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INTRODUCTION AND PURPOSE Physical activity during pregnancy has numerous health benefits, including reducing the risk of excessive gestational weight gain, gestational diabetes, preeclampsia, and preterm birth. Quality of life (QOL) often decreases during pregnancy which may be linked to reduced physical activity (PA). This article emphasizes the importance of exercise during pregnancy and postpartum. METHODS An extensive examination of articles published in scientific journals was carried out through online research platforms PubMed and Google Scholar. We searched articles by entering keywords in appropriate configuration: “physical activity”, “pregnancy”, “pregnant exercises”, “pregnant woman”, “quality of life”, “QOL”. DESCRIPTIONS OF THE STATE OF KNOWLEDGE AND RECOMMENDATIONS Gestational overweight and obesity are linked to negative outcomes for both mother and child. Additionally, physical activity plays a vital role in reducing postpartum depressive disorders and managing conditions such as gestational diabetes and hypertensive disorders. WHO recommends to get at least 150 minutes of moderate-intensity aerobic activity per week during pregnancy and the postpartum period. The American College of Obstetricians and Gynecologists (ACOG) similarly advises engaging in a minimum of 150 minutes of moderate-intensity aerobic activity, like brisk walking, each week during and after pregnancy. SUMMARY Physical activity can play a crucial role in preventing depressive disorders in women during the postpartum period. A systematic review and meta-analysis conducted in 2017 revealed that women who engaged in aerobic exercise for 30 to 60 minutes, 2 to 7 times a week, had a significantly lower risk of gestational hypertensive disorders, gestational hypertension, and cesarean delivery compared to those who were more sedentary.

The result of a kidney transplantation may be affected by certain congenital or acquired urological diseases that need to be addressed before, during or after the kidney transplant. Complications accompanying kidney transplantation are not fundamentally different from the events that accompany other difficult surgical procedures. However, their course is usually modified by adverse circumstances in the recipient - uremia, dialysis treatment, immunosuppression. The incidence of urological complications is reported in the range of 1 to 30 % of the transplants, and they represent up to one half of all surgical complications. They can cause a significant morbidity and mortality and can lead to a delayed onset of the function and even to a loss of the transplanted kidney. Urological complications that need to be addressed before kidney transplantation include anomalies or pathological changes in the lower urinary tract, pelvic involvement in atherosclerosis or previous kidney transplants, infectious foci in lithiasis or pyonephrosis, large polycystic kidneys and malignancies. During the kidney transplantation itself, vascular complications, and complications connected with the reconstruction of the lower urinary tract can occur. Other complications are bacterial and viral infections and malignancies. All these complications require a rapid and accurate diagnosis and subsequent targeted treatment with intention to maintain a functional kidney transplant. [ABSTRACT FROM AUTHOR]

(1) Background: Compared to medical personnel, SARS-CoV-2mRNA vaccination-related positive immunity rates, levels, and preservation over time in dialysis and kidney transplant patients are reduced. We hypothesized that COVID-19 pre-exposure influences both vaccination-dependent immunity development and preservation in a group-dependent manner. (2) Methods: We evaluated 2- and 9-month follow-up data in our observational Dia-Vacc study, exploring specific cellular (interferon-γ release assay = IGRA) and/or humoral immune responses (IgA/IgG/RBD antibodies) after two SARS-CoV-2mRNA vaccinations in 2630 participants, including medical personnel (301-MP), dialysis patients (1841-DP), and kidney transplant recipients (488-KTR). Study participants were also separated into COVID-19 pre-exposure (hybrid immunity) positive (n = 407) versus negative (n = 2223) groups. (3) Results: COVID-19 pre-exposure improved most vaccination-related positive immunity rates in KTR and DP at 2 months but not in MP, where rates reached almost 100% independent of hybrid immunity. In the COVID-19-negative study, patients’ immunity faded between two and nine months, evaluated via the percentage of patients with an RBD antibody decrease >50%, and was markedly group- (MP-17.8%, DP-52.2%, and KTR-38.6%) and vaccine type-dependent. In contrast, in all patient groups with COVID-19, pre-exposure RBD antibody decreases of >50% were similarly rare (MP-4.3%, DP-7.2%, and KTR-0%) but still vaccine type-dependent, with numerically reduced numbers in mRNA-1273- versus BNT162b2mRNA-treated patients. Multivariable regression analysis of RBD antibody changes between two and nine months by interval scale categorization confirmed COVID-19 pre-exposure as a factor in inhibiting strong RBD Ab fading. COVID-19 pre-exposure in MP and DP also numerically reduced T-cell immunity fading. In DP, symptomatic (versus asymptomatic) COVID-19 pre-exposure was identified as a factor in reducing strong RBD Ab fading after vaccination. (4) Conclusions: After mRNA vaccination, immunity positivity rates in DP and KTR but not MP, as well as immunity preservation in MP/DP/KTR, are markedly improved via prior COVID-19 infection. In DP, prior symptomatic compared to asymptomatic COVID-19 disease was particularly effective in blocking immunity fading after mRNA vaccination.

