MEDICAL HYPOTHESES医学假说
MEDICAL HYPOTHESES(英文缩写 MED HYPOTHESES),ISSN 0306-9877,eISSN 1532-2777,中文译名:医学假说 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.411 | Q2 |
| 2022 | 4.700 | Q2 |
| 2023 | 2.100 | Q3 |
| 2024 | 0.800 | Q4 |
| 2025 | 1.000 | Q4 |
MEDICAL HYPOTHESES 最新收录文献
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1. Subclinical mastitis during lactation: a modifiable risk factor for breast cancer?
1. 哺乳期亚临床乳腺炎：乳腺癌症的可改变危险因素？PMID:日期:2025-12-01Chronic inflammation likely contributes to breast cancer risk, but epidemiologic studies are inconclusive. Two types of inflammatory episodes in breast tissue, referred to here as clinical mastitis and subclinical mastitis, have received little to no attention as risk factors for breast cancer. Clinical mastitis represents an painful inflammatory state of the breast that in most cases will be quickly treated and resolved. In contrast, subclinical mastitis remains undetected in most cases and may represent inflammation. Based on the concentration of sodium (Na) and cytokines in milk, several publications suggest that subclinical mastitis is relatively common and can persist for extended periods. We propose that subclinical mastitis is a modifiable risk factor for breast cancer. This chronic subclinical inflammatory profile in breast tissue may cause genetic instability and perturb epigenetic mechanisms leading to cancer. We suggest studies to determine the extent that subclinical mastitis is associated with breast cancer risk.
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2. The Role of Hemispheric Sensory Shifts: Impacts on Stretch Reflex and Motor Plasticity Post-Stroke.
PMID:日期:2025-06-01Previous studies have found that post-stroke motor impairments are associated with damage to the lesioned corticospinal tract and the hyperexcitability of the cortico-reticulospinal tract at the hemisphere opposite to the lesion side, i.e., the contralesional hemisphere. While motor deficits and recovery mechanisms have been extensively studied, the role of sensory feedback in motor control has received less attention. We hypothesize that sensory-motor reorganization influences the stretch reflex and contributes to post-stroke spasticity. Effective motor function depends on the sensorimotor network, which integrates proprioceptive, tactile, and vibratory sensory inputs to guide movement and facilitate sensorimotor plasticity. Following stroke, these sensory pathways may undergo significant reorganization, leading to disrupted feedback loops and maladaptive changes in motor pathways. Recent studies have reported a hemispheric shift of somatosensory processing following a stroke. We propose to test our hypothesis by quantitatively analyzing the extent to which reorganization of sensory feedback pathways affects the stretch reflex. Testing our hypothesis will provide novel insights into the pathophysiological mechanisms underlying post-stroke spasticity. This will facilitate the development of customized rehabilitation strategies tailored to individual patient needs including improving their sensory feedback during movement exercise and other therapeutical intervention.
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3. Calcitonin Gene-Related Peptide-Induced Central Sensitization: A Hypothesis for Long COVID Symptoms.
PMID:日期:2025-02-01Central sensitization (CS) denotes aberrant processing of sensory stimuli within the central nervous system, wherein innocuous inputs activate pain pathways, leading to pain hypersensitivity. Features observed in CS conditions are often present in patients with long COVID, suggesting a potentially shared pathophysiological mechanism. We hypothesize that elevated levels of calcitonin gene-related peptide (CGRP), a neuropeptide known to play an integral role in the development of CS, may contribute to the persistent symptoms observed in long COVID. This article explores the role of CGRP within the context of CS and proposes its potential relationship to long COVID.
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4. How the Somatosensory System Adapts to the Motor Change in Stroke: A Hemispheric Shift?
PMID:日期:2024-11-01Previous studies found that post-stroke motor impairments are associated with damage to the lesioned corticospinal tract and a maladaptive increase in indirect contralesional motor pathways. How the somatosensory system adapts to the change in the use of motor pathways and the role of adaptive sensory feedback to the abnormal movement control of the paretic arm remains largely unknown. We hypothesize that following a unilateral stroke, there is an adaptive hemispheric shift of somatosensory processing toward the contralesional sensorimotor areas to provide sensory feedback support to the contralesional indirect motor pathways. This research could provide new insights related to somatosensory reorganization after stroke, which could enrich future hypothesis-driven therapeutic rehabilitation strategies from a sensory or sensory-motor perspective. Understanding how somatosensory information shifts may provide a target for a novel method to therapeutically prevent and mitigate the emergence and expression of upper limb motor impairments, following a stroke.
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5. Unstable Plaque is a Treatable Cause of Cognitive Decline.
PMID:日期:2024-09-01While many risk factors are modifiable, there remains a compelling need for novel approaches to prevent cognitive impairment. We propose that unstable carotid plaque causes microemboli that, in turn, cause microinfarcts and other adverse pathophysiological cerebral processes, which individually do not manifest clinically but cumulatively manifest as cognitive decline and ultimately cognitive impairment. Animal models support multiple cerebral microemboli having adverse effects on cognition. By addressing the source for microembolization by endarterectomy or stenting, patients with high-grade atherosclerotic stenosis may have better cognitive outcomes. If our hypothesis is verified, then treatment of carotid plaque at elevated risk of generating cerebral microemboli would be effective in preserving cognition, regardless of whether the stenosis is high-grade or causing cerebral hemispheric hypoperfusion.
