Piston Sensing for Golay-6 Sparse Aperture System with Double-Defocused Sharpness Metrics via ResNet-34.

In pursuit of high imaging quality, optical sparse aperture systems must correct piston errors quickly within a small range. In this paper, we modified the existing deep-learning piston detection method for the Golay-6 array, by using a more powerful single convolutional neural network based on ResNet-34 for feature extraction; another fully connected layer was added, on the basis of this network, to obtain the best results. The Double-defocused Sharpness Metric (DSM) was selected first, as a feature vector to enhance the model performance; the average RMSE of the five sub-apertures for valid detection in our study was only 0.015λ (9 nm). This modified method has higher detecting precision, and requires fewer training datasets with less training time. Compared to the conventional approach, this technique is more suitable for the piston sensing of complex configurations.

Potential role of BAY11-7082, a NF-κB blocker inhibiting experimental autoimmune encephalomyelitis in C57BL/6J mice via declining NLRP3 inflammasomes.

Multiple sclerosis (MS) is an inflammatory autoimmune demyelinating disease of the central nervous system. NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is implicated in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which NLRP3 inflammasome is involved in the development of MS and EAE is not clear. NF-kappaB (NF-κB) is associated with the activity of NLRP3 inflammasomes, but the role of NF-κB is controversial. We sought to demonstrate that both NF-κB and NLRP3 contribute to development of MS and EAE, and NF-κB pathway is positively correlated with NLRP3 activation in EAE. The inhibitor of NF-κB and NLRP3, BAY11-7082, can prevent and treat EAE. BAY11-7082 (5 and 20 mg/kg/i.p.) was intraperitoneally administered to EAE mice at the time of second injection of pertussis toxin (BAY11-7082 prevention group) or at the onset of symptoms (BAY11-7082 treatment group). mRNA expressions of NLRP3 were determined by qPCR. Protein expressions of NLRP3, NF-κB p65, and phosphorylated p65 were determined by western blotting. Serum levels of inflammatory cytokines were measured by cytometric bead array. Mice treated with BAY11-7082 (both prevention and treatment groups) showed lower clinical scores and attenuated pathological changes. NLRP3 inflammasome and activity of NF-κB in spinal cord of EAE mice was higher than that in control group. However, the level of NLRP3 inflammasome decreased in BAY11-7082 prevention and treatment groups. BAY11-7082 is a promising therapeutic agent for MS. NLRP3 activation in EAE maybe related with NF-κB pathway.

Autophagy modulation in multiple sclerosis and experimental autoimmune encephalomyelitis.

Multiple sclerosis (MS), a white matter demyelinating disease of the central nervous system (CNS), is characterized by neuroinflammatory and neurodegenerative. Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model for investigating pathogenic mechanisms of MS, representing the destruction of the blood-brain barrier (BBB), the activation of T cells, and the infiltration of myeloid cells. An increasing number of studies have documented that autophagy plays a critical role in the pathogenesis of both MS and EAE. Autophagy maintains CNS homeostasis by degrading the damaged organelles and abnormal proteins. Furthermore, autophagy is involved in inflammatory responses by regulating the activation of immune cells and the secretion of inflammatory factors. However, the specific mechanisms of autophagy involved in MS and EAE are not completely understood. In this review, we will summarize the complex mechanisms of autophagy in MS and EAE, providing potential therapeutic approaches for the management of MS.

Nuclear factor kappa B inhibitor suppresses experimental autoimmune neuritis in mice via declining macrophages polarization to M1 type.

Guillain-Barré syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of the peripheral nervous system (PNS). Macrophages play a central role in its animal model, experimental autoimmune neuritis (EAN), which has been well accepted. Additionally, nuclear factor (NF)-κB inhibitors have been used to treat cancers and have shown beneficial effects. Here, we investigated the therapeutic effect of M2 macrophage and the NF-κB pathway's correlation with macrophage activation in EAN in C57BL/6 mice. We demonstrate that M2 macrophage transfusion could alleviate the clinical symptoms of EAN by reducing the proportion of M1 macrophage in the peak period, inhibiting the phosphorylation of NF-κB p65. The NF-κB inhibitor (BAY-11-7082) could alleviate the clinical symptoms of EAN and shorten the duration of symptoms by reducing the proportion of M1 macrophages and the expression of proinflammatory cytokines. Consequently, BAY-11-7082 exhibits strong potential as a therapeutic strategy for ameliorating EAN by influencing the balance of M1/M2 macrophages and inflammatory cytokines.

