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The intestinal microbiota refers to the collection of microorganisms that exist in the human gut. It has been said that bacteria influence the development of metabolic diseases, such as diabetes mellitus, as they have roles in immunomodulation, protection against pathogens, blood vessel growth, repairing the intestinal wall, and the development of the neurological system. In this review, we look at the latest research regarding interactions between gut microbiota and oral antihyperglycemic drugs and we present data suggesting that the microbiome may help counteract the reduced glucose tolerance and insulin resistance associated with metabolic disorders. We found that antidiabetic drugs can have significant impacts on gut microbiota composition and function, potentially influencing both the efficacy and side effects of these medications. Additionally, we discovered that microbial-based therapeutics, including probiotics, prebiotics, and postbiotics, and fecal microbiota can be considered when discussing preventive measures and personalized treatment options for type 2 diabetes mellitus. Understanding how antidiabetic drugs modulate gut microbiota composition and function is essential for optimizing their therapeutic efficacy and minimizing potential adverse effects. The relationship between the gut microbiota and glycemic agents, not fully understood, is currently the subject of increasing research and discussion. It has been proven that the microbiome can impact the effectiveness of the medications, but further research in this field may uncover novel therapeutic strategies for diabetes and other metabolic disorders by targeting the gut microbiota. [ABSTRACT FROM AUTHOR]

Recent epidemiologic studies carried out in Romania confirmed an ascending trend for cardiovascular disease (CVD) risk factor prevalence such as diabetes mellitus (DM), obesity and dyslipidemia. The aim of this study is to describe the CVD risk factor profile and preventative behavior in a representative sample of the general adult population of an Eastern Romanian urban area. More than 70% of the studied population had a body mass index (BMI) above the normal range for their age, with 36.7% of the subjects residing in obesity and severe obesity clusters. For overweight and obese subjects, the number of comorbidities (CVD, arterial hypertension and DM type 2) was higher than in the population with normal weight (44% vs. 31%, 22% vs. 14% and 18% vs. 10%, respectively). The prevalence of high blood pressure was almost double that reported in previous Romanian studies (69.3% vs. 36.6%) and higher than expected, based on self-reported known CVD diagnoses (37.5%). There was a visible difference between the results obtained for quantifiable CVD risk factors and self-reported lifestyle ones. Routine blood test monitoring may be an easy and inexpensive tool to guide educational and medical interventions to address modifiable CV risk factors in the adult population in order to prevent the fatal consequences of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Cervical cancer (CC) is the fourth most common cause of cancer‐related deaths amongst women worldwide. CC represents a major global healthcare issue, and Romania ranks the worst in mortality rates amongst EU countries. However, the early detection of CC can be lifesaving. To understand the testing process undergone by women in Romania, we performed a retrospective study, and investigated a cohort of 83 785 cervical cases from Romanian women aged 15−70, obtained in private‐based opportunistic screening. We examined the correlation between Pap smear results, human papilloma virus (HPV) genotyping, and the expression of cell cycle markers p16 and Ki‐67. Analysis of Pap results revealed approximately 10% abnormal cases, of which high‐grade squamous intraepithelial lesions constituted 4.9%. HPV genotyping of 12 185 cases with available Pap results unveiled a range of high‐risk HPV (hrHPV) types associated with cervical abnormalities. Notably, 26% of hrHPV‐positive cases showed no observable abnormalities. In a subset of cases with abnormal Pap and a type of hrHPV, P16/Ki‐67 double‐staining was also positive. This study suggests the importance of an integrated diagnostic algorithm that should consider the HPV genotype, Pap smear, and p16/Ki‐67 staining. This algorithm should enhance the CC screening accuracy and its management strategies, particularly in those regions with a high disease burden, such as Romania. [ABSTRACT FROM AUTHOR]

Objectives. Muscle contusion is the most common form of muscle injury and the muscle endogenous regenerative capacity can compensate for non-extensive damage. However, severe traumatic injuries may overcome this capacity. More effective therapeutic strategies are still needed, so the exploration of the molecular context during muscle regeneration might provide new insights. Materials and methods. We investigated the expression pattern of a reputed angiogenic molecule, CD105/endoglin, by measuring the tissue and serum concentration by multiplex assay in normal and Dmdmdx dystrophic mice by following the distribution of the cellular sources by immunofluorescence in a mouse model of acute muscle contusion. Results. Maximal tissue concentration in normal animals was obtained 48h post-injury, and then started to decline, with only one other significantly increased value 5 days after injury. In dystrophic mice, tissue levels were globally much higher than in normal animals and started rising 1h post-injury and were maintained elevated all along the regeneration process. In situ immunolabelling highlighted the increased positive population mostly in the inflammatory areas. Double staining separates distinct subsets based on hematopoietic marker CD45 and the endothelial marker CD31 co-expression in endoglin positive cells. Conclusions. This study offers a timeline of endoglin expression during normal and pathologic muscle regeneration, providing evidence that the major wave corresponds to the inflammatory stage of muscle regeneration, deriving from multiple cellular sources such as endothelial cells, blood cells and also other interstitial cells that become activated during this process. [ABSTRACT FROM AUTHOR]

