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In this Letter, we report continuous-wave (CW) lasers with wavelengths beyond 3â µm in homemade Ho3+/Pr3+ co-doped AlF3-based glass fibers. The laser cavity was established through the integration of a dichroic mirror (DM, HR@3-3.1â µm) positioned at the pump end and a partial reflectivity (PR) fiber Bragg grating (FBG) situated at the laser emission end. The FBGs in AlF3-based glass fibers were fabricated by a fs laser direct-writing method, and the resonant wavelengths were 3.009, 3.036, and 3.064â µm, respectively. Under the pump of 1.15â µm laser, a maximum unsaturated output power of 1.014â W was obtained at 3.009â µm with an overall laser efficiency of 11.8% and FWHM bandwidth of 0.88â nm. Furthermore, in order to enhance the optical-thermal stability, the FBG was heat-treated at 200°C for 30â min, and a higher output power of 1081â mW (348â mW without heat treatment) at 3.036â µm was achieved. To the best of our knowledge, this is the first demonstration of 3-3.1â µm lasers by using FBGs in Ho3+/Pr3+ co-doped AlF3-based fibers.
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In this Letter, we report an Ho3+-doped fluorotellurite glass all-fiber laser at 2075 nm. The gain fiber is pumped in-band with a 1976-nm fiber laser and connected by fusion splicing. A high-quality fusion splicing point with a loss of < 0.1â dB was obtained by finely adjusting the splicing power and offset. In addition, by optimizing the writing parameters, a third-order fiber Bragg grating (FBG) with a reflectivity of 98% was achieved at 2075 nm using the femtosecond laser direct-writing method. Using the FBG as the laser cavity mirror and a relatively short 28-cm-long home-made Ho3+-doped fluorotellurite fiber as the laser medium, a laser with a maximum unsaturated output power of 7.33 W was obtained, and the corresponding slope efficiency was as high as 93.4%. The first, to the best of our knowledge, demonstration of the fluorotellurite glass all-fiber â¼2.1-µm laser presented in this work may pave the way for a high-power 2.1-µm fiber laser with a compact structure.
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In this Letter, we report the fabrication of fiber Bragg gratings (FBGs) in home-made Ho3+/Pr3+ co-doped single-cladding fluoroaluminate (AlF3) glass fibers and its application in watt-level lasing at the mid-infrared (MIR) wavelength of 2.86 µm. The FBGs were inscribed using an 800 nm femtosecond (fs) laser direct-writing technique. The FBG properties were investigated for different pulse energies, inscription speeds, grating orders, and transversal lengths. A second-order FBG with a high reflectivity of 99% was obtained at one end of a 16.5-cm-long gain fiber. Under 1150 nm laser pumping, this fiber yielded a power exceeding 1 W at 2863.9 nm with an overall laser efficiency of 17.7%. The fiber laser showed a FWHM bandwidth of 0.46 nm and long-term spectral stability.
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A room-temperature watt-level continuous-wave-output power mid-infrared fiber laser operating at $\lambda\sim 3\; \unicode{x00B5}{\rm m}$ is demonstrated using a ${{\rm Ho}^{3 +}}/{{\rm Pr}^{3 +}}$ co-doped ${{\rm AlF} _3}$ based glass fiber as a gain fiber. This fixed-wavelength laser had maximum output power of 1.13 W with a slope efficiency of 10.3% and a long-term operating stability of ${\gt}{40}\;{\min }$ without any additional packaging or active thermal management. A fiber laser with tunability from 2.842 to 2.938 µm showed a maximum output power of 110 mW.
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Ho3+/Pr3+ co-doped AlF3-based glass fibers were fabricated by using a rod-in-tube method based on the matrix glass composition of AlF3-BaF2-CaF2-YF3-SrF2-MgF2-LiF-ZrF4-PbF2. Under the pump of a 1150 mW Raman fiber laser, a 2.9 µm laser was observed in a 19 cm long Ho3+/Pr3+ co-doped AlF3-based glass fiber with an output power of 173 mW and a slope efficiency of 10.4%. Ho3+/Pr3+ co-doped AlF3-based glasses were fabricated to investigate the deactivation effects of Pr3+ ions on the Ho3+:5I7 level. Our results showed that the Ho3+/Pr3+ co-doped AlF3-based glass fibers are potential gain media for â¼2.9µm lasers.
