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The dynamic and surface manipulation of the M13 bacteriophage via the meeting application demands the creation of a pathway to design efficient applications with high selectivity and responsivity rates. Here, we report the role of the M13 bacteriophage thin film layer that is deposited on an optical nanostructure involving gold nanoparticles/SiO2/Si, as well as its influence on optical and geometrical properties. The thickness of the M13 bacteriophage layer was controlled by varying either the concentration or humidity exposure levels, and optical studies were conducted. We designed a standard and dynamic model based upon three-dimensional finite-difference time-domain (3D FDTD) simulations that distinguished the respective necessity of each model under variable conditions. As seen in the experiments, the origin of respective peak wavelength positions was addressed in detail with the help of simulations. The importance of the dynamic model was noted when humidity-based experiments were conducted. Upon introducing varied humidity levels, the dynamic model predicted changes in plasmonic properties as a function of changes in NP positioning, gap size, and effective index (this approach agreed with the experiments and simulated results). We believe that this work will provide fundamental insight into understanding and interpreting the geometrical and optical properties of the nanostructures that involve the M13 bacteriophage. By combining such significant plasmonic properties with the numerous benefits of M13 bacteriophage (like low-cost fabrication, multi-wavelength optical characteristics devised from a single structure, reproducibility, reversible characteristics, and surface modification to suit application requirements), it is possible to develop highly efficient integrated plasmonic biomaterial-based sensor nanostructures.
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Bacteriófagos , Nanopartículas del Metal , Nanoestructuras , Oro , Dióxido de Silicio , Reproducibilidad de los Resultados , Nanoestructuras/química , Bacteriófago M13/químicaRESUMEN
Under strong laser fields, electrons in solids radiate high-harmonic fields by travelling through quantum pathways in Bloch bands in the sub-laser-cycle timescales. Understanding these pathways in the momentum space through the high-harmonic radiation can enable an all-optical ultrafast probe to observe coherent lightwave-driven processes and measure electronic structures as recently demonstrated for semiconductors. However, such demonstration has been largely limited for semimetals because the absence of the bandgap hinders an experimental characterization of the exact pathways. In this study, by combining electrostatic control of chemical potentials with HHG measurement, we resolve quantum pathways of massless Dirac fermions in graphene under strong laser fields. Electrical modulation of HHG reveals quantum interference between the multi-photon interband excitation channels. As the light-matter interaction deviates beyond the perturbative regime, elliptically polarized laser fields efficiently drive massless Dirac fermions via an intricate coupling between the interband and intraband transitions, which is corroborated by our theoretical calculations. Our findings pave the way for strong-laser-field tomography of Dirac electrons in various quantum semimetals and their ultrafast electronics with a gate control.
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MV was reported to have beneficial effects in ameliorating insulin resistance in db/db mice, but the intrinsic mechanisms for glucose homeostasis are unclear. This study examined the anti-diabetic mechanism of MV using HepG2 cells and C57BL/KsJ-db/db mice. MV increased insulin sensitivity by promoting insulin-dependent glucose uptake and activating glycogen accumulation in HepG2 cells. Furthermore, the glucose homeostasis was enhanced in db/db mice administered 1 mg/kg/day of MV for eight weeks by activating the IRS-1/PI3K/Akt and AMPK pathways in the skeletal muscle and liver tissue. In addition, MV promoted glycogen synthesis by regulating the key enzymes, including GSK-3ß and GS, and suppressed gluconeogenesis by inhibiting the mRNA expressions of G6pase and PEPCK. These findings show that MV regulates both signaling pathways and improves the glucose metabolism disorder. Thus, MV might be an alternative functional food or nutraceutical in ameliorating T2DM. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-022-01146-4.
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BACKGROUND: Headache is a common complication of regional anesthesia. The treatment of post spinal anesthesia headache varies depending on the cause. Although meningitis is rare, it can cause significant harm to the patient. Post dural puncture headache and septic meningitis are the most commonly suspected causes of post spinal anesthesia headache; however, other causes should also be considered. CASE SUMMARY: A 69-year-old woman was scheduled for varicose vein stripping surgery under spinal anesthesia. The procedure was performed aseptically, and surgery was completed without any complications. After 4 d, the patient visited the emergency room with complaints of headache, nausea, and anorexia. Clinical examination revealed that the patient was afebrile. Considering the history of spinal anesthesia, post dural puncture headache and septic meningitis was initially suspected, and the patient was treated with empirical antibiotics. Subsequently, varicella-zoster virus PCR test result was positive, and all other test results were negative. The patient was diagnosed with meningitis caused by varicella-zoster virus and was treated with acyclovir for 5 d. The headache improved, and the patient was discharged without any problems. CONCLUSION: Viral meningitis due to virus reactivation may cause headache after regional anesthesia. Therefore, clinicians should consider multiple etiologies of headache.
