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<title cf:type="text"><![CDATA[Progress in Biochemistry and Biophysics -->News and Views]]></title>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Identification and Function of Cardiac Nexus Glia]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220132]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[神经胶质细胞在神经系统的发育和分化中扮演着重要角色。近期，研究人员在心脏中发现一种新型神经胶质细胞，命名为连接胶质细胞（Nexus glia）。该细胞具有神经胶质细胞的特性，能够影响心脏内神经细胞的发育，继而调节心脏节律。连接胶质细胞的发现为胶质细胞在外周器官中的功能机制研究提供了重要的物质基础，也为临床维持心脏稳态和控制心脏自主节律提供了潜在的药物靶标。]]></description>
<pubDate>2022/4/22 0:00:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[Song Li-Juan,YANG Rong-Fang and ZHANG Shu-Li]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>Song Li-Juan,YANG Rong-Fang and ZHANG Shu-Li</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220132]]></guid><cfi:id>15</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Two types of new glia were detected in adult V-VSZ]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220142]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate>2022/4/22 0:00:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[JI Juan-Juan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>JI Juan-Juan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220142]]></guid><cfi:id>14</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Efficiency Evaluation of Listed Enterprises in China"s Biological Industry Based on DEA Model]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200199]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> With the rapid development of the bio-industry, more and more biological enterprises, mainly biomedical enterprises, have emerged. How to promote the output efficiency of biological enterprises is the most concern of the government and enterprises themselves.<b>Methods</b> This paper constructs a DEA model to evaluate the input-output efficiency of 370 listed companies in China’s biological industry.<b>Results</b> The research results show that the average comprehensive technical efficiency of listed companies in China"s biological industry is 0.596, and there is still much room for improvement.<b>Conclusion</b> The main factor restricting the overall technical efficiency of listed companies in China’s biological industry is pure technical efficiency. Large-scale listed biological companies should optimize investment and reduce redundancy, while smaller-scale listed biological companies need to expand their scale.]]></description>
<pubDate>2022/2/21 0:00:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[DING Jun-Qi,BAI Jing-Yu and LIN Xiao-Feng]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DING Jun-Qi,BAI Jing-Yu and LIN Xiao-Feng</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20200199]]></guid><cfi:id>13</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Zoonotic Transmission of <i>Orthohepevirus C</i>（Rat Hepatitis E Virus）]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220384]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[]]></description>
<pubDate>2022/12/20 0:00:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[CONG Chao,ZHAO Wan-Qiu,LIU Jian-Kun and HUANG Fen]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CONG Chao,ZHAO Wan-Qiu,LIU Jian-Kun and HUANG Fen</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220384]]></guid><cfi:id>12</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[An Overview of The Functions of The GlyCosmos Portal in Glycosciences Research]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220001]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[As research in various fields of biology has reached new heights in recent years, glycans have gradually attracted the attention of scientists. Many studies have shown that glycans have multiple activities, which has caused more and more relevant researchers to pay attention to the role of sugar in life and how sugar works. Glycobiology has become a hot research area in biology. It is very important to have a good tool for newcomers to glycobiology research or just entering the field. GlyCosmos, as a comprehensive and unified open portal for glycoscience, whose data is freely available to the public, provides access to glycan-related data, including the following: (1) repository; (2) various databases related to glycogen, glyco proteins, cell pathways and diseases and various visualization databases of Glycome; (3) the most advanced and unified multiple standardized polysaccharide representation methods and other functions. Although the website has only been completed in the past two years, due to the convenience, uniformity and standardized model provided by the website, it has provided a standardized database and representation method for many international glycan studies, so the website has been widely used at present. The use is also well known by glycobiologists, so this website is very helpful for newcomers to glycobiology research. This article summarizes the functions in the GlyCosmos portal, hoping to help those who intend to engage in glycobiology to better understand and use the website, which will be helpful and provide reference value for subsequent research.]]></description>
