Business Customer Satisfaction Measurement in the Food Company

Import 22/07/2015Práca je zameraná na analýzu spokojnosti zákazníkov v potravinárskej spoločnosti. Cieľom práce je zistiť celkovú spokojnosť zákazníkov s kvalitou predávaných výrobkov a čiastkové spokojnosti týkajúce sa ceny výrobkov, distribúcie a komunikácie so zástupcami spoločnosti. Najskôr je vymedzený pojem zákazník, spokojnosť zákazníka a charakterizovaná daná spoločnosť. Výskum je realizovaný prostredníctvom písomného ale aj online dotazníka. Výskum je zároveň zameraný len na regionálnych B2B zákazníkov spoločnosti. Na základe výsledkov sú stanovené návrhy a odporučenia pre management spoločnosti, ktoré môže viesť k prípadnému zvýšeniu zákazníckej spokojnosti.The bachelor thesis is mainly focused on customer satisfaction measurement in the food company. The aim of this thesis is to discover total customer satisfaction with quality of received products and partial satisfaction regarding their price, distribution and communication with company’s representatives. The theoretical part includes the definition of the terms customer, customer satifaction and characterization of the company. The reaserch is realized via both written and online questionare and is focused only on local B2B customers of the company. On the basis of the results were given recommendations for the management of the company to help increase the customer satisfaction.116 - Katedra marketingu a obchoduvelmi dobř

Whole genome sequencing identifies missense mutation in MTBP in Shar-Pei affected with Autoinflammatory Disease (SPAID)

Abstract Background Autoinflammatory diseases in dogs are characterized by complex disease processes with varying clinical signs. In Shar-Pei, signs of inflammation including fever and arthritis are known to be related with a breed-specific predisposition for Shar-Pei Autoinflammatory Disease (SPAID). Results Clinical and histopathological examinations of two severely SPAID-affected Shar-Pei revealed signs of inflammation including fever, arthritis, and perivascular and diffuse dermatitis in both dogs. A multifocal accumulation of amyloid in different organs was found in one SPAID-affected case. Whole genome sequencing resulted in 37 variants, which were homozygous mutant private mutations in SPAID-affected Shar-Pei. Nine SNVs with predicted damaging effects and three INDELs were further investigated in 102 Shar-Pei affected with SPAID, 62 unaffected Shar-Pei and 162 controls from 11 different dog breeds. The results showed the missense variant MTBP:g.19383758G > A in MTBP to be highly associated with SPAID in Shar-Pei. In the region of this gene a large ROH (runs of homozygosity) region could be detected exclusively in the two investigated SPAID-affected Shar-Pei compared to control dog breeds. No further SPAID-associated variant with predicted high or moderate effects could be found in genes identified in ROH regions. This MTBP variant was predicted to affect the MDN2-binding protein domain and consequently promote proinflammatory reactions. In the investigated group of Shar-Pei older than six years all dogs with the mutant genotype A/A were SPAID-affected whereas SPAID-unaffected dogs harbored the homozygous wildtype (G/G). Shar-Pei with a heterozygous genotype (G/A) were shown to have a 2.13-fold higher risk for disease development, which gave evidence for an incomplete dominant mode of inheritance. Conclusions The results of this study give strong evidence for a variant in MTBP related with proinflammatory processes via MTBP-MDM2 pathway. Thus, these results enable a reliable detection of SPAID in Shar-Pei dogs

Cytotoxic CD8+ T cell ablation enhances the capacity of regulatory T cells to delay viral elimination in Theiler's murine encephalomyelitis

