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The infusion of Serjania erecta Radlk (Sapindaceae) (popular name "cipó-cinco-folhas") leaves is used in popular medicine to treat back pain. The anti-inflammatory, anti-hyperalgesic and anti-nociceptive properties of the ethanolic extract from S. erecta leaves (EESE) has not been yet completely clarified.

Multiple sclerosis (MS) is the most common demyelinating disease that attacks the central nervous system. Dietary intake of cuprizone (CPZ) produces demyelination resembling that of patients with MS. Given the role of the vagus nerve in gut-microbiota-brain axis in development of MS, we performed this study to investigate whether subdiaphragmatic vagotomy (SDV) affects demyelination in CPZ-treated mice. SDV significantly ameliorated demyelination and microglial activation in the brain compared with sham-operated CPZ-treated mice. Furthermore, 16S ribosomal RNA analysis revealed that SDV significantly improved the abnormal gut microbiota composition of CPZ-treated mice. An untargeted metabolomic analysis demonstrated that SDV significantly improved abnormal blood levels of metabolites in CPZ-treated mice compared with sham-operated CPZ-treated mice. Notably, there were correlations between demyelination or microglial activation in the brain and the relative abundance of several microbiome populations, suggesting a link between gut microbiota and the brain. There were also correlations between demyelination or microglial activation in the brain and blood levels of metabolites. Together, these data suggest that CPZ produces demyelination in the brain through the gut-microbiota-brain axis via the subdiaphragmatic vagus nerve.

In advanced cancer, although performance status (PS), systemic inflammatory response and nutritional status are known to have prognostic value, geographical variations and sociodemographic indexes may also impact survival. This study compares validated prognostic factors in two international cohorts and establishes a prognostic framework for treatment.

Chronic wounds fail to heal through the three normal stages of healing (inflammatory, proliferative, and remodelling), resulting in a chronic tissue injury that is not repaired within the average time limit. Patients suffering from type 1 and type 2 diabetes are prone to develop diabetic foot ulcers (DFUs), which commonly develop into chronic wounds that are non treatable with conventional therapies. DFU develops due to various risk factors, such as peripheral neuropathy, peripheral vascular disease, arterial insufficiency, foot deformities, trauma and impaired resistance to infection. DFUs have gradually become a major problem in the health care system worldwide. In this review, we not only focus on the pathogenesis of DFU but also comprehensively summarize the outcomes of preclinical and clinical studies thus far and the potential therapeutic mechanism of bone marrow-derived mesenchymal stem cells (BMSCs) for the treatment of DFU. Based on the published results, BMSC transplantation can contribute to wound healing through growth factor secretion, anti-inflammation, differentiation into tissue-specific cells, neovascularization, re-epithelialization and angiogenesis in DFUs. Moreover, clinical trials showed that BMSC treatment in patients with diabetic ulcers improved ulcer healing and the ankle-brachial index, ameliorated pain scores, and enhanced claudication walking distances with no reported complications. In conclusion, although BMSC transplantation exhibits promising therapeutic potential in DFU treatment, additional studies should be performed to confirm their efficacy and long-term safety in DFU patients.

Non steroidal anti-inflammatory drugs (NSAIDs) are those of the most common over the counter (OTC) medications widely used by millions of people every day. Unfortunately, despite their popularity those drugs can cause serious side effect in the digestive system (ulcers, bleeding, and pain). These inconveniences are caused by the changes in the structures of the outer phospholipid layers of gastric mucus and mucosa. As a result the H ions from the stomach acid can pass easily through these natural protective barriers and damage the epithelial cells which causes ulcers and bleeding. Chitosan as a polysaccharide known for its unique biocompatibility, drug delivery possibilities and wound healing effect has been chosen to examine if it can induce the reduction of undesirable effects of naproxen. This paper focuses on the interactions of the naproxen with a model biological membrane with and without the presence of chitosan. Applying the Langmuir technique coupled with the surface potential measurements and the Brewster angle microscope imaging allowed to characterize successfully examined systems in terms of the monolayer fluidity changes, compressibility, thickness, stability, electric properties and morphology. The results proved that the presence of naproxen alters the mechanical and electrical properties of the model membrane depending on its surface pressure. Moreover, the addition of chitosan to the lipid-drug system causes significant changes in the properties of the layer, i.e. a reduction of its compressibility, thickness and morphology modification. Nevertheless, chitosan suppressed some changes induced by naproxen such as alteration of the dipole moment and film stability.

