The Role of Oxidative Stress Enhanced by Adiposity in Cardiometabolic Diseases.

Cardiometabolic diseases (CMDs), including cardiovascular disease (CVD), metabolic syndrome (MetS), and type 2 diabetes (T2D), are associated with increased morbidity and mortality. The growing prevalence of CVD is mostly attributed to the aging population and common occurrence of risk factors, such as high systolic blood pressure, elevated plasma glucose, and increased body mass index, which led to a global epidemic of obesity, MetS, and T2D. Oxidant-antioxidant balance disorders largely contribute to the pathogenesis and outcomes of CMDs, such as systemic essential hypertension, coronary artery disease, stroke, and MetS. Enhanced and disturbed generation of reactive oxygen species in excess adipose tissue during obesity may lead to increased oxidative stress. Understanding the interplay between adiposity, oxidative stress, and cardiometabolic risks can have translational impacts, leading to the identification of novel effective strategies for reducing the CMDs burden. The present review article is based on extant results from basic and clinical studies and specifically addresses the various aspects associated with oxidant-antioxidant balance disorders in the course of CMDs in subjects with excess adipose tissue accumulation. We aim at giving a comprehensive overview of existing knowledge, knowledge gaps, and future perspectives for further basic and clinical research. We provide insights into both the mechanisms and clinical implications of effects related to the interplay between adiposity and oxidative stress for treating and preventing CMDs. Future basic research and clinical trials are needed to further examine the mechanisms of adiposity-enhanced oxidative stress in CMDs and the efficacy of antioxidant therapies for reducing risk and improving outcome of patients with CMDs.

The Role of Selected Trace Elements in Oxidoreductive Homeostasis in Patients with Thyroid Diseases.

Impaired levels of selenium (Se), zinc (Zn), copper (Cu), iron (Fe), manganese (Mn) and iodine (I) in the organism may adversely affect the thyroid endocrine system. These trace elements play a role in the fight against oxidative stress as components of enzymes. Oxidative-antioxidant imbalance is considered a possible factor in many pathological conditions, including various thyroid diseases. In the available literature, there are few scientific studies showing a direct correlation of the effect of supplementation of trace elements on slowing down or preventing the occurrence of thyroid diseases in combination with the improvement of the antioxidant profile, or through the action of these elements as antioxidants. Among the available studies, it has been shown that an increase in lipid peroxidation levels and a decrease in the overall antioxidant defense status occur during such thyroid diseases as thyroid cancer, Hashimoto's thyroiditis and dysthyroidism. In studies in which trace elements were supplemented, the following were observed: a decrease in the level of malondialdehyde after supplementation with Zn during hypothyroidism and reduction in the malondialdehyde level after Se supplementation with a simultaneous increase in the total activity status and activity of antioxidant defense enzymes in the course of autoimmune thyroiditis. This systematic review aimed to present the current state of knowledge about the relationship between trace elements and thyroid diseases in terms of oxidoreductive homeostasis.

Genotype-phenotype correlation in two Polish neonates with alveolar capillary dysplasia.

BACKGROUND: Alveolar capillary dysplasia (ACD) is a rare cause of severe pulmonary hypertension and respiratory failure in neonates. The onset of ACD is usually preceded by a short asymptomatic period. The condition is refractory to all available therapies as it irreversibly affects development of the capillary bed in the lungs. The diagnosis of ACD is based on histopathological evaluation of lung biopsy or autopsy tissue or genetic testing of FOXF1 on chromosome 16q24.1. Here, we describe the first two Polish patients with ACD confirmed by histopathological and genetic examination. CASE PRESENTATION: The patients were term neonates with high Apgar scores in the first minutes of life. They both were diagnosed prenatally with heart defects. Additionally, the first patient presented with omphalocele. The neonate slightly deteriorated around 12th hour of life, but underwent surgical repair of omphalocele followed by mechanical ventilation. Due to further deterioration, therapy included inhaled nitric oxide (iNO), inotropes and surfactant administration. The second patient was treated with prostaglandin E1 since birth due to suspicion of aortic coarctation (CoA). After ruling out CoA in the 3rd day of life, infusion of prostaglandin E1 was discountinued and immediately patient's condition worsened. Subsequent treatment included re-administration of prostaglandin E1, iNO and mechanical ventilation. Both patients presented with transient improvement after application of iNO, but died despite maximized therapy. They were histopathologically diagnosed post-mortem with ACD. Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact. CONCLUSIONS: Both patients presented with a distinct course of ACD, extra-pulmonary manifestations and response to medications. Surgery and ceasing of prostaglandin E1 infusion should be considered as potential causes of this variability. We further highlight the necessity of thorough genetic testing and histopathological examination and propose immunostaining for CD31 and CD34 to facilitate the diagnostic process for better management of infants with ACD.