Theiler's murine encephalomyelitis (TME) of susceptible mouse strains is a commonly used infectious animal model for multiple sclerosis. The study aim was to test the hypothesis whether cytotoxic T cell responses account for the limited impact of regulatory T cells on antiviral immunity in TME virus-induced demyelinating disease (TMEV-IDD) resistant C57BL/6 mice. TME virus-infected C57BL/6 mice were treated with (i) interleukin-2/-anti-interleukin-2-antibody-complexes to expand regulatory T cells (“Treg-expansion”), (ii) anti-CD8-antibodies to deplete cytotoxic T cells (“CD8-depletion”) or (iii) with a combination of Treg-expansion and CD8-depletion (“combined treatment”) prior to infection. Results showed that “combined treatment”, but neither sole “Treg-expansion” nor “CD8-depletion,” leads to sustained hippocampal infection and virus spread to the spinal cord in C57BL/6 mice. Prolonged infection reduces myelin basic protein expression in the spinal cord together with increased accumulation of β-amyloid precursor protein in axons, characteristic of myelin loss and axonal damage, respectively. Chronic spinal cord infection upon “combined treatment” was also associated with increased T and B cell recruitment, accumulation of CD107b+ microglia/macrophages and enhanced mRNA expression of interleukin (IL)-1α, IL-10 and tumor necrosis factor α. In conclusion, data revealed that the suppressive capacity of Treg on viral elimination is efficiently boosted by CD8-depletion, which renders C57BL/6 mice susceptible to develop chronic neuroinfection and TMEV-IDD

Intact interleukin-10 receptor signaling protects from hippocampal damage elicited by experimental neurotropic virus infection of SJL mice

Abstract Theiler’s murine encephalomyelitis virus (TMEV) infection represents an experimental mouse model to study hippocampal damage induced by neurotropic viruses. IL-10 is a pleiotropic cytokine with profound anti-inflammatory properties, which critically controls immune homeostasis. In order to analyze IL-10R signaling following virus-induced polioencephalitis, SJL mice were intracerebrally infected with TMEV. RNA-based next generation sequencing revealed an up-regulation of Il10, Il10rα and further genes involved in IL-10 downstream signaling, including Jak1, Socs3 and Stat3 in the brain upon infection. Subsequent antibody-mediated blockade of IL-10R signaling led to enhanced hippocampal damage with neuronal loss and increased recruitment of CD3+ T cells, CD45R+ B cells and an up-regulation of Il1α mRNA. Increased expression of Tgfβ and Foxp3 as well as accumulation of Foxp3+ regulatory T cells and arginase-1+ macrophages/microglia was detected in the hippocampus, representing a potential compensatory mechanism following disturbed IL-10R signaling. Additionally, an increased peripheral Chi3l3 expression was found in spleens of infected mice, which may embody reactive regulatory mechanisms for prevention of excessive immunopathology. The present study highlights the importance of IL-10R signaling for immune regulation and its neuroprotective properties in the context of an acute neurotropic virus infection

Theiler’s murine encephalomyelitis virus (TMEV)-infection exacerbates enteric disease following interleukin-10 receptor (IL-10R) blockade.

<p>(A) Note changes of colonic mucosa with severe lymphohistiocytic to neutrophilic inflammation (arrow heads), crypt abscess formation (#), and loss of crypt epithelium (arrow). H&E staining, bar = 60 μm (B) Significantly increased severity of colitis at 14 days post infection (dpi) in TMEV-infected mice with IL10R antibody (Ab) treatment (group “IL10R↓_early/TMEV”) compared to Ab treated animals without infection (group “IL10R↓_early/mock”). Animals receiving isotype control instead of IL-10R Ab did not show any intestinal inflammation. IL-10R Ab treated SJL mice with TMEV-infection (group “IL10R↓_early/TMEV”), TMEV-infected mice without IL-10R Ab treatment (group “isotype_early/TMEV”), IL-10R Ab treated SJL mice without TMEV-infection (group “IL10R↓_early/mock”). Box and whisker plots display median, minimum and maximum values as well as upper and lower quartiles, 5 animals used in all groups, Wilcoxon rank-sum tests, *  =  p < 0.05.</p

Motor coordination in Theiler’s murine encephalomyelitis virus (TMEV)-infected SJL mice.

<p>(A) <i>Experiment I</i>: RotaRod^® performance test after early application of the IL-10 receptor blocking antibody (IL-10R Ab) at 0, 7, 14 and 21 dpi (arrows) revealed motor coordination deficits in TMEV-infected animals compared to mock-infected mice at 42 dpi. However, no differences were determined between IL-10R Ab- and isotype-treated animals. white box = TMEV-infected mice without IL-10R Ab treatment (group “isotype_early/TMEV”), grey box = TMEV-infected mice with IL-10R treatment (group “IL10R↓_early/TMEV”), black box = mock-infected mice with IL-10R treatment (group “IL10R↓_early/mock”). (B) <i>Experiment II</i>: application of IL-10R Ab at 35 and 42 dpi (arrows) caused also deterioration of motor coordination starting at 42 dpi. However, no differences were observed between IL-10R Ab- and isotype-treated animals (groups “IL-10R↓_late/TMEV” and “isotype_late/TMEV”). white box = TMEV-infected mice without IL-10R Ab treatment (group “isotype_late/TMEV”), grey box = TMEV-infected mice with IL-10R treatment (group “IL10R↓_late/TMEV”), black box = mock-infected mice with IL-10R treatment (group “IL10R↓_late/mock”). Box and whisker plots display median, minimum and maximum values as well as upper and lower quartiles, 5 animals used at all investigated time points, Wilcoxon rank-sum tests, *  =  p < 0.05.</p

