Transitional Justice in Taiwan: Changes and Challenges

Taiwan’s experience with transitional justice over the past three decades suggests that dealing with historical injustice is a dynamic and fluid process that is fundamentally shaped and constrained by the balance of power and socio-political reality in a particular transitional society. This Article provides a contextualized legal-political analysis of the evolution of Taiwan’s transitional justice regime, with special attention to its limits and challenges. Since Taiwan’s democratization began, the transitional justice project developed by the former authoritarian Chinese Nationalist Party (Kuomintang, KMT) has been rather disproportionately focused on restorative over retributive mechanisms, with the main emphasis placed on reparations and apology and little consideration of truth recovery and individual accountability. But since the Democratic Progressive Party began to control the government and legislature in 2016, its new transitional justice initiatives have introduced significant changes, including, among others, investigating the KMT’s “illicit party assets” and removing authoritarian symbols such as Chiang Kai-shek’s statues, eliciting various contentions and contestations along the way. In our view, Taiwan is now confronted with profound challenges in developing a holistic, thoughtful transitional justice regime: fierce partisan politics that could interrupt progress at any time, conflation of transitional justice and identity politics, pending legal complications and a general distrust of the judiciary, and limited public engagement in transitional justice issues. Whether Taiwan can continue to thrive depends on how it grapples with these challenges in pursuit of justice and reconciliation that will strengthen and sustain tomorrow’s democratic Taiwan

The Effectiveness of Traditional Chinese Medicine in Treating Patients with Leukemia

Leukemia is the most common malignancy among all childhood cancers and is associated with a low survival rate in adult patients. Since 1995, the National Health Insurance (NHI) program in Taiwan has been offering insurance coverage for Traditional Chinese Medicine (TCM), along with conventional Western medicine (WM). This study analyzes the status of TCM utilization in Taiwan, in both pediatric and adult patients with leukemia. A retrospective cohort study was conducted using population-based National Health Insurance Research Database of Registry of Catastrophic Illness, involving patient data from 2001 to 2010 and follow-up data through 2011. The effectiveness of TCM use was evaluated. Relevant sociodemographic data showed that both pediatric and adult patients who were TCM users one year prior to leukemia diagnosis were more likely to utilize TCM services for cancer therapy. A greater part of medical expenditure of TCM users was lower than that of TCM nonusers, except little discrepancy in drug fee of adult patients. The survival rate is also higher in TCM users. Altogether, these data show that TCM has the potential to serve as an adjuvant therapy when combined with conventional WM in the treatment of patients with leukemia

Training strategy for a lightweight countermeasure model for automatic speaker verification

The countermeasure (CM) model is developed to protect Automatic Speaker Verification (ASV) systems from spoof attacks and prevent resulting personal information leakage. Based on practicality and security considerations, the CM model is usually deployed on edge devices, which have more limited computing resources and storage space than cloud-based systems. This work proposes training strategies for a lightweight CM model for ASV, using generalized end-to-end (GE2E) pre-training and adversarial fine-tuning to improve performance, and applying knowledge distillation (KD) to reduce the size of the CM model. In the evaluation phase of the ASVspoof 2021 Logical Access task, the lightweight ResNetSE model reaches min t-DCF 0.2695 and EER 3.54%. Compared to the teacher model, the lightweight student model only uses 22.5% of parameters and 21.1% of multiply and accumulate operands of the teacher model.Comment: ASVspoof202

The polarity protein VANG-1 antagonizes Wnt signaling by facilitating Frizzled endocytosis

Signaling that instructs the migration of neurons needs to be tightly regulated to ensure precise positioning of neurons and subsequent wiring of the neuronal circuits. Wnt-Frizzled signaling controls neuronal migration in metazoans, in addition to many other aspects of neural development. We show that Caenorhabditis elegans VANG-1, a membrane protein that acts in the planar cell polarity (PCP) pathway, antagonizes Wnt signaling by facilitating endocytosis of the Frizzled receptors. Mutations of vang-1 suppress migration defects of multiple classes of neurons in the Frizzled mutants, and overexpression of vang-1 causes neuronal migration defects similar to those of the Frizzled mutants. Our genetic experiments suggest that VANG-1 facilitates Frizzled endocytosis through β-arrestin2. Co-immunoprecipitation experiments indicate that Frizzled proteins and VANG-1 form a complex, and this physical interaction requires the Frizzled cysteine-rich domain. Our work reveals a novel mechanism mediated by the PCP protein VANG-1 that downregulates Wnt signaling through Frizzled endocytosis

The crystal structure of the DNase domain of colicin E7 in complex with its inhibitor Im7 protein

AbstractBackground: Colicin E7 (ColE7) is one of the bacterial toxins classified as a DNase-type E-group colicin. The cytotoxic activity of a colicin in a colicin-producing cell can be counteracted by binding of the colicin to a highly specific immunity protein. This biological event is a good model system for the investigation of protein recognition.Results: The crystal structure of a one-to-one complex between the DNase domain of colicin E7 and its cognate immunity protein Im7 has been determined at 2.3 Å resolution. Im7 in the complex is a varied four-helix bundle that is identical to the structure previously determined for uncomplexed Im7. The structure of the DNase domain of ColE7 displays a novel α/β fold and contains a Zn2+ ion bound to three histidine residues and one water molecule in a distorted tetrahedron geometry. Im7 has a V-shaped structure, extending two arms to clamp the DNase domain of ColE7. One arm (α1∗–loop12–α2∗; where ∗ represents helices in Im7) is located in the region that displays the greatest sequence variation among members of the immunity proteins in the same subfamily. This arm mainly uses acidic sidechains to interact with the basic sidechains in the DNase domain of ColE7. The other arm (loop 23–α3∗–loop 34) is more conserved and it interacts not only with the sidechain but also with the mainchain atoms of the DNase domain of ColE7.Conclusions: The protein interfaces between the DNase domain of ColE7 and Im7 are charge-complementary and charge interactions contribute significantly to the tight and specific binding between the two proteins. The more variable arm in Im7 dominates the binding specificity of the immunity protein to its cognate colicin. Biological and structural data suggest that the DNase active site for ColE7 is probably near the metal-binding site

BET Bromodomain Inhibition Triggers Apoptosis of NF1-Associated Malignant Peripheral Nerve Sheath Tumors through Bim Induction

SummaryMalignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive sarcomas that develop sporadically or in neurofibromatosis type 1 (NF1) patients. There is no effective treatment for MPNSTs and they are typically fatal. To gain insights into MPNST pathogenesis, we utilized an MPNST mouse model that allowed us to study the evolution of these tumors at the transcriptome level. Strikingly, in MPNSTs we found upregulation of a chromatin regulator, Brd4, and show that BRD4 inhibition profoundly suppresses both growth and tumorigenesis. Our findings reveal roles for BET bromodomains in MPNST development and report a mechanism by which bromodomain inhibition induces apoptosis through induction of proapoptotic Bim, which may represent a paradigm shift in therapy for MPNST patients. Moreover, these findings indicate epigenetic mechanisms underlying the balance of anti- and proapoptotic molecules and that bromodomain inhibition can shift this balance in favor of cancer cell apoptosis