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6. Elevated Circulating Procathepsin L as a Potential Biomarker of Inflamm-aging.
PMID:日期:2024-05-01Inflamm-aging is a condition of low-grade and chronic systemic inflammation characterized by a systemic increase in multiple inflammatory biomarkers such as tumor necrosis factor (TNF), interleukin 6 (IL-6), C-reactive protein (CRP), and CXCL9 (MIG) in experimental and clinical settings. However, despite the recent identification of extracellular procathepsin L (pCTS-L) as a novel mediator of inflammatory diseases such as sepsis, its possible role in inflamm-aging was previously not investigated. In the present study, we compared blood levels of pCTS-L and other 62 cytokines and chemokines between young and aged Balb/C mice by Western blotting and Cytokine Antibody Arrays. In light of the surprising finding of a marked increase in blood pCTS-L levels in aged mice, we propose that blood pCTS-L levels may serve as another biomarker of inflamm-aging. Given the capacity of pCTS-L in inducing various cytokines (e.g., TNF and IL-6), it will be important to test the hypothetic role of pCTS-L in inflamm-aging under experimental and clinical conditions.
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8. Potential Therapeutic Targets for Hypotension in Duchenne Muscular Dystrophy.
PMID:日期:2024-04-01Duchenne Muscular Dystrophy (DMD) is marked by genetic mutations occurring in the DMD gene, which is widely expressed in the cardiovascular system. In addition to developing cardiomyopathy, patients with DMD have been reported to be susceptible to the development of symptomatic hypotension, although the mechanisms are unclear. Analysis of single-cell RNA sequencing data has identified potassium voltage-gated channel subfamily Q member 5 (KCNQ5) and possibly ryanodine receptor 2 (RyR2) as potential candidate hypotension genes whose expression is significantly upregulated in the vascular smooth muscle cells of DMD mutant mice. We hypothesize that heightened KCNQ5 and RyR2 expression contributes to decreased arterial blood pressure in patients with DMD. Exploring pharmacological approaches to inhibit the KCNQ5 and RyR2 channels holds promise in managing the systemic hypotension observed in individuals with DMD. This avenue of investigation presents new prospects for improving clinical outcomes for these patients.
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9. Neuron-Targeted Exosome Therapy: A Novel Approach for Treating Cardiogenic Dementia via RyR2 Inhibition.
PMID:日期:2024-02-01Cardiogenic dementia (CD), recognized since the late 1970s, manifests as altered consciousness and cognition due to heart conditions. Its elusive molecular mechanisms present diagnostic and management challenges. Emerging research implicates ryanodine receptor type 2 (RyR2) mediated intracellular Ca2+ leaks in myocardial infarction (MI)-linked cognitive impairment. We hypotheses that intravenous delivery of neuron-targeted exosomes loaded with RyR2-targeting siRNA (si-RyR2) to cerebral regions could rectify Ca2+ imbalance, curbing neurotoxic protein generation tied to CD. To investigate, si-RyR2 exosomes will be administered to MI-induced mice, with hippocampal samples analyzed for Ca2+ levels, β-amyloid, and p-tau. Results hold promise for advancing CD treatment insights.
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10. Reprogramming endothelial and vascular smooth muscle cells to prevent and treat hypertension.
PMID:日期:2023-10-01The major pathophysiological characteristic of hypertension is the occurrence of small artery remodeling and endothelial dysfunction. There is also solid evidence showing that microcirculation abnormalities occur prior to the onset of hypertension. However, the mechanism(s) that trigger these changes prior to the elevation of blood pressure are unknown, and this may limit our ability to identify the cause of this disease and effectively treat it. In hypertension, as with aging, the vasculature becomes less susceptible to repair. One of the reasons is because endothelial cells start to deteriorate and present with exacerbated endothelial-to-mesenchymal transition (EndMT). Likewise, vascular smooth muscle cells (VSMC) also dedifferentiate into a synthetic phenotype, whereby they start to produce and secrete extracellular vesicles with a high migration and proliferation capacity for repairing vascular injury. Uncontrolled EndMT and/or VSMC phenotype switching contributes to vascular diseases, but the initial trigger for these conditions is unidentified. Importantly, EndMT and synthetic VSMC exhibit plasticity and can return to adopt an endothelial cell-like fate and present contractile phenotype again, respectively. Therefore, in this hypothesis we will take advantage of this plasticity, and we propose to manipulate this fate by inducing partial cellular reprogramming without passing through the pluripotent state. Specifically, we suggest that activation of the three master transcription factors, Oct-4, Sox-2, and Klf-4 (collectively termed OSK) will reprogram endothelial cells and prevent and reduce EndMT and VSMC synthetic phenotype. It was recently shown that activation of OSK was able to restore lost vision in old mice, and cancer risk was reduced by excluding c-Myc. Therefore, OSK treatment could provide new possibilities for vascular rejuvenation and treatment of hypertension.