Clinical effects of Theiler’s murine encephalomyelitis virus (TMEV)-infection in SJL mice following IL-10R blockade.

<p>(A) <i>Experiment I</i>: TMEV-infection causes worsening of systemic clinical signs (increased clinical scores) at 22 dpi in SJL mice with early anti-IL-10 receptor antibody (IL-10R Ab) treatment compared to non-infected mice following anti-IL-10R Ab treatment (<b>red asterisks</b>) and TMEV-infected mice without anti-IL-10R Ab treatment (<b>black asterisks</b>), suggestive of a triggering effect of virus infection upon IL-10R deficiency-mediated systemic signs. (B) <i>Experiment II</i>: Ab treatment during the late infection phase leads to similar clinical scores between TMEV-infected mice with and without IL-10R blockade. 5 animals used in all three groups and at all investigated time points, Wilcoxon rank-sum tests, arrows = administration of IL-10R Ab or isotype control, respectively, red asterisks = significant differences (p < 0.05) between TMEV-infected mice with and without IL-10R blockade, black asterisks = significant differences (p < 0.05) between IL-10R blocked mice with and without TMEV-infection, green asterisks significant differences (p < 0.05) between TMEV-infected mice and IL-10R blocked mice.</p

Enteric disease following interleukin-10 receptor (IL-10R) blockade in non-infected SJL mice.

<p>(A) Unformed feces and mucosal edema in an animal at 14 days after onset of IL-10R antibody (Ab) treatment. (B) Colon of a control animal (group “isotype”) at day 21 with normal mucosal architecture. (C) Colon of an animal receiving IL-10R Ab (group “IL-10R↓”) at the same time point. Note infiltration of neutrophilic granulocytes (arrows) and loss of goblet cells (#). B, C: H&E staining, bar = 20 μm. (D) IL-10R blockade causes progressive colitis compared to control animals. grey box with vertical lines = control animals (group “isotype”), white box with vertical lines = IL-10R blocked animals (group “IL-10R↓”). Box and whisker plot display median, minimum and maximum values as well as upper and lower quartiles, 5 animals used at all investigated time points, Wilcoxon rank-sum tests, *  =  p < 0.05.</p

Effect of IL-10 receptor (IL-10R) blockade upon leukomyelitis in Theiler’s murine encephalomyelitis virus (TMEV)-infected SJL mice.

<p>(A) TMEV-infection and concurrent intraperitoneal application of IL-10R antibody lead to an increase of CD3⁺ T cells in the spinal cord at 49 days post infection (dpi) compared to (B) TMEV-infected control animals. A,B: immunohistochemistry, bar = 20 μm. (C) Statistical analyses revealed a significant increase of CD3⁺ T cells in TMEV-infected mice with IL-10R blockade compared to isotype-treated animals at 49 dpi. Almost no CD3⁺ T cells were present in spinal cord cross sections of mock-infected animals. (D) Simultaneously, IL-6 mRNA expression significantly decreased in TMEV-infected animals following IL-10R blockade. white box = TMEV-infected mice without IL-10R Ab treatment (group “isotype_late/TMEV”), grey box = TMEV-infected mice with IL-10R treatment (group “IL10R↓_late/TMEV”), black box = mock-infected mice with IL-10R treatment (group “IL10R↓_late/mock”). Box and whisker plots display median, minimum and maximum values as well as upper and lower quartiles, 5 animals used in all groups, Wilcoxon rank-sum tests, *  =  p < 0.05.</p

Summary of primer pairs used for polymerase chain reaction.

<p>Summary of primer pairs used for polymerase chain reaction.</p