Medical hypotheses最新文献_第2页

Fibroblast-to-myofibroblast differentiation in gut wall and abdominal soft tissue corrupts normal bowel function in “irritable bowel syndrome”: A hypothesis 肠易激综合征患者肠壁和腹部软组织中成纤维细胞向肌成纤维细胞的分化破坏了正常的肠功能：一种假说

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-09 DOI: 10.1016/j.mehy.2026.111905

Shiloh Plaut

Irritable Bowel Syndrome (IBS) is a common gastrointestinal disorder characterized by chronic abdominal discomfort, pain, and altered bowel habits, as well as extraintestinal manifestations such as fatigue, musculoskeletal pain, gastroesophageal reflux, depression, and anxiety. Despite prevalences of approximately 10% in the general population, its fundamental etiopathogenesis remains unclear. Current theories mainly point toward a multifactorial aetiology crediting psychological stress with a prominent role. The paradigms currently embraced for IBS are mainly based on, and emphasize, the gut-brain axis, visceral hypersensitivity, central sensitization, neuroendocrinology, dysbiosis, motility abnormalities, and post-infectious persistent low-grade mucosal inflammation. Yet, they don’t fully explain its diverse clinical presentations nor IBS’s symptomatic overlap with conditions such as fibrositis/fibromyalgia syndrome. Available treatments are mostly symptomatic and provide limited relief, indicating a still major gap in our mechanistic understanding. This paper proposes a hypothesis for IBS etiopathogenesis as an organic disease of the extracellular matrix driven by myofibroblast overactivity in the gut wall and abdominal soft tissue, along with downstream consequences stemming from tissue stiffness. This process is theorized to mechanically compress visceral structures and nerves, impair synchronized organ motility, and induce substrate stiffness-mediated visceral hypersensitivity. In this theoretical framework the extraintestinal manifestations reflect mechanistic overlap with fibromyalgia, which helps unify functional-psychosomatic syndromes as a medical entity with a shared organic mechanism. This mechanism, along with known mechanisms of gut dysbiosis and the gut-brain axis, helps explain “medically unexplained symptoms” of fibromyalgia-type syndromes and offers testable predictions for future research and suggests new avenues for IBS diagnosis and treatment.

肠易激综合征（IBS）是一种常见的胃肠道疾病，其特征是慢性腹部不适、疼痛和排便习惯改变，以及肠外表现，如疲劳、肌肉骨骼疼痛、胃食管反流、抑郁和焦虑。尽管在一般人群中患病率约为10%，但其根本病因尚不清楚。目前的理论主要指向一个多因素的病因学，认为心理压力起着突出的作用。目前，肠易激综合征的治疗模式主要基于并强调肠-脑轴、内脏超敏反应、中枢致敏、神经内分泌、生态失调、运动异常和感染后持续性低级别粘膜炎症。然而，他们并不能完全解释肠易激综合征不同的临床表现，也不能完全解释肠易激综合征与纤维炎/纤维肌痛综合征等疾病的症状重叠。现有的治疗大多是对症治疗，提供有限的缓解，表明我们对机制的理解仍然存在重大差距。本文提出一种假设，认为IBS的发病机制是由肠壁和腹部软组织中肌成纤维细胞过度活跃驱动的细胞外基质器质性疾病，以及由组织僵硬引起的下游后果。理论上，这一过程会机械地压迫内脏结构和神经，损害器官同步运动，并诱导底物刚度介导的内脏超敏反应。在这一理论框架下，肠外表现反映了与纤维肌痛的机制重叠，这有助于将功能-心身综合征统一为具有共同有机机制的医学实体。这一机制，连同已知的肠道生态失调机制和肠-脑轴，有助于解释纤维肌痛型综合征的“医学上无法解释的症状”，并为未来的研究提供可测试的预测，并为肠易激综合征的诊断和治疗提供新的途径。

