Eosinophilic leukocytes function in host protection against parasitic worms. In turn, helminthic parasites harbor specific molecules to evade or paralyze eosinophil-associated host immune responses; these molecules facilitate the migration and survival of parasitic helminths in vivo. This competition between eosinophil and worm leads to stable equilibria between them. An understanding of such dynamic host-eosinophil interactions will help us to uncover mechanisms of cross talk between host and parasite in helminth infection. In this review, we examine recent findings regarding the innate immune responses of eosinophils to helminthic parasites, and discuss the implications of these findings in terms of eosinophil-mediated tissue inflammation in helminth infection.
Animals ; Eosinophils/*immunology/parasitology ; Helminthiasis/*immunology/*parasitology ; Helminths/*immunology ; Host-Parasite Interactions ; Humans

PURPOSE: The symptoms of female urethral syndrome (FUS) can originate from mechanical or functional obstructions of the bladder neck or urethra. From retrospective reviews of women referred for evaluation of lower urinary tract symptoms (LUTS), 2.7 to 23% had urodynamic evidence of a bladder outlet obstruction (BOO). However, few urodynamic studies (UDS) have been performed on the prevalence of BOO in FUS. This study was aimed at identifying the causative factors of FUS symptoms, including BOO, as evidenced by UDS. MATERIALS AND METHODS: One hundred and sixteen women with FUS were enrolled in our UDS evaluations. An additional 247 patients, presenting for evaluation of stress urinary incontinence (SUI), served as controls. Comparisons of the maximum flow rate (Qmax), voided volume, post-void residual, detrusor pressure at maximum flow rate (PdetQmax), maximum detrusor pressure (Pdetmax) were made between the FUS and SUI cases. By definition, the FUS cases were divided into normal, BOO, detrusor under activity, detrusor instability and low compliance. These sub-groups were compared with controls in a similar way. RESULTS: Women with FUS showed a lower Qmax (15.9 versus 23.8ml/sec, p<0.05), higher post-void residual (86 versus 22ml, p<0.05), PdetQmax (24.0 versus 18.0 cmH2O, p<0.05) and Pdetmax (33.3 versus 27.9cmH2O, p<0.05) compared to those with SUI. The incidence of BOO, detrusor under activity and detrusor instability were 31.9, 25 and 16%, respectively, in the FUS group. Only 22% of women with FUS showed normal UDS findings. CONCLUSIONS: These results indicated the importance of UDS in identifying the causative factors of the symptoms of FUS. Treatment of a BOO will help provide new treatment modalities for FUS.
Classification* ; Compliance ; Female* ; Humans ; Incidence ; Lower Urinary Tract Symptoms ; Neck ; Prevalence ; Retrospective Studies ; Urethra ; Urinary Bladder ; Urinary Bladder Neck Obstruction ; Urinary Incontinence ; Urodynamics*

PURPOSE: The symptoms of female urethral syndrome (FUS) can originate from mechanical or functional obstructions of the bladder neck or urethra. From retrospective reviews of women referred for evaluation of lower urinary tract symptoms (LUTS), 2.7 to 23% had urodynamic evidence of a bladder outlet obstruction (BOO). However, few urodynamic studies (UDS) have been performed on the prevalence of BOO in FUS. This study was aimed at identifying the causative factors of FUS symptoms, including BOO, as evidenced by UDS. MATERIALS AND METHODS: One hundred and sixteen women with FUS were enrolled in our UDS evaluations. An additional 247 patients, presenting for evaluation of stress urinary incontinence (SUI), served as controls. Comparisons of the maximum flow rate (Qmax), voided volume, post-void residual, detrusor pressure at maximum flow rate (PdetQmax), maximum detrusor pressure (Pdetmax) were made between the FUS and SUI cases. By definition, the FUS cases were divided into normal, BOO, detrusor under activity, detrusor instability and low compliance. These sub-groups were compared with controls in a similar way. RESULTS: Women with FUS showed a lower Qmax (15.9 versus 23.8ml/sec, p<0.05), higher post-void residual (86 versus 22ml, p<0.05), PdetQmax (24.0 versus 18.0 cmH2O, p<0.05) and Pdetmax (33.3 versus 27.9cmH2O, p<0.05) compared to those with SUI. The incidence of BOO, detrusor under activity and detrusor instability were 31.9, 25 and 16%, respectively, in the FUS group. Only 22% of women with FUS showed normal UDS findings. CONCLUSIONS: These results indicated the importance of UDS in identifying the causative factors of the symptoms of FUS. Treatment of a BOO will help provide new treatment modalities for FUS.
Classification* ; Compliance ; Female* ; Humans ; Incidence ; Lower Urinary Tract Symptoms ; Neck ; Prevalence ; Retrospective Studies ; Urethra ; Urinary Bladder ; Urinary Bladder Neck Obstruction ; Urinary Incontinence ; Urodynamics*

No abstract available.

No abstract available.
Pityriasis Rubra Pilaris ; Pityriasis ; Ustekinumab

No abstract available.
Hyperlipoproteinemia Type IV* ; Hyperlipoproteinemias ; Xanthomatosis*

No abstract available.
Nevus, Blue* ; Nose*

No abstract available.
Lichen Sclerosus et Atrophicus* ; Lichens*

The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.
*Apoptosis ; Caspases/metabolism ; Entamoeba histolytica/*enzymology/*growth & development ; Humans ; Hydrolysis ; Jurkat Cells ; Phosphatidylinositol 3-Kinases/*metabolism ; Protein Kinase C/*metabolism ; T-Lymphocytes/*parasitology/*physiology

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-kappaB (p65) in Caco-2 cells. However, IkappaB, an inhibitor of NF-kappaB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-kappaB was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-kappaB and STATs in colonic epithelial cells, which ultimately accelerates cell death.
Caco-2 Cells ; Calcium-Binding Proteins ; Calpain/genetics/metabolism ; Caspase 3/genetics/metabolism ; Caspases ; *Cell Death ; Colon/cytology ; Entamoeba histolytica/*physiology ; Epithelial Cells/cytology/parasitology ; Humans ; I-kappa B Proteins/metabolism ; Intestinal Mucosa/cytology ; NF-kappa B/genetics/*metabolism ; RNA Interference ; RNA, Small Interfering ; STAT3 Transcription Factor/genetics/*metabolism ; STAT5 Transcription Factor/genetics/*metabolism ; Signal Transduction