Many common thermographic cameras have quite good sensitivity (0.05 °C or better) but limited accuracy, often about ±2 °C. This is not sufficient for quantitative measurements such as human body temperature diagnostics, where an accuracy of 0.3 °C is assumed. A thermographic device with a built-in active reference element for enhanced precision measurement was developed for these purposes. It was adapted for human body temperature diagnostics using face temperature measurements. It is based on a micro-bolometers detector and the reference element is heated to a temperature of 37 °C, which is mostly assumed as decisive for an increased temperature indication. As the reference element is embedded into the device housing, the use of the device can be very flexible. The performed human temperature measurement experiments showed that the accuracy of the introduced device is comparable with the thermographic measurements obtained using an external black body, which is often used for these applications.

IntroductionThe prognosis of glioblastoma remains unfavorable. TTFields utilize low intensity electric fields (frequency 150–300 kHz) that disrupt cellular processes critical for cancer cell viability and tumor progression. TTFields are delivered via transducer arrays placed on the patients’ scalp. Methods: Between the years 2004 and 2022, 55 patients (20 female), aged 21.9–77.8 years (mean age 47.3±11.8 years; median 47.6 years) were treated with TTFields for newly-diagnosed GBM, and compared to 54 control patients (20 females), aged 27.0–76.7 years (mean age 51.4±12.2 years; median 51.7 years) (p=0.08). All patients underwent gross total or partial resection of GBM. One patient had biopsy only. When available, MGMT promoter methylation status and IDH mutation was detected.ResultsPatients on TTFields therapy demonstrated improvements in PFS and OS relative to controls (hazard ratio: 0.64, p=0.031; and 0.61, p=0.028 respectively). TTFields average time on therapy was 74.8% (median 82%): median PFS of these patients was 19.75 months. Seven patients with TTFields usage ≤60% (23–60%, mean 46.3%, median 53%) had a median PFS of 7.95 months (p=0.0356). Control patients with no TTFields exposure had a median PFS of 12.45 months. Median OS of TTF patients was 31.67 months compared to 24.80 months for controls.DiscussionThis is the most extensive study on newly-diagnosed GBM patients treated with TTFields, covering a period of 18 years at a single center and presenting not only data from clinical trials but also a group of 36 patients treated with TTFields as a part of routine clinical practice.

The juxtaglomerular niche occupied by renin cells (RCN) plays an important role in glomerular repair but the precise temporal and spatial interrelations remain unclear. This study proposes the hypothesis of a local intra-extraglomerular regenerative feedback system and establishes a new quantifiable system for RCN responses in individual glomeruli in vivo. A strictly intraglomerular two-photon laser-induced injury model was established. Labeled renin cells (RC) in transgenic renin reporter mice were fate-traced in healthy and injured glomeruli over several days by intravital microscopy and quantified via new three-dimensional image processing algorithms based on ray tracing. RC in healthy glomeruli demonstrated dynamic extraglomerular protrusions. Upon intraglomerular injury the corresponding RCN first increased in volume and then increased in area of dynamic migration up to threefold compared to their RCN. RC started migration reaching the site of injury within 3 hours and acquired a mesangial cell phenotype without losing physical RCN-contact. During intraglomerular repair only the corresponding RCN responded via stimulated neogenesis, a process of de novo differentiation of RC to replenish the RCN. Repeated continuous intravital microscopy provides a state-of-the-art tool to prove and further study the local intraglomerular RCN repair feedback system in individual glomeruli in vivo in a quantifiable manner.

Background: Diabetic kidney disease is the leading cause of end-stage renal disease. Administration of ACE inhibitors or/and SGLT2 inhibitors show renoprotective effects in diabetic and other kidney diseases. The underlying renoprotective mechanisms of SGLT2 inhibition, especially in combination with ACE inhibition, are incompletely understood. We used longitudinal intravital microscopy to directly elucidate glomerular hemodynamics on a single nephron level in response to the ACE inhibitor enalapril or/and the SGLT2 inhibitor empagliflozin.Methods: Five weeks after the induction of diabetes by streptozotocin, male C57BL/6 mice were treated with enalapril, empagliflozin, enalapril/empagliflozin or placebo for 3 days. To identify hemodynamic regulation mechanisms, longitudinal intravital multiphoton microscopy was employed to measure single nephron glomerular filtration rate (snGFR) and afferent/efferent arteriole width.Results: Diabetic mice presented a significant hyperfiltration. Compared to placebo treatment, snGFR was reduced in response to enalapril, empagliflozin, or enalapril/empagliflozin administration under diabetic conditions. While enalapril treatment caused significant dilation of the efferent arteriole (12.55 ± 1.46 µm vs. control 11.92 ± 1.04 µm, p < 0.05), empagliflozin led to a decreased afferent arteriole diameter (11.19 ± 2.55 µm vs. control 12.35 ± 1.32 µm, p < 0.05) in diabetic mice. Unexpectedly under diabetic conditions, the combined treatment with enalapril/empagliflozin had no effects on both afferent and efferent arteriole diameter change.Conclusion: SGLT2 inhibition, besides ACE inhibition, is an essential hemodynamic regulator of glomerular filtration during diabetes mellitus. Nevertheless, additional mechanisms—independent from hemodynamic regulation—are involved in the nephroprotective effects especially of the combination therapy and should be further explored in future studies.

