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Intracardiac echocardiography (ICE) enables cardiac imaging with a wide field of view, deep imaging depth, and high frame rate during surgery. However, strong sidelobe and grating lobe artifacts created by the ultra-compact transducer degrade its image quality, making diagnosis and monitoring of treatment difficult. Conventionally, aperture apodization algorithms are often used to suppress sidelobe and grating lobe artifacts at the expense of lateral resolution, which is undesirable in ICE. In this study, we present comparative results of the beamforming methods specifically in ICE application. We demonstrate and compare five nonlinear beamforming algorithms in ICE: nonlinear pthroot delay and sum (NL-p-DAS), nonlinear pthroot spectral magnitude scaling (NL-p-SMS), delay-and-sum with coherence factors (DAS + SCF), delay and sum with apodization (DAS + apodization) and delay and sum (DAS). Phantom and ex-vivoexperiment compare the performance of each algorithm in static and dynamic conditions. DAS + SCF shows the best lateral resolution, and all four algorithms improve the image contrast and sidelobe suppression over conventional DAS. NL-p-SMS stands out for the best axial resolution and suppression of grating lobe artifacts. For motion tracking, NL-p-SMS shows better temporal resolution than other methods. Overall, all the beamforming algorithms other than DAS showed improved image quality. Among them, NL-p-SMS, which has a high temporal resolution, showed the potential for providing more accurate information regards movement tracking.

We present the clinicopathological and molecular genetic characteristics of a neuroepithelial tumor (NET), EWSR1::PATZ1fusion-positive with a literature review. This fusion has recently been discovered in rare central nervous system tumors and soft tissue sarcomas and was not included in the fifth edition of the WHO classifications. We identified this fusion in 2 NETs. The first case involved a 7-year-old girl and the second case occurred in a 53-year-old man; both presented with headaches and vomiting. The pediatric case initially showed an intermediate grade of the tumor, but upon recurrences, it transformed into a high-grade tumor with 2 relapses in 8.3 years. This case exhibited high mitotic activity (20/10 high-power fields), and a high Ki-67 index (21%). The TERTpromoter (TERTp) mutation was present in both initial and recurrent tumors. In contrast, the adult case was a low-grade tumor with no mitotic activity or recurrence over 13.5 months after subtotal resection and gamma knife surgery. Interestingly, the pediatric case demonstrated a longer survival time compared to conventional glioblastoma. The TERTpmutation, similar to being a molecular signature in adult-type glioblastoma, could also be an indicator of high-grade behavior in PATZ1 fusion NET.

This study examined hope as a mediator between school connectedness and childhood career development. Participants included 456 elementary school students in Grades 4 through 6. The results of structural equation modeling supported the hypothesized mediation model, indicating that school connectedness leads to childhood career development both directly and indirectly via hope. The findings suggest that when children feel connected to school, they are likely to demonstrate a greater level of hope, which in turn leads to enhanced career development. The results of this study highlight the importance of developmental assets in promoting childhood career development and has important implications for counseling practice in school settings.

Mismatch repair-deficient (MMRD) brain tumors are rare among primary brain tumors and can be induced by germline or sporadic mutations. Here, we report 13 MMRD-associated (9 sporadic and 4 Lynch syndrome) primary brain tumors to determine clinicopathological and molecular characteristics and biological behavior. Our 13 MMRD brain tumors included glioblastoma (GBM) IDH-wildtype (n= 9) including 1 gliosarcoma, astrocytoma IDH-mutant WHO grade 4 (n= 2), diffuse midline glioma (DMG) H3K27M-mutant (n= 1), and pleomorphic xanthoastrocytoma (PXA) (n= 1). Next-generation sequencing using a brain tumor-targeted gene panel, microsatellite instability (MSI) testing, Sanger sequencing for germline MMR gene mutation, immunohistochemistry of MMR proteins, and clinicopathological and survival analysis were performed. There were many accompanying mutations, suggesting a high tumor mutational burden (TMB) in 77%, but TMB was absent in one case of GBM, IDH-wildtype, DMG, and PXA, respectively. MSH2, MLH1, MSH6, and PMS2mutations were found in 31%, 31%, 31% and 7% of patients, respectively. MSI-high and MSI-low were found in 50% and 8% of these gliomas, respectively and 34% was MSI-stable. All Lynch syndrome-associated GBMs had MSI-high. In addition, 77% (10/13) had histopathologically multinucleated giant cells. The progression-free survival tended to be poorer than the patients with no MMRD gliomas, but the number and follow-up duration of our patients were insufficient to get statistical significance. In the present study, we found that the most common MMRD primary brain tumor was GBM IDH-wildtype. The genetic profile of MMRD GBM was different from that of conventional GBM. MMRD gliomas with TMB and MSI-H may be sensitive to immunotherapy but resistant to temozolomide. Our findings can help develop better treatment options.

