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The effect of high pressure thermal (HPT) treatments on the inactivation of spores of non-proteolytic type E Clostridium botulinum TMW 2.990 was investigated at high pressures (300 to 600 MPa) and elevated temperatures (80 to 100 °C) in four low-acid foods (steamed sole, green peas with ham, vegetable soup, braised veal) and imidazole phosphate buffer (IPB). In addition, corresponding conventional thermal treatments at ambient pressure were performed to expose possible synergisms of pressure and temperature on spore inactivation. In general, spore count reduction was more efficient by combining pressure and temperatures < 100 °C and the overall process duration could be shortened due to accelerated heating rates (adiabatic effect). Processing at 90 °C and 600 MPa resulted in inactivation below the detection limit after 5 min in all foods except steamed sole. Traditional thermal processing of spores at 90 °C for 10 min, on the other hand, did not result in an estimated 6-log reduction. Additional HPT treatments in steamed sole and IPB did not reveal pronounced food matrix dependent protective effects. Here, varying pressure levels did not appear to be the driving force for spore count reduction in steamed sole at any temperature. By applying a Weibull distribution on destruction kinetics of isobaric/isothermal holding times, 6D-values were calculated. Compression and decompression phase (1 s pressure holding time) had a considerable impact on spore count reduction (max. -2.9 log units) in both, foods and buffer. Hence, compression and decompression phases should directly be included into the total lethal effect of HPT treatments to avoid prolonged holding times and overprocessing.

The effect of high pressure thermal (HPT) processing on the inactivation of spores of proteolytic type B Clostridium botulinum TMW 2.357 in four differently composed low-acid foods (green peas with ham, steamed sole, vegetable soup, braised veal) was studied in an industrially feasible pressure range and temperatures between 100 and 120°C. Inactivation curves exhibited rapid inactivation during compression and decompression followed by strong tailing effects. The highest inactivation (approx. 6-log cycle reduction) was obtained in braised veal at 600 MPa and 110°C after 300 s pressure-holding time. In general, inactivation curves exhibited similar negative exponential shapes, but maximum achievable inactivation levels were lower in foods with higher fat contents. At high treatment temperatures, spore inactivation was more effective at lower pressure levels (300 vs. 600 MPa), which indicates a non-linear pressure/temperature-dependence of the HPT spore inactivation efficiency. A comparison of spore inactivation levels achievable using HPT treatments versus a conventional heat sterilization treatment (121.1°C, 3 min) illustrates the potential of combining high pressures and temperatures to replace conventional retorting with the possibility to reduce the process temperature or shorten the processing time. Finally, experiments using varying spore inoculation levels suggested the presence of a resistant fraction comprising approximately 0.01% of a spore population as reason for the pronounced tailing effects in survivor curves. The loss of the high resistance properties upon cultivation indicates that those differences develop during sporulation and are not linked to permanent modifications at the genetic level.

This study investigated the effect of growth temperature (8–32 °C), process temperature (−17 to 32 °C), and sodium chloride concentration (0–3 %) on the lethality of pressure to Listeria monocytogenes . Pressure treatments were performed using a 5-strain cocktail of L. monocytogenes . Cultures grown at 8 °C were more resistant to pressure than cultures grown at 20 or 32 °C. Pressure treatments of the Listeria cocktail indicated that Listeria were most resistant to pressure at −5 or +5 °C. The effect of pressure was further evaluated at 500 MPa and +5 °C in buffer containing 1 or 3 % NaCl. Cultures treated in the presence of 3 % NaCl were more resistant than cultures treated in the presence of 1 % NaCl. Results obtained in buffer were compared to treatment of cooked ham containing 1 or 3 % NaCl. L. monocytogenes was more resistant in ham with 3 % NaCl when compared to ham with 1 % NaCl. L. monocytogenes grown at 32 °C were slightly more resistant to pressure when compared to cultures grown at 8 °C. Refrigerated storage of treated samples for 4 weeks demonstrated that L. monocytogenes recovered from all treatments with a pressure-holding time of 8 min or less. In conclusion, the effect of high-pressure processing strongly depends on growth temperature, process temperature, and the food matrix. To generally achieve a 5-log reduction of L. monocytogenes on ready-to-eat meats, combinations of pressure with elevated temperature or other antimicrobial hurdles are necessary.