Corticotropin releasing factor (CRF) receptors have been implicated in stress-induced hyperalgesia. The present study examined the role of CRF receptors Type 1&2 (CRFR1, CRFR2) in stress-induced bladder hyperalgesia in female rats by quantifying changes in receptor and agonist content following chronic (CFS, 7 daily episodes), acute (AFS, single episode) and control (NFS, no episodes) footshock protocols. ELISAs demonstrated that CFS lead to an increase in spinal thoracolumbar and lumbosacral spinal cord CRFR2 content and a decrease in lumbosacral spinal cord CRFR1 content. Content of the endogenous CRFR2 agonist, urocortin 2, was also increased in lumbosacral spinal cord and bladder tissues of CFS-pretreated rats, but urocortin 3 was decreased. Correlative single unit studies of lumbosacral dorsal horn neurons excited by bladder distension, in anesthetized rats that had undergone CFS, AFS or NFS protocols, used a before-after methodology with administration of a CRFR1 antagonist (antalarmin, 24 μg), CRFR2 antagonist (aSVG30, 12 μg) or normal saline topically to the exposed spinal cord following primary characterization. aSVG30 produced a reduction of neuronal responses evoked by bladder distension in CFS-pretreated rats but no statistically significant effects of aSVG30, antalarmin or vehicle were noted in other groups tested with the exception that antalarmin had an inhibitory effect on spontaneous activity in NFS-pretreated rats. The present findings are consistent with previous experiments using reflex responses to bladder distension as endpoints and further support a role for CRFR2-related mechanisms in stress-induced bladder hypersensitivity. This suggests CRFR2 antagonists may have efficacy in the treatment of bladder pain.

Post-surgical bone defects require new alternative approaches for a better healing process. For this matter, photobiomodulation therapy (PBMT) has been used in order to improve the process of healing, pain, and inflammation reduction and tissue rejuvenation. This study is set to evaluate the effect of PBMT on angiogenic and inflammatory factors for bone regeneration in rat post-surgical cranial defects. Thirty male Wistar rats were distributed accidentally into two groups (Subdivided into 3 groups according to their follow-up durations). During operation, an 8-mm critical-sized calvarial defect was made in each rat. A continuous diode laser was used (power density 100 mW/cm, wavelength 810 nm, the energy density of 4 J/cm). Bone samples were assessed histomorphometrically and histologically after hematoxylin and eosin (H&E) staining. ALP, PTGIR, OCN, and IL-1 levels were measured by RT-PCR. VEGF expression was studied by immunohistochemistry analysis. The level of IL-1 expression decreased significantly in the PBMT group compared to the control after 7 days (p < 0.05), while, the PTGIR level was improved significantly compared to the control group after 7 days. Furthermore, levels of OCN and ALP improved after PBM use; however, the alterations were not statistically meaningful (p > 0.05). Evaluation with IHC displayed a significant rise in VEGF expression after 3 days in the PBMT group compared to the control (p > 0.05). In this study's conditions, the results showed a meaningful alteration in osteogenic, inflammatory, and angiogenic mediators in post-surgical calvarial defect following PBMT. It appears that PBM can accelerate angiogenesis in the bone healing procedure which can be helpful in bone tissue engineering.

Chronic itch is the most prominent feature of atopic dermatitis (AD), and antihistamine treatment is often less effective in clinical pruritus severity in AD. Multiple studies have shown that histamine-independent itch pathways is thought to predominate in AD-induced chronic itch. Mas-related G-protein-coupled receptor (Mrgpr) A3 sensory neurons have been identified as one of the major itch-sensing neuron populations, and transient receptor potential (TRP) channel A1 is the key downstream of MrgprA3 mediated histamine-independent itch. MrgprA3-TRPA1 signal pathway is necessary for the development of chronic itch and may be the potentially promising target of chronic itch in AD. Dictamnine is one of the main quinoline alkaloid components of Cortex Dictamni (a traditional Chinese medicine widely used in clinical treatment of skin diseases). However, the anti-inflammatory and anti-pruritic effect of dictamnine on AD have not been reported. In this study, we used the 2,4-dinitrofluorobenzene (DNFB)-induced AD mouse model to observe the scratching behavior, inflammatory manifestations, and to detect the expression of MrgprA3 and TRPA1 in skin and DRG. The data demonstrated that dictamnine effectively inhibited AD-induced chronic itch, inflammation symptoms, epidermal thickening, inflammatory cell infiltration, and downregulates the expression of MrgprA3 and TRPA1. Furthermore, dictamnine restrained the excitability of MrgprA3 and TRPA1 neurons. Molecular docking also indicated that dictamnine has better binding affinity with MrgprA3. These results suggest that dictamnine may inhibit chronic itch caused by AD through the MrgprA3-TRPA1 mediated histamine-independent itch pathway, and may have a potential utility in AD treatment.

Muscle fatigue and pain are key symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Although the pathophysiology is not yet fully understood, there is ample evidence for hypoperfusion which may result in electrolyte imbalance and sodium overload in muscles. Therefore, the aim of this study was to assess levels of sodium content in muscles of patients with ME/CFS and to compare these to healthy controls.

We report a novel presentation of deficit in anterior pituitary function with variable immune deficiency (DAVID) syndrome in a healthy young girl presenting in Addisonian crisis with raised intracranial pressure. Nearly all cases of DAVID syndrome described in the literature have presented with recurrent infections and variable immunodeficiency. Pseudotumour cerebri has not been reported in DAVID syndrome to date.