The therapeutic effects of ginkgolides in Guillain-Barré syndrome and experimental autoimmune neuritis.

BACKGROUND: Guillain-Barré syndrome (GBS) is an acquired immune-mediated inflammatory peripheral neuropathy. The immune regulation of ginkgolides have been revealed in recent years. We herein investigate the potential therapeutic effects of ginkgolides both on GBS and its animal model, experimental autoimmune neuritis (EAN). METHODS: EAN in C57BL/6 mice induced by subcutaneous injection with peripheral nerve myelin P0 protein peptide 180-199 (P0 peptide) were treated with ginkgolides at three different doses. GBS patients were randomly divided into two groups, the experimental group and the control group. The experimental group were treated with ginkgolides as soon as diagnosed. RESULTS: Our data indicated that ginkgolides administration daily ameliorated the score of EAN and delayed the peak of disease in EAN mice. Ginkgolides also down-regulated the proportions of T helper (Th) 17 cells in EAN spleens. Furthermore, we also found that administration of ginkgolides significantly decreased the levels of interferon (IFN)-γ and interleukin-12 (IL)-12 in GBS patients. CONCLUSIONS: Our results suggested that ginkgolides ameliorated the clinical score of EAN through down-regulating the proportions of Th 17 cells. Ginkgolides also suppressed inflammation response by decreasing pro-inflammatory cytokines IFN-γ and IL-12, suggesting ginkgolides had potential therapeutic effects on GBS patients and EAN in the future.

Characteristics of an elliptical Airy beam with a circular concentric vortex and its realization.

We theoretically and experimentally study the propagation characteristics of elliptical Airy vortex beams (EAVBs) with a circular concentric vortex. It is found that EAVBs inherit the abruptly autofocusing properties of the circular Airy beams (CABs), but EAVBs will have a better autofocusing performance than circular Airy vortex beams (CAVBs) under certain conditions. It is also found that the initial m-order concentric vortex of EAVBs splits into |m| first-order vortices at the autofocusing plane, and the focusing pattern splits into |m|+1 bright spots with the pattern's tilting direction related to the sign of m [m is the topological charge (TC) of the vortex]. These characteristics of EAVBs may have potential applications in TC detection, optical micromanipulation, communications, and other fields.

Role of Resolvins in the Inflammatory Resolution of Neurological Diseases.

The occurrence of neurological diseases including neurodegenerative disorders, neuroimmune diseases, and cerebrovascular disorders is closely related to neuroinflammation. Inflammation is a response against infection or injury. Genetic abnormalities, the aging process, or environmental factors can lead to dysregulation of the inflammatory response. Our immune system can cause massive damage when the inflammatory response becomes dysregulated. Inflammatory resolution is an effective process that terminates the inflammatory response to maintain health. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega-three polyunsaturated fatty acids that play a crucial regulatory role in the development of inflammation. Resolvins (Rvs) derived from EPA and DHA constitute the Rvs E and Rvs D series, respectively. Numerous studies on the effect of Rvs over inflammation using animal models reveal that they have both anti-inflammatory and pro-resolving capabilities. Here, we review the current knowledge on the classification, biosynthesis, receptors, mechanisms of action, and role of Rvs in neurological diseases.

Generation and propagation of a new kind of power-exponent-phase vortex beam.

A general analytical formula for the propagation of the new kind of power-exponent-phase vortex beam through a paraxial ABCD optical system is derived. With two different calculation methods, the evolution of the intensity distribution and phase contour of such a beam in free space is investigated. Some experiments are carried out to verify the theoretical predictions. Both of the theoretical and experimental results show that the beam's profile can be modulated by the topological charge and the power order. In addition, the orbital angular momentum (OAM) density and the normalized OAM of such a beam are also studied.

Measuring the topological charge of optical vortices with a twisting phase.

We analyzed the propagation characteristics of the intensity of a vortex beam after it passes through a twisting phase. It was found that the doughnut-like intensity pattern of a vortex beam would separate into several bright and dark fringes. The number of dark fringes between two bright spots is equal to the topological charge (TC) of the vortex beam. Meanwhile, the intensity pattern varies with the sign of the TC. Based on this property, we proposed a convenient method to measure the TC of a vortex beam by observing its intensity pattern after passing through a twisting phase. This detection technique is mainly based on the use of a twisting phase, and the effect of parameters in the twisting phase is demonstrated and clearly studied. By choosing proper parameters in the twisting phase, the separation speed of a vortex beam's intensity could be controlled in the experiment. The experimental results are in good agreement with the theoretical analyses.

