Prevalence of Dry Eye Symptoms and Associated Risk Factors among University Students in Poland

International Journal of Environmental Research and Public Health, Journal Year: 2023, Volume and Issue: 20(2), P. 1313 - 1313

Published: Jan. 11, 2023

Aim: The aim of the study was to demonstrate prevalence and risk factors dry eye symptoms (DES) among university students in Poland. Material methods: A cross-sectional survey conducted 312 Polish students. questionnaire consisted Ocular Surface Disease Index (OSDI), 5-Item Dry Eye Questionnaire (DEQ-5) questions regarding medical history factors. Results: According OSDI, more than half respondents (57.1%) have ocular surface disease. Time spent using electronic devices is correlated with scores gathered both OSDI DEQ-5 (p < 0.001). There a statistically significant dependence between psychotropics = 0.002), glucocorticosteroids usage 0.026), presence depression 0.001), diabetes 0.01) or allergy 0.008) proved questionnaires. Respondents refractive errors those living metropolitan areas higher symptom intensity(p 0.022). Stress felt by associated DES risk. No correlation smoking habits observed. SARS-CoV-2 infection severity 0.036). Conclusion: Pathogenesis multifactorial its depends on several factors, genetic environmental. Its young population underestimated. Determining will enable implementation appropriate prophylaxis early diagnosis.

Language: Английский

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Progressive Irreversible Proprioceptive Piezo2 Channelopathy-Induced Lost Forced Peripheral Oscillatory Synchronization to the Hippocampal Oscillator May Explain the Onset of Amyotrophic Lateral Sclerosis Pathomechanism

Cells, Journal Year: 2024, Volume and Issue: 13(6), P. 492 - 492

Published: March 12, 2024

Amyotrophic lateral sclerosis (ALS) is a mysterious lethal multisystem neurodegenerative disease that gradually leads to the progressive loss of motor neurons. A recent non-contact dying-back injury mechanism theory for ALS proposed primary damage an acquired irreversible intrafusal proprioceptive terminal Piezo2 channelopathy with underlying genetic and environmental risk factors. Underpinning this excessively prolonged mechanotransduction under allostasis may induce dysfunctionality in mitochondria, leading channelopathy. This microinjury suggested provide one gateway from physiology pathophysiology. The chronic, but not irreversible, form implicated many diseases unknown etiology. Dry eye them where replenishing synthetic proteoglycans promote nerve regeneration. Syndecans, especially syndecan-3, are as first critical link hierarchical ordered depletory pathomechanism proton-collecting/distributing antennas; hence, they play role onset. Even more importantly, shedding or charge-altering variants Syndecan-3 contribute channelopathy-induced disruption Piezo2-initiated proton-based ultrafast long-range signaling through VGLUT1 VGLUT2. Thus, these alterations only cause hippocampus conscious proprioception, could disrupt feedback motoneurons. Correspondingly, inert signaled skeletal system coming light be progressively lost ALS. In addition, functional MyoD family inhibitor proteins, auxiliary subunits Piezo2, theorized channelopathy, explain how microinjured ion channels evolve principal transcription activators.

Language: Английский

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Likely pathogenic variants of SDC3, KCNA2, KCNK1, KCNK16 and HSF1 are in support of acquired irreversible PIEZO2 channelopathy in ALS onset

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 3, 2025

Amyotrophic lateral sclerosis is a multisystem progressive neurodegenerative disease. A recent theory of ALS proposed that the disease initiating primary damage an acquired irreversible intrafusal proprioceptive terminal PIEZO2 channelopathy with underlying genetic and environmental risk factors. Underpinning this these ion channels initiate ultrafast proton-based oscillatory signaling to motor neurons through VGLUT1 hippocampus VGLUT2. This may gradually degenerate in which process K_v1.2 are depleted. Furthermore, it also depletes heat shock transcription factor-1 hippocampus, hence negatively affecting adult hippocampal neurogenesis. In addition, not only PIEZO2-PIEZO2 crosstalk fully disrupted progressively between afferent terminals due lost initiated cross-coupled Huygens synchronization, but PIEZO2-PIEZO1 on periphery. Syndecans, especially syndecan-3 nervous system, critical players maintenance PIEZO crosstalk. The detected charge altering variants likely promotes impairment crosstalk, loss as well. Variants KCNA2 facilitate faster function when prevails, mention potassium current rectifying encoding KCNK1 KCNK16 propel provide autoimmune-like pathogenic background. Moreover, diminishing presence identified HSF1 variants, leading impaired

