Activity

re is associated with a lower risk of dying in hospital. Therefore, patients who are cared for by physicians with higher rates of referral to palliative care are less likely to die in hospital and more likely to die at home. Standardizing referral to palliative care may help reduce physician-level variation as a barrier to access.

Pediatric intensive care units (PICUs) are increasingly staffed with advanced practice providers (APPs), supplementing traditional physician staffing models.

We evaluate the effect of APP-inclusive staffing models on clinical outcomes and resource utilization in US PICUs.

Retrospective cohort study of children admitted to PICUs in 9 states in 2016 using the Healthcare Cost and Utilization Project’s State Inpatient Databases. PICU staffing models were assessed using a contemporaneous staffing survey. We used multivariate regression to examine associations between staffing models with and without APPs and outcomes.

The primary outcome was in-hospital mortality. Secondary outcomes included odds of hospital acquired conditions and ICU and hospital lengths of stay.

The sample included 38,788 children in 40 PICUs. Patients admitted to PICUs with APP-inclusive staffing were younger (6.1±5.9 vs. 7.1±6.2 y) and more likely to have complex chronic conditions (64% vs. 43%) and organ failure on admission (25% vysician-only staffing. Further research can inform APP integration strategies which optimize outcomes.In the conventional view a muscle is composed of intermediate structures before its further division into microscopic muscle fibers. Our experiments in mice have confirmed this intermediate structure is composed of the lamella cluster formed by motor endplates, the innervating nerve branches and the corresponding muscle fibers, which can be viewed as an independent structural and functional unit. In this study, we verified the presence of these muscle construction units in rabbits. The results showed that the muscular branch of the femoral nerve sent out 4-6 nerve branches into the quadriceps and the tibial nerve sent out 4-7 nerve branches into the gastrocnemius. When each nerve branch of the femoral nerve was stimulated from the most lateral to the medial, the contraction of the lateral muscle, intermediate muscle and medial muscle of the quadriceps could be induced by electrically stimulating at least one nerve branch. When stimulating each nerve branch of the tibial nerve from the lateral to the medial, the muscle contraction of the lateral muscle 1, lateral muscle 2, lateral muscle 3 and medial muscle of the gastrocnemius could be induced by electrically stimulating at least one nerve branch. Electrical stimulation of each nerve branch resulted in different electromyographical waves recorded in different muscle subgroups. Hematoxylin-eosin staining showed most of the nerve branches around the neuromuscular junctions consisted of one individual neural tract, a few consisted of two or more neural tracts. The muscles of the lower limb in the rabbit can be subdivided into different muscle subgroups, each innervated by different nerve branches, thereby allowing much more complex muscle activities than traditionally stated. Together, the nerve branches and the innervated muscle subgroups can be viewed as an independent structural and functional unit. This study was approved by the Animal Ethics Committee of Peking University People’s Hospital (approval No. 2019PHE027) on October 20, 2019.Our previous RNA sequencing study showed that the long non-coding RNA ischemia-related factor Vof-16 (lncRNA Vof-16) was upregulated after spinal cord injury, but its precise role in spinal cord injury remains unclear. mTOR cancer Bioinformatics predictions have indicated that lncRNA Vof-16 may participate in the pathophysiological processes of inflammation and apoptosis. PC12 cells were transfected with a pHBLV-U6-MCS-CMV-ZsGreen-PGK-PURO vector to express an lncRNA Vof-16 knockdown lentivirus and a pHLV-CMVIE-ZsGree-Puro vector to express an lncRNA Vof-16 overexpression lentivirus. The overexpression of lncRNA Vof-16 inhibited PC12 cell survival, proliferation, migration, and neurite extension, whereas lncRNA Vof-16 knockdown lentiviral vector resulted in the opposite effects in PC12 cells. Western blot assay results showed that the overexpression of lncRNA Vof-16 increased the protein expression levels of interleukin 6, tumor necrosis factor-α, and Caspase-3 and decreased Bcl-2 expression levels in PC12 cells. Furthery. The experiments were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China.In Alzheimer’s disease and ischemic stroke, intranasal insulin can act as a neuroprotective agent. However, whether intranasal insulin has a neuroprotective effect in intracerebral hemorrhage and its potential mechanisms remain poorly understood. In this study, a mouse model of autologous blood-induced intracerebral hemorrhage was treated with 0.5, 1, or 2 IU insulin via intranasal delivery, twice per day, until 24 or 72 hours after surgery. Compared with saline treatment, 1 IU intranasal insulin treatment significantly reduced hematoma volume and brain edema after cerebral hemorrhage, decreased blood-brain barrier permeability and neuronal degeneration damage, reduced neurobehavioral deficits, and improved the survival rate of mice. Expression levels of p-AKT and p-GSK3β were significantly increased in the perihematoma tissues after intranasal insulin therapy. Our findings suggest that intranasal insulin therapy can protect the neurological function of mice after intracerebral hemorrhage through the AKT/GSK3β signaling pathway. The study was approved by the Ethics Committee of the North Sichuan Medical College of China (approval No. NSMC(A)2019(01)) on