Hypoxia of renal medulla is a key factor implicated in the development of drug-induced renal failure. Drugs are known to influence renal hemodynamics and, subsequently, affect renal tissue oxygenation. Changes in renal oxygenation can be assessed non-invasively in humans using blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI). This study was designed to test the acute effects of administration of specific drugs in healthy human kidney oxygenation using BOLD-MRI. Acute changes in renal tissue oxygenation induced by the non-steroidal anti-inflammatory drug indomethacin, the iodinated radio-contrast media (RCM) iopromidum, and the calcineurin inhibitors cyclosporine micro-emulsion (CsA-ME) and tracrolimus were studied in 30 healthy volunteers. A modified Multi Echo Data Image Combination sequence was used to acquire 12 T(2)(*)-weighted images. Four coronal slices were selected to cover both kidneys. The mean R(2)(*) (1/T(2)(*)) values determined in medulla and cortex showed no significant changes induced by indomethacin and tacrolimus administration. CsA-ME decreased medullary (P=0.008) and cortical (P=0.004) R(2)(*) values 2 h after ingestion. Iopromidum caused a significant increase in medullary R(2)(*) within the first 20 min after injection (P<0.001), whereas no relevant changes were observed in renal cortex. None of the measurements showed left-right kidney differences. Significant differences in renal medullary oxygenation were evidenced between female and male subjects (P=0.013). BOLD-MRI was efficient to show effects of specific drugs in healthy renal tissue. Cyclosporine increased renal medullary oxygenation 2 h after ingestion of a single dose, whereas indomethacin and tacrolimus showed no effect on renal oxygenation. Injection of iodinated RCM decreased renal medullary oxygenation.

Insulin resistance is documented in clamp studies in 75% of women with polycystic ovary syndrome (PCOS). Although it is not included in the diagnostic criteria of PCOS, there is a crucial role of this metabolic impairment, which along with hormonal abnormalities, increase each other in a vicious circle of PCOS pathogenesis. Insulin resistance in this group of patients results from defects at the molecular level, including impaired insulin receptor-related signaling pathways enhanced by obesity and its features: Excess visceral fat, chronic inflammation, and reactive oxygen species. While lifestyle intervention has a first-line role in the prevention and management of excess weight in PCOS, the role of anti-obesity pharmacological agents in achieving and maintaining weight loss is being increasingly recognized. Glucagon-like peptide-1 receptor agonists (GLP1-RAs) not only act by reducing body weight but also can affect the mechanisms involved in insulin resistance, like an increasing expression of glucose transporters in insulin-dependent tissues, decreasing inflammation, reducing oxidative stress, and modulating lipid metabolism. They also tend to improve fertility either by increasing LH surge in hypothalamus-pituitary inhibition due to estrogen excess connected with obesity or decreasing too high LH levels accompanying hyperinsulinemia. GLP1-RAs seem promising for effective treatment of obese PCOS patients, acting on one of the primary causes of PCOS at the molecular level.

We aimed to evaluate the relationship between selected serum sex hormones and lipid profiles in a group of women with polycystic ovary syndrome (PCOS) dividing according to four phenotypes, value of body mass index (BMI), and presence of hyperlipidemia. The study included 606 Caucasian women. Lipids and selected hormones were estimated using commercially available procedures during hospitalization in 2017. Phenotype of PCOS, BMI value, and hyperlipidemia were significant factors that influenced androgen hormone concentrations, such as total and free testosterone and androstenedione as well as the value of free androgen index (FAI). Moreover, significant changes in concentrations of dehydroepiandrosterone sulphate and sex hormone binding globulin (SHBG) were found between those groups. Higher quartiles of triglyceride concentrations increased the odds ratio of decreased concentrations of SHBG or increased values of FAI, while an adverse relation was found in case of HDL-C. The concentration of estradiol in the blood of women with PCOS was not associated with lipid profile parameters in any investigated groups. Probably, irregularities in sex hormone concentrations during PCOS is not directly associated with lipid profile parameters but could be reflective of the concentration of SHBG or the ratio of SHBG and total testosterone and their association with lipids.

We investigated the relationship between selected body composition (BC) parameters and included 55 women diagnosed with PCOS and 29 women in which PCOS was excluded. Hormone concentration and BC parameters were assessed during hospitalization. Women with PCOS had higher concentration of luteinizing hormones, total testosterone, androstenedione, and Anti-Müllerian hormones compared to women that were not diagnosed with PCOS. We did not observe any significant differences in the BC parameters between both groups as well as between four PCOS phenotype subgroups. Only in the group of women with PCOS was the concentration of sex hormone binding globulin and free testosterone correlated with all investigated BC parameters. Correspondence analysis did not confirm unambiguously associations between phenotypes of PCOS and the value of BC parameters, while logistic regression revealed that increased Anti-Müllerian hormone concentration and the value of body mass index could be useful parameters in differentiating women with PCOS and women with other disorders. The ROC analysis performed on the entire group of women also confirmed that the concentration of Anti-Müllerian hormones could be a powerful parameter to categorize women as suffering from PCOS.

Asthma is a heterogeneous disease characterized by chronic inflammation of the airways with symptoms such as wheezing, shortness of breath, chest tightness and coughing of varying frequency and severity, with varying degrees of airway obstruction. Many factors have a significant influence on the course of asthma, including smoking. The harmful effects of cigarettes have been known for a long time and pose a unique threat to people suffering from asthma. Exposure to passive inhalation of tobacco smoke and active smoking can lead to exacerbation of the disease, wheezing, coughing and shortness of breath. Tobacco smoke irritates the respiratory system and damages the cilia. Continued exposure to cigarette smoke in the environment also increases the risk of other respiratory diseases such as bronchitis, pneumonia and lung cancer.