Analysis of Training Deep Learning Models for PCB Defect Detection.

Recently, many companies have introduced automated defect detection methods for defect-free PCB manufacturing. In particular, deep learning-based image understanding methods are very widely used. In this study, we present an analysis of training deep learning models to perform PCB defect detection stably. To this end, we first summarize the characteristics of industrial images, such as PCB images. Then, the factors that can cause changes (contamination and quality degradation) to the image data in the industrial field are analyzed. Subsequently, we organize defect detection methods that can be applied according to the situation and purpose of PCB defect detection. In addition, we review the characteristics of each method in detail. Our experimental results demonstrated the impact of various degradation factors, such as defect detection methods, data quality, and image contamination. Based on our overview of PCB defect detection and experiment results, we present knowledge and guidelines for correct PCB defect detection.

Precise control of mitophagy through ubiquitin proteasome system and deubiquitin proteases and their dysfunction in Parkinson's disease.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the elderly population and is caused by the loss of dopaminergic neurons. PD has been predominantly attributed to mitochondrial dysfunction. The structural alteration of α-synuclein triggers toxic oligomer formation in the neurons, which greatly contributes to PD. In this article, we discuss the role of several familial PD-related proteins, such as α-synuclein, DJ-1, LRRK2, PINK1, and parkin in mitophagy, which entails a selective degradation of mitochondria via autophagy. Defective changes in mitochondrial dynamics and their biochemical and functional interaction induce the formation of toxic α-synucleincontaining protein aggregates in PD. In addition, these gene products play an essential role in ubiquitin proteasome system (UPS)-mediated proteolysis as well as mitophagy. Interestingly, a few deubiquitinating enzymes (DUBs) additionally modulate these two pathways negatively or positively. Based on these findings, we summarize the close relationship between several DUBs and the precise modulation of mitophagy. For example, the USP8, USP10, and USP15, among many DUBs are reported to specifically regulate the K48- or K63-linked de-ubiquitination reactions of several target proteins associated with the mitophagic process, in turn upregulating the mitophagy and protecting neuronal cells from α-synuclein-derived toxicity. In contrast, USP30 inhibits mitophagy by opposing parkin-mediated ubiquitination of target proteins. Furthermore, the association between these changes and PD pathogenesis will be discussed. Taken together, although the functional roles of several PD-related genes have yet to be fully understood, they are substantially associated with mitochondrial quality control as well as UPS. Therefore, a better understanding of their relationship provides valuable therapeutic clues for appropriate management strategies. [BMB Reports 2021; 54(12): 592-600].

The central regulator p62 between ubiquitin proteasome system and autophagy and its role in the mitophagy and Parkinson's disease.

The ubiquitin-proteasome system (UPS) and autophagy are two major degradative pathways of proteins in eukaryotic cells. As about 30% of newly synthesized proteins are known to be misfolded under normal cell conditions, the precise and timely operation of the UPS and autophagy to remove them as well as their tightly controlled regulation, is so important for proper cell function and survival. In the UPS, target proteins are labeled by small proteins called ubiquitin, which are then transported to the proteasome complex for degradation. Alternatively, many greatly damaged proteins are believed to be delivered to the lysosome for autophagic degradation. Although these autophagy and UPS pathways have not been considered to be directly related, many recent studies proposed their close link and dynamic interconversion. In this review, we'll focus on the several regulatory molecules that function in both UPS and autophagy and their crosstalk. Among the proposed multiple modulators, we will take a closer look at the so-called main connector of UPS-autophagy regulation, p62. Last, the functional role of p62 in the mitophagy and its implication for the pathogenesis of Parkinson's disease, one of the major neurodegenerative diseases, will be briefly reviewed. [BMB Reports 2020; 53(1): 56-63].

Comparison of Oncologic Outcomes and Complications According to Surgical Approach to Radical Prostatectomy: Special Focus on the Perineal Approach.