Mismatch repair-deficient (MMRD) brain tumors are rare among primary brain tumors and can be induced by germline or sporadic mutations. Here, we report 13 MMRD-associated (9 sporadic and 4 Lynch syndrome) primary brain tumors to determine clinicopathological and molecular characteristics and biological behavior. Our 13 MMRD brain tumors included glioblastoma (GBM) IDH-wildtype (n= 9) including 1 gliosarcoma, astrocytoma IDH-mutant WHO grade 4 (n= 2), diffuse midline glioma (DMG) H3K27M-mutant (n= 1), and pleomorphic xanthoastrocytoma (PXA) (n= 1). Next-generation sequencing using a brain tumor-targeted gene panel, microsatellite instability (MSI) testing, Sanger sequencing for germline MMR gene mutation, immunohistochemistry of MMR proteins, and clinicopathological and survival analysis were performed. There were many accompanying mutations, suggesting a high tumor mutational burden (TMB) in 77%, but TMB was absent in one case of GBM, IDH-wildtype, DMG, and PXA, respectively. MSH2, MLH1, MSH6, and PMS2mutations were found in 31%, 31%, 31% and 7% of patients, respectively. MSI-high and MSI-low were found in 50% and 8% of these gliomas, respectively and 34% was MSI-stable. All Lynch syndrome-associated GBMs had MSI-high. In addition, 77% (10/13) had histopathologically multinucleated giant cells. The progression-free survival tended to be poorer than the patients with no MMRD gliomas, but the number and follow-up duration of our patients were insufficient to get statistical significance. In the present study, we found that the most common MMRD primary brain tumor was GBM IDH-wildtype. The genetic profile of MMRD GBM was different from that of conventional GBM. MMRD gliomas with TMB and MSI-H may be sensitive to immunotherapy but resistant to temozolomide. Our findings can help develop better treatment options.

The purpose of this content analysis was to examine the use of theory in school-counselor-led interventions. Specifically, we examined intervention characteristics, evaluation design, and use of theory in school-counselor-led intervention studies that were published by the American Counseling Association, the American School Counselor Association (ASCA), and in other school-counseling-related journals from 2003 to 2022. Drawing from 45 published articles, results indicated that few school counseling articles explicitly included ASCA Mindsets & Behaviors (ASCA, 2021) or integrated formal counseling theory to inform student outcomes.

Lung cancer has a high incidence worldwide, and most lung cancer-associated deaths are attributable to cancer metastasis. Although several medicinal properties of Panax ginsengMeyer have been reported, the effect of ginsenosides Rk1 and Rg5 on epithelial-mesenchymal transition (EMT) stimulated by transforming growth factor beta 1 (TGF- β1) and self-renewal in A549 cells is relatively unknown.

This study examined the correlation between burnout, mentoring, and turnover intentions among 106 full‐time junior counseling faculty members at U.S. universities. Using the job demands–resources model, the authors aimed to provide a better understanding of the risk and protective environmental factors (i.e., burnout and mentoring) that affect turnover intentions among junior counseling faculty. Burnout was found to be predictive of high turnover intentions. Findings also supported the moderating role of faculty mentoring in the association between burnout and turnover intentions. Implications for counseling programs and institutions are addressed.