January 7, 2019.Lycium barbarum (LB) is a traditional Chinese medicine that has been demonstrated to exhibit a wide variety of biological functions, such as antioxidation, neuroprotection, and immune modulation. One of the main mechanisms of Alzheimer’s disease is that microglia activated by amyloid beta (Aβ) transform from the resting state to an M1 state and release pro-inflammatory cytokines to the surrounding environment. In the present study, immortalized microglial cells were pretreated with L. barbarum extract for 1 hour and then treated with oligomeric Aβ for 23 hours. The results showed that LB extract significantly increased the survival of oligomeric Aβ-induced microglial cells, downregulated the expression of M1 pro-inflammatory markers (inducible nitric oxide synthase, tumor necrosis factor α, interleukin-6, and interleukin-1β), and upregulated the expression of M2 anti-inflammatory markers (arginase-1, chitinase-like protein 3, and interleukin-4). LB extract also inhibited the oligomeric Aβ-induced secretion of tumor necrosis factor α, interleukin-6, and interleukin-1β in microglial cells. The results of in vitro cytological experiments suggest that, in microglial cells, LB extract can inhibit oligomeric Aβ-induced M1 polarization and concomitant inflammatory reactions, and promote M2 polarization.Mesenchymal stem cell (MSC) transplantation is a promising treatment strategy for spinal cord injury, but immunological rejection and possible tumor formation limit its application. The therapeutic effects of MSCs mainly depend on their release of soluble paracrine factors. Exosomes are essential for the secretion of these paracrine effectors. Bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) can be substituted for BMSCs in cell transplantation. However, the underlying mechanisms remain unclear. In this study, a rat model of T10 spinal cord injury was established using the impact method. Then, 30 minutes and 1 day after spinal cord injury, the rats were administered 200 μL exosomes via the tail vein (200 μg/mL; approximately 1 × 106 BMSCs). Treatment with BMSC-EXOs greatly reduced neuronal cell death, improved myelin arrangement and reduced myelin loss, increased pericyte/endothelial cell coverage on the vascular wall, decreased blood-spinal cord barrier leakage, reduced caspase 1 expression, inhibited interleukin-1β release, and accelerated locomotor functional recovery in rats with spinal cord injury. In the cell culture experiment, pericytes were treated with interferon-γ and tumor necrosis factor-α. Then, Lipofectamine 3000 was used to deliver lipopolysaccharide into the cells, and the cells were co-incubated with adenosine triphosphate to simulate injury in vitro. Pre-treatment with BMSC-EXOs for 8 hours greatly reduced pericyte pyroptosis and increased pericyte survival rate. These findings suggest that BMSC-EXOs may protect pericytes by inhibiting pyroptosis and by improving blood-spinal cord barrier integrity, thereby promoting the survival of neurons and the extension of nerve fibers, and ultimately improving motor function in rats with spinal cord injury. All protocols were conducted with the approval of the Animal Ethics Committee of Zhengzhou University on March 16, 2019.Spinal cord injury (SCI) is associated with high production and excessive accumulation of pathological 4-hydroxy-trans-2-nonenal (4-HNE), a reactive aldehyde, formed by SCI-induced metabolic dysregulation of membrane lipids. Reactive aldehyde load causes redox alteration, neuroinflammation, neurodegeneration, pain-like behaviors, and locomotion deficits. Pharmacological scavenging of reactive aldehydes results in limited improved motor and sensory functions. In this study, we targeted the activity of mitochondrial enzyme aldehyde dehydrogenase 2 (ALDH2) to detoxify 4-HNE for accelerated functional recovery and improved pain-like behavior in a male mouse model of contusion SCI. N-(1,3-benzodioxol-5-ylmethyl)-2,6-dichlorobenzamide (Alda-1), a selective activator of ALDH2, was used as a therapeutic tool to suppress the 4-HNE load. SCI was induced by an impactor at the T9-10 vertebral level. Injured animals were initially treated with Alda-1 at 2 hours after injury, followed by once-daily treatment with Alda-1 foneurodegeneration, promotes the neurorepair process, and improves functional outcomes. Consequently, we suggest that Alda-1 may have therapeutic potential for the treatment of human SCI. Animal procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of MUSC (IACUC-2019-00864) on December 21, 2019.Excess extracellular glutamate leads to excitotoxicity, which induces neuronal death through the overactivation of N-methyl-D-aspartate receptors (NMDARs). Excitotoxicity is thought to be closely related to various acute and chronic neurological disorders, such as stroke and Alzheimer’s disease. Polygalasaponin F (PGSF) is a triterpenoid saponin monomer that can be isolated from Polygala japonica, and has been reported to protect cells against apoptosis. To investigate the mechanisms underlying the neuroprotective effects of PGSF against glutamate-induced cytotoxicity, PGSF-pretreated hippocampal neurons were exposed to glutamate for 24 hours. The results demonstrated that PGSF inhibited glutamate-induced hippocampal neuron death in a concentration-dependent manner and reduced glutamate-induced Ca2+ overload in the cultured neurons. In addition, PGSF partially blocked the excess activity of NMDARs, inhibited both the downregulation of NMDAR subunit NR2A expression and the upregulation of NMDAR subunit NR2B expression, and upregulated the expression of phosphorylated cyclic adenosine monophosphate-responsive element-binding protein and brain-derived neurotrophic factor.