Rejected

PURPOSE OF THE STUDY To investigate the pressure levels on the axillary nerve at different plate positions after plate fixation of a proximal humerus fracture. MATERIAL AND METHODS Eight fresh-frozen cadaveric specimens were used. The plates were applied on the lateral side of the humerus. A FlexiForce pressure sensor was placed between the nerve and the plate, and the pressure on the nerve was measured (Group 1). The plates were then placed in two different positions such that distal portion of the plates would have 30° anterior and 30° posterior angles to the anatomical axis of the humerus (Group 2 and 3). The anterior of the distal attachment of the deltoid muscle was then elevated and the plates were placed in the middle of the anatomical axis of the humerus (Group 4). The position of the plates were controlled by fluoroscopy and the pressure was measured for each configuration sequentially. RESULTS The mean age of the cadavers was 70.5 ± 6.8 years (range: 61-80 years). Mean pressure values of the groups were 2.65 ± 0.8, 2.52 ± 0.8, 5.65 ± 1.4, and 2.56 ± 0.9 N, respectively. Group 3 had statistically highest-pressure values than the other groups, while no difference was found among groups 1, 2, and 4. DISCUSSION Numbness and weakness of the shoulder muscles are other clinical findings. If numbness on the deltoid muscle is reported, then atrophy is noted in the deltoid muscle in later stages. Persistent pain may be seen even if fracture union occurs after PHF surgery. Axillary nerve entrapment may be considered after the removal of common complications such as avascular necrosis due to fracture, screw migration, infection, and biceps tendon and rotator cuff problems. The sensory branch of the axillary nerve provides the sensation of the anterior joint capsule and lateral part of the deltoid muscle. CONCLUSIONS Proximal humerus plates, which are angled posteriorly along, lead to an increased pressure on the axillary nerve. Anterior orientation of the plate or elevation of deltoid insertion may be used to prevent the possible complications related to axillary nerve. Level of evidence Level II. Key words: proximal humerus fracture, Philos, axillary nerve, nerve injury.

Trigeminal neuralgia pain remains a challenge to treat. Natural compounds may be promising options for relieving pain. This study was aimed at investigating the effects of aconitine in a rat model of trigeminal neuralgia pain. Infraorbital nerve chronic constriction injury was performed in adult Wistar Albino rats. After the neuropathic pain developed, the rats were assigned to one of the treatment groups: carbamazepine 40 or 80 mg/kg; aconitine 0.25, 0.50, or 0.75 mg/kg; or saline injection (control group). Behavioral testing with von Frey filaments and the rotarod test were carried out before the surgical procedure and on the 24th to 29th postoperative days. Following the completion of tests, ipsilateral and contralateral spinal cords were harvested for Western blot analyses to assess NR-1 protein expression. ANOVA followed by Mann-Whitney test was performed for the statistical analyses. values of <0.05 were considered significant. Aconitine significantly reduced mechanical sensitivity in a dose-dependent manner. A significant reduction in motor coordination was noted for the higher doses of aconitine which was similar with the 40 and 80 mg/kg doses of carbamazepine. NR-1 expression was reduced in the ipsilateral spinal cord, whereas no significant difference was noted between the groups in the expression of NR-1 in the contralateral spinal cord. Aconitine had a significant pain relieving effect, which was similar to carbamazepine, in a dose-dependent manner. Aconitine may be an alternative pharmacological agent for the control of trigeminal neuralgia pain.

