Acceptance of COVID-19 booster vaccination based on the protection motivation theory: A cross-sectional study in China.

The promotion of the booster shots against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is an open issue to be discussed. Little is known about the public intention and the influencing factors regarding the booster vaccine. A cross-sectional survey in Chinese adults was conducted using an online questionnaire, which designed on the basis of protection motivation theory (PMT) scale and vaccine hesitancy scale (VHS). Hierarchical multiple regression was used to compare the fitness of the PMT scale and VHS for predicting booster vaccination intention. Multivariable logistic regression was used to analyze the factors associated with the acceptance. Six thousand three hundred twenty-one (76.8%) of participants were willing to take the booster shot. However, the rest of the participants (23.2%) were still hesitant to take the booster vaccine. The PMT scale was more powerful than the VHS in explaining the vaccination intention. Participants with high perceived severity (adjusted odds ratio [aOR] = 0.69) and response cost (aOR = 0.47) were less willing to take the booster shots, but participants with high perceived susceptibility (aOR = 1.19), response efficacy (aOR = 2.13), and self-efficacy (aOR = 3.33) were more willing to take the booster shots. In summary, interventions based on PMT can provide guidance to ensure the acceptance of the booster vaccine.

MicroRNA-200c Inhibits the Metastasis of Triple-Negative Breast Cancer by Targeting ZEB2, an Epithelial-Mesenchymal Transition Regulator.

OBJECTIVE: Triple-negative breast cancer (TNBC) is one of the most common malignant, highly heterogeneous tumors in women. MicroRNAs (miRNAs), such as miR-200c, play an important role in various types of malignant cancer, including TNBC. However, the biological role of miRNA-200c in TNBC is not well understood. In this study, we investigated the mechanism of miR-200c in the growth of TNBC. METHODS: Reverse transcription quantitative polymerase chain reaction was used to detect the expression of miR-200c in TNBC tissues and TNBC cells. Cell Counting Kit-8 (CCK-8) assays, wound healing, and transwell assays were used to observe the effects of miR-200c on TNBC cell proliferation, migration, and invasion, respectively. The expression of epithelial-mesenchymal transition (EMT) markers were detected by Western blotting. Dual luciferase reporter assays were used to test whether ZEB2 is a novel target of miR-200c. RESULT: Our results show that ZEB2 is a novel target of miR-200c and that ZEB2 mediates the metastasis of triple-negative breast cancer via EMT. CONCLUSION: miR-200c attenuates TNBC cell invasion and EMT by targeting ZEB2. Our data therefore suggest that miR-200c may be used to develop novel early-stage diagnostic and therapeutic strategies for TNBC.

[The mitochondrial tRNAMet/tRNAGlnA4401G and tRNACysG5821A mutations may be associated with hypertension in two Han Chinese families].

Mitochondrial tRNA genes are the hot spots for mutations associated with essential hypertension. We report here the clinical and molecular genetic characterization of two Han Chinese pedigrees with materially inherited essential hypertension. Clinical evaluation revealed the variable severity and age-at-onset of hypertension among matrilineal relatives. In particular, the age-at-onset of hypertension in the maternal kindred ranged from 36 years to 79 years. The sequence analysis of entire mitochondrial genome in two probands showed that two probands carried the identical homoplasmic tRNAMet/tRNAGlnA4401G and tRNACysG5821A mutations and distinct sets of polymorphisms belonging to East Asian haplogroup C. The A4401G mutation may affect the processing of the precursors of tRNAMet and tRNAGln , thereby altering the tRNA metabolism. The tRNACys G5821A mutation is located in the acceptor stem of tRNACys. This mutation may abol-ish the predicted G6-C67 pairing and consequently affect the structure and stability of mitochondrial tRNACys, thereby leading to mitochondrial dysfunction. Therefore, these data suggested that the tRNAMet/tRNAGlnA4401G and tRNACys G5821A mutations are likely associated with essential hypertension in these two Chinese pedigrees.

Mitochondrial tRNA variants in Chinese subjects with coronary heart disease.