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This publisher's note contains corrections to Opt. Lett. 45, 1216 (2020).
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Sleep disturbance led by BMAL1-deficiency has been recognized both in rodent and non-human primate models. Yet it remained unclear how their diurnal brain oscillations were affected upon BMAL1 ablation and what caused the discrepancy in the quantity of sleep between the two species. Here, we investigated diurnal electroencephalographs of BMAL1-deficient mice and cynomolgus monkeys at young adult age and uncovered a shared defect of dysregulated high-frequency oscillations by Kullback-Leibler divergence analysis. We found beta and gamma oscillations were significantly disturbed in a day versus night manner in BMAL1-deficient monkeys, while in mice the beta band difference was less evident. Notably, the dysregulation of beta oscillations was particularly associated with psychiatric behaviors in BMAL1-deficient monkeys, including the occurrence of self-injuring and delusion-like actions. As such psychiatric phenotypes were challenging to uncover in rodent models, our results offered a unique method to study the correlation between circadian clock dysregulation and psychiatric disorders.
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Circadian dysregulation associates with numerous diseases including metabolic dysfunction, sleep disorder, depression and aging. Given that declined circadian amplitude is a trait commonly found with compromised health, interventions that design in precluding circadian amplitude from dampening will aid to mitigate complex, circadian-related diseases. Here we identify a neurogenic small molecule ISX-9 that is able to support persistent and higher amplitude of circadian oscillations. ISX-9 improves diurnal metabolic rhythms in middle-aged mice. Moreover, the ISX-9-treated mice show better sleep homeostasis with increased delta power during the day time and higher locomotive activity in the dark period. ISX-9 augments CaMKIIδ expression and increases BMAL1 activity via eliciting CaMKIIδ-mediated phosphorylation on BMAL1 residues S513/S515/S516, accordingly composes a positive feedback effect on enhancing circadian amplitude. CaMKIIδ-targeting, and the use of ISX-9 may serve as decent choices for treating circadian-related disorders.
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Factores de Transcripción ARNTL , Ritmo Circadiano , Factores de Transcripción ARNTL/genética , Factores de Transcripción ARNTL/metabolismo , Envejecimiento , Animales , Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina , Ritmo Circadiano/fisiología , Homeostasis , Isoxazoles , Ratones , Sueño , TiofenosRESUMEN
Mastitis is a serious and prevalent disease caused by infection by pathogens such as Staphylococcus aureus. We evaluated the anti-inflammatory effects and mechanism of luteolin, a natural flavonoid with a wide range of pharmacological activities, in a mouse model of S. aureus mastitis. We also treated cultured mouse mammary epithelial cells (mMECs) with S. aureus and luteolin. Histopathological changes were examined by H&E staining and the levels of inflammatory cytokine proteins were analyzed using ELISAs. We determined mRNA levels with qPCR and the level of NF-κB and matrix metalloproteinase (MMP) proteins by Western blotting. The observed histopathological changes showed that luteolin protected mammary glands with S. aureus infection from tissue destruction and inflammatory cell infiltration. Luteolin inhibited the expression of TNF-α, IL-1ß, and IL-6, all of which were increased with S. aureus infection of mammary tissues and mMECs. S. aureus-induced TLR2 and TLR4 was suppressed by luteolin, as were levels of IκBα and NF-κB p65 phosphorylation and expression of MMP-2 and MMP-9. Levels of tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 were enhanced. These findings suggest luteolin is a potentially effective new treatment to reduce tissue damage and inflammation from S. aureus-induced mastitis.
