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Multiprincipal element alloys usually exhibit earlier pop-in events than pure metals and dilute solid solutions during nanoindentation experiments. To understand the origin of this phenomenon, large-scale atomic simulations of nanoindentation were performed on a series of metallic materials to investigate the underlying physics of incipient plasticity at the nanoscale. Statistical result shows that lattice distortion δ and normalized critical pressure pc/Es follow a power-law relationship. Via quantitative analysis on the relative positions of the atoms within the nearest neighbor shell, the physical origin of premature incipient plasticity is revealed as severe lattice distortion induces large relative atomic displacement, so only a small indentation strain is required to meet the critical displacement threshold that triggers incipient plasticity. Therefore, for perfect crystals, lattice distortion is an intrinsic and determinative factor that affects the first pop-in event.
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Objective: The purpose of this study was to evaluate the protective effect of Shengmai Zhenwu decoction on patients with chronic heart failure (CHF) based on the levels of soluble interleukin 1 receptor-like 1 (ST2). Methods: We included a total of 80 outpatients and inpatients with CHF who were undergoing treatment at the Shanghai Municipal Hospital of Traditional Chinese Medicine between March 2020 and March 2022. We randomly divided them into the observation group (n = 40) and the control group (n = 40). Patients in the control group received treatments as per conventional Western medicine, while those in the observation group were treated with the Shengmai Zhenwu decoction in conjunction with Western medicine for eight consecutive weeks. We then compared the pre- and post-treatment levels of ST2 and N-terminal pro-brain natriuretic peptide (NT-proBNP) of the patients in the two groups. Results: There were no significant differences in the pre-treatment levels of ST2 and NT-proBNP indexes between the two groups (P > 0.05), while the post-treatment comparison between the two groups in terms of ST2 and NT-proBNP levels suggested that the effect in the observation group was better, with statistical significance (P < 0.05). Conclusion: Shengmai Zhenwu decoction was beneficial in patients with CHF, suggesting that it could be a promising and effective method for the treatment of CHF.
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Context: Duchesnea indica is effective against hepatocellular carcinoma (HCC); however, its underlying mechanism of action remains unclear. Objective: The present study aimed to investigate the potential mechanism of action and effects of D. indica components against HCC. Materials and methods: First, the effects of D. indica against HCC were investigated in vitro and in vivo. For in vitro experiments, HCC cell lines were treated with D. indica solutions at different concentrations (0, 1, 2 mg/mL) and then assessed for cell apoptosis, proliferation, migration, invasion, and angiogenic ability. For in vivo experiments, 24 mice were randomly divided into the following four groups: model group and D. indica low-, medium-, and high-dose groups. Tumor growth and CD34 and Ki67 expression levels were assessed to determine the effects of D. indica on cell proliferation and angiogenic ability. Furthermore, transcriptome sequencing and differential expression analyses were used to identify D. indica-induced differentially expressed genes (DEGs) in HCC cells. Additionally, mass spectrometry was conducted to identify the chemical components of D. indica. Four databases were used to predict the target proteins of these chemical components in HCC. HCC-associated genes were identified from two databases. By intersecting the identified DEGs; target proteins; and HCC-associated genes, key D. indica-regulated HCC-related genes were identified. Subsequently, protein-protein interaction network, network pharmacology, and molecular docking were used to identify the active compounds in D. indica and their likely gene targets. Results: In vitro experiments demonstrated that D. indica induced tumor cell apoptosis and inhibited cell proliferation, migration, invasion, and angiogenic potential. In vivo experiments demonstrated that D. indica inhibited tumor growth in a dose-dependent manner. Bioinformatic analyses identified 49 key D. indica-regulated HCC-related genes, of which FOS, SERPINE1, AKR1C3, and FGF2 were the most significant. Mass spectrometry identified the following five molecules in D. indica with potential anti-HCC activity: 4', 5, 7-trihydroxyflavone; ethyl protocatechuate; 3, 5-dihydroxy-benzoic acid; curculigosaponin A; and curculigine G. Molecular docking validated the interaction between D. indica active compounds and their target proteins in HCC. Conclusions: The present study confirmed the therapeutic effects of D. indica against HCC and identified the key genes and active components that may contribute to its mechanism of action, thereby providing a basis for further research on targeted therapeutics for HCC.
