Enhancement of Antioxidant Capacity and Phenolic Composition in Pine Pollen by Using Macro-Fungi Fermentation.

Fermentation is an effective method to enhance the bioactivity and bioavailability of bioactive compounds in plant foods. In this study, the effects of fermentations with Wolfiporia cocos, Morchella sp., and Ganoderma lingzhi on the total phenolics, total flavonoids, monomeric phenolic compounds, and antioxidant activities of fermented pine pollen were investigated.

Skeleton Enhanced Dispersed Lubricant Particle Based Triboelectric Nanogenerator for Droplet Energy Harvesting.

Liquid-solid triboelectric nanogenerators (LS-TENGs) can be widely utilized for droplet energy harvesting, in which slippery modification of triboelectric layer is crucial for output enhancement. However, classical slippery lubricant-infused surfaces suffer from the blocked triboelectric effect and the poor durability. Herein, a controllable phase separation method is reported to disperse skeleton-enhanced lubricant particles on triboelectric layer, leading to the development of a stretchable slippery triboelectric nanogenerator (SS-TENG) based on a modified slippery triboelectric layer and a liquid metal electrode.

Effects of global genetic deficiency in aged mice following experimental ischemic stroke.

Besides the loss of blood and oxygen reaching the ischemic tissue, many secondary effects of ischemic stroke can cause additional tissue damage, including inflammation, oxidative stress, and proteomic disturbances. Receptor-interacting serine/threonine kinase 2 (RIPK2) is an important mediator in the post-stroke inflammatory cascade that responds to signals and molecular patterns released by dead or dying cells in the ischemic area. We hypothesize that RIPK2 signaling worsens injury and neurological recovery post-stroke and that global deletion of is protective following ischemic stroke in aged mice.

Effects of Global Genetic Deficiency in Aged Mice following Experimental Ischemic Stroke.

Besides the loss of blood and oxygen reaching the ischemic tissue, many secondary effects of ischemic stroke can cause additional tissue death, including inflammation, oxidative stress, and proteomic disturbances. Receptor-interacting serine/threonine kinase 2 (RIPK2) is an important mediator in the post-stroke inflammatory cascade that responds to signals and molecular patterns released by dead or dying cells in the ischemic area. We hypothesize that RIPK2 signaling worsens injury and neurological recovery post-stroke and that global deletion of will be protective following ischemic stroke in aged mice.

Application of enhanced recovery after surgery in pediatric patients with obstructive sleep apnea-hypopnea syndrome.

BackgroundEnhanced Recovery After Surgery (ERAS) has demonstrated effectiveness in accelerating recovery and reducing complications across surgical fields, with limited application in Ear-Nose-Throat surgeries. Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS), a prevalent condition affecting pediatric patients, calls for innovative management due to its impact on health and the need for surgical interventions like tonsillectomy.ObjectiveThe present study aimed to investigate the efficacy of ERAS in pediatric patients with OSAHS.

Changes in adropin levels in brain and peripheral tissues with aging.

Adropin is a bioactive peptide found in the brain and various peripheral tissues. Evidence suggests that aging significantly decreases brain adropin levels, and interventions that elevate adropin may help alleviate age-related neurological disorders such as ischemic stroke and cognitive decline. However, the impact of aging on peripheral tissue adropin levels and its relationship with the neural recognition molecule NB-3/contactin-6 in the brain remains unclear.

RIPK2 Is Crucial for the Microglial Inflammatory Response to Bacterial Muramyl Dipeptide but Not to Lipopolysaccharide.

Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a kinase that is essential in modulating innate and adaptive immune responses. As a downstream signaling molecule for nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs), it is implicated in the signaling triggered by recognition of microbe-associated molecular patterns by NOD1/2 and TLRs. Upon activation of these innate immune receptors, RIPK2 mediates the release of pro-inflammatory factors by activating mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB).

RIPK2 is crucial for the microglial inflammatory response to bacterial muramyl dipeptide but not to lipopolysaccharide.

Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a kinase that plays an essential role in the modulation of innate and adaptive immune responses. As a downstream signaling molecule for nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs), it is implicated in the signaling triggered by recognition of microbe-associated molecular patterns by NOD1/2 and TLRs. Upon activation of these innate immune receptors, RIPK2 mediates the release of pro-inflammatory factors by activating mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB).

Pharmacological inhibition of receptor-interacting protein kinase 2 (RIPK2) elicits neuroprotective effects following experimental ischemic stroke.

Ischemic stroke induces a debilitating neurological insult, where inflammatory processes contribute greatly to the expansion and growth of the injury. Receptor-interacting protein kinase 2 (RIPK2) is most well-known for its role as the obligate kinase for NOD1/2 pattern recognition receptor signaling and is implicated in the pathology of various inflammatory conditions. Compared to a sham-operated control, ischemic stroke resulted in a dramatic increase in the active, phosphorylated form of RIPK2, indicating that RIPK2 may be implicated in the response to stroke injury.

Functional regulation of microglia by vitamin B12 alleviates ischemic stroke-induced neuroinflammation in mice.

Ischemic stroke is the second leading cause of death and disability worldwide, and efforts to prevent stroke, mitigate secondary neurological damage, and promote neurological recovery remain paramount. Recent findings highlight the critical importance of microbiome-related metabolites, including vitamin B12 (VB12), in alleviating toxic stroke-associated neuroinflammation. Here, we showed that VB12 tonically programmed genes supporting microglial cell division and activation and critically controlled cellular fatty acid metabolism in homeostasis.

Receptor-interacting protein kinase 2 (RIPK2) profoundly contributes to post-stroke neuroinflammation and behavioral deficits with microglia as unique perpetrators.

Background: Receptor-interacting protein kinase 2 (RIPK2) is a serine/threonine kinase whose activity propagates inflammatory signaling through its association with pattern recognition receptors (PRRs) and subsequent TAK1, NF-κB, and MAPK pathway activation. After stroke, dead and dying cells release a host of damage-associated molecular patterns (DAMPs) that activate PRRs and initiate a robust inflammatory response. We hypothesize that RIPK2 plays a damaging role in the progression of stroke injury by enhancing the neuroinflammatory response to stroke and that global genetic deletion or microglia-specific conditional deletion of Ripk2 will be protective following ischemic stroke.

Overexpression of complement C5a indicates poor survival and therapeutic response in metastatic renal cell carcinoma.

Introduction: Complement C5a is an important component of the innate immune system. An increasing number of reports have revealed the relevance of C5a in tumor progression; however, its exact role in metastatic renal cell carcinoma (mRCC) remains unknown.

Methods: We evaluated C5a expression in tumor tissue microarrays of 231 mRCC patients and analyzed the relationship between C5a levels and clinical outcomes, and the expression of epithelial-mesenchymal transition (EMT)-related proteins, programmed cell death protein 1 (PD-1), and programmed cell death-ligand 1 (PD-L1).

Neuroprotection by the cannabidiol aminoquinone VCE-004.8 in experimental ischemic stroke in mice.

Synthetic cannabidiol (CBD) derivative VCE-004.8 is a peroxisome proliferator-activated receptor gamma (PPARγ) and cannabinoid receptor type 2 (CB) dual agonist with hypoxia mimetic activity. The oral formulation of VCE-004.

Protective roles of adropin in neurological disease.

Adropin is a highly conserved secreted peptide encoded by the Energy Homeostasis Associated gene (). It is expressed in many tissues throughout the body, including the liver and brain, and plays a crucial role in maintaining lipid homeostasis and regulating insulin sensitivity. Adropin also participates in several other pathophysiological processes of multiple central nervous system (CNS) diseases.

[Pseudotargeted metabolomics analysis of pine pollen intervention in the liver of premature ovarian failure rats].

Premature ovarian failure (POF) is a prevalent gynecological disease. In traditional Chinese medicine, it is believed that POF is directly related to abnormal function of the liver and kidneys. As such, regulation of the liver metabolism through the use of medicinal and edible substances is important for the treatment of POF.

