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Notes: Abstract  We report a 55-year-old man, the recipient of a cardiac allograft for ischemic cardiomyopathy 9 years earlier, who presented with progressive aortic root dilation, worsening aortic insufficiency, and an incidentally discovered chronic type A aortic dissection limited to the donor aorta. The patient was taken to the operating room, and the aortic dissection successfully repaired using standard reoperative techniques. This is the sixth case reported in the literature, and only the fourth survivor. To our knowledge, this case represents the first successful repair, of a limited aortic dissection of the donor aorta postcardiac transplantation, using a composite valve graft and modified-Cabrol coronary reconstruction.

Notes: Background The Th2 immune response in the nasal mucosa of subjects with allergic rhinitis is mediated by allergen-specific IgE. Moreover, these subjects show positive responses for markers of systemic atopy, including allergen-specific skin sensitivity and raised serum IgE titres. In contrast, idiopathic rhinitis (IR) subjects with similar histological nasal mucosal features differ in being defined as non-allergic because they have negative atopic responses.Objective We hypothesized that it is possible to have an allergic Th2 disease pathway localized in the nasal mucosa of ‘non-allergic’ rhinitis subjects despite an absence of atopic responses.Methods The presence of house dust mite and grass pollen-specific IgE antibodies was investigated in non-atopic (n=10) and atopic (n=11) subjects with persistent rhinitis and compared to normal (n=12) control subjects. Biotin-labelled allergen was used to localize specific allergen-binding antibodies in situ in sections of nasal mucosa.Results Grass pollen allergen binding was detected in the nasal mucosa of 3/10 non-atopic IR subjects but, in contrast, dust mite-specific antibodies were not detected. Specific antibodies were present in a total of 8/11 mucosal samples from the allergic group, but none was detected in normal control tissues.Conclusion These findings support the concept of localized nasal allergy in ‘non-atopic’ rhinitis subjects. We propose the term ‘entopy’ to define this phenomenon and believe that this concept has a wider implication for localized allergic responses in other mucosal sites.

Notes: Background The pathophysiology of idiopathic rhinitis is unknown but the disease is classified as being non-allergic on the basis of negative serum IgE radioallergosorbent assay (RAST) and skin prick tests. In contrast, allergic rhinitis has a Th2 type inflammatory pathology mediated by IgE and mast cells.Objective To test the null hypothesis that there would be no difference in the cellular infiltrate for key Th2-associated inflammatory cells between allergic and idiopathic rhinitis.Methods We applied strict selection criteria in the recruitment of allergic and idiopathic rhinitis cases. In contrast to previous studies which used cytology or small biopsies, we studied all layers of the mucosa by using whole, full-thickness nasal turbinate specimens with an average length of 2.5 cm. Immunohistochemistry and in situ hybridization techniques were used to compare the distribution and cell populations of mast cells, IgE positive (IgE+) cells, eosinophils and plasma cells in perennial allergic (n = 11) and idiopathic (n = 17) rhinitis, and control nasal mucosal tissue (n = 9).Results Mast cells and IgE+ cells were significantly increased within the epithelium of allergic and idiopathic mucosa compared to normal mucosa (P 〈 0.05). More IgE+ cells were present in the allergic group compared to the idiopathic group with the majority of IgE+ cells being mast cells. Both rhinitic groups showed increased eosinophilia localized to the superficial submucosa compared to normal mucosa (P 〈 0.05). More plasma cells were present in the allergic rhinitic tissue.Conclusion Idiopathic and allergic rhinitic mucosa show similarities in their inflammatory infiltrate suggesting that both groups share a highly localized Th2, IgE-mediated cellular immunopathology.