Despite disadvantages, such as high cost and their poor predictive value, animal experiments are still the state of the art for pharmaceutical substance testing. One reason for this problem is the inability of standard cell culture methods to emulate the physiological environment necessary to recapitulate in vivo processes. Microphysiological systems offer the opportunity to close this gap. In this study, we utilize a previously employed microphysiological system to examine the impact of pressure and flow on the transportation of substances mediated by multidrug resistance protein 1 (MDR1) across an artificial cell-based tubular barrier. By using a miniaturized fluorescence measurement device, we could continuously track the MDR1-mediated transport of rhodamine 123 above the artificial barrier over 48 h. We proved that applying pressure and flow affects both active and passive transport of rhodamine 123. Using experimental results and curve fittings, the kinetics of MDR1-mediated transport as well as passive transport were investigated; thus, a kinetic model that explains this transport above an artificial tubular barrier was identified. This kinetic model demonstrates that the simple Michaelis–Menten model is not an appropriate model to explain the MDR1-mediated transport; instead, Hill kinetics, with Hill slope of n = 2, is a better fit. The kinetic values, Km, Vmax, and apparent permeability (Papp), obtained in this study are comparable with other in vivo and in vitro studies. Finally, the presented proximal tubule-on-a-chip can be used for pharmaceutical substance testing and to investigate pharmacokinetics of the renal transporter MDR1.

Abstract It was evidenced that saturated fatty acids (FAs) have a detrimental effect on pancreatic β-cells function and survival, leading to endoplasmic reticulum (ER) calcium release, ER stress, and apoptosis. In the present study, we have tested the effect of three calcium influx inhibitors, i.e., diazoxide, nifedipine, and verapamil, on the apoptosis-inducing effect of saturated stearic acid (SA) in the human pancreatic β-cell lines NES2Y and 1.1B4. We have demonstrated that the application of all three calcium influx inhibitors tested has no inhibitory effect on SA-induced ER stress and apoptosis in both tested cell lines. Moreover, these inhibitors have pro-apoptotic potential per se at higher concentrations. Interestingly, these findings are in contradiction with those obtained with rodent cell lines and islets. Thus our data obtained with human β-cell lines suggest that the prospective usage of calcium channel blockers for prevention and therapy of type 2 diabetes mellitus, developed with the contribution of the saturated FA-induced apoptosis of β-cells, seems rather unlikely.

Background. Unlike leukoplakia, the smokers' lesion - a type of oral white lesion spontaneously regressing following cessation of smoking - is generally considered a non-serious condition and there is no recommendation for subsequent follow-up of such patients. Case report. Here, however, we present the case of a patient (female, 56, smoker) in whom we detected a smoker's lesion which regressed completely, without any signs of abnormality or malignity. The only shadow of a doubt that led us to inviting her for another examination was an additional examination using a VELscope® autofluorescence device that revealed autofluorescence suppression on the site of the former lesion. Another examination one month later revealed a patch of epithelium with a normal color but a negligibly different light reflection in the center of the former lesion; VELscope® indicated the questionable area to still be suspect. Following excision using margins indicated by VELscope® (+2-3 mm), histopathology revealed a squamous cell carcinoma. The secondary excision was carcinoma free and even after 5 years, the carcinoma has not recurred. Conclusion. We would like to point out that apparent spontaneous regressions of oral white lesions following smoking cessation still need attention and close follow-up to make sure that a developing squamous cell carcinoma cannot pass undetected.

Kidney transplant recipients (KTR) show significantly lower seroconversion rates after SARS-CoV-2 mRNA vaccination compared to dialysis patients (DP). Mycophenolate mofetil or mycophenolic acid (MMF/MPA) in particular has been identified as a risk factor for seroconversion failure. While the majority of all KTR worldwide receive MMF/MPA for immunosuppressive therapy, its impact on antibody decline in seroconverted KTR still remains unclear. In an observational study (NCT04799808), we investigated whether 132 seroconverted KTR (anti-spike S1 IgG or IgA positive after 2 vaccinations) show a more rapid antibody decline with MMF/MPA than those without this medication. A total of 2 months after mRNA vaccination, average anti-spike S1 IgG levels of KTR with MMF/MPA were lower than without (p = 0.001), while no differences between these two groups were observed after 6 months (p = 0.366). Similar results were obtained for anti-RBD IgG antibodies (T2 p = 0.003 and T3 p = 0.135). The probability of severe IgG decline with MMF/MPA was three times lower than without (p = 0.003, OR 0.236, 95% CI 0.091–0.609). In the multivariate analysis, neither immunosuppressants, such as calcineurin inhibitors, mTOR inhibitors (mTOR-I; mechanistic target of rapamycin), glucocorticoids, nor vaccine type, sex, or age showed a significant influence on IgG titer decline between 2 and 6 months. For the decision on additional booster vaccinations, we consider immunosurveillance to be needed as an integral part of renal transplant follow-up after SARS-CoV-2 mRNA vaccination. Not only the lack of seroconversion but also the peak and titer decline of the specific IgG and RBD IgG antibody formation after two mRNA vaccinations is significantly influenced by MMF/MPA.

