Mycobacterium marinum hand infection: a case report and literature review.

Mycobacterium marinum, a photochromogenic, slow-growing mycobacterium, thrives in both marine and freshwater environments. Optimal growth occurs between 25°C and 35°C, with survival becoming challenging above 37°C. Typically, M. marinum enters the body via skin abrasions, often leading to infections of the upper extremities. Diagnosis of M. marinum infection is frequently challenging and delayed due to the difficult pathogen identification. At present, a standardized treatment protocol has yet to be established. Presented herein is a case study detailing an infection of the right hand's middle finger caused by M. marinum. Notably, his occupation as a chef, handling fish and seafood post-injury, was a significant factor. Histological examination of the skin biopsy and positive acid-fast staining were consistent with a diagnosis of mycobacterial infection. Pathological examination confirmed a skin infection with infectious granuloma, and tissue section acid-fast staining revealed acid-fast bacill. Cultures on Columbia blood agar yielded rough, flattened, yellow-fleshy colonies after 10 days, which was identified as M. marinum through 16S rRNA sequencing. The patient responded well to a 3-month regimen of oral moxifloxacin (0.4 qd) and linezolid (0.6 qd), resulting in rash resolution and pain relief, with no recurrence observed for 1-year follow-up. This report presents the first documented acid-fast staining images of M. marinum tissue sections and colony morphology photographs, offering an in-depth view of M. marinum's morphological characteristics. It aims to enhance awareness of M. marinum infections, underscore the necessity for clinicians to delve into patient histories, and provide a review of the clinical manifestations, diagnostic techniques, therapeutic approaches, and pathogenic mechanisms associated with M. marinum.

Description of Nesterenkonia aerolata sp. nov., an actinobacterium isolated from air of manufacturing shop in a pharmaceutical factory.

During our studies on the microorganism diversity from air of manufacturing shop in a pharmaceutical factory in Shandong province, China, a Gram-stain-positive, aerobic, cocci-shaped bacterium, designated LY-0111T, was isolated from a settling dish. Strain LY-0111T grew at temperature of 10-42 °C (optimum 35 °C), pH of 5.0-10.0 (optimum pH 7.0) and NaCl concentration of 1-12% (optimum 0.5-3%, w/v). Based on the 16S rRNA gene sequence analysis, the strain shared the highest sequence similarities to Nesterenkonia halophila YIM 70179T (96.2%), and was placed within the radiation of Nesterenkonia species in the phylogenetic trees. The genome of the isolate was sequenced, which comprised 2,931,270 bp with G + C content of 66.5%. A supermatrix tree based on the gene set bac120 indicated that LY-0111T was close related to Nesterenkonia xinjiangensis YIM 70097T (16S rRNA gene sequence similarity 95.3%). Chemotaxonomic analysis indicated that the main respiratory quinones were MK-7, MK-8, and MK-9, the predominant cellular fatty acids were anteiso-C15:0 and iso-C15:0, and the major polar lipids consisted of diphosphatidylglycerol, phosphatidylglycerol and phosphatidylinositol. According to the phenotypic, chemotaxonomic and phylogenetic features, strain LY-0111T is considered to represent a novel species, for which the name Nesterenkonia aerolata sp. nov. is proposed. The type strain is LY-0111T (= JCM 36375T = GDMCC 1.3945T). In addition, Nesterenkonia jeotgali was proposed as a later synonym of Nesterenkonia sandarakina, according to the ANI (96.8%) and dDDH (72.9%) analysis between them.

Rare occurrence of pulmonary coinfection involving Aspergillus fumigatus and Nocardia cyriacigeorgica in immunocompetent patients based on NGS: A case report and literature review.

