Background: This study aimed to estimate temporal trends in metabolically unhealthy obesity (MUO) among United States (US) adults by age, sex, race/ethnicity, and income from 1999 to 2018. Methods: We included 17,230 non-pregnant adults from a nationally representative cross-sectional study, the National Health and Nutrition Examination Survey (NHANES). MUO was defined as body mass index ≥30 kg/m2 with any metabolic disorders in blood pressure, blood glucose, and blood lipids. The age-adjusted percentage of MUO was calculated, and linear regression models estimated trends in MUO. Results: The weighted mean age of adults was 47.28 years; 51.02% were male, 74.64% were non-Hispanic White. The age-adjusted percentage of MUO continuously increased in adults across all subgroups during 1999–2018, although with different magnitudes (all P<0.05 for linear trend). Adults aged 45 to 64 years consistently had higher percentages of MUO from 1999–2000 (34.25%; 95% confidence interval [CI], 25.85% to 42.66%) to 2017–2018 (42.03%; 95% CI, 35.09% to 48.97%) than the other two age subgroups (P<0.05 for group differences). The age-adjusted percentage of MUO was the highest among non-Hispanic Blacks while the lowest among non-Hispanic Whites in most cycles. Adults with high-income levels generally had lower MUO percentages from 1999–2000 (22.63%; 95% CI, 17.00% to 28.26%) to 2017–2018 (32.36%; 95% CI, 23.87% to 40.85%) compared with the other two subgroups. Conclusion This study detected a continuous linear increasing trend in MUO among US adults from 1999 to 2018. The persistence of disparities by age, race/ethnicity, and income is a cause for concern. This calls for implementing evidence-based, structural, and effective MUO prevention programs.

Background: This study aimed to estimate temporal trends in metabolically unhealthy obesity (MUO) among United States (US) adults by age, sex, race/ethnicity, and income from 1999 to 2018. Methods: We included 17,230 non-pregnant adults from a nationally representative cross-sectional study, the National Health and Nutrition Examination Survey (NHANES). MUO was defined as body mass index ≥30 kg/m2 with any metabolic disorders in blood pressure, blood glucose, and blood lipids. The age-adjusted percentage of MUO was calculated, and linear regression models estimated trends in MUO. Results: The weighted mean age of adults was 47.28 years; 51.02% were male, 74.64% were non-Hispanic White. The age-adjusted percentage of MUO continuously increased in adults across all subgroups during 1999–2018, although with different magnitudes (all P<0.05 for linear trend). Adults aged 45 to 64 years consistently had higher percentages of MUO from 1999–2000 (34.25%; 95% confidence interval [CI], 25.85% to 42.66%) to 2017–2018 (42.03%; 95% CI, 35.09% to 48.97%) than the other two age subgroups (P<0.05 for group differences). The age-adjusted percentage of MUO was the highest among non-Hispanic Blacks while the lowest among non-Hispanic Whites in most cycles. Adults with high-income levels generally had lower MUO percentages from 1999–2000 (22.63%; 95% CI, 17.00% to 28.26%) to 2017–2018 (32.36%; 95% CI, 23.87% to 40.85%) compared with the other two subgroups. Conclusion This study detected a continuous linear increasing trend in MUO among US adults from 1999 to 2018. The persistence of disparities by age, race/ethnicity, and income is a cause for concern. This calls for implementing evidence-based, structural, and effective MUO prevention programs.

Background: This study aimed to estimate temporal trends in metabolically unhealthy obesity (MUO) among United States (US) adults by age, sex, race/ethnicity, and income from 1999 to 2018. Methods: We included 17,230 non-pregnant adults from a nationally representative cross-sectional study, the National Health and Nutrition Examination Survey (NHANES). MUO was defined as body mass index ≥30 kg/m2 with any metabolic disorders in blood pressure, blood glucose, and blood lipids. The age-adjusted percentage of MUO was calculated, and linear regression models estimated trends in MUO. Results: The weighted mean age of adults was 47.28 years; 51.02% were male, 74.64% were non-Hispanic White. The age-adjusted percentage of MUO continuously increased in adults across all subgroups during 1999–2018, although with different magnitudes (all P<0.05 for linear trend). Adults aged 45 to 64 years consistently had higher percentages of MUO from 1999–2000 (34.25%; 95% confidence interval [CI], 25.85% to 42.66%) to 2017–2018 (42.03%; 95% CI, 35.09% to 48.97%) than the other two age subgroups (P<0.05 for group differences). The age-adjusted percentage of MUO was the highest among non-Hispanic Blacks while the lowest among non-Hispanic Whites in most cycles. Adults with high-income levels generally had lower MUO percentages from 1999–2000 (22.63%; 95% CI, 17.00% to 28.26%) to 2017–2018 (32.36%; 95% CI, 23.87% to 40.85%) compared with the other two subgroups. Conclusion This study detected a continuous linear increasing trend in MUO among US adults from 1999 to 2018. The persistence of disparities by age, race/ethnicity, and income is a cause for concern. This calls for implementing evidence-based, structural, and effective MUO prevention programs.