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BACKGROUND: As highly-conserved types of lipid flippases among fungi, P4-ATPases play a significant role in various cellular processes. Cdc50 acts as the regulatory subunit of flippases, forming heterodimers with Drs2 to translocate aminophospholipids. Cdc50 homologs have been reported to be implicated in protein trafficking, drug susceptibility, and virulence in Saccharomyces cerevisiae, Candida albicans and Cryptococcus neoformans. It is likely that Cdc50 has an extensive influence on fungal cellular processes. The present study aimed to determine the function of Cdc50 in Candida glabrata by constructing a Δcdc50 null mutant and its complemented strain. RESULTS: In Candida glabrata, the loss of Cdc50 led to difficulty in yeast budding, probably caused by actin depolarization. The Δcdc50 mutant also showed hypersensitivity to azoles, caspofungin, and cell wall stressors. Further experiments indicated hyperactivation of the cell wall integrity pathway in the Δcdc50 mutant, which elevated the major cell wall contents. An increase in exposure of ß-(1,3)-glucan and chitin on the cell surface was also observed through flow cytometry. Interestingly, we observed a decrease in the phagocytosis rate when the Δcdc50 mutant was co-incubated with THP-1 macrophages. The Δcdc50 mutant also exhibited weakened virulence in nematode survival tests. CONCLUSION: The results suggested that the lipid flippase subunit Cdc50 is implicated in yeast budding and cell wall integrity in C. glabrata, and thus have a broad influence on drug susceptibility and virulence. This work highlights the importance of lipid flippase, and offers potential targets for new drug research.
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Adenosina Trifosfatases , Saccharomyces cerevisiae , Adenosina Trifosfatases/metabolismo , Saccharomyces cerevisiae/metabolismo , Candida glabrata/genética , Candida glabrata/metabolismo , Caspofungina , Parede Celular/metabolismo , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismoRESUMO
Psoriasis is a chronic inflammatory skin disease characterized by infiltration of inflammatory cells and excessive proliferation of epidermal keratinocytes. SERPINB4, as a serine protease inhibitor, has been clearly expressed in the skin lesions and serum of patients with psoriasis, but the specific mechanism of action is not yet clear. Here, we showed that SERPINB4 expression was increased in skin lesions from the imiquimod (IMQ)-treated mice and M5-(a mixture of five proinflammatory cytokines: IL-17A, IL-22, IL-1α, oncostatin M, and TNF-α) treated human immortalized keratinocyte (HaCaT). Knockdown of SERPINB4 by short hairpin RNA attenuated the M5-induced keratinocyte inflammation. Conversely, lentiviral expression of SERPINB4 promoted keratinocyte inflammation. Finally, we observed that SERPINB4 stimulation activated the p38MAPK signaling pathway. Taken together, these results suggest that SERPINB4 has a critical role in psoriasis pathogenesis.
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Queratinócitos , Psoríase , Humanos , Animais , Camundongos , Queratinócitos/metabolismo , Pele/patologia , Psoríase/genética , Inflamação/metabolismo , Transdução de Sinais , Modelos Animais de Doenças , Camundongos Endogâmicos BALB C , Proliferação de CélulasRESUMO
Introduction: Candida glabrata has emerged as a fungal pathogen with high infection and mortality rates, and its primary virulence factors are related to adhesion and biofilm formation. These virulence factors in C.glabrata are primarily mediated by epithelial adhesins (Epas), most of which are encoded in subtelomeric regions and regulated by subtelomeric silencing mechanisms. The transcription factor Mss11, known for its regulatory role in adhesion, biofilm formation, and filamentous growth in Saccharomyces cerevisiae and Candida albicans, has also been implicated in the expression of EPA6, suggesting its potential influence on C.glabrata virulence. The present study aims to determine the regulatory role of Mss11 in the virulence of C. glabrata. Methods: In this work, a Δmss11 null mutant and its complemented strain were constructed from a C.glabrata standard strain. The impact of the transcription factor Mss11 on the virulence of C.glabrata was investigated through a series of phenotypic experiments, including the microbial adhesion to hydrocarbons (MATH) test, adherence assay, biofilm assay, scanning electron microscopy and Galleria mellonella virulence assay. Furthermore, transcriptome sequencing, quantitative reverse transcription polymerase chain reaction (RT-qPCR), and chromatin immunoprecipitation sequencing (ChIP-seq) were employed to investigate the molecular mechanisms behind the regulation of Mss11. Results: In C.glabrata, the loss of MSS11 led to a significant reduction in several virulence factors including cell surface hydrophobicity, epithelial cell adhesion, and biofilm formation. These observations were consistent with the decreased virulence of the Δmss11 mutant observed in the Galleria mellonella infection model. Further exploration demonstrated that Mss11 modulates C. glabrata virulence by regulating EPA1 and EPA6 expression. It binds to the upstream regions of EPA1 and EPA6, as well as the promoter regions of the subtelomeric silencing-related genes SIR4, RIF1, and RAP1, indicating the dual regulatory role of Mss11. Conclusion: Mss11 plays a crucial role in C. glabrata adhesion and biofilm formation, and thus has a broad influence on virulence. This regulation is achieved by regulating the expression of EPA1 and EPA6 through both promoter-specific regulation and subtelomeric silencing.
