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Bioinformation 2024First identified as a pathogen in Malaysia and Singapore in 1999, Nipah virus (NiV) caused nearly 300 human cases and over 100 fatalities. It also killed about 1 million...
First identified as a pathogen in Malaysia and Singapore in 1999, Nipah virus (NiV) caused nearly 300 human cases and over 100 fatalities. It also killed about 1 million pigs. Three years later (2002), it was reported in Pteropus bats in Malaysia, in Cambodia & Thailand, (2005), and as far as Madagascar (2007) and Ghana (2008). India (Kerala) reported its first human NiV-caused fatalities in September 2023. Taken together, these trends emphasize its public health threat. In humans, NiV infection initially leads to fever, headache, body aches and muscle pain, nausea and vomiting. The symptoms rapidly evolve into sore throat, cough and atypical pneumonia leading to severe respiratory distress. The cadre of NiV-induced pathology (Nipah disease, NiD) then includes severe dizziness and drowsiness, progressive alteration in cognition and consciousness, acute encephalitis and seizures. Public health protocols (e.g., mask-wearing, quarantine), essential to contain and control CoViD-19, seem insufficient to contain NiD spread because NiV transmission occurs primarily via direct contacts with body fluids of infected carriers, but presumably not by airborne transmission. As in the case of SARS-C0V2, health care providers (i.e., physicians, dentists, nurses, dental assistants) are greatest risks not only of contracting but of spreading NiV infection. NiV is a high-pathogenicity pathogen, against which, at present, we have no anti-viral medications or preventive vaccine. Taken together, the evidence to date heightens the threat of an upcoming NiD pandemic.
PubMed: 38352906
DOI: 10.6026/973206300200001 -
Journal of Global Health Dec 2023Unhealthy lifestyle and diet may contribute to the development of cardiovascular disease (CVD), but limited evidence exists regarding the association between sleep...
Interplay of sleep patterns and oxidative balance score on total cardiovascular disease risk: Insights from the National Health and Nutrition Examination Survey 2005-2018.
BACKGROUND
Unhealthy lifestyle and diet may contribute to the development of cardiovascular disease (CVD), but limited evidence exists regarding the association between sleep patterns, oxidative stress-related exposures to diet and lifestyle, and CVD risk.
METHODS
We analysed data from 10 212 adults in the National Health and Nutrition Examination Survey (NHANES) database (2005-2018). Self-report questionnaires were used to collect data on sleep duration, sleepiness, and trouble sleeping, classified into three categories: healthy, intermediate, and poor sleep patterns. Healthy sleep was defined as sleeping seven to nine hours per night with no self-reported sleepiness or trouble sleeping, while intermediate and poor sleep patterns indicated one and two to three sleep problems, respectively. The oxidative balance score (OBS) was calculated based on twenty oxidative stress-related exposures to dietary and lifestyle factors, with a higher score indicating greater antioxidant exposure. Survey-based multivariable-adjusted regression analysis was conducted to examine the association of sleep patterns or OBS alone and combined with the total and specific CVD risk.
RESULTS
Participants with poor sleep patterns had a higher likelihood of developing CVD (odds ratio (OR) = 1.76; 95% confidence interval (CI) = 1.26-2.45, P < 0.05), while an inverse association was found between OBS and CVD risk (quartile (Q) 4 vs Q1: OR = 0.67; 95% CI = 0.47-0.94, P = 0.02, P for trend <0.05). There was an interaction between sleep patterns and OBS (P for interaction = 0.03). Participants with unhealthy (intermediate and poor) sleep patterns and pro-oxidant OBS (Q1 and Q2) were significantly associated with increased risk of total CVD (OR = 2.31; 95% CI = 1.42-3.74, P < 0.05), as well as angina and congestive heart failure, but not coronary heart disease (CHD). Stratified analysis showed that among individuals without hyperlipidaemia, participants with both unhealthy sleep patterns and pro-oxidant OBS exhibited a higher risk of CHD compared to those with healthy sleep patterns and antioxidative OBS.
CONCLUSIONS
Unhealthy sleep patterns and reduced oxidative balance are positively associated with an increased risk of overall and specific CVD. Interventions that target healthy sleep habits and antioxidant-rich diets and lifestyles may be important for reducing the risk of CVD.
Topics: Adult; Humans; Nutrition Surveys; Cardiovascular Diseases; Antioxidants; Reactive Oxygen Species; Risk Factors; Sleepiness; Oxidative Stress; Sleep
PubMed: 38085249
DOI: 10.7189/jogh.14.04170 -
Journal of Biological Rhythms Aug 2023Late chronotype, which often leads to higher social jetlag (SJL), is strongly associated with the prevalence of smoking. Any circadian disruption, strain, or...
Late chronotype, which often leads to higher social jetlag (SJL), is strongly associated with the prevalence of smoking. Any circadian disruption, strain, or misalignment, results in people not being able to live according to their biological time as is described by SJL, which we will therefore use as umbrella term. We hypothesized two scenarios potentially explaining the association between smoking and SJL: (A) If smoking delays the clock, circadian phase should advance upon quitting. (B) If people smoke more to compensate the consequences of SJL, circadian phase should not change upon quitting. To distinguish between these two hypotheses, we accompanied participants of a smoking cessation program (not involving nicotine replacement products) across the cessation intervention (3 weeks prior and 6 weeks after) by monitoring their circadian behavior, sleep quality, and daytime sleepiness via questionnaires and actimetry. Our results show no effects of cessation on SJL, chronotype, sleep quality, or daytime sleepiness, thereby favoring scenario (B). Thus, smoking may be a consequence of rather than a cause for SJL. Daytime sleepiness was a significant predictor for the outcome in our model but did not improve with cessation.
Topics: Humans; Circadian Rhythm; Nicotine; Chronotype; Smoking Cessation; Social Behavior; Tobacco Use Cessation Devices; Jet Lag Syndrome; Disorders of Excessive Somnolence; Sleep; Surveys and Questionnaires
PubMed: 37345295
DOI: 10.1177/07487304231177197 -
Genes Aug 2023The circadian rhythm is a self-sustaining 24 h cycle that regulates physiological processes within the body, including cycles of alertness and sleepiness. Cells have... (Review)
Review
The circadian rhythm is a self-sustaining 24 h cycle that regulates physiological processes within the body, including cycles of alertness and sleepiness. Cells have their own intrinsic clock, which consists of several proteins that regulate the circadian rhythm of each individual cell. The core of the molecular clock in human cells consists of four main circadian proteins that work in pairs. The CLOCK-BMAL1 heterodimer and the PER-CRY heterodimer each regulate the other pair's expression, forming a negative feedback loop. Several other proteins are involved in regulating the expression of the main circadian genes, and can therefore also influence the circadian rhythm of cells. This review focuses on the existing knowledge regarding circadian gene variants in both the main and secondary circadian genes, and their association with various diseases, such as tumors, metabolic diseases, cardiovascular diseases, and sleep disorders.
PubMed: 37761843
DOI: 10.3390/genes14091703