Application of Self-Attention Generative Adversarial Network for Electromagnetic Imaging in Half-Space.

In this paper, we introduce a novel artificial intelligence technique with an attention mechanism for half-space electromagnetic imaging. A dielectric object in half-space is illuminated by TM (transverse magnetic) waves. Since measurements can only be made in the upper space, the measurement angle will be limited. As a result, we apply a back-propagation scheme (BPS) to generate an initial guessed image from the measured scattered fields for scatterer buried in the lower half-space. This process can effectively reduce the high nonlinearity of the inverse scattering problem. We further input the guessed images into the generative adversarial network (GAN) and the self-attention generative adversarial network (SAGAN), respectively, to compare the reconstruction performance. Numerical results prove that both SAGAN and GAN can reconstruct dielectric objects and the MNIST dataset under same measurement conditions. Our analysis also reveals that SAGAN is able to reconstruct electromagnetic images more accurately and efficiently than GAN.

Quantification of the Safe Zone of the First to Third Sacral Segments for Transiliac-Transsacral Screw Fixation in Normal and Dysmorphic Sacra.

Transiliac-transsacral screw fixation is widely used to stabilize unstable posterior pelvic ring injuries. Preoperative radiographic assessment of the safe osseous corridor is necessary because the safe space of sacrum is narrower for transiliac-transsacral screw placement than for traditional iliosacral screw placement. However, the radiographic assessment has rarely been studied in the Taiwanese population. We retrospectively analyzed 100 patients with pelvic computed tomography images and divided them into normal and dysmorphic pelvis groups. To determine the safe osseous space, we recorded cross-section area, cross-sectional diameter of the safe zone (CS-szD), and safe zone width on axial view (Ax-szW) in the S1 to S3 segments. The prevalence of dysmorphic pelvis was 48% among all patients. In the S1 segment, no differences were found in the cross-section area and CS-szD been the two groups. However, the Ax-szW was significantly smaller in the dysmorphic pelvis group. In the S2 segment, the cross-section area, CS-szD, and Ax-szW were all significantly larger in the dysmorphic pelvis group. In the S3 segment, the cross-section area and CS-szD of the normal pelvis group were both significantly smaller. No differences were found in the Ax-szW between the two groups. Based on our findings in a Taiwanese population, S1 was the most suitable segment for transiliac-transsacral screw fixation in a normal pelvis, whereas S2, followed by S3, was most suitable in a dysmorphic pelvis. This study offers surgeons information on identifying the optimal sacral segment for transiliac-transsacral screw placement for each pelvic morphology. [Orthopedics. 2024;47(1):e13-e18.].

Microwave Imaging of Anisotropic Objects by Artificial Intelligence Technology.

In this paper, we present the microwave imaging of anisotropic objects by artificial intelligence technology. Since the biaxial anisotropic scatterers have different dielectric constant components in different transverse directions, the problems faced by transverse electronic (TE) polarization waves are more complex than those of transverse magnetic (TM) polarization waves. In other words, measured scattered field information can scarcely reconstruct microwave images due to the high nonlinearity characteristic of TE polarization. Therefore, we first use the dominant current scheme (DCS) and the back-propagation scheme (BPS) to compute the initial guess image. We then apply a trained convolution neural network (CNN) to regenerate the microwave image. Numerical results show that the CNN possesses a good generalization ability under limited training data, which could be favorable to deploy in image processing. Finally, we compare DCS and BPS reconstruction images for anisotropic objects by the CNN and prove that DCS is better than BPS. In brief, successfully reconstructing biaxial anisotropic objects with a CNN is the contribution of this proposal.

Rupture of finger distal interphalangeal collateral ligament treated with a mini soft anchor.