The dorsolateral prefrontal cortex (dlPFC) generates the mental representations that are the foundation of abstract thought, and provides top-down regulation of emotion through projections to the medial PFC and cingulate cortices. Physiological recordings from dlPFC Delay cells have shown that the generation of mental representations during working memory relies on NMDAR neurotransmission, with surprisingly little contribution from AMPAR. Systemic administration of low "antidepressant" doses of the NMDAR antagonist, ketamine, erodes these representations and reduces dlPFC Delay cell firing. In contrast to the dlPFC, V1 neuronal firing to visual stimuli depends on AMPAR, with much less contribution from NMDAR. Similarly, neurons in the dlPFC that respond to sensory events (cue cells, response feedback cells) rely on AMPAR, and systemic ketamine increases their firing. Insults to NMDAR transmission, and the impaired ability for dlPFC to generate mental representations, may contribute to cognitive deficits in schizophrenia, e.g., from genetic insults that weaken NMDAR transmission, or from blockade of NMDAR by kynurenic acid. Elevated levels of kynurenic acid in dlPFC may also contribute to cognitive deficits in other disorders with pronounced neuroinflammation (e.g., Alzheimer's disease), or peripheral infections where kynurenine can enter brain (e.g., delirium from sepsis, "brain fog" in COVID19). Much less is known about NMDAR actions in the primate cingulate cortices. However, NMDAR neurotransmission appears to process the affective and visceral responses to pain and other aversive experiences mediated by the cingulate cortices, which may contribute to sustained alterations in mood state. We hypothesize that the very rapid, antidepressant effects of intranasal ketamine may involve the disruption of NMDAR-generated aversive mood states by the anterior and subgenual cingulate cortices, providing a "foot in the door" to allow the subsequent return of top-down regulation by higher PFC areas. Thus, the detrimental vs. therapeutic effects of NMDAR blockade may be circuit dependent.

To document longitudinal symptom, quality-of-life and imaging response in patients with recurrent gynecological tumors treated with magnetic resonance guided high intensity focused ultrasound (MRgHIFU), and compare changes in patients with intra- versus extra-pelvic lesions.

Little is known about the impact of occupational seafaring on lower limb conditions. The aim of the study was to estimate the prevalence of dermatological diseases affecting the feet and lower extremities of seafarers, as well as the possible impact of working conditions on the development of the pathologies analysed.

Mesenchymal stem cell (MSC) therapies have been used as cell-based treatments for decades, owing to their anti-inflammatory, immunomodulatory, and regenerative properties. With high expectations, many ongoing clinical trials are investigating the safety and efficacy of MSC therapies to treat arthritic diseases. Studies on osteoarthritis (OA) have shown positive clinical outcomes, with improved joint function, pain level, and quality of life. In addition, few clinical MSC trials conducted on rheumatoid arthritis (RA) patients have also displayed some optimistic outlook. The largely positive outcomes in clinical trials without severe side effects establish MSCs as promising tools for arthritis treatment. However, further research is required to investigate its applicability in clinical settings. This review discusses the most recent advances in clinical studies on MSC therapies for OA and RA.

Aging is associated with changes in hormones, slowing of metabolism, diminished physiological processes, chronic inflammation and high exposure to oxidative stress factors, generally described as the biological cost of living. Lifestyle interventions of diet and exercise can improve the quality of life during aging and lower diet-related chronic disease. The endocannabinoid system (ECS) has important effects on systemic metabolism and physiological systems, including the central and peripheral nervous systems. Exercise can reduce the loss of muscle mass and improve strength, and increase the levels of endocannabinoids (eCB) in brain and blood. Although the ECS exerts controls on multiple systems throughout life it affords benefits to natural aging. The eCB are synthesized from polyunsaturated fatty acids (PUFA) and the primary ones are produced from arachidonic acid (n-6 PUFA) and others from the n-3 PUFA, namely eicosapentaenoic and docosahexaenoic acids. The eCB ligands bind to their receptors, CB1 and CB2, with effects on appetite stimulation, metabolism, immune functions, and brain physiology and neuroplasticity. Dietary families of PUFA are a primary factor that can influence the types and levels of eCB and as a consequence, the downstream actions when the ligands bind to their receptors. Furthermore, the association of eCB with the synthesis of oxylipins (OxL) is a connection between the physiological actions of eCB and the lipid derived immunological OxL mediators of inflammation. OxL are ubiquitous and influence neuroinflammation and inflammatory processes. The emerging actions of eCB on neuroplasticity, well-being and pain are important to aging. Herein, we present information about the ECS and its components, how exercise and diet affects specific eCB, their role in neuroplasticity, neuroinflammation, pain, mood, and relationship to OxL. Poor nutrition status and low nutrient intakes observed with many elderly are reasons to examine the role of dietary PUFA actions on the ECS to improve health.

