Changing profiles of the burden of Alzheimer's disease and other dementias attributable to smoking in the belt and road initiative countries: A secondary analysis of global burden of disease 2019.

Objectives: This study was aimed at analyzing the burden and trend of Alzheimer's disease and other dementias attributed to smoking (SADD) in the Belt and Road Initiative (BRI) countries during 1990-2019. Methods: Data from The 2019 Global Burden of Disease Study was used to extract information on the burden of SADD in terms of the numbers and age-standardized rate of mortality (ASMR) and disability-adjusted life years (ASDALR) in the BRI countries for 1990-2019. The average annual percent change (AAPC) was used to analyze the temporal trends of ASDALR from 1990 to 2019 and in the final decade by Joinpoint regression analysis. Results: The DALYs of SADD were the highest in China, India, and the Russian Federation in 1990 and in Lebanon, Montenegro and Bosnia, and Herzegovina in 2019. From 1990 to 2019, the ASDALR in China had increased from 55.50/105 to 66.18/105, but decreased from 2010 to 2019, while that of India had declined from 32.84/105 to 29.35/105, but increased from 2010 to 2019. The ASDALR showed the fastest increase in the Russian Federation, with AAPC of 1.97% (95% confidence interval [CI]: 1.77%, 2.16%), and the fastest decline in Sri Lanka, with AAPC of -2.69% (95% CI: 2.79%, -2.59%). ASMR and ASDALR from SADD showed a substantial decline during 1990-2019 both globally and in the different socio-demographic index (SDI) regions (all P < 0.05, except for the high-middle-SDI region). Compared to the rates in males, the AAPC in ASDALR of females was significantly greater in 20 countries(all P < 0.05). In the age group of 20-54 years, the DALYs rate showed a decreasing trend only in 13 members in the low-SDI region (all P < 0.05). Conclusion: Under the premise of eliminating the differences, mobilizing resources in the country itself, the BRI organization, and globally will help reduce the global SADD burden and achieve healthy and sustainable development.

The association between cadmium exposure and the risk of chronic obstructive pulmonary disease: A systematic review and meta-analysis.

According to the World Health Organization, chronic obstructive pulmonary disease (COPD) was one of the top ten causes of death worldwide in 2019. The ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC) provides a useful indicator for the diagnosis of COPD. Existing data have demonstrated that cadmium (Cd) exposure is associated with COPD. However, data concerning the incidence and progression of cadmium-induced COPD is inconsistent. To explore the relationship between cadmium exposure and the risk of COPD in humans, through January 12, 2023, we conducted a thorough search of the PubMed, Cochrane, Web of Science, Embase and Scopus databases for relevant material. In this study, a meta-analysis was conducted to evaluate the association between cadmium and COPD. This meta-analysis indicated that exposure to cadmium (per 1 µg/L increase) was associated with reduced FEV1/FVC (% change = -47.54%, 95% CI: -54.99% to -40.09%). Subgroup analysis showed that the combined effect estimates were significantly higher in the COPD patient group (% change = -54.66%, 95% CI: -83.32% to -26.00%) than in the general population (% change = -52.11%, 95%CI: -60.53% to -43.70%). Therefore, we conclude that cadmium exposure is associated with reduced FEV1/FVC, which suggests a risk for COPD.

Neuroprotective Effects of Melittin Against Cerebral Ischemia and Inflammatory Injury via Upregulation of MCPIP1 to Suppress NF-κB Activation In Vivo and In Vitro.

Melittin, a principal constituent of honeybee venom, exhibits diverse biological effects, encompassing anti-inflammatory capabilities and neuroprotective actions against an array of neurological diseases. In this study, we probed the prospective protective influence of melittin on cerebral ischemia, focusing on its anti-inflammatory activity. Mechanistically, we explored whether monocyte chemotactic protein-induced protein 1 (MCPIP1, also known as ZC3H12A), a recently identified zinc-finger protein, played a role in melittin-mediated anti-inflammation and neuroprotection. Male C57/BL6 mice were subjected to distal middle cerebral artery occlusion to create a focal cerebral cortical ischemia model, with melittin administered intraperitoneally. We evaluated motor functions, brain infarct volume, cerebral blood flow, and inflammatory marker levels within brain tissue, employing quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assays, and western blotting. In vitro, an immortalized BV-2 microglia culture was stimulated with lipopolysaccharide (LPS) to establish an inflammatory cell model. Post-melittin exposure, cell viability, and cytokine expression were examined. MCPIP1 was silenced using siRNA in LPS-induced BV-2 cells, with the ensuing nuclear translocation of nuclear factor-κB assessed through cellular immunofluorescence. In vivo, melittin enhanced motor functions, diminished infarction, fostered blood flow restoration in ischemic brain regions, and markedly inhibited the expression of inflammatory cytokines (interleukin-1ß, interleukin-6, tumor necrosis factor-α, and nuclear factor-κB). In vitro, melittin augmented MCPIP1 expression in LPS-induced BV-2 cells and ameliorated inflammation-induced cell death. The neuroprotective effect conferred by melittin was attenuated upon MCPIP1 knockdown. Our findings establish that melittin-induced tolerance to ischemic injury is intrinsically linked with its anti-inflammatory capacity. Moreover, MCPIP1 is, at the very least, partially implicated in this process.