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Candida glabrata , Proteínas de Saccharomyces cerevisiae , Candida glabrata/genética , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismo , Virulência/genética , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Saccharomyces cerevisiae/metabolismo , Adesão Celular , Biofilmes , Fatores de Virulência/genética , Fatores de Virulência/metabolismo , Proteínas Repressoras/metabolismo , Proteínas de Saccharomyces cerevisiae/metabolismo , Proteínas de Ligação a Telômeros/metabolismoRESUMO
BACKGROUND: The Candida glabrata does not develop into a pathogenic hiphal form; however, it has become the second most common pathogen of fungal infections in humans, partly because of its adhesion ability and virulence. OBJECTIVES: The present study aimed to determine whether Flo8, a transcription factor that plays an important role in the virulence and drug resistance in Candida albicans, has a similar role in C. glabrata. METHODS: We constructed FLO8 null strains of a C. glabrata standard strain and eight clinical strains from different sources, and a FLO8 complemented strain. Real-time quantitative PCR, biofilm formation assays, hydrophobicity tests, adhesion tests, Caenorhabditis elegans survival assay, and drug-susceptibility were then performed. RESULTS: Compared with the wild-type strains, the biofilm formation, hydrophobicity, adhesion, and virulence of the FLO8-deficient strains decreased, accompanied by decreased expression of EPA1, EPA6, and EPA7. On the other hand, it showed no changes in antifungal drug resistance, although the expression levels of CDR1, CDR2, and SNQ2 increased after FLO8 deletion. CONCLUSIONS: These results indicated that Flo8 is involved in the adhesion and virulence of C. glabrata, with FLO8 deletion leading to decreased expression of EPA1, EPA6, and EPA7 and decreased biofilm formation, hydrophobicity, adhesion, and virulence.
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Candida glabrata , Proteínas Fúngicas , Antifúngicos/farmacologia , Biofilmes , Candida albicans/metabolismo , Candida glabrata/genética , Candida glabrata/metabolismo , Farmacorresistência Fúngica , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismo , Humanos , VirulênciaRESUMO
The translational failure of neuroprotective therapies in stroke may be influenced by the mismatch of existing comorbidities between animal models and patients. Previous studies found that single-target neuroprotective agents reduced infarction in Sprague-Dawley but not in spontaneously hypertensive rats. It is of great interest to explore whether multi-target neuroprotectants and stroke models with comorbidities should be used in further translational researches. Ischemic stroke was induced in normotensive or hypertensive rats by 90- or 120-min middle cerebral artery occlusion (MCAO) and reperfusion. Intra-Arterial Selective Cooling Infusion (IA-SCI) was started at the onset of reperfusion for 30 minutes. Acute neurological deficits, infarct volumes, gene expression and markers of A1-like and A2-like astrocytes were evaluated. In further analysis, TNFα and IL-1α were administrated intracerebroventricularly, phenotype shifting of astrocytes and infarct volumes were assessed. Normobaric oxygen treatment, as a negative control, was also assessed in hypertensive rats. IA-SCI led to similar benefits in normotensive rats with 120-min MCAO and hypertensive rats with both 90-min and 120-min MCAO, including mitigated functional deficit and reduced infarct volumes. IA-SCI shifted astrocyte phenotypes partly by downregulating A1-like astrocytes and upregulating A2-like astrocytes in both RNA and protein levels. Upregulated A1-type astrocyte markers levels, induced by intracerebroventricular injection of TNFα and IL-1α, were closely related to increased infarct volumes in hypertensive rats, despite receiving IA-SCI treatment. In addition, infarct volumes and A1/A2-like genes were not affected by normobaric oxygen treatment. IA-SCI reduced infarction in both normotensive and hypertensive rats. Our results demonstrated the neuroprotective effects of IA-SCI in hypertensive rats may be related with phenotype shifting of astrocytes.