Language: Английский

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Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 2319 - 2319

Published: March 5, 2025

Unaccustomed and/or strenuous eccentric contractions are known to cause delayed-onset muscle soreness. In spite of this fact, their exact and mechanism have been unknown for more than 120 years. The exploration the diverse functionality Piezo2 ion channel, as principal proprioceptive component, its autonomously acquired channelopathy may bring light apparently simple but mysterious pain condition. Correspondingly, neurocentric non-contact acute compression axonopathy theory soreness suggests two damage phases affecting compartments, including intrafusal (within spindle) extrafusal (outside ones. secondary phase in space is relatively well explored. However, suggested primary within spindle far from being entirely known. current manuscript describes how proposed channelopathy-induced could be initiating transient neural switch unfolding This results a quantum mechanical free energy-stimulated ultrafast proton-coupled signaling rapid glutamate-based along muscle-brain axis. addition, it induces metabolic or, even importantly, an energy generation Type Ia terminals that eventually leads glutaminolysis deficit mitochondrial deficiency, not mention force switch. summary, or likely inward unidirectional proton pathway reversal between auxiliary ligands, leading channelopathy.

Language: Английский

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Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

Biomolecules, Journal Year: 2022, Volume and Issue: 12(9), P. 1207 - 1207

Published: Aug. 31, 2022

Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction for proprioception. Recently, it was postulated that could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time window when unaccustomed or strenuous eccentric contractions are executed. One consequence of this proposed transient microinjury VGLUT1/Ia synaptic disconnection motoneurons, we can learn from platinum-analogue chemotherapy. A secondary, harsher injury phase with involvement polymodal Aδ and nociceptive C-fibers follow primary impairment proprioception delayed onset muscle soreness. Repetitive reinjury these form repeated bout effects is to tertiary phase. Notably, use associated motor learning memory. The monosynaptic static firing sensory encoding affected stretch reflex immediate microdamage leading impaired proprioception, exaggerated reduced range motion. These channelopathies afferent constitute critical gateway pathophysiology Correspondingly, fatiguing contraction-based pathological hyperexcitation afferents induces reactive oxygen species production-associated neuroinflammation neuronal activation spinal cord

Language: Английский

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Miswired Proprioception in Amyotrophic Lateral Sclerosis in Relation to Pain Sensation (and in Delayed Onset Muscle Soreness)—Is Piezo2 Channelopathy a Principal Transcription Activator in Proprioceptive Terminals Besides Being the Potential Primary Damage?

Life, Journal Year: 2023, Volume and Issue: 13(3), P. 657 - 657

Published: Feb. 27, 2023

Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative multisystem disease, with an unknown pathomechanism, resulting in progressive motoneuron loss. In 90-95% of cases, ALS sporadic, but close to 10% familial inherited gene mutations from family members. Recently, non-contact dying-back injury mechanism theory postulated that irreversible intrafusal proprioceptive terminal degeneration induces the non-resolving impairment circuitry, leading loss, overloading and depletion central nervous system, eventually death. The current manuscript proposes Piezo2 channelopathy this constantly activated dysregulated transcription process ALS, providing access underlying pathogenic variants letting cell-type-specific noncoding DNA become more apparent. This opinion piece genes are associated both downstream upstream, their mutations, along aging process, could explain ALS. Moreover, microinjury ion channel be primary damage or root cause death Finally, also depicts pathomechanism as why considered painless disease.

