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Early and premature menopause, or premature ovarian insufficiency (POI), affects 1% of women under the age of 40 years. This paper reviews the main aspects of early and premature menopause and their impact on cognitive decline. Based on the literature, cognitive complaints are more common near menopause: a phase marked by a decrease in hormone levels, especially estrogen. A premature reduction in estrogen puts women at a higher risk for cardiovascular disease, parkinsonism, depression, osteoporosis, hypertension, weight gain, midlife diabetes, as well as cognitive disorders and dementia, such as Alzheimer’s disease (AD). Experimental and epidemiological studies suggest that female sex hormones have long-lasting neuroprotective and anti-aging properties. Estrogens seem to prevent cognitive disorders arising from a cholinergic deficit in women and female animals in middle age premature menopause that affects the central nervous system (CNS) directly and indirectly, both transiently and in the long term, leads to cognitive impairment or even dementia, mainly due to the decrease in estrogen levels and comorbidity with cardiovascular risk factors, autoimmune diseases, and aging. Menopausal hormone therapy from menopause to the age of 60 years may provide a “window of opportunity” to reduce the risk of mild cognitive impairment (MCI) and AD in later life. Women with earlier menopause should be taken care of by various specialists such as gynecologists, endocrinologists, neurologists, and psychiatrists in order to maintain their mental health at the highest possible level.

Old age increases the risk of Alzheimer’s disease (AD), the most common neurodegenerative disease, a devastating disorder of the human mind and the leading cause of dementia. Worldwide, 50 million people have the disease, and it is estimated that there will be 150 million by 2050. Today, healthcare for AD patients consumes 1% of the global economy. According to the amyloid cascade hypothesis, AD begins in the brain by accumulating and aggregating Aβ peptides and forming β-amyloid fibrils (Aβ42). However, in clinical trials, reducing Aβ peptide production and amyloid formation in the brain did not slow cognitive decline or improve daily life in AD patients. Prevention studies in cognitively unimpaired people at high risk or genetically destined to develop AD also have not slowed cognitive decline. These observations argue against the amyloid hypothesis of AD etiology, its development, and disease mechanisms. Here, we look at other avenues in the research of AD, such as the presenilin hypothesis, synaptic glutamate signaling, and the role of astrocytes and the glutamate transporter EAAT2 in the development of AD.

Background Device-associated health care-associated infections (DA-HAIs) in intensive care unit (ICU) patients constitute a major therapeutic issue complicating the regular hospitalisation process and having influence on patients’ condition, length of hospitalisation, mortality and therapy cost. Methods The study involved all patients treated > 48 h at ICU of the Medical University Teaching Hospital (Poland) from 1.01.2015 to 31.12.2017. The study showed the surveillance and prevention of DA-HAIs on International Nosocomial Infection Control Consortium (INICC) Surveillance Online System (ISOS) 3 online platform according to methodology of the INICC multidimensional approach (IMA). Results During study period 252 HAIs were found in 1353 (549F/804M) patients and 14,700 patient-days of hospitalisation. The crude infections rate and incidence density of DA-HAIs was 18.69% and 17.49 ± 2.56 /1000 patient-days. Incidence density of ventilator-associated pneumonia (VAP), central line-associated bloodstream infection (CLA-BSI) and catheter-associated urinary tract infection (CA-UTI) per 1000 device-days were 12.63 ± 1.49, 1.83 ± 0.65 and 6.5 ± 1.2, respectively. VAP(137) constituted 54.4% of HAIs, whereas CA-UTI(91) 36%, CLA-BSI(24) 9.6%.The most common pathogens in VAP and CA-UTI was multidrug-resistant (MDR) Acinetobacter baumannii (57 and 31%), and methicillin-resistant Staphylococcus epidermidis (MRSE ) in CLA-BSI (45%). MDR Gram negative bacteria (GNB) 159 were responsible for 63.09% of HAIs. The length of hospitalisation of patients with a single DA-HAI at ICU was 21(14–33) days, while without infections it was 6.0 (3–11) days; p  = 0.0001. The mortality rates in the hospital-acquired infection group and no infection group were 26.1% vs 26.9%; p  = 0.838; OR 0.9633;95% CI (0.6733–1.3782). Extra cost of therapy caused by one ICU acquired HAI was US$ 11,475/Euro 10,035. Hand hygiene standards compliance rate was 64.7%, while VAP, CLA-BSI bundles compliance ranges were 96.2–76.8 and 29–100, respectively. Conclusions DA-HAIs was diagnosed at nearly 1/5 of patients. They were more frequent than in European Centre Disease Control report (except for CLA-BSI), more frequent than the USA CDC report, yet less frequent than in limited-resource countries (except for CA-UTI). They prolonged the hospitalisation period at ICU and generated substantial additional costs of treatment with no influence on mortality. The Acinetobacter baumannii MDR infections were the most problematic therapeutic issue. DA-HAIs preventive methods compliance rate needs improvement.

