Epilepsy is a common nervous system disease. It has been found that the pathogenesis of epilepsy is associated mutations in various genes, including genes encoding voltage-dependent ion channel, genes encoding ligand-gated ion channel, and solute carrier family genes. Different types of epilepsy caused by different mutations have different responses to drugs, and therefore, diagnosis and medication guidance based on genes are new thoughts for developing therapies. With the application of next-generation sequencing technology, more and more genes will be determined, which helps to further study the pathogenic mechanism of mutant genes and provides a basis for precision drug therapy for epilepsy.
Epilepsy ; drug therapy ; etiology ; genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Ion Channels ; genetics ; Precision Medicine

Microbial keratitis(MK)is a common corneal blind eye disease in the world. Severe keratitis can cause irreversible complications and even lead to blindness. Rapididentification of pathogen is the key for early and accurate MK treatment and a large of clinical data indicated that identifying the type of infected microorganisms accurately and quickly is still a challenge for ophthalmologists. The in vivo confocal microscopy(IVCM)is a non-invasive imaging technology that can provide high-resolution images of all corneal layers in a fast and real-time manner, has been used in the diagnosis and follow-up of corneal diseases. In recent years, with the intersection and integration of disciplines, artificial intelligence has been used to identify the characteristic structures in microbial keratitis IVCM images, which has brought important value for accurate and rapid diagnosis of microbial keratitis. Therefore, this article will review the characteristics of confocal microscopy in the diagnosis of microbial keratitis and the application of artificial intelligence in the diagnosis of microbial keratitis. It is of great significance to promote the diagnosis and treatment of keratitis in the future.

Hepatic fibrosis refers to the pathological process of abnormal proliferation of intrahepatic connective tissue caused by various pathogenic factors, resulting in the excessive accumulation of extracellular matrix (ECM) in the liver and the formation of fibrous scar. Its continuous deterioration will gradually develop into liver cirrhosis, liver failure, liver cancer and other serious liver diseases. Because liver fibrosis and early liver cirrhosis can be reversed, it is very important to control the reversible process of liver fibrosis for the prevention and treatment of liver cirrhosis and liver cancer. In recent years, it has been found that traditional Chinese medicine(TCM) has the characteristics of multi-target, less toxic and side effects and good effect in the treatment of liver fibrosis. In this paper, the mechanism of anti-hepatic fibrosis of TCM and its compound was summarized. TCM can regulate transforming growth factor-β (TGF-β), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and other growth factors to inhibit the activation of (HSCs) and induce the apoptosis of activated HSCs, promote the expression of adiponectin and inhibit the secretion of leptin, inhibit the inflammatory reaction of liver, resist oxidant stress, inhibit the capillarization of hepatic sinusoidal endothelial cells, so as to effectively prevent the progress of liver fibrosis. Therefore, TCM can inhibit the development of liver fibrosis through multi-mechanism and multi-level, and is one of the important means to treat liver fibrosis.

OBJECTIVE： To establish the method for content determination of total flavonoids from Combretum alfrdii， and to optimize the extraction technology of total flavonoids from C. alfrdii. METHODS： Using aluminium trichloride as， chromogenic agent， UV spectrum was adopted to determine the content of total flavonoids from C. alfrdii. Based on single factor test， ethanol volume fraction， material-liquid ratio， extraction time， extraction temperature and times were selected as investigation factors， and the content of total flavonoids was selected as response value， Plackett-Burman design was used to screen the factors that had significant influence on the content of total flavonoidsfrom C. alfrdii. Then steepest climbing test was adopted to confirm the optimum valuing range； the extraction technology of total flavonoids was optimized by Box-Behnken response methodology. RESULTS： The linear range of total flavonoids were 0.012-0.036 mg/mL （r＝0.999 9）； RSDs of precision， stability and repeatability tests were less than 3％； the recovery ranged from 92.98％ to 99.86％ （RSD＝2.71％， n＝6）. The optimal extraction technology included that 60％ ethanol， material-liquid ratio of 1 ∶ 34 （g/mL）， extracting for 3 times， lasting for 60 min， extraction temperature of 80 ℃. Under this technology， average content of total flavonoids from C. alfrdii was 2.71％ （RSD＝1.69％， n＝6）， and the relative error was 2.65％ compared with predicted value of the model （2.64％）. CONCLUSIONS： Established method is stable and reproducible， and can be used for content determination of total flavonoids from C. alfrdii. The optimized extraction method is stable and feasible.

