334 research outputs found
Combined effects of aerobic exercise and 40-Hz light flicker exposure on early cognitive impairments in Alzheimer’s disease of 3×Tg mice
Alzheimer’s disease (AD) is a progressive degenerative brain disease and the primary cause of dementia. At an early stage, AD is generally characterized by short-term memory impairment, owing to dysfunctions of the cortex and hippocampus. We previously reported that a combination of exercise and 40-Hz light flickering can protect against AD-related neuroinflammation, gamma oscillations, reduction in Aβ, and cognitive decline. Therefore, we sought to extend our previous findings to the 5-mo-old 3×Tg-AD mouse model to examine whether the same favorable effects occur in earlier stages of cognitive dysfunction. We investigated the effects of 12 wk of exercise combined with 40-Hz light flickering on cognitive function by analyzing neuroinflammation, mitochondrial function, and neuroplasticity in the hippocampus in a 3×Tg-AD mouse model. Five-month-old 3×Tg-AD mice performed 12 wk of exercise with 40-Hz light flickering administered independently and in combination. Spatial learning and memory, long-term memory, hippocampal Aβ, tau, neuroinflammation, proinflammatory cytokine expression, mitochondrial function, and neuroplasticity were analyzed. Aβ and tau proteins levels were significantly reduced in the early stage of AD, resulting in protection against cognitive decline by reducing neuroinflammation and proinflammatory cytokines. Furthermore, mitochondrial function improved, apoptosis was reduced, and synapse-related protein expression increased. Overall, exercise with 40-Hz light flickering was significantly more effective than exercise or 40-Hz light flickering alone, and the improvement was comparable to the levels in the nontransgenic aged-match control group. Our results indicate a synergistic effect of exercise and 40-Hz light flickering on pathological improvements in the hippocampus during early AD-associated cognitive impairment
Management of Complex Regional Pain Syndrome Type 1 With Total Spinal Block
Complex regional pain syndrome (CRPS) is a painful and disabling disorder that can affect one or more extremities. Unfortunately, the knowledge concerning its natural history and mechanism is very limited and many current rationales in treatment of CRPS are mainly dependent on efficacy originated in other common conditions of neuropathic pain. Therefore, in this study, we present a case using a total spinal block (TSB) for the refractory pain management of a 16-year-old male CRPS patient, who suffered from constant stabbing and squeezing pain, with severe touch allodynia in the left upper extremity following an operation of chondroblastoma. After the TSB, the patient's continuous and spontaneous pain became mild and the allodynia disappeared and maintained decreased for 1 month
IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways
Recent studies of the pathogenesis of rheumatoid arthritis (RA) have revealed that both synovial fibroblasts and T cells participate in the perpetuation of joint inflammation as dynamic partners in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. In this study, we investigated the role of IL-17, a major Th1 cytokine produced by activated T cells, in the activation of RA synovial fibroblasts. Transcripts of IL-17R (IL-17 receptor) and IL-17RB (IL-17 receptor B) were present in fibroblast-like synoviocytes (FLS) of RA patients. IL-17R responded with increased expression upon in vitro stimulation with IL-17, while the level of IL-17RB did not change. IL-17 enhanced the production of IL-6 and IL-8 in FLS, as previously shown, but did not affect the synthesis of IL-15. IL-17 appears to be a stronger inducer of IL-6 and IL-8 than IL-15, and even exerted activation comparable to that of IL-1β in RA FLS. IL-17-mediated induction of IL-6 and IL-8 was transduced via activation of phosphatidylinositol 3-kinase/Akt and NF-κB, while CD40 ligation and p38 MAPK (mitogen-activated protein kinase) are not likely to partake in the process. Together these results suggest that IL-17 is capable of more than accessory roles in the activation of RA FLS and provide grounds for targeting IL-17-associated pathways in therapeutic modulation of arthritis inflammation
Acute dural venous sinus thrombosis in a child with idiopathic steroid-dependent nephrotic syndrome: a case report
Nephrotic syndrome (NS) is a hypercoagulable state in which children are at risk of venous thromboembolism. A higher risk has been reported in children with steroid-resistant NS than in those with steroid-sensitive NS. The mortality rate of cerebral venous sinus thrombosis (CVST) is approximately 10% and generally results from cerebral herniation in the acute phase and an underlying disorder in the chronic phase. Our patient initially manifested as a child with massive proteinuria and generalized edema. He was treated with albumin replacement and diuretics, angiotensin-converting enzyme inhibitor, and deflazacort. Non-contrast computed tomography showed areas of hyperattenuation in the superior sagittal sinus when he complained of severe headache and vomiting. Subsequent magnetic resonance imaging revealed empty delta signs in the superior sagittal, lateral transverse, and sigmoid sinuses, suggesting acute CVST. Immediate anticoagulation therapy was started with unfractionated heparin, antithrombin III replacement, and continuous antiproteinuric treatment. The current report describes a life-threatening CVST in a child with steroid-dependent NS, initially diagnosed by contrast non-enhanced computed tomography and subsequently confirmed by contrast-enhanced magnetic resonance imaging, followed by magnetic resonance venography for recanalization, addressing successful treatment
Altered Resting-State Functional Connectivity in Wernicke's Encephalopathy With Vestibular Impairment
Objectives: To reveal the neural basis of Wernicke's encephalopathy (WE) with impaired vestibulo-ocular reflex (VOR), we evaluated resting-state functional connectivity (rs-fc) in the vestibular processing brain regions.