INTRODUCTION: The objective of the study was to compare oncologic outcomes and complications in patients with prostate cancer who underwent radical perineal prostatectomy (RPP), radical retropubic prostatectomy (RRP), laparoscopic radical prostatectomy (LRP), or robotic-assisted radical prostatectomy (RARP). MATERIALS AND METHODS: We retrospectively reviewed 2617 patients who underwent RPP (n = 673), RRP (n = 396), LRP (n = 223), or RARP (n = 1325) between 1995 and 2013. Clinicopathological outcomes were compared according to surgical approach. Kaplan-Meier and Cox regression analyses were carried out to assess oncologic outcomes. Complications were stratified according to the Clavien classification system. RESULTS: The 5-year biochemical recurrence (BCR)-free survival after RPP was 75.3%, which was higher than for RRP (71.4%; P = .007) and comparable with LRP (76.1%; P = .666) and RARP (75.3%; P = .898). In multivariate analysis, RPP was comparable with LRP (P = .591) and RARP (P = .089) whereas RRP was associated with increased BCR (P < .001). No significant difference was seen in 5-year cancer-specific survival (RPP, 99.0%; RRP, 98.7%; LRP, 100.0%; and RARP, 99.8%; P = .071). The 5-year overall survival after RPP was 97.0%, which was lower than for RARP (99.6%; P = .007), but comparable with RRP (96.2%; P = .792) and LRP (99.1%; P = .606). Overall complication rates were 25.1% for RPP, 36.4% for RRP, 16.1% for LRP, and 9.4% for RARP (P < .001), respectively. After RPP, wound dehiscence (10.3%) was the most common complication. However, approximately 75% of complications were minor. CONCLUSION: RPP showed acceptable oncologic outcomes compared with other surgical approaches. Careful attention is required to prevent wound dehiscence.

Validation of the Korean Version of the Manchester-Oxford Foot Questionnaire in Patients With Hallux Valgus.

The Manchester-Oxford Foot Questionnaire (MOXFQ) is a practical, reliable, and valid questionnaire for hallux valgus surgery and has been translated into several languages. However, the MOXFQ has not been translated into Korean. In the present study, we aimed to translate and evaluate the validity and reliability of the Korean version of the MOXFQ for patients affected by hallux valgus. In accordance with the guidelines of cross-cultural adaptation, we translated the English version of MOXFQ into Korean and then backward translated it into English. We sent out letters that included the Korean version of the MOXFQ, a visual analog scale measure of pain, and a validated Korean version of the short-form 36-item Health Survey to 135 patients with hallux valgus. A retest was administered after 2 weeks. Of the 135 patients, 104 responded to the first questionnaire, and 82 of the first-time responders returned their second questionnaires. We evaluated the test-retest reliability, internal consistency, concurrent validity, and construct validity of the Korean version of the MOXFQ. The intraclass correlation coefficient for test-retest reliability was 0.82 for the total MOXFQ and ranged from 0.81 to 0.82 for the 3 subscales. Cronbach's alpha for the total MOXFQ was 0.85 and ranged from 0.8 to 0.92 for the 3 subscales. Concurrent and construct validity was supported by significant correlation with the visual analog scale and short-form 36-item Health Survey subscale scores. The Korean version of the MOXFQ was tested, and it was found to be a valid and reliable instrument for patients with hallux valgus.

Reliability and Validity of the Korean Version of the Foot Function Index.

Although translated versions of the Foot Function Index (FFI) in several languages are available, the absence of a Korean version has precluded comparing the data from Korea with the data from other countries using the FFI. We, therefore, evaluated the reliability and validity of the adapted Korean version of the FFI. We translated the English version of the FFI into Korean and back into English. We mailed the Korean version of the visual analog scale, FFI, and the previously validated Medical Outcomes Study Short-Form 36-item questionnaire (SF-36) to 121 patients with treated foot complaints. To evaluate the test-retest reliability and internal consistency, we used the intraclass correlation coefficient and Cronbach's α, respectively. We also evaluated the concurrent and construct validity of Korean version of the FFI by comparing the visual analog scale and SF-36. Cronbach's α was 0.91 and 0.95 for the pain and disability subscales, respectively. The reproducibility was good, and a strong correlation between the FFI and the SF-36 and visual analog scale with related content was observed, indicating good construct validity.The Korean version of the FFI is a reliable and valid questionnaire for the self-assessment of pain and disability in Korean patients with foot complaints.