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引用次数: 0

Percutaneous pedicle screws may be one of the causes of intermuscular hematoma following minimally invasive percutaneous treatment for thoracolumbar fractures 经皮椎弓根螺钉可能是胸腰椎骨折微创经皮治疗后肌间血肿的原因之一

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-23 DOI: 10.1016/j.mehy.2026.111920

Lei Wu, Yuda Xu, Jun Zhang, Yanli Zhu, Rongming Xu, Changming Zhao

Percutaneous pedicle screw fixation has emerged as a minimally invasive surgical approach for the treatment of thoracolumbar fractures, presenting benefits like diminished tissue trauma, minimal blood loss, and accelerated recovery. Despite these benefits, a number of patients still suffer from the occurrence of intermuscular hematoma after undergoing surgery. This hypothesis proposes that the structural characteristics of percutaneous pedicle screws, especially their hollow design, might play a role in the development of intermuscular hematoma. We explore the underlying potential mechanisms of this phenomenon and provide evidence from existing literature to support our hypothesis.

经皮椎弓根螺钉固定已成为治疗胸腰椎骨折的一种微创手术方法，其优点包括减少组织损伤、减少失血和加速恢复。尽管有这些好处，许多患者在手术后仍然遭受肌间血肿的发生。这一假设提出，经皮椎弓根螺钉的结构特点，特别是其中空设计，可能在肌间血肿的发展中起作用。我们探索这一现象的潜在机制，并从现有文献中提供证据来支持我们的假设。

引用次数: 0

Neuro-entero-cardiac bridge: could gut-derived catecholamine-loaded extracellular vesicles synchronize the pathogenesis of Parkinson’s disease, irritable bowel syndrome, and stress-triggered arrhythmias? 神经-肠-心桥：肠源性负载儿茶酚胺的细胞外囊泡能否同步帕金森病、肠易激综合征和应激性心律失常的发病机制？

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-07 DOI: 10.1016/j.mehy.2026.111896

Okechukwu Paul-Chima Ugwu , Mariam Basajja , Fabian C. Ogenyi , Chinyere N. Ugwu , Michael Ben Okon , Mustafa M. Mundu

The gut–brain–heart axis is increasingly recognized as a clinically relevant interface in chronic and stress-responsive disorders. Parkinson’s disease (PD), irritable bowel syndrome (IBS), and stress-triggered arrhythmias show epidemiologic and mechanistic convergence through autonomic dysregulation, mucosal immune activation, barrier dysfunction, and systemic inflammatory signaling. However, the molecular messengers that could help “couple” these organ systems over time remain incompletely defined. Extracellular vesicles (EVs) represent a plausible integrative mechanism because they can transport regulatory cargo (RNAs, proteins, lipids) and influence distant tissues, including during inflammation and stress responses. We hypothesize that stress-responsive gut-linked EVs originating from intestinal epithelial, immune, enteroendocrine, and enteric neural compartments may contribute to shared vulnerability across PD, IBS, and arrhythmias by distributing inflammatory and neuroactive regulatory signals (especially microRNAs) systemically. Importantly, direct evidence that gut-derived EVs are “highly enriched” with catecholamines (dopamine, norepinephrine) in PD, IBS, or arrhythmia contexts is currently lacking; therefore, EV-mediated catecholamine transport is presented here as a testable sub-hypothesis rather than an established driver of pathology. Even if EV-associated catecholamines are detectable, they may constitute a minor fraction relative to synaptic/autonomic catecholamine signaling and could represent an epiphenomenon of stress biology rather than a dominant transport route. We outline falsifiable predictions and a rigorous experimental strategy that explicitly addresses EV heterogeneity, contamination by non-EV particles, and causality controls. If supported, gut-linked EV cargo profiles could provide biomarkers that stratify tri-system risk and point toward adjunctive therapeutic approaches that complement established gut–brain–heart pathways (vagus/autonomic signaling and microbiota-derived metabolites, including TMAO-related pathways).