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Acetic acid has been proposed to improve lifestyle-related diseases, including hyperlipidemia and hyperglycemia. This study compared the hypoglycemic and hypolipogenic effects of acetic acid vinegar (AV, contains only 4% acetic acid) and Monascus-fermented grain vinegar (MV) containing various bioactive compounds in 3T3L1 cells and C57BL/KsJ-db/db mice (DB). The DB were divided randomly into three treatment groups containing nine mice each; DB-, AV-, and MV-groups were orally administered 1 mL/kg/day of distilled water, acetic acid vinegar, and Monascus vinegar, respectively, for 8 weeks. Exposure to AV and MV inhibited the adipogenic differentiation of 3T3L1 preadipocytes and lipid accumulation during differentiation. Oral administration of AV or MV to the mice resulted in a marked reduction in the body weight, liver weight, and hepatic triglyceride content compared to the control DB-group. Moreover, treatment with AV and MV clearly increased the expression of cyclic adenosine monophosphate (cAMP) and AMP-activated protein kinase (AMPK) and suppressed the expression of fatty acid synthetase in liver tissues of DB. Significantly, lower levels of fasting blood glucose, insulin, leptin, and the glycosylated hemoglobin (HbA1c) as well as higher levels of the skeletal muscle GLUT4 expression were obtained in the AV- or MV-groups than levels determined in the control DB-group (P < .05). Although MV has the potential to be a natural alternative treatment for obesity-associated type 2 diabetes, this study suggests that acetic acid is the central ingredient in MV responsible for the hypoglycemic and hypolipogenic effects in the DB mice.
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Diabetes Mellitus Tipo 2 , Monascus , Ácido Acético/metabolismo , Animales , Glucemia/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Hipoglucemiantes/metabolismo , Hipoglucemiantes/farmacología , Insulina , Hígado/metabolismo , Ratones , Ratones Endogámicos C57BL , Monascus/metabolismoRESUMEN
The aim of this work was to evaluate the inhibitory activities of organic acids identified from commercial vinegars on α-amylase and α-glucosidase. Six organic acids (acetic, citric, lactic, malic, succinic, and tartaric) were identified in nine commercial vinegars, whose contents varied considerably depending on the raw materials. Most of the fruit vinegars, comprised of various organic acids, were found to be more effective inhibitors against digestive enzymes than grain vinegars containing mainly acetic acid. Citric acid had the lowest IC50 values for α-amylase and α-glucosidase activities 0.64±0.04 µM/mL and 8.95±0.05 µM/mL, respectively, and thus exhibited the strongest antidiabetic effect. Mulberry fruit vinegar containing the highest content of total organic acid (111.02±1.50 mg/mL) showed the strongest digestive enzyme inhibitory impact. The results indicate that vinegars with higher contents of various organic acids hold strong potential against digestive enzymes.
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CASP9 (caspase 9) is a well-known initiator caspase which triggers intrinsic apoptosis. Recent studies also suggest various non-apoptotic roles of CASP9, including macroautophagy/autophagy regulation. However, the involvement of CASP9 in autophagy and its molecular mechanisms are not well understood. Here we report the non-apoptotic function of CASP9 in positive regulation of autophagy through maintenance of mitochondrial homeostasis. Growth factor or amino acid deprivation-induced autophagy activated CASP9, but without apoptotic features. Pharmacological inhibition or genetic ablation of CASP9 decreased autophagy flux, while ectopic expression of CASP9 rescued autophagy defects. In CASP9 knockout (KO) cells, initiation and elongation of phagophore membranes were normal, but sealing of the membranes and autophagosome maturation were impaired, and the lifetime of autophagosomes was prolonged. Ablation of CASP9 caused an accumulation of inactive ATG3 and decreased lipidation of the Atg8-family members, most severely that of GABARAPL1. Moreover, it resulted in abnormal mitochondrial morphology with depolarization of the membrane potential, reduced reactive oxygen species production, and aberrant accumulation of mitochondrial fusion-fission proteins. CASP9 expression or exogenously added H2O2 in the CASP9 KO cells corrected the ATG3 level and lipidation status of Atg8-family members, and restored autophagy flux. Of note, only CASP9 expression but