Value evaluation of serum (sdLDLc*HCYc)/HDLc ratio in the stability of intracranial arterial plaques in patients with acute cerebral infarction.

BACKGROUND: We aimed to analyze the value of serum (sdLDLc*HCYc)/HDLc ratio in the stability of intracranial arterial plaques among patients with acute cerebral infarction. METHODS: A retrospective analysis was conducted on 140 patients with acute cerebral infarction admitted to the neurology department and 101 healthy individuals for regular examinations in our hospital from 2013 to 2019, who were respectively allocated into the study group and the control group. Participants in both groups were measured for serum sdLDLc, HDLc, and HCYc using peroxidase method, enzyme-linked immunosorbent assay, and enzyme method, respectively. The laboratory indexes of the two groups were compared. The multivariate logistic regression analysis was done to analyze the influencing factors of the stability of intracranial artery plaque in patients with acute cerebral infarction. The value of high-density lipoprotein cholesterol (HDL-C), homocysteine, sdLDLc, (sdLDLc*HCYc)/HDLc in diagnosing the stability of intracranial artery plaque was also evaluated in patients with acute cerebral infarction. RESULTS: There was no distinct difference in height, hypertension, diabetes, coronary heart disease, smoking history and drinking history between the two groups (P>0.05). The study group showed statistically significant differences in age, gender, weight, and BMI (P<0.05). The current study demonstrated no statistical difference in the levels of TG, low-density lipoprotein cholesterol (LDL-C), α-lipoprotein, and HCYc between the two groups (P>0.05). However, the levels of TC, HDL-C, sdLDLc, (sdLDLc*HCYc)/HDLc in the study group were significantly different when comparing with the control group (P<0.05). No statistically significant difference was found in the levels of TG, triglycerides, LDL-C, α-lipoprotein, and HCYc among patients with different degrees of stenosis in the study group (P>0.05). The level of HDL-C was significantly lower in cases of severe stenosis compared to no stenosis, mild stenosis and moderate stenosis, with severe stenosis showing the lowest levels; mild stenosis had lower levels than no stenosis, while moderate stenosis had lower levels than both no stenosis and mild stenosis (P<0.05). The levels of sdLDLc, (sdLDLc*HCYc)/HDLc exhibited a significant increase in cases of severe stenosis as compared tono stenosis, mild stenosis, and moderate stenosis. Furthermore, the levels of sdLDLc, (sdLDLc*HCYc)/HDLc were found to be higher in moderate stenosis as compared to no stenosis and mild stenosis. Similarly, the levels of sdLDLc, (sdLDLc*HCYc)/HDLc were observed to be higher in mild stenosis than no stenosis (P<0.05).The independent variables were set as the indicators with difference in single factor comparison, including age, gender, BMI, TC, LDL-C, HDL-C, HCYc, sdLDLc, (sdLDLc*HCYc)/HDLc. The dependent variable was the stability of intracranial artery plaque in patients with acute cerebral infarction. After variable selection, the results showed that the factors influencing the stability of intracranial artery plaque in patients with acute cerebral infarction were age, BMI, (sdLDLc*HCYc)/HDLc. The degree of plaque enhancement was used as a criterion to reflect the stability of plaque. ROC curve analysis showed that (sdLDLc*HCYc)/HDLc had a higher evaluation value for the stability of intracranial artery plaque than HDL-C, homocysteine, and sdLDLc in patients with acute cerebral infarction. CONCLUSION: The serum (sdLDLc*HCYc)/HDLc ratio was found to have potential in evaluating the stability of intracranial arterial plaques in patients with acute cerebral infarction.

Association of urinary arsenic with the oxidative DNA damage marker 8-hydroxy-2 deoxyguanosine: A meta-analysis.