Roles of macrophage migration inhibitory factor in Guillain-Barré syndrome and experimental autoimmune neuritis: beneficial or harmful?

INTRODUCTION: Macrophage migration inhibitory factor (MIF) plays an important role in the pathogenesis of Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN), which may offer an opportunity for the development of the novel therapeutic strategies for GBS. Areas covered: 'macrophage migration inhibitory factor' and 'Guillain-Barré syndrome' were used as keywords to search for related publications on Pub-Med, National Center for Biotechnology Information (NCBI), USA. MIF is involved in the etiology of various inflammatory and autoimmune disorders. However, the roles of MIF in GBS and EAN have not been summarized in the publications we identified. Therefore, in this review, we described and analyzed the major roles of MIF in GBS/EAN. Primarily, this molecule aggravates the inflammatory responses in this disorder. However, multiple studies indicated a protective role of MIF in GBS. The potential of MIF as a therapeutic target in GBS has been recently demonstrated in experimental and clinical studies, although clinical trials have been unavailable to date. Expert opinion: MIF plays a critical role in the initiation and progression of GBS and EAN, and it may represent a potential therapeutic target for GBS.

Role of Inflammasomes in Neuroimmune and Neurodegenerative Diseases: A Systematic Review.

Inflammasomes are multiprotein complexes that can sense pathogen-associated molecular patterns and damage-associated molecular signals. They are involved in the initiation and development of inflammation via activation of IL-1ß and IL-18. Many recent studies suggest a strong correlation between inflammasomes and neurological diseases, such as multiple sclerosis (MS), Alzheimer's disease (AD), and Parkinson's disease (PD). Several components of inflammasomes, such as nucleotide-binding oligomerization domain- (NOD-) like receptor, absent in melanoma 2- (AIM2-) like receptors (ALRs), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1, as well as the upstream factors and downstream effectors, are associated with the initiation and development of MS and its animal model, experimental autoimmune encephalomyelitis. Additionally, inflammasomes affect the efficacy of interferon-ß therapy in patients with MS. Finally, the strong association of inflammasomes with AD and PD needs to be further studied. In this review of latest literatures, we comprehensively tease out diverse roles of different kinds of inflammasomes in neuroimmune and neurodegenerative diseases, especially in the perspective of double roles involved in pathogenesis, and identify future research priorities.

Beneficial or Harmful Role of Macrophages in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis.

Guillain-Barré syndrome (GBS), an immune-mediated demyelinating peripheral neuropathy, is characterized by acute weakness of the extremities and areflexia or hyporeflexia. Experimental autoimmune neuritis (EAN) is a common animal model for GBS, which represents a CD4+ T cell-mediated inflammatory autoimmune demyelination of the peripheral nervous system (PNS), and is used to investigate the pathogenic mechanism of GBS. It has been found that macrophages play a critical role in the pathogenesis of both GBS and EAN. Macrophages have been primarily classified into two major phenotypes: proinflammatory macrophages (M1) and anti-inflammatory macrophages (M2). The two different macrophage subsets M1 and M2 may play a decisive role in initiation and development of GBS and EAN. However, recently, it has been indicated that the roles of macrophages in immune regulation and autoimmune diseases are more complex than those suggested by a simple M1-M2 dichotomy. Macrophages might exert either inflammatory or anti-inflammatory effect by secreting pro- or anti-inflammatory cytokines, and either inducing the activation of T cells to mediate immune response, resulting in inflammation and demyelination in the PNS, or promoting disease recovery. In this review, we summarize the dual roles of macrophages in GBS and EAN and explore the mechanism of macrophage polarization to provide a potential therapeutic approach for GBS in the future.

Gut Microbiota in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis: Current Applications and Future Perspectives.