Summary: Background: Vulnerable dialysis and kidney transplant patients show impaired seroconversion rates compared to medical personnel eight weeks after SARS-CoV-2mRNA vaccination. Methods: We evaluated six months follow up data in our observational Dia-Vacc study exploring specific cellular (interferon-γ release assay) or/and humoral immune responses after 2x SARS-CoV-2mRNA vaccination in 1205 participants including medical personnel (125 MP), dialysis patients (970 DP) and kidney transplant recipients (110 KTR) with seroconversion (de novo IgA or IgG antibody positivity by ELISA) after eight weeks. Findings: Six months after vaccination, seroconversion remained positive in 98% of MP, but 91%/87% of DP/KTR (p = 0·005), respectively. Receptor binding domain-IgG (RBD-IgG) antibodies were positive in 98% of MP, but only 68%/57% of DP/KTR (p

Plasmalemma vesicle-associated protein (PLVAP) is the main component of endothelial diaphragms in fenestrae, caveolae, and transendothelial channels. PLVAP is expressed in the adult kidney glomerulus upon injury. Glomerular endothelial injury is associated with progressive loss of kidney function in diabetic kidney disease (DKD). This study aimed to investigate whether PLVAP could serve as a marker for glomerular endothelial damage in DKD. Glomerular PLVAP expression was analyzed in different mouse models of DKD and their respective healthy control animals using automatic digital quantification of histological whole kidney sections. Transgenic mice expressing a dominant-negative GIP receptor (GIPRdn) in pancreatic beta-cells as a model for diabetes mellitus (DM) type 1 and black and tan brachyuric (BTBR) ob/ob mice, as a model for DM type 2, were used. Distinct PLVAP induction was observed in all diabetic models studied. Traces of glomerular PLVAP expression could be identified in the healthy control kidneys using automated quantification. Stainings for other endothelial injury markers such as CD31 or the erythroblast transformation-specific related gene (ERG) displayed no differences between diabetic and healthy groups at the time points when PLVAP was induced. The same was also true for the mesangial cells marker α8Integrin, while the podocyte marker nephrin appeared to be diminished only in BTBR ob/ob mice. Glomerular hypertrophy, which is one of the initial morphological signs of diabetic kidney damage, was observed in both diabetic models. These findings suggest that PLVAP is an early marker of glomerular endothelial injury in diabetes-induced kidney damage in mice.

Background: Intravital microscopy is an emerging technique in life science with applications in kidney research. Longitudinal observation of (patho-)physiological processes in living mice is possible in the smallest functional unit of the kidney, a single nephron (sn). In particular, effects on glomerular filtration rate (GFR) - a key parameter of renal function - can be assessed. Methods: After intravenous injection of a freely filtered, non-resorbable, fluorescent dye in C57BL/6 mice, a time series was captured by multiphoton microsopy. Filtration was observed from the glomerular capillaries to the proximal tubule (PT) and the tubular signal intensity shift was analyzed to calculate the snGFR. Results: Previously described methods for snGFR analysis relied on two manually defined measurement points in the PT and the tubular volume was merely estimated in 2D images. We present an extended image processing workflow by adding continuous measurement of intensity along the PT in every frame of the time series using ImageJ. Automatic modelling of actual PT volume in a 3D dataset replaced 2D volume estimation. Subsequent data analysis in R, with a calculation of intensity shifts in every frame and normalization against tubular volume, allowed exact assessment of snGFR by linear regression. Repeated analysis of image data obtained in healthy mice showed a striking increase of reproducibility by reduction of user interaction. Conclusions: These improvements in image processing and data analysis maximize the reliability of a sophisticated intravital microscopy technique for the precise assessment of snGFR, a highly relevant predictor of kidney function.

The article deals with the issue of electromagnetic disturbances caused by electromechanical relays. Electromagnetic compatibility (EMC) is important for the reliable work of electrical and electronic devices. Our research focused on the low-voltage relay, which is the source of electrical fast transients (EFT)/burst disturbances. The voltage and current waveforms were tested on the constructed stand while opening the relays’ contacts. We investigated one-circuit topology with varied element parameters in order to observe their influence on the burst phenomenon. The new technologies in the measurement equipment allow us to observe many detailed aspects of the burst phenomenon, which were not reported up to now. In order to analyze the disturbances, they have been fragmented into restoration, ignition and arc times. The number of disturbance cycles differs depending on the value of the circuit capacitance on the load side. The effect of capacity on times of restoration, ignition and burning arc was also observed. The division into cycles allowed us to observe changes in the studied phenomenon along with the increased distance between the relay contacts during its opening. There were also discrepancies between the presentation of the phenomenon in the standard defining the method of measuring the resistance to interference EFT/burst and the measurement results.

Newly constructed devices must meet a number of requirements in terms of the level of generated disturbances. To achieve an acceptable level in such devices, filters are installed—one of the cheapest ways to reduce interference in devices. One of the key elements of the filter that is responsible for the effectiveness of noise reduction are ferrites. Unfortunately, for various devices, an individual approach should be used in the selection of filters and, accordingly, ferrites. Due to the fact that ferrites from different manufacturers do not have standardized characteristics and information on their effectiveness, the selection of the right ferrite is a very time-consuming process. Therefore, this article will present the possibilities of quickly determining selected ferrite parameters in order to ensure the necessary level of noise reduction. For this purpose, assumptions from the CISPR 17 standard will be used. For selected types of ferrites, a large number of measurements were carried out in order to determine the optimal computational algorithm for adjusting ferrite characteristics to the designed conditions. The performance of these tests will be the basis for conducting tests on a larger number of ferrites, as well as for the development of possible standardization procedures.

