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Poultry meat, an essential source of animal protein, requires stringent safety and quality measures to address public health concerns and growing international attention. This review examines both direct and indirect factors that compromise poultry meat quality in intensive farming systems. It highlights the integration of rapid and micro-testing with traditional methods to assess meat safety. The paper advocates for adopting probiotics, prebiotics, and plant extracts to improve poultry meat quality.
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Alteration of synaptic function in the dorsal horn (DH) has been implicated as a cellular substrate for the development of neuropathic pain, but certain details remain unclear. In particular, the lack of information on the types of synapses that undergo functional changes hinders the understanding of disease pathogenesis from a synaptic plasticity perspective. Here, we addressed this issue by using optogenetic and retrograde tracing ex vivo to selectively stimulate first-order nociceptors expressing Nav1.8 (NRsNav1.8) and record the responses of spinothalamic tract neurons in spinal lamina I (L1-STTNs). We found that spared nerve injury (SNI) increased excitatory postsynaptic currents (EPSCs) in L1-STTNs evoked by photostimulation of NRsNav1.8 (referred to as Nav1.8-STTN EPSCs). This effect was accompanied by a significant change in the failure rate and paired-pulse ratio of synaptic transmission from NRsNav1.8 to L1-STTN and in the frequency (not amplitude) of spontaneous EPSCs recorded in L1-STTNs. However, no change was observed in the ratio of AMPA to NMDA receptor-mediated components of Nav1.8-STTN EPSCs or in the amplitude of unitary EPSCs constituting Nav1.8-STTN EPSCs recorded with extracellular Ca2+ replaced by Sr2+ In addition, there was a small increase (approximately 10%) in the number of L1-STTNs showing immunoreactivity for phosphorylated extracellular signal-regulated kinases in mice after SNI compared with sham. Similarly, only a small percentage of L1-STTNs showed a lower action potential threshold after SNI. In conclusion, our results show that SNI induces presynaptic modulation at NRNav1.8 (consisting of both peptidergic and nonpeptidergic nociceptors) synapses on L1-STTNs forming the lateral spinothalamic tract.
Assuntos
Potenciais Pós-Sinápticos Excitadores , Canal de Sódio Disparado por Voltagem NAV1.8 , Nociceptores , Tratos Espinotalâmicos , Transmissão Sináptica , Animais , Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo , Canal de Sódio Disparado por Voltagem NAV1.8/genética , Nociceptores/metabolismo , Nociceptores/fisiologia , Tratos Espinotalâmicos/metabolismo , Potenciais Pós-Sinápticos Excitadores/fisiologia , Masculino , Transmissão Sináptica/fisiologia , Camundongos , Optogenética , Camundongos Endogâmicos C57BL , Camundongos TransgênicosAssuntos
Hérnia Inguinal , Herniorrafia , Hipertermia Maligna , Humanos , Hérnia Inguinal/cirurgia , Hérnia Inguinal/diagnóstico , Masculino , Herniorrafia/métodos , Herniorrafia/efeitos adversos , Hipertermia Maligna/etiologia , Hipertermia Maligna/diagnóstico , Pessoa de Meia-Idade , Parada Cardíaca/etiologia , Laparoscopia , VirilhaRESUMO
This study investigates the correlation between REM sleep patterns, as measured by the Apple Watch, and depressive symptoms in an undiagnosed population. Employing the Apple Watch for data collection, REM sleep duration and frequency were monitored over a specified period. Concurrently, participants' depressive symptoms were evaluated using standardized questionnaires. The analysis, primarily using Spearman's correlation, revealed noteworthy findings. A significant correlation was observed between an increased REM sleep proportion and higher depressive symptom scores, with a correlation coefficient of 0.702, suggesting a robust relationship. These results highlight the potential of using wearable technology, such as the Apple Watch, in early detection and intervention for depressive symptoms, suggesting that alterations in REM sleep could serve as preliminary indicators of depressive tendencies. This approach offers a non-invasive and accessible means to monitor and potentially preempt the progression of depressive disorders. This study's implications extend to the broader context of mental health, emphasizing the importance of sleep assessment in routine health evaluations, particularly for individuals exhibiting early signs of depressive symptoms.