The gut environment and gut microbiome dysbiosis have been demonstrated to significantly influence a range of disorders in humans, including obesity, diabetes, rheumatoid arthritis, and multiple sclerosis (MS). MS is an autoimmune disease affecting the central nervous system (CNS). The etiology of MS is not clear, and it should involve both genetic and extrinsic factors. The extrinsic factors responsible for predisposition to MS remain elusive. Recent studies on MS and its animal model, experimental autoimmune encephalomyelitis (EAE), have found that gastrointestinal microbiota may play an important role in the pathogenesis of MS/EAE. Thus, gut microbiome adjustment may be a future direction of treatment in MS. In this review, we discuss the characteristics of the gut microbiota, the connection between the brain and the gut, and the changes in gut microbiota in MS/EAE, and we explore the possibility of applying microbiota therapies in patients with MS.

Kainic Acid Impairs the Memory Behavior of APP23 Mice by Increasing Brain Amyloid Load through a Tumor Necrosis Factor-α-Dependent Mechanism.

Kainic acid (KA) was recently identified as an epileptogenic and neuroexcitotoxic agent that is responsible for inducing learning and memory deficits in various neurodegenerative diseases, such as Alzheimer's disease (AD). However, the mechanism by which KA acts upon AD remains unclear. To this end, we presently investigated the roles of KA in processing amyloid-ß protein precursor (AßPP) and amyloid-ß protein (Aß) loads during the course of AD development and progression. Specifically, KA treatment clearly caused the upregulation of tumor necrosis factor α (TNF-α) via activation of the PI3-K/AKT, ERK1/2, and p65 pathways in glial cells. TNF-α secreted from glial cells was then found to be responsible for stimulating the expression of BACE-1 and PS1/2, which resulted in the production and deposition of Aß in neurons. Finally, the accumulation and aggregation of Aß lead to the cognitive decline of APP23 mice. These results indicate that KA accelerates the progression of AD by inducing the crosstalk between glial cells and neurons.

The roles of macrophages and microglia in multiple sclerosis and experimental autoimmune encephalomyelitis.

Multiple sclerosis (MS) is an autoimmune and neurodegenerative disorder characterized by chronic inflammation, demyelination, as well as axonal and neuronal loss in the central nervous system (CNS). Macrophages and microglia are important components of the innate immune system. They participate in the primary response to microorganisms and play a role in inflammatory responses, homeostasis, and tissue regeneration. In the initial phase of MS and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, macrophages from peripheral tissues infiltrate into the CNS and, together with residential microglia, contribute to the pathogenesis of MS. In the early stages, microglia and macrophages are expressed as the M1 phenotype, which can release proinflammatory cytokines, leading to tissue damage in the CNS. However, in the later stage, the M2 phenotype, which is the phenotype that is associated with resolving inflammation and tissue repair, becomes predominant in the CNS. Therefore, it is hypothesized that the M1/M2 phenotype balance plays an important role in disease progression and that the transition from the proinflammatory M1 phenotype to the regulatory or anti-inflammatory M2 phenotype can lead to restoration of homeostasis and improved functional outcomes. This review of recent literature focuses on the discussion of the M1/M2 phenotypes of microglia and macrophages as well as their relevance in the pathophysiology and treatment of MS and EAE. Furthermore, the possibility of directing the polarization of microglia and macrophages toward the M2 phenotype as a therapeutic and preventative strategy for MS is discussed.

Incidental pulmonary embolism in suspected stroke patients undergoing carotid CT angiography.

PURPOSE: The purpose of this study was to investigate the prevalence of incidental pulmonary embolism (IPE) in suspected stroke patients receiving carotid computed tomography angiography (CTA) and its characteristics. MATERIALS AND METHODS: A total of 4873 cases receiving carotid CTA between January 2013 and December 2016 were retrospectively reassessed by one radiologist. Patients with previous or suspected PE were excluded. The remaining prior contrast-enhanced carotid CTA studies were regarded as a "potentially incidental" IPE when a filling defect was found in one or more pulmonary arteries and subjected to the other two thoracic radiologists independently for reviewing and assessing for characteristics of the IPE and the image quality of the PE. The differences were noted between inpatients and outpatients in prevalence of IPE. Characteristics of the patients with IPE were also studied in terms of gender, age, as well as clinical indication. RESULTS: The prevalence of IPE among these suspected stroke patients was 0.8% on carotid CT angiography, and 24 (96%) of all IPEs had not been previously diagnosed by the original reporting radiologists. Most of the IPEs were at the lobar or segmental levels, single and in right upper lobe of pulmonary arteries. In most of the cases, the reviewing radiologists judged the contrast bolus as good. The outpatient group had a lower percentage of patients with IPE when compared with the inpatient counterpart (p = 0.024). The prevalence of IPE in patients with suspected stroke was higher with the increasing of age (p = 0.013). CONCLUSIONS: IPE can occur in suspected stroke patients on carotid CT angiography, and most of them have been previously neglected in clinical practice. Radiologists should check the higher pulmonary arterial vasculature carefully on the contrast-enhanced carotid CTA scans.