The paper is a continuation of the research works of the authors. The aim of it is identifying the electromagnetic environment in which the control equipment of the short-circuit test stand operates. Exceptional attention was devoted to the issues related to the operation of the time-phase controller system. Measurements and identification of the electromagnetic environment were carried out on a specific short-circuit test stand, where short-circuit currents are generated by the medium-voltage (MV) short-circuit transformers. Short circuit tests are always preceded by powering the MV side of the test transformer by unloading the low-voltage (LV) side. Thereafter, the controller must wait for the release of the operator to start the test. Sometimes an electromagnetically disturbed controller starts the test without release. Such situation is undesired and can be destructive for the tested objects. Identification of the transient fields during the powering of the test transformer is indispensable for assessing the hazard of EM interference of the controller. Earlier research by the authors showed that the repetitive damped oscillating waves (DOW) are a component of the electromagnetic environment. Adequate instrumentation to cope with the problem are D-dot and B-dot field probes is needed. The paper reports such measurements along with recording the voltage signals. It was suspected that repetitive ignition and extinction of the short arc by closing the circuit breaker in the MV circuit is the origin of the DOW. Additional investigation of the circuit breaker in stand-alone operation is excluded in this hypothesis. The only possibility of the DOW is pulse traveling back and forth in the MV circuit, which is a line with distributed parameters.

The paper presents problems related to the processing of signals recorded with differential field probes E and H. The fundamental problem to which special attention has been paid is the result of the integration operation. Due to the presence of constant/slowly-varying components in the raw signal, there is a drift present in the outcome of integration. This line wander can be enormous. This is particularly evident if the integration is performed in a standard manner, uniformly over the entire recorded waveform. The paper contains the Authors’ proposition to segment the signal and perform the integration independently in each of the sub-regions. This approach is based on the assumption of a local mean value instead of its global character for the recorded waveform. Although this leads to more complex signal processing, it gives significantly better results as it is suppressing the deterioration drift in the integrated signal more than 400 times. The results are presented on laboratory recordings and outdoor tests. In the first case, voltage pulses with durations of about 50 ns and rise times in the range of single ns were recorded. In the second case, high-energy electromagnetic pulse signals were used. It was formed by sinusoidal waveforms packets of 3 GHz frequency with a single packet duration of 5 μs and packet repetition frequency f ≤ 300 Hz.

Many compounds have the potential to harm pancreatic beta-cells; organochlorine pollutants belong to those compounds. In this work, we aimed to find markers of acute toxicity of p,p'-DDT exposure among proteins expressed in NES2Y human pancreatic beta-cells employing 2-D electrophoresis. We exposed NES2Y cells to a high concentration (150 μM, LC96 after 72 hours) of p,p'-DDT for 24 and 30 hours and determined proteins with changed expression using 2-D electrophoresis. We have found 22 proteins that changed their expression. They included proteins involved in ER stress (GRP78, and endoplasmin), mitochondrial proteins (GRP75, ECHM, IDH3A, NDUS1, and NDUS3), proteins involved in the maintenance of the cell morphology (EFHD2, TCPA, NDRG1, and ezrin), and some other proteins (HNRPF, HNRH1, K2C8, vimentin, PBDC1, EF2, PCNA, biliverdin reductase, G3BP1, FRIL, and HSP27). The proteins we have identified may serve as indicators of p,p'-DDT toxicity in beta-cells in future studies, including long-term exposure to environmentally relevant concentrations.

Epilepsy as a chronic neurological disorder is characterized by recurrent, unprovoked epileptic seizures. In about half of the people who suffer from epilepsy, the root cause of the disorder is unknown. In the other cases, different factors can cause the onset of epilepsy. In recent years, the role of gut microbiota has been recognized in many neurological disorders, including epilepsy. These data are based on studies of the gut microbiota–brain axis, a relationship starting by a dysbiosis followed by an alteration of brain functions. Interestingly, epileptic patients may show signs of dysbiosis, therefore the normalization of the gut microbiota may lead to improvement of epilepsy and to greater efficacy of anticonvulsant drugs. In this descriptive review, we analyze the evidences for the role of gut microbiota in epilepsy and hypothesize a mechanism of action of these microorganisms in the pathogenesis and treatment of the disease. Human studies revealed an increased prevalence of Firmicutes in patients with refractory epilepsy. Exposure to various compounds can change microbiota composition, decreasing or exacerbating epileptic seizures. These include antibiotics, epileptic drugs, probiotics and ketogenic diet. Finally, we hypothesize that physical activity may play a role in epilepsy through the modulation of the gut microbiota.