Surgical Wound Fluids from Patients with Breast Cancer Reveal Similarities in the Biological Response Induced by Intraoperative Radiation Therapy and the Radiation-Induced Bystander Effect-Transcriptomic Approach.

In patients with breast cancer who undergo breast-conserving surgery (BCS), more than 90% of local recurrences occur in the same quadrant as the primary cancer. Surgical wound fluids (SWF) are believed to play a role in this process by inducing an inflammatory process in the scar tissue area. Despite strong clinical data demonstrating the benefits of intraoperative radiotherapy (IORT), the biological basis underlying this process remains poorly understood. Ionizing radiation (IR) directly affects cells by damaging DNA, thereby altering the cell phenotype. IR directly affects cancer cells and also influences unirradiated cells located nearby, a phenomenon known as the radiation-induced bystander effect (RIBE), significantly modifying the tumor microenvironment. We hypothesized that SWF obtained from patients after BCS and IORT would induce a radiobiological response (due to RIBE) in unirradiated cells, thereby modifying their phenotype. To confirm this hypothesis, breast cancer cells were incubated with SWF collected from patients after BCS: (1) without IORT (wound fluid (WF) group), (2) with IORT (radiotherapy wound fluid (RT-WF) group), and (3) WF with conditioned medium from irradiated cells (WF+RIBE group) and then subjected to microarray analysis. We performed gene set enrichment analysis to determine the biological processes present in these cells. This analysis showed that the RT-WF and WF+RIBE groups shared common biological processes, including the enhancement of processes involved in cell-cycle regulation, DNA repair, and oxidative phosphorylation. The WF group was characterized by overrepresentation of pathways involved in the INF-α and INF-γ response, inflammatory response, and the IL6 JAK/STAT3 signaling pathway. These findings show that MDA-MB-468 cells stimulated with surgical wound fluids obtained from patients who underwent BCS plus IORT and from cells stimulated with SWF plus RIBE share common biological processes. This confirms the role of the radiation-induced bystander effect in altering the biological properties of wound fluids.

Cutting Edge: Lymphotoxin Signaling Is Essential for Clearance of Salmonella from the Gut Lumen and Generation of Anti-Salmonella Protective Immunity.

The immunological components that control resolution of Salmonella infection and successful vaccination are poorly defined. In a model of chronic gastrointestinal infection, we observed that the lymphotoxin (LT) pathway is essential for the clearance and resolution of primary infection of attenuated Salmonella enterica Typhimurium strain SL3261 ΔaroA Using gnotobiotic mice, we show that LTß receptor (LTßR) signaling and the microbiota are required to promote clearance of attenuated S. enterica Typhimurium from the gut lumen. We also found that LTßR signaling was required for successful immunization and subsequent protection upon challenge with a virulent strain of S enterica Typhimurium. LTßR signaling promoted the development of specific IgG recognizing S enterica Typhimurium during infection, as well as Ag-driven IFN-γ responses. B cell- and type 3 innate lymphoid cell-derived LT signaling, but not T cell-derived LT, contributes to anti-S enterica Typhimurium protective responses. Collectively, our results suggest that LT signaling is essential for multiple steps of anti-S enterica Typhimurium immune responses.

MicroRNA Profiling During Neural Differentiation of Induced Pluripotent Stem Cells.

MicroRNAs (miRNA) play an essential role in the regulation of gene expression and influence signaling networks responsible for several cellular processes like differentiation of pluripotent stem cells. Despite several studies on the neurogenesis process, no global analysis of microRNA expression during differentiation of induced pluripotent stem cells (iPSC) to neuronal stem cells (NSC) has been done. Therefore, we compared the profile of microRNA expression in iPSC lines and in NSC lines derived from them, using microarray-based analysis. Two different protocols for NSC formation were used: Direct and two-step via neural rosette formation. We confirmed the new associations of previously described miRNAs in regulation of NSC differentiation from iPSC. We discovered upregulation of miR-10 family, miR-30 family and miR-9 family and downregulation of miR-302 and miR-515 family expression. Moreover, we showed that miR-10 family play a crucial role in the negative regulation of genes expression belonging to signaling pathways involved in neural differentiation: WNT signaling pathway, focal adhesion, and signaling pathways regulating pluripotency of stem cells.