not H2O2 rescued mitochondrial defects, revealing regulation of mitochondrial homeostasis by CASP9. Our findings suggest a new regulatory link between mitochondria and autophagy through CASP9 activity, especially for the proper operation of the Atg8-family conjugation system and autophagosome closure and maturation. ABBREVIATIONS: AA: amino acid; ACD: autophagic cell death; ACTB: actin beta; ANXA5: annexin A5; APAF1: apoptotic peptidase activating factor 1; Atg: autophagy related; ATG16L1: autophagy related 16 like 1; BafA1: bafilomycin A1; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; CARD: caspase recruitment domain containing; CASP: caspase; CM-H2DCFDA: chloromethyl-2',7'-dichlorodihydrofluorescein diacetate; Δψm: mitochondrial membrane potential; DN: dominant-negative; DNM1L/DRP1: dynamin 1 like; EBSS: Earle's balanced salt solution; GABARAP: GABA type A receptor-associated protein; GABARAPL1: GABA type A receptor associated protein like 1; GABARAPL2: GABA type A receptor associated protein like 2; HCN: hippocampal neural stem cells; IAM: inner autophagosome membrane; INS: insulin; KO: knockout; LEHD: Z-LEHD-fmk; MAP1LC3: microtubule associated protein 1 light chain 3; MFN1: mitofusin 1; MFN2: mitofusin 2; MTORC1: mechanistic target of rapamycin kinase complex 1; PARP1: poly(ADP-ribose) polymerase 1; PBS: phosphate-buffered saline; PE: phosphatidylethanolamine; ROS: reactive oxygen species; sgRNA: single guide RNA; SR-SIM: super-resolution structured illumination microscopy; SQSTM1: sequestosome 1; STS: staurosporine; STX17: syntaxin 17; TMRE: tetramethylrhodamine ethyl ester; TUBB: tubulin beta class I; ULK1: unc-51 like autophagy activating kinase 1; WT: wild type; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1.
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Autofagosomas/metabolismo , Caspasa 9/metabolismo , Homeostasis , Mitocondrias/metabolismo , Animales , Factor Apoptótico 1 Activador de Proteasas/metabolismo , Autofagia , Caspasa 9/deficiencia , Células HeLa , Hipocampo/citología , Humanos , Dinámicas Mitocondriales , Proteínas Mitocondriales/metabolismo , Modelos Biológicos , Células-Madre Neurales/metabolismo , Ratas , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Macroautophagy/autophagy is generally regarded as a cytoprotective mechanism, and it remains a matter of controversy whether autophagy can cause cell death in mammals. Here, we show that chronic restraint stress suppresses adult hippocampal neurogenesis in mice by inducing autophagic cell death (ACD) of hippocampal neural stem cells (NSCs). We generated NSC-specific, inducible Atg7 conditional knockout mice and found that they had an intact number of NSCs and neurogenesis level under chronic restraint stress and were resilient to stress- or corticosterone-induced cognitive and mood deficits. Corticosterone treatment of adult hippocampal NSC cultures induced ACD via SGK3 (serum/glucocorticoid regulated kinase 3) without signs of apoptosis. Our results demonstrate that ACD is biologically important in a mammalian system in vivo and would be an attractive target for therapeutic intervention for psychological stress-induced disorders.Abbreviations: AAV: adeno-associated virus; ACD: autophagic cell death; ACTB: actin, beta; Atg: autophagy-related; ASCL1/MASH1: achaete-scute family bHLH transcription factor 1; BafA1: bafilomycin A1; BrdU: Bromodeoxyuridine/5-bromo-2'-deoxyuridine; CASP3: caspase 3; cKO: conditional knockout; CLEM: correlative light and electron microscopy; CORT: corticosterone; CRS: chronic restraint stress; DAB: 3,3'-diaminobenzidine; DCX: doublecortin; DG: dentate gyrus; GC: glucocorticoid; GFAP: glial fibrillary acidic protein; HCN: hippocampal neural stem; i.p.: intraperitoneal; MAP1LC3B: microtubule-associated protein 1 light chain 3 beta; MKI67/Ki67: antigen identified by monoclonal antibody Ki 67; MWM: Morris water maze; Nec-1: necrostatin-1; NES: nestin; NR3C1/GR: nuclear receptor subfamily 3, group C, member 1; NSC: neural stem cell; PCD: programmed cell death; PFA: paraformaldehyde; PX: Phox homology; PtdIns3P: phosphatidylinositol-3-phosphate; RBFOX3/NeuN: RNA binding protein, fox-1 homolog (C. elegans) 3; SGK: serum/glucocorticoid-regulated kinases; SGZ: subgranular zone; SOX2: SRY (sex determining region Y)-box 2; SQSTM1: sequestosome 1; STS: staurosporine; TAM: tamoxifen; Ulk1: unc-51 like kinase 1; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VIM: vimentin; WT: wild type; ZFYVE1: zinc finger, FYVE domain containing 1; Z-VAD/Z-VAD-FMK: pan-caspase inhibitor.