Pancreatic β-cell failure and death contribute significantly to the pathogenesis of type 2 diabetes. One of the main factors responsible for β-cell dysfunction and subsequent cell death is chronic exposure to increased concentrations of FAs (fatty acids). The effect of FAs seems to depend particularly on the degree of their saturation. Saturated FAs induce apoptosis in pancreatic β-cells, whereas unsaturated FAs are well tolerated and are even capable of inhibiting the pro-apoptotic effect of saturated FAs. Molecular mechanisms of apoptosis induction by saturated FAs in β-cells are not completely elucidated. Saturated FAs induce ER stress, which in turn leads to activation of all ER stress pathways. When ER stress is severe or prolonged, apoptosis is induced. The main mediator seems to be the CHOP transcription factor. Via regulation of expression/activity of pro- and anti-apoptotic Bcl-2 family members, and potentially also through the increase in ROS production, CHOP switches on the mitochondrial pathway of apoptosis induction. ER stress signalling also possibly leads to autophagy signalling, which may activate caspase-8. Saturated FAs activate or inhibit various signalling pathways, i.e., p38 MAPK signalling, ERK signalling, ceramide signalling, Akt signalling and PKCδ signalling. This may lead to the activation of the mitochondrial pathway of apoptosis, as well. Particularly, the inhibition of the pro-survival Akt signalling seems to play an important role. This inhibition may be mediated by multiple pathways (e.g., ER stress signalling, PKCδ and ceramide) and could also consequence in autophagy signalling. Experimental evidence indicates the involvement of certain miRNAs in mechanisms of FA-induced β-cell apoptosis, as well. In the rather rare situations when unsaturated FAs are also shown to be pro-apoptotic, the mechanisms mediating this effect in β-cells seem to be the same as for saturated FAs. To conclude, FA-induced apoptosis rather appears to be preceded by complex cross talks of multiple signalling pathways. Some of these pathways may be regulated by decreased membrane fluidity due to saturated FA incorporation. Few data are available concerning molecular mechanisms mediating the protective effect of unsaturated FAs on the effect of saturated FAs. It seems that the main possible mechanism represents a rather inhibitory intervention into saturated FA-induced pro-apoptotic signalling than activation of some pro-survival signalling pathway(s) or metabolic interference in β-cells. This inhibitory intervention may be due to an increase of membrane fluidity.

In today’s agriculture, maize is considered to be one of the major feed, food and industrial crops. Cultivation of maize by inappropriate agricultural practices and on unsuitable sites is connected with specific risks of soil degradation, mainly due to water erosion of the soil. The aim of this study was to evaluate the yielding parameters, fodder quality and anti-erosion efficiency of different methods of conservation tillage for maize in two areas (Jevíčko—JEV and Skoupý—SKO) with different climate and soil conditions in the Czech Republic in the period 2016–2018, using multivariate exploratory techniques such as principal component analysis (PCA) and factor analysis (FA). Four variants of soil tillage methods were analysed: Conventional Tillage (CT), two slightly different Strip-Till techniques (ST) and Direct Sowing (DS). The analysed parameters were: dry mass of the plants, height of the plants, starch content (SC), organic matter digestibility (OMD) and content of neutral detergent fibre (NDF), soil loss by erosion and surface runoff. The multivariate exploratory techniques PCA and FA significantly differed in two categories of techniques in both locations. The first category consists of soil conservation techniques (SCT): ST (JEV/SKO) and DS (JEV). These techniques are characterised by lower yields of dry mass, lower height of plants, forage quality equal to CT, but a high level of protection of the soil against erosion. The second category consists of CT (JEV and SKO) and partially of DS (SKO). These treatments are characterised by high dry mass production, higher plants, high forage quality, but a feeble capacity of protection of the soil against erosion. The results of the study confirm the presumption of the positive influence of introduction and application of new agronomical practices in the areas of interest and other areas with similar natural conditions in the sense of sustainable management for agricultural management of agricultural land for the conditions of the Czech Republic and therefore of Central and Eastern Europe. PCA and FA were used as an effective method for comprehensive evaluation of the use of STC in agricultural practice.

Currently, various types of software compensations are applied to machine tools. Their aim is to increase the working accuracy of the tools. The improvement in working accuracy is then further assessed according to the increase in the dimensional and shape accuracy or the surface quality of the workpiece. This publication describes the effects of the volumetric accuracy of a machine tool on the working accuracy of a workpiece, where total roundness (RONt) is evaluated in multiple cuts. In the experiment, two test workpieces are manufactured on a three-axis milling machining centre. The first is made using a standard machine setup while the second with activated volumetric compensation. The LaserTRACER self-tracking laser interferometer is used to compensate for volumetric accuracy. In the second part, verification measurements are performed with a Ballbar, where roundness error is evaluated according to ISO 230-4. Then two test workpieces are machined, and, in the last part, measurement is performed on Talyrond 595S roundness measuring equipment. Finally, the results are analysed and the dependence between the volumetric accuracy, the circularity error of the machine and the working accuracy of the CNC machine tool is established, represented by the RONt of the workpiece. This paper presents new and unpublished relations between the volumetric accuracy of the machine tool and the RONt of the workpiece.

Intradural spinal arteriovenous fistulas (sAVF) are spinal vascular lesions that usually manifest due to myelopathy or local symptoms caused by venous congestion and ischemia. In addition, perimedullary arteriovenous fistulas (PMAVF) in particular may rupture and cause subarachnoid or intramedullary hemorrhage along with relevant symptoms. Subarachnoid hemorrhage (SAH) can propagate into cranial space with clinically dominant symptoms and signs of typical aneurysmal intracranial SAH. The standard workup for cerebral SAH, after excluding an intracranial source of hemorrhage, is usually limited to a cervical spine MRI; therefore, thoracolumbar sources of hemorrhage can be missed, or their diagnosis may be delayed. Here we present a case of a pregnant patient who presented with cerebral SAH. The source of hemorrhage was not initially identified, leading to a presumptive diagnosis of benign pretruncal non-aneurysmal SAH. The correct diagnosis of spinal thoracolumbar PMAVF was revealed 2.5 months later due to the progression of local symptoms. While the diagnosis was being refined and endovascular treatment was being planned (but delayed due to pregnancy), there was a recurrence of intraconal hemorrhage followed by brainstem hemorrhage. This led to significant clinical deterioration. The PMAVF was then treated microsurgically and the patient experienced partial recovery.