Introduction. Since the beginning of the 1990s, with the discovery of the first “cancer genes”, numerous genetic factors have been identified through a great number of studies to be associated with the susceptibility for hereditary cancers. Hundreds of genes have been detected, with thousands of variants involved in the development of the disease. Next Generation Sequencing (NGS) technology has been the most important tool in cancer research and cancer diagnosis as well, during the past decades. Most of the laboratories worldwide use multigene NGS panels to identify the genetic causes or the genetic predisposition for cancer. Materials and method. NGS sequencing on an Illumina platform has been performed using multigene panels for the different types of cancer. The study included individuals tested during February-September 2021. Results. Apart from the BRCA1 and BRCA2 genes mutations, identified in the greater majority of cases, pathogenic variants in other genes, such as PALB2, CHEK2, MSH6, MLH1, ATM, NF1 etc., have been detected. The most frequent pathology identified in our cohort was breast cancer, followed by colorectal and ovarian cancers. Other types of cancer reported in these individuals were melanoma, cerebral tumors, pancreatic cancer, endocrine tumors, renal cancer, gastrointestinal tumors and prostate cancer. Conclusions. NGS panels are the test of choice for the diagnosis of the disease in hereditary cancer patients and for identifying the risk for developing the disease in healthy individuals. Both pre-testing and post-testing genetic counseling are of great importance for the selection of patients for genetic testing and for choosing the most eloquent genetic test for each individual in particular, and also for the clinical interpretation of the results, which in many cases may raise numerous problems and discussions. [ABSTRACT FROM AUTHOR]

Background: Psoriasis vulgaris is a chronic inflammatory hyper-proliferative disease of the skin, scalp, nails, and joints. It has been hypothesized that prolactin (PRL) may modulate the skin immune system and be involved in the pathogenesis of psoriasis. Psoriasis exerts significant, negative impact on patients' quality of life. Relatively high rates of depression are reported in patients with psoriasis. Objectives: The aim of this work was to study the possible role of PRL in the pathogenesis of psoriasis and its correlation with the disease activity, clinically, molecular and emotional status of patients. Subjects and methods: A total of 41 samples were analyzed - 21 new patients with psoriasis vulgaris before treatment and 20 after therapy - were included in this study. In all patients, we determined skin disease activity according to the PASI index, the psychological impact measured with HAMA and HAMD scales and the quality of their life measured by DLQI. The concentration of prolactin in the serum was measured by enzyme-linked immunosorbent assay (ELISA), and the concentration of soluble receptor of IL-2 was measured with automated immune chemiluminescent system - IMMULITE procedure. Results: The PRL and sIL2R serum levels were significantly decreased after three months of therapy, at least 50% with a p value <0.00001. Clinical, hormonal, molecular correlations between before and after therapy were measured with a statistically significant result. Correlations between HAMA-PRL and DLQI-PRL before therapy were not statistically significant, only the relationship between HAMD and PRL was demonstrated. After treatment, we obtained a significant clinical, psychological and paraclinical (especially serum levels of prolactin and sIL2R) decreased and relevant response on all the patients treated and analyzed. Conclusion: Prolactin seems to have a role in the pathogenesis of psoriasis and may represent a cause and/or a consequence of psoriasis pathology. The most likely scenario is that PRL enhances interferon-induced chemokine production in keratinocytes, thereby facilitating cutaneous T-cell infiltration. This raises the intriguing light that PRL may offer a novel future therapeutic target in psoriasis and other skin diseases that worsen in response to psychological distress. [ABSTRACT FROM AUTHOR]

Introduction: The polypeptide hormone prolactin (PRL) represents the pituitary modulator of lactation and reproduction. Currently, we discuss the wide range of PRL actions "beyond the mammary horizon". Multiple studies had showed the role of PRL as a cytokine, with comparable structural motifs, similar receptor structures and signal transduction pathways. Almost two decades ago it was fi rst hypothesized that PRL acts as a neuroendocrine modulator of both skin epithelial growth and the skin immune system. Moreover, it was described the PRL circuit between the skin and the central nervous system. Psoriasis vulgaris, an immunologically mediated skin disease, is a common disorder, having as main pathogenetic mechanisms the chronic infl ammation and keratinocytes hyperproliferation. Psoriasis vulgaris is not a life threatening disease, but aff ects seriously the quality of life; there is still no causative treatment., Methods: After we describe the essentials of general PRL biology, the almost ubiquitous distribution of its receptors and the vast list of extrapituitary PRL-expressing tissues, our aim is to summarize clinical observations that provide insights into how PRL may impact on the psoriatic skin and defi ne research for be% er characterize the complex role of PRL in human skin biology and pathology., Results: Focusing on psoriasis, as a stress-related disease, we then discuss the possible role of PRL/ PRLR in its pathology and may identify one potential biological marker and therapeutic targets for the management of this autoimmune skin disorder., Conclusion: This theory/concept can now be integrated into current views on the multilevel neuroendocrine- immune communication along the brain-skin axis in health and disease. Due to the pathogenic complexity, there is no curative treatment for psoriasis and pharmacological modulation of PRL may represent a future target to restrict the lesions in psoriatic patients.