Consumers increasingly have worn-out batteries as electrical and electronic equipment with new technical developments are introduced into the market and quickly replace older models. As a result, large amounts of end-of-life (EOL) or waste batteries are generated. Such batteries may contain a variety of materials that includes valuable resources as well as toxic elements. Thus, the proper recycling and management of batteries is very important from the perspective of resource conservation and environmental effect. The collection and recycling of EOL batteries is relatively low in South Korea compared to other countries, although an extended producer responsibility (EPR) policy was adopted for battery recycling in 2003. In this study, the management and material flow of EOL batteries is presented to determine potential problems and quantitative flow, based on literature review, site visits to battery recycling facilities, and interviews with experts in the Korea Battery Recycling Association (KBRA), manufacturers, and regulators in government. The results show that approximately 558 tons of manganese-alkaline batteries, the largest fraction among recycling target items, was disposed in landfills or incinerators in 2015, while approximately 2,000 tons of batteries were recovered at a recycling facility by simple sorting and crushing processes. By raising environmental awareness, more diverse and effective collection systems could be established for consumers to easily dispose of EOL batteries in many places. Producers, retailers and distributors in South Korea should also play an important role in the collection of EOL batteries from consumers. Lithium-ion batteries from many electronic devices must be included in the EPR system for resource recovery.

Central neurocytoma (CN) is a low-grade neuronal tumor that mainly arises from the lateral ventricle (LV). This tumor remains poorly understood in the sense that no driver gene aberrations have been identified thus far. We investigated immunomarkers in fetal and adult brains and 45 supratentorial periventricular tumors to characterize the biomarkers, cell of origin, and tumorigenesis of CN. All CNs occurred in the LV. A minority involved the third ventricle, but none involved the fourth ventricle. As expected, next-generation sequencing performed using a brain-tumor-targeted gene panel in 7 CNs and whole exome sequencing in 5 CNs showed no driver mutations. Immunohistochemically, CNs were robustly positive for FGFR3 (100%), SSTR2 (92%), TTF-1 (Nkx2.1) (88%), GLUT-1 (84%), and L1CAM (76%), in addition to the well-known markers of CN, synaptophysin (100%) and NeuN (96%). TTF-1 was also positive in subependymal giant cell astrocytomas (100%, 5/5) and the pituicyte tumor family, including pituicytoma and spindle cell oncocytoma (100%, 5/5). Interestingly, 1 case of LV subependymoma (20%, 1/5) was positive for TTF-1, but all LV ependymomas were negative (0/5 positive). Because TTF-1-positive cells were detected in the medial ganglionic eminence around the foramen of Monro of the fetal brain and in the subventricular zone of the LV of the adult brain, CN may arise from subventricular TTF-1–positive cells undergoing neuronal differentiation. H3K27me3 loss was observed in all CNs and one case (20%) of LV subependymoma, suggesting that chromatin remodeling complexes or epigenetic alterations may be involved in the tumorigenesis of all CNs and some ST-subependymomas. Further studies are required to determine the exact tumorigenic mechanism of CN.

Ag+(AgNO3) and As3+(As2O3) exposures resulted in dose-dependent decreases in the growth rate of Lemna paucicostatawith IC50values of 0.101±0.004 mg/mL and 0.753±0.127 mg/mL, respectively. Both Ag+and As3+caused dose-dependent increases in lipid peroxidation, a key oxidative damage marker. Additionally, Ag+and As3+caused increases in some components of antioxidant system, namely, ascorbate content and peroxidase activities such as ascorbate peroxidase, glutathione peroxidase, and guaiacol peroxidase. However, notable differences between Ag+and As3+were found in their effects on the glutathione (GSH) system. Ag+caused significant decreases in the GSH content and activities of glutamate cysteine ligase (GCL) and glutathione reductase (GR), the enzymes involved in the GSH synthesis and redox recycling, respectively. In contrast, As3+caused increases in the GSH content and GCL activity. Our results suggest that the Ag+-induced decrease in GSH content accompanied by the decreases in its synthesis and redox recycling is a critical component that further predisposes L. paucicostatato Ag+toxicity.

