Risk factors for anxiety in patients with epilepsy: A meta-analysis.

BACKGROUND: Epilepsy is a very common neurological disease, and it is important to focus on both controlling seizures and alleviating the psychological problems associated with this disease.Anxiety is an important risk factor for epilepsy and seriously affects the quality of life of patients with epilepsy (PWE). However, several risk factors for anxiety in PWE are relatively controversial and understudied. This meta-analysis was performed to identify potential risk factors for anxiety in PWE with the aim of reducing the incidence of anxiety and improving the quality of life among the individuals. METHOD: The PubMed, Embase and Cochrane Library databases were systematically searched up to July 2023 to find eligible original English studies. All the search results were reviewed based on our inclusion and exclusion criteria. We calculated the combined odds ratios (ORs), standard mean differences (SMDs) and their corresponding 95% confidence intervals (CIs) to evaluate the effect of the included risk factors on anxiety in PWE. RESULTS: Twenty-four studies involving 5,403 PWE were ultimately included. The pooled results of our meta-analysis showed that female sex (OR = 1.67; 95 % CI: 1.30,2.15; p < 0.001), unmarried/divorced/widowed (OR = 0.83; 95 % CI: 0.72,0.96; p = 0.011), low socioeconomic status (OR = 0.47; 95 % CI: 0.33,0.67; p < 0.001), education levels below high school (OR = 1.74; 95 % CI: 1.36,2.23; p < 0.001), a history of trauma (OR = 2.53; 95 % CI: 1.69,3.78; p < 0.001), monotherapy (OR = 0.49; 95 % CI: 0.39,0.62; p < 0.001), AED-induced psychiatric side effects (OR = 2.45; 95 % CI: 1.20,4.98); p = 0.014), depression (OR = 5.45 95 % CI: 2.49,11.94; p < 0.001), a history of suicide (OR = 3.56; 95 % CI: 1.72,7.38; p = 0.001), and illness-related shame (OR = 2.76; 95 % CI: 2.17,3.52; p < 0.001) were risk factors for anxiety. CONCLUSION: This meta-analysis showed that female, unmarried, low socioeconomic status, education level below senior high school, a history of trauma, monotherapy, AED-induced psychiatric side effects, depression, a history of suicide, and shame were risk factors for anxiety in PWE. However, further research is needed to determine the effect of other potential risk factors on anxiety in PWE. In addition, most of the studies included in this meta-analysis were not uniform in scale, and the risk factors were not comprehensive; therefore, larger prospective studies in different countries are needed to further investigate these risk factors.

MiR-767-3p promotes the progression of hepatocellular carcinoma via targeting CASP-3/-9.

OBJECTIVE: The aim of this study was to investigate the relationship between miR-767-3p and hepatocellular carcinoma (HCC). METHOD: We examined the expression of miR-767-3p in both HCC tissues and HCC cell lines by qRT-PCR and western blot assay. We also investigated the influence of miR-767-3p on HCC by transfecting HCC cells with either miR-767-3p mimics or inhibitors. RESULT: MiR-767-3p expression was increased in HCCs and cell lines. Functional analyses demonstrated that miR-767-3p increased HCC cell proliferation and prevented apoptosis both in vitro and in vivo, whereas miR-767-3p inhibition had the opposite effect. Caspase-3 and caspase-9 were found to be direct targets of miR-767-3p in HCC cell lines, and overexpression of miR-767-3p suppressed caspase-3/-9 production. Caspase-3 and caspase-9 siRNA knockdown revealed similar promoting of cell proliferation and inhibiting of cell apoptosis produced by miR-767-3p overexpression, whereas caspase-3/-9 siRNAs inhibited miR-767-3p knockdown-induced inhibition of cell proliferation and promotion of cell apoptosis. CONCLUSION: MiR-767-3p promoted proliferation and prevented apoptosis in human hepatocellular carcinoma (HCC) through inhibiting the caspase-3/caspase-9 pathway.

COX10-AS1-mediated miR-361-5p regulated cell invasion and migration by targeting SPRY1 in oral squamous cell carcinoma.

BACKGROUND: COX10-AS1 belongs to the class of lncRNA and has been shown to influence carcinogenesis; however, its function and underlying mechanism in oral squamous cell carcinoma are still unclear (OSCC). METHOD: Western blotting, immunohistochemistry, and RT-PCR were used to identify gene expression. Cell invasion and migration were discovered using Transwell and Scratch-Wound analyses. The interaction between lncRNA and miRNA was examined using dual-luciferase and immunofluorescence assays. RESULTS: We discovered that COX10-AS1 was significantly downregulated in OSCC tissues when compared to matched noncancerous tissues, indicating a dismal prognosis for OSCC patients. By raising the expression of MMP-2/-9 and Snail and lowering the expression of E-cadherin, COX10-AS1 deletion increased OSCC cell invasion and migration. Next, three binding sites between COX10-AS1 and miR-361-5p were shown in the StarBase V2.0 database. Pearson's correlation analysis revealed a negative association between the expression of COX10-AS1 and that of miR-361-5p, and miR-361-5p transfection reduced COX10-AS1's influence on OSCC cell invasion and migration. Furthermore, COX10-AS1 favorably regulated SPRY1, a miR-361-5p target gene. CONCLUSION: Through the miR-361-5p/SPRY1 axis, COX10-AS1 can act as a tumor suppressor and is decreased in OSCC.