DNA-PK triggers histone ubiquitination and signaling in response to DNA double-strand breaks produced during the repair of transcription-blocking topoisomerase I lesions.

Although defective repair of DNA double-strand breaks (DSBs) leads to neurodegenerative diseases, the processes underlying their production and signaling in non-replicating cells are largely unknown. Stabilized topoisomerase I cleavage complexes (Top1cc) by natural compounds or common DNA alterations are transcription-blocking lesions whose repair depends primarily on Top1 proteolysis and excision by tyrosyl-DNA phosphodiesterase-1 (TDP1). We previously reported that stabilized Top1cc produce transcription-dependent DSBs that activate ATM in neurons. Here, we use camptothecin (CPT)-treated serum-starved quiescent cells to induce transcription-blocking Top1cc and show that those DSBs are generated during Top1cc repair from Top1 peptide-linked DNA single-strand breaks generated after Top1 proteolysis and before excision by TDP1. Following DSB induction, ATM activates DNA-PK whose inhibition suppresses H2AX and H2A ubiquitination and the later assembly of activated ATM into nuclear foci. Inhibition of DNA-PK also reduces Top1 ubiquitination and proteolysis as well as resumption of RNA synthesis suggesting that DSB signaling further enhances Top1cc repair. Finally, we show that co-transcriptional DSBs kill quiescent cells. Together, these new findings reveal that DSB production and signaling by transcription-blocking Top1 lesions impact on non-replicating cell fate and provide insights on the molecular pathogenesis of neurodegenerative diseases such as SCAN1 and AT syndromes, which are caused by TDP1 and ATM deficiency, respectively.

Three-dimensional printing of complex biological structures by freeform reversible embedding of suspended hydrogels.

We demonstrate the additive manufacturing of complex three-dimensional (3D) biological structures using soft protein and polysaccharide hydrogels that are challenging or impossible to create using traditional fabrication approaches. These structures are built by embedding the printed hydrogel within a secondary hydrogel that serves as a temporary, thermoreversible, and biocompatible support. This process, termed freeform reversible embedding of suspended hydrogels, enables 3D printing of hydrated materials with an elastic modulus <500 kPa including alginate, collagen, and fibrin. Computer-aided design models of 3D optical, computed tomography, and magnetic resonance imaging data were 3D printed at a resolution of ~200 µm and at low cost by leveraging open-source hardware and software tools. Proof-of-concept structures based on femurs, branched coronary arteries, trabeculated embryonic hearts, and human brains were mechanically robust and recreated complex 3D internal and external anatomical architectures.

A Case of Osmotic Demyelination Presenting with Severe Hypernatremia.

Osmotic demyelination syndrome is a demyelinating disorder associated with rapid correction of hyponatremia. But, it rarely occurs in acute hypernatremia, and it leads to permanent neurologic symptoms and is associated with high mortality. A 44-year-old woman treated with alternative medicine was admitted with a history of drowsy mental status. Severe hypernatremia (197mEq/L) with hyperosmolality (415mOsm/kgH2O) was evident initially and magnetic resonance imaging revealed a high signal intensity lesion in the pons, consistent with central pontine myelinolysis. She was treated with 0.45% saline and 5% dextrose water and intravenous corticosteroids. Serum sodium normalized and her clinical course gradually improved. Brain lesion of myelinolysis also improved in a follow-up imaging study. This is the first report of a successful treatment of hypernatremia caused by iatrogenic salt intake, and it confirms the importance of adequate fluid supplementation in severe hypernatremia.

