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Prunus africana (Hook.f.) Kalkman (Rosaceae), commonly known as "Pygeum" or "African cherry", occurs in mainland montane forest "islands" scattered across sub-Saharan Africa, Madagascar, and some surrounding islands. Traditionally, decoctions of the stem-bark are taken orally for the treatment of a wide variety of conditions, such as benign prostatic hyperplasia (BPH), stomach ache, chest pain, malaria, heart conditions, and gonorrhoea, as well as urinary and kidney diseases. The timber is used to make axe handles and for other household needs. The dense wood is also sawn for timber.

Severe acute respiratory syndrome (SARS) due to the novel coronavirus has become the highest priority that threatens human health. This situation demands widespread vaccination and the innovation of new therapeutic methods. Despite drug discoveries, the need for approving new medicaments is felt because of adverse effects and lack of efficacy. Several medicinal plants including Viola odorata L. are recommended in traditional Persian medicine for alleviating respiratory infection symptoms. Recent studies showed anti-inflammatory, antioxidant, anti-asthmatic, antitussive, analgesic, and antibacterial activities of sweet violet. These enhance respiratory functions, reduce pulmonary inflammation, and decline mucous membrane edema. This study aimed to evaluate the efficacy of sweet violet syrup in alleviating the manifestations of COVID-19 infection.

Patellofemoral pain (PFP) is a common cycling-related injury, and independent factors need to be identified to enable effective injury prevention strategies. We aim to determine factors associated with PFP in cyclists entering mass community-based events.

We assessed whether race or ethnicity was associated with the incidence of high-impact chronic pain (cLBP) among adults consulting a primary care provider for acute low back pain (aLBP).

Previous studies have suggested that administration of epidural 3% 2-chloroprocaine (CP) before epidural morphine results in decreased analgesic efficacy of epidural morphine. We sought to determine whether these observations were a result of antagonism or a window period between the conclusion of surgical anesthesia for cesarean delivery and the peak onset time of epidural morphine, and whether a method to preserve the analgesic efficacy of epidural morphine exists.

Asperuloside (ASP) and geniposide (GP) are iridoids that have shown various biological properties, such as reduction of inflammation, oxidative stress, and neuroprotection. The aim of this study was to investigate the mechanism of action of ASP and GP through the experimental model of pilocarpine-induced seizures. Mice were treated daily with saline, valproic acid (VPA), GP (5, 25, or 50 mg/kg), or ASP (20 or 40 mg/kg) for 8 days. Pilocarpine (PILO) treatment was administered after the last day of treatment, and the epileptic behavior was recorded for 1 h and analyzed by an adapted scale. Afterward, the hippocampus and blood samples were collected for western blot analyses, ELISA and comet assay, and bone marrow to the micronucleus test. We evaluated the expression of the inflammatory marker cyclooxygenase-2 (COX-2), GluN2B, a subunit of the NMDA receptor, pGluR1, an AMPA receptor, and the enzyme GAD-1 by western blot and the cytokine TNF-α by ELISA. The treatments with GP and ASP were capable to decrease the latency to the first seizure, although they did not change the latency to status epilepticus (SE). ASP demonstrated a genotoxic potential analyzed by comet assay; however, the micronuclei frequency was not increased in the bone marrow. The GP and ASP treatments were capable to reduce COX-2 and GluN2B receptor expression after PILO exposure. This study suggests that GP and ASP have a protective effect on PILO-induced seizures, decreasing GluN2B receptor and COX-2 expression.

Enhanced recovery after surgery (ERAS) protocols have been propagated in general surgery since the mid-1990s due to medical and health economic advantages for patients as well as hospitals. A comprehensive implementation in Germany is not yet established, although the demographic change requires more than ever concepts for the safe treatment of multimorbid frail patients. The aim of this review is to present modern ERAS concepts, to discuss an extension to prehabilitation measures for frail patients and to present aspects of structural feasibility.