Dual-mode colorimetric and fluorescence sensing system for the detection of captopril based on Fe/NC nanozymes and carbon dots.

Metal nitrogen-doped carbon (MNC) nanozymes have received increasing attention in bio-catalysis filed due to adequate catalytic activity, outstanding stability and reusability. Herein, the Fe/NC nanozymes (Fe/NC NZs) with peroxidase-like activity was successfully synthesized and a fluorescence turn on and colorimetric dual-mode sensing system was developed for quantification of captopril (CP) based on Fe/NC NZs and orange-emitting carbon dots (O-CDs). The Fe/NC NZs as an enzyme mimic can efficiently catalyze the 3,3',5,5'-tetramethylbenzidine (TMB) chromogenic reaction, forming blue-colored oxidized TMB product (oxTMB) with the presence of H2O2, leading to the fluorescence quenching of O-CDs simultaneously via the inner filter effect (IFE). When CP was present, the blue oxTMB was reduced to colorless TMB, resulting in the inhibition of IFE and the recovery of fluorescence of O-CDs. The fluorescence increase of O-CDs and absorbance decrease of oxTMB depended on CP concentration. Good linear relationships of fluorescence and colorimetric sensing towards CP were obtained in the range from 1 to 50 µM, and the detection limits were 0.47 and 0.56 µM, respectively. Moreover, this as-constructed dual-mode sensor was used to detect CP in pharmaceutical products with satisfactory results.

USP36 promotes tumor growth of non-small cell lung cancer via increasing KHK-A expression by regulating c-MYC-hnRNPH1/H2 axis.

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer with poor prognosis. This study designated to figure out the effects of Ubiquitin Specific Peptidase 36 (USP36) on NSCLC. Data of this study demonstrated that upregulation of USP36 was observed in NSCLC tissues and cell lines. Overexpression of USP36 promoted NSCLC cell proliferation and inhibited NSCLC cell apoptosis. Knockdown of USP36 decreased Ketohexokinase A (KHK-A) and increased KHK-C expression at both RNA and protein levels. Expression of c-MYC and hnRNPH1/H2 was positively correlated with the expression of USP36. Upregulation of c-MYC reversed the downregulation of hnRNPH1/H2 induced inhibition of USP36. Overexpression of hnRNPH1/H2 reversed the downregulation of KHK-A induced inhibition of USP36. Results of in vivo xenograft model were consistent with the findings of in vitro experiments. In summary, overexpression of USP36 in NSCLC accelerated tumor growth through upregulation of KHK-A, which was medicated by stabilizing c-MYC to increase hnRNPH1/H2 expression.

Novel sodalite stabilized zero-valent iron for super stable and outstanding efficiency in activating persulfate for organic pollutants fast removal.

In this study, novel porous sodalite (SOD) was synthesized through Reactive Oxidation Species (ROS) route from industrial waste lithium silicon fume (LSF) to stabilize nZVI (SOD@nZVI), and used as an outstanding persulfate (PS) activator for efficient organic degradation. Characterization results revealed nZVI evenly distributed on SOD via ion-exchange, and the fabricated SOD@nZVI exhibited high stability and superior reactivity over a wide pH range of 2-12 during oxidation reaction. The mechanism responsible for fast organic degradation in the SOD@nZVI+PS system was carefully investigated, and weak magnetic field (WMF) and friction were found to contribute to improved SOD@nZVI performance. The fast redox cycle of Fe2+/Fe3+ on SOD@nZVI can be stimulated by changing the mixing condition and altering the friction layer to harvest mechanical energy during the reaction, which can maximum persulfate activation to generate more reactive radicals for organic fast degradation. This study is of great significance, as it offers a practical route turning waste into excellent PS activator for in-situ organic pollution remediation, as well as proposing a new idea to maximum PS activation performance by manipulating the inner lining of reactor.

GDAP2 Overexpression Affects the Development of Neurons and Dysregulates Neuronal Excitatory Synaptic Transmission.