Cell-penetrating peptides (CPPs) are commonly used as delivery vehicles for the introduction of a variety of macromolecules into cells. Trans-activator of transcription (TAT) is the most commonly used CPP and, as a delivery vehicle, is assumed to be biologically inert. In this study, we pretreated human lung epithelial cells with TAT prior to stimulation with phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator. Surprisingly, TAT alone inhibited the production of multiple cytokines induced by PKC activation. Furthermore, PKC activation-induced IκBα degradation was partially reduced by TAT. Moreover, TAT treatment alone induced apoptosis in a dose-dependent manner, influenced expression of several B cell lymphoma 2 (Bcl-2) family members and increased caspase 3 cleavage at a high dose. These findings suggest that TAT as a delivery vehicle should be used cautiously, as it may affect the inflammatory response, as well as signals related to apoptosis.

Phenol exposure caused a significant reduction in the growth rate of Lemna paucicostatawith an IC50of 234.5±5.8 mg/L. Additionally, phenol caused a dose-dependent increase in the formation of reactive oxygen species (ROS). However, lipid peroxidation was not significantly affected, implying that the membrane lipids are protected by antioxidants under phenol-induced oxidative stress. The ascorbate content decreased in a phenol dose-dependent manner in accordance with the increase in ROS formation, and ascorbate peroxidase activity increased at a low phenol concentration. In contrast, phenol caused remarkable increases in both the total glutathione content and the activities of enzymes involved in glutathione redox- cycling, i.e., glutathione peroxidase and glutathione reductase. Catalase and guaiacol peroxidase activities were also increased, while superoxide dismutase activity decreased. Our results suggest that the phenol-induced increases in glutathione, glutathione redox-cycling enzymes, and H2O2-scavenging enzymes are important components of the adaptive response to phenol exposure. Thus, these increases can be used as indicators of the oxidative stress caused by phenol.

ABSTRACTEnterohemorrhagic Escherichia coliserotype O157:H7 causes outbreaks of diarrhea, hemorrhagic colitis, and the hemolytic-uremic syndrome. E. coliO157:H7 intimately attaches to epithelial cells, effaces microvilli, and recruits F-actin into pedestals to form attaching and effacing lesions. Lipid rafts serve as signal transduction platforms that mediate microbe-host interactions. The aims of this study were to determine if protein kinase C (PKC) is recruited to lipid rafts in response to E. coliO157:H7 infection and what role it plays in attaching and effacing lesion formation. HEp-2 and intestine 407 tissue culture epithelial cells were challenged with E. coliO157:H7, and cell protein extracts were then separated by buoyant density ultracentrifugation to isolate lipid rafts. Immunoblotting for PKC was performed, and localization in lipid rafts was confirmed with an anti-caveolin-1 antibody. Isoform-specific PKC small interfering RNA (siRNA) was used to determine the role of PKC in E. coliO157:H7-induced attaching and effacing lesions. In contrast to uninfected cells, PKC was recruited to lipid rafts in response to E. coliO157:H7. Metabolically active bacteria and cells with intact lipid rafts were necessary for the recruitment of PKC. PKC recruitment was independent of the intimin gene, type III secretion system, and the production of Shiga toxins. Inhibition studies, using myristoylated PKC? pseudosubstrate, revealed that atypical PKC isoforms were activated in response to the pathogen. Pretreating cells with isoform-specific PKC siRNA showed that PKC? plays a role in E. coliO157:H7-induced attaching and effacing lesions. We concluded that lipid rafts mediate atypical PKC signal transduction responses to E. coliO157:H7. These findings contribute further to the understanding of the complex array of microbe-eukaryotic cell interactions that occur in response to infection.