RATIONALE: In our search on PubMed, we found that reports of co-infections involving Aspergillus fumigatus and Nocardia cyriacigeorgica in the literature are notably scarce. Most cases have been documented in patients with compromised immune systems or underlying pulmonary conditions. In contrast, our patient did not present with any of these risk factors. Furthermore, there have been no recent incidents such as near-drowning or other accidents in the patient history. To the best of our knowledge, this case represents a hitherto unreported clinical scenario. To enhance comprehension, we conducted a comprehensive literature review by compiling a total of 20 case reports (spanning from 1984 to 2023) on co-infections involving Aspergillus and Nocardia species, retrieved from PubMed. PATIENT CONCERNS AND DIAGNOSIS: Chest CT revealed the presence of multiple nodules and clustered high-density shadows in both lungs. Bronchoscopy revealed mucosal congestion and edema in the apical segment of the right upper lobe of the lung, along with the presence of 2 spherical polypoid new organisms. The pathological analysis reported severe chronic inflammation with evidence of Aspergillus within the tissue. Next-Generation Sequencing of bronchoalveolar lavage fluid revealed the presence of reads corresponding to A fumigatus and N cyriacigeorgica. Positive cultures for A fumigatus and the Nocardia genus were yielded by prolonging the incubation of samples in the microbiology laboratory. INTERVENTIONS: Treatment with voriconazole for A fumigatus and sulfamethoxazole-trimethoprim for N cyriacigeorgica infection was given. OUTCOMES: The patient improved and was discharged. After 6 months of telephone follow-up, the patient reported no clinical symptoms, discontinued the medication on his own. LESSONS: A fumigatus and N cyriacigeorgica can manifest as a co-infection in immunocompetent patients. Clinicians should prioritize the significant advantages and value of NGS in detecting rare and mixed pathogens associated with pulmonary infections.

Dehydration Accelerates Cytogenesis and Cyst Growth in Pkd1-/- Mice by Regulating Macrophage M2 Polarization.

Adult autosomal dominant polycystic kidney disease (ADPKD) has been shown to be related as a "third hit" to the occurrence of acute or chronic kidney injury. Here, we examined whether dehydration, as a common kidney risk factor, could cause cystogenesis in chronic-onset Pkd1-/- mice by regulating macrophage activation. First, we confirmed that dehydration accelerated cytogenesis in Pkd1-/- mice and that macrophages infiltrated the kidney tissues even earlier than macroscopic cyst formation. Then, microarray analysis suggested that glycolysis pathway may be involved in macrophage activation in Pkd1-/- kidneys under conditions of dehydration. Further, we confirmed glycolysis pathway was activated and lactic acid (L-LA) was overproduced in the Pkd1-/- kidney under conditions of dehydration. We have already proved that L-LA strongly stimulated M2 macrophage polarization and overproduction of polyamine in macrophage in vitro, and in the present study, we further discovered that M2 polarization-induced polyamine production shortened the primary cilia length by disrupting the PC1/PC2 complex. Finally, the activation of L-LA-arginase 1-polyamine pathway contributed to cystogenesis and progressive cyst growth in Pkd1-/- mice recurrently exposed to dehydration.

Macrophages promote heat stress nephropathy in mice via the C3a-C3aR-TNF pathway.

Heat-stress nephropathy (HSN) is associated with recurrent dehydration. However, the mechanisms underlying HSN remain largely unknown. In this study, we evaluated the role of dehydration in HSN and kidney injury in mice. Firstly, we found that complement was strongly activated in the mice that were exposed to dehydration; and among complement components, the interaction between C3a and its receptor, C3aR, was more closely associated with kidney injury. Then two-month-old mice were intraperitoneally injected with 2% dimethyl sulfoxide (DMSO) or the C3aR inhibitor SB290157 during dehydration. DMSO-treated mice exhibited excessive macrophage infiltration, renal cell apoptosis, and kidney fibrosis. In contrast, SB290157-treated mice had no apparent kidney injury. By fluorescence-activated cell sorting (FACS), we found that SB290157 treatment in mice remarkably inhibited macrophage infiltration and suppressed CCR2 expression in macrophages. In addition, C3a binding to C3aR promoted macrophage polarization toward the M1 phenotype and increased the production of TNF-α, which induced renal tubular epithelial cell (RTEC) apoptosis in vivo and in vitro. Interestingly, C3a treatment failed to directly induce TNF-α production and apoptosis in RTECs. However, TNF-α production in response to C3a treatment was significantly elevated when RTECs were cocultured with macrophages, suggesting that macrophages rather than RTECs are the target of C3a-C3aR interaction. At last, we proved that infusion of macrophages which highly expressed TNF-α would significantly deteriorate HSN in TNF-KO mice when they were exposed to recurrent dehydration. This study uncovers a novel mechanism underlying the pathogenesis of HSN, and a potential pathway to prevent kidney injury during dehydration.