GDAP2 is a gene highly expressed in the human brain and encodes ganglioside-induced differentiation-associated protein 2 (GDAP2). At present, little is known about the function of GDAP2. In recent years, it has been reported that mutations in the GDAP2 gene may be involved in hereditary cerebellar ataxia. In this study, we first conducted a preliminary study on the effect of GDAP2 overexpression on cultured primary hippocampal neurons in vitro. By analysing neuronal morphology, it was found that the complexity of neurons and the number of dendritic spines increased when GDAP2 was upregulated. The electrophysiological recordings showed that GDAP2 overexpression significantly increased the frequency of mEPSCs, suggesting that GDAP2 overexpression dysregulates excitatory synaptic transmission in cultured primary hippocampal neurons in vitro. On the other hand, behavioural and field-potential recordings of epileptic mouse models showed that GDAP2 overexpression was associated with increased seizure frequency. In summary, this preliminary study suggested that GDAP2 overexpression may have a certain pathogenic effect, providing a new perspective for the study of gene-related diseases such as epilepsy.

Pre- and postoperative heart rate variability and vagus nerve stimulation in patients with drug-resistant epilepsy - A meta-analysis.

OBJECTIVE: The effect of vagus nerve stimulation (VNS), an important auxiliary therapy for treating drug-resistant epilepsy (DRE), on autonomic nerve function is still controversial. Heart rate variability is a widely used indicator of autonomic nerve function. To clarify the relationship between VNS and heart rate variability (HRV), we performed a meta-analysis to systematically evaluate the effect of VNS on HRV in patients with epilepsy. METHODS: We performed a systematic review by searching the following online databases: PubMed, Web of Science, EMBASE and the Cochrane Library. The key search terms were "vagal nerve stimulation," "epilepsy" and "heart rate variability". Other features of VNS in patients with epilepsy include postoperative changes in low-frequency (LF), high-frequency (HF) and low-frequency/high-frequency (LF/HF) heart rate variability, which were used as evaluation indices, and the Newcastle-Ottawa Quality Assessment Scale and Stata 14.0 statistical software were used for literature quality evaluation and meta-analysis. RESULTS: Twelve studies published in English were obtained, and 229 patients with epilepsy who underwent VNS were ultimately included after elimination of duplicate articles and those that did not meet the inclusion criteria. Regarding LF heart rate variability, in the response subgroup, patients with DRE with VNS presented a lower value (-0.58) before surgery than after surgery, with a 95% confidence interval (CI) ranging from -1.00 to -0.15. For HF heart rate variability, patients with DRE with VNS had a lower value (-0.45) before surgery than after surgery in the response subgroup, with a 95% CI ranging from -0.74 to -0.17. No differences were found for LF/HF values or the LF and HF values of other subgroups. CONCLUSION: VNS has little effect on the balance of sympathetic and parasympathetic nerve activity and would not be expected to cause cardiovascular autonomic dysfunction in patients with DRE. For patients with DRE, VNS can control seizures and has little effect on autonomic nervous function.

Development of carbon dot-thiochrome-based sensing system for ratiometric fluorescence detection of D-penicillamine.

A simple and rapid ratiometric fluorescent sensing system for D-penicillamine (D-PA) determination is developed based on yellow carbon dots (Y-CDs) combined with thiochrome (oxVB1) for the first time. The oxidization of thiamine (VB1) can be catalyzed by Alkaline-hydrolyzed artemisinin (a-ART) to form oxVB1, which leads to the occurrence of fluorescence emission peak at 466 nm. Furthermore, the oxidation reaction between a-ART and VB1 could be inhibited by D-PA, and accompanied with the decrease of fluorescence at 466 nm. However, the fluorescence peak of Y-CDs as an internal reference at 566 nm was almost unchanged. The ratiometric signal changes contributed to a robust and sensitive D-PA sensing. Under the optimal condition, a good linear response for the D-PA detection was obtained in the ranges of 0.5-50 µM with a detection limit of 0.33 µM. In addition, Y-CDs and thiochrome-based sensing system was applied to D-PA determination in real samples and obtained acceptable results. We developed a new carbon dots/thiochrome fluorescent nanoprobe for ratiometric fluorescence sensing of D-penicillamine.

ARF3 inhibits proliferation and promotes apoptosis in gastric cancer by regulating AKT and ERK pathway.

ADP-ribosylation factor 3 (ARF3) has confirmed participate in diverse biological processes in many cancers. However, the expression patterns and roles of ARF3 in gastric cancer (GC) remains largely unknown. In our study, by using qRT-PCR and western blot, we found that, in In GC tissues and cells, the expression of ARF3 was significantly down-regulated. Functional experiments demonstrated that ARF3 inhibited proliferation, induced cycle arrest and enhanced apoptosis of GC cells. Moreover, by performing western blot, we found that ARF3 could regulate the protein expression of key factors of AKT and ERK pathway. Using orthotopic xenograft mouse models, it is showed that ARF3 could inhibit GC tumorigenesis in vivo. To sum up, ARF3 may suppress proliferation, induced cycle arrest and promotes apoptosis of GC by modulating AKT and ERK pathway. It might act as a potential biomarker for GC prognosis.