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Luteolina/farmacología , Mastitis/genética , Mastitis/metabolismo , Metaloproteinasas de la Matriz/genética , Metaloproteinasas de la Matriz/metabolismo , FN-kappa B/metabolismo , Infecciones Estafilocócicas/genética , Infecciones Estafilocócicas/metabolismo , Staphylococcus aureus/fisiología , Animales , Línea Celular , Supervivencia Celular/efectos de los fármacos , Citocinas/genética , Citocinas/metabolismo , Modelos Animales de Enfermedad , Femenino , Regulación de la Expresión Génica/efectos de los fármacos , Mediadores de Inflamación/metabolismo , Luteolina/química , Glándulas Mamarias Animales/efectos de los fármacos , Glándulas Mamarias Animales/metabolismo , Glándulas Mamarias Animales/patología , Mastitis/tratamiento farmacológico , Mastitis/microbiología , Ratones , Transducción de Señal/efectos de los fármacos , Infecciones Estafilocócicas/tratamiento farmacológico , Receptor Toll-Like 2/genética , Receptor Toll-Like 2/metabolismo , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/metabolismoRESUMEN
Mastitis is defined as the inflammation of the mammary gland. LPS, which is widely used to induce mastitis models for the study of this disease, triggers similar inflammation as Escherichia coli. Sophocarpine, isolated from Sophora alopecuroides L., exhibits multiple biological properties. The aim of the present study was to determine the anti-inflammatory effect and mechanism of action of sophocarpine on mastitis within an LPS-induced mouse model. ELISA and western blotting were performed to detect protein levels. The qPCR was performed to detect mRNA levels. The ELISA and qRT-PCR results showed that sophocarpine inhibited the expression of TNF-α, IL-1ß and IL-6 in a dose-dependent manner. However, sophocarpine suppressed TLR4 expression. Further study showed that sophocarpine could suppress the phosphorylation of IκBα, p65 and p38. These results confirm that sophocarpine played an anti-inflammatory role in LPS-induced mastitis by regulating TLR4 and the NF-κB and MAPK signaling pathways in mammary gland tissues. Therefore, sophocarpine may be a potential therapeutic drug for the treatment of mastitis.
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Alcaloides/uso terapéutico , Antiinflamatorios/uso terapéutico , Glándulas Mamarias Humanas/efectos de los fármacos , Mastitis/tratamiento farmacológico , Sophora/inmunología , Receptor Toll-Like 4/metabolismo , Animales , Modelos Animales de Enfermedad , Regulación hacia Abajo , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Femenino , Humanos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Lipopolisacáridos/inmunología , Glándulas Mamarias Humanas/inmunología , Mastitis/inducido químicamente , Mastitis/inmunología , Ratones , Ratones Endogámicos BALB C , FN-kappa B/metabolismo , Transducción de Señal/efectos de los fármacos , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
Endometritis is commonly caused by pathogenic microorganisms, including Staphylococcus aureus (S. aureus). Piperine, which is a natural medicine, has shown a variety of biological activities. To explore the effect and mechanism of piperine on S. aureus endometritis, a mouse model of S. aureus endometritis was successfully established in the present study. Histopathological changes were observed with H&E staining, cytokines were analyzed by ELISA, mRNA was analyzed by qPCR, and proteins were detected by western blot. The results showed that piperine could significantly alleviate inflammatory injury in S. aureus endometritis. The qPCR and ELISA results showed that piperine effectively reduced the S. aureus-induced overexpression of TNF-α, IL-1ß, and IL-6 but increased the expression of IL-10. The S. aureus-induced inflammation was related to TLR-2 and TLR-4 because the results showed that their expression was increased in S. aureus infection but then decreased with piperine treatment. To further confirm that piperine caused an anti-inflammatory response by targeting NF-κB and MAPKs, the expression of I-κB, p65, p38, ERK, and JNK was measured. The phosphorylation of I-κB, p65, p38, ERK, and JNK was inhibited by piperine in a dose-dependent manner. All of the results indicated that piperine may be a potential anti-inflammatory drug both in endometritis and in other S. aureus-induced diseases.