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Hipertensão , AVC Isquêmico , Fármacos Neuroprotetores , Acidente Vascular Cerebral , Animais , Astrócitos/metabolismo , Modelos Animais de Doenças , Humanos , Hipertensão/complicações , Hipertensão/terapia , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/terapia , Fármacos Neuroprotetores/farmacologia , Oxigênio/metabolismo , Oxigênio/farmacologia , Fenótipo , Ratos , Ratos Sprague-Dawley , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/terapia , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Introduction: This study aimed to screen for oxidative stress-related genes (OSRGs) and build an oxidative stress-related signature to predict the prognosis of liver cancer. Methods: OSRGs with a protein domain correlation score ≥ 6 were downloaded from the GeneCards database and intersected with The Cancer Genome Atlas (TCGA) data for subsequent analyses. Differential immune cells (DICs) and immune and stromal scores between the normal and tumor samples were determined, followed by unsupervised hierarchical cluster analysis. Immune-related OSRGs were identified using weighted gene co-expression network analysis. An OSRG-related risk signature was then built, and the GSE14520 dataset was used for validation. A nomogram evaluation model was used to predict prognosis. Results: Nine DICs were determined between the normal and tumor groups, and three subtypes were obtained: clusters 1, 2, and 3. Cluster 1 had the best prognosis among the clusters. One hundred thirty-eight immune-related OSRGs were identified, and seven prognosis-related OSRGs were used to build the OSRG score prognostic model. Patients in the high OSRG score group had a poorer prognosis than those in the low OSRG score group. Six immune cell infiltration and enrichment scores of the 16 immune gene sets showed significant differences between the high and low OSRG score groups. Moreover, a nomogram was constructed based on the prognostic signature and clinicopathological features and had a robust predictive performance and high accuracy. Conclusion: The OSRG-related risk signature and the prognostic nomogram accurately predicted patient survival.
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The A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family is gradually being recognized as an important family of mediators that, along with the matrix metalloproteinases (MMPs), control the degradation process in osteoarthritis (OA). The objective of this study was to uncover the detailed alterations of ADAMTS1, ADAMTS2, and ADAMTS5 in the knee joint of OA mice. The OA model was established by anterior cruciate ligament transection (ACLT) on the knee joints of C57BL/6 J mice. The mice showed representative phenotypes of ACLT-induced OA, including obvious deterioration of the cartilage, reductions in the collagen and proteoglycan components in the cartilage matrix of OA mice, and increased inflammation and osteoclast activity. By qPCR, the gene expression levels of Adamts1, -2, and -5 were the top-ranked among Adamts1-5 in cartilage/chondrocytes, osteogenic tissue/osteoblasts, and cortical bone/osteocytes. Moreover, the protein expression levels of ADAMTS1, -2, and -5 were all increased in articular cartilage, the growth plate, and subchondral bone of the knee joint. The results suggest the important roles of ADAMTS1, -2, and -5 in OA disease, which will be helpful in further research on degenerative changes in OA.
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Desintegrinas , Metaloproteinases da Matriz , Osteoartrite , Animais , Articulação do Joelho , Camundongos , Camundongos Endogâmicos C57BL , Osteoartrite/genética , TrombospondinasRESUMO
OBJECTIVE: The aim of this study was to demonstrate the influence of the virulence factor GroEL on osteoblast behavior by characterizing the changes of secreted gelatinases. DESIGN: ELISA was performed to detect GroEL from samples from patients with or without apical periodontitis. An apical periodontitis model was established in rats and the expression of MMP-2, MMP-9 and NF-κB was evaluated by immunofluorescence staining. The primary osteoblasts and osteoblast-like MC3T3 cells were stimulated with recombinant GroEL, and gelatin zymography was used to determine the activity and expression of MMP-2 and MMP-9. Western blot was used to screen signaling pathways, and immunofluorescence staining was performed to confirm the activated signaling. RESULTS: First, we found expression of GroEL to be higher in oral saliva, gingival crevicular fluid and periradicular granulation tissue of patients with apical periodontitis than it was in healthy control patients. We next found that recombinant GroEL could increase the activity of the gelatinases, MMP-2 and MMP-9, which were secreted by both primary osteoblasts and MC3T3 cells. In a rat apical periodontitis model, strong expression of gelatinases was confirmed. Then, we found that GroEL-enhanced gelatinase activity was mediated through activation of NF-κB signaling. Acetylated NF-κB accumulated in the cell nucleus and bound to the promoter of MMP-2 and MMP-9 genes, thus initiating their high expression. CONCLUSION: This study reveals a direct interaction between oral bacteria and adult cells by demonstrating that gelatinase secretion is induced by GroEL, which partially explains bone resorption through gelatinase activation.
