Cooling effect on growth of intermetallic compounds in lead-free solder joints

Předkládaná práce se zabývá problémy optimalizace procesu bezolovnatého pájení. Cílem mé práce bylo dokázat vliv intenzity chlazení na růst intermetalických vrstev v bezolovnatém pájeném spoji a vliv intenzity chlazení na jeho jakost. V experimentu byly použity dva druhy pájecích past: Sn/Ag/Cu a Sn/Bi/Zn. Výsledné vzorky byly hodnoceny z hlediska smáčivosti, velikosti intermetalickych vrstev, optického zhodnocení pájky a střihové zkoušky.This work deals with issues of process optimalization of lead-free soldering. The aim of this work is demonstrate of cooling on grow intermetallic layers during lead-free solde ring process and a hold intensity of cooling on joint quality. The experiment was performed with two types of solder pastes: Sn/Ag/Cu a Sn/Bi/Zn. The final samples were appraised in light of wet-ting, size of intermetallic layers, optical estimation solder and sudar stress test.

Porcine mononuclear phagocyte subpopulations in the lung, blood and bone marrow: dynamics during inflammation induced by Actinobacillus pleuropneumoniae

Mononuclear phagocytes (MP) are cells of nonspecific immunity, playing an essential role in defense against bacterial pathogens. Although various MP subpopulations have been described in the pig, relations among these populations in vivo are unknown to date. The present study was aimed at describing porcine MP subpopulations infiltrating inflamed tissue of pigs under in vivo conditions. Actinobacillus pleuropneumoniae (APP) infection was used to induce an inflammatory response. CD172α, CD14, CD163, MHCII and CD203α cell surface molecules were used to identify MP by flow cytometry. Changes in MP subpopulations in the peripheral blood (PB) and bone marrow (BM) compartments along with the analysis of MP appearing in the inflamed lungs were assessed to elucidate the possible origin and maturation stages of the infiltrating MP. The MP population migrating to the inflamed lungs was phenotype CD14+ CD163+ CD203α+/− MHCII+/−. Concomitantly, after APP infection there was an increase in the PB MP CD14+ CD163+ CD203α− MHC II− population, suggesting that these cells give rise to inflammatory monocytes/macrophages. The CD203α and MHCII molecules appear on these cells after leaving the PB. In healthy animals, the BM MP precursors were represented by CD14− CD163− cells maturing directly into CD14+ CD163− that were then released into the PB. After infection, an altered maturation pathway of MP precursors appeared, represented by CD14− CD163− CD203α− MHCII− MP directly switching into CD14+ CD163+ CD203α− MHCII− MP. In conclusion, two different MP maturation pathways were suggested in pigs. The use of these pathways differs under inflammatory and noninflammatory conditions

Neutrophil apoptosis during experimentally induced Staphylococcus aureus mastitis

Abstract -The objective of this study was to determine whether neutrophil apoptosis and their consequent elimination by macrophages from the mammary gland is modulated by an infection caused by Staphylococcus aureus (S. aureus). The study was performed on twenty mammary glands of 5 virgin heifers. A buffered physiological solution (PBS) was administered as a means of control into the mammary glands of the heifers and after 168 h, the glands were inoculated with S. aureus. The samples of cell populations were obtained by lavages of the mammary glands in 4 intervals (24, 48, 72 and 168 h) after the experimental infection. Flow cytometry was used for determination of Annexin-V positivity and propidium iodide (PI) negativity of neutrophils. Light microscopy was used for determination of neutrophil karyopyknosis. Cytochemistry was used for the detection of myeloperoxidase-positive (MPO+) macrophages. Instillation of S. aureus resulted in an intramammary infection which persisted during the following experimental period. The total number of both Annexin-V-positive and PI negative neutrophils and karyopyknotic neutrophils peaked at 24 h after both of PBS and S. aureus administration. The highest percentages of Annexin-V-positive and PI negative neutrophils and karyopyknotic neutrophils were detected 48 and 168 h after PBS and S. aureus administration, respectively. The total number of MPO+ macrophages was the highest 24 h and 48 h after PBS and S. aureus administration, respectively; the percentage of MPO+ macrophages was the highest at 72 h in both cases. The dynamics of resolution of mastitis caused by S. aureus was very similar to the resolution of inflammatory response of the mammary gland after PBS administration. Mechanisms of cell pathogen elimination as well as inflammation resolution were very intensively involved; nevertheless, the mammary gland infection persisted. An early inclusion of the mechanisms of an acute inflammatory resolution thus paradoxically led to chronic infection

