The purpose of this study was to compare the neurotrophic factor response following one session of high-intensity exercise, resistance training or both in a cohort of physically inactive overweight adults aged 18–30 years old. A randomized, parallel-group clinical trial of 51 men (23.6 ± 3.5 years; 83.5 ± 7.8 kg; 28.0 ± 1.9 kg/m2) who are physically inactive (i.e., < 150 min of moderate-intensity exercise per week or IPAQ score of <600 MET min/week for >6 months) and are either abdominally obese (waist circumference ≥90 cm) or have a body mass index, BMI ≥25 and ≤ 30 kg/m2 were randomized to the following four exercise protocols: high-intensity exercise (4 × 4 min intervals at 85–95% maximum heart rate [HRmax] interspersed with 4 min of recovery at 75–85% HRmax) (n = 14), resistance training (12–15 repetitions per set, at 50–70% of one repetition maximum with 60 s of recovery) (n = 12), combined high-intensity and resistance exercise (n = 13), or non-exercising control (n = 12). The plasma levels of neurotrophin-3 (NT-3), neurotrophin-4 (also known as neurotrophin 4/5; NT-4 or NT-4/5), and brain-derived neurotrophic factor (BDNF) were determined before (pre-exercise) and 1-min post-exercise for each protocol session. Resistance training induced significant increases in NT-3 (+39.6 ng/mL [95% CI, 2.5–76.6; p = 0.004], and NT-4/5 (+1.3 ng/mL [95% CI, 0.3–2.3; p = 0.014]), respectively. Additionally, combined training results in favorable effects on BDNF (+22.0, 95% CI, 2.6–41.5; p = 0.029) and NT-3 (+32.9 ng/mL [95% CI, 12.3–53.4; p = 0.004]), respectively. The regression analysis revealed a significant positive relationship between changes in BDNF levels and changes in NT-4/5 levels from baseline to immediate post-exercise in the combined training group (R2 = 0.345, p = 0.034) but not the other intervention groups. The findings indicate that acute resistance training and combined exercise increase neurotrophic factors in physically inactive overweight adults. Further studies are required to determine the biological importance of changes in neurotrophic responses in overweight men and chronic effects of these exercise protocols.Trial Registration: ClinicalTrials.gov, NCT02915913 (Date: September 22, 2016).

Therapeutic drug monitoring (TDM) is a fundamental tool when administering drugs that have a limited dosage or high toxicity, which could endanger the lives of patients. To carry out this monitoring, one can use different biological fluids, including blood, plasma, serum, and urine, among others. The help of specialized methodologies for TDM will allow for the pharmacodynamic and pharmacokinetic analysis of drugs and help adjust the dose before or during their administration. Techniques that are more versatile and label free for the rapid quantification of drugs employ biosensors, devices that consist of one element for biological recognition coupled to a signal transducer. Among biosensors are those of the optical biosensor type, which have been used for the quantification of different molecules of clinical interest, such as antibiotics, anticonvulsants, anti-cancer drugs, and heart failure. This review presents an overview of TDM at the global level considering various aspects and clinical applications. In addition, we review the contributions of optical biosensors to TDM.

Diabetes mellitus (DM) is the most commonly occurring cause of neuropathy around the world and is beginning to grow in countries where there is a risk of obesity. DM Type II, (T2DM) is a common age-related disease and is a major health concern, particularly in developed countries in Europe where the population is aging. T2DM is a chronic disease which is characterised by hyperglycemia, hyperinsulinemia and insulin resistance, together with the body's inability to use glucose as energy. Such metabolic disorder produces a chronic inflammatory state, as well as changes in lipid metabolism leading to hypertriglyceridemia, thereby producing chronic deterioration of the organs and premature morbidity and mortality. The pathology's effects increase cerebral damage, leading to the rapid onset of neurodegenerative diseases. Hyperglycemia causes oxidative stress in tissues which are susceptible to the complications involved in diabetes, including peripheral nerves. Other additional mechanisms include activation of polyol aldose reductase signalling accompanied by protein kinase C (PKC)-ß activation, poly(ADP ribose) polymerase activation, cyclooxygenase (COX) 2 activation, endothelial dysfunction, altered Na+/K+ ATPase pump function, dyslipidaemia and perturbation of calcium balance. All the forgoing has an impact on neuron activity, mitochondrial function, membrane permeability and endothelial function. These biochemical processes directly affect the neurons and endothelial tissue, thereby accelerating cerebral aging by means of peroxidation of the polyunsaturated fatty acids and thus injuring cell membrane integrity and inducing apoptosis in the glial cells. The Central Nervous System (CNS) includes two types de glial cells: microglia and macroglia (astrocytes, oligodendrocytes and radial cells which include Bergmann cells and Müller cells). Glial cells constitute more than 90% of the CNS cell population. Human studies have shown that some oral antidiabetic drugs can improve cognition in patients suffering mild cognitive impairment (MCI) and dementia [1, 2]. While it is still unclear whether diabetes management will reduce MCI and Alzheimer's disease (AD), incidence, emerging evidence suggests that diabetes therapies may improve cognitive function. This review focuses three aspects: the clinical manifestation of diabetes regarding glial and neuronal cells, the association between neurodegeneration and diabetes and summarises some of the pharmacogenomic data obtained from studies of T2DM treatment, focusing on polymorphisms in genes affecting pharmacokinetics, pharmacodynamics and treatment outcome of the most commonly-prescribed oral anti-diabetic drugs (OADs).

Genetics has led to a new focus regarding approaches to the most prevalent diseases today. Ascertaining the molecular secrets of neurodegenerative diseases will lead to developing drugs that will change natural history, thereby affecting the quality of life and mortality of patients. The sequencing of candidate genes in patients suffering neurodegenerative pathologies is faster, more accurate, and has a lower cost, thereby enabling algorithms to be proposed regarding the risk of neurodegeneration onset in healthy persons including the year of onset and neurodegeneration severity. Next generation sequencing has resulted in an explosion of articles regarding the diagnosis of neurodegenerative diseases involving exome sequencing or sequencing a whole gene for correlating phenotypical expression with genetic mutations in proteins having key functions. Many of them occur in neuronal glia, which can trigger a proinflammatory effect leading to defective proteins causing sporadic or familial mutations. This article reviews the genetic diagnosis techniques and the importance of bioinformatics in interpreting results from neurodegenerative diseases. Risk scores must be established in the near future regarding diseases with a high incidence in healthy people for defining prevention strategies or an early start for giving drugs in the absence of symptoms.

Antimicrobial resistance to antibiotic treatment has significantly increased during recent years, causing this to become a worldwide public health problem. More than 70% of pathogenic bacteria are resistant to at least one of the currently used antibiotics. Polymyxin E (colistin) has recently been used as a “last line” therapy when treating Gram-negative multi-resistant bacteria. However, little is known about these molecules’ pharmacological use as they have been discontinued because of their high toxicity. Recent research has been focused on determining colistimethate sodium’s pharmacokinetic parameters to find the optimal dose for maintaining a suitable benefit–risk balance. This review has thus been aimed at describing the use of colistin on patients infected by multi-drug resistant bacteria and the importance of measuring this drug’s plasma levels in such patients.