Chondrogenic Differentiation of Pluripotent Stem Cells under Controllable Serum-Free Conditions.

The repair of damaged articular cartilage using currently available implantation techniques is not sufficient for the full recovery of patients. Pluripotent stem cells (iPSC)-based therapies could bring new perspectives in the treatment of joint diseases. A number of protocols of in vitro differentiation of iPSC in chondrocytes for regenerative purposes have been recently described. However, in order to use these cells in clinics, the elimination of animal serum and feeder cells is essential. In our study, a strictly defined and controllable protocol was designed for the differentiation of pluripotent stem cells (BG01V, ND 41658*H, GPCCi001-A) in chondrocyte-like cells in serum- and a feeder cell-free system, using the embryoid bodies step. The extension of the protocol and culture conditions (monolayer versus 3D culture) was also tested after the initial 21 days of chondrogenic differentiation. Promotion of the chondrogenic differentiation in 3D culture via the elevated expression of genes related to chondrogenesis was achieved. Using immunofluorescence and immunohistochemistry staining techniques, the increased deposition of the specific extracellular matrix was indicated. As a result, chondrocyte-like cells in the early stages of their differentiation using pellet culture under fully controlled and defined conditions were obtained.

Expression of Pluripotency Genes in Chondrocyte-Like Cells Differentiated from Human Induced Pluripotent Stem Cells.

Human induced pluripotent stem cells (hiPSCs) constitute an important breakthrough in regenerative medicine, particularly in orthopedics, where more effective treatments are urgently needed. Despite the promise of hiPSCs only limited data on in vitro chondrogenic differentiation of hiPSCs are available. Therefore, we compared the gene expression profile of pluripotent genes in hiPSC-derived chondrocytes (ChiPS) to that of an hiPSC cell line created by our group (GPCCi001-A). The results are shown on heatmaps and plots and confirmed by Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) analysis. Unlike the ChiPS, our GPCCi001-A cells maintained their pluripotency state during long-term culture, thus demonstrating that this cell line was comprised of stable, fully pluripotent hiPSCs. Moreover, these chondrocyte-like cells not only presented features that are characteristic of chondrocytes, but they also lost their pluripotency, which is an important advantage in favor of using this cell line in future clinical studies.

[Consumption of polyunsaturated fatty acids by young hypertensive adults].

Background: A properly balanced diet is a key factor in preventing the development of diet-related diseases and may assist the pharmacological treatment of many conditions. Some studies indicate on relationship between consumption of polyunsaturated fatty acids (PUFA) and positive health outcomes. Aim: To evaluate sources in diet and frequency of consumption of PUFA by young adults suffering from arterial hypertension and to identify differences in PUFA and saturated fatty acids intake de-pending on gender, age, education, BMI, history of hypertension, BP values and the number of an-tihypertensive drugs used. Material and methods: The study group consisted of 100 hypertensive patients, 60 males and 40 females, aged 20 ­ 45 years (mean age 33.4±6.6 years), without concomitant diseases. Study tool constituted the self-reported questionnaire of food products intake, its frequency and intensity assessed during last one month period. The questionnaire involved 7 groups of typical food products, which were also divided into 2 baskets: "basket of 10 healthy" and "basket of 10 unhealthy" products. Results: Patients more often consumed products containing saturated fatty acids than PUFA. In the study group dairy products and meat dominated the diet, especially in hypertensive men. Olive oil was the most popular healthy product consumed by patients (42% of responders). People living in the city ate more often fish and plant products than those from rural areas, but overall fish consump-tion was low ­ only 6 to 12% of patients consumed omega-3 rich fish at least once a week. Regard-less of gender, place of living, education and other clinical factors our hypertensive patients choose more products from the "unhealthy" than "healthy" basket in the last month. Conclusion: Young people suffering from hypertension are characterized by unfavorable eating habits, especially low frequency of PUFA containing products consumption. Intensive educational programs to increase knowledge of young hypertensives about diet beneficial for health are still required.

Molecular mechanisms of induced pluripotency.