肠-脑-心轴越来越被认为是慢性和应激反应性疾病的临床相关界面。帕金森病（PD）、肠易激综合征（IBS）和应激性心律失常通过自主神经失调、粘膜免疫激活、屏障功能障碍和全身炎症信号传导表现出流行病学和机制上的趋同。然而，随着时间的推移，能够帮助这些器官系统“配对”的分子信使仍未完全确定。细胞外囊泡（EVs）代表了一种合理的综合机制，因为它们可以运输调节货物（rna、蛋白质、脂质）并影响远端组织，包括炎症和应激反应。我们假设来自肠上皮室、免疫室、肠内分泌室和肠神经室的应激性肠联EVs可能通过在系统中分布炎症和神经活性调节信号（尤其是microrna）而导致PD、IBS和心律失常的共同易感性。重要的是，目前缺乏直接证据表明肠源性ev在PD、IBS或心律失常情况下“高度富集”儿茶酚胺（多巴胺、去肾上腺素）；因此，ev介导的儿茶酚胺运输在这里被提出作为一个可测试的子假设，而不是一个既定的病理驱动程序。即使可以检测到ev相关的儿茶酚胺，它们也可能只占突触/自主神经儿茶酚胺信号传导的一小部分，并且可能代表应激生物学的副现象，而不是主要的运输途径。我们概述了可证伪的预测和严格的实验策略，明确解决EV异质性，非EV粒子污染和因果关系控制。如果得到支持，肠道相关的EV货物谱可以提供生物标志物，对三系统风险进行分层，并指出补充已建立的肠-脑-心通路（迷走神经/自主神经信号和微生物衍生代谢物，包括tmao相关途径）的辅助治疗方法。

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引用次数: 0

Arm elevation as a compensatory neuromechanical strategy during smartphone use: a hypothesis on segmental reweighting for postural stability 手臂抬高作为一种代偿性神经力学策略在智能手机的使用：对姿势稳定性的节段重加权的假设

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-08 DOI: 10.1016/j.mehy.2026.111900

Noppharath Sangkarit, Weerasak Tapanya, Saisunee Konsanit

Contemporary smartphone interaction involves prolonged static postures and attentional diversion, both of which challenge sensorimotor regulation of balance. Yet, emerging evidence suggests that subtle changes in arm elevation may paradoxically enhance postural stability during smartphone use. We hypothesize that arm elevation constitutes a compensatory neuromechanical adaptation that improves whole-body equilibrium through dynamic segmental reweighting. By elevating the arms, users may shift the center of segmental mass upward, engaging tonic activation of scapular and trunk musculature, which in turn increases mechanical coupling and stabilizing stiffness across the axial chain. This redistribution may reduce uncontrolled trunk oscillations and enhance sensorimotor efficiency of balance control, despite concurrent cognitive loading. Preliminary smartphone-based accelerometry observations indicate lower center-of-mass sway magnitudes under elevated-arm conditions, consistent with this proposed stabilization mechanism. If validated, this hypothesis reframes arm elevation during smartphone use as an active, goal-directed stabilizing strategy—rather than a passive by-product of mechanical load—and highlights ergonomic interventions that leverage segmental mechanics to preserve postural stability during mobile multitasking.

当代智能手机互动涉及长时间的静态姿势和注意力转移，这两者都挑战了平衡的感觉运动调节。然而，新出现的证据表明，在使用智能手机时，手臂高度的细微变化可能会矛盾地增强姿势稳定性。我们假设手臂抬高是一种代偿性神经机械适应，通过动态节段加权改善全身平衡。通过抬高手臂，使用者可以将节段质量中心向上移动，参与肩胛骨和躯干肌肉组织的强直激活，从而增加机械耦合并稳定轴链上的刚度。这种重新分配可以减少不受控制的主干振荡，增强平衡控制的感觉运动效率，尽管同时存在认知负荷。基于智能手机的初步加速度测量结果表明，在手臂抬高的情况下，质心摆动幅度较小，与所提出的稳定机制一致。如果这一假设得到证实，那么在智能手机使用过程中，手臂抬高将成为一种主动的、目标导向的稳定策略，而不是机械负荷的被动副产品，并强调了利用节段力学来保持移动多任务处理过程中姿势稳定性的人体工程学干预措施。