Ischemic Stroke Impacts the Gut Microbiome, Ileal Epithelial and Immune Homeostasis.

Ischemic stroke critically impacts neurovascular homeostasis, potentially resulting in neurological disorders. However, the mechanisms through which stroke-induced inflammation modifies the molecular and metabolic circuits, particularly in ileal epithelial cells (iECs), currently remain elusive. Using multiomic approaches, we illustrated that stroke impaired the ileal microbiome and associated metabolites, leading to increased inflammatory signals and altered metabolites, potentially deteriorating the iEC homeostasis.

Therapeutic Benefits of Adropin in Aged Mice After Transient Ischemic Stroke via Reduction of Blood-Brain Barrier Damage.

Background: Adropin is a peptide encoded by the energy homeostasis-associated gene () that is highly expressed in the brain. Aging and stroke are associated with reduced adropin levels in the brain and plasma. We showed that treatment with synthetic adropin provides long-lasting neuroprotection in permanent ischemic stroke.

An Unexplored Role for MMP-7 (Matrix Metalloproteinase-7) in Promoting Gut Permeability After Ischemic Stroke.

Poststroke infections are common complications of stroke and are highly associated with poor outcomes for patients. Stroke induces profound immunodepression coupled with alterations to autonomic signaling, which together render the body more susceptible to infection from without (nosocomial/community-acquired infection) and from within (commensal bacterial infection). Critical to the hypothesis of commensal infection is the phenomenon of poststroke gut permeability and gut dysbiosis.

Conservative treatment of urinary fistula: Case report.

Radical cystectomy is the gold standard treatment for muscular invasive bladder cancer. Bricker surgery is the most common technique used for urinary diversion; however, troublesome complications such as postoperative anastomotic stenosis or fistula may occur. The case of a patient who had a urinary fistula after Bricker surgery performed at our hospital, is described.

Targeted BRD4 protein degradation by dBET1 ameliorates acute ischemic brain injury and improves functional outcomes associated with reduced neuroinflammation and oxidative stress and preservation of blood-brain barrier integrity.

Bromodomain-containing protein 4 (BRD4), a member of the bromodomain and extra-terminal domain (BET) protein family, plays a crucial role in regulating inflammation and oxidative stress that are tightly related to stroke development and progression. Consequently, BRD4 blockade has attracted increasing interest for associated neurological diseases, including stroke. dBET1 is a novel and effective BRD4 degrader through the proteolysis-targeting chimera (PROTAC) strategy.

Neurovascular protection by adropin in experimental ischemic stroke through an endothelial nitric oxide synthase-dependent mechanism.

Adropin is a highly-conserved peptide that has been shown to preserve endothelial barrier function. Blood-brain barrier (BBB) disruption is a key pathological event in cerebral ischemia. However, the effects of adropin on ischemic stroke outcomes remain unexplored.

Role of BET Proteins in Inflammation and CNS Diseases.

Bromodomain and extra-terminal domain (BET) proteins consist of four mammalian members (BRD2, BRD3, BRD4, and BRDT), which play a pivotal role in the transcriptional regulation of the inflammatory response. Dysregulated inflammation is a key pathological process in various CNS disorders through multiple mechanisms, including NF-κB and Nrf2 pathways, two well-known master regulators of inflammation. A better mechanistic understanding of the BET proteins' role in regulating the inflammatory process is of great significance since it could reveal novel therapeutic targets to reduce neuroinflammation associated with many CNS diseases.

Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice.

The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias.

Altered cellular localisation and expression, together with unconventional protein trafficking, of prion protein, PrP, in type 1 diabetes.

Aims/hypothesis: Normal cellular prion protein (PrP) is a conserved mammalian glycoprotein found on the outer plasma membrane leaflet through a glycophosphatidylinositol anchor. Although PrP is expressed by a wide range of tissues throughout the body, the complete repertoire of its functions has not been fully determined. The misfolded pathogenic isoform PrP (the scrapie form of PrP) is a causative agent of neurodegenerative prion diseases.