Platelet-rich plasma, platelet-rich fibrin, and enamel matrix derivative for oral mucosal wound healing

Different approaches to enhance healing of hard or soft tissues include the use of cytokines and growth factors to modify cellular behaviour. Numerous growth factors are found in autologous blood concentrates – platelet rich plasma (PRP) and platelet rich fibrin (PRF). Enamel matrix derivative (EMD) may improve tissue healing via amelogenins. Bilayered collagen matrix (CM) is used for soft tissue augmentation. The aim of the present study was to assess potential benefits of PRP, PRF and EMD in combination with bilayered collagen matrix or CM alone in treatment of oral mucosal defects in rabbits. Twenty-seven New Zealand white rabbits were included in this randomized controlled trial. Artificial oral mucosal defects were treated with one of these five approaches: PRP+CM, PRF+CM, EMD+CM, CM alone, or left untreated as a negative control (CO). The animals were euthanized 1 day, 7 days, or 28 days after surgery and necropsies were harvested. Histological and molecular biological analyses were performed. All defects were healed by day 28. No differences between PRP+CM, PRF+CM, CM alone and CO groups were recorded at any time point. Slower angiogenesis and a higher presence of inflammatory infiltrate were observed in the EMD+CM group 28 days after surgery. Molecular biological analyses did not reveal any statistically significant changes. In conclusion, no improvement in mucosal healing of wounds covered with a collagen membrane and PRP, PRF, or EMD was observed, compared with CM alone or untreated controls.Different approaches to enhance healing of hard or soft tissues include the use of cytokines and growth factors to modify cellular behaviour. Numerous growth factors are found in autologous blood concentrates – platelet rich plasma (PRP) and platelet rich fibrin (PRF). Enamel matrix derivative (EMD) may improve tissue healing via amelogenins. Bilayered collagen matrix (CM) is used for soft tissue augmentation. The aim of the present study was to assess potential benefits of PRP, PRF and EMD in combination with bilayered collagen matrix or CM alone in treatment of oral mucosal defects in rabbits. Twenty-seven New Zealand white rabbits were included in this randomized controlled trial. Artificial oral mucosal defects were treated with one of these five approaches: PRP+CM, PRF+CM, EMD+CM, CM alone, or left untreated as a negative control (CO). The animals were euthanized 1 day, 7 days, or 28 days after surgery and necropsies were harvested. Histological and molecular biological analyses were performed. All defects were healed by day 28. No differences between PRP+CM, PRF+CM, CM alone and CO groups were recorded at any time point. Slower angiogenesis and a higher presence of inflammatory infiltrate were observed in the EMD+CM group 28 days after surgery. Molecular biological analyses did not reveal any statistically significant changes. In conclusion, no improvement in mucosal healing of wounds covered with a collagen membrane and PRP, PRF, or EMD was observed, compared with CM alone or untreated controls

Granulation tissue enriched by aspirin and omega-3 fatty acids in healing experimental periodontal lesion

Aims. Granulation tissue (GT) and specialized proresolving mediators such as lipoxins and resolvins are key elements in the successful resolution of periodontitis. Aspirin triggered lipoxins and resolvins are even more powerful than their natural analogues. Their biosynthesis can be accelerated by omega3 fatty acids. The aim of this study was to evaluate the use of GT enriched by aspirin and omega‑3 fatty acids during the surgical treatment of periodontitis in an experimental animal model (rabbit). Methods. In each of 24 rabbits, two experimental periodontal defects were created. In total, 47 defects were treated with open flap debridement and one of three procedures: (1) GT extracted and soaked with aspirin and omega‑3 fatty acids (ASA+OMEGA3 group); (2) GT soaked with saline (PLACEBO group); or (3) GT left untreated (CONTROL group). Then, the GT was replaced in situ. Primary evaluated criteria were the probing pocket depth (PPD) and the clinical at‑ tachment level (CAL). Necropsies were harvested 2, 6, and 12 weeks after surgery. The samples were used for histological and molecular biological assessment. Results. A trend of greater PPD and CAL in the ASA+OMEGA3 group was observed at 6 weeks. However, there was no significant difference between them. During the observation period, tissue levels of FGF‑7, IL1β and TIMP1 showed a statistically significant decrease (P<0.05). For the other variables, the ASA+OMEGA3 group was comparable with the PLACEBO and CONTROL groups. Conclusion. This experiment did not demonstrate the superiority of the proposed approach. However, the enriched granulation tissue did not impair healing outcomes