Neurostimulation techniques for the treatment of chronic low back pain (LBP) have been rapidly evolving; however, questions remain as to which modalities provide the most efficacious and durable treatment for intractable axial symptoms. Modalities of spinal cord stimulation, such as traditional low-frequency paresthesia based, high-density or high dose (HD), burst, 10-kHz high-frequency therapy, closed-loop, and differential target multiplexed, have been limitedly studied to determine their efficacy for the treatment of axial LBP. In addition, stimulation methods that target regions other than the spinal cord, such as medial branch nerve stimulation of the multifidus muscles and the dorsal root ganglion may also be viable treatment options. Here, current scientific evidence behind neurostimulation techniques have been reviewed with a focus on the management of chronic axial LBP.

Infrared (IR) inhibition can selectively block peripheral sensory nerve fibers, a potential treatment for autonomic-dysfunction-related diseases (e.g., neuropathic pain and interstitial cystitis). Lowering the IR inhibition threshold can increase its translational potentials. Infrared induces inhibition by enhancing potassium channel activation. We hypothesized that the IR dose threshold could be reduced by combining it with isotonic ion replacement. We tested the IR inhibition threshold on the pleural-abdominal connective of . Using a customized chamber system, the IR inhibition was applied either in normal saline or in isotonic ion-replaced saline, which could be high glucose saline, high choline saline, or high glucose/high choline saline. Each modified saline was at a subthreshold concentration for inhibiting neural conduction. We showed that isotonically replacing ions in saline with glucose and/or choline can reduce the IR threshold and temperature threshold of neural inhibition. Furthermore, the size selectivity of IR inhibition was preserved when combined with high glucose/high choline saline. The present work of IR inhibition combined with isotonic ion replacement will guide further development of a more effective size-selective IR inhibition modality for future research and translational applications.

An analytical review of the methods of cancer patients' rehabilitation with peripheral polyneuropathy induced by cytostatics (PNPIC) was carried out. Studies from electronic databases were investigated: Scopus, Web of Science, MedLine, World Health Organization, The Cochrane Central Register of Controlled Trials, ScienceDirect, US National Library of Medicine National Institutes of Health, PubMed Cancer, eLIBRARY, CyberLeninka. Despite the improvement of anticancer therapy and an increase in patients' life expectancy, the emerging peripheral polyneuropathy remains an urgent problem, since it significantly affects both the patients' life quality and the selection of adequate therapy. The frequency of detection of PNPIC is 90%, after discontinuation of treatment; symptoms of damaged peripheral nerve fibers remain in 30% of patients. The clinical symptoms of PNPIC are varied and most often include numbness in the extremities and / or increased sensitivity to thermal or mechanical stimuli, neuropathic pain. Currently, to prevent PNPIC, treatment is being modified with a reduction in the duration of courses and doses of cytostatics, and interruption of treatment. Official guidelines do not recommend any prophylaxis other than the possible use of duloxetine or a topical gel containing baclofen, amitriptyline, and ketamine. Over the past few years, there has been no significant progress in the prevention and treatment of PNPIC. The most common drug treatment method in clinical practice is the prescription of vitamins B. Among the non-drug treatment methods of PNPIC, the authors used acupuncture, electro-acupuncture, manual therapy, massage, gymnastics, yoga, sensorimotor training, general vibration therapy, percutaneous electro-neuro-stimulation, electro-analgesia, local cryotherapy, hydrotherapy, low-intensity alternating magnetic radiation. The studies included in the review are heterogeneous in design and protocol, number of patients, and time points for assessing outcomes. In connection with the existing differences, it is not possible to carry out a comparative analysis of the results of these rehabilitation types and to give an unambiguous answer about their effectiveness. As the analysis has shown, peripheral PNPIC is well known all over the world, however, the search for methods of its treatment is far from complete.