Gastric cancer is a malignant tumor with a high incidence in the world, and the incidence rate only increases every year. Because of the loss of mental property caused by surgery and postoperative recovery treatment, it has become a difficult problem for many families to solve. Exploring the factors affecting the recovery of gastrointestinal function after surgery to accelerate the recovery has become one of the important research topics of current medical experts and scholars. The purpose of this article is to explore the factors affecting the recovery of gastrointestinal function after gastrointestinal malignancies. In this paper, firstly through experimental investigation, the fasting time and operation method of patients undergoing gastrointestinal malignant tumor surgery are used as variables to conduct a controlled experiment, and the first defecation time, exhaust time, and bowel sound recovery of the experimental subjects after surgery are recorded. Changes in time and other indicators are compared to verify whether they affect the recovery of gastrointestinal function. Experimental data showed that the recovery time of bowel sounds was 29.10 ± 11.09 h in patients with fasting time less than or equal to 2 days after operation, the time of first exhaustion was 28.75 ± 27.80 h, and the time of first defecation was 54.70 ± 39.40 h. The recovery time of bowel sounds in patients with fasting time longer than 2 days was 40.47 ± 9.40 h, the first exhaust time was 71.40 ± 17.54 h, and the first defecation time was 98.30 ± 28.16 h. Therefore, resuming diet as soon as possible after operation is beneficial to the recovery of gastrointestinal function in patients with gastrointestinal malignancies.

Lung transplant (LTX) can provide a survival benefit and improve physical function for selected patients with advanced pulmonary disease. Sarcopenia is a systemic muscle-failure that can be found in a variety of life stages and disabilities. In this study, we follow the evolution of each variable defined in sarcopenia and the outcomes in LTX recipients with post-transplant sarcopenia.

Autonomic dysfunction may occur during the acute phase of COVID-19. Heart rate variability (HRV) is a useful tool for the assessment of cardiac sympathetic and parasympathetic balance. We aimed to evaluate cardiac autonomic function by using HRV in subjects after recovery from COVID-19 who had previously symptomatic and were followed outpatiently.

This study was aimed at investigating whether quercetin (Q) may improve the recovery of neuromuscular function and biochemical parameters in the 7 days following an eccentric exercise-induced muscle damage (EEIMD). Sixteen men (25.9 ± 3.3 y) ingested Q (1000 mg/day) or placebo (PLA) for 14 days following a double-blind crossover study design. A neuromuscular (NM) test was performed pre-post, 24 h, 48 h, 72 h, 96 h and 7 days after an intense eccentric exercise. The force-velocity relationship of the elbow flexor muscles and their maximal voluntary isometric contraction (MVIC) were recorded simultaneously to the electromyographic signals (EMG). Pain, joint angle, arm circumference, plasma creatine kinase (CK) and lactate-dehydrogenase (LDH) were also assessed. The results showed that Q supplementation significantly attenuated the strength loss compared to PLA. During the recovery, force-velocity relationship and mean fibers conduction velocity (MFCV) persisted significantly less when participants consumed PLA rather than Q, especially at the highest angular velocities (p < 0.02). A greater increase in biomarkers of damage was also evident in PLA with respect to Q. Q supplementation for 14 days seems able to ameliorate the recovery of eccentric exercise-induced weakness, neuromuscular function impairment and biochemical parameters increase probably due to its strong anti-inflammatory and antioxidant action.

[Figure: see text].

Innate lymphoid cells type 2 (ILC2s) play critical homeostatic functions in peripheral tissues. ILC2s reside in perivascular niches and limit atherosclerosis development.

Mechanical ventilation (MV) induces diaphragmatic muscle fiber atrophy and contractile dysfunction (ventilator induced diaphragmatic dysfunction, VIDD). It is unknown how rapidly diaphragm muscle recovers from VIDD once spontaneous breathing is restored. We hypothesized that following extubation, the return to voluntary breathing would restore diaphragm muscle fiber size and contractile function using an established rodent model.

If bilateral thyroid surgery is planned and staged thyroidectomy considered in case of loss of neuromonitoring signal (LOS), a waiting time of 20 minutes is suggested for evaluation of early nerve recovery. This recommendation is based on clinical observations and has not been thoroughly validated experimentally.