<pubDate>2022/12/20 0:00:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[JI Teng-Qi and ZHANG Ji]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>JI Teng-Qi and ZHANG Ji</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220001]]></guid><cfi:id>11</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Neurological Insights into Attentional Deficits in High Trait Anxiety: a Commentary on Hu <i>et al</i>.’s Paper in <i>Cerebral Cortex</i> (2023)]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20240302]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[In a recent publication, Hu <i>et al</i>. (2023) have reported that individuals with high trait anxiety exhibit attentional deficits characterized by reduced inhibition of distractors and delayed attentional selection of targets, indicating impaired top-down attentional control. This commentary underscores their significant contributions to the cognitive theory of anxiety. Based on their findings, we propose a novel training approach called attentional inhibition training (AIT), aimed at improving top-down attentional control to alleviate symptoms of anxiety. Furthermore, we explore the potential application of non-invasive transcranial magnetic stimulation (TMS) for rapidly enhancing attentional control function.]]></description>
<pubDate>2024/10/30 20:34:41</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[MA Hao-Yun,LIANG Jian-Hui and LIU Dong-Qiang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MA Hao-Yun,LIANG Jian-Hui and LIU Dong-Qiang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20240302]]></guid><cfi:id>10</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Fast Object Perception in The Subcortical Pathway: a Commentary on Wang <i>et al</i>.’s Paper in <i>Human Brain Mapping </i>(2023)]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250077]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The subcortical visual pathway is generally thought to be involved in dangerous information processing, such as fear processing and defensive behavior. A recent study, published in <i>Human Brain Mapping</i>, shows a new function of the subcortical pathway involved in the fast processing of non-emotional object perception. Rapid object processing is a critical function of visual system. Topological perception theory proposes that the initial perception of objects begins with the extraction of topological property (TP). However, the mechanism of rapid TP processing remains unclear. The researchers investigated the subcortical mechanism of TP processing with transcranial magnetic stimulation (TMS). They find that a subcortical magnocellular pathway is responsible for the early processing of TP, and this subcortical processing of TP accelerates object recognition. Based on their findings, we propose a novel training approach called subcortical magnocellular pathway training (SMPT), aimed at improving the efficiency of the subcortical M pathway to restore visual and attentional functions in disorders associated with subcortical pathway dysfunction.]]></description>
<pubDate>2025/5/19 14:18:10</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[MA Hao-Yun,WEI Yu-Yin and HU Li-Ping]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MA Hao-Yun,WEI Yu-Yin and HU Li-Ping</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20250077]]></guid><cfi:id>9</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Structural Basis of Microtubule-regulated “Sequestration and Release” of GEF-H1 in Signal Transduction]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260164]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Microtubules have long been regarded as structural scaffolds that maintain cell shape, mediate intracellular transport, and drive cell division. Over the past two decades, this view has shifted, with accumulating evidence demonstrating that microtubules are dynamic and active participants in cellular signaling networks, regulating key physiological processes such as cell survival and differentiation through multiple mechanisms. Recently, the team led by Michel O. Steinmetz reported in <i>Cell</i> the first structural elucidation of how microtubules regulate immune responses by “sequestering and releasing” the guanine nucleotide exchange factor GEF-H1 protein. This work addresses a central question in microtubule-mediated signal transduction, provides a conceptual and methodological framework for basic research, and offers new targets and strategies for cancer immunotherapy and targeted drug development.]]></description>
<pubDate>2026/5/30 21:52:46</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[REN Jin-Qi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>REN Jin-Qi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260164]]></guid><cfi:id>8</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Improvements and Recent Advances of Metadynamics Enhanced Sampling Method]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260145]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The functional realization of proteins and other biological macromolecules depends on conformational dynamics and allosteric regulation, and elucidating their molecular mechanisms is an important foundation for understanding life processes. Molecular dynamics simulations are a powerful tool for investigating conformational evolution at the atomic level. However, traditional methods are limited by simulation timescales and high free-energy barriers, making it difficult to effectively capture rare conformations and their transition pathways. As a result, the development of enhanced sampling techniques has become key to overcoming this bottleneck. As a classical enhanced sampling technique, metadynamics suffers from several shortcomings, including strong dependence on collective variables and significant errors caused by bias potential accumulation. This article reviews three major improvement strategies. The first combines stochastic resetting with metadynamics, using trajectory-resetting mechanisms to improve sampling efficiency while avoiding the difficulty of optimizing collective variables. The second, SinkMeta, employs a “sinking” bias effect to enable efficient exploration of specific regions and paths. The third, OPES-based hybrid methods, improve the stability of free-energy estimation by optimizing the target distribution or the way the bias is constructed. These methods provide new ideas for characterizing free-energy landscapes and studying conformational transitions in complex biological systems, while also promoting the continued development of enhanced sampling methodologies.]]></description>
