[Clinical features of long segmental myelopathy caused by nitrous oxide].

OBJECTIVE: To analyze the clinical and imaging characteristics of the neurological damage caused by nitrous oxide (N2O). METHODS: In the study, 10 patients in the Department of Neurology of China-Japan Friendship Hospital from October 2015 to February 2018 were retrospectively analyzed for the demographic data, the history of inhaled N2O, clinical features, blood examination, electrophysiological examination, spinal magnetic resonance imaging and therapeutic efficacy profiles. RESULTS: The male-to-female ratio was 4:6 and it presented with an age-of-onset 17-26 years [the average age: (20.80±3.12) years]. The time from inhaled N2O to onset was 1 month to 1 year [the average time: (6.95±4.19) months]. Paralysis in all the patients and numbness in 9 patients were the main clinical features, while positive Lhermitte's sign in 3 patients, urinary and defecation disturbance in 4 patients were also found. Blood examination indicated anemia in 2 patients, giant cell anemia in 1 case and small cell hypochromic anemia in 1 case. 3 cases had been treated with vitamin B12 in an external hospital, and the other 7 cases had abnormal increase in homocysteine levels. Electrophysiological examinations showed sensory and motor nerve involvement in 9 patients, and motor nerve involvement in 1 patient. The severity of lower extremity lesion was significantly heavier than that of upper extremity. Spinal magnetic resonance imagings showed that long segmental lesions were present in the cervical spinal cord of all the patients, 3 cases with long segmental lesions of the thoracic cord and 2 cases with spinal cord swelling. In 6 cases, the horizontal axis had an "inverted V-type" T2 high signal, 1 case was classified as "crescent", and 3 cases were "eight-shaped". The symptoms in these 10 cases were alleviated in varying degrees after stopping the inhalation of nitrous oxide, actively supplementing high doses of vitamin B12 and doing early rehabilitation exercises. CONCLUSION: Myelopathy with nitrous oxide presents as paralysis and numbness in limb extremities. In imaging, cervical spinal cord damage is common, accompanied by thoracic spinal cord damage. The horizontal axis is more common in the "inverted V-type". Treatment with high doses of vitamin B12 is effective.

LncRNA CASC2 regulates high glucose-induced proliferation, extracellular matrix accumulation and oxidative stress of human mesangial cells via miR-133b/FOXP1 axis.

OBJECTIVE: Diabetic nephropathy (DN) is one of the primary complications of diabetes. Long non-coding RNA cancer susceptibility candidate 2 (CASC2) has been established to function in DN, while its role in high glucose (HG)-induced human mesangial cells (HMCs) remains limited. MATERIALS AND METHODS: The expression level of CASC2 and miR-133b was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using cell counting kit-8 (CCK-8) assay. Extracellular matrix (ECM) accumulation was monitored through the expression levels of collagen IV (Col IV) and fibronectin (FN) using qRT-PCR and western blot analyses. Oxidative stress was observed through the expression of NADPH oxidase2 (NOX2) and the activity of malondialdehyde (MDA) and superoxide dismutase (SOD) using western blot or corresponding detection kit. The expression of forkhead box P1 (FOXP1) at mRNA and protein levels was determined by qRT-PCR and Western blot, respectively. The relationship between miR-133b and CASC2 or FOXP1 was predicted by online bioinformatics tools and verified by dual-luciferase reporter assay or RNA pull-down. RESULTS: The expression of CASC2 was reduced in serum from DN patients and HG-induced HMCs. CASC2 upregulation inhibited HG-induced HMCs proliferation, ECM accumulation and oxidative stress. MiR-133b was a target of CASC2 with a high level in serum from DN patients and HG-induced HMCs, and its enrichment reversed the effects of CASC2 upregulation. Besides, FOXP1 was a target of miR-133b with a low level in HG-induced HMCs, and its knockdown abolished the impacts of CASC2 upregulation. CONCLUSIONS: CASC2 upregulation suppressed HG-induced proliferation, ECM accumulation and oxidative stress of HMCs through miR-133b /FOXP1 regulatory axis, suggesting that CASC2 was a novel biomarker for DN treatment.

Regulation of Lnc-NTF3-5 on islet ß-cell dysfunction in high glucose environment and related mechanisms.

OBJECTIVE: The pathogenesis of diabetes is closely related to islet ß-cell dysfunction. Lnc-NTF3-5 participates in the occurrence and development of various diseases. However, Lnc-NTF3-54's effect on islet ß-cell dysfunction in high glucose environment remains unclear. MATERIALS AND METHODS: The islet ß cell MIN6 cells were cultured in vitro and randomly divided into control group, high glucose group, NTF3-5 siRNA group, and NTF3-5 group, which was respectively transfected with Lnc-NTF3-5 siRNA and Lnc-NTF3-5 plasmid under high glucose condition. Lnc-NTF3-5 expression was measured by real time PCR and cell proliferation was assessed by MTT assay. In addition, Caspase 3 activity, SOD activity, and ROS content were also detected along with the secretion of IL-10 and IL-1 by enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared with control group, Lnc-NTF3-5 expression in MIN6 cells was significantly increased in high glucose environment (p<0.05). In high glucose environment, Lnc-NTF3-5 plasmid transfection up-regulated Lnc-NTF3-5 expression, inhibited cell proliferation, increased Caspase 3 activity, and decreased SOD activity. Meanwhile, Lnc-NTF3-5 plasmid also increased ROS content and IL-1 level, and decreased IL-10 level and insulin secretion. Compared with high glucose group, the differences were statistically significant (p<0.05). However, transfection of Lnc-NTF3-5 siRNA down-regulated Lnc-NTF3-5 expression under high glucose environment and reversed the above changes. Compared with high glucose group, the differences were statistically significant (p<0.05). CONCLUSIONS: Lnc-NTF3-5 expression is increased in high glucose environment. Targeting Lnc-NTF3-5 can inhibit islet cell apoptosis, oxidative stress, and promote islet cell proliferation and insulin secretion.