Association of platelet-to-white blood cell ratio and platelet-to-neutrophil ratio with the risk of fatal stroke occurrence in middle-aged to older Chinese.

BACKGROUND: White blood cell (WBC) and neutrophil (NEUT) counts, which are commonly inflammatory markers, have been related to an increased risk of fatal stroke. However, it is unclear whether platelet-to-white blood cell ratio (PWR) and platelet-to-neutrophil ratio (PNR) are related to the risk of fatal stroke in middle-aged to older populations. METHOD: In total, 27,811 participants without a stroke history at baseline were included and followed up for a mean of 14.3 years (standard deviation = 3.2), and 838 stroke deaths were recorded. The Cox proportional hazards regression was used to assess the relationships between the PWR and the PNR and the risk of fatal strokes. RESULTS: Compared to the 1st quartile, an increased risk of fatal all stroke showed among the participants in the highest quartiles of both the WBC (adjusted hazard ratio (aHR) = 1.35, 95% confidence interval (CI) 1.09-1.66) and the NEUT (aHR = 1.45, 95% CI 1.18-1.79). The restricted cubic splines showed decreased trends in associations of the PWR and the PNR with the risk of fatal all stroke. A decreased risk of fatal all stroke showed in those with the highest quartiles for both the PWR (aHR = 0.73, 95% CI 0.53-1.00) and the PNR (aHR = 0.74, 95% CI 0.54-1.01). The participants with the 2nd, the 3rd and the 4th change quartiles for the PWR and the PNR had weak decreasing trends for the risk of fatal all stroke, compared to those in the 1st change quartile, and the significant associations were observed in those with an increase of 20% for the PWR with the risk of fatal haemarragic stroke (aHR = 0.47, 95% CI 0.22-0.95) and a decrease of 20% for the PNR with the risk of fatal all stroke (aHR = 1.33, 95% CI 0.99-1.79), compared to those with stable dynamic changes. CONCLUSIONS: Higher neutrophil count and platelet-to-neutrophil ratio were associated with a contrary risk of fatal stroke, with an increased for the former and a decreased for the later. A potentially chronic inflammation should be paid close attention to stroke occurrence in relatively healthy middle-aged to older populations.

Association of Neutrophil-to-Lymphocyte Ratio with the Risk of Fatal Stroke Occurrence in Older Chinese.

BACKGROUND: Associations of neutrophil-to-lymphocyte ratio (NLR) and its longitudinal change with risk of fatal strokes are unclear in older populations. METHODS: In this retrospective analysis, a total of 27,799 participants were included and followed up for a mean of 14.3 years (standard deviation = 3.2). 838 stroke deaths were recorded. Cox proportional hazards regression was used to assess associations of NLR with fatal strokes. RESULTS: Compared to those in the first quartile and after adjustment for a series of factors, the participants in the highest neutrophil quartile had an increased risk of fatal all stroke (adjusted hazard ratio (aHR) = 1.45, 95% confidence interval (CI), 1.18-1.79) and fatal ischaemic stroke (aHR = 1.58, 95% CI, 1.17-2.12). Restricted cubic splines showed an increased trend of relationship between the NLR and fatal all stroke. The participants with the highest NLR quartile had an increased risk of fatal all stroke (aHR = 1.52, 95% CI, 1.23-1.88) and fatal ischaemic stroke (aHR = 1.59, 95% CI, 1.13-2.26), respectively; Similar associations repeated after further C-reactive protein adjustment; a 21% and a 32% increased risk of fatal all stroke and fatal ischaemic stroke showed in a continuous variable model. Those in NLR change with 5% increase had a 70% increased risk of fatal all stroke (aHR = 1.70, 95%CI, 1.13-2.57), compared to those in stable (-5%∼5%). CONCLUSIONS: Higher NLR was associated with an increased risk of fatal all stroke and fatal ischaemic stroke, and its longitudinal change increase of ≥ 5% was associated with an increased risk of fatal all stroke in a relatively healthy older population.

Age at menarche, age at menopause, reproductive years and risk of fatal stroke occurrence among Chinese women: the Guangzhou Biobank Cohort Study.