Components made of nickel-based alloys are typically used for high-temperature applications because of their high corrosion resistance and very good creep and fatigue strength, even at temperatures around 1000 °C. Corrosive damage can significantly reduce the mechanical properties and the expected remaining service life of components. In the present study, a new method was introduced to continuously determine the change in microstructure occurring as a result of exposure to high temperature and cyclic mechanical loading. For this purpose, the conventional low-cycle fatigue test procedure was modified and a non-destructive, electromagnetic testing technique was integrated into a servohydraulic test rig to monitor the microstructural changes. The measured values correlate with the magnetic material properties of the specimen, allowing the microstructural changes in the specimen’s subsurface zone to be analyzed upon high-temperature fatigue. Specifically, it was possible to show how different loading parameters affect the maximum chromium depletion as well as the depth of chromium depletion, which influences the magnetic properties of the nickel-based material. It was also observed that specimen failure is preceded by a certain degree of microstructural change in the subsurface zone. Thus, the integration of the testing technology into a test rig opens up new possibilities for improved prediction of fatigue failure via the continuous recording of the microstructural changes.

In meta‐analyses, it is critical to assess the extent to which publication bias might have compromised the results. Classical methods based on the funnel plot, including Egger's test and Trim‐and‐Fill, have become the de facto default methods to do so, with a large majority of recent meta‐analyses in top medical journals (85%) assessing for publication bias exclusively using these methods. However, these classical funnel plot methods have important limitations when used as the sole means of assessing publication bias: they essentially assume that the publication process favors large point estimates for small studies and does not affect the largest studies, and they can perform poorly when effects are heterogeneous. In light of these limitations, we recommend that meta‐analyses routinely apply other publication bias methods in addition to or instead of classical funnel plot methods. To this end, we describe how to use and interpret selection models. These methods make the often more realistic assumption that publication bias favors “statistically significant” results, and the methods also directly accommodate effect heterogeneity. Selection models have been established for decades in the statistics literature and are supported by user‐friendly software, yet remain rarely reported in many disciplines. We use a previously published meta‐analysis to demonstrate that selection models can yield insights that extend beyond those provided by funnel plot methods, suggesting the importance of establishing more comprehensive reporting practices for publication bias assessment.

Prader-Willi syndrome (PWS) is a rare neurodevelopmental disorder caused by a loss of usually paternally expressed, maternally imprinted genes located on chromosome 15q11-q13. Individuals with PWS display a specific behavioral phenotype and have a higher susceptibility than the general population for certain psychiatric conditions, especially psychosis. An impairment of the oxytocin system has been described in Prader-Willi syndrome, but has not yet been investigated in detail on the epigenetic level. Recent studies have pointed out altered methylation patterns of the oxytocin receptor gene ( OXTR ) in various psychiatric disorders, including psychosis. In this study, we investigated methylation rates of CpG dinucleotides in the promoter region of the oxytocin receptor gene via bisulfite-sequencing using DNA extracted from peripheral blood samples of 31 individuals with PWS and 14 controls matched for age, sex, and BMI. Individuals with PWS show significantly lower methylation in the intron 1 region of the OXTR than neurotypical controls ( p  = 0.012). Furthermore, male PWS subjects with psychosis show significantly lower methylation of the OXTR exon 1 region than those without psychosis ( p  = 0.002). Transcription factor binding site analysis revealed E2F1 as a transcription factor potentially binding to the exon 1 region. E2F1 is physiologically regulated by Necdin , an anti-apoptotic protein whose corresponding gene is located within the PWS locus. This study provides evidence of a disruption of the Oxytocin system on an epigenetic level in PWS in general and in individuals with PWS and psychosis.

