1.Impact of metabolic syndrome on cardio-cerebral vascular events in pre-hypertensive population.
Shou-ling WU ; Ying ZHANG ; Chun-yu RUAN ; Qi TIAN ; Cheng JIN ; Jin-feng LI ; Yu-yan SUN ; Wei HUANG ; Ji-wen ZHONG ; Jun CAI
Chinese Journal of Cardiology 2012;40(5):397-401
OBJECTIVEThis study investigated the impact of metabolic syndrome on the development of cardio-cerebral vascular (CVD) events in a pre-hypertensive population.
METHODSThe data used in this prospective study was derived from the Kailuan study cohort (n = 101 510). Prehypertension was diagnosed in 29 968 (mean age: 50 ± 9 years and 23 744 males) individuals by the JNC VII criteria and these subjects were further classified into metabolic syndrome positive (MS+, n = 3447) and MS negative (MS-, n = 26 521) groups according to the modified 2004 Chinese Diabetes Society criteria. Subjects were followed up for 38 - 53 (mean 47 ± 5) months and first-ever CVD events were recorded. Baseline anthropometric and laboratory features were obtained by physical examination from June 2006 to October 2007 and the last follow-up day was December 31, 2010. Multivariable Cox proportional hazards regression models were used to analyze the risk factors of first-ever CVD events.
RESULTSThere were 354 CVD events during follow up. The incidences of CVD events (1.80% vs. 1.28%) and cerebral infarction (1.10% vs. 0.57%) were significantly higher in the MS+ group than in the MS- group (all P < 0.05). After adjustment for other established CVD risk factors, the hazards ratio was 1.45 (95%CI: 1.10 - 1.92) for total CVD events and 1.84 (95%CI: 1.27 - 2.67) for cerebral infarction events in MS+ group.
CONCLUSIONSIn this cohort, metabolic syndrome is linked with increased risk for CVD events.
Adult ; Cardiovascular Diseases ; etiology ; Cerebrovascular Disorders ; etiology ; Cohort Studies ; Female ; Humans ; Male ; Metabolic Syndrome ; complications ; Middle Aged ; Prehypertension ; complications ; Prospective Studies ; Risk Factors
2.SARS-CoV-2 with transcription regulatory sequence motif mutation poses a greater threat.
Jin Long BEI ; Guo Feng XU ; Jia CHANG ; Xin Yu WANG ; Dong An QIU ; Ji Shou RUAN ; Xin LI ; Shan GAO
Journal of Southern Medical University 2022;42(3):399-404
OBJECTIVE:
To analyze the mutations in transcription regulatory sequences (TRSs) of coronaviruss (CoV) to provide the basis for exploring the patterns of SARS-CoV-2 transmission and outbreak.
METHODS:
A combined evolutionary and molecular functional analysis of all sets of publicly available genomic data of viruses was performed.
RESULTS:
A leader transcription regulatory sequence (TRS-L) usually comprises the first 60-70 nts of the 5' UTR in a CoV genome, and the body transcription regulatory sequences (TRS-Bs) are located immediately upstream of the genes other than ORF1a and 1b. In each CoV genome, the TRS-L and TRS-Bs share a specific consensus sequence, namely the TRS motif. Any changes of nucleotide residues in the TRS motifs are defined as TRS motif mutations. Mutations in the TRS-L or multiple TRS-Bs result in superattenuated variants. The spread of super-attenuated variants may cause an increase in asymptomatic or mild infections, prolonged incubation periods and a decreased detection rate of the viruses, thus posing new challenges to SARS-CoV-2 prevention and control. The super-attenuated variants also increase their possibility of long-term coexistence with humans. The Delta variant is significantly different from all the previous variants and may lead to a large-scale transmission. The Delta variant (B.1.617.2) with TRS motif mutation has already appeared and shown signs of spreading in Singapore, which, and even the Southeast Asia, may become the new epicenter of the next wave of SARS-CoV-2 outbreak.
CONCLUSION
TRS motif mutation will occur in all variants of SARS-CoV-2 and may result in super-attenuated variants. Only super-attenuated variants with TRS motif mutations will eventually lose the abilities of cross-species transmission and causing outbreaks.
COVID-19/virology*
;
Genome, Viral
;
Humans
;
Mutation
;
SARS-CoV-2/genetics*