Methods: Rs-fc between the vestibular regions and the rest of the brain were compared with neurotological features including the head-impulse tests (vHIT) and caloric responses in patients with WE (n = 5, mean age 53.4 ± 10 years) and healthy controls (n = 20, mean age 55.0 ± 9.2 years). Rs-fc analyses employed a region of interest (ROI)-based approach using regions selected a priori that participate in vestibular processing including the cerebellar vermis, insula, parietal operculum, and calcarine cortex.
Results: The main neurologic findings for patients with WE were mental changes; gait ataxia; spontaneous and gaze-evoked nystagmus (GEN); and bilaterally positive HIT for the horizontal canals. Video HIT documented bilateral horizontal canal dysfunction with decreased gain and corrective saccades. Caloric irrigation and rotation chair testing revealed prominent bilateral horizontal canal paresis. Patients with WE also had decreased spatial memory, which substantially recovered after treatments. Functional connections at the predefined seed regions, including the insular cortex and parietal operculum, were attenuated in the WE group compared to healthy controls.
Conclusions: WE is related to impaired VOR and visuospatial dysfunction, and fMRI documented changes in the rs-fc of multisensory vestibular processing regions including the insula, parietal operculum, and superior temporal gyrus, which participate in integration of vestibular perception
Six-Month Comparison of Coronary Endothelial Dysfunction Associated With Sirolimus-Eluting Stent Versus Paclitaxel-Eluting Stent
ObjectivesThis study was designed to investigate whether endothelial dysfunction is related to drug-eluting stent (DES) implantation at 6 months after stenting.BackgroundCurrent available DES could delay vessel healing and subsequently impair endothelial function.MethodsEndothelial function was estimated at 6-month follow-up in 75 patients (31 men, mean age 62.1 years) with a DES (39 sirolimus-eluting stents [SES], 36 paclitaxel-eluting stents [PES]), and 10 patients with a bare-metal stent (BMS) to the left anterior descending artery, by incremental acetylcholine (Ach) infusion (20 μg/min, 50 μg/min, 100 μg/min) and nitrate (200 μg/min) into the left coronary ostium. Vascular responses were quantitatively measured in arterial segments 5 mm proximal and distal to DES and compared with corresponding segments in the BMS group and midsegments in the left circumflex artery as a reference nonstented artery. All antianginal agents were withheld for at least 72 h before coronary angiography.ResultsGreater vasoconstriction to Ach was observed in both the SES and PES groups than in the BMS group or control segments of left circumflex artery. Vasoconstriction to Ach was more prominent in arterial segments distal to stents in both SES and PES groups compared with those in the BMS group (p < 0.001). The degree of vasoconstriction to Ach was similar between the SES and PES groups. Endothelium-independent vasodilatation to nitrate did not differ significantly between the study groups.ConclusionsAbnormal vasoconstriction to Ach was found in the SES and PES groups, especially in arterial segments distal to DES at 6 months after stenting, which suggests that DES has a potential long-term adverse effect on local coronary endothelial dysfunction
A Prospective, Randomized, 6-Month Comparison of the Coronary Vasomotor Response Associated With a Zotarolimus- Versus a Sirolimus-Eluting Stent Differential Recovery of Coronary Endothelial Dysfunction
ObjectivesWe prospectively compared coronary endothelial dysfunction in patients with zotarolimus-eluting stent (ZES) versus sirolimus-eluting stent (SES) implantation at 6-month follow-up.BackgroundA ZES has been associated with uniform and rapid healing of the endothelium.MethodsFifty patients were randomly treated with intravascular ultrasound-guided stenting with a single stent to the mid-segment of the left anterior descending artery (20 ZES, 20 SES, and 10 bare-metal stents), and endothelial function was estimated before and after intervention at 6-month follow-up by incremental acetylcholine (Ach) (10, 20, 50, and 100 μg/min) and nitrate (200 μg/min) infusions into the left coronary ostium. The vascular response was quantitatively measured in the 5-mm segments proximal and distal to the stent.ResultsIn the drug-eluting stent groups, more intense vasoconstriction to incremental doses of Ach was observed at 6-month follow-up compared with the responses before stenting. Endothelial function associated with the ZES was more preserved at 6-month follow-up compared with the SES. Vasoconstriction to Ach was more prominent in the distal segments than the proximal segments in both the ZES and SES groups. Endothelium-independent vasodilation to nitrate did not differ significantly among the study groups.ConclusionsVasoconstriction in response to Ach in the peri-stent region was less pronounced in the ZES group than the SES group at 6-month follow-up, which suggests that endothelial function associated with ZES can be more preserved than the SES
A Case Report of Carbon Monoxide Poisoning Induced Cardiomyopathy Complicated with Left Ventricular Thrombus
The heart and the brain, most oxygen-dependent organs, may be severely affected after carbon monoxide (CO) exposure. CO induced cardiotoxicity may occur as a consequence of moderate to severe CO poisoning, including angina attack, myocardial infarct, arrhythmias, and heart failure. We present a rare case of CO poisoning induced cardiomyopathy with left ventricular (LV) thrombus. It is thought that LV thrombus may have been caused severely decreased LV function with dyskinesis. After short-term anticoagulant therapy, echocardiography findings revealed complete recovery of LV dyskinesis and resolution of LV thrombus
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