Quantitative analyses of the correlation between dynamic contrast-enhanced MRI and intravoxel incoherent motion DWI in thyroid nodules.

This study investigated the correlation between dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and intravoxel incoherent motion diffusion-weighted imaging (IVIM DWI) to differentiate thyroid nodules. Quantitative DCE-MRI parameters, including the transfer constant (K trans), rate constant (K ep) and volume fraction of the extracellular extravascular space (V e), were calculated. The diffusion coefficient (D), pseudo-diffusion coefficient (D* ), and perfusion fraction (f) were derived from biexponential fitting of IVIM DWI. A total of 38 nodules, including 22 malignant and 16 benign nodules, were analyzed. The K trans, K ep and V e for benign lesions were 1.32 ± 0.76 min-1, 6.44 ± 1.44 min-1, and 2.02 ± 0.89 min-1, respectively, and for malignant lesions, the values were 0.84 ± 0.30 min-1, 5.43 ± 1.38 min-1, and 1.71 ± 0.83 min-1, respectively (P = 0.027, 0.036, and 0.257, respectively). The D, f, and D* for benign lesions were 1.51 ± 0.52 mm2/s, 26.63 ± 8.75%, and 15.84 ± 8.71 mm2/s, respectively, and for malignant lesions, the values were 0.68 ± 0.17 mm2/s, 31.63 ± 10.72%, and 11.10 ± 4.21 mm2/s, respectively (P [< 0.0001, 0.135, 0.058], respectively). No significant correlations were found between IVIM DWI and DCE-MRI quantitative parameters (all P > 0.05). In benign nodules, a moderate inverse correlation was found between D and K ep (r = -0.54, P = 0.031). IVIM DWI shows no significant correlation with perfusion parameters derived from DCE-MRI; however, IVIM DWI combined with quantitative DCE-MRI may be a useful imaging tool for the assessment of thyroid nodules in clinical studies.

Matrix metalloproteinase-7 in platelet-activated macrophages accounts for cardiac remodeling in uremic mice.

Heart failure is the leading cause of mortality in patients with end-stage renal disease, and progressive cardiac remodeling is the key pathological basis of heart failure. However, the mechanism by which uremia-induced cardiac remodeling occurs is not well understood. Here, we showed that platelets were significantly activated in 5/6 nephrectomy-operated mice, and cardiac remodeling in the uremic mice was significantly improved when platelets were effectively depleted. A cardiac fibrosis-related gene expression profile revealed that Mmp7, encoding matrix metalloproteinase-7 (MMP-7), exhibited the greatest degree of downregulation in the hearts of uremic mice with platelets depleted. Using fluorescence-activated cell sorting, we discovered that MMP-7 was mainly expressed in M1 and M4 cardiac macrophages, although it was also extensively expressed in heart tissues. For the upstream therapeutic target, neutralization of platelet factor 4 (PF4) with monoclonal antibody not only significantly suppressed M4 macrophages in vivo, but also notably prevented collagen destruction in heart tissues. For the downstream therapeutic target, the pharmacological inhibition of MMP-7 with selective inhibitor failed to notably affect the platelet status, but significantly reduced heart collagen destruction in mice, a further indication that MMP-7 is a crucial downstream molecular target of platelet activation. In vitro, platelets interacted with macrophages and drove them to upregulate MMP-7 expression via free molecules, especially PF4. Taken together, the data suggest that MMP-7 is a key downstream target of platelet activation during uremia. Thus, MMP-7 is a likely and novel therapeutic target for intervention of cardiac remodeling during uremia.