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引用次数: 0

The role of spinal cord pulsatility in the pathogenesis of Post-traumatic syringomyelia: A novel hypothesis 脊髓搏动在创伤后脊髓空洞发病机制中的作用：一个新的假说

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-24 DOI: 10.1016/j.mehy.2026.111924

Feifan Xu , Fengzeng Jian , Jian Guan , Zhiqiang Yi , Xingwen Wang

This paper proposes a novel hypothesis that impaired spinal cord pulsatility is a critical factor in the pathogenesis of post-traumatic syringomyelia (PTS). Beyond established theories on cerebrospinal fluid dynamics and intramedullary changes, we posit that post-traumatic adhesions and compression diminish spinal cord motion and compliance. This loss of normal kinematics disrupts fluid homeostasis, facilitating syrinx formation and progression. Supporting evidence includes consistent intraoperative observation of reduced pulsatility in PTS, which improves after decompression and adhesion release, correlating with syrinx collapse. Literature confirms pulsatility’s role in cord protection and cerebrospinal fluid dynamics. If validated, this hypothesis reframes PTS pathophysiology, suggesting spinal cord pulsatility as a biomarker for diagnosis, a real-time surgical guide for decompression, and a target for future therapies aimed at restoring mechanical homeostasis.

本文提出了一个新的假设，即脊髓搏动功能受损是创伤后脊髓空洞症（PTS）发病的关键因素。除了脑脊液动力学和髓内变化的既定理论外，我们假设创伤后粘连和压迫会减少脊髓的运动和顺应性。这种正常运动学的丧失破坏了流体稳态，促进了鼻窦的形成和发展。支持性证据包括术中一致观察到PTS患者搏动性降低，减压和粘连释放后搏动性改善，与鼻管塌陷相关。文献证实了搏动在脊髓保护和脑脊液动力学中的作用。如果得到证实，这一假设将重新构建PTS病理生理学，表明脊髓搏动可作为诊断的生物标志物、减压的实时手术指南，以及旨在恢复机械稳态的未来治疗目标。

引用次数: 0

Aquaporin dysregulation and persistent hyperosmolar microenvironments as a barrier to tissue recovery 水通道蛋白失调和持续高渗透性微环境是组织恢复的障碍

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-17 DOI: 10.1016/j.mehy.2026.111916

Susie Sarkozy

Chronic inflammatory conditions frequently persist despite anti-inflammatory treatment, suggesting that inflammation alone does not fully explain incomplete tissue recovery. Many affected tissues exhibit localized extracellular hyperosmolarity, which can impose sustained biophysical stress independent of inflammatory signaling. We hypothesize that persistent hyperosmolar microenvironments represent an underappreciated barrier to tissue recovery and that aquaporin-mediated water equilibration plays a critical role in resolving, but not initiating, this stress. When aquaporin function is dysregulated, compensatory water movement may be insufficient, permitting hyperosmolar stress to persist even as inflammatory markers improve. We hypothesize that persistent hyperosmolar microenvironments can represent an underappreciated barrier to tissue recovery and that aquaporin-mediated water equilibration may play a critical role in resolving this stress, while upstream initiators vary by condition and subtype.