BACKGROUND: Ruptured finger distal interphalangeal (DIP) collateral ligament is a rare injury, with controversial treatment until the present. Our case series aimed to demonstrate feasible surgical intervention using a mini anchor. METHODS: The present study includes four patients with ruptured finger DIP collateral ligaments who received primary repair in a single institute. They have suffered from joint instability due to ligament loss caused by infection, motorcycle accidents, and work-related accidents. All patients were operated on similarly using a 1.0 mm mini anchor for ligament reattachment. RESULTS: The finger DIP joint range of motion (ROM) was documented in all patients during follow-up. Joint ROM recovered to almost normal degrees, and the pinch strength recovered to > 90% compared to the contralateral side in all patients. Additionally, collateral ligament re-rupture, DIP joint subluxation or re-dislocation, and infection were not noted during follow-up. CONCLUSIONS: Ruptured finger DIP joint ligament requiring surgery is usually based on a combination with other soft tissue injuries and defects. However, repair with a 1.0 mm mini anchor is a feasible surgical intervention to reattach the ligament with minimal complication.

Epidemiological profiles and pathogenicity of Vancomycin-resistant Enterococcus faecium clinical isolates in Taiwan.

The emerging Vancomycin-resistant Enterococcus faecium (VRE-fm) is an opportunistic pathogen causing nosocomial infections. The identification of VRE-fm is important for successful prevention and control in healthcare settings. VRE-fm clinical isolates obtained from regional hospitals in northern Taiwan were characterized for antimicrobial susceptibility, virulence genes and biofilm production. Most isolates exhibited multi-drug resistance and carried the virulence genes, esp and hyl. While all isolates produce biofilms, those isolates that carried esp exhibited greater biofilm production. Isolates with different virulence gene carriages were examined for pathogenicity by using a nematode model, Caenorhabditis elegans, for determining microbial-host interactions. The survival assay showed that C. elegans was susceptible to Linezolid-resistant VRE-fm isolates with hyl. Combining the molecular epidemiological profiles regarding pathogenesis in C. elegans can serve as a guide for physicians in limiting opportunistic infections caused by VRE-fm.

Impaired immune response and barrier function in GSPD-1-deficient C. elegans infected with Klebsiella pneumoniae.

gspd-1-RNAi knockdown Caenorhabditis elegans was used as an immune-compromised model to investigate the role of G6PD in host-pathogen interactions. A shorted lifespan, increased bacterial burden and bacterial translocation were observed in gspd-1-knockdown C. elegans infected with Klebsiella pneumoniae (KP). RNAseq revealed that the innate immune pathway, including clc-1 and tsp-1, was affected by gspd-1 knockdown. qPCR confirmed that tight junction (zoo-1, clc-1) and immune-associated genes (tsp-1) were down-regulated in gspd-1-knockdown C. elegans and following infection with KP. The down-regulation of antimicrobial effector lysozymes, including lys-1, lys-2, lys-7, lys-8, ilys-2 and ilys-3, was found in gspd-1-knockdown C. elegans infected with KP. Deletion of clc-1, tsp-1, lys-7, and daf-2 in gspd-1-knockdown C. elegans infected with KP abolished the shorten lifespan seen in the Mock control. GSPD-1 deficiency in C. elegans resulted in bacterial accumulation and lethality, possibly due to a defective immune response. These findings indicate that GSPD-1 has a protective role in microbial defense in C. elegans by preventing bacterial colonization through bacterial clearance.

Glucose-6-Phosphate Dehydrogenase, Redox Homeostasis and Embryogenesis.

Normal embryogenesis requires complex regulation and precision, which depends on multiple mechanistic details. Defective embryogenesis can occur by various mechanisms. Maintaining redox homeostasis is of importance during embryogenesis. NADPH, as produced from the action of glucose-6-phosphate dehydrogenase (G6PD), has an important role in redox homeostasis, serving as a cofactor for glutathione reductase in the recycling of glutathione from oxidized glutathione and for NADPH oxidases and nitric oxide synthases in the generation of reactive oxygen (ROS) and nitrogen species (RNS). Oxidative stress differentially influences cell fate and embryogenesis. While low levels of stress (eustress) by ROS and RNS promote cell growth and differentiation, supra-physiological concentrations of ROS and RNS can lead to cell demise and embryonic lethality. G6PD-deficient cells and organisms have been used as models in embryogenesis for determining the role of redox signaling in regulating cell proliferation, differentiation and migration. Embryogenesis is also modulated by anti-oxidant enzymes, transcription factors, microRNAs, growth factors and signaling pathways, which are dependent on redox regulation. Crosstalk among transcription factors, microRNAs and redox signaling is essential for embryogenesis.