Pin1 promotes neuronal death in stroke by stabilizing Notch intracellular domain.

OBJECTIVE: Stroke is a leading cause of mortality and disability. The peptidyl-prolyl cis/trans isomerase Pin1 regulates factors involved in cell growth. Recent evidence has shown that Pin1 plays a major role in apoptosis. However, the role of Pin1 in ischemic stroke remains to be investigated. METHODS: We used Pin1 overexpression and knockdown to manipulate Pin1 expression and explore the effects of Pin1 in cell death on ischemic stress in vitro and in a mouse stroke model. We also used Pin 1 inhibitor, γ-secretase inhibitor, Notch1 intracellular domain (NICD1)-deleted mutant cells, and Pin1 mutant cells to investigate the underlying mechanisms of Pin1-NICD1-mediated cell death. RESULTS: Our findings indicate that Pin1 facilitates NICD1 stability and its proapoptotic function following ischemic stroke. Thus, overexpression of Pin1 increased NICD1 levels and enhanced its potentiation of neuronal death in simulated ischemia. By contrast, depletion or knockout of Pin1 reduced the NICD1 level, which in turn desensitized neurons to ischemic conditions. Pin1 interacted with NICD1 and increased its stability by inhibiting FBW7-induced polyubiquitination. We also demonstrate that Pin1 and NICD1 levels increase following stroke. Pin1 heterozygous (+/-) and knockout (-/-) mice, and also wild-type mice treated with an inhibitor of Pin1, each showed reduced brain damage and improved functional outcomes in a model of focal ischemic stroke. INTERPRETATION: These results suggest that Pin1 contributes to the pathogenesis of ischemic stroke by promoting Notch signaling, and that inhibition of Pin1 is a novel approach for treating ischemic stroke.

Reliability and validity of the Korean version of Obsessive-Compulsive Inventory-Revised in a non-clinical sample.

PURPOSE: The reliability and validity of a Korean version of the Obsessive-Compulsive-Inventory-Revised (OCI-R) was examined in non-clinical student samples. MATERIALS AND METHODS: The Korean version of OCI-R was administered to a total of 228 Korean college students. The Maudsley Obsessive Compulsive Inventory (MOCI), Beck's Depression Inventory (BDI), and Beck's Anxiety Inventory (BAI) were administered to 228 students. RESULTS: The total and each of subscale of the Korean OCI-R demonstrated excellent internal consistency, good test-retest reliability, moderate convergent validity and good divergent validity. CONCLUSION: It was concluded that the Korean version of the OCI-R has strong psychometric properties as the original version.

Identification and characterization of Paragonimus westermani leucine aminopeptidase.

Paragonimus westermani is a tissue-invading trematode parasite that causes inflammatory lung disease as well as systemic infections including cerebral invasion in carnivorous mammals. While aminopeptidases play important roles in trematodes in the catabolism of host hemoglobin, an essential source of nutrient for the parasite, little is known about aminopeptidase in Paragonimus. Presently, we isolated a cDNA encoding a 58 kDa P. westermani leucine aminopeptidase (PwLAP). Deduced amino acid sequence of PwLAP exhibited significant sequence homology with LAP from Schistosoma spp. and Fasciola hepatica. Biochemical analysis of the recombinant PwLAP protein demonstrated preferential substrate specificity for Leu-NHMec and inhibition by EDTA, 1,10-phenanthroline, and bestatin, which are conserved characteristics of the M17 family of leucine aminopeptidase. PwLAP exhibited relatively higher enzyme activity in the presence of Mn2+ compared to Schistosoma mansoni LAP. Based on the biochemical properties and immunohistochemical analysis, PwLAP is concluded to represent a leucine aminopeptidase. The enzyme is most likely responsible for the catabolism of host hemoglobin, and, hence, represents a potential target of Paragonimus chemotherapy.