To determine which factors affect the recovery of visual function in macula off rhegmatogenous retinal detachment (RRD).

Injury to mature neurons induces downregulated KCC2 expression and activity, resulting in elevated intracellular [Cl-] and depolarized GABAergic signaling. This phenotype mirrors immature neurons wherein GABA-evoked depolarizations facilitate neuronal circuit maturation. Thus, injury-induced KCC2 downregulation is broadly speculated to similarly facilitate neuronal circuit repair. We test this hypothesis in spinal cord motoneurons injured by sciatic nerve crush, using transgenic (CaMKII-KCC2) mice wherein conditional CaMKIIα promoter-KCC2 expression coupling selectively prevents injury-induced KCC2 downregulation. We demonstrate, via an accelerating rotarod assay, impaired motor function recovery in CaMKII-KCC2 mice relative to wild-type mice. Across both cohorts, we observe similar motoneuron survival and re-innervation rates, but differing post-injury reorganization patterns of synaptic input to motoneuron somas-for wild-type, both VGLUT1-positive (excitatory) and GAD67-positive (inhibitory) terminal counts decrease; for CaMKII-KCC2, only VGLUT1-positive terminal counts decrease. Finally, we recapitulate the impaired motor function recovery of CaMKII-KCC2 mice in wild-type mice by administering local spinal cord injections of bicuculline (GABAA receptor blockade) or bumetanide (lowers intracellular [Cl-] by NKCC1 blockade) during the early post-injury period. Thus, our results provide direct evidence that injury-induced KCC2 downregulation enhances motor function recovery and suggest an underlying mechanism of depolarizing GABAergic signaling driving adaptive reconfiguration of presynaptic GABAergic input.

The strategies concerning modification of the complex immune pathological inflammatory environment during acute spinal cord injury remain oversimplified and superficial. Inspired by the acidic microenvironment at acute injury sites, a functional pH-responsive immunoregulation-assisted neural regeneration strategy was constructed. With the capability of directly responding to the acidic microenvironment at focal areas followed by triggered release of the IL-4 plasmid-loaded liposomes within a few hours to suppress the release of inflammatory cytokines and promote neural differentiation of mesenchymal stem cells in vitro, the microenvironment-responsive immunoregulatory electrospun fibers were implanted into acute spinal cord injury rats. Together with sustained release of nerve growth factor (NGF) achieved by microsol core-shell structure, the immunological fiber scaffolds were revealed to bring significantly shifted immune cells subtype to down-regulate the acute inflammation response, reduce scar tissue formation, promote angiogenesis as well as neural differentiation at the injury site, and enhance functional recovery in vivo. Overall, this strategy provided a delivery system through microenvironment-responsive immunological regulation effect so as to break through the current dilemma from the contradiction between immune response and nerve regeneration, providing an alternative for the treatment of acute spinal cord injury.

The goal of the present study was to determine the neuroprotective efficacy of ischemic preconditioning using behavioral, electrophysiological and histological endpoints at various time points up to 90 days postischemia. Gerbils were exposed to a brief, non-injurious episode of forebrain ischemia (1.5 min) on each of 2 consecutive days. Three days following this preconditioning procedure, the animals received a 5 min occlusion. Other animals underwent sham surgery or a 5 min occlusion without preconditioning. Ischemic preconditioning appeared to provide striking histological protection at both rostral (approximately 80% and approximately 67% of sham) and posterior levels of hippocampus (approximately 94% and approximately 78% of sham) at 3 and 10 days survival, respectively. However, in spite of the near normal number of CA1 neurons, animals displayed marked impairments in an open field test of habituation as well as reduced dendritic field potentials in the CA1 area. Additionally, in ischemic animals the basal and apical dendritic regions of CA1 were nearly devoid of the cytoskeletal protein microtubule associated protein 2 (MAP2). Staining levels of MAP2 in preconditioned and sham animals were similar. With increasing survival time, open field behavior as well as CA1 field potential amplitude recovered. Nonetheless, CA1 cell death in ischemic preconditioned animals continued over the 90-day survival period (P<0.05, vs. sham levels). Ischemic preconditioning provides a significant degree of neuroprotection characterized by a complex interplay of protracted cell death and neuroplasticity (recovery of function). These competing processes are best elucidated using a combination of functional and histological endpoints as well as multiple and extended survival times (i.e., greater than 7-10 days).

