Metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) are diseases that can be influenced by the structure of gut microbiota, whose improvement is often neglected in metabolic pathology. This review highlights the following main aspects: the relationship between probiotics/gut microbes with the pathogenesis of MetS, the particular positive roles of Akkermansia muciniphila supplementation in the onset of MetS, and the interaction between dietary polyphenols (prebiotics) with gut microbiota. Therefore, an extensive and in-depth analysis of the often-neglected correlation between gut microbiota and chronic metabolic diseases was conducted, considering that this topic continues to fascinate and stimulate researchers through the discovery of novel strains and their beneficial properties.

Withaferin A (WA), a manifold studied, C28-steroidal lactone withanolide found in Withania somnifera. Given its unique beneficial effects, it has gathered attention in the era of modern science. Cancer, being considered a “hopeless case and the leading cause of death worldwide, and the available conventional therapies have many lacunae in the form of side effects. The poly pharmaceutical natural compound, WA treatment, displayed attenuation of various cancer hallmarks by altering oxidative stress, promoting apoptosis, and autophagy, inhibiting cell proliferation, reducing angiogenesis, and metastasis progression. The cellular proteins associated with antitumor pathways were also discussed. WA structural modifications attack multiple signal transduction pathways and enhance the therapeutic outcomes in various diseases. Moreover, it has shown validated pharmacological effects against multiple neurodegenerative diseases by inhibiting acetylcholesterinases and butyrylcholinesterases enzyme activity, antidiabetic activity by upregulating adiponectin and preventing the phosphorylation of peroxisome proliferator-activated receptors (PPARγ), cardioprotective activity by AMP-activated protein kinase (AMPK) activation and suppressing mitochondrial apoptosis. The current review is an extensive survey of various WA associated disease targets, its pharmacokinetics, synergistic combination, modifications, and biological activities.

Current therapies for Parkinson’s disease (PD) are palliative, of which the levodopa/carbidopa therapy remains the primary choice but is unable to modulate the progression of neurodegeneration. Due to the complication of such a multifactorial disorder and significant limitations of the therapy, numerous genetic approaches have been proved effective in finding out genes and mechanisms implicated in this disease. Following the observation of a higher frequency of PD in Gaucher’s disease (GD), a lysosomal storage condition, mutations of glycosylceramidase beta (GBA) encoding glucocerebrosidase (GCase) have been shown to be involved and have been explored in the context of PD. GBA mutations are the most common genetic risk factor of PD. Various studies have revealed the relationships between PD and GBA gene mutations, facilitating a better understanding of this disorder. Various hypotheses delineate that the pathological mutations of GBA minimize the enzymatic activity of GCase, which affects the proliferation and clearance of α-synuclein; this affects the lysosomal homeostasis, exacerbating the endoplasmic reticulum stress or encouraging the mitochondrial dysfunction. Identification of the pathological mechanisms underlying the GBA-associated parkinsonism (GBA + PD) advances our understanding of PD. This review based on current literature aims to elucidate various genetic and clinical characteristics correlated with GBA mutations and to identify the numerous pathological processes underlying GBA + PD. We also delineate the therapeutic strategies to interfere with the mutant GCase function for further improvement of the related α-synuclein–GCase crosstalks. Moreover, the various therapeutic approaches such as gene therapy, chaperone proteins, and histone deacetylase inhibitors for the treatment of GBA + PD are discussed.

One of the most commonly occurring neurodegenerative disorders, Alzheimer’s disease (AD), encompasses the loss of cognitive and memory potential, impaired learning, dementia and behavioral defects, and has been prevalent since the 1900s. The accelerating occurrence of AD is expected to reach 65.7 million by 2030. The disease results in neural atrophy and disrupted inter-neuronal connections. Amongst multiple AD pathogenesis hypotheses, the amyloid beta (Aβ) cascade is the most relevant and accepted form of the hypothesis, which suggests that Aβ monomers are formed as a result of the cleavage of amyloid precursor protein (APP), followed by the conversion of these monomers to toxic oligomers, which in turn develop β-sheets, fibrils and plaques. The review targets the events in the amyloid hypothesis and elaborates suitable therapeutic agents that function by hindering the steps of plaque formation and lowering Aβ levels in the brain. The authors discuss treatment possibilities, including the inhibition of β- and γ-secretase-mediated enzymatic cleavage of APP, the immune response generating active immunotherapy and passive immunotherapeutic approaches targeting monoclonal antibodies towards Aβ aggregates, the removal of amyloid aggregates by the activation of enzymatic pathways or the regulation of Aβ circulation, glucagon-like peptide-1 (GLP-1)-mediated curbed accumulation and the neurotoxic potential of Aβ aggregates, bapineuzumab-mediated vascular permeability alterations, statin-mediated Aβ peptide degradation, the potential role of ibuprofen and the significance of natural drugs and dyes in hindering the amyloid cascade events. Thus, the authors aim to highlight the treatment perspective, targeting the amyloid hypothesis, while simultaneously emphasizing the need to conduct further investigations, in order to provide an opportunity to neurologists to develop novel and reliable treatment therapies for the retardation of AD progression.

Background and Objectives: This study evaluated the clinical characteristics of the acute coronary syndromes (ACS) in chronic kidney disease (CKD) patients and established prognostic values of the biomarkers and echocardiography. Materials and Methods: 273 patients admitted to the cardiology department of the Clinical County Emergency Hospital of Oradea, Romania, with ACS diagnosis were studied. Two study groups were formed according to the presence of CKD (137 patients with ACS + CKD and 136 with ACS without CKD). Kidney Disease: Improving Global Outcomes (KDIGO) threshold was used to assess the stages of CKD. Results: Data regarding the medical history, laboratory findings, biomarkers, echocardiography, and coronary angiography were analysed for both groups. ACS parameters were represented by ST-segment elevation myocardial infarction (STEMI), which revealed a greater incidence in subjects without CKD (43.88%); non-ST-segment elevation myocardial infarction (NSTEMI), characteristic for the CKD group (28.47%, with statistically significance p = 0.04); unstable angina and myocardial infarction with nonobstructive coronary arteries (MINOCA). Diabetes mellitus, chronic heart failure, previous stroke, and chronic coronary syndrome were more prevalent in the ACS + CKD group (56.93%, p < 0.01; 41.61%, p < 0.01; 18.25%, p < 0.01; 45.26%, p < 0.01). N-terminal pro b-type natriuretic peptide (NT-proBNP) was statistically higher (p < 0.01) in patients with CKD; Killip class 3 was evidenced more frequently in the same group (p < 0.01). Single-vessel coronary artery disease (CAD) was statistically more frequent in the ACS without CKD group (29.41%, p < 0.01) and three-vessel CAD or left main coronary artery disease (LMCA) were found more often in the ACS + CKD group (27.01%, 14.6%). Conclusions: Extension of the CAD in CKD subjects revealed an increased prevalence of the proximal CAD, and the involvement of various coronary arteries is characteristic in these patients. Biomarkers and echocardiographic elements can outline the evolution and outcomes of ACS in CKD patients.

Obesity and overweight are major contributors to the morbidity and mortality of modern civilization. This study determined the prevalence of certain risk factors for adiposity and assesses their impact on overweight/obesity prevalence. Nine hundred individuals were evaluated, aged between 18-65 years, including clinical examination, evaluation of medical history, BMI determination and completion on questionnaires assessing nutritional intake and presence of depression symptoms. Overweight prevalence was 29.56% and obesity prevalence was 21.33%. Fast-food consumption was the most frequent risk factor for adiposity found in 61.67% of individuals, eating <3 meals/day was found in 58.89%, sedentary lifestyle in 53.33%, sleeping time <6 h/day in 44.22%, hypercaloric nutrition in 43.56%, excessive alcohol consumption in 42.89% and depression symptoms in 31.78%. Unhealthy lifestyle a composite risk factor was identified in 67.33% of individuals. Fast-food consumption increases the risk for adiposity by 1.85-fold while sedentary lifestyle by 1.79-fold. Risk factors for adiposity play an important role in increasing the prevalence of overweight and obesity. Public health measures are necessary in order to educate the general population regarding the importance of healthy nutrition and physical exercise.

Metabolic syndrome is associated with increased risk of cardiovascular disease. This study investigated the correlation between adipocyte and inflammation biomarkers, and metabolic syndrome and its components. The study included 80 patients with normal body-mass index and 80 obese patients. The groups were assessed for serum values of adiponectin, leptin and highly sensitive C reactive protein (hsCRP), the homeostatic model assessment of insulin resistance (HOMA-IR), as well as the influence of these biochemical markers on the prevalence of metabolic syndrome and its components. Leptin, HOMA-IR and hsCRP had statistically significant (P<0.01) higher values in the group of obese subjects, while adiponectin had statistically significant (P<0.01) lower values. The prevalence of metabolic syndrome was 35% in the obese group and 5% in the normal weight group. Adiponectin and HOMA-IR were the variables significantly associated with metabolic syndrome (P<0.01), adiponectin/HOMA-IR ratio and leptin/adiponectin ratio were also associated with metabolic syndrome (P<0.01). No relationship was found between metabolic syndrome and hsCRP. Adiponectin and adiponectin/HOMA-IR were associated with all the components of metabolic syndrome and they can be useful to identify patients with high risk of diabetes mellitus and cardiovascular disease.

The spectrum and antibiotic sensitivity of isolated strains vary between departments, hospitals, countries; the discrepancies are related to the use and dosage of these antibiotics. The purpose of our research was to compare the type of pathogens and the susceptibility of the isolated strains, as well as the use of antibiotics in the surgical departments of the Emergency Clinical County Hospital, Oradea, Romania; for one year, all the patients admitted to the mentioned sections were monitored. Antibiotic sensitivity of isolated strains was expressed using cumulative antibiogram. The total consumption of antibiotics was 479.18 DDD/1000 patient-days in the surgical sections. The most commonly used drugs were cephalosporins third and first generation, and clindamycin. Infections of wounds, urinary tract and fluids were most commonly diagnosed, and the most isolated was Escherichia coli, followed by Staphylococcus aureus and Enterococcus faecalis. The most commonly prescribed antimicrobial was ceftriaxone, but its sensitivity was low. This study revealed that the intake of antimicrobials in the surgical sections is increased and the comparison of antimicrobial prescriptions, sensitivity rates, and the spectrum of isolated pathogens showed differences between antimicrobials.