BACKGROUND: Coronary heart disease is the leading cause of death worldwide. Mitochondrial genetic determinants for the development of this disorder remain less explored. METHODS AND RESULTS: We performed a clinical and genetic evaluation and mutational screening of 22 mitochondrial tRNA genes in a cohort of 80 genetically unrelated Han Chinese subjects and 125 members of 4 families with coronary heart disease and 512 Chinese control subjects. This analysis identified 16 nucleotide changes among 9 tRNA genes. Of these, the T5592C mutation creates a highly conservative base pairing (5G-68C) on the acceptor stem of tRNA(Gln), whereas the G15927A mutation destabilizes a highly conserved base pairing (28C-42G) in the anticodon stem of tRNA(Thr). However, the other tRNA variants were polymorphisms. The pedigrees of BJH24 carrying the T5592C mutation, BJH15, and BJH45 harboring the G15927A mutation exhibited maternal transmission of coronary heart disease. Sequence analysis of their mitochondrial genomes revealed the presence of T5592C or G15927A mutation but the absence of other functionally significant mutations in all matrilineal relatives of these families. CONCLUSIONS: Our previous observations showed that altered structures of tRNAs by these mtDNA mutations caused mitochondrial dysfunction. These may be the first evidence that mtDNA mutations increase the risk of coronary heart disease. Our findings may provide new insights into the pathophysiology of this disorder.

Frequency and spectrum of mitochondrial ND6 mutations in 1218 Han Chinese subjects with Leber's hereditary optic neuropathy.

PURPOSE: To investigate the molecular pathogenesis of Leber's hereditary optic neuropathy (LHON) in Chinese families. METHODS: A cohort of 1218 Han Chinese subjects with LHON and 316 control subjects underwent the clinical and genetic evaluation and molecular analysis of mitochondrial (mt)DNA. RESULTS: The age at onset of optic neuropathy in these subjects ranged from 5 to 55 years, with the average of 18 years. Mutational analysis of ND6 gene identified 92 (73 known and 19 novel) variants in these subjects. These variants included 29 (9 novel and 20 known) missense mutations and 63 silence variants. A total of 94 subjects carrying one of the known T14484C, T14502C, and G14459A mutations accounted for 7.7% cases of this cohort, particularly 4.4% for T14484C mutation. Furthermore, eight putative LHON-associated ND6 mutations accounted for 1.1% case of this cohort. Thus, 106 subjects carrying one of ND6 mutations accounted for 8.7% cases of this cohort. Low penetrance of optic neuropathy in pedigrees carrying one of eight putative mutations indicated that the mutation(s) is necessary, but itself insufficient to produce a clinical phenotype. Mitochondrial DNAs in 98 probands carrying the ND6 mutation(s) were widely dispersed among 12 Eastern Asian subhaplogroups. In particular, the occurrences of haplogroups M9, M10, M11, and H2 in patients carrying the ND6 mutations were higher than those in controls. CONCLUSIONS: These data further support that the ND6 gene is the hot spot for mutations associated with LHON. Thus, our findings may provide valuable information for the further understanding of pathophysiology and management of LHON.

[Research progress in heritable dyslipidemia].

Dyslipidemia is defined as high levels of serum cholesterol and/or triglycerides. Dyslipidemia often leads to severe cardiovascular diseases including coronary heart disease and stroke as the first clinical manifestation, thus threatening the health of human beings. Dyslipidemia diseases can be caused by the genetic factors, including the Mandelian or polygenic inheritance. Traditional methods of identifying genes associated with dyslipidemia are mainly DNA sequencing and linkage analysis, suitable for Mendelian genetic dyslipidemia disease. The rise of next-generation sequencing technology applies to not only Mandelian inheritance, but also complex forms of dyslipidemia diseases. Since 2006, genome-wide association studies (GWAS) screened out many causative genes associated with dyslipidemia, and most of these genes were the previously identified ones by the pedigree-based classic approaches. Furthermore, GWAS revealed that there were the different frequencies of gene variations related to complex forms of dyslipidemia diseases. Most of the identified single nucleotide polymorphisms (SNPs) associated with dyslipidemia are located in non-coding regions and thus people gradually focus on the gene variations of these loci. The identification of the causative genes will provide new insights into the pathophysiology of dyslipidemia diseases and a step toward therapeutic intervention. This review summarized recent pro-gress in heritable dyslipidemia.