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Associative learning involves complex interactions of multiple cognitive factors. While adult subjects can articulate these factors verbally, for model animals such as macaques, we rely on behavioral outputs. In our study, we used pupillary responses as an alternative measure to capture these underlying cognitive changes. We recorded the dynamic changes in the pupils of three male macaques when they learned the associations between visual stimuli and reward sizes under the classical Pavlovian experimental paradigm. We found that during the long-term learning process, the gradual changes in the pupillary response reflect the changes in the cognitive state of the animals. The pupillary response can be explained by a linear combination of components corresponding to multiple cognitive factors. These components reflect the impact of visual stimuli on the pupils, the prediction of reward values associated with the visual stimuli, and the macaques' understanding of the current experimental reward rules. The changing patterns of these factors during interday and intraday learning clearly demonstrate the enhancement of current reward-stimulus association and the weakening of previous reward-stimulus association. Our study shows that the dynamic response of pupils can serve as an objective indicator to characterize the psychological changes of animals, understand their learning process, and provide important tools for exploring animal behavior during the learning process.
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Aprendizagem por Associação , Cognição , Condicionamento Clássico , Pupila , Recompensa , Animais , Masculino , Aprendizagem por Associação/fisiologia , Pupila/fisiologia , Condicionamento Clássico/fisiologia , Cognição/fisiologia , Estimulação Luminosa/métodos , Macaca mulatta , Reflexo Pupilar/fisiologiaAssuntos
Laparoscopia , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/cirurgia , Gastrectomia/efeitos adversos , Duodeno/cirurgia , Laparoscopia/efeitos adversos , Estudos Retrospectivos , Complicações Pós-Operatórias/diagnóstico , Complicações Pós-Operatórias/etiologia , Complicações Pós-Operatórias/cirurgiaRESUMO
Stroke damage to the primary visual cortex (V1) causes severe visual deficits, which benefit from perceptual retraining. However, whereas training with high-contrast stimuli can locally restore orientation and motion direction discrimination abilities at trained locations, it only partially restores luminance contrast sensitivity (CS). Recent work revealed that high-contrast discrimination abilities may be preserved in the blind field of some patients early after stroke. Here, we asked if CS for orientation and direction discrimination is similarly preserved inside the blind field, to what extent, and whether it could benefit from a visual training intervention. Thirteen subacute patients (<3 months post-V1-stroke) and 12 chronic patients (>6 months post-V1-stroke) were pre-tested, then trained to discriminate either orientation or motion direction of Gabor patches of progressively lower contrasts as their performance improved. At baseline, more subacute than chronic participants could correctly discriminate the orientation of high-contrast Gabors in their blind field, but all failed to perform this task at lower contrasts, even when 10Hz flicker or motion direction were added. Training improved CS in a greater portion of subacute than chronic participants, but no-one attained normal CS, even when stimuli contained flicker or motion. We conclude that, unlike the near-complete training-induced restoration of high-contrast orientation and motion direction discrimination abilities, V1 damage in adulthood may severely limit the residual visual system's ability to regain normal CS. Our results support the notion that CS involves different neural substrates and computations than those required for orientation and direction discrimination in V1-damaged visual systems.Significance statement Stroke-induced V1 damage in adult humans induces a rapid and severe impairment of contrast sensitivity for orientation and motion direction discrimination in the affected hemifield, although discrimination of high-contrast stimuli can persist for several months. Adaptive training with Gabor patches of progressively lower contrasts improves contrast sensitivity for both orientation and motion discriminations in the blind-field of subacute (<3 months post-stroke) and chronic (>6 months post-stroke) participants; however, it fails to restore normal contrast sensitivity. Nonetheless, more subacute than chronic stroke participants benefit from such training, particularly when discriminating the orientation of static, non-flickering targets. Thus, contrast sensitivity appears critically dependent on processing within V1, with perceptual training displaying limited potential to fully restore it after V1 damage.