Endothelial cells (EC) frequently undergo primary or secondary injury during kidney disease such as thrombotic microangiopathy or glomerulonephritis. Renin Lineage Cells (RLCs) serve as a progenitor cell niche after glomerular damage in the adult kidney. However, it is not clear whether RLCs also contribute to endothelial replenishment in the glomerulus following endothelial injury. Therefore, we investigated the role of RLCs as a potential progenitor niche for glomerular endothelial regeneration. We used an inducible tet-on triple-transgenic reporter strain mRen-rtTAm2/LC1/LacZ to pulse-label the renin-producing RLCs in adult mice. Unilateral kidney EC damage (EC model) was induced by renal artery perfusion with concanavalin/anti-concanavalin. In this model glomerular EC injury and depletion developed within 1 day while regeneration occurred after 7 days. LacZ-labelled RLCs were restricted to the juxtaglomerular compartment of the afferent arterioles at baseline conditions. In contrast, during the regenerative phase of the EC model (day 7) a subset of LacZ-tagged RLCs migrated to the glomerular tuft. Intraglomerular RLCs did not express renin anymore and did not stain for glomerular endothelial or podocyte cell markers, but for the mesangial cell markers α8-integrin and PDGFRβ. Accordingly, we found pronounced mesangial cell damage parallel to the endothelial injury induced by the EC model. These results demonstrated that in our EC model RLCs are not involved in endothelial regeneration. Rather, recruitment of RLCs seems to be specific for the repair of the concomitantly damaged mesangium.

Real and scenario prognosis in engineering hydrology often involves using simulation techniques of mathematical modelling the rainfall-runoff processes in small catchments. These catchments are often up to 50 km2 in area, their character is torrential, and the type of water flow is super-critical. Many of them are ungauged. The damage in the catchments is enormous, and the length of the torrents is about 23% of the total length of small rivers in the Czech Republic. The Smědá experimental mountainous catchment (with the Bílý potok downstream gauge) in the Jizerské hory Mts. was chosen as a model area for simulating extreme rainfall-runoff processes using two different models. For the purposes of evaluating and simulating significant rainfall-runoff episodes, we chose the KINFIL physically-based 2D hydrological model, and ANN, an artificial neural network mathematical "learning" model. A neural network is a model of the non-linear functional dependence between inputs and outputs with free parameters (weights), which are created by iterative gradient learning algorithms utilizing calibration data. The two models are entirely different. They are based on different principles, but both require the same time series (rainfall-runoff) data. However, the parameters of the models are fully different, without any physical comparison. The strength of KINFIL is that there are physically clear parameters corresponding to adequate hydrological process equations, while the strength of ANN lies in the "learning procedure". Their common property is the rule that the greater the number of measured rainfall-runoff events (pairs), the better fitted the simulation results can be expected.

Saturated fatty acids (FAs) induce apoptosis in the human pancreatic NES2Y β-cell line while unsaturated FAs have nearly no detrimental effect. Moreover, unsaturated FAs are capable of inhibiting the pro-apoptotic effect of saturated FAs. Hypoxia is also known to have deleterious effects on β-cells function and viability. In the present study, we have tested the modulatory effect of hypoxia on the effect of FAs on the growth and viability of the human pancreatic NES2Y β-cells. This study represents the first study testing hypoxia effect on effects of FAs in pancreatic β-cells as well as in other cell types. We showed that hypoxia increased the pro-apoptotic effect of saturated stearic acid (SA). Endoplasmic reticulum stress signaling seemed to be involved while redistribution of FA transporters fatty acid translocase/cluster of differentiation 36 (FAT/CD36) and fatty acid-binding protein (FABP) do not seem to be involved in this effect. Hypoxia also strongly decreased the protective effect of unsaturated oleic acid (OA) against the pro-apoptotic effect of SA. Thus, in the presence of hypoxia, OA was unable to save SA-treated β-cells from apoptosis induction. Hypoxia itself had only a weak detrimental effect on NES2Y cells. Our data suggest that hypoxia could represent an important factor in pancreatic β-cell death induced and regulated by FAs and thus in the development of type 2 diabetes mellitus.

Background: Fatty acid-induced apoptosis and ER stress of pancreatic β-cells contribute to the development of type 2 diabetes, however, the molecular mechanisms involved are unclear. Aims: In this study we have tested the role of caspase-2 and suggested ER stress mediator JNK in saturated fatty acid-induced apoptosis of the human pancreatic β-cells NES2Y. Results: We found that stearic acid at apoptosis-inducing concentration activated ER stress signaling pathways, i.e. IRE1α, PERK and ATF6 pathways, in NES2Y cells. During stearic acid-induced apoptosis, JNK inhibition did not decrease the rate of apoptosis nor the activation of caspase-8, -9, -7 and -2 and PARP cleavage. In addition, inhibition of JNK activity did not affect CHOP expression although it did decrease the induction of BiP expression after stearic acid treatment. Caspase-2 silencing had no effect on PARP as well as caspase-8, -9 and -7 cleavage and the induction of CHOP expression, however, it also decreased the induction of BiP expression. Surprisingly, caspase-2 silencing was accompanied by increased phosphorylation of c-Jun. Conclusions: We have demonstrated that caspase-2 as well as JNK are not key players in apoptosis induction by saturated fatty acids in human pancreatic β-cells NES2Y. However, they appear to be involved in the modulation of saturated fatty acid-induced ER stress signaling, probably by a mechanism independent of c-Jun phosphorylation.

