

Analysis on the control of the black tiger shrimp in the America from the perspective of international cooperation.

The invasive black tiger shrimp has caused serious ecological problems in the America. However, since it can be directly eaten or made into feed, it may be beneficial to other countries. In order to ensure ecological security, it is necessary to control the invasion of the black tiger shrimp through international cooperation. Common control modes of the black tiger shrimp include the introducing natural enemy mode, making feed mode and the "bringing to the table" mode. In order to derive the applicable scope of various control modes of the black tiger shrimp and provide suggestions for the security and sustainability of the ecological supply chain of the America and cooperative country, this article constructs three differential game models and compares and analyzes the equilibrium results obtained by the models. Finally, the study shows that the higher the price of feed and the price of black tiger shrimp, the greater the degree of control of the black tiger shrimp. If the price of the black tiger shrimp and the reputation of the America for controlling the black tiger shrimp are lower, the America can gain more benefits under the feed production mode. Otherwise, the America prefers to sell the black tiger shrimp directly, thus directly "bringing to the table". Compared with the feed production or "bringing to the table" mode, cooperative country prefer to control the black tiger shrimp flooding through the natural enemy introduction mode.

Equal allocation, demand priority or negotiated allocation? How to allocate water resources in the Tigris and Euphrates River Basin efficiently.

The Tigris and Euphrates River Basin is an important water supply, but it suffers from water scarcity. It is necessary to carry out reasonable allocation of water resources in this region. Since water resources issues in this region are of multinational interest, international cooperative distribution efforts are needed. Common water resources allocation modes include equal allocation, demand priority or negotiation allocation. In order to derive the applicable range of various water resources allocation modes, this article constructs three differential game models and compares and analyzes the equilibrium results obtained by the models. Finally, the study shows that when the cost of developing water resources is small and the revenue obtained from developing water resources is large, the water-scarce region can obtain the maximum benefit by adopting the demand priority mode. Otherwise, the water-scarce region can obtain the maximum benefit by adopting the negotiation allocation mode. This study can inform the allocation, strategic interaction and cooperation of dynamic water resources in the two river basins.

The Dual Spillover Spiraling Effects of Family Incivility on Workplace Interpersonal Deviance: From the Conservation of Resources Perspective.

In recent years, interest in family-to-work interference and its consequences has increased dramatically. Drawing on conservation of resources theory, we propose and test a dual spillover spiraling model which examines the indirect effects of family incivility on workplace interpersonal deviance through increasing family-to-work conflict (resource loss spiral) and decreasing family-to-work enrichment (resource gain spiral). We also examine the moderating effects of family-supportive supervisor behaviors on these indirect effects. The findings from a three-wave survey, with 455 employees and their coworkers in 60 teams, reveal that experienced family incivility (Time 1) induces more interpersonal deviance at work (Time 3) through facilitating family-to-work conflict (Time 2) and inhibiting family-to-work enrichment (Time 2). Such indirect deviation amplifying effects are mitigated by higher supervisor-level family-supportive supervisor behaviors (Time 1). Theoretical and practical implications are discussed.

From depression to wellbeing: How to protect the mental health of isolated people under the "dynamic clearance" of patients with COVID-19.

In 2020, COVID-19 became a global pandemic. The Chinese government's quarantine measures tend to cause anxiety, tension and depression among the quarantined people. This article constructs a differential game model of self-regulation, government guidance and social forces guidance. Then, the psychological benefits of the masses and the benefits of the whole society under the three modes are obtained, and the applicable conditions of various connection modes are compared. The research results show that: compared with social power channeling, the public under the government channeling mode can obtain more psychological benefits. However, with the increase of guidance, the difference between the psychological benefits of different ways of guidance first decreases and then tends to be stable. Under the guidance mode, the social benefits of the government decrease, and the more guidance, the smaller the social benefits. Therefore, both the government and social forces should make use of limited resources to conduct appropriate psychological counseling for the isolated population.

Remote monitoring, personnel extinguishment or helicopter extinguishment? How to control forest fires more effectively.

Forest fires have a great impact on the ecological environment. The government needs to take measures to control forest fires. Forest fires are easily affected by wind speed and other weather conditions, and the difficulty of extinguishing forest fires is easily affected by terrain complexity. Effective management methods can protect the important ecological functions of forests, thereby maintaining long-term development and economic efficiency. The government can put out the fire by remote monitoring, personnel extinguishing and helicopter extinguishing. Different from most articles on how to eliminate forest fires from the technical point of view, this article mainly analyzes from the two aspects of optimizing resource allocation and guiding policy formulation. This article constructs the differential game model under these three modes, and then obtains the equilibrium result. And the comparative analysis. Finally, the conclusion is drawn. The stronger the wind, the more residents need to flee. However, strong winds are not conducive to crews and helicopters fighting the fire. Rather than fighting fires, residents are more inclined to detect forest fires in time through remote monitoring. When the personnel can effectively control the fire, the personnel fire extinguishing mode is preferentially selected. Otherwise, helicopter firefighting mode should be selected.