Recovery from sensory deprivation is slow and incomplete in adult visual cortex. In this study, we show that visual stimulation during locomotion, which increases the gain of visual responses in primary visual cortex, dramatically enhances recovery in the mouse. Excitatory neurons regained normal levels of response, while narrow-spiking (inhibitory) neurons remained less active. Visual stimulation or locomotion alone did not enhance recovery. Responses to the particular visual stimuli viewed by the animal during locomotion recovered, while those to another normally effective stimulus did not, suggesting that locomotion promotes the recovery only of the neural circuits that are activated concurrent with the locomotion. These findings may provide an avenue for improving recovery from amblyopia in humans.DOI: http://dx.doi.org/10.7554/eLife.02798.001.

Hurdles in the treatment of retinal degeneration include managing the functional rewiring of surviving photoreceptors and integration of any newly added cells into the remaining second-order retinal neurons. Zebrafish are the premier genetic model for such questions, and we present two new transgenic lines allowing us to contrast vision loss and recovery following conditional ablation of specific cone types: UV or blue cones. The ablation of each cone type proved to be thorough (killing 80% of cells in each intended cone class), specific, and cell-autonomous. We assessed the loss and recovery of vision in larvae via the optomotor behavioural response (OMR). This visually mediated behaviour decreased to about 5% or 20% of control levels following ablation of UV or blue cones, respectively (P<0.05). We further assessed ocular photoreception by measuring the effects of UV light on body pigmentation, and observed that photoreceptor deficits and recovery occurred (p<0.01) with a timeline coincident to the OMR results. This corroborated and extended previous conclusions that UV cones are required photoreceptors for modulating body pigmentation, addressing assumptions that were unavoidable in previous experiments. Functional vision recovery following UV cone ablation was robust, as measured by both assays, returning to control levels within four days. In contrast, robust functional recovery following blue cone ablation was unexpectedly rapid, returning to normal levels within 24 hours after ablation. Ablation of cones led to increased proliferation in the retina, though the rapid recovery of vision following blue cone ablation was demonstrated to not be mediated by blue cone regeneration. Thus rapid visual recovery occurs following ablation of some, but not all, cone subtypes, suggesting an opportunity to contrast and dissect the sources and mechanisms of outer retinal recovery during cone photoreceptor death and regeneration.

Peripheral nerve injury (PNI) can result in neurodegenerative changes leading to motor, sensory and autonomic dysfunction. Injury to the rat sciatic nerve is used to model pathophysiologic processes following PNI and assess the efficacy of therapeutic interventions. Frequently, temporal changes in the sciatic functional index (SFI), a measure of sensorimotor integration are measured in rats to assess functional recovery following sciatic nerve injury. However, multiple rat strains and behavioral endpoints have been employed to investigate pathophysiology of PNI and impact of therapeutic intervention on recovery, raising the possibility that rat strain may influence the outcome of such studies.

Following the discovery of Mirror Neuron System (MNS), Action Observation Training (AOT) has become an emerging rehabilitation tool to improve motor functions both in neurologic and orthopedic pathologies. The aim of this study is to present the state of the art on the use of AOT in experimental studies to improve motor function recovery in any disease. The research was performed in PubMed, PEDro, Embase, CINAHL and Cochrane Central Register of Controlled Trials (last search July 2015). Randomized controlled trials (RCTs) that analyse efficacy of AOT for recovery of motor functions, regardless of the kind of disease, were retrieved. The validity of the included studies was assessed using the Cochrane Collaboration tool for evaluating risk of bias. Twenty RCTs were eligible. Four studies showed AOT efficacy in improving upper limb functional recovery in participants with chronic stroke, two studies in sub-acute ones and one in acute ones. Six articles suggested its effectiveness on walking performance in chronic stroke individuals, and three of them also suggested an efficacy in improving balance. The use of AOT was also recommended in individuals with Parkinson's disease to improve autonomy in activities of daily living, to improve spontaneous movement rate of self-paced finger movements and to reduce freezing of gait. Other two studies also indicated that AOT improves upper limb motor function in children with cerebral palsy. The last two studies, showed the efficacy of AOT in improving motor recovery in postsurgical orthopedic participants. Overall methodological quality of the considered studies was medium. The majority of analyzed studies suggest the efficacy of AOT, in addition to conventional physiotherapy, to improve motor function recovery in individuals with neurological and orthopedic diseases. However, the application of AOT is very heterogeneous in terms of diseases and outcome measures assessed, which makes it difficult to reach, to date, any conclusion that might influence clinical practice.