<pubDate>2026/5/14 11:42:00</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[TONG Ming-Qiong,YIN Yue-Wen,SHI Zhi-Hong and CAO Zan-Xia]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>TONG Ming-Qiong,YIN Yue-Wen,SHI Zhi-Hong and CAO Zan-Xia</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260145]]></guid><cfi:id>7</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Novel Subset-specific Functions of Dendritic Cells: From Spatiotemporal Regulation of Lymph Node Immunity to Precision Targeting StrategiesA Commentary on The Study by Huang & Gerner (Cell, 2026)]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260177]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Dendritic cells (DCs) serve as a crucial link between innate and adaptive immunity and represent key modulatory nodes in the initiation of adaptive immune responses. Although DC-targeted vaccines and therapeutic strategies show great promise, their development remains in the early stages due to a limited understanding of the regulatory mechanisms governing distinct DC subsets in response to various immunogens and types of immune responses. Recently, a study by Jessica Y. Huang and Michael Y. Gerner published in <i>Cell</i> has uncovered a novel functional dimension of DCs. Beyond their classical roles in antigen presentation and T cell priming, DCs dynamically regulate the spatiotemporal organization of innate and adaptive immune responses within lymph nodes. During early type I immune responses, tissue-resident DC2s recruit innate immune cells and promote their trafficking, effectively limiting pathogen spread; however, this comes at the cost of disrupting lymph node architecture and suppressing the initiation of adaptive immunity. Following effective pathogen restraint, DCs shift their role to mediate the removal of apoptotic neutrophils and facilitate the restoration of lymph node structure, thereby reinstating adaptive immunity. These findings suggest that a deeper understanding of subset-specific regulatory networks of DCs in various immune contexts may enhance the precision and efficacy of DC-targeted immunotherapies.]]></description>
<pubDate>2026/5/25 11:00:44</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[YANG Shao-Jun and ZHANG Xu-Yuan]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>YANG Shao-Jun and ZHANG Xu-Yuan</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260177]]></guid><cfi:id>6</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Low-input Proteomics Reshapes Our Understanding of Regulatory Mechanisms in Early Embryonic Development]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260069]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Early mammalian embryogenesis represents a central question in life sciences, yet its molecular regulation has long been inferred primarily from transcriptomic and translatomic analyses. Recently, a study by Zhu <i>et al.</i> (2025) based on low-input proteomic approaches systematically charted protein dynamics from oocytes to blastocysts in both mice and humans, further interrogating molecular signatures of developmentally compromised human embryos at the single-embryo level. This work not only substantially expands proteome coverage during early development, but also reveals a pervasive uncoupling between transcriptional activation, translational initiation, and protein accumulation. These findings provide new perspectives on the relationship between zygotic genome activation (ZGA) and lineage specification. This paper discussed the central role of low-input proteomics in this study, highlighted its implications for reshaping current paradigms of early embryonic development, and considered its potential applications across broader areas of biomedical research.]]></description>
<pubDate>2026/3/17 15:02:15</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[CHEN Hong-Yu]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Hong-Yu</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260069]]></guid><cfi:id>5</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[His-ADPR: Revealing The Chemical Milestones of Immune Signal Evolution]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260002]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The evolutionary arms race between life and pathogens drives diversification in immune system signaling mechanisms. Recent research has found that the TIR protein of the bacterial type II Thoeris defense system can produce a novel “hybrid” immune signaling molecule—histidine-ADP-ribose (His-ADPR). This molecule, formed by the direct linkage of an amino acid and a nucleotide, challenges the traditional view that TIR enzymes generate only pure nucleotide derivatives. This signal is specifically recognized by the Macro domain of an effector protein, triggering the transmembrane domain to disrupt the membrane for defense. The study further reveals that phages can evade immunity by expressing “signal sponge” proteins that bind and sequester His-ADPR. This offensive-defensive pressure drives TIR enzymes to continuously expand their “chemical arsenal” of signaling molecules. The discovery not only confirms the shared biochemical core of bacterial TIR signaling molecules (based on NAD<sup>+</sup> modification), but also highlights their remarkable chemical plasticity and evolutionary innovative capacity. It provides a new perspective for understanding the origin and diversity of immune signaling.]]></description>