尽管进行了抗炎治疗，慢性炎症仍经常持续存在，这表明炎症本身并不能完全解释不完全的组织恢复。许多受影响的组织表现出局部的细胞外高渗，这可以施加独立于炎症信号的持续生物物理应激。我们假设，持续的高渗透性微环境代表了组织恢复的一个未被充分认识的障碍，而水通道蛋白介导的水平衡在解决而不是引发这种压力方面起着关键作用。当水通道蛋白功能失调时，代偿性水运动可能不足，即使炎症标志物改善，也会导致高渗应激持续存在。我们假设，持续的高渗透性微环境可能是组织恢复的一个未被充分认识的障碍，而水通道蛋白介导的水平衡可能在解决这种压力中发挥关键作用，而上游的启动物因条件和亚型而异。

引用次数: 0

A substrate-competition hypothesis for type 2 diabetes driven by nutrient excess rather than a primary insulin-signaling defect 2型糖尿病的基质竞争假说是由营养过剩而非原发性胰岛素信号缺陷驱动的

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-23 DOI: 10.1016/j.mehy.2026.111926

John M. Poothullil

Type 2 diabetes (T2D) is most commonly framed within a dominant insulin-resistance paradigm characterized by reduced insulin-stimulated glucose disposal and inadequate suppression of hepatic glucose output. While this framework describes reproducible physiological phenotypes, the causal status and temporal ordering of insulin-signaling–associated changes in the development of chronic hyperglycemia remain debated. Clinical observations—including variable diabetes risk across BMI strata and frequent glycemic improvement with dietary change—motivate consideration of alternative causal models.

This article proposes an alternative hypothesis for the pathogenesis of T2D with an explicit causal sequence that does not invoke a primary insulin-signaling defect. In this framework, chronic dietary substrate surplus—particularly refined-carbohydrate exposure—exceeds an individual’s capacity to buffer and safely store lipid in adipose tissue (“personal fat threshold”). As adipose buffering becomes constrained, lipid overflow into the circulation and non-adipose tissues increases, leading to ectopic lipid accumulation in liver and skeletal muscle. This metabolic state promotes a preferential shift toward fatty-acid oxidation via substrate competition (the Randle cycle), functionally displacing glucose utilization. Within this framework, reduced insulin effectiveness emerges as a context-dependent physiological phenotype rather than as evidence of a required insulin-signaling defect or a necessary causal mediator of dysglycemia.

The model yields falsifiable predictions regarding temporal ordering and measurable intermediates and outlines cohort and controlled feeding-trial designs that allow direct empirical adjudication between this framework and insulin-resistance–first models, with implications for dietary strategies in T2D prevention and treatment.

2型糖尿病（T2D）最常见的特点是胰岛素抵抗模式，其特征是胰岛素刺激的葡萄糖处理减少和肝脏葡萄糖输出抑制不足。虽然这一框架描述了可复制的生理表型，但胰岛素信号相关变化在慢性高血糖发展中的因果状态和时间顺序仍存在争议。临床观察——包括不同BMI水平的糖尿病风险和饮食改变导致的血糖改善——激发了对其他因果模型的考虑。本文提出了T2D发病机制的另一种假说，该假说具有明确的因果关系，不涉及原发性胰岛素信号缺陷。在这个框架下，长期的饮食底物过剩——特别是精制碳水化合物暴露——超过了个体缓冲和安全储存脂肪组织的能力（“个人脂肪阈值”）。由于脂肪缓冲受到限制，脂质溢出进入循环，非脂肪组织增加，导致肝脏和骨骼肌的异位脂质积累。这种代谢状态通过底物竞争（兰德尔循环）促进脂肪酸氧化的优先转变，在功能上取代了葡萄糖的利用。在这个框架内，胰岛素有效性降低是一种环境依赖的生理表型，而不是胰岛素信号缺陷或血糖异常的必要因果介质的证据。该模型产生了关于时间顺序和可测量中间物的可证伪预测，并概述了队列和控制喂养试验设计，允许在该框架和胰岛素抵抗优先模型之间进行直接的经验判断，对糖尿病预防和治疗的饮食策略具有指导意义。