Although physical exercise is an effective strategy for treatment of ischemic stroke, the underlying protective mechanisms are still not well understood. It has been recently demonstrated that neural progenitor cells play a vital role in the recovery of neurological function (NF) through differentiation into mature neurons. In the current study, we observed that physical exercise significantly reduced the infarct size and improved damaged neural functional recovery after an ischemic stroke. Furthermore, we found that the treatment not only exhibited a significant increase in the number of neural progenitor cells and neurons but also decreased the apoptotic cells in the peri-infarct region, compared to a control in the absence of exercise. Importantly, the insulin-like growth factor-1 (IGF-1)/Akt signaling pathway was dramatically activated in the peri-infarct region of rats after physical exercise training. Therefore, our findings suggest that physical exercise directly influences the NF recovery process by increasing neural progenitor cell count via activation of the IGF-1/Akt signaling pathway.

The plasticity of brain function, especially reorganization after stroke or sensory loss, has been investigated extensively. Based upon its special characteristics, the olfactory system allows the investigation of functional networks in patients with smell loss, as it holds the unique ability to be activated by the sensorimotor act of sniffing, without the presentation of an odor. In the present study, subjects with chronic peripheral smell loss and healthy controls were investigated using functional magnetic resonance imaging (fMRI) to compare functional networks in one of the major olfactory areas before and after an olfactory training program. Data analysis revealed that olfactory training induced alterations in functional connectivity networks. Thus, olfactory training is capable of inducing neural reorganization processes. Furthermore, these findings provide evidence for the underlying neural mechanisms of olfactory training.

Promotion of new blood vessel formation is a new strategy for treating ischemic stroke. Non-coding miRNAs have been recently considered potential therapeutic targets for ischemic stroke. miR-181b has been shown to promote angiogenesis in hypoxia and traumatic brain injury model, while its effect on ischemic stroke remains elusive. In this study, we found that overexpression of miR-181b in brain microvascular endothelial cells subjected to oxygen-glucose deprivation in vitro restored cell proliferation and enhanced angiogenesis. In rat models of focal cerebral ischemia, overexpression of miR-181b reduced infarction volume, promoted angiogenesis in ischemic penumbra, and improved neurological function. We further investigated the molecular mechanism by which miR-181b participates in angiogenesis after ischemic stroke and found that miR-181b directly bound to the 3'-UTR of phosphatase and tensin homolog (PTEN) mRNA to induce PTEN downregulation, leading to activation of the protein kinase B (Akt) pathway, upregulated expression of vascular endothelial growth factors, down-regulated expression of endostatin, and promoted angiogenesis. Taken together, these results indicate that exogenous miR-181b exhibits neuroprotective effects on ischemic stroke through activating the PTEN/Akt signal pathway and promoting angiogenesis.

Adult mammalian injured axons regenerate over short-distance in the peripheral nervous system (PNS) while the axons in the central nervous system (CNS) are unable to regrow after injury. Here, we demonstrated that Lycium barbarum polysaccharides (LBP), purified from Wolfberry, accelerated long-distance axon regeneration after severe peripheral nerve injury (PNI) and optic nerve crush (ONC). LBP not only promoted intrinsic growth capacity of injured neurons and function recovery after severe PNI, but also induced robust retinal ganglion cell (RGC) survival and axon regeneration after ONC. By using LBP gene expression profile signatures to query a Connectivity map database, we identified a Food and Drug Administration (FDA)-approved small-molecule glycopyrrolate, which promoted PNS axon regeneration, RGC survival and sustained CNS axon regeneration, increased neural firing in the superior colliculus, and enhanced visual target re-innervations by regenerating RGC axons leading to a partial restoration of visual function after ONC. Our study provides insights into repurposing of FDA-approved small molecule for nerve repair and function recovery.