Notes: Aims  To investigate the problem of children drowning in bath seats by examining case reports, by looking at the epidemiology of bath drowning in children under two years of age and by reviewing the literature.Methods  We describe two babies: one who drowned and one nearly drowned in the bath whilst in a bath seat. We examined the RoSPA/RLSS UK database of cases of children under two years drowning in the bath for the years 1989–2003. Cases are ascertained through a press cutting system. We conducted an all language literature search of original articles, references, textbooks and conference abstracts 1951 – October 2004 in 11 standard databases.Results  The two cases illustrate how parents can have a false sense of security with bath seats. We found six cases of babies under two years drowning in the UK associated with bath seats in the time period 1989–2003. They were all boys: five of the six were under one year of age. This compared with 47 children of similar age drowning in the bath not associated with a bath seat. The literature is sparse with only four papers since 1966.Discussion  A baby drowning after being placed in a bath seats is a rare but definite cause of death. Bath seats appear to give a false sense of security (even if not encouraged by the manufacturers). It is unclear whether putting a baby in a bath seat represents an increased risk of drowning compared with a baby without a seat. Without knowing the numbers of mothers that use bath seats it is difficult to come to firm conclusions on the risks to babies. New research is needed to clarify this issue. Whether in a seat or not it is clear that the main risk to babies in the bath is being left unsupervised.

Notes: Aims: Preinvasive endocervical glandular lesions, termed cervical glandular intraepithelial neoplasia, are increasing in incidence. The distinction of cervical glandular intraepithelial neoplasia from benign mimics, especially tubo-endometrial metaplasia, endometriosis and microglandular hyperplasia, can be difficult. This study investigates the value of immunohistochemical staining with MIB1, bcl2 and p16 in the distinction of cervical glandular intraepithelial neoplasia from these benign mimics.Methods and results: Immunohistochemical staining using the monoclonal antibodies MIB1, bcl2 and p16 was performed on cases of cervical glandular intraepithelial neoplasia (n=21), tubo-endometrial metaplasia (n=13), endometriosis (n=7) and microglandular hyperplasia (n=14). With tubo-endometrial metaplasia and microglandular hyperplasia staining with MIB1 was either negative or involved 〈10% of cells, while with cervical glandular intraepithelial neoplasia the majority of cases (86%) exhibited 〉10% positive cells. Two cases of endometriosis exhibited a MIB1 index of 10–30% while in the other cases 〈10% cells stained. With bcl2 the cells of microglandular hyperplasia were negative although there was staining of associated reserve cells in 43% of cases. All cases of tubo-endometrial metaplasia except one and all cases of endometriosis stained diffusely positive with bcl2. Cases of cervical glandular intraepithelial neoplasia were negative or exhibited focal staining. With p16 all cases of cervical glandular intraepithelial neoplasia exhibited diffuse strong positivity, generally involving 100% of cells, while all cases of microglandular hyperplasia were negative. Sixty-two percent of cases of tubo-endometrial metaplasia showed focal positivity, the remainder being negative. Cases of tubo-endometrial metaplasia were never diffusely positive with p16. In three cases of endometriosis there was staining of 〉50% of cells while the other cases were either focally positive or negative.Conclusions: A panel of antibodies, comprising MIB1, bcl2 and p16, is a useful adjunct to histology in distinguishing cervical glandular intraepithelial neoplasia from tubo-endometrial metaplasia, endometriosis and microglandular hyperplasia. Cases of cervical glandular intraepithelial neoplasia are diffusely positive for p16 and generally exhibit a high proliferation index with MIB1, while bcl2 is negative or, at most, focally positive. Tubo-endometrial metaplasia and endometriosis are characterized by strong diffuse positivity with bcl2 and a low proliferation index with MIB1 (although occasional cases of endometriosis show moderate proliferative activity). p16 is negative or exhibits focal positivity in tubo-endometrial metaplasia but in endometriosis there may be quite widespread positivity. Microglandular hyperplasia shows a low proliferation index with MIB1 and is negative for bcl2 and p16.

Notes: Background : Post-infectious irritable bowel syndrome is associated with increased serotonin-containing enterochromaffin cells and lymphocytes in rectal biopsies. Animal studies have suggested that steroids reduce the lymphocyte response and suppress some of the post-infectious changes in neuromuscular function.Aim : To evaluate whether steroids reduce the number of enterochromaffin cells and improve the symptoms of post-infectious irritable bowel syndrome.Methods : Twenty-nine patients with post-infectious irritable bowel syndrome underwent a randomized, double-blind, placebo-controlled trial of 3 weeks of oral prednisolone, 30 mg/day. Mucosal enterochromaffin cells, T lymphocytes and mast cells were assessed in rectal biopsies before and after treatment, and bowel symptoms were recorded in a daily diary.Results: Initial enterochromaffin cell counts were increased and correlated with initial lamina propria T-lymphocyte counts (r = 0.460, P = 0.014). Enterochromaffin cell counts did not change significantly after either prednisolone (− 0.8% ± 9.2%) or placebo (7.9% ± 7.9%) (P = 0.5). Although lamina propria T-lymphocyte counts decreased significantly after prednisolone (22.0% ± 5.6%, P = 0.003), but not after placebo (11.5% ± 8.6%, P = 0.1), this was not associated with any significant treatment-related improvement in abdominal pain, diarrhoea, frequency or urgency.Conclusions : Prednisolone does not appear to reduce the number of enterochromaffin cells or cause an improvement in symptoms in post-infectious irritable bowel syndrome. Other approaches to this persistent condition are indicated.