BACKGROUND: The relationship between women's reproductive characteristics and stroke events is unclear. We aimed to investigate age at menarche, age at menopause and number of reproductive years in relation to fatal stroke occurrence in the Guangzhou Biobank Cohort Study. METHODS: In total, 16,504 postmenopausal women without stroke, heart disease or a cancer history at baseline were included and followed up for a median of 12.0 years. After review of available records, 222 stroke deaths were recorded. Cox proportional hazards regression was used to assess the associations between the risk of fatal stroke occurrence and age at menarche, age at menopause and number of reproductive years. RESULTS: In the whole cohort, compared with those aged 15 years at menarche, an increased risk of fatal stroke among women at menarche showed respectively in those aged 12 years (aHR (adjusted hazard ratio) = 1.86, 95% confidence interval (CI) 0.96-3.60), aged 13 years (aHR = 1.69, 95% CI 0.98-2.92), aged 17 years (aHR = 1.83, 95% CI 1.10-3.05) and aged ≥ 18 years (aHR = 1.66, 95% CI 1.03-2.70), wherein the associations revealed an atypically U-shaped; similar U-shaped association to the cohort of postmenopausal women born before 1940 released a range of incremental risks of fatal stroke in women at menarche aged ≤ 12 years (aHR = 3.68, 95% CI 1.68-8.05), aged 13 years (aHR = 2.11, 95% CI 1.02-4.34), aged 14 years (aHR = 2.07, 95% CI 1.04), aged 17 years (aHR = 2.30, 95% CI 1.20-4.39) and aged 18 years (aHR = 2.50, 95% CI 1.37-4.57), respectively. Compared with menopausal women aged 51-52 years, those aged < 43 years at menopause had an increased risk for fatal stroke among postmenopausal women born in and after 1940 (aHR = 1.64, 95% CI 0.97-2.78) and postmenopausal women born before 1940 (aHR = 1.97, 95% CI 1.05-3.69). Additionally, compared with those with 32-34 reproductive years, women with ≤ 28 reproductive years had an increased risk for fatal stroke in the whole cohort (aHR = 1.91, 95% CI 1.28-2.86) and the cohort of postmenopausal women born before 1940 (aHR = 1.79, 95% CI 1.15-2.80). CONCLUSIONS: Younger and older age at menarche, younger age at menopause and fewer reproductive ages were related to an increased risk of fatal stroke in postmenopausal women.

Higher total white blood cell and neutrophil counts are associated with an increased risk of fatal stroke occurrence: the Guangzhou biobank cohort study.

BACKGROUND: Chronic inflammatory diseases are linked to an increased risk of stroke events. The white blood cell (WBC) count is a common marker of the inflammatory response. However, it is unclear whether the WBC count, its subpopulations and their dynamic changes are related to the risk of fatal stroke in relatively healthy elderly population. METHODS: In total, 27,811 participants without a stroke history at baseline were included and followed up for a mean of 11.5 (standard deviation = 2.3) years. After review of available records, 503 stroke deaths (ischaemic 227, haemorrhagic 172 and unclassified 104) were recorded. Cox proportional hazards regression was used to assess the associations between the WBC count, its subpopulations and their dynamic changes (two-phase examination from baseline to the 1st follow-up) and the risk of fatal all stroke, fatal ischaemic stroke and fatal haemorrhagic stroke. RESULTS: (i) Regarding the WBC count in relation to the risk of fatal stroke, restricted cubic splines showed an atypically U-curved association between the WBC count and the risk of fatal all stroke occurrence. Compared with those in the lowest WBC count quartile (< 5.3*10^9/L), the participants with the highest WBC count (> 7.2*10^9/L) had a 53 and 67% increased risk for fatal all stroke (adjusted hazard ratio [aHR] = 1.53, 95% confidence interval (CI) 1.16-2.02, P = 0.003) and fatal haemorrhagic stroke (aHR = 1.67, 95% CI 1.10-2.67, P = 0.03), respectively; compared with those in the lowest quartile (< 3.0*10^9/L), the participants with the highest NEUT count (> 4.5*10^9/L) had a 45 and 65% increased risk for fatal all stroke (aHR = 1.45, 95% CI 1.10-1.89, P = 0.008) and fatal ischaemic stroke (aHR = 1.65, 95%CI 1.10-2.47 P = 0.02), respectively. With the additional adjustment for C-reactive protein, the same results as those for all stroke and ischaemic stroke, but not haemorrhagic stroke, were obtained for the WBC count (4 ~ 10*10^9/L) and the NEUT count (the NEUT counts in the top 1% and bottom 1% at baseline were excluded). (ii) Regarding dynamic changes in the WBC count in relation to the risk of fatal stroke, compared with the stable group (- 25% ~ 25%, dynamic changes from two phases of examination (baseline, from September 1st, 2003 to February 28th, 2008; 1st follow-up, from March 31st 2008 to December 31st 2012)), the groups with a 25% increase in the WBC count and NEUT count respectively had a 60% (aHR = 1.60, 95% CI 1.07-2.40, P = 0.02) and 45% (aHR = 1.45, 95% CI1.02-2.05, P = 0.04) increased risk of fatal all stroke occurrence. CONCLUSIONS: The WBC count, especially the NEUT count, was associated with an increased risk of fatal all stroke occurrence. Longitudinal changes in the WBC count and NEUT count increase in excess of 25% were also associated with an increased risk of fatal all stroke occurrence in the elderly population.