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引用次数: 0

Temporal coding instability in tinnitus: The temporal jitter hypothesis 耳鸣的时间编码不稳定性：时间抖动假说

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-15 DOI: 10.1016/j.mehy.2026.111913

Halime Sümeyra Sevmez

Despite decades of investigation, the pathophysiological basis of tinnitus remains incompletely understood. Prevailing models have largely emphasized peripheral deafferentation, central hyperactivity, maladaptive plasticity, aberrant neural synchrony, and deficits in sensory gating. While these frameworks account for selected features of tinnitus, they do not fully explain several persistent observations, including the heterogeneity of electrophysiological findings, the occurrence of tinnitus in individuals with clinically normal audiograms, and the frequently inconsistent associations between tinnitus and conventional neural amplitude or latency measures. Against this background, the Temporal Jitter Hypothesis is proposed as a complementary conceptual framework that identifies temporal auditory coding fidelity as a potentially underrecognized dimension of tinnitus pathophysiology, particularly within a mechanistically coherent subgroup of individuals characterized by preserved audiometric thresholds yet disrupted temporal processing. The hypothesis posits that increased variability in neural spike timing and reduced phase locking across the auditory pathway may give rise to temporally unstable neural representations even in the absence of overt threshold elevation. Such instability may subsequently interact with central gain and predictive processes, increasing the likelihood that internally generated auditory activity attains perceptual salience and persistence. Rather than constituting a universal explanation, this framework is intended to complement existing models by providing a constrained and empirically testable account of tinnitus within this specific physiological context. By shifting the explanatory emphasis from neural response magnitude toward temporal precision, the Temporal Jitter Hypothesis integrates behavioral, electrophysiological, and computational evidence while establishing a structured foundation for future experimental and translational research.

尽管经过数十年的研究，耳鸣的病理生理基础仍然不完全清楚。主流模型主要强调外周神经传递障碍、中枢亢进、适应性不良可塑性、异常神经同步和感觉门控缺陷。虽然这些框架解释了耳鸣的特定特征，但它们并不能完全解释一些持续的观察结果，包括电生理结果的异质性，耳鸣在临床听音正常的个体中的发生，以及耳鸣与传统神经振幅或潜伏期测量之间经常不一致的关联。在此背景下，时间抖动假说被提出作为一个补充的概念框架，它确定了时间听觉编码保真度是耳鸣病理生理的一个潜在未被认识的维度，特别是在一个机制一致的个体亚群中，其特征是保留了听力阈值，但破坏了时间处理。该假设认为，即使在没有明显阈值升高的情况下，神经脉冲时间的变异性增加和听觉通路上相锁的减少也可能导致暂时不稳定的神经表征。这种不稳定性可能随后与中枢增益和预测过程相互作用，增加内部产生的听觉活动获得感知显著性和持久性的可能性。而不是构成一个普遍的解释，这个框架旨在补充现有的模型，提供一个限制和经验可测试的耳鸣在这种特定的生理背景下的解释。通过将解释重点从神经反应量级转向时间精度，时间抖动假说整合了行为、电生理和计算证据，同时为未来的实验和转化研究奠定了结构化的基础。

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引用次数: 0

An environmental–sensorimotor cascade hypothesis: Spatial and mechanical affordances shape segmental trunk control in preterm infants 环境-感觉-运动级联假说：空间和机械启示影响早产儿节段性躯干控制

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-02-18 DOI: 10.1016/j.mehy.2026.111918