Growing knowledge concerning transcriptional control of cellular pluripotency has led to the discovery that the fate of differentiated cells can be reversed, which has resulted in the generation, by means of genetic manipulation, of induced pluripotent stem cells. Overexpression of just four pluripotency-related transcription factors, namely Oct3/4, Sox2, Klf4, and c-Myc (Yamanaka factors, OKSM), in fibroblasts appears sufficient to produce this new cell type. Currently, we know that these factors induce several changes in genetic program of differentiated cells that can be divided in two general phases: the initial one is stochastic, and the subsequent one is highly hierarchical and organised. This review briefly discusses the molecular events leading to induction of pluripotency in response to forced presence of OKSM factors in somatic cells. We also discuss other reprogramming strategies used thus far as well as the advantages and disadvantages of laboratory approaches towards pluripotency induction in different cell types.

Protocol to generate scaffold-free, multicomponent 3D melanoma spheroid models for preclinical drug testing.

Three-dimensional (3D) models play an increasingly important role in preclinical drug testing as they faithfully mimic interactions between cancer cells and the tumor microenvironment (TME). Here, we present a protocol for generating scaffold-free 3D multicomponent human melanoma spheroids. We describe steps for characterizing models using live-cell imaging and histology, followed by drug testing and assessment of cell death through various techniques such as imaging, luminescence-based assays, and flow cytometry. Finally, we demonstrate the models' adaptability for co-cultures with immune cells.

Exploring the Link between Inflammatory Biomarkers and Head and Neck Cancer: Understanding the Impact of Smoking as a Cancer-Predisposing Factor.

Head and neck cancer (HNC) is associated with significant morbidity globally, with smoking recognized as a key risk factor. This study investigates the interplay between smoking and inflammatory biomarkers in HNC development. The study involved 50 HNC patients, divided into smoking and non-smoking groups, and a control group of 30 healthy individuals. Serum levels of 48 cytokines, chemokines, growth factors, and other inflammatory markers were meticulously assessed. Significant differences in the levels of an extensive panel of inflammatory markers were observed between the patient groups and healthy controls. Elevated macrophage colony-stimulating factor (M-CSF) in both HNC groups implicated increased activity in pathways known for immunomodulation, proliferation, and angiogenesis during HNC cancerogenesis. In contrast, non-smokers with HNC demonstrated higher levels of interleukin 10 (IL-10) and interleukin 15 (IL-15), suggesting a more robust immune response. Platelet-derived growth factor BB (PDGF-BB) levels were particularly high in smokers with HNC. Smoking seems to alter the levels of crucial biomarkers in HNC, potentially affecting disease progression and responses to treatment. The data indicate that smokers may experience a more aggressive cancer phenotype, while non-smokers maintain a profile suggestive of a more active and effective immune response against HNC.

Feasibility and Cardiometabolic Effects of Time-Restricted Eating in Patients with Metabolic Syndrome.

Metabolic syndrome (MetS) and a prolonged daily eating window (EW) are associated with circadian rhythm disruption and increased cardiometabolic risk. Misalignment between circadian timing system and daily rhythms of food intake adversely impacts metabolic regulatory mechanisms and cardiovascular function. Restricting the daily EW by imposing an eating-fasting cycle through time-restricted eating (TRE) can restore robust circadian rhythms, support cellular metabolism, and improve cardiometabolic health. The aim of this study was to assess a feasibility of 12-week TRE intervention with self-selected 10 h EW and effects of TRE on EW duration, cardiometabolic outcomes, daily rhythms of behavior, and wellbeing in Polish patients with MetS and EW ≥ 14 h/day. Dietary intake was monitored with a validated myCircadianClock application (mCC app). Adherence to TRE defined as the proportion of days recorded with mCC app in which participants satisfied 10-h TRE was the primary outcome. A total of 26 patients (aged 45 ± 13 years, 62% women, 3.3 ± 0.5 MetS criteria, EW 14 ± 1.5 h/day) were enrolled. Coexistence of increased waist circumference (WC) (96% of patients), elevated fasting plasma glucose (FPG) (77%), and elevated blood pressure (BP) (69%) was the most common MetS pattern (50%). TRE intervention (mean duration of 81.6 ± 12.6 days) led to reducing daily EW by 28% (p < 0.0001). Adherence to TRE was 87 ± 13%. Adherence to logging food intake on mCC app during TRE was 70 ± 27%. Post TRE, a decrease in body weight (2%, 1.7 ± 3.6 kg, p = 0.026), body mass index (BMI) (1%, 0.5 ± 1.2 kg/m2, p = 0.027), WC (2%, 2.5 ± 3.9 cm, p = 0.003), systolic BP (4%, 4.8 ± 9.0 mmHg, p = 0.012), FPG (4%, 3.8 ± 6.9 mg/dL, p = 0.037), glycated hemoglobin (4%, 0.2 ± 0.4%, p = 0.011), mean fasting glucose level from continuous glucose monitor (CGM) (4%, 4.0 ± 6.1 mg/dL, p = 0.002), and sleepiness score (25%, 1.9 ± 3.2 points, p = 0043) were observed. A significant decrease in body weight (2%), BMI (2%), WC (3%), mean CGM fasting glucose (6%), sleepiness score (27%), and depression score (60%) was found in patients with mean post-TRE EW ≤ 10 h/day (58% of total), and not in patients with EW > 10 h/day. Adherence to TRE was higher in patients with post-TRE EW ≤ 10 h/day vs. patients with EW > 10 h/day (94 ± 6% vs. 77 ± 14%, p = 0.003). Our findings indicate that 10-h TRE was feasible in the European MetS population. TRE resulted in reducing daily EW and improved cardiometabolic outcomes and wellbeing in patients with MetS and prolonged EW. Use of the mCC app can aid in implementing TRE. This pilot clinical trial provides exploratory data that are a basis for a large-scale randomized controlled trial to determine the efficacy and sustainability of TRE for reducing cardiometabolic risks in MetS populations. Further research is needed to investigate the mechanisms of TRE effects, including its impact on circadian rhythm disruption.