Abstract: The new concept micro devices consisting of various biomolecules have been developed in clinical, pharmaceutical, and environmental fields. Particularly, various diagnostics using biomolecule related device have been investigated and commercialized to detect specific molecules in complex matrix. In recent days, biomolecules have been employed to electronic device to generate new alternatives of silicon based nano electronics by applying natural behaviors of biomolecules. We reviewed here the bioelectronic device consisting of proteins developed by mimicking natural phenomena. We surveyed the working principle, fabrication technologies, and memory function validation of metalloprotein based biomemory device.

High levels of factor XI have been implicated as a risk factor for deep venous thrombosis and possibly cardiovascular disease; however, the relationship between elevated factor XI activity and stroke has yet to be established. We retrospectively evaluated factor XI activity, factor XI antigen, and high-sensitivity C-reactive protein (hs-CRP) values in samples from 65 patients with stroke, 13 with transient ischemic attack (TIA), and 17 with venous thrombosis, younger than 55 years with normal prothrombin and partial thromboplastin times who underwent evaluation for a hypercoagulable state. Factor XI activity levels were more than normal in 22% of patients with stroke or TIA and 18% of patients with venous thrombosis, producing odds ratios of 5.3 and 4.1 for stroke or TIA and venous thrombosis, respectively. Factor XI activity levels correlate with factor XI antigen levels by Deming regression analysis (slope, 1.3; R = 0.667) and a lack of correlation of both with hs-CRP suggests that factor XI is not an acute phase reactant. Our findings suggest an association between elevated factor XI activity and stroke.

Human adenovirus-based vectors have emerged as a new promising vehicle for in vivo gene transfer-mediated therapy. However, the full potential of this methodology has not been fully realized because of the nonspecific tissue distribution of adenoviral vectors. Adenovirus infection is initiated by forming a complex between the fiber protein and a ubiquitously expressed host cell membrane protein, coxsackie B virus and adenovirus receptor (CAR). Therefore, ablating the adenovirus vector's ability to bind to the CAR is the first step in redirecting adenoviral tropism. To ablate CAR binding, we mutated the Bβ sheet of the fiber knob, generating CAR-binding ablated replication-incompetent (dl-K420A-Z) and replication-competent (YKLK420A) adenoviral vectors. The in vitro transduction efficiency of dl-K420A-Z was significantly reduced in comparison to dl-LacZ carrying the wild-type fiber in CAR-positive cells but not in CAR-negative cells, suggesting that the mutation introduced in the Bβ sheet of the fiber knob could disable the CAR-dependent transduction pathway. The in vivo transduction was also dramatically reduced in the liver and other organs for mice treated with dl-K420A-Z, compared with a cognate control vector, dl-LacZ. Concomitant with this attenuated gene transfer efficiency in vivo was a substantial reduction in the amount of general toxicity observed in the YKL-K420A–treated mice. Diminished toxicity was surmised from quantitative measurement of serum level of enzymes for liver and kidney function, hematologic chemistries, histopathology, and differences in lethality. Significant decrease in serum transaminases (alanine transferase [ALT] and aspartate transferase [AST]) was observed in mice treated with YKL-K420A. In addition, the lethality was lower in the YKLK420A– treated groups compared to the YKL-1–treated groups at all doses examined. Furthermore, the hepatopathologic analysis revealed that YKL-1 induced focal zonal necrosis and hepatocyte degeneration, while YKL-K420A induced mild spotty necrosis. In summary, this decreased vector tropism of CAR-binding ablated adenoviruses in normal tissues may increase the amount of virus available for infecting tumor cells and thus increase the antitumor efficacy with fewer unwanted side effects.

Addressing mental health in urban schools with youth who are often disadvantaged requires an understanding of protective individual and school contextual influences. Using hierarchical multiple regression analyses, we investigated school connectedness (SC) as a moderator between social skills (SS) and emotional/behavioral difficulties (ED/BD) among 319 urban middle school students (Grades 6–8; 65% self-identified as Black). SS levels predicted ED/BD. SC moderated the association between SS and mental health concerns. We address implications for school counseling practice.