BackgroundDietary sodium restriction remains a guidelines-approved lifestyle recommendation for chronic heart failure (CHF) patients. However, its efficacy in clinical outcome improvement is dubious.ObjectiveThe study evaluated whether dietary sodium restriction in CHF reduces clinical events.MethodsWe performed a systematic review of the following databases: Academic Search Ultimate, ERIC, Health Source Nursing/Academic Edition, MEDLINE, Embase, Clinicaltrials.gov and Cochrane Library (trials) to find studies analysing the impact of sodium restriction in the adult CHF population. Both observational and interventional studies were included. Exclusion criteria included i.e.: sodium consumption assessment based only on natriuresis, in-hospital interventions or mixed interventions—e.g. sodium and fluid restriction in one arm only. The review was conducted following PRISMA guidelines. Meta-analysis was performed for the endpoints reported in at least 3 papers. Analyses were conducted in Review Manager (RevMan) Version 5.4.1.ResultsInitially, we screened 9175 articles. Backward snowballing revealed 1050 additional articles. Eventually, 9 papers were evaluated in the meta-analysis. All-cause mortality, HF-related hospitalizations and the composite of mortality and hospitalisation were reported in 8, 6 and 3 articles, respectively. Sodium restriction was associated with a higher risk of the composite endpoint (OR 4.12 [95% CI 1.23–13.82]) and did not significantly affect the all-cause mortality (OR 1.38 [95% CI 0.76–2.49]) or HF hospitalisation (OR 1.63 [95% CI 0.69–3.88]).ConclusionsIn a meta-analysis, sodium restriction in CHF patients worsened the prognosis in terms of a composite of mortality and hospitalizations and did not influence all-cause mortality and HF hospitalisation rate.

Background/Objectives: Recent advancements in cardiovascular imaging have opened new avenues for integrating novel biomarkers into risk assessment models, enhancing their predictive accuracy. One such emerging biomarker is the left atrioventricular coupling index (LACI). The study aims to evaluate the relationship between the SCORE (Systematic Coronary Risk Evaluation) and LACI derived from cardiac computed tomography (CCT). Methods: This study included 137 participants (56.09 ± 7.64 years). Cardiovascular risk was assessed using the SCORE system. CCT was performed using the standard coronary computed tomography angiography protocol. LACI was calculated as the ratio of left atrial end-diastolic volume (LA EDV) to left ventricular end-diastolic volume (LV EDV), expressed as a percentage. Results: The subgroup with SCORE ≥5% had higher LACI than the subgroup with SCORE < 5%. Similarly, the subgroup with SCORE ≥10% had higher LACI than the subgroup with SCORE < 10%. LACI demonstrated a significant positive correlation with the SCORE (r = 0.29, p = 0.01). Prediction analysis showed that LACI ≥ 53.34% as a predictor of SCORE ≥ 10% had the highest accuracy of 78.1%, with a high sensitivity of 79.8% and a moderate specificity of 61.5%. High specificity (80.6%) is characterized by LACI ≥ 29.52% as a predictor of SCORE ≥ 5. Conclusions: LACI is a novel and significant biomarker associated with cardiovascular risk, as reflected by its relationship with the SCORE system.

Oxidative stress is proven to increase cardiovascular risk and to diminish healthy life expectancy. Sleep bruxism (SB) is a prevalent masticatory muscle activity during sleep characterized by heterogeneous etiology and inadequately recognized pathophysiology. Recent theories have proposed a potential association between SB and oxidative stress. The aim of the research was to compare the antioxidant status between individuals with SB in contrast to those without SB. A total of 80 adults participated in a full-night polysomnography, assessed according to the American Academy of Sleep Medicine (AASM) standards. Blood samples were subsequently drawn via venipuncture for analysis. Participants were stratified into two groups based on their bruxism episode index (BEI). Using successive receiver operating characteristic (ROC) curves, optimal cut-off values were identified, enabling the detection of correlations with moderate (BEI > 2) and severe (BEI > 4) sleep bruxism. In the investigated group of patients we observed the relationship between bruxism and the examined parameters: total antioxidant status (TAS), advanced protein products (AOPP) and thiobarbituric acid-reacting substances (TBARS). Low TAS (≤ 0.14 mM and ≤ 0. 16 mM), high AOPP (≥ 82.44 µmol/l) and high TBARS (≥ 723.03 µmol/l and ≥ 1585.45 µmol/l) serum levels result in significantly higher sleep bruxism parameters. Sleep bruxism is related to oxidative stress markers. Elevated markers of lipid and protein peroxidation may be associated with endovascular damage and cardiovascular risk in sleep bruxers, but further research is needed in this topic.