The clinical characteristics and short-term prognosis in elderly patients with Guillain-Barré syndrome.

To investigate the clinical characteristics and short-term prognosis of elderly patients with Guillain-Barré syndrome (GBS).We retrospectively analyzed the clinical data of adult GBS. According to the age, the enrolled subjects were divided into 2 groups, that is, patients ≥60 years (elderly group) and those aged 18 to 59 years (nonelderly group). The clinical characteristics and short-term prognosis of the patients in the 2 groups were compared.In total, 535 patients were enrolled. There were 67 patients fell into the elderly group with a mean age of 69 years old; while 468 patients fell into the nonelderly group with a mean age of 39 years old. We found that the elderly patients had significantly lower incidence of antecedent infections (49.3% vs 66.2%, P < 0.01). The time from onset to admission (5 vs 4 days, P < 0.05) and time from onset to nadir (7 vs 6 days, P < 0.05) were significantly longer in the elderly patients. It was noteworthy that more elderly patients were found with lymphocytopenia (55.4% vs 37.3%, P < 0.01), hyponatremia (25.0% vs 10.2%, P < 0.01), hypoalbuminemia (9.0% vs 2.6%, P < 0.05), and hyperglycemia (34.3% vs 15.2%, P < 0.01). Importantly, the elderly patients had longer duration of hospitalization (17 vs 14 days, P < 0.05), higher incidence of pneumonia (29.9% vs 18.8%, P < 0.05), and poorer short-term prognosis (58.2% vs 42.7%, P < 0.05). In patients with severe GBS, no significant differences were observed in disease severity, treatment modality, incidence of pneumonia, and duration of hospitalization between the 2 groups. However, more patients in the elderly group showed poor short-term prognosis (84.1% vs 63.8%, P < 0.01). Further, old age (≥60 years) (OR = 2.906, 95% CI: 1.174-7.194, P < 0.05) and lower Medical Research Council (MRC) score at nadir (OR = 0.948, 95% CI: 0.927-0.969, P < 0.01) were risk factors for poor short-term prognosis in severe GBS patients.The clinical characteristics and short-term prognosis of elderly patients with GBS are distinct from nonelderly adults. Old age (≥60 years) and lower nadir MRC score serve as predictor for poor short-term prognosis in severe GBS patients.

Distinct Clinical Characteristics of Pediatric Guillain-Barré Syndrome: A Comparative Study between Children and Adults in Northeast China.

OBJECTIVE: Clinical characteristics of pediatric Guillain-Barré syndrome (GBS) have been extensively studied whereas scarcely been compared with those of adult GBS. Herein we compared the clinical features of GBS between pediatric and adult patients. METHODS: We retrospectively collected the clinical data of 750 patients with GBS (541 adults and 209 children), and compared the clinical characteristics between children and adults. RESULTS: Pain was a more frequent complaint in children (17.2% vs 9.6%, p < 0.01), who were also found with shorter interval from disease onset to nadir (6.3d vs 7.3d, p < 0.01) and higher incidence of bulbar dysfunction (22.0% vs 14.8%, p < 0.05). The disease severity in children was comparable with adults. In addition, a higher incidence of pediatric GBS was found in summer, especially in July and August (both p < 0.01). However, the incidence of antecedent infections of different seasons in adult and pediatric patients was comparable (p > 0.05). The clinical features of acute motor axonal neuropathy (AMAN) and acute inflammatory demyelinating polyneuropathy (AIDP) in children were overall comparable with adult ones (p > 0.05). Similar to adults, bulbar dysfunction (odds ratio [OR]: 4.621, 95% confidence interval [CI]: 1.240-17.218, p < 0.05) and lower nadir Medical Research Council (MRC) sum score (OR: 0.897, 95% CI: 0.855-0.941, p < 0.01) were also risk factors for mechanical ventilation in children. However, distinct from adult ones, autonomic dysfunction was significantly higher in mechanically ventilated childhood GBS (39.1% vs 8.8%, p < 0.01), which also served as a predictor for mechanical ventilation in pediatric GBS (OR: 70.415, 95% CI: 9.265-535.158, p < 0.01). As to the efficacy of intravenous immunoglobulin, insignificant difference was identified between children and adults. CONCLUSION: The clinical features of pediatric GBS differ from those of adults. Autonomic dysfunction is an independent risk factor for mechanical ventilation in pediatric patients.