Intravoxel incoherent motion and ADC measurements for differentiating benign from malignant thyroid nodules: utilizing the most repeatable region of interest delineation at 3.0 T.

BACKGROUND: There is a growing need for a reproducible and effective imaging method for the quantitative differentiation of benign from malignant thyroid nodules. This study aimed to investigate the performances of intravoxel incoherent motion (IVIM) parameters and the apparent diffusion coefficient (ADC) in differentiating malignant from benign thyroid nodules derived from the most repeatable region of interest (ROI) delineation. METHODS: Forty-three patients with 46 pathologically confirmed thyroid nodules underwent diffusion-weighted imaging (DWI) with 8 b values. Two observers measured the intravoxel incoherent motion (IVIM) parameters (D, f and D*) and the apparent diffusion coefficient (ADC), ADC600 and ADC990 values using whole-lesion (W-L) ROI and IVIM parameters using single-section (S-S) ROI delineation. The intraclass correlation coefficients (ICCs) and Bland-Altman plots were used to evaluate the intra- and interobserver variability. The diagnostic performance of these parameters was evaluated by generating receiver operating characteristic (ROC) curves. RESULTS: The ICC values of all IVIM with W-L ROI delineation were higher than those with S-S ROI delineation, and excellent intra- and interobserver reproducibility was obtained. According to the Bland-Altman plots, the 95% limits of agreement of the IVIM parameters determined by the W-L ROIs revealed smaller absolute intra- and interobserver variability than those determined by S-S ROIs. The D and ADC600 values obtained from the W-L ROIs were the most powerful parameters in differentiating benign from the malignant nodules [area under the ROC curve = 0.962 and 0.970, P = 0.771]. CONCLUSIONS: The W-L ROI of the thyroid was considered an effective method for obtaining IVIM measurements with excellent reproducibility for differentiating benign from malignant nodules.

The role of the complement factor B-arginase-polyamine molecular axis in uremia-induced cardiac remodeling in mice.

The role of complement system in heart diseases is controversial. Besides, the mechanisms by which complement components participate in cardiac remodeling (CR) and heart failure during uremia are unclear. In this study, 5/6 nephrectomy was performed to adult mice to establish the uremic model and CR deteriorated over the course of uremia. Although complement pathways were not further activated over the course of the disease, soluble complement factor B (CFB) was upregulated at post-nephrectomy day 90 (PNx90) compared with PNx30. Further, CFB notably deteriorated CR in uremic mice but this effect was reversed by depletion of macrophages with liposomal clodronate. In vivo and in vitro CFB upregulated arginase 1 (ARG1) expression, increased ARG1 enzymatic activity, and stimulated the syntheses of ornithine, leading to polyamine overproduction in macrophages. Putrescine, an important polyamine, promoted cardiac fibroblast proliferation and collagen production, resulting in progressive CR. In vivo the inhibition of ARG1 activity with Nω -hydroxyl-l-arginine remarkably improved the general survival rates, inhibited the infiltration of cardiac fibroblasts, and alleviated progression of CR in uremic mice. Taken together, the CFB-ARG1-putrescine axis is related to progression of CR and ARG1 hyperactivity in macrophages may provide a novel therapeutic target against the heart injury in uremia.

FGFR1 Induces Acquired Resistance Against Gefitinib By Activating AKT/mTOR Pathway In NSCLC.

