Objective:To summarize the clinical manifestations, diagnosis, treatment and prognosis of acute flaccid myelitis (AFM) in children.Methods:Clinical characteristics of 4 AFM cases from Department of Neurology, Children′s Hospital Affiliated to Capital Institute of Pediatrics, from September 2018 to November 2022, were analyzed retrospectively.Results:The age of 4 children with AFM was 7 years, 4 years and 3 months, 7 years and 1 month, 6 years and 5 months, respectively. There were 2 boys and 2 girls. Prodromal infection status showed 3 children of respiratory tract infection and 1 child of digestive tract infection. The main manifestation was asymmetrical limb weakness after infection, and the affected limb range was from monoplegia to quadriplegia. Cranial nerve injury was involved in 1 child, no encephalopathy. Magnetic resonance imaging in the spinal cord of all 4 children showed long T1 and T2 signals, mainly involving gray matter. Cerebrospinal fluid cell-protein separation was observed in 2 children. Pathogen detected in 1 child pharyngeal swab was enterovirus D68. Antibody IgM to adenovirus was positive in the blood of 1 child. Antibody IgG against Echo and Coxsackie B virus were positive in the blood of another child. After glucocorticoid, human immunoglobulin or simple symptomatic treatment and at the same time under later rehabilitation training, muscle strength recovered to different degrees, but there were disabilities left in 3 children.Conclusions:AFM should be considered in children with acute and asymmetrical flaccid paralysis accompanied by abnormal magnetic resonance imaging signal in the central region of spinal cord, especially post-infection. The effective treatment is limited and the prognosis is poor.

Objective To develop a Behavioral Decision-making Scale for Glycemic Management in pregnant women with gestational diabetes and to test its reliability and validity.Methods Based on the trans-theoretical model and behavioral decision theory,the test version of the scale was formed through literature review,semi-structured interview,brainstorming,2 rounds of expert consultation and cognitive interview.A total of 560 pregnant women with gestational diabetes mellitus were recruited from 10 hospitals in Quanzhou,Fujian Province by convenience sampling method from 21 July to November 2023.The data were divided into 2 parts by random number method for exploratory factor analysis and confirmatory factor analysis.Results The scale included 4 dimensions of"behavioral decision-making motivation""behavioral decision-making influencing factors""behavioral decision-making intention"and"behavioral decision-making effectiveness"with 34 items.The Cronbach's αcoefficient of the total scale was 0.971;the split-half reliability was 0.919;the test-retest reliability was 0.863;the content validity index of the scale was 0.853.The exploratory factor analysis extracted 4 common factors,and the cumulative variance contribution rate was 78.28％.The confirmatory factor analysis showed that the factor structure of the scale was stable.Conclusion The scale has ideal reliability and validity,which can be used to measure the level of glycemic management behavior decision-making of pregnant women with gestational diabetes mellitus.

More than 85% of patients with uveal melanoma (UM) carry a GNAQ or GNA11 mutation at a hotspot codon (Q209) that encodes G protein α subunit q/11 polypeptides (Gα_q/11). GNAQ/11 relies on palmitoylation for membrane association and signal transduction. Despite the palmitoylation of GNAQ/11 was discovered long before, its implication in UM remains unclear. Here, results of palmitoylation-targeted mutagenesis and chemical interference approaches revealed that the loss of GNAQ/11 palmitoylation substantially affected tumor cell proliferation and survival in UM cells. Palmitoylation inhibition through the mutation of palmitoylation sites suppressed GNAQ/11^Q209L-induced malignant transformation in NIH3T3 cells. Importantly, the palmitoylation-deficient oncogenic GNAQ/11 failed to rescue the cell death initiated by the knock down of endogenous GNAQ/11 oncogenes in UM cells, which are much more dependent on Gα_q/11 signaling for cell survival and proliferation than other melanoma cells without GNAQ/11 mutations. Furthermore, the palmitoylation inhibitor, 2-bromopalmitate, also specifically disrupted Gα_q/11 downstream signaling by interfering with the MAPK pathway and BCL2 survival pathway in GNAQ/11-mutant UM cells and showed a notable synergistic effect when applied in combination with the BCL2 inhibitor, ABT-199, in vitro. The findings validate that GNAQ/11 palmitoylation plays a critical role in UM and may serve as a promising therapeutic target for GNAQ/11-driven UM.
Humans ; Mice ; Animals ; Lipoylation ; NIH 3T3 Cells ; Uveal Neoplasms/genetics* ; Melanoma/genetics* ; Cell Proliferation ; Proto-Oncogene Proteins c-bcl-2 ; GTP-Binding Protein alpha Subunits, Gq-G11/genetics*