Liver failure （LF） is a great trouble to the majority of patients due to its severe onset， many complications， difficult treatment， poor prognosis and other characteristics. This disease is liver injury caused by infection， hepatotoxic substances， autoimmunity， circulation disorders and other factors. It is a group of common clinical symptoms mainly manifested by coagulation disorders， jaundice， hepatic encephalopathy， ascites， and so on. In traditional Chinese medicine， it falls under the categories of "tympanites"， "jaundice" and other diseases. At present， the research progress of Western medicine in the treatment of LF is slow， and its clinical application effect is still not ideal. In contrast， traditional Chinese medicine has a long history in the treatment of this disease， with over thousands of years of clinical practice and verification. It is characterized by exact efficacy and fewer side effects. The pathological mechanism of LF is extremely complex， involves a variety of signaling pathways， and is mainly related to inflammation， oxidative stress， liver fibrosis， cell apoptosis and other processes. In recent years， many studies have shown that traditional Chinese medicine can intervene in the occurrence and development of LF by mediating relevant signaling pathways in vivo， but there is still a lack of relevant summary. Therefore， this review summarized several signaling pathways related to the intervention of traditional Chinese medicine in LF by referring to and sorting out relevant literature worldwide， including nuclear factor kappa B （NF-κB）， mitogen-activated protein kinase （MAPK）， phosphatidylin-ositol-3-kinase/protein kinase B （PI3K/Akt）， transforming growth factor-β/ drosophila mothers against decapentaplegic proteins （TGF-β/Smads）， and nuclear factor erythroid 2-related factor 2/heme oxygenase-1 （Nrf2/HO-1）， and elaborated the specific mechanism of their intervention in LF. This paper aims to provide practical and effective pathways and corresponding mechanisms for the treatment of LF by traditional Chinese medicine， and to provide new ideas and a theoretical basis for the clinical treatment of LF and further scientific research.

Objective: Tracking the information on 1.69 million fetal cases across Guangxi Zhuang Autonomous Region (Guangxi) so as to study the occurrences of total and major birth defects in order to evaluate the ability on related prevention and control programs in Guangxi. Methods: Using the self-developed "Gui Women’s System" to establish a database of 1.69 million fetal cases in Guangxi and to analyze the distribution of time, space and population, as well as the outcomes of pregnancy, using the big data. Results: During the 29 months of observation, the overall live birth rate was 99.25%, with stillbirth rate during pregnancy as 0.44%, stillbirth rate during birth as 0.02%, and the 0-6 days mortality rate as 0.14%. The total detection rate on birth defects was 197.63/10 000; the incidence rate was 103.04/10 000, the birth rate was 102.55/10 000. The overall discovery rate of major birth defects was 48.33/10 000, with the incidence rate as 783 000, the birth rate as 0.58/10 000. The discovery rates of major birth defects in 14 cities were between 35 and 68/10 000, and the birth rate dropped significantly to less than 1.00 in 10 000. Nationalities showed that the number of pregnant women with birth defects more than 50 000 would include Hui (9.68/10 000), Yao (9.57/10 000), and Jing (9.37/10 000). With the increasing age of gestation, number of birth defects, incidence of major birth defects also increased. Ninety-five percent of the major birth defects were found within <28 weeks and with the top 5 kinds of major birth defects as complicated congenital heart disease (9.11/10 000), alpha thalassemia (8.36/10 000), and 21-trisomy syndrome (7.85/10 000), beta thalassemia (5.32/10 000) and fetal edema syndrome (4.92/10 000). The top 5 major birth defects appeared as complicated congenital heart disease (9.11/10 000), alpha thalassemia (8.36/10 000), and 21-trisomy syndrome (7.85/10 000), beta thalassemia (5.32/10 000) and fetal edema syndrome (4.92/10 000). Conclusion Programs leading to increase the rate on discovery of major birth defects were fundamental in effectively reducing the major birth defects.

At present, hepatic encephalopathy has a relatively high mortality and thus greatly affects patients’ quality of life. This article describes the changes of intestinal flora in patients with hepatic encephalopathy and analyzes the mechanism of action of intestinal flora in hepatic encephalopathy and related treatment methods. It is pointed out that the development of hepatic encephalopathy is closely associated with intestinal flora, and clinical treatment by regulating intestinal flora has achieved a marked effect in patients with hepatic encephalopathy. In the future, the research on intestinal flora in patients with hepatic encephalopathy can be deepened to provide better regimens for the treatment of hepatic encephalopathy.