OBJECTIVE: As an epidermal growth factor, receptor-tyrosine kinase inhibitor (EGFR-TKI), gefitinib demonstrates a good therapeutic effect in patients with EGFR-mutant non-small-cell lung cancer (NSCLC). However, an overwhelming majority of these patients inevitably develop resistance against gefitinib. Unfortunately, the mechanism underlying this phenomenon is still not fully understood. Here we aim to reveal the mechanism of gefitinib resistance in NSCLC induced by FGFR1. MATERIALS AND METHODS: We used high-throughput sequencing to compare the mRNA expression profiles of PC9 and PC9-GR (gefitinib-resistant) cells. The clinical significance of fibroblast growth factor receptor 1 (FGFR1) in NSCLC was also investigated using immunohistochemistry and Kaplan-Meier survival analysis. Finally, the in vitro molecular mechanisms were analyzed using confocal laser microscopy, Western blotting, transwell assay, colony formation assay, CCK-8 assay, and apoptosis assay. RESULTS: We observed that FGFR1 was highly expressed in NSCLC tissues and was closely associated with poor prognosis. Cytological experiments showed that FGFR1 promoted the proliferation and migration of PC9-GR cells and mediated their resistance to gefitinib. Furthermore, studies aimed at unraveling this mechanism revealed that FGFR1 activated the AKT/mTOR signaling pathway. These findings show that the FGFR1/AKT/mTOR signaling pathway plays a vital role in acquired resistance against gefitinib in NSCLC. CONCLUSION: This work provides new evidence that FGFR1 functions as a key regulator of gefitinib resistance, thereby demonstrating its potential as a novel biomarker and therapeutic target for NSCLC.

A new nanoscale metastable iron phase in carbon steels.

Metastable ω phase is common in body-centred cubic (bcc) metals and alloys, including high-alloying steels. Recent theoretical calculations also suggest that the ω structure may act as an intermediate phase for face-centred cubic (fcc)-to-bcc transformation. Thus far, the role of the ω phase played in fcc-bcc martensitic transformation in carbon steels has not been reported. In previous investigations on martensitic carbon steels, extra electron diffraction spots were frequently observed by transmission electron microscopy (TEM), and these spots were historically ascribed to the diffraction arising from either internal twins or carbides. In this paper, an intensive TEM investigation revealed that the extra spots are in fact attributed to the metastable ω phase in particle-like morphology with an overall size of several or dozens of nanometres. The strict orientation relationships between the ω phase and the ferrite matrix are in good agreement with those of the hexagonal (P6/mmm) ω phase in other bcc metals and alloys. The identification of the ω phase as well as the extra diffraction spots might provide a clue to help understand the physical mechanism of martensitic transformation in steels.

Evaluating renal biopsy-associated hemorrhage complications by the equation and providing an early intervention: a single-center experience.

BACKGROUND: The aim was to evaluate the risk for major hemorrhage complications (MHC) prior to percutaneous renal biopsy and apply a specific procedure in high-risk patients to decrease their incidence. Hemorrhage complications that required blood transfusion or other interventions were diagnosed as MHC. METHODS: One retrospective (Group A, n = 1314) and two prospective cohorts (Group B, n = 249 and Group C, n = 422) were involved in the study. Group A was used to establish a risk equation for MHC, Group B to test its performance, and Group C to evaluate the efficacy of the proposed procedure to reduce MHC incidence. Group C was classified, based on the equation, into high-risk (C1) and low-risk (C2) patients, who received different interventions. The intervention in Group C1 consisted of use of 18-gauge needles, a 12-h rest period post-operation, and reptilase injection; in Group C2, 16-gauge needles were used, with a 6-h rest, and no reptilase injection. Group B was also divided into B1 (high-risk) and B2 (low-risk) using the same cut-off, for further comparison. RESULTS: (1) In Group A, 4.8% of patients experienced MHC and the equation: Logit (PMHC) = 0.022 × mean arterial pressure (mmHg) + 0.216 × bleeding time (min) - 0.011 × eGFR [ml/(min 1.73 m(2))] - 0.894 × kidney length (cm) - 2.100 × renal cortical thickness (cm) + 6.225 (cutoff = -1.664) was established. (2) The area under the receiver operating characteristic curve was 0.848 (95 % CI 0.797-0.890) for Group B. (3) MHC occurred in 4.8 and 2.8% of patients in Group B and C, respectively; Group B1 suffered significantly more frequent gross hematuria, hematoma and MHC than Group C1; however, no significant difference except for large hematoma was found between Groups B2 and C2 for all complications. CONCLUSIONS: The equation is reliable to predict the risk for MHC; the interventions proposed can decrease the incidence of MHC in high-risk patients.