Language: Английский

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Significantly Delayed Medium-Latency Response of the Stretch Reflex in Delayed-Onset Muscle Soreness of the Quadriceps Femoris Muscles Is Indicative of Sensory Neuronal Microdamage

Journal of Functional Morphology and Kinesiology, Journal Year: 2022, Volume and Issue: 7(2), P. 43 - 43

Published: May 27, 2022

Unaccustomed or strenuous eccentric exercise is known to cause delayed-onset muscle soreness. A recent hypothesis postulated that mechano-energetic microinjury of the primary afferent sensory neuron terminals in spindles, namely a transient Piezo2 channelopathy, could be critical soreness form bi-phasic non-contact injury mechanism. This theory includes this microlesion delay medium-latency response stretch reflex. Our aim with study was investigate hypothesis. According our knowledge, no has examined effect on findings demonstrated significant reflex observed right after multi-stage fitness test quadriceps femoris muscles Hungarian professional handball players who consequently experienced The long-latency and most likely short-latency were unaffected by study, which line earlier findings. We translate these as indicative proprioceptive Type Ia terminal microdamage spindle aforementioned new acute compression axonopathy

Language: Английский

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Should We Void Lactate in the Pathophysiology of Delayed Onset Muscle Soreness? Not So Fast! Let’s See a Neurocentric View!

Metabolites, Journal Year: 2022, Volume and Issue: 12(9), P. 857 - 857

Published: Sept. 13, 2022

The pathophysiology of delayed onset muscle soreness is not entirely known. It seems to be a simple, exercise-induced pain condition, but has remained mystery for over 120 years. buildup lactic acid used blamed fatigue and soreness; however, studies in the 1980s largely refuted role lactate soreness. Regardless, this belief widely held even today, only general public, within medical scientific community as well. Current opinion highlighting lactate's soreness, if neural dimension neuro-energetics are overlooked. By doing so, have an essential initiation primary damage phase intrafusal space. Unaccustomed or strenuous eccentric contractions suggested facilitate nourishment proprioceptive sensory neurons spindle under hyperexcitation. However, excessive acidosis could eventually contribute impaired proprioception increased nociception pathological condition. Furthermore, also secondary extrafusal space, primarily by potentiating bradykinin. After all, interpretation may help us dispel 40-year-old controversy about

Language: Английский

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Delayed-Onset Muscle Soreness Mimics a Tendency Towards a Positive Romberg Test

Published: May 16, 2025

Delayed-onset muscle soreness (DOMS) is induced by unaccustomed and/or strenuous repetitive eccentric or isometric contractions. However, the exact mechanism of DOMS far from entirely known for more than 120 years. A recent neurocentric theory proposes that a non-contact acute compression axonopathy initiated on intrafusal proprioceptive Type Ia terminal, in form an autonomously acquired transient Piezo2 channelopathy under eccentric/isometric contractions and allostatic stress. The current study was executed seventeen young male handball players Hungarian National Handball Academy. dynamometer-based exercise protocol used order to induce stabilometry measure postural sway before right after aforementioned inducing protocol. findings this contrast fatigue related ones, namely it decreased with open eyes. Furthermore, closed eyes did not reduce antero-posterior due effect, like observed fatigue, fact increased it. Hence, both eye are where when were reduced closed. finding effect analogous tendency towards positive Romberg test. Indeed, test indicative impaired signaling neurology principal mechanosensory ion channel responsible proprioception. In summary, our suggests reflex-like compensatory control enhancement response underlying factor, however resulting enhanced left-right sway. This observation may have relevance higher risk sport injuries mention provides differential diagnostic method distinguish between microdamage.

Language: Английский

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Proton-Mediated PIEZO2 Channelopathy: Linking Oxaliplatin Treatment to Impaired Proprioception and Cognitive Deficits

Cancers, Journal Year: 2024, Volume and Issue: 16(23), P. 3898 - 3898

Published: Nov. 21, 2024

Oxaliplatin induces acute neuropathy within a few hours post-treatment, with symptoms persisting for several days. Delayed onset muscle soreness also causes the delayed of mechanical pain sensation starting at about 6-8 h and lasting up to week after exercise. Both conditions come impaired proprioception could be chronic if these bouts are repeated frequently. The involvement PIEZO2 ion channels, as principal mechanosensory channels responsible proprioception, is theorized in both well. current opinion manuscript meant explain how minor stretch-related microdamage on Type Ia proprioceptive terminals aforementioned proprioception. This includes platinum-induced proton affinity 'switch' endings content, resulting this being likely initiating cause. Furthermore, it postulates proton-based ultrafast long-range oscillatory synchronization hippocampus due terminals. Finally, provides insight into impairment PIEZO2-initiated muscle-brain axis may contribute chemobrain its associated cognitive memory deficits.

Language: Английский

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