BACKGROUND: The International Agency for Research on Cancer has classified arsenic as a class I carcinogen. Oxidative DNA damage is a typical early precursor to recognized malignancies. The most sensitive early independent marker of oxidative DNA damage is believed to be 8-hydroxy-2 deoxyguanosine (8-OHdG). To date, research on the link between urinary arsenic and 8-OHdG has not been consistent. OBJECTIVE: This study was aimed at exploring the effects of urinary arsenic on 8-OHdG in human urine. METHODS: A literature search until January 2023 was performed on the PubMed, Cochrane Library, Web of Science, Embase, and Scopus databases through a combination of computer and manual retrieval. Stata 12.0 was used to examine the degree of heterogeneity among included studies. The percentage change and 95 % confidence interval (95 % CI) of 8-OHdG were calculated between populations exposed to different doses. We used a random effect model because the degree of heterogeneity exceeded 50 %. Sensitivity analysis and testing for publication bias were performed. RESULTS: This meta-analysis included nine studies, most of which were performed in China. After exposure to arsenic, urinary arsenic (per 10 µg/g creatinine increase) was associated with the increased 8-OHdG (% change = 41.49 %, 95 % CI: 19.73 %, 63.25 %). Subgroup analysis indicated that the percentage change in 8-OHdG in urine was more pronounced in people exposed to arsenic <50 µg/L (% change = 24.60 %, 95 % CI: 17.35 %, 37.85 %). In studies using total urinary arsenic content as an indicator, the percentage change in 8-OHdG in urine was more significant (% change = 60.38 %, 95 % CI: 15.08 %, 105.68 %). CONCLUSION: The 8-OHdG levels in human urine significantly increased after exposure to environmental arsenic, thus suggesting that arsenic exposure is correlated with oxidative DNA damage.

A patient with MELAS syndrome combined with autoimmune abnormalities: a case report.

Background: Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is a group of maternally inherited disorders caused by mutations or deletions in mitochondrial genes with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes as the main clinical manifestations. Case presentation: We reported a 20-year-old female patient with MELAS syndrome combined with autoimmune abnormalities. She suffered from an intermittent headache in the right temporal region with no obvious cause, and then, after strenuous exercise in dance class, the headache became aggravated, accompanied by unresponsiveness, blurred vision, and diplopia. Her blood lactate levels were elevated, her antinuclear antibodies were positive, and the antimetabolic glutamate receptors 5 in her serum were positive. Brain DWI showed a hypertensive signal in the right temporo-parietal-occipital cortex and subcortical area. Brain MRS showed decreased NAA peak and increased Lac peak. Muscle biopsy showed myogenic damage, and the modified Gomori trichrome (MGT) staining showed ragged red fibers (RRF). A genetic study revealed a mitochondrial DNA A3243G mutation. Conclusion: Mitochondrial encephalomyopathy is a rare clinical condition; however, the association with autoimmune diseases is not yet clear and still needs further research and analysis.

dbMisLoc: A Manually Curated Database of Conditional Protein Mis-localization Events.

Over the last few years, an increasing number of protein mis-localization events have been reported under various conditions. It is important to understand these events and their relationship with complex disorders. Although many efforts had been made in establishing models with statistical or machine learning algorithms, a comprehensive database resource is still missing. Since the records of experimental-validated protein mis-localization events spread across many literatures, a collection of all these reports in a unique website is demanded. In this paper, we created the dbMisLoc database by manually curating conditional protein mis-localization events from various literatures. The dbMisLoc database records the protein localizations, mis-localizations, conditions for mis-localization, and the original reports. The dbMisLoc database allows the users to intuitively view, search, visualize and download protein mis-localization records. The dbMisLoc database integrates a BLAST search engine, which can search mis-localized proteins that are similar to user queries. The dbMisLoc database can be accessed directly through ( https://dbml.pufengdu.org ). The source code of dbMisLoc database is available from the GitHub repository ( https://github.com/quinlanW/dbMisLoc ) for free. Users can host their own mirrors of dbMisLoc database on their own servers. dbMisLoc is database for manually curated protein mis-localization events. It contains mis-localization events in 14 categories of conditions such as diseases, drug treatments and environmental stresses.

Construction of a novel necroptosis-related lncRNA signature for prognosis prediction in esophageal cancer.