Objective: To investigate the distribution and related factors of birth weight of live births and full-term infants in Guangxi Zhuang Autonomous Region of China. Methods: Based on Guangxi women and children information system from 2016 to 2018, a large real-time database about maternal and live-birth information was established. It covered 1 712 midwifery institutions in Guangxi. A total of 2 394 240 cases of live births were collected and 2 243 129 cases of which were full-term infants. The multivariate logistic regression model was used to analyze the related factors of low birth weight. Results: The birth weight of 2 394 240 live births, (3 123.49±461.08) g, in Guangxi was approximately normal distribution with a peak distribution to the left. The incidence of low birth weight was 8.05%, and the incidence of macrosomia was 2.07%. The incidence of low birth weight was 10.92% for the puerpera with body mass index (BMI, kg/m²) <18.5, 16.82% for the puerpera with height <145 cm, 8.92% for the puerpera with age <20 years old, 7.67% for the puerpera with age ≥35 years old, and 54.65% for the puerpera with premature birth. The birth weight of 2 243 129 full-term infants, (3 176.01±400.78) g, was approximately normal distribution with a peak distribution to the right. The incidence of low birth weight was 2.97%, and the incidence of macrosomia was 2.19%. The incidence of low birth weight was 4.73% for puerpera with BMI<18.5, 8.17% for puerpera with height<145 cm, 4.83% for puerpera with age <20 years old, and 3.05% for puerpera with age ≥35 years old. The risks of low birth weight [OR (95%CI) value] of pregnant women aged <20, 25-29 and 30-34 years old were 1.31 (1.28-1.35), 0.88 (0.86-0.90) and 0.89 (0.87-0.91) times of those aged ≥35 years old. The risks of low birth weight [OR (95%CI) value] of pregnancy BMI <18.5 and 18.5-23.9 kg/m² group were 1.98 (1.94-2.03) and 1.20 (1.18-1.23) times of those pregnancy BMI ≥24 kg/m². The risks of low birth weight [OR (95%CI) value] of pregnant women′s height (cm)<145, 145-154, 155-159 and 160-164 cm were 4.67 (4.39-4.97), 2.36 (2.29-2.44), 1.58 (1.53-1.63) and 1.22 (1.18-1.26) times of those heights ≥165 cm group. The risks of low birth weight [OR (95%CI) value] of pregnant women′s gestational age <28, 28-31 and 32-36 years old were 136.65 (124.33-150.20), 1 704.37 (1 509.02-1 925.02) and 33.45 (32.98-33.94) times of those gestational age ≥37 years old. Conclusion The incidence of low birth weight of live births was higher in Guangxi from 2016 to 2018. There is a higher risk of low birth weight for younger, older, low height, low BMI and preterm women in Guangxi from 2016 to 2018.

The purpose of the present study was to investigate the effect and potential mechanism of knockdown of sphingosine kinase-1 (SPHK1) on the proliferation, cell cycle and apoptosis of non-small cell lung cancer (NSCLC) cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect SPHK1 mRNA expression in human healthy lung fibroblasts (MRC-5 cells) and four NSCLC cell lines. Then, A549 and H1299 cells were transfected with SPHK1-shRNA and corresponding negative control. CCK-8, Annexin V-FITC/PI dual staining and cell cycle assay were performed to evaluate cell proliferation, apoptosis and cell cycle distribution, respectively. JC-1 mitochondrial membrane potential measurement kit was adopted to measure mitochondrial membrane potential. Western blot was used to detect the protein expression levels of cell cycle and mitochondrial apoptotic pathway-related proteins, as well as MEK/ERK signaling pathway. The results showed that the mRNA expression of SPHK1 in NSCLC cells was higher than that in MRC-5 cells. SPHK1-shRNA significantly inhibited the proliferation of A549 and H1299 cells, blocked the cell cycle in G0/G1 phase, and promoted cell apoptosis through the mitochondrial pathway. Compared with the control group, the expression of p-MEK and p-ERK proteins in the SPHK1-shRNA group was significantly down-regulated. Moreover, MEK/ERK inhibitor could dramatically suppress cell proliferation and promote cell apoptosis. These results suggest that SPHK1 knockdown can inhibit the proliferation of NSCLC cells and might promote mitochondrial apoptotic pathway by inhibiting MEK/ERK signaling pathway.
Apoptosis ; Carcinoma, Non-Small-Cell Lung/genetics* ; Cell Line, Tumor ; Cell Proliferation ; Gene Knockdown Techniques ; Humans ; Lung Neoplasms/genetics* ; Phosphotransferases (Alcohol Group Acceptor)/genetics*

OBJECTIVEShellfish are recognized as important vehicles of norovirus-associated gastroenteritis. The present study aimed to monitor norovirus contamination in oysters along the farm-to-fork continuum in Guangxi, a major oyster production area in Southwestern China.

METHODSOyster samples were collected monthly from farms, markets, and restaurants, from January to December 2016. Norovirus was detected and quantified by one-step reverse transcription-droplet digital polymerase chain reaction (RT-ddPCR).

RESULTSA total of 480 oyster samples were collected and tested for norovirus genogroups I and II. Norovirus was detected in 20.7% of samples, with genogroup II predominating. No significant difference was observed in norovirus prevalence among different sampling sites. The norovirus levels varied widely, with a geometric mean of 19,300 copies/g in digestive glands. Both norovirus prevalence and viral loads showed obvious seasonality, with a strong winter bias.

CONCLUSIONThis study provides a systematic analysis of norovirus contamination 'from the farm to the fork' in Guangxi. RT-ddPCR can be a useful tool for detection and quantification of low amounts of norovirus in the presence of inhibitors found particularly in foodstuffs. This approach will contribute to the development of strategies for controlling and reducing the risk of human illness resulting from shellfish consumption.