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Sjögren’s syndrome (SS) is a chronic autoimmune disease with a wide spectrum of possible organ involvement. Peripheral (PNS) and central nervous system (CNS)-related symptoms may occur in the course of the disease. The aim of this study was to compare the health-related quality of life (HR-QOL) in SS patients with and without peripheral neuropathy. The study involved 50 patients with primary Sjögren’s syndrome (pSS). All patients underwent neurological clinical examination followed by nerve conduction studies (NCS) and rheumatological examination. Thirty-six-item Short Form Health Survey (SF-36) was used for evaluating HR-QOL. To assess pSS activity, the EULAR Sjögren’s Syndrome Disease Activity Index (ESSDAI) and EULAR Sjögren’s Syndrome Patient Reported Index (ESSPRI) were used. For the assessment of clinical disability due to peripheral neuropathy, the Overall Disability Sum Score scale (ODSS) was used. Additional evaluation of pain was performed with the use of the Visual Analogue Scale (VAS) and a semistructured interview. Twenty-three (46%) patients were diagnosed with peripheral neuropathy. The most common PNS manifestation was sensorimotor neuropathy (47%). Neurological symptoms preceded the diagnosis of pSS in eight patients. The following domains of the SF-36 form were significantly lower scored by patients with peripheral nervous system involvement role-physical [0 (0-100) vs. 75 (0-100)], role-emotional [67 (0-100) vs. 100 (0-100)], vitality [40 (10-70) vs. 50 (20-75)], bodily pain [45 (10-75) vs. 55 (0-100)], and general health [20 (5-50) vs. 30 (0-50)] (p ≤ 0.05). Our study showed that peripheral neuropathy was a common organ-specific complication in SS patients. In pSS patients, coexisting neurological involvement with symptoms such as pain and physical disability may be responsible for diminished HR-QOL.BACKGROUNDS The width of mucosal defects after endoscopic submucosal dissection (ESD) of esophageal squamous cell carcinoma (ESCC) is known to be a risk factor for esophageal strictures. Although steroid injection and oral steroid have recently been reported as prophylactic treatments, these were shown to be ineffective in a subset of patients with post-ESD mucosal defects involving the entire circumference of the esophagus. The aim of this study was to demonstrate outcome with prophylactic steroid administration for post-ESD mucosal defects involving the entire circumference, and to explore risk factors for esophageal strictures except for circumference of the esophagus. METHODS Between November 2012 and August 2018, we enrolled patients with post-ESD mucosal defects involving the entire circumference of the esophagus who had received steroid injection (triamcinolone acetonide 50-100 mg, given immediately after ESD) followed by oral steroid (prednisolone 30 mg/day, tapered gradually over 8 weeks) as prophylapreading ESCC involving the entire circumference of esophagus given its high stricture risk.The majority of patients hospitalized for heart failure (HF) are admitted to internal medicine (IM) rather than to cardiology (CA) units, but to date few studies have analyzed the characteristics of these two populations. In this snapshot survey, we compared consecutive patients admitted for HF in six IM units vs. one non-intensive CA unit. During the 6-month survey period, 467 patients were enrolled (127 in CA, 27.2% vs. 340 in IM, 72.8%). IM patients were almost 10 years older (CA 75 ± 10, IM 82 ± 8 years; p  less then  0.001), more frequently female (CA 39%, IM 55%; p = 0.002) and living at home alone (CA 12%, IM 21%; p = 0.017). The leading cause of hospitalization in both groups was acute worsening of HF (CA 42%, IM 53%; p = 0.031), followed by atrial fibrillation (CA 29%, IM 12%; p  less then  0.001) and infections (CA 24%, IM 27%; p = 0.563). Ischemic (CA 43%, IM 30%; p = 0.008) and dilated cardiomyopathy patients (CA 21%, IM 12%; p  less then  0.001) were primarily admitted to CA unit, whereas those with hypertensive heart disease to IM (CA 3%, IM 39%; p  less then  0.001). Left ventricular ejection fraction (LVEF) was available in 96% of CA patients, but only in 60% of IM patients (p = 0.001). Among patients with LVEF measured, those with LVEF  less then  40% were predominantly admitted to CA (CA 60%, IM 14%; p  less then  0.001), whereas those with LVEF ≥ 50% were admitted to IM (CA 21%, IM 33%; p = 0.019); 26% of IM patients were discharged without a known LVEF. Medical treatments also significantly differed, according to patients’ clinical and instrumental characteristics in each unit. Tacedinaline nmr This study demonstrates important differences between HF patients hospitalized in CA vs. IM, and the need for a greater interaction between these two medical specialties for a better care of HF patients.The excitatory neurotransmitter glutamate evokes physiological responses within the astrocytic network that lead to fine morphological changes. However, the mechanism by which astrocytes couple glutamate sensing with cellular calcium rise remains unclear. We tested a possible connection between L-type voltage-gated calcium channels (Cav) and glutamate-induced response in U118-MG astrocytoma cells. While astrocytoma cells differ from primary astrocytes, they demonstrate the same response to glutamate. In this study, the extension of U118-MG processes upon glutamate exposure was shown to depend on extracellular calcium entry via L-type Cav’s. Drugs known to bind to the pore-forming subunit of Cav’s decreased the astrocytic filopodia extension caused by glutamate, and ligands of the α2δ auxiliary subunit inhibited all process growth (e.g., gabapentinoids). The observed phenotypic responses suggest that α2δ is a main contributor to the role of Cavs in glutamate-dependent filopodiagenesis, thereby opening new avenues of research on the role of α2δ in astrocytic neurochemical signaling.Neurons of the central nervous system (CNS) that project long axons into the spinal cord have a poor axon regenerative capacity compared to neurons of the peripheral nervous system. The corticospinal tract (CST) is particularly notorious for its poor regeneration. Because of this, traumatic spinal cord injury (SCI) is a devastating condition that remains as yet uncured. Based on our recent observations that direct neuronal interleukin-4 (IL-4) signaling leads to repair of axonal swellings and beneficial effects in neuroinflammation, we hypothesized that IL-4 acts directly on the CST. Here, we developed a tissue culture model for CST regeneration and found that IL-4 promoted new growth cone formation after axon transection. Most importantly, IL-4 directly increased the regenerative capacity of both murine and human CST axons, which corroborates its regenerative effects in CNS damage. Overall, these findings serve as proof-of-concept that our CST regeneration model is suitable for fast screening of new treatments for SCI.