[The evaluation of lipolytic activity of strains of Enterococcus faecium]. / Ocena aktywnosci lipolitycznej szczepów Enterococcus faecium.

INTRODUCTION: Little is known about the involvement of hydrolytic enzymes such as lipases as virulence factors in infections involving Enterococcus spp. METHODS: A total of 45 isolates of E. faecium were investigated. Lipolytic activity of enterococcal strains was determined by Tryptic Soy Agar containing Tween 20, Tween 40, Tween 60, Tween 80 and egg yolk. RESULTS: We detected that E. fecium strains produced lipases more frequently on Tween 20 agar (71.1% strains) than on Tween 40 agar, Tween 60 agar, Tween 80 agar, egg yolk agar (respectively 33.3%, 24.4%, 20.0%, 31.1%). Our results indicate that lipase may be a virulence factor in E. faecium. CONCLUSIONS: Studies suggest that source of isolation from clinical materials (blood, wound and fluid from the abdominal cavity) does not have an influence on the ability hydrolysis esters.

The Role of Glutathione in Selected Viral Diseases.

During inflammatory processes, immunocompetent cells are exposed to substantial amounts of free radicals and toxic compounds. Glutathione is a cysteine-containing tripeptide that is an important and ubiquitous antioxidant molecule produced in human organs. The intracellular content of GSH regulates the detoxifying capacity of cells, as well as the inflammatory and immune response. GSH is particularly important in the liver, where it serves as the major non-protein thiol involved in cellular antioxidant defense. There are numerous causes of hepatitis. The inflammation of the liver can be caused by a variety of infectious viruses. The relationship between oxidative stress and the hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis E virus (HEV) infection is not fully known. The aim of this study was to examine the relationship between hepatotropic viruses and glutathione status, including reduced glutathione (GSH) and oxidized glutathione (GSSG), as well as antioxidant enzymes, e.g., glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) in liver diseases.

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection.

Ferroptosis is a recently discovered form of programmed cell death. It is characterized by the accumulation of iron and lipid hydroperoxides in cells. Vitamin K is known to have antioxidant properties and plays a role in reducing oxidative stress, particularly in lipid cell membranes. Vitamin K reduces the level of reactive oxygen species by modulating the expression of antioxidant enzymes. Additionally, vitamin K decreases inflammation and potentially prevents ferroptosis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leading to coronavirus disease 2019 (COVID-19) is associated with oxidant-antioxidant imbalance. Studies have shown that intensified ferroptosis occurs in various tissues and cells affected by COVID-19. Vitamin K supplementation during SARS-CoV-2 infection may have a positive effect on reducing the severity of the disease. Preliminary research suggests that vitamin K may reduce lipid peroxidation and inhibit ferroptosis, potentially contributing to its therapeutic effects in COVID-19 patients. The links between ferroptosis, vitamin K, and SARS-CoV-2 infection require further investigation, particularly in the context of developing potential treatment strategies for COVID-19.

Single-cell transcriptomics of NRAS-mutated melanoma transitioning to drug resistance reveals P2RX7 as an indicator of early drug response.

