Lymphome non hodgkinien Ki-1 positif révélé par des ulcérations cutanéomuqueuses et une glomérulonéphrite

Malignant lymphoma particularly of T phenotype can be associated with specific or non specific cutaneous lesions. These cutaneous manifestations can occur at the onset of the disease being sometimes the revealing sign or they can appear during the course of the lymphoreticular malignancies. Glomerulonephritis was also described in lymphoma. Ki- positive large cell lymphoma was recently identified. A new case is reported with lymphadenopathy and intestinal localisation revealed by cutaneous and mucosal ulcerations principally in the mouth and a focal segmental glomerulonephritis with endo- and extracapillary proliferation. The absence of lymphoma in cutaneous and renal lesions and the clinical presentation support the hypothesis of paraneoplastic manifestations, may be related to a vasculitis.     

Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates

Summary— Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 ± 10 ppb in the control group (n = 20), and 210 ± 10, 198 ± 20 and 159 ± 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean ± standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 ± 19 ppb during NO-releasing drug treatment and increased to 231 ± 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 ± 32 ppb without nitrate treatment and decreased to 188 ± 28 ppb 7 days after nitrate addition (P = 0.02 using paired (test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 ± 25 ppb without nitrate treatment and was similar (207 ± 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.     

Effects of SR 48968 on the neuropeptide gamma-induced contraction of the human isolated bronchus

Summary— Neuropeptide gamma (NPγ) induced a contractile response of the human isolated bronchus which was potentiated by the neutral endopeptidase inhibitor, phosphoramidon, but was not modified by atropine and indomethacin. NPγ was 3.31-fold more potent than NKA. Contractile response curves to NPγ were shifted to the right and maximal responses reduced by the non-peptide NK₂-receptor antagonist, SR 48968. The pK_B of SR 48968 (8.94 ± 0.18, n = 15), calculated according to Kenakin (1987) was very close to that reported for [Nle¹⁰]-NKA (4–10), a specific agonist of neurokinin NK₂-receptors (8.86 ± 0.13, n = 13), suggesting that the contractile effects of NPγ on the human isolated bronchus were mediated through NK_2A-receptors.     

Kidney aminopeptidase A and hypertension, part I: spontaneously hypertensive rats

Tissue and plasma levels of aminopeptidase A (APA), the principal enzyme that hydrolyzes angiotensin II (Ang II) to angiotensin III, were measured in spontaneously hypertensive rats (SHR) and their normotensive control strain at 3 different ages corresponding to prehypertensive (4 weeks), developing (8 weeks), and established (16 weeks) phases of hypertension. Plasma APA activity was significantly but modestly elevated in SHR at all 3 ages compared with normotensive Wistar-Kyoto rats. Likewise, levels of APA in brain, heart, and adrenal gland were generally, but again only moderately, elevated in SHR at all ages. However, a large increase in APA activity was seen within the kidney in which APA levels were elevated 41%, 51%, and 68% in SHR at 4, 8, and 16 weeks of age, respectively. Kidney APA levels were also significantly increased in immunoblots from 8- and 16-week-old SHR. Glomeruli isolated from 16-week-old SHR had 57% higher APA activity and increased immunoreactivity compared with Wistar-Kyoto rats. To determine whether the increase in kidney APA activity in SHR was related to Ang II levels, SHR were treated for 2 weeks with the angiotensin-converting enzyme inhibitor captopril. Captopril treatment reduced blood pressure to normotensive values and resulted in a 25% reduction in kidney APA activity. These results suggest that APA expression in the kidney may be regulated by activity of the renin-angiotensin system. If so, this would further suggest that upregulation of APA during conditions in which Ang II levels were elevated would have a protective effect against Ang II-mediated cardiovascular diseases, whereas a decrease in APA expression or a failure to upregulate would exacerbate such conditions.     

Lack of differential pattern in central adiposity and metabolic syndrome in Barrett's esophagus and gastroesophageal reflux disease

Obesity is an established risk factor for esophageal adenocarcinoma, although the mechanism is unclear. A pathway from reflux to inflammation through metaplasia is the dominant hypothesis, and an added role relating to visceral adiposity and the metabolic syndrome has been mooted in Barrett's esophagus (BE) patients. Whether BE differs from gastroesophageal reflux disease (GERD) in obesity and metabolic syndrome profiles is unclear, and this was the focus of this study. Patients with proven BE or GERD were randomly selected from the unit data registry and invited to attend for metabolic syndrome screening, anthropometry studies including segmental body composition analysis, and laboratory tests including fasting lipids, insulin, and C‐reactive protein. Metabolic syndrome was defined using the National Cholesterol Education Program (NCEP) and the International Diabetes Federation (IDF) criteria. One hundred and eighteen BE patients and 113 age‐ and sex‐matched GERD controls were studied. The incidence of obesity (body mass index >30 kg/m²) was 36% and 38%, respectively, with the pattern of fat deposition predominantly central and an estimated trunk fat mass of 13 and 14 kg, respectively. Using the NCEP criteria, metabolic syndrome was significantly more common in the BE cohort (30% vs 20%, P < 0.05), but there was no significant difference using IDF criteria (42% vs 37%, P= 0.340). Central obesity and the metabolic syndrome are common in both Barrett's and GERD cohorts, but not significantly different, suggesting that central obesity and the metabolic syndrome does not per se impact on the development of BE in a reflux population. In BE, the importance of obesity and the metabolic syndrome in disease progression merits further study.     

Spontaneous communication in autism spectrum disorder: A review of topographies and interventions

Lack of spontaneous communicative initiations appears to be a consistent problem in individuals with a diagnosis of autism spectrum disorder (ASD; Fujiki & Brinton, 2009). Spontaneous communication is emitted at a much lower frequency compared to individuals with language impairment and typically developing persons. Deficits of spontaneity in social interaction have been identified explicitly in the diagnostic criteria for autism, regardless of communication level or ability (American Psychiatric Association, 1994). In addition, without intervention 21–66% of children with ASD do not develop communicative speech (Lord & McGee, 2001). Individuals with autism rarely initiate appropriate speech and often fail to engage in typical social interactions such as asking questions, requesting information, expