Ovidiu Gabriel Bratu

Uric acid (UA), a key purine metabolite associated with metabolic, cardiovascular, and renal disorders, has been extensively investigated using electrochemical sensors. Increasing efforts now focus on translating these technologies into commercial point-of-care (POC) platforms for rapid, decentralized detection. Commercial screen-printed electrodes (SPEs) are widely employed as substrates for such platforms, typically after surface modification with nanomaterials or recognition elements; however, their inherent, unmodified analytical capabilities remain largely uncharacterized. This gap is significant, as the baseline performance of the underlying electrode ultimately constrains or enables the benefits of any subsequent modification. Here, we systematically compare two commercially available SPEs, DRP-110 and DRP-150, for UA detection using differential pulse voltammetry under standardized conditions. Both electrodes exhibited two distinct UA oxidation peaks. The first peak gave linear calibration over 0.02–0.5 µM (R² = 0.9863 DRP-110, 0.9928 DRP-150), with validated LOD/LOQ of 0.076/0.230 µM (DRP-110) and 0.055/0.166 µM (DRP-150); the second peak extended the linear working range to 1–1000 µM (DRP-110, R² = 0.9833) and 1–2000 µM (DRP-150, R² = 0.9928), with LOD/LOQ of 3.37/10.20 µM and 2.23/6.77 µM, respectively, derived from its low-concentration segment. DRP-150 demonstrated superior sensitivity at both peaks. However, both electrodes showed low selectivity toward ascorbic acid. Spike recovery testing in modified artificial urine gave recoveries of 68.0–98.49%, supporting preliminary feasibility in a defined urine-like matrix.

Primary retroperitoneal tumors are a rare group of neoplasms that often prove to be a real therapeutic challenge. The clinical picture is in most cases nonspecific, being the result of nearby tissue and organ compression, displacement and/or invasion, and it usually includes a variety of deceiving signs and symptoms that may lead to diagnostic errors. During the course of the disease, up to half of the patients diagnosed with retroperitoneal tumors can develop gastrointestinal symptoms, the incidence of such symptoms significantly increasing with tumor size. Therefore, symptoms such as abdominal distension, diffuse abdominal pain or epigastric pain mimicking acute pancreatitis, diarrhea, constipation, jaundice, hematemesis, melena and hematochezia can be found. The mainstream treatment for primary retroperitoneal tumors is surgical excision, chemotherapy and radiotherapy but associated with poor results. Due to their rarity, as well as to the complexity of these tumors, patients should be managed in high volume centers that allow the possibility of a multidisciplinary approach.

Genital self‑mutilation is a pathology that leads to numerous and important discussions, rarely presented in the medical literature. There have been many attempts to explain the reasons behind these medical phenomena, but single cases have been generally reported, making it extremely difficult to draw valid conclusions. It is acknowledged that there are psychotic and non‑psychotic causes, from psychiatric problems and sexual identity disorders to cultural or religious reasons, alcohol or recreational drug consumption, unconventional types of sexual satisfaction or self‑satisfaction. Recent theories consider self‑mutilation as a phenomenon of reducing distress or tension, as an expression of feelings of anger or sorrow. It is believed that 55‑85% of those who have resorted to self‑mutilation have at least once in their life tried to commit suicide. There is evidence that early discovery and intervention as well as proper treatment in regards to psychosis can significantly reduce the number of self‑mutilation episodes, with a protective role of these individuals. Cases of genital self‑mutilation may be considered real medical emergencies, sometimes extremely challenging and accompanied by severe complications. Injury of the genital area is usually accompanied by numerous early or long‑term complications due to the marked vascular area and to the microbial flora present in this part of the body. The degree of mutilation is an unforeseen aspect that the medical staff may have to encounter during the intervention, sometimes testing their imagination and surgical skills when dealing with such a case. Understanding the causes of these self‑aggressive behaviors, which may be life‑threatening, is critical and multidisciplinary mobilization is needed after treatment of the acute phases. The outcome of these patients depends on integrated collaborative work. These cases represent a serious reason for frustration for the physicians involved in solving them, and knowledge of these issues is valuable to urologists, psychiatrists and other health professionals.

Androgen insensitivity syndrome (AIS) is an X-linked recessive genetic syndrome that occurs as result of an androgen receptor mutation; it affects the normal masculinization process in chromosomal male patients. More than 900 androgen receptor mutations that can lead to AIS have been identified. The complete androgen insensitivity is characterized by a total lack of response to androgens, usually in patients with 46XY karyotype but with feminine phenotype. Primary amenorrhoea and inguinal swellings in female patients are the main signs that could raise suspicion for this syndrome. Patients with partial androgen insensitivity have ambiguous genitalia at birth and gynecomastia during puberty, whereas those with mild androgen insensitivity present a normal male phenotype but altered spermatogenesis during adulthood and pubertal gynecomastia. The diagnosis of AIS often proves to be a challenge; its management is complex and requires a multidisciplinary approach to meet decision-making challenges in sex assignment, fertility and timing of gonadectomy, psychological outcomes and genetic counselling.