Relationships of urinary VEGF/CR and IL-6/CR with glomerular pathological injury in asymptomatic hematuria patients.

BACKGROUND: Interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) have important functions in injury and repair processes of glomerular intrinsic cells. A study was conducted to analyze the urinary VEGF/creatinine (CR) and IL-6/CR levels in simple hematuria patients after excluding the interference of creatinine. We aimed to investigate the function and relationships of the above indices in the glomerular pathological injury process, and to elaborate the values of urinary VEGF and IL-6 changes in the diagnosis of asymptomatic hematuria or hematuria with proteinuria. MATERIAL/METHODS: A total of 121 renal hematuria patients diagnosed by clinical and laboratory tests were included as research subjects. The midstream fresh morning urine was collected on the day renal biopsy was performed. RESULTS: The IL-6/CR value of the group III was significantly greater than in group I (Z=-2.478, P<0.05), with a statistically significant difference between these 2 groups. The VEGF/CR value of group III was significantly greater than in group II (P<0.01). Compared with group I, the VEGF/CR of group III was significantly greater (Z=-4.65, P<0.01), with a statistically significant difference. CONCLUSIONS: The VEGF/CR and IL-6/CR values in simple hematuria patients were positively correlated with glomerular pathological injury scores. VEGF/CR and IL-6/CR might be used as biological diagnostic indicators in determining the extent of simple hematuria glomerular injury.

Clinicopathologic analysis of isolated hematuria in child/adolescent and adult patients.

To our knowledge, no in-depth clinicopathologic study of isolated hematuria (IH) is currently available. To address this gap, we analyzed the clinicopathologic features of IH as it manifests in child/adolescent and adult patients. The clinical data and pathological types of 543 IH patients who underwent renal pathological examinations from January 2005 to June 2010 were retrospectively analyzed. Clinical manifestations differed among the age groups: children/adolescents exhibited the highest percentage of mesangial proliferative glomerulonephritis (41.78%), whereas adults showed the highest percentage of immunoglobulin A nephropathy (IgAN) (52.39%). In addition, the percentage of IH patients who were classified according to clinical pathology differed from that of patients who were classified according to renal pathological type. Patients with IgAN who were found to have minimal proteinuria had more severe IH. For IH patients, especially those with a small amount of proteinuria, renal biopsy should be performed as early as possible in order to develop a long-term treatment plan and prognosis evaluation.

Clinical values of urinary IL-6 in asymptomatic renal hematuria and renal hematuria with proteins.