Fibromyalgia (FM) is a chronic and systemic condition that causes widespread chronic pain, asthenia, and muscle stiffness, as well as in some cases depression, anxiety, and disorders of the autonomic system. The exact causes that lead to the development of FM are still unknown today. In a percentage of individuals, the symptoms of FM are often triggered and/or exacerbated by proximity to electrical and electromagnetic devices. Plasma metabolomic profile of 54 patients with fibromyalgia and self-reported electromagnetic sensitivity (IEI-EMF) were compared to 23 healthy subjects using gas chromatography-mass spectrometry (GC-MS) coupled with multivariate statistical analysis techniques. Before the GC-MS analysis the plasma samples were extracted with a modified Folch method and then derivatized with methoxamine hydrochloride in pyridine solution and N-trimethylsilyltrifuoroacetamide. The combined analysis allowed to identify a metabolomic profile able of distinguishing IEI-EMF patients and healthy subjects. IEI-EMF patients were therefore characterized by the alteration of 19 metabolites involved in different metabolic pathways such as energy metabolism, muscle, and pathways related to oxidative stress defense and chronic pain. The results obtained in this study complete the metabolomic "picture" previously investigated on the same cohort of IEI-EMF patients with H-NMR spectroscopy, placing a further piece for better understanding the pathophysiological mechanisms in patients with IEI-EMF.

Chronic pain is a common and often debilitating problem that affects 100 million Americans. A better understanding of pain's molecular mechanisms is necessary for developing safe and effective therapeutics. Microglial activation has been implicated as a mediator of chronic pain in numerous preclinical studies; unfortunately, translational efforts using known glial modulators have largely failed, perhaps at least in part due to poor specificity of the compounds pursued, or an incomplete understanding of microglial reactivity. In order to achieve a more granular understanding of the role of microglia in chronic pain as a means of optimizing translational efforts, we utilized a clinically-informed mouse model of complex regional pain syndrome (CRPS), and monitored microglial activation throughout pain progression. We discovered that while both males and females exhibit spinal cord microglial activation as evidenced by increases in Iba1, activation is attenuated and delayed in females. We further evaluated the expression of the newly identified microglia-specific marker, TMEM119, and identified two distinct populations in the spinal cord parenchyma after peripheral injury: TMEM119+ microglia and TMEM119- infiltrating myeloid lineage cells, which are comprised of Ly6G + neutrophils and Ly6G- macrophages/monocytes. Neurons are sensitized by inflammatory mediators released in the CNS after injury; however, the cellular source of these cytokines remains somewhat unclear. Using multiplex hybridization in combination with immunohistochemistry, we demonstrate that spinal cord TMEM119+ microglia are the cellular source of cytokines IL6 and IL1β after peripheral injury. Taken together, these data have important implications for translational studies: 1) microglia remain a viable analgesic target for males and females, so long as duration after injury is considered; 2) the analgesic properties of microglial modulators are likely at least in part related to their suppression of microglial-released cytokines, and 3) a limited number of neutrophils and macrophages/monocytes infiltrate the spinal cord after peripheral injury but have unknown impact on pain persistence or resolution. Further studies to uncover glial-targeted therapeutic interventions will need to consider sex, timing after injury, and the exact target population of interest to have the specificity necessary for translation.

There is growing literature supporting cannabinoids as a potential therapeutic for pain conditions. The development of chronic pain has been associated with reduced concentrations of the endogenous cannabinoid anandamide (AEA) in the midbrain dorsal periaqueductal gray (dPAG), and microinjections of synthetic cannabinoids into the dPAG are antinociceptive. Therefore, the goal of this study was to examine the role of the dPAG in cannabinoid-mediated sensory inhibition. Given that cannabinoids in the dPAG also elicit sympathoexcitation, a secondary goal was to assess coordination between sympathetic and antinociceptive responses. AEA was microinjected into the dPAG while recording single unit activity of wide dynamic range (WDR) dorsal horn neurons (DHNs) evoked by high intensity mechanical stimulation of the hindpaw, concurrently with renal sympathetic nerve activity (RSNA), in anesthetized male rats. AEA microinjected into the dPAG decreased evoked DHN activity (n = 24 units), for half of which AEA also elicited sympathoexcitation. AEA actions were mediated by cannabinoid 1 receptors as confirmed by local pretreatment with the cannabinoid receptor antagonist AM281. dPAG microinjection of the synaptic excitant DL-homocysteic acid (DLH) also decreased evoked DHN activity (n = 27 units), but in all cases this was accompanied by sympathoexcitation. Thus, sensory inhibition elicited from the dPAG is not exclusively linked with sympathoexcitation, suggesting discrete neuronal circuits. The rostrocaudal location of sites may affect evoked responses as AEA produced sensory inhibition without sympathetic effects at 86 % of caudal compared to 25 % of rostral sites, supporting anatomically distinct neurocircuits. These data indicate that spatially selective manipulation of cannabinoid signaling could provide analgesia without potentially harmful autonomic activation.