The paper deals with the measuring of the density profile of unevenly pressed wood of European aspen (Populus tremula L.). The main aim of the work is to examine in an experimental way the possibilities of using the X – RAY DENSE – LAB laboratory equipment designed for the determination of density profiles of agglomerated and plied large-area materials. The work uses the X – RAY DENSE – LAB equipment to determine the density profile of the cross-section of unevenly pressed aspen wood, plasticized hydrothermically, without the presence of chemical substances. The work also presents calculations of the level of compression/densification in dependence on the density and it describes the factors that can influence the density profile of compressed/densified wood; at the same time, it presents the possible ways to determine the density profile in the cross-section. Further, it includes the creation of the methodology for sample preparation so that the results do not get distorted during measuring. It describes the preparation of sample pieces, the orientation of the anatomic structure, the methodology of pressing, air conditioning, sample preparation, their measuring and analysis. The paper also describes the theory and the principles of measuring with use of X – RAY DENSE – LAB and its calibration. The paper analyses the obtained results of density profiles and searches for and describes the causes of the uneven distribution of the density in the cross-section. It concludes by summarizing the results and recommending the procedure for future measuring.

It has been shown that saturated fatty acids (FAs) have a detrimental effect on pancreatic β-cells function and survival, leading to apoptosis, whereas unsaturated FAs are well tolerated and are even capable of inhibiting the pro-apoptotic effect of saturated FAs. Molecular mechanisms of apoptosis induction and regulation by FAs in β-cells remain unclear; however, mitogen-activated protein (MAP) kinase and endoplasmic reticulum (ER) stress signaling pathways may be involved. In this study, we tested how unsaturated oleic acid (OA) affects the effect of saturated stearic acid (SA) on the p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathways as well as the ER stress signaling pathways during apoptosis induction in the human pancreatic β-cells NES2Y. We demonstrated that OA is able to inhibit all effects of SA. OA alone has only minimal or no effects on tested signaling in NES2Y cells. The point of OA inhibitory intervention in SA-induced apoptotic signaling thus seems to be located upstream of the discussed signaling pathways.

Pancreatic β-cell failure and death is considered to be one of the main factors responsible for type 2 diabetes. It is caused by, in addition to hyperglycemia, chronic exposure to increased concentrations of fatty acids, mainly saturated fatty acids. Molecular mechanisms of apoptosis induction by saturated fatty acids in β-cells are not completely clear. It has been proposed that kinase signaling could be involved, particularly, c-Jun N-terminal kinase (JNK), protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt kinases and their pathways. In this review, we discuss these kinases and their signaling pathways with respect to their possible role in apoptosis induction by saturated fatty acids in pancreatic β-cells.

Saturated stearic acid (SA) induces apoptosis in the human pancreatic β-cells NES2Y. However, the molecular mechanisms involved are unclear. We showed that apoptosis-inducing concentrations of SA activate the p38 MAPK signaling pathway in these cells. Therefore, we tested the role of p38 MAPK signaling pathway activation in apoptosis induction by SA in NES2Y cells. Crosstalk between p38 MAPK pathway activation and accompanying ERK pathway inhibition after SA application was also tested. The inhibition of p38 MAPK expression by siRNA silencing resulted in a decrease in MAPKAPK-2 activation after SA application, but it had no significant effect on cell viability or the level of phosphorylated ERK pathway members. The inhibition of p38 MAPK activity by the specific inhibitor SB202190 resulted in inhibition of MAPKAPK-2 activation and noticeable activation of ERK pathway members after SA treatment but in no significant effect on cell viability. p38 MAPK overexpression by plasmid transfection produced an increase in MAPKAPK-2 activation after SA exposure but no significant influence on cell viability or ERK pathway activation. The activation of p38 MAPK by the specific activator anisomycin resulted in significant activation of MAPKAPK-2. Concerning the effect on cell viability, application of the activator led to apoptosis induction similar to application of SA (PARP cleavage and caspase-7, -8, and -9 activation) and in inhibition of ERK pathway members. We demonstrated that apoptosis-inducing concentrations of SA activate the p38 MAPK signaling pathway and that this activation could be involved in apoptosis induction by SA in the human pancreatic β-cells NES2Y. However, this involvement does not seem to play a key role. Crosstalk between p38 MAPK pathway activation and ERK pathway inhibition in NES2Y cells seems likely. Thus, the ERK pathway inhibition by p38 MAPK activation does not also seem to be essential for SA-induced apoptosis.

Apres la victoire de l’armee de l’Empereur Justinien le Grand, remportee sur les Vandales en Afrique latine (533), l’Eglise locale avait la chance de guerir ses blessures et de se renforcer.

The process of preparation for priesthood in Church of the early centuries was accomplished by means of the system: master and his disciples. Such was the legacy inherited from ancient philosophers and Jewish rabbis. Such was also the example set by Christ himself and many of his followers — among others St Paul.

BRAK

Saint Augustin a demeure a Rome deux fois, a savoir au debut et a la fin de a la fin de son sejour en Italie, dans les annees 383-388.

sprawozdanie

recenzja

En raison du 1600-eme anniversaire du synode d'Aquilee celebre recemment, l’auteur rappelle son histoire presque entierement passee sous silence dans l’historiographie polonaise.

recenzja