Pro-inflammatory diets promote the formation of hyperuricemia.

Background: Hyperuricemia, as a very prevalent chronic metabolic disease with increasing prevalence year by year, poses a significant burden on individual patients as well as on the global health care and disease burden, and there is growing evidence that it is associated with other underlying diseases such as hypertension and cardiovascular disease. The association between hyperuricemia and dietary inflammatory index (DII) scores was investigated in this study. Methods: This study enrolled 13, 040 adult subjects (aged ≥ 20 years) from the US National Health and Nutrition Survey from 2003 to 2018. The inflammatory potential of the diet was assessed by the DII score, and logistic regression was performed to evaluate the relationship between the DII score and the development of hyperuricemia; subgroup analyses were used to discuss the influence of other factors on the relationship. Results: Participants in the other quartiles had an increased risk of hyperuricemia compared to those in the lowest quartile of DII scores. Stratification analyses stratified by body mass index (BMI), sex, hypertension, drinking, diabetes, education level and albumin-creatinine-ratio (ACR) revealed that the DII score was also associated with the risk of hyperuricemia (P<0.05). There was an interaction in subgroup analysis stratified by sex, age, and hypertension (P for interaction <0.05). The results showed a linear-like relationship between DII and hyperuricemia, with a relatively low risk of developing hyperuricemia at lower DII scores and an increased risk of developing hyperuricemia as DII scores increased. Conclusions: This study showed that the risk of hyperuricemia increased at slightly higher DII scores (i.e., with pro-inflammatory diets), but not significantly at lower levels (i.e., with anti-inflammatory diets). The contribution of the DII score to the development of hyperuricemia increased with higher scores. The relationship between inflammatory diets and hyperuricemia requires more research on inflammation, and this study alerts the public that pro-inflammatory diets may increase the risk of developing hyperuricemia.

COVID-19 vaccination effectiveness and safety in vulnerable populations: a meta-analysis of 33 observational studies.

Background: Even 3 years into the COVID-19 pandemic, questions remain about how to safely and effectively vaccinate vulnerable populations. A systematic analysis of the safety and efficacy of the COVID-19 vaccine in at-risk groups has not been conducted to date. Methods: This study involved a comprehensive search of PubMed, EMBASE, and Cochrane Central Controlled Trial Registry data through 12 July 2022. Post-vaccination outcomes included the number of humoral and cellular immune responders in vulnerable and healthy populations, antibody levels in humoral immune responders, and adverse events. Results: A total of 23 articles assessing 32 studies, were included. The levels of IgG (SMD = -1.82, 95% CI [-2.28, -1.35]), IgA (SMD = -0.37, 95% CI [-0.70, -0.03]), IgM (SMD = -0.94, 95% CI [-1.38, -0.51]), neutralizing antibodies (SMD = -1.37, 95% CI [-2.62, -0.11]), and T cells (SMD = -1.98, 95% CI [-3.44, -0.53]) were significantly lower in vulnerable than in healthy populations. The positive detection rates of IgG (OR = 0.05, 95% CI [0.02, 0.14]) and IgA (OR = 0.03, 95% CI [0.01, 0.11]) antibodies and the cellular immune response rates (OR = 0.20, 95% CI [0.09, 0.45]) were also lower in the vulnerable populations. There were no statistically significant differences in fever (OR = 2.53, 95% CI [0.11, 60.86]), chills (OR = 2.03, 95% CI [0.08, 53.85]), myalgia (OR = 10.31, 95% CI [0.56, 191.08]), local pain at the injection site (OR = 17.83, 95% CI [0.32, 989.06]), headache (OR = 53.57, 95% CI [3.21, 892.79]), tenderness (OR = 2.68, 95% CI [0.49, 14.73]), and fatigue (OR = 22.89, 95% CI [0.45, 1164.22]) between the vulnerable and healthy populations. Conclusion: Seroconversion rates after COVID-19 vaccination were generally worse in the vulnerable than healthy populations, but there was no difference in adverse events. Patients with hematological cancers had the lowest IgG antibody levels of all the vulnerable populations, so closer attention to these patients is recommended. Subjects who received the combined vaccine had higher antibody levels than those who received the single vaccine.

Complete chloroplast genome of Zanthoxylum avicennae (Lam.) DC (Rutaceae: Zanthoxylum).

In this study, the chloroplast (Cp) genome of Zanthoxylum avicennae (Lam.) DC was sequenced by high-throughput sequencing technology. The length of the Cp genome of Zanthoxylum avicennae was 158,568 bp, and the total GC content was 38.4%, including a large single-copy (LSC) region of 86,318 bp, a small single-copy (SSC) region of 18,250 bp, and 27,000 bp of inverted repeats (IRs). The Cp genome encoded 131 genes, including 88 protein-coding, 37 tRNA, and six rRNA genes. Phylogenetic analysis of the genome sequence showed that Zanthoxylum avicennae was closely related to Zanthoxylum nitidum, Zanthoxylum esquirolii and Zanthoxylum motuoense of the Rutaceae family.

Complete chloroplast genome of Euphorbia micractina Boiss (Euphorbiaceae: Euphorbia).