BACKGROUND: Esophageal cancer (EC), one highly malignant gastrointestinal cancer, is the 6th leading cause of cancer-related deaths worldwide. Necroptosis and long non-coding RNA (lncRNA) play important roles in the occurrence and development of EC, but the research on the role of necroptosis-related lncRNA in EC is not conclusive. This study aims to use bioinformatics to investigate the prognostic value of necroptosis-related lncRNA in EC. METHODS: Transcriptome data containing EC and normal samples, and clinical information were obtained from the Cancer Genome Atlas database. 102 necroptosis-related genes were obtained from Kanehisa Laboratories. Necroptosis-related lncRNAs were screened out via univariate, multivariate Cox and the least absolute shrinkage and selection operator regression analyses to construct the risk predictive model. The reliability of the risk model was evaluated mainly through quantitative real-time PCR (qRT-PCR), the receiver operating characteristic (ROC) curves and the constructed nomogram. KEGG pathways were explored in the high- and low-risk groups of EC patients via gene set enrichment analyses (GSEA) software. Immune microenvironment and potential therapeutic agents in risk groups were also analyzed. RESULTS: A 6 necroptosis-related lncRNAs risk model composed of AC022211.2, Z94721.1, AC007991.2, SAMD12-AS1, AL035461.2 and AC051619.4 was established to predict the prognosis level of EC patients. qRT-PCR analysis showed upregulated Z94721.1 and AL035461.2 mRNA levels and downregulated AC051619.4 mRNA level in EC tissues compared with normal tissues. According to clinical characteristics, the patients in the high-risk group had a shorter overall survival than the low-risk group. The ROC curve and nomogram confirmed this model as one independent and predominant predictor. GSEA analysis showed metabolic and immune-related pathways enriched in the risk model. Most of the immune cells and immune checkpoints were positively correlated with the risk model, mainly active in the high-risk group. For the prediction of potential therapeutic drugs, 16 compounds in the high-risk group and 2 compounds in the low-risk group exhibited higher sensitivity. CONCLUSIONS: Our results supported the necroptosis-related lncRNA signature could independently predict prognosis of EC patients, and provided theoretical basis for improving the clinical treatment of EC.

Estimation of the LDL subclasses in ischemic stroke as a risk factor in a Chinese population.

BACKGROUND: Acute ischemic stroke (AIS) is one of the leading causes of mortality and long-term disability worldwide. Our study aims to clarify the role of low-density lipoproteins (LDL) subclasses in the occurrence of AIS and develop a risk xprediction model based on these characteristics to identify high-risk people. METHODS: Five hundred and sixty-six patients with AIS and 197 non-AIS controls were included in this study. Serum lipids and other baseline characteristics including fasting blood glucose (GLU), serum creatinine (Scr), and blood pressure were investigated in relation to occurrence of AIS. The LDL subfractions were classified and measured with the Lipoprint System by a polyacrylamide gel electrophoresis technique. RESULTS: Levels of LDL-3, LDL-4 and LDL-5 subclasses were significantly higher in the AIS group compared to the non-AIS group and lower level of LDL-1 was prevalent in the AIS patients. Consistently, Spearman correlation coefficient demonstrated that sd-demonevels, especially LDL-3 and LDL-4 levels, were significantly positively correlated with AIS. Furthermore, there is a significant positive correlation between small dense LDL (sd-LDL, that is LDL-3 to 7) levels and serum lipids including total cholesterol (TC), Low density lipoprotein cholesterol (LDL-C), and Triglyceride (TG). Increased LDL-3 and LDL-4 as well as decreased LDL-1 and LDL-2 were correlated to the occurrence of AIS, even in the people with normal LDL-C levels. A new prediction model including 12 variables can accurately predict the AIS risk in Chinese patients (AUC = 0.82 ± 0.04). CONCLUSIONS: Levels of LDL subclasses should be considered in addition to serum LDL-C in assessment and management of AIS. A new prediction model based on clinical variables including LDL subtractions can help clinicians identify high of AIS, even in the people with norm.

Taxane-derived compounds protect SK-N-SH cells against oxidative stress injury induced by H2O2.

OBJECTIVE: Discussed the protection of taxane-derived compounds, 7-deacetyl-taxine B and 5-cinnamoyloxy-taxin B, against oxidative stress injury. METHODS: SK-N-SH cells were pretreated with 7-deacetyl-taxine B, 5-cinnamoyloxy-taxin B or DMSO (control) and then incubated with H2O2 for another 24 h. Cell viability was measured by MTT colorimetric assay. Apoptosis rate, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were detected using flow cytometry assay. Ultrastructure was detected by Transmission electron microscope. RESULTS: Taxane-derived compounds improved H2O2 mediated loss of cell viability in SK-N-SH cell. Ultrastructure of control group cells showed nucleus shrinkage, dense aggregation of chromatin, appearance of apoptotic body and mitochondrial dilation. Treated group showed alleviation of mitochondrial dilation and chromatin margination, and reduction of apoptosis cells induced by H2O2. The apoptosis rate was decreased in treated group compared with control group. DCFH-DA staining showed that ROS were significantly decreased in cells treated with taxane-derived compounds compared with control group. Rhodamine123 staining showed that MMP was significantly decreased in cells treated with taxane-derived compounds compared with control group. CONCLUSION: The anti-oxidative stress and neuroprotective effect of taxane-derived compounds was verified here, wherein it could protect neurocytes from H2O2-induced oxidative stress injury.