Treatment options for patients with NRAS-mutant melanoma are limited and lack an efficient targeted drug combination that significantly increases overall and progression-free survival. In addition, targeted therapy success is hampered by the inevitable emergence of drug resistance. A thorough understanding of the molecular processes driving cancer cells' escape mechanisms is crucial to tailor more efficient follow-up therapies. We performed single-cell RNA sequencing of NRAS-mutant melanoma treated with MEK1/2 plus CDK4/6 inhibitors to decipher transcriptional transitions during the development of drug resistance. Cell lines resuming full proliferation (FACs [fast-adapting cells]) and cells that became senescent (SACs [slow-adapting cells]) over prolonged treatment were identified. The early drug response was characterized by transitional states involving increased ion signaling, driven by upregulation of the ATP-gated ion channel P2RX7. P2RX7 activation was associated with improved therapy responses and, in combination with targeted drugs, could contribute to the delayed onset of acquired resistance in NRAS-mutant melanoma.

An evaluation of oligonucleotide-based therapeutic strategies for polyQ diseases.

BACKGROUND: RNA interference (RNAi) and antisense strategies provide experimental therapeutic agents for numerous diseases, including polyglutamine (polyQ) disorders caused by CAG repeat expansion. We compared the potential of different oligonucleotide-based strategies for silencing the genes responsible for several polyQ diseases, including Huntington's disease and two spinocerebellar ataxias, type 1 and type 3. The strategies included nonallele-selective gene silencing, gene replacement, allele-selective SNP targeting and CAG repeat targeting. RESULTS: Using the patient-derived cell culture models of polyQ diseases, we tested various siRNAs, and antisense reagents and assessed their silencing efficiency and allele selectivity. We showed considerable allele discrimination by several SNP targeting siRNAs based on a weak G-G or G-U pairing with normal allele and strong G-C pairing with mutant allele at the site of RISC-induced cleavage. Among the CAG repeat targeting reagents the strongest allele discrimination is achieved by miRNA-like functioning reagents that bind to their targets and inhibit their translation without substantial target cleavage. Also, morpholino analog performs well in mutant and normal allele discrimination but its efficient delivery to cells at low effective concentration still remains a challenge. CONCLUSIONS: Using three cellular models of polyQ diseases and the same experimental setup we directly compared the performance of different oligonucleotide-based treatment strategies that are currently under development. Based on the results obtained by us and others we discussed the advantages and drawbacks of these strategies considering them from several different perspectives. The strategy aimed at nonallele-selective inhibiting of causative gene expression by targeting specific sequence of the implicated gene is the easiest to implement but relevant benefits are still uncertain. The gene replacement strategy that combines the nonallele-selective gene silencing with the expression of the exogenous normal allele is a logical extension of the former and it deserves to be explored further. Both allele-selective RNAi approaches challenge cellular RNA interference machinery to show its ability to discriminate between similar sequences differing in either single base substitutions or repeated sequence length. Although both approaches perform well in allele discrimination most of our efforts are focused on repeat targeting due to its potentially higher universality.

[Occurrence and antimicrobial susceptibility of Morganella morganii strains isolated from clinical samples]. / Wystepowanie oraz lekowrazliwosc szczepów Morganella morganiiizolowanych z materialu klinicznego.

The aim of this study was the evaluation of occurrence and antimicrobial susceptibility of M morganii rods isolated from clinical samples. This study included 201 strains isolated in the Clinical Microbiology Department of Dr. A. Jurasz University Hospital in 2008-2010. Identification to species was carried out on the basis of the results of biochemical reactions included in the tests ID 32E and VITEK2 GN. Antimicrobial susceptibility of M. morganii rods was determined by the disk-diffusion method on Mueller-Hinton II Agar. Strains of M morganii most commonly isolated from skin and soft tissue, and material taken from the urinary tract, mainly from patients of Anesthesiology and Intensive Care Unit, Department of General and Vascular Surgery and Department of General Surgery and Endocrinology. All of M morganii strains isolated during the three years were susceptible to carbapenems. We reported decrease of strains susceptible to piperacillin and chloramphenicol. In 2010 we showed a higher percentage of strains intermediate to tigecycline, compared with 2009. We observed increase in the percentage of strains resistant to cefoperazone with sulbactam and reported decrease in the percentage of strains resistant and intermediate to aminoglycosides. Extended Spectrum Beta-Lactamases were produced by 13 (6,5%) of M morganii strains.