Notes: We report a case of isolated extragenital bowenoid papulosis (BP) in a young man with an idiopathic low CD4 count. The lesions occurred on the dorsal aspect of his left middle finger and were not associated with genital involvement. Polymerase chain reaction studies of a biopsy demonstrated human papillomavirus 18. As far as we are aware, this is the first documented case of BP (genital or extragenital) associated with idiopathic CD4 lymphocytopenia.

Notes: Background:  Allergic rhinitis is characterized by selective expansion of T cell subsets with a CD4+ phenotype. Recently, we identified a subpopulation of nonallergic rhinitis subjects with increased epithelial mast cell and eosinophil populations, suggestive of local mucosal allergy. Previously, T cell subsets have not been characterized in this subselection of nonallergic subjects and furthermore, their relationship to mast cell and basophil effector cells remain unidentified.Objective:  To determine if a subpopulation of nonallergic subjects with idiopathic rhinitis (IR) have localized allergy confined to their nasal mucosa by comparing the T cell subsets and major histocompatibility complex (MHC) II expressing cells to persistent allergic rhinitis (PAR). Furthermore, the relationship between T cell subsets and mast cells/basophils was investigated.Methods:  None of the symptomatic patients in this study were clinically allergen-challenged. Nasal turbinate mucosa was removed from patients with PAR, IR and normal controls. Morphometry was performed on immunostained sections for T cell subset populations including CD3+, CD4+, CD8+, CD25+, CD45RA+, CD45RO+, human leucocyte antigen (HLA)-DRα (MHC class II), mast cell tryptase and for basophils.Results:  Subjects with persistent allergic rhinitis differed to normal controls in showing significantly increased numbers of total (CD3+), activated (CD25+) and allergen-naïve (CD45RA+) T lymphocytes in their nasal mucosa (P 〈 0.025). The naïve CD45RA+ memory T cells correlated to mucosal mast cells in PAR (P = 0.03). IR patients differ to allergic subjects in showing significantly reduced numbers of epithelial HLA-DRα+ cells (P = 0.007), but increased numbers of CD8+ lymphocytes (P = 0.02). The CD8+ T cells correlated with mucosal mast cell numbers (P = 0.02). In both rhinitis groups, basophils were present in very low numbers obviating the need for statistical analysis.Conclusion:  PAR is characterized by increased numbers of CD3+, CD25+ and CD45RA+ T lymphocytes compared with normal mucosa. Allergic and nonallergic rhinitis groups can be separated by significant differences in the number of epithelial antigen presenting cells (APCs) (HLA-DRα+) and sub-epithelial activated (CD25+) T cells. Moreover, IR patients do not significantly differ to their allergic counterparts with respect to total (CD3+) and naïve (CD45RA+) T cell numbers, or numbers of epithelial activated (CD25+) lymphocytes. IR subjects show significantly increased numbers of CD8+ lymphocytes compared with control mucosa and although our findings suggest that the initiating inflammatory events may differ, both rhinitis groups show a similarity in pathology involving mucosal mast cells with an association to infiltrating T cells.

Notes: Abstract. In recent years (1996-2001) the recoil-decay tagging technique has been employed with great success at the Department of Physics of the University of Jyväskylä. Various arrays of germanium detectors have been coupled to the RITU gas-filled separator in order to study nuclei far from stability. An overview of the physics studied with these arrays, along with discussion of technical development of the RITU separator, is presented. Even with a comparatively modest array of germanium detectors it has been possible to study nuclei produced with cross-sections as low as 200 nb.