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Chaperonina 60/metabolismo , Gelatinases/metabolismo , Osteoblastos/enzimologia , Periodontite/enzimologia , Animais , Bactérias/patogenicidade , Reabsorção Óssea , Linhagem Celular , Humanos , Metaloproteinase 2 da Matriz , Metaloproteinase 9 da Matriz , Camundongos , NF-kappa B , Ratos , Fatores de Virulência/metabolismoRESUMO
BACKGROUND: Increasing evidence demonstrates that high-sensitivity C-reactive protein (hs-CRP) is an independent prognostic predictor in acute ischemic stroke (AIS) patients. The purpose of this study is to investigate the association between hs-CRP levels and clinical outcomes in AIS patients receiving endovascular therapy (EVT). METHODS: This observational study was based on a prospective registry study. AIS patients receiving EVT from December 2012 to January 2019 were included. The modified Rankin Scale (mRS) scores at the 90-day and long-term follow-up were evaluated as clinical outcomes. Multivariable logistic regression analysis was conducted to adjust for confounders. Receiver operating characteristic (ROC) curve analysis was performed based on significant predictors of favorable outcomes in the logistic regression analysis. Patients were divided into two groups according to the cutoff value. Clinical outcomes were compared between groups. Survival probability was assessed using Kaplan-Meier survival analysis. RESULTS: Multivariable logistic regression analysis of the 362 enrolled AIS patients demonstrated that age (P=0.030), National Institutes of Health Stroke Scale (NIHSS) score (P=0.023), hs-CRP levels (P<0.001), and symptomatic intracranial hemorrhage (sICH) (P=0.006) were independently predictive of favorable outcomes. ROC curve analysis indicated that the hs-CRP level was predictive of favorable outcomes at the 90-day follow-up with a cutoff value of 8.255 mg/L. The mRS scores between patients with hs-CRP <8.255 mg/L and patients with hs-CRP ≥8.255 mg/L at the 90-day [2 (IQR, 1-2) vs. 4 (IQR, 3-6), P<0.001] and long-term follow-up [1 (IQR, 0-2) vs. 4 (IQR, 2-6), P<0.001] were significantly different. Patients with hs-CRP ≥8.255 mg/L had significantly increased risk of poor clinical outcomes at the 90-day and long-term follow-up compared with those with hs-CRP <8.255 mg/L (P<0.001 each). CONCLUSIONS: Elevated hs-CRP levels were associated with poor clinical outcomes in AIS patients receiving EVT.
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Isquemia Encefálica , Hipotermia Induzida , Neuroproteção , Acidente Vascular Cerebral , Isquemia Encefálica/complicações , Isquemia Encefálica/fisiopatologia , Isquemia Encefálica/terapia , Humanos , Acidente Vascular Cerebral/fisiopatologia , Acidente Vascular Cerebral/prevenção & controleAssuntos
Isquemia Encefálica , Hipertensão , Acidente Vascular Cerebral , Animais , Pressão Sanguínea , Ratos , Ratos WistarRESUMO
We report a refractive-index matching method to measure nonabsorbing solid ultraviolet (UV) Raman cross-sections that avoids the local field correction and interface scattering of incident light. We used refractive-index-matched chloroform as an internal standard to determine the solid-state 995 cm(-1) Na(2)SO(4) 244 nm Raman cross-sections. The pure liquid chloroform 668 cm(-1) 244 nm Raman cross-section was determined by using acetonitrile as an internal standard and by calculating the local field corrections for the observed Raman intensities. Our measured 244 nm UV Raman cross-section of the solid-state 995 cm(-1) SO4(2-) band of 1.97 ± 0.07 × 10(-28) cm(2)/(molc·sr) is about half of its aqueous solution Raman cross-section, indicating interactions between the sulfate species in the solid that decrease the Raman polarizability.