<pubDate>2026/2/10 17:19:05</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[LU Qiang and CHENG Rui]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LU Qiang and CHENG Rui</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260002]]></guid><cfi:id>4</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Mitoxyperilysis——a Novel Pathway of Cell Death Connecting Dietary Interventions and Innate Immune Activation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260075]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Dietary interventions such as fasting are gaining increasing attention for their synergistic effects in anti-tumor therapy, yet the precise underlying mechanisms remain incompletely understood. Recent research has unveiled a novel mode of cell death named “mitoxyperilysis”, providing a fresh perspective on the molecular mechanisms by which fasting may interfere with tumor treatment. This form of death is primarily triggered by the synergy between metabolic dysfunction and innate immune activation. Its mechanism involves the mTORC2 signaling pathway mediating prolonged abnormal contact between damaged mitochondria and the plasma membrane. This leads to massive local release of reactive oxygen species (ROS), which further induces lipid peroxidation of the plasma membrane, ultimately resulting in the physical rupture and death of the cell. The most significant distinction between mitoxyperilysis and classical cell death pathways lies in its independence from caspases and GSDMD. This comment aims to systematically elucidate the process, molecular mechanisms, and differences from other classical cell death pathways of mitoxyperilysis, while also exploring its potential for clinical translation in oncological diseases. Targeting induction of mitoxyperilysis may enhance the efficacy of existing anti-tumor drugs and overcome chemotherapy resistance. However, intervention protocols require further optimization to achieve an optimal balance between safety and therapeutic effectiveness in clinical application.]]></description>
<pubDate>2026/3/4 14:24:32</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[WANG Yi,CHEN Zhe,LI Xin and CHEN Lin-Xi]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>WANG Yi,CHEN Zhe,LI Xin and CHEN Lin-Xi</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260075]]></guid><cfi:id>3</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[RAD6A-RAD18 Ubiquitination Complex-mediated Nuclear-cytoplasmic Trafficking and Viral Budding of Henipavirus M Protein]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260027]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The ubiquitination modification of henipavirus (HNV) M protein is essential for its nuclear-cytoplasmic trafficking and viral budding, but the precise regulatory mechanism has remained unclear. A recent study published in <i>Emerging Microbes & Infections</i> demonstrated that the RAD6A-RAD18 ubiquitination complex plays a unique and pivotal role in the nuclear-cytoplasmic trafficking of the HNV M protein and the process of viral budding. Furthermore, this study revealed that treating cells with TZ9 (a RAD6 inhibitor) or RAD18 RING domain-binding peptides markedly impaired the ubiquitination level of HNV M protein, resulting in its nuclear retention and subsequent impairment of viral budding and replication. These findings lay a theoretical foundation for the development of novel antiviral drugs and specific antiviral therapies targeting HNV infections, and provide valuable references for investigating the biological functions of M protein’s ubiquitination as well as the replication and pathogenic mechanisms of other paramyxoviruses.]]></description>
<pubDate>2026/2/2 11:45:41</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[DUAN Zhi-Qiang]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DUAN Zhi-Qiang</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260027]]></guid><cfi:id>2</cfi:id><cfi:read>true</cfi:read></item>
<item>
<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Reshaping “Cerebellar Inhibition”: Mechanistic Insights and Precision Medicine Perspectives for rTMS in Machado-Joseph Disease]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260006]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Machado-Joseph disease, or spinocerebellar ataxia type 3 (SCA3), represents the most common autosomal dominant cerebellar ataxia worldwide. Despite its progressive and debilitating nature, disease-modifying therapies remain elusive. Repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising non-invasive intervention; however, its clinical application has been hindered by inconsistent protocols and a lack of mechanistic understanding. A recent landmark study published in <i>Brain Stimulation</i> by Chen<i> et al.</i> addressed these challenges by combining a high-dose intermittent theta-burst stimulation (iTBS) protocol with concurrent transcranial magnetic stimulation-electroencephalography (TMS-EEG). This commentary provides an in-depth analysis of their findings, highlighting the restoration of cerebello-cortical inhibition (CBI) as a key therapeutic mechanism. Furthermore, we discuss the broader implications of this work, proposing that future translational research should integrate accelerated iTBS (aiTBS) paradigms, cortical response measurements (CRM), and individualized neuro-navigation to establish a new era of precision neuromodulation for ataxia.]]></description>
<pubDate>2026/2/2 8:46:54</pubDate>
<category><![CDATA[News and Views]]></category>
<author><![CDATA[HAN Ya-Zhen,ZHOU Jie,CHEN Yu-Chao,GAO Zhong-Ming and CHE Xian-Wei]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HAN Ya-Zhen,ZHOU Jie,CHEN Yu-Chao,GAO Zhong-Ming and CHE Xian-Wei</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20260006]]></guid><cfi:id>1</cfi:id><cfi:read>true</cfi:read></item>
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