Weerasak Tapanya, Noppharath Sangkarit

Preterm infants frequently display delayed postural control and segmental instability, yet the environmental mechanisms influencing this neuromechanical development remain poorly understood. Conventional views emphasize intrinsic neuromuscular immaturity, overlooking how daily environments constrain sensorimotor calibration. Drawing from longitudinal observations of moderate-to-late preterm infants, we propose an environmental–sensorimotor cascade hypothesis. This framework posits that spatial and mechanical affordance within infant home containers (e.g., playpens, cribs/cots, and other bounded spaces)—specifically usable play area and surface compliance—may modulate the quality and frequency of postural perturbations, thereby shaping the maturation of segmental trunk control. Limited spatial area restricts center-of-mass excursions and reduces opportunities for anticipatory and reactive adjustments, while excessively firm surfaces may impose lower demands on proprioceptive reweighting. Conversely, moderately compliant surfaces stimulate multi-segment coordination and feedforward stabilization. Over time, these constraints produce distinct trajectories of static, active, and reactive trunk control, influencing upright locomotor milestones. We hypothesize that such affordance-dependent calibration operates through adaptive tuning of trunk muscle synergies and sensory feedback gain. If confirmed, this hypothesis redefines the environment as an active biomechanical teacher, offering new targets for early intervention in preterm infants.

早产儿经常表现出姿势控制迟缓和节段性不稳定，然而影响这种神经力学发展的环境机制仍然知之甚少。传统观点强调内在的神经肌肉不成熟，忽视了日常环境如何限制感觉运动校准。根据对中度至晚期早产儿的纵向观察，我们提出了一个环境-感觉-运动级联假说。该框架假设婴儿家庭容器（例如，围栏、婴儿床/婴儿床和其他有界空间）中的空间和机械功能-特别是可用的游戏区域和表面依从性-可能调节姿势扰动的质量和频率，从而塑造节段躯干控制的成熟。有限的空间区域限制了质心的偏移，减少了预期和反应性调整的机会，而过于坚固的表面可能会降低本体感觉重加权的要求。相反，适度柔顺的表面刺激多段协调和前馈稳定。随着时间的推移，这些限制产生了静态、主动和被动躯干控制的不同轨迹，影响直立运动的里程碑。我们假设这种能力依赖的校准是通过躯干肌肉协同作用和感觉反馈增益的自适应调节来操作的。如果得到证实，这一假设将环境重新定义为一个活跃的生物力学老师，为早产儿的早期干预提供了新的目标。

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引用次数: 0

A novel multilayered drug-releasing stent for actively accelerating thrombosis in aneurysm therapy 一种新型多层药物释放支架在动脉瘤治疗中积极加速血栓形成

IF 0.8 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Medical hypotheses

Pub Date : 2026-04-01 Epub Date: 2026-03-01 DOI: 10.1016/j.mehy.2026.111930

Peng Zhang , Xiaoyan Deng , Xiao Liu , Fan Zhang , Jun Li , Chun Guo , Shangming Liu

Current endovascular treatments such as flow diverters promote aneurysm occlusion through passive changes in blood flow, but are limited by a high-risk transition period during which delayed thrombus formation may lead to sac enlargement and rupture. We hypothesize that engineering a porous stent with a localized, controlled-release system for pro-thrombotic agents can actively accelerate the formation of stable thrombus, thereby mitigating this risk. The proposed stent device combines flow stagnation via overlapping struts, a structural support for endothelialization, and targeted delivery of thrombotic agents into the aneurysm sac. If confirmed, this approach may introduce a new treatment strategy that combines device design with targeted drug therapy to improve occlusion effectiveness and patient safety.

目前的血管内治疗，如分流器，通过被动改变血流促进动脉瘤闭塞，但受限于高风险过渡期，延迟血栓形成可能导致囊增大和破裂。我们假设，设计一种具有局部、促血栓药物控释系统的多孔支架可以积极地加速稳定血栓的形成，从而降低这种风险。提出的支架装置结合了通过重叠支柱的血流停滞，内皮化的结构支持，以及将血栓形成剂靶向递送到动脉瘤囊中。如果得到证实，该方法可能会引入一种新的治疗策略，将设备设计与靶向药物治疗相结合，以提高闭塞效果和患者安全性。

引用次数: 0