Alzheimer’s disease (AD) is the most common cause of dementia worldwide. Pathological deposits of neurotoxin proteins within the brain, such as amyloid-β and hyperphosphorylated tau tangles, are prominent features in AD. The prion protein (PrP) is involved in neurodegeneration via its conversion from the normal cellular form (PrPC) to the infection prion protein scrapie (PrPSc) form. Some studies indicated that post-translationally modified PrPC isoforms play a fundamental role in AD pathological progression. Several studies have shown that the interaction of Aβ oligomers (Aβos) with the N-terminal residues of the PrPC protein region appears critical for neuronal toxicity. PrPC-Aβ binding always occurs in AD brains and is never detected in non-demented controls, and the binding of Aβ aggregates to PrPC is restricted to the N-terminus of PrPC. In this study, we aimed to gather all of the recent information about the connections between PrPC and AD, with potential clinical implications.

Beginning with the various strategies of the SARS-CoV-2 virus to invade our bodies and manifest infection, and ending with the recent long COVID, we are witnessing the evolving course of the disease in addition to the pandemic. Given the partially controlled course of the COVID-19 pandemic, the greatest challenge currently lies in managing the short- and long-term complications of COVID-19. We have assembled current knowledge of the broad spectrum of cardiovascular, pulmonary, and neuropsychiatric sequelae following SARS-CoV-2 infection to understand how these clinical manifestations collectively lead to a severe form of the disease. The ultimate goal would be to better understand these complications and find ways to prevent clinical deterioration.

Sleep bruxism (SB) is a sleep-related behavior characterized as rhythmic (phasic) or non-rhythmic (tonic) masticatory muscle activity. SB is a common sleep behavior with a predominantly central origin. The aim of this systematic review was to evaluate the relationship between inflammatory status and SB according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 (PRISMA 2020). The research was registered at PROSPERO (CRD42023395985). We performed a systematic literature analysis using five different databases. Furthermore, the backward snowballing technique was applied to identify additional papers. Initially, 28 papers were screened from the database search, and 162 papers were revealed in the backward snowballing process. Eventually, five articles were included. Data concerning the inflammatory status of patients experiencing SB were investigated and summarized. Due to the heterogeneity of the compared studies, only a qualitative comparison and narrative summary were performed. The results suggest that SB could be associated with systemic inflammation. In fact, this systematic review revealed that there are no papers conclusively showing that the inflammatory status in bruxers is comparable to non-bruxers. However, each of the examined studies utilized different methods of assessing systemic inflammation, which makes the results dubious.

Objectives. Many studies have confirmed the existence of a relationship between SARS-CoV-2 virus infection and an increased incidence of arrhythmia in the population of adults, children and adolescents. It is believed that one of the potential side effects of COVID-19 vaccination is arrhythmia. However, large-scale studies confirming the relationship between COVID-19 vaccination and cardiac arrhythmia are currently lacking. The objective of this study was to analyze the occurrence of arrhythmias in 24 h Holter ECG monitoring among patients who had experienced COVID-19, comparing those who were vaccinated against SARS-CoV-2 with those who were unvaccinated. Methods. The study was performed on a study group of 237 patients, who underwent 24 h Holter monitoring. Results. Ventricular extrasystoles (VEs) were distinctively more common in patients, who had COVID-19 infection and were not vaccinated for COVID-19 comparing to the control group. Similarly, research has shown that supraventricular extrasystoles (SVEs) occurred remarkably more frequently in both unvaccinated and vaccinated patients after COVID-19 infection in relation to control groups. Multivariable regression analysis demonstrates that, in the whole study group, obesity, arterial hypertension, previous myocardial infarction and lack of vaccination against COVID-19 are independent risk factors for higher VE rates. Obesity, diabetes type 2 and lack of vaccination against COVID-19 are independent risk factors for higher SVE rates. The use of β-blockers is an independent protective factor against higher VE and SVE rates, and the use of ACE inhibitors against higher SVE rates. Conclusions. In this study, the authors obtained promising results for the future, facilitating further discussion and research on the topic of the antiarrhythmic advantages of COVID-19 vaccination. Moreover, the knowledge acquired in this study serves as a valuable tool for effectively promoting COVID-19 vaccination among patients.