Nucleolar control by a non-apoptotic p53-caspases-deubiquitinylase axis promotes resistance to bacterial infection.

The nucleolus is best known for its cellular role in regulating ribosome production and growth. More recently, an unanticipated role for the nucleolus in innate immunity has recently emerged whereby downregulation of fibrillarin and nucleolar contraction confers pathogen resistance across taxa. The mechanism of this downregulation, however, remains obscure. Here we report that rather than fibrillarin itself being the proximal factor in this pathway, the key player is a fibrillarin-stabilizing deubiquitinylase USP-33. This was discovered by a candidate-gene search of Caenorhabditis elegans in which CED-3 caspase was revealed to execute targeted cleavage of USP-33, thus destabilizing fibrillarin. We also showed that cep-1 and ced-3 mutant worms altered nucleolar size and decreased antimicrobial peptide gene, spp-1, expression rendering susceptibility to bacterial infection. These phenotypes were reversed by usp-33 knockdown, thus linking the CEP-1-CED-3-USP-33 pathway with nucleolar control and resistance to bacterial infection in worms. Parallel experiments with the human analogs of caspases and USP36 revealed similar roles in coordinating these two processes. In summary, our work outlined a conserved cascade that connects cell death signaling to nucleolar control and innate immune response.

Size scaling of nucleolus in Caenorhabditis elegans embryos.

Nucleolus is viewed as a plurifunctional center in the cell, tightly linked to ribosome biosynthesis. As a non-membranous structure, how the size of nucleolus is determined is a long outstanding question, and the possibility of "direct size scaling to the nucleus" was raised by genetic studies in fission yeast. Here, we used the model organism Caenorhabditis elegans to test this hypothesis in multi-cellular organisms. We depleted ani-2, ima-3, or C27D9.1 by RNAi feeding, which altered embryo sizes to different extents in ncl-1 mutant worms. DIC imaging provided evidence that in size-altering embryo nucleolar size decreases in small cells and increases in large cells. Furthermore, analyses of nucleolar size in four blastomeres (ABa, ABp, EMS, and P2) within the same embryo of ncl-1 mutants consistently demonstrated the correspondence between cell and nucleolar sizes - the small cells (EMS and P2) have smaller nucleoli in comparison to the large cells (ABa).

A Genetic Cascade of let-7-ncl-1-fib-1 Modulates Nucleolar Size and rRNA Pool in Caenorhabditis elegans.

Ribosome biogenesis takes place in the nucleolus, the size of which is often coordinated with cell growth and development. However, how metazoans control nucleolar size remains largely unknown. Caenorhabditis elegans provides a good model to address this question owing to distinct tissue distribution of nucleolar sizes and a mutant, ncl-1, which exhibits larger nucleoli than wild-type worms. Here, through a series of loss-of-function analyses, we report that the nucleolar size is regulated by a circuitry composed of microRNA let-7, translation repressor NCL-1, and a major nucleolar pre-rRNA processing protein FIB-1/fibrillarin. In cooperation with RNA binding proteins PUF and NOS, NCL-1 suppressed the translation of FIB-1/fibrillarin, while let-7 targeted the 3'UTR of ncl-1 and inhibited its expression. Consequently, the abundance of FIB-1 is tightly controlled and correlated with the nucleolar size. Together, our findings highlight a novel genetic cascade by which post-transcriptional regulators interplay in developmental control of nucleolar size and function.