SPI-1-encoded type III secretion system of Salmonella enterica is required for the suppression of porcine alveolar macrophage cytokine expression

Genes localized at Salmonella pathogenicity island-1 (SPI-1) are involved in Salmonella enterica invasion of host non-professional phagocytes. Interestingly, in macrophages, SPI-1-encoded proteins, in addition to invasion, induce cell death via activation of caspase-1 which also cleaves proIL-1β and proIL-18, precursors of 2 proinflammatory cytokines. In this study we were therefore interested in whether SPI-1-encoded type III secretion system (T3SS) may influence proinflammatory response of macrophages. To test this hypothesis, we infected primary porcine alveolar macrophages with wild-type S. Typhimurium and S. Enteritidis and their isogenic SPI-1 deletion mutants. ΔSPI1 mutants of both serovars invaded approx. 5 times less efficiently than the wild-type strains and despite this, macrophages responded to the infection with ΔSPI1 mutants by increased expression of proinflammatory cytokines IL-1β, IL-8, TNFα, IL-23α and GM-CSF. Identical macrophage responses to that induced by the ΔSPI1 mutants were also observed to the infection with sipB but not the sipA mutant. The hilA mutant exhibited an intermediate phenotype between the ΔSPI1 mutant and the wild-type S. Enteritidis. Our results showed that the SPI-1-encoded T3SS is required not only for cell invasion but in macrophages also for the suppression of early proinflammatory cytokine expression

Interleukin-17 producing cells in swine induced by microbiota during the early postnatal period - a brief research report

Interleukin-17A (IL-17) is a pro-inflammatory cytokine involved in the immune response to many pathogens playing also a role in certain chronic and autoimmune diseases. The presented study focused on the early postnatal development of IL-17 producing cells in swine. In agreement with previous studies, αβ T-helper (CD3+CD4+) and γδ T (CD3+TCRγδ+) cells were found to be the major producers of IL-17. In newborn conventional piglets, αβ T-helper cells positive for IL-17 were almost undetectable, but their frequency increased markedly with age in all issues examined, i.e., blood, spleen, and mesenteric lymph nodes (MLN). Additional analyses of CD8 and CD27 expression showed that the main αβ T-helper producers of IL-17 has CD8+CD27- phenotype in all tissues. IL-17 positive CD8+CD27+ αβ T-helper subpopulation was found only in blood and spleen. The production of IL17 in CD8-CD27+ αβ T-helper cells was always minor. In contrast, γδ T cells positive for IL-17 did not show a similar age-dependent increase in blood and spleen, whereas they increased in MLN. Because of the age-dependent increase in conventional animals, we included a comparison with germ-free piglets to show that the increase in IL-17 positive cells was clearly depended on the presence of the microbiota as the production in germ-free animals was negligible without any age-dependent increase

MALDI MSI reveals the spatial distribution of protein markers in tracheobronchial lymph nodes and lung of pigs after respiratory infection

Respiratory infections are a real threat for humans, and therefore the pig model is of interest for studies. As one of a case for studies, Actinobacillus pleuropneumoniae (APP) caused infections and still worries many pig breeders around the world. To better understand the influence of pathogenic effect of APP on a respiratory system-lungs and tracheobronchial lymph nodes (TBLN), we aimed to employ matrix-assisted laser desorption/ionization time-of-flight mass spectrometry imaging (MALDI-TOF MSI). In this study, six pigs were intranasally infected by APP and two were used as non-infected control, and 48 cryosections have been obtained. MALDI-TOF MSI and immunohistochemistry (IHC) were used to study spatial distribution of infectious markers, especially interleukins, in cryosections of porcine tissues of lungs (necrotic area, marginal zone) and tracheobronchial lymph nodes (TBLN) from pigs infected by APP. CD163, interleukin 1 beta (IL-1 beta) and a protegrin-4 precursor were successfully detected based on their tryptic fragments. CD163 and IL-1 beta were confirmed also by IHC. The protegrin-4 precursor was identified by MALDI-TOF/TOF directly on the tissue cryosections. CD163, IL-1 beta and protegrin-4 precursor were all significantly (p < 0.001) more expressed in necrotic areas of lungs infected by APP than in marginal zone, TBLN and in control lungs