Here we show that soluble CD83 induces the resolution of inflammation in an antigen-induced arthritis (AIA) model. Joint swelling and the arthritis-related expression levels of IL-1β, IL-6, RANKL, MMP9, and OC-Stamp were strongly reduced, while Foxp3 was induced. In addition, we observed a significant inhibition of TRAP + osteoclast formation, correlating with the reduced arthritic disease score. In contrast, cell-specific deletion of CD83 in human and murine precursor cells resulted in an enhanced formation of mature osteoclasts. RNA sequencing analyses, comparing sCD83- with mock treated cells, revealed a strong downregulation of osteoclastogenic factors, such as Oc-Stamp, Mmp9 and Nfatc1, Ctsk, and Trap. Concomitantly, transcripts typical for pro-resolving macrophages, e . g ., Mrc1/2, Marco, Klf4, and Mertk, were upregulated. Interestingly, members of the metallothionein (MT) family, which have been associated with a reduced arthritic disease severity, were also highly induced by sCD83 in samples derived from RA patients. Finally, we elucidated the sCD83-induced signaling cascade downstream to its binding to the Toll-like receptor 4/(TLR4/MD2) receptor complex using CRISPR/Cas9-induced knockdowns of TLR4/MyD88/TRIF and MTs, revealing that sCD83 acts via the TRIF-signaling cascade. In conclusion, sCD83 represents a promising therapeutic approach to induce the resolution of inflammation and to prevent bone erosion in autoimmune arthritis.

To facilitate the recovery process of chronic and hard-to-heal wounds novel pro-resolving treatment options are urgently needed. We investigated the pro-regenerative properties of soluble CD83 (sCD83) on cutaneous wound healing, where sCD83 accelerated wound healing not only after systemic but also after topical application, which is of high therapeutic interest. Cytokine profile analyses revealed an initial upregulation of inflammatory mediators such as TNFα and IL-1β, followed by a switch towards pro-resolving factors, including YM-1 and IL-10, both expressed by tissue repair macrophages. These cells are known to mediate resolution of inflammation and stimulate wound healing processes by secretion of growth factors such as epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), which promote vascularization as well as fibroblast and keratinocyte differentiation. In conclusion, we have found strong wound healing capacities of sCD83 beyond the previously described role in transplantation and autoimmunity. This makes sCD83 a promising candidate for the treatment of chronic- and hard-to-heal wounds.

Alterations in macrophage (Mφ) polarization, function, and metabolic signature can foster development of chronic diseases, such as autoimmunity or fibrotic tissue remodeling. Thus, identification of novel therapeutic agents that modulate human Mφ biology is crucial for treatment of such conditions. Herein, we demonstrate that the soluble CD83 (sCD83) protein induces pro-resolving features in human monocyte-derived Mφ biology. We show that sCD83 strikingly increases the expression of inhibitory molecules including ILT-2 (immunoglobulin-like transcript 2), ILT-4, ILT-5, and CD163, whereas activation markers, such as MHC-II and MSR-1, were significantly downregulated. This goes along with a decreased capacity to stimulate alloreactive T cells in mixed lymphocyte reaction (MLR) assays. Bulk RNA sequencing and pathway analyses revealed that sCD83 downregulates pathways associated with pro-inflammatory, classically activated Mφ (CAM) differentiation including HIF-1A, IL-6, and cytokine storm, whereas pathways related to alternative Mφ activation and liver X receptor were significantly induced. By using the LXR pathway antagonist GSK2033, we show that transcription of specific genes (e.g., PPARG , ABCA1 , ABCG1 , CD36 ) induced by sCD83 is dependent on LXR activation. In summary, we herein reveal for the first time mechanistic insights into the modulation of human Mφ biology by sCD83, which is a further crucial preclinical study for the establishment of sCD83 as a new therapeutical agent to treat inflammatory conditions.

Over the last decade, acoustic methods, including acoustic emission (AE) and ultrasonic testing (UT), have been increasingly deployed for process diagnostics and health monitoring of electrochemical power devices, including batteries, fuel cells, and water electrolysers. These techniques are non-invasive, highly sensitive, and low-cost, providing a high level of spatial and temporal resolution and practicality. Their application in electrochemical devices is based on identifying changes in acoustic signals emitted from or propagated through materials as a result of physical, structural, and electrochemical changes within the material. These changes in acoustic signals are then correlated to critical processes and the health status of these devices. This review summarises progress in the use of acoustic methods for the process and health monitoring of major electrochemical energy conversion and storage devices. First, the fundamental principles of AE and UT are introduced, and then the application of these acoustic techniques to electrochemical power devices are discussed. Conclusions and perspectives on some of the key challenges and potential commercial and academic applications of the devices are highlighted. It is expected that, with further developments, acoustic techniques will form a key part of the suite of diagnostic techniques routinely used to monitor electrochemical devices across various processes, including fabrication, post-mortem examination and recycle decision support to aid the deployment of these devices in increasingly demanding applications.