This study explored the link between insulin sensitivity, insulin resistance and leptinaemia in people with prediabetes with and without non‑alcoholic fatty liver disease (NAFLD). A total of 143 prediabetes patients were evaluated in the study. Ultrasonography was used for diagnosis of NAFLD, and fasting insulin, postprandial insulin, leptin levels, common clinical/biochemical determinations were determined. In total, 69 (48.25%) of the patients were diagnosed with NAFLD and 74 (51.75%) without NAFLD. Leptin values correlated statistically with fasting insulin in prediabetes patients, while in the patients that were also diagnosed with NAFLD the correlation was stronger. Values of log‑leptin <1 ng/ml were found in 64% of patients with prediabetes without NAFLD, and in 2% of patients with prediabetes and NAFLD. In the context of the association between serum leptin levels and a worse biochemical profile in prediabetes patients on one hand, and fatty liver disease and a worse biochemical profile in prediabetes patients on the other, leptin can be considered a possible candidate molecule that mediates the biochemical alterations identified in these patients.

Non‑alcoholic fatty liver disease (NAFLD) is a component of metabolic syndrome that significantly increases the cardiovascular risk of patients with glucose metabolism alterations. This study identified the prevalence of NAFLD, predictors of NAFLD and explored the link between insulin sensitivity, insulin resistance and leptinemia in 143 patients registered with prediabetes. Abdominal ultrasound was performed, and fasting insulin, postprandial insulin, leptin levels, common clinical/biochemical determinations were assessed. Certain variables that can predict NAFLD existence were determined and it was found that there is a high prevalence of NAFLD in patients with prediabetes. In univariate analysis, statistically significant associations (P<0.05) were found between waist circumference, systolic blood pressure, diastolic blood pressure, triglycerides, HDL‑cholesterol, insulin sensitivity, β‑cell function, leptin and NAFLD presence. The coefficients for the variables which obtain statistically significant association (P<0.05) are low, except for leptin which is the biochemical parameter that (in both univariate and multivariate analysis) is a strong predictor of NAFLD presence.

Despite major progress in the prevention and treatment of cardiovascular diseases, women remain an underdiagnosed and insufficiently treated group, with higher hospitalization and death rates compared to men. Obesity, more frequently encountered in women, raises the risk of metabolic syndrome and cardiovascular diseases as women age. There are some differences based on sex regarding the screening, diagnosis, and treatment of dyslipidemia, as it has been observed that women are less frequently prescribed statins and, when they are, they receive lower doses, even after myocardial infarction or coronary revascularization. Real-life data show that, compared to men, women are at higher risk of non-adherence to statin treatment and are more predisposed to discontinue treatment because of side effects. Statin metabolism has some particularities in women, due to a lower glomerular filtration rate, higher body fat percentage, and overall faster statin metabolism. In women of fertile age, before initiating statin treatment, contraception methods should be discussed because statins may have teratogenic effects. Older women have a higher likelihood of polypharmacy, with greater potential for drug interactions when prescribing a statin.

Within the last few years, there have been an increased number of clinical studies involving urinary microbiota. Low-biomass microbiome sequencing (e.g., urine, lung, placenta, blood) is easily biased by contamination or cross-contamination. So far, a few critical steps, from sampling urine to processing and analyzing, have been described (e.g., urine collection modality, sample volume size, snap freezing, negative controls usage, laboratory risks for contamination assessment, contamination of negative results reporting, exploration and discussion of the impact of contamination for the final results, etc.) We performed a literature search (Pubmed, Scopus and Embase) and reviewed the published articles related to urinary microbiome, evaluating how the aforementioned critical steps to obtain unbiased, reliable results have been taken or have been reported. We identified different urinary microbiome evaluation protocols, with non-homogenous reporting systems, which can make gathering results into consistent data for similar topics difficult and further burden the already so complex emerging field of urinary microbiome. We concluded that to ease the progress in this field, a joint approach from researchers, authors and publishers would be necessary in order to create mandatory reporting systems which would allow to recognize pitfalls and avoid compromising a promising field of research.

Botulinum toxin is a substance produced by Clostridium Botulinum and is responsible for human botulism. This substance is a poison, a neurotoxin, but used in limited quantities it can be a cure for some diseases. It is well connected to a large variety of medical applications. The mechanism of action relies on blocking the acetylcholine at the neuromuscular junction, which blocks the transmission of the nervous impulse with secondary flaccid paralysis. In urology, its role in idiopathic overactive bladder and neurogenic bladder is well known. We performed a thorough review using PubMed and other databases, revising the mechanisms of botulinum toxin action in urologic pathology, treatment procedures and other options. Botulinum toxin is a well‑studied substance with a large number of applications in medicine. In urologic pathology, overactive bladder and neurogenic bladder are backed by robust studies that support the therapeutic role of this substance. The toxin has multiple effects, such as inhibition of the nerve growth factor, blocking the bladder sensory afferent pathway and apoptotic effect on the prostate tissue, by inhibiting the substance P, altering the nociceptive pathways. Interstitial cystitis and other rare pathologies show promising results, but further studies are needed. The role of botulinum toxin in benign prostatic hyperplasia is still not elucidated.