Renal hematuria is caused by glomerular disease. Under pathological conditions, the distribution of interleukin-6 (IL-6) in kidney tissue is abnormal and urinary IL-6 levels are increased. Abnormal IL-6 secretion promotes the hyperplasia of mesangial cells and matrix and, thus, affects the permeability of the glomerular filtration membrane. Therefore, the detection of urinary IL-6 levels in patients with renal hematuria is beneficial for disease evaluation. A total of 82 patients with primary renal hematuria were divided into group 1 (UPr/24 h < 150 mg; pure hematuria group), group 2 (150 mg ≤ UPr/24 h ≤ 1,000 mg) and group 3 (UPr/24 h > 1,000 mg). A total of 30 normal individuals were selected as the controls. The urinary IL-6 levels were detected by the enzyme-linked immunosorbent assay (ELISA) method and a renal biopsy was conducted. The urinary IL-6 levels and renal pathological damage scores in groups 1 and 2 were significantly reduced compared with those in group 3, (P<0.001 and 0.01, respectively), with no significant difference between groups 1 and 2 (P>0.05). The correlation coefficient (r) of urinary IL-6 with 24 h urinary protein (UPr/24 h) in groups 1, 2 and 3 was 0.017, 0.045 and 0.747, respectively, and that of urinary IL-6 with renal pathological damage score was 0.627, 0.199 and 0.119, respectively. The UPr/24 h was significantly correlated with IL-6 level (r=0.7320, P<0.000). In group 1, the urinary IL-6 levels were correlated with the degree of renal pathological damage. A positive correlation was observed between urinary IL-6 levels and UPr/24 h.

Cultured cell-derived extracellular matrix scaffolds for tissue engineering.

Cell-derived extracellular matrix (ECM) scaffolds have received considerable interest for tissue engineering applications. In this study, ECM scaffolds derived from mesenchymal stem cell (MSC), chondrocyte, and fibroblast were prepared by culturing cells in a selectively removable poly(lactic-co-glycolic acid) (PLGA) template. These three types of ECM scaffolds were used for in vitro cultures of MSC and fibroblasts to examine their potential as scaffolds for cartilage and skin tissue engineering. The MSC were cultured in MSC- and chondrocyte-derived ECM scaffolds. The ECM scaffolds supported cell adhesion, promoted both cell proliferation and the production of ECM and demonstrated a stronger stimulatory effect on the chondrogenesis of MSC compared with a conventional pellet culture method. Histological and immunohistochemical staining indicated that cartilage-like tissues were regenerated after the MSC were cultured in ECM scaffolds. Fibroblasts were cultured in the fibroblast-derived ECM scaffolds. Fibroblasts proliferated and produced ECM to fill the pores and spaces in the scaffold. After 2 weeks of culture, a uniform multilayered tissue was generated with homogenously distributed fibroblasts. Cell-derived ECM scaffolds have been demonstrated to facilitate tissue regeneration and will be a useful tool for tissue engineering.

Detection of iron-oxide layer on the surface of iron nitride using high-resolution electron microscopy and Fourier filtering.

High-resolution electron microscopy (HREM) was used to detect the surface Fe3O4 iron-oxide layer formed on [011] Fe4N iron nitride due to electron irradiation in the transmission electron microscope. The existence of a surface oxide layer was confirmed by both image processing and through-focus observation. Images of the iron oxide were revealed using the process of fast Fourier transformation (FFT) of experimental HREM images, filtering of the FFT patterns and inverse FFT. By through-focus observation, HREM images of iron oxide were obtained based on the tuning of contrast transfer function. Fourier filtering is effective for examining the beginning of phase transformation, because at this stage the diffraction spots of iron oxide are too weak to be detected. At the time when the iron oxide layer has developed to some extent, through-focus observation is useful to obtain an image of oxide layers.

Ordering in a fluid inert gas confined by flat surfaces.

High-resolution transmission electron microscopy images of room-temperature fluid xenon in small faceted cavities in aluminum reveal the presence of three well-defined layers within the fluid at each facet. Such interfacial layering of simple liquids has been theoretically predicted, but observational evidence has been ambiguous. Molecular dynamics simulations indicate that the density variation induced by the layering will cause xenon, confined to an approximately cubic cavity of volume approximately 8 cubic nanometers, to condense into the body-centered cubic phase, differing from the face-centered cubic phase of both bulk solid xenon and solid xenon confined in somewhat larger (>/=20 cubic nanometer) tetradecahedral cavities in face-centered cubic metals. Layering at the liquid-solid interface plays an important role in determining physical properties as diverse as the rheological behavior of two-dimensionally confined liquids and the dynamics of crystal growth.