Background: This study aimed to estimate temporal trends in metabolically unhealthy obesity (MUO) among United States (US) adults by age, sex, race/ethnicity, and income from 1999 to 2018. Methods: We included 17,230 non-pregnant adults from a nationally representative cross-sectional study, the National Health and Nutrition Examination Survey (NHANES). MUO was defined as body mass index ≥30 kg/m2 with any metabolic disorders in blood pressure, blood glucose, and blood lipids. The age-adjusted percentage of MUO was calculated, and linear regression models estimated trends in MUO. Results: The weighted mean age of adults was 47.28 years; 51.02% were male, 74.64% were non-Hispanic White. The age-adjusted percentage of MUO continuously increased in adults across all subgroups during 1999–2018, although with different magnitudes (all P<0.05 for linear trend). Adults aged 45 to 64 years consistently had higher percentages of MUO from 1999–2000 (34.25%; 95% confidence interval [CI], 25.85% to 42.66%) to 2017–2018 (42.03%; 95% CI, 35.09% to 48.97%) than the other two age subgroups (P<0.05 for group differences). The age-adjusted percentage of MUO was the highest among non-Hispanic Blacks while the lowest among non-Hispanic Whites in most cycles. Adults with high-income levels generally had lower MUO percentages from 1999–2000 (22.63%; 95% CI, 17.00% to 28.26%) to 2017–2018 (32.36%; 95% CI, 23.87% to 40.85%) compared with the other two subgroups. Conclusion This study detected a continuous linear increasing trend in MUO among US adults from 1999 to 2018. The persistence of disparities by age, race/ethnicity, and income is a cause for concern. This calls for implementing evidence-based, structural, and effective MUO prevention programs.

Hyperhomocysteinemia (HHcy) is one of the independent risk factors for youth cerebral infarction. Gene mutation of key enzymes in homocysteine metabolism is the main cause of HHcy. Few cases of cystathionine beta-synthase (CBS) compound heterozygous mutation complicated with pulmonary embolism and lower extremity artery embolism have been reported. This article reported a young cerebral infarction patient complicated with pulmonary embolism and lower extremity artery embolism, who was subsequently detected with significantly elevated blood Hcy, and finally etiologically diagnosed with CBS 833 T>C/1082C>T compound heterozygous mutation. With the treatment of folic acid, methyl cobalt amine, vitamin B 6 and anticoagulant, the blood Hcy has been gradually declined, and no new thrombotic events occurred during the follow-up period of a year.

Objective:To explore the effect of Syncytin-1 overexpression in the skeletal muscle cells on changes of sodium-dependent neutral amino acid transporter 1 (ASCT1), inflammatory factors and neuroprotective factors in co-culture model of spinal cord anterior horn motor neurons, Schwann cells, and skeletal muscle cells.Methods:(1) Spinal cord anterior horn motor neurons, skeletal muscle cells, and Schwann cells were primarily cultured in vitro; the expressions of choline acetyltransferase (ChAT), α-smooth muscle actin (α-SMA) and calcium-binding protein B (S100B) in the neurons, muscle cells, and Schwann cells were detected by immunofluorescence staining, respectively. (2) Plasmids containing Syncytin-1 or control plasmids were transfected into the skeletal muscle cells, respectively; 24 h after that, these transfected skeletal muscle cells were co-cultured with spinal cord anterior horn motor neurons and Schwann cells, respectively (Syncytin-1 recombinant plasmid transfection group or control plasmid transfection group); changes of morphology and junction of co-culture cells were observed under inverted microscope. Forty-eighty h after co-culture, enzyme-linked immunosorbent assay (ELISA) was used to detect the tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS) and vascular endothelial growth factor (VEGF) concentrations in the supernatant of co-culture cells; real-time quantitative (qRT)-PCR and Western blotting were used to detect the Syncytin-1, ASCT1, TNF-α, iNOS, and VEGF mRNA and protein expressions in the co-culture cells Results:(1) Immunofluorescent staining showed that more than 95% spinal cord anterior horn motor neurons were with positive CHAT expression, more than 95% skeletal muscle cells were with positive α-SMA expression, and more than 95% Schwann cells were with positive S100B expression; all of which were localized in the cytoplasm. (2) There were no obvious differences in number or morphology of co-culture cells between the Syncytin-1 recombinant plasmid transfection group and control plasmid transfection group. As compared with the control plasmid transfection group, Syncytin-1 recombinant plasmid transfection group had significantly increased concentrations of TNF-α, iNOS and VEGF in the supernatant of co-cultured cells, and statistically increased mRNA and protein expressions of TNF-α, iNOS, syncytin-1 and VEGF, and significantly decreased ASCT1 mRNA and protein expressions ( P<0.05). Conclusion:Syncytin-1 overexpression in the skeletal muscle cells may decrease the ASCT1 expression, induce the inflammatory factor release, and increase the neuroprotective factor VEGF expression.