Euphorbia micractina Boiss is a plant with high medicinal value. Yet, its molecular biology is not fully understood. In this study, we sequenced the whole chloroplast genome (CP) sequence of E. micractina to study its phylogenetic relationship in Euphorbiaceae. The total length of the chloroplast genome of E. micractina is 162,056 bp, including a large single-copy (LSC) region of 89,936bp bp, a small single-copy (SSC) region of 18,376 bp, and a pair of identical inverted repeat regions (IRs) of 11,367 bp. The genome has 128 genes, including 84 protein-coding genes, 36 transfer RNA (tRNA) genes, and 8 ribosomal RNA (rRNA) genes. The overall GC content of the plastome is 35.7%. The phylogenetic analysis of E. micractina with 30 related species suggested a closest taxonomical relationship with Euphorbia pekinensis in the Euphorbiaceae family.

MTRR silencing inhibits growth and cisplatin resistance of ovarian carcinoma via inducing apoptosis and reducing autophagy.

Methionine synthase reductase (MTRR) is involved in the DNA synthesis and production of S-adenosylmethionine (SAM) and plays an important role in the carcinogenesis. However, the role of MTRR in the resistance of ovarian cancer (OC) to chemotherapy has yet to be elucidated. In order to investigate the clinical significance of MTRR in OC, MTRR expression was reduced by using the RNA interference technique, and therefore, and the tumor growth and cisplatin-resistance were evaluated in vitro and in vivo. Results showed MTRR expression increased orderly from normal tissues, benign ovarian tumor to OC tissue. MTRR over-expression in OC tissue was correlated with pathologic type (P=0.005), grade (P=0.037), FIGO stage (P=0.001), organ metastasis (P=0.009) and platinum resistance (P=0.038). MTRR silencing inhibited cell proliferation, cisplatin resistance and autophagy, and induced apoptosis of OC cells. In addition, MTRR silencing also affected the caspase expression as well as mTOR signaling pathway. Further, the tumor volume in MTRR-suppressed SKOV3/DDP mice treated with cisplatin significantly decreased when compared with controls (P<0.05). In summary, MTRR expression, which is increased in human OC, is related to the differentiation and cisplatin resistance of OC cells. MTRR silencing inhibits cell growth and cisplatin resistance by regulating caspase expression and mTOR signaling pathway in OC cells. It is suggested that MTRR may be a potential target for the therapy of OC.

Novel microRNAs expression of patients with chemotherapy drug-resistant and chemotherapy-sensitive epithelial ovarian cancer.

The aim of this study is to examine the microRNA (miRNA) expression of epithelial ovarian cancer (EOC) in both drug-resistant and drug-sensitive tissues and to explore the pathogenic characteristics of drug-resistant miRNAs in EOC. The samples with 10 cases of drug-resistant and drug-sensitive EOC tissue were obtained from undergoing surgical resection of ovarian cancer (OC). Total miRNAs were extracted and isolated, respectively. Hybridization was carried out on miRNA microarray chip. Real-time polymerase chain reaction (RT-PCR) was performed to confirm the difference of miRNA expression. Bioinformatic software was used to predict the possible target genes of each miRNA which expressed differently. The results indicated that four miRNAs related drug-resistance been identified, and the expression of hsa-miR-152 and hsa-miR-381 in drug-resistant OC tissue was significantly higher compared with those in drug-sensitive tissue (P < 0.01). However, expression of hsa-miR-200a-3p and hsa-miR-429 were downregulated in drug-resistant tissues (P < 0.01). The results obtained by miRNA microarrays of differential expression with hsa-miR-106b-3p, hsa-miR-152, hsa-miR-200a-3p, hsa-miR-381, and hsa-miR-429 were confirmed by real-time PCR. There were 62 significantly different miRNAs, including 42 significant upregulated miRNAs and 20 significant downregulated miRNAs in the drug-resistant tissue. Five databases, including Target Scan, miRanda, miRDB, PicTar5, and RNA22, were used for bioinformatics prediction. In conclusion, miRNA microarray analysis has become a fast and efficient molecular biological technology for the study of biological information. hsa-miR-152, hsa-miR-200a-3p, hsa-miR-381, and hsa-miR-429 may participate in the formation of drug resistance in EOC through the target genes predicted.

Effects of HLEC on the secreted proteins of epithelial ovarian cancer cells prone to metastasize to lymph nodes.

OBJECTIVE: To study explores the effect of HLEC on the secreted proteins of epithelial ovarian cancer (EOC) cells (SKOV3-PM4) with directional highly lymphatic metastasis. METHODS: Supernatants of four groups of cultured cells, namely, SKOV3 (A), SKOV3+HLEC (B), SKOV3-PM4 (C), SKOV3-PM4+HLEC (D), were collected, and their proteins were detected by antibody arrays and iTRAQ-2D-LC-MALDI-TOF/TOF/MS. Significantly differential proteins were further analyzed via bioinformatics and validated in human serums and cell media via ELISA. RESULTS: Results of antibody arrays and mass spectrometry demonstrated that GRN and VEGFA were upregulated in group C (compared with group A), whereas IGFBP7 and SPARC were downregulated in group D (compared with group C). Comprehensive bioinformatics analysis results showed that IGFBP7 and VEGFA were closely linked to each other. Further validation with serums showed statistical significance in VEGFA and IGFBP7 levels among groups of patients with ovarian cancers, benign tumors, and control groups. Two proteins were upegulated in the first group. VEGFA in the control group was downregulated. For IGFBP, upregulation in the control group and down-regulation in the first group were also observed. CONCLUSION: The HLEC microenvironment is closely associated with directional metastasis to lymph nodes and with differential proteins including cell stromal proteins and adhesion factors. The upregulation of VEGFA and GRN and the downregulation of SPARC and IGFBP7 are closely associated with directional metastasis to lymph nodes in EOC cells.