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We developed a facile method to fabricate deep ultraviolet (UV) photonic crystal crystalline colloidal array (CCA) Bragg diffraction devices. The CCAs were prepared through the self-assembly of small, monodisperse, highly surface charged silica particles (~50 nm diameter) that were synthesized by using a modified Stöber process. The particle surfaces were charged by functionalizing them with the strong acid, non-UV absorbing silane coupling agent 3-(trihydroxylsilyl)-1-propane-sulfonic acid (THOPS). These highly charged, monodisperse silica particles self assemble into a face-centered cubic CCA that efficiently Bragg diffracts light in the deep UV. The diffracted wavelength was varied between 237 nm to 227 nm by tilting the CCA orientation relative to the incident beam between glancing angles from 90° to ~66°. Theoretical calculations predict that the silica CCA diffraction will have a full width at half-maximum (FWHM) of 2 nm with a transmission of ~10(-11) at the band center. We demonstrate the utility of this silica CCA filter to reject the Rayleigh scattering in 229 nm deep UV Raman measurements of highly scattering Teflon.
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Coloides/química , Dióxido de Silício/química , Espectrofotometria Ultravioleta/instrumentação , Análise Espectral Raman/instrumentação , Desenho de Equipamento , Tamanho da Partícula , Politetrafluoretileno/químicaRESUMO
We developed a convenient and fast approach to preparing close-packed two-dimensional (2-D) particle arrays on mercury surfaces. Addition of cosolvents, such as alcohols, to aqueous colloidal particle suspensions induces spreading and self-assembly of the particles into 2-D arrays on top of the mercury surface. We can fabricate large-area close-packed 2-D arrays (>70 cm(2)) within 30 s. We attached these 2-D arrays to functional hydrogel films such that the 2-D array spacings were altered by the hydrogel volume response to the environment. We directly observed the hydrogel volume induced 2-D array spacing changes by using confocal laser scanning microscopy to monitor the spacings of fluorescent polystyrene particle 2-D arrays in response to changes in pH, solvent composition, temperature, etc.
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We have developed the first high-diffraction-efficiency two-dimensional (2-D) photonic crystals for molecular recognition and chemical sensing applications. We prepared close-packed 2-D polystyrene particle arrays by self-assembly of spreading particle monolayers on mercury surfaces. The 2-D particle arrays amazingly diffract 80% of the incident light. When a 2-D array was transferred onto a hydrogel thin film showing a hydrogel volume change in response to a specific analyte, the array spacing was altered, shifting the 2-D array diffraction wavelength. These 2-D array photonic crystals exhibit ultrahigh diffraction efficiencies that enable them to be used for visual determination of analyte concentrations.
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Técnicas de Química Analítica/instrumentação , Fótons , Hidrogéis , Concentração de Íons de Hidrogênio , Polímeros/química , Propriedades de SuperfícieRESUMO
We examined the deep UV 229 nm photochemistry of NaNO(3) in solution and in the solid state. In aqueous solution excitation within the deep UV NO(3)¯ strong π â π* transition causes the photochemical reaction NO(3)¯ â NO(2)¯ + O·. We used UV resonance Raman spectroscopy to examine the photon dose dependence of the NO(2)¯ band intensities and measure a photochemical quantum yield of 0.04 at pH 6.5. We also examined the response of solid NaNO(3) samples to 229 nm excitation and also observe formation of NO(2)¯. The quantum yield is much smaller at â¼10(-8). The solid state NaNO(3) photochemistry phenomena appear complex by showing a significant dependence on the UV excitation flux and dose. At low flux/dose conditions NO(2)¯ resonance Raman bands appear, accompanied by perturbed NO(3)¯ bands, indicating stress in the NaNO(3) lattice. Higher flux/dose conditions show less lattice perturbation but SEM shows surface eruptions that alleviate the stress induced by the photochemistry. Higher flux/dose measurements cause cratering and destruction of the NaNO(3) surface as the surface layers are converted to NO(2)¯. Modest laser excitation UV beams excavate surface layers in the solid NaNO(3) samples. At the lowest incident fluxes a pressure buildup competes with effusion to reach a steady state giving rise to perturbed NO(3)¯ bands. Increased fluxes result in pressures that cause the sample to erupt, relieving the pressure.