Small nerve fibers refer to peripheral afferent small diameter, thinly myelinated Aδ-fibers and unmyelinated C-fibers. Small nerve fiber impairment caused by various mechanisms calls small fiber neuropathy (SFN). Small nerve fiber impairment caused by immune injury in Guillain-Barre Syndrome (GBS) is a common cause of SFN, which is currently reported as a variant of GBS; the main manifestations of small nerve fiber impairment of GBS are sense disturbance to pain and temperature and autonomic nerve dysfunction. Small nerve fiber impairment of GBS is widely correlated with the prognosis and mortality of GBS. At present, researches on small nerve fiber impairment of GBS are mainly based on case reports, and its diagnosis mainly relies on pathological examination and electrophysiological examination, which is easy to be missed in the early stage. Early recognition and appropriate management of small nerve fiber impairment of GBS are keys to reduce GBS mortality. In this paper, the pathogenesis, clinical manifestations, diagnosis, treatment and other aspects of small nerve fiber impairment of GBS are reviewed to provide clinicians with a comprehensive understanding of small nerve fiber impairment of GBS.

Amyotrophic lateral sclerosis (ALS) is a series of upper and lower motor neuron degenerative disorders,characterized by muscle weakness and atrophy,bulbar paralysis and pyramidal signs.Recent studies showed that ALS may present with many atypical clinical manifestations,such as cognitive impairment,autonomic dysfunction,extrapyramidal disorders,paresthesia,and abnormal eye movements.This review summarized the recent understanding of atypical clinical manifestations in ALS.

Objective To study the relationship between serum uric acid (UA) level and cerebrovascular stenosis in acute ischemic stroke (AIS) patients.Methods Five hundred and thirteen patients with AIS or old IS admitted to our hospital from April 2014 to April 2016 were divided into primary IS group (n=236),recurrent IS group (n=136),and old IS group (n=141).Venous blood samples were taken on admission for biochemical testing.The patients were further divided into serum UA≤255 μmol/L group (n=128),serum UA=256-312μmol/L group (n=129),serum UA=313-371 μmol/L group (n=129),and serum UA＞371 μmol/L group (n=127).Their cerebrovascular stenosis was assessed by CT angiography or magnetic resonance angiography after admission.Results The severity of cerebrovascular stenosis,hypertension,diabetes and hyperlipidemia was significantly different in primary IS group,recurrent IS group and old IS group (27.5％ vs 33.8％ vs 12.8％、24.2％ vs 28.7％ vs 46.8％、61.9％ vs 49.3％ vs 40.4％、71.6％ vs 61.8％ vs 46.8％,P=0.000).Logistic regression analysis showed that serum UA≤ 255 μmol/L was an independent risk factor for cerebrovascular stenosis (OR =2.787,95 ％CI:2.209-3.365,P=0.001).The risk of cerebrovascular stenosis decreased gradually with the elevated serum UA level.Conclusion Serum UA level is not directly related with recurrent IS.Low serum UA level is a risk factor for cerebrovascular stenosis in AIS.

Objective To analyze the related influencing factors of progressive ischemic stroke, and to investigate the value of serum markers for prediction of progressive ischemic stroke. Methods Three hundred and six patients with acute cerebral infarction were divided into progressive ischemic stroke (PIS) group (n=91) and non-progressive ischemic stroke (NPIS) group (n=215). Data of gender, age, past medical history, personal history and serum markers were collected and compared in two groups. Binary Logistic regression was used to analyze the influencing factors of PIS. The receiver operating characteristic (ROC) curves of neutrophils to lymphocytes ratio (NLR), fibrinogen and fasting blood glucose were analyzed in two groups. Results Positive rates of hypertension history, diabetes history, hypercholesterolemia history, incidence of large artery atherosclerotic (LAA) stroke were significantly higher in PIS group than those in NPIS group ( P<0.05). The levels of neutrophils, NLR, fibrinogen and fasting blood glucose were significantly higher, but the level of lymphocytes was significantly lower in patients with PIS than those in patients with NPIS (P<0.05). Logistic regression analysis confirmed that diabetes, LAA stroke, NLR, fibrinogen and fasting blood glucose were independent risk factors for the PIS ( P<0.05). The areas under ROC curve by NLR, fibrinogen and fasting blood glucose were 0.777, 0.560 and 0.574, respectively. The sensitivities of NLR, fibrinogen and fasting blood glucose were 72.5%, 59.8%and 47.3%, respectively;and the specificities were 76.7%, 51.2% and 69.8%, respectively. Conclusion The occurrence of PIS is related with blood pressure, blood lipids, inflammatory cells in peripheral bolld, fibrinogen and fasting blood glucose. The level of NLR in peripheral blood can predict the occurrence of PIS, which can be used as an important reference index for early diagnosis of PIS.