Tetrandrine alleviates cerebral ischemia/reperfusion injury by suppressing NLRP3 inflammasome activation via Sirt-1.

BACKGROUND & AIMS: Tetrandrine (Tet) has been reported to have anti-inflammatory effects and protect from the ischemic strokes. The NLRP3 inflammasome plays a key role in cerebral ischemia/reperfusion (I/R)-induced inflammatory lesions. However, the molecular mechanisms of Tet related to the progression of cerebral ischemia are still unclear. Therefore, the aim of this study was to investigate the possible effects of Tet on cerebral ischemia and the related mechanisms involved in NLRP3 inflammasome. METHODS: C57BL/6J mice used as a cerebral I/R injury model underwent middle cerebral artery occlusion (MCAO) for 2 h following reperfusion for 24 h. Tet (30 mg/kg/day, i.p.) was administered for seven days and 30 min before and after MCAO. Their brain tissues were evaluated for NLRP3 inflammasome and Sirtuin-1 (Sirt-1) expression. An intracerebroventricular injection of Sirt-1 siRNA was administered to assess the activation of the NLRP3 inflammasome. RESULTS: Tet significantly reduced the neurological deficits, infarction volume, and cerebral water content in MCAO mice. Moreover, it inhibited I/R-induced over expression of NLRP3, cleaved caspase-1, interleukin (IL)-1ß, IL-18, and Sirt-1. Sirt-1 knockdown with siRNA greatly blocked the Tet-induced reduction of neurological severity score and infarct volume, and reversed the inhibition of NLRP3 inflammasome activation. CONCLUSION: Our results demonstrate that Tet has benefits for cerebral I/R injury, which are partially related to the suppression of NLRP3 inflammasome activation via upregulating Sirt-1.

Rare earth elements recycling from waste phosphor by dual hydrochloric acid dissolution.

This paper is a comparative study of recycling rare earth elements from waste phosphor, which focuses on the leaching rate and the technical principle. The traditional and dual dissolution by hydrochloric acid (DHA) methods were compared. The method of dual dissolution by hydrochloric acid has been developed. The Red rare earth phosphor (Y0.95Eu0.05)2O3 in waste phosphor is dissolved during the first step of acid leaching, while the Green phosphor (Ce0.67Tb0.33MgAl11O19) and the Blue phosphor (Ba0.9Eu0.1MgAl10O17) mixed with caustic soda are obtained by alkali sintering. The excess caustic soda and NaAlO2 are removed by washing. The insoluble matter is leached by the hydrochloric acid, followed by solvent extraction and precipitation (the DHA method). In comparison, the total leaching rate of the rare earth elements was 94.6% by DHA, which is much higher than 42.08% achieved by the traditional method. The leaching rate of Y, Eu, Ce and Tb reached 94.6%, 99.05%, 71.45%, and 76.22%, respectively. DHA can decrease the consumption of chemicals and energy. The suggested DHA method is feasible for industrial applications.

Perinatal outcome of recurrent pre-eclampsia versus pre-eclampsia in nulliparas.

AIM: The aim of the study was to compare the perinatal outcome of recurrent pre-eclampsia in multiparas with that of pre-eclampsia in nulliparas. METHODS: This retrospective study was performed by collecting maternal and perinatal data from records of women with pre-eclampsia who delivered at Mackay Memorial Hospital over a 10-year period. Fifty women with recurrent pre-eclampsia were compared with 207 women who developed pre-eclampsia as nulliparas. In the 50 multiparas, the outcome of recurrent pre-eclampsia was also compared with that of their earlier episodes of pre-eclampsia. Maternal and fetal variables compared included maternal blood pressure, serum biochemistry, rate of preterm delivery, rate of abruptio placentae and neonatal outcome. RESULTS: Compared with nulliparous women with pre-eclampsia (n = 50), women with recurrent pre-eclampsia (n = 207) had a smaller increase in mean maternal blood pressure (27.0 +/- 18.9 mmHg vs 34.3 +/- 19.3 mmHg, P = 0.021), less dipstick proteinuria (>or=++; 36.0 vs 58.5%, P = 0.004), and bore children with a heavier mean birthweight (2909.1 +/- 895.5 g vs 2551.1 +/- 933.0 g, P = 0.017). No significant statistical difference was found in the gestational age of delivery, maternal serum biochemical levels and rate of abruptio placentae or preterm delivery. Within the multiparous group (n = 50), recurrent disease was associated with a lower mean maternal blood pressure and dipstick proteinuria and with higher birthweight than in their previous pre-eclamptic pregnancies. CONCLUSION: Recurrent pre-eclampsia appears to be less severe and to have a better perinatal outcome than pre-eclampsia in nulliparas.