Risk of group aggregative behavior during COVID-19 outbreak: A case report.

BACKGROUND: At the end of 2019, a new epidemic of viral pneumonia emerged in China and was determined to be caused by a novel coronavirus, which was named coronavirus disease 2019 (COVID-19) by the World Health Organization. The epidemic quickly spread, causing a worldwide pandemic. Scientists and clinicians across the globe have shifted their research efforts towards understanding the virus itself and its epidemiology. CASE SUMMARY: In mid-January 2020, a Chinese family made a visit to a local city, and within the next 2 wk one after another fell ill with COVID-19. At the beginning of their first illness onset, the family had eaten in a restaurant, which led to the subsequent illness onset in another two families. All cases were diagnosed as COVID-19 by real-time fluorescent reverse transcription-polymerase chain reaction. Epidemiological investigation showed that the transmission chain was complete. CONCLUSION: This chain of social exposure highlights the danger of group aggregative behavior for spread of COVID-19.

Microarray analysis of altered long non-coding RNA expression profile in liver cancer cells treated by ginsenoside Rh2.

Microarray expression profiles of lncRNAs and mRNAs were investigated in HepG2 cells treated with 20 µg/ml ginsenoside Rh2 as well as in ginsenoside Rh2-untreated cells. Microarray analysis showed 618 upregulated lncRNAs and 161 downregulated lncRNAs in HepG2 cells treated with ginsenoside Rh2 compared with the control group. Moreover, three differentially expressed lncRNAs were validated by quantitative real-time polymerase chain reaction (qRT-PCR). This may be beneficial to patients as an anti-cancer treatment and potentially provide novel targets for HCC (hepatocellular carcinoma) therapy.

[Mercury concentration in cerebrospinal fluid in patients with chronic mercury poisoning].

OBJECTIVE: To investigate the changes of mercury (Hg) levels in cerebrospinal fluid (CSF) in patients with chronic mercury poisoning and elucidate the neurotoxic mechanism of mercury. METHODS: Nine patients with chronic mercury poisoning (poisoning group) as well as eight patients without exposure to mercury were included in this study. Mercury concentrations of 24 hour urine (U-Hg) and CSF (CSF-Hg) were measured with cold-vapor atomic absorption spectrometry-alkali stannous chloride method. The concentration of blood (B-Hg) at the same day was measured with cold-vapor atomic absorption spectrometry-acidic stannous chloride method. In five patients of poisoning group, these concentrations before chelation therapy were compared with those after chelation therapy. RESULTS: The levels of B-Hg, U-Hg, and CSF-Hg in poisoning group (250.00 +/- 48.54, 160.07 +/- 91.15, 20.22 +/- 10.21 nmol/L, respectively) were significantly higher than those in control group (81.04 +/- 63.01, 24.73 +/- 9.96 nmol/L, undetectable, respectively; P < 0.01). In nine patients of poisoning group, CSF-Hg concentrations were correlated with B-Hg (r = 0.675, P < 0.05), but not U-Hg. After chelation therapy with dimercaptopropane sulfonate in five patients of poisoning group, the levels of B-Hg, U-Hg, and CSF-Hg were decreased significantly (P < 0.05). The reduction of CSF-Hg was not related with B-Hg and U-Hg. CONCLUSION: CSF-Hg concentration in chronic mercury poisoning patient is increased with the rise of B-Hg, but not U-Hg. When the levels of B-Hg and U-Hg drop to normal, the CSF-Hg level is still high enough to be detected. It indicates that mercury is combined with protein after entering brain and this complex is difficult to cross through blood-cerebral barrier. The complex may cause neuromuscular disorder and fremitus in chronic mercury poisoning.