Objective To investigate the effects of enteral immunonutrition supplemented with omega-3 polyunsaturated fatty acid (ω-3 PUFA) on inflammatory response,intestinal mucosal barrier function and the prognosis in patients with severe traumatic brain injury (sTBI).Methods 122 patients of sTBI hospitalized between January 2015 and December 2016 were randomly divided into experimental group (ω-3 PUFA,n=61) and control group (n =61).The serum levels of tumor necrosis factor-α (TNF-α),interleukin (IL)-6 and neuron specific enolase (NSE) were tested with enzyme linked immunosorbent assay.Meanwhile,D-lactate acid and intestinal fat acid binding protein (I-FABP) were evaluated by enzymology spectrophotometer method.After 14 days of treatment,the Glasgow Coma Scale (GCS) scores,Acute Physiology and Chronic Health Evaluation (APACHE) Ⅱ scores and prognoses of both groups were compared.Results The serum levels of inflammatory factors (TNF-α and IL-6),intestinal mucosal barrier function indicators (D-lactate acid and I-FABP) and NSE proteins significantly increased after sTBI (P =0.01).Compared with the control group,the experimental group on day 3 had significantly lower serum levels of inflammatory factors [TNF-α:(107.77± 19.79) μg/Lvs.(151.76±21.65) μg/L,P=0.01;IL-6:(76.85±7.15) μg/Lvs.(105.27±10.12) μg/L,P=0.01] and intestinal mucosal barrier function indicators [D-lactate:(69.81 ±6.32) μg/L vs.(89.80± 8.75) μg/L,P=0.03;I-FABP:(40.81±6.73) μg/Lvs.(56.60±8.58) μg/L,P=0.01].On day 7,the experimental group had significantly lower expression of NSE proteins than the control group [(13.63± 2.53) μg/L vs.(19.12±3.00) μg/L,P=0.02].The experimental group received better prognosis compared to the control group on day 14 [GCS scores:(9.74±0.76) vs.(8.44±0.53),P=0.04;APACHE Ⅱ scores:(14.67±1.37) vs.(17.53±1.47),P=0.03].The experimental group also had fewer days in hospitalization [(19.37±2.27) d vs.(25.42±2.61) d,P=0.01].Conclusion Enteral immunonutrition supplemented with ω-3 PUFA can effectively regulate the inflammatory response,and reduce impairment to the intestinal mucosal barrier function and damage to neurons in patients with sTBI.

AIM:To observe the effects of the combination of berberin and epirubicin on the cell cycle of T24 bladder cancer cells and the underlying mechanisms.METHODS:The cancer cells were exposed to epirubicin in the presence or absence of different concentrations of berberin.The viability of the cancer cells was determined by MTT assay.The cell cycle distribution was detected by flow cytometry, and the protein levels of cyclin D1, CDK2, CDK4, P21 and P27 were detected by Western blot.RESULTS:Berberine markedly enhanced the inhibitory effect of epirubicin on the viability of T24 cells and promoted epirubicin-induced cell cycle arrest at G0/G1 phase as compared with the negative control cells.Epirubicin increased the protein expression of P27 and P21, both of which were enhanced by treatment with berberin.In contrast, berberin exposure further decreased the protein expression of cyclin D1, CDK2 and CDK4 in epirubicin-treated T24 cells.CONCLUSION:Berberine significantly promotes epirubicin-induced G0 /G1 phase arrest in human bladder cancer cells by up-regulating P27 and P21 expression and inhibiting the expression of cyclin D1, CDK2 and CDK4.

Objective To explore the effects of different degrees of intermittent hypoxia (IH) on the activation and the secretion of extracellular matrix in MLg lung fibroblast cell line. Methods MLg lung fibroblast cells in logarithmic growth phase were exposed for 5%O2 for 100 seconds and 21%O2 for 120 seconds in 1 h, 4 h and 8 h groups (IH1, IH4 and IH8) and normoxia group (21%O2 for 8 h, N group). The cells in each group were collected at the end of experiment. Real-time PCR was used to measure the mRNA expression levels ofα-SMA and typeⅠcollagen (COL1) A1, and Western blot assay was used to detect the protein expression levels ofα-SMA and COL1. Results The mRNA and protein expression levels ofα-SMA and COL1 were significantly increased in IH1, IH4 and IH8 groups than those in N group (all P < 0.05). Furthermore, expression levels of α-SMA and COL1 showed a time-dependent increase with IH exposure time. Conclusion The intermittent hypoxia can promote the cell activation and the extracellular matrix secretion of mouse lung fibroblast cells, which may be related with the oxidative stress.

Objective To explore the effects of cobalt chloride (CoCl2)-induced hypoxia on migration of melanoma cells, and to detect the transcription, expression and secretion of Follistatin-like 1(FSTL1) in this process. Methods B16F10 melanoma cell line was treated with CoCl2 in order to mimic hypoxia. Experimental cells were divided into three groups: 0μmol/L, 50μmol/L and 100μmol/L CoCl2 treatment groups. MTT assay was used to assure cell viability, and to determine the treatment concentration of CoCl2. Transwell assay was used to determine the migration ability of B16F10 melanoma cell line. Real-time PCR was used to measure the mRNA expression of Fstl1. Western blot assay was used to detect the intracel?lular and extracellular protein expression of FSTL1. Results The cell viability of B16F10 melanoma cell line was signifi?cantly reduced by CoCl2 treatment, with a time and concentration-dependent manner. The migration ability of B16F10 cell line was significantly increased in CoCl2 treated group compared with that of control group (P<0.05). The mRNA level of Fstl1 was obviously higher in CoCl2 treated group than that of control group (P<0.05). The intracellular expression of FSTL1 protein was consistent with the expression trend of Fstl1 mRNA. Simultaneously, the extracellular protein level of FSTL1 was significantly decreased compared with that of control group. There was no expression of FSTL1 in 100μmol/L CoCl2 treat?ment group. Conclusion The migration ability of melanoma cell line is enhanced by CoCl2 treatment, which may be associ?ated with expression and secretion of FSTL1, however, the relevant mechanism still needs further investigation.

Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for atherosclerosis. Accumulated evidence has revealed that OSAS can induce systemic inflammation, oxidative stress, and endothelial dysfunction, which will contribute to the pathogenesis of atherosclerosis. T lymphocytes can be activated by inflammation and oxidative stress, resulting in the elevated cytotoxicity towards vascular endothelial cells. Thus, T lymphocytes play a key role in OSAS-related atherosclerosis development or progression via immuno-inflammatory alterations. This review described the current development of the role of T lymphocytes in OSAS-related atherosclerosis.

Objective To observe the curative effect of continuous airway positive pressure ventilation (CPAP) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and cough syncope. Methods Forty-three hospitalized patients with OSAHS and cough syncope were collected in the Department of Respiration of Tianjin General Hospital, and analyzed the related information. They were given CPAP treatment, and were divided into good compliance group (n=26) and poor compliance group (n=17) according to CPAP compliance after a half-year treatment. The apnea hypoventilation index (AHI) and c-reactive protein (CRP) were compared before and after treatment between two groups. Results The positive correlation was found between the frequency of the cough syncope and indicators of OSAHS, such as AHI, body mass index (BMI), CRP, sleepiness score (ESS) and circumference of abdomen and neck (r=0.612, 0.431, 0.224, 0.654, 0.435 and 0.344,P<0.05). All these patients were cured after the treatment of both CPAP and medication for 1 or 2 weeks. During a half-year follow-up, the cough syncope didn’t occur in those patients of good compliance group, otherwise cough syncope still happened but with less frequency in patitents of poor compliance group. Before the treatment , there was no significant difference in AHI (45.00±15.69 vs. 48.70±16.47) and CRP (3.46± 1.15 vs. 3.38±0.72) between the two groups. After treatment, AHI (26.97±14.06 vs. 48.18±15.96) and CRP (1.56±0.76 vs. 3.18± 0.78) were significantly lower in the good compliance group than those of the poor compliance group (P<0.01). Conclusion Timely and sustained treatment of OSAHS may help reduce the incidence of cough syncope and significantly improve AHI, CRP and cough symptoms.

Objective To investigate the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) supplementation on neuron apoptosis,brain edema,activation of microglia,inflammatory response and neural function after traumatic brain injury (TBI) in rats,so as to understand the protection of ω-3 PUFA in rats following TBI and its mechanism.Methods TBI model was established using Feeney's method.Ninety SD rats were randomly divided into 5 groups:sham operation group (sham group),TBI group,TBI + selective activator of c-Jun N-terminal kinase (JNK) anisomycin group (TBI + Aniso group),TBI + ω-3 PUFA supplementation group (TBI + ω-3 group),and TBI + ω-3 PUFA supplementation + JNK activation group (TBI + ω-3 + Aniso group).We measured rat behavioral outcomes by modified neurological severity score (mNSS) on day 1,3,and 7 after TBI.Brain water content was measured with wet-dry weight method.The neuron apoptosis and microglial activation (identified by specific marker IBA-1) in TBI cerebral cortex were determined by TUNEL staining and immunofluorescence.Inflammatory cytokines [tumor necrosis factor-α (TNF-α),interleukin (IL)-1α,IL-1β,and IL-6] and the JNK signaling pathway (JNK,pJNK) were tested with reverse transcription-polymerase chain reaction and Western blot,respectively.Results Compared with the sham group,the levels of brain cell apoptosis,brain edema,neuron apoptosis,and inflammatory-relatived factors (TNF-α,IL-1 α,IL-1β,and IL-6) were significantly increased in the other four groups (P ＜ 0.05).Compared with the TBl group,ω-3 PUFA supplementation reduced brain water content following TBI,especially on day 3 after TBI [(78.14 ± 0.57) ％ vs.(82.31 ± 0.81) ％,P ＜ 0.01],and improved neurological function score (P ＜ 0.05).Meanwhile,ω-3 PUFA supplementation suppressed neuron apoptosis,the activation of microglia,and the mRNA and protein expressions of inflammatory cytokines (TNF-α,IL-1α,IL-1 β,IL-6).The activation of JNK signaling pathway was also inhibited by ω-3 PUFA.Conclusion ω-3 PUFA supplementation may markedly reduce brain edema,suppress neuron apoptosis,and improve neurological outcomes after TBI in rats,possibly mediated by inhibiting JNK signaling pathway and microglial activation,reducing microglia-induced cerebral inflammatory responses,demonstrated as down-regulated expression of TNF-α,IL-1α,IL-1β,and IL-6.