Allergic conversion of protective mucosal immunity against nasal bacteria in patients with chronic rhinosinusitis with nasal polyposis

1. Download high-res image (155KB)
2. Download full-size image

     

Ischaemia-reperfusion injury of the peripheral nerve: An experimental study

Although the neuropathology of ischaemic fibre degeneration is relatively well known, its pathogenesis is poorly understood. One of the presumed mechanisms is oxidative stress, causing the breakdown of the blood-nerve barrier (BNB) and ending in lipid peroxidation. We evaluated the effect of ischaemia and reperfusion on the sciatic-tibial nerve of the rat and investigated the biochemical, pathological, and functional evidence of BNB disruption and lipid peroxidation. The distal portion and trifurcation of the sciatic nerve were rendered ischaemic by clamping the femoral vessels for 3 h and followed by varying durations of reperfusion. Reperfusion resulted in an increase in lipid peroxidation beginning from the first hour and increasing until the seventh day, followed by a gradual decline over the following weeks. Nerve oedema and ischaemic fibre degeneration (IFD) consistently became more severe and prominent with reperfusion, indicating that oxidative stress damages the BNB and causes IFD. Results of functional testing by the sciatic function index correlated with other parameters as walking track analysis results got worse as reperfusion periods increased. Impairment of walking patterns was more striking after the first day and continued up to the third week. These data indicate that severe ischaemia of the peripheral nerve results in reperfusion injury, functional impairment, and disruption of the BNB. Microvascular events, which may occur during reperfusion, may be important in amplifying the nerve fibre degeneration that initiated during ischaemia.     

Anti‐angiogenic therapy (bevacizumab) in the management of oral lichen planus

Oral lichen planus (OLP), a mucocutaneous chronic inflammatory disease, is conventionally managed using topical corticosteroid therapy. Given the fact that OLP is strongly linked to angiogenesis, anti‐angiogenic drugs, such as bevacizumab, might be introduced as an alternative treatment for contraindicated, non‐responsive patients. The aim of the present study was to report the short‐term effectiveness and safety of intralesional bevacizumab injection in the management of atrophic/erosive OLP. A case series study was conducted in patients with atrophic/erosive OLP in the buccal mucosa, assigned to receive either 2.5 mg of bevacizumab, by intralesional injection (n = 20, test), or topical 0.1% triamcinolone acetonide ointment (n = 20, control). The size, score, and pain intensity of the lesions were assessed pre‐ and post‐treatment. Tissue biopsies were collected for histopathologic, immunohistochemical, and ultrastructural examination. After 1 wk, the test group had significant reductions both in lesion seize and in pain scores compared with controls. A marked decrease in vascular endothelial growth factor (VEGF) and interleukin‐8 immunoexpression was noted in tissue biopsies from bevacizumab‐treated lesions compared with control lesions. Furthermore, ultrastructural examination of OLP tissue specimens revealed significant healing signs associated with bevacizumab treatment. Short‐term data suggest that intralesional bevacizumab injection effectively and safely achieved resolution of atrophic/erosive OLP lesions without disease exacerbations during a 3‐month follow‐up period.     

Activation of central GABAB receptors offsets the cyclosporine counteraction of endotoxic cardiovascular outcomes in conscious rats

We have previously shown that cyclosporine (CSA) counteracts cardiovascular manifestations induced by endotoxemia (lipopolysaccharide, LPS) such as hypotension and cardiac autonomic dysfunction in conscious rats. In this study, we investigated whether the facilitation of central γ‐amino butyric acid (GABA) neurotransmission blunts these favorable influences of CSA. The LPS‐CSA interaction was determined in the absence and presence of drugs that activate GABA_A or GABA_B receptors or elevate synaptic GABA levels in the central nervous system. The consequent i.v. administration of CSA (10 mg/kg) blunted the LPS‐evoked hypotension, tachycardia, and reductions in time‐ and frequency‐domain indices of heart rate variability (measures of cardiac autonomic control) evoked by LPS (10 mg/kg i.v.). The ability of CSA to reverse the LPS effects disappeared in rats treated intracisternally (i.c.) with baclofen (selective GABA_B agonist, 2 μg/rat) but not muscimol (selective GABA_A agonist, 1 μg/rat), indicating a preferential compromising action for central GABA_B receptors on the advantageous effects of CSA. Moreover, the improvement by CSA of LPS‐evoked cardiovascular derangements was also eliminated after concurrent i.c. administration of vigabatrin (GABA transaminase inhibitor, 200 μg/rat) or tiagabine (GABA reuptake inhibitor, 100 μg/rat). These results demonstrate that the activation of central GABA_B receptors either directly via baclofen or indirectly following interventions that boost GABA levels in central synapses counterbalances the rectifying action of CSA on endotoxemia.     

Robotic Rehabilitation and Spinal Cord Injury: a Narrative Review

Mobility after spinal cord injury (SCI) is among the top goals of recovery and improvement in quality of life. Those with tetraplegia rank hand function as the most important area of recovery in their lives, and those with paraplegia, walking. Without hand function, emphasis in rehabilitation is placed on accessing one’s environment through technology. However, there is still much reliance on caretakers for many activities of daily living. For those with paraplegia, if incomplete, orthoses exist to augment walking function, but they require a significant amount of baseline strength and significant energy expenditure to use. Options for those with motor complete paraplegia have traditionally been limited to the wheelchair. While wheelchairs provide a modified level of independence, wheelchair users continue to face difficulties in access and mobility. In the past decade, research in SCI rehabilitation has expanded to include external motorized or robotic devices that initiate or augment movement. These robotic devices are used with 2 goals: to enhance recovery through repetitive, functional movement and increased neural plasticity and to act as a mobility aid beyond orthoses and wheelchairs. In addition, lower extremity exoskeletons have been shown to provide benefits to the secondary medical conditions after SCI such as pain, spasticity, decreased bone density, and neurogenic bowel. In this review, we discuss advances in robot-guided rehabilitation after SCI for the upper and lower extremities, as well as potential adjuncts to robotics.