Short-Term Prognosis of Mechanically Ventilated Patients With Guillain-Barré Syndrome Is Worsened by Corticosteroids as an Add-On Therapy.

Intravenous immunoglobulin (IVIg) has been proven most effective in treating Guillain-Barré syndrome (GBS). Corticosteroids as an add-on therapy have been prescribed in severe GBS cases. However, the efficacy of intravenous corticosteroids combined with IVIg in dealing with severe GBS remains unclear. We explored the therapeutic effects of different therapeutic regimens on the short-term prognosis of GBS patients, especially the severe cases.We retrospectively analyzed the clinical data of 527 adult patients with GBS who were prescribed to different treatments from 2003 to 2014. The therapeutic effect of a treatment was evaluated by the improvement of Hughes Functional Grading Scale (HFGS) and Medical Research Council (MRC) sum score.With comparable incidence of infectious complications (P > 0.05), more mechanically ventilated patients were found improvement after IVIg treatment than combination IVIg with intravenous corticosteroids (MRC: 97% vs. 72.4%, P < 0.05; HFGS: 97% vs. 72.4%, P < 0.05). As to bedridden patients without mechanical ventilation, incidence of infectious complications (P > 0.05) and ratio of patients who were improved after IVIg were insignificantly different from the combination therapy (MRC: 89.6% vs. 86.5%; HFGS: 69.6% vs. 61.5%; both P > 0.05), even if the intravenous corticosteroids were initiated within 7 days after onset (P > 0.05). In addition, supportive treatment was sufficient for patients who were able to walk with help (HFGS = 3) and mildly affected (HFGS < 3) when compared with IVIg and intravenous corticosteroids.IVIg is sufficient to GBS patients who are unable to walk (HFGS > 3), while corticosteroids are detrimental for short-term prognosis in mechanically ventilated patients when used in combination with IVIg. Further prospective and randomized studies are warranted to validate this finding.

Predictors for mechanical ventilation and short-term prognosis in patients with Guillain-Barré syndrome.

INTRODUCTION: Guillain-Barré syndrome (GBS) is an immune-mediated disorder of the peripheral nervous system. Respiratory failure requiring mechanical ventilation (MV) is a serious complication of GBS. Identification of modifiable risk factors for MV and poor short-term prognosis in mechanically ventilated patients with GBS may contribute to the individualized management and may help improve the outcome of the patients. METHODS: We retrospectively analyzed the clinical data of 541 patients who were diagnosed with GBS from 2003 to 2014. Independent predictors for MV and short-term prognosis in mechanically ventilated patients were identified via multivariate logistic regression analysis. RESULTS: The mean age was 41.6 years with a male predilection (61.2%). Eighty patients (14.8%) required MV. Multivariate analysis revealed that shorter interval from onset to admission (p < 0.05), facial nerve palsy (p < 0.01), glossopharyngeal and vagal nerve deficits (p < 0.01) and lower Medical Research Council (MRC) sum score at nadir (p < 0.01) were risk factors for MV; disease occurrence in summer (p < 0.01) was a protective factor. As to prognostic factors, absence of antecedent infections (p < 0.01) and lower MRC sum score at nadir (p < 0.01) were predictors of poor short-term prognosis in mechanically ventilated patients regardless of treatment modality. We further investigated the predictors of poor short-term prognosis in patients requiring MV with different nadir MRC sum scores. Combined use of intravenous corticosteroids with intravenous immunoglobulin (odds ratio 10.200, 95% confidence interval 1.068-97.407, p < 0.05) was an independent predictor of poor short-term prognosis in mechanically ventilated patients with a nadir MRC sum score from 0 to 12 points, regardless of existence of antecedent infection. CONCLUSIONS: Clinical predictors of MV and poor short-term prognosis in mechanically ventilated GBS patients were distinct. Add-on use of intravenous corticosteroids was a risk factor for poor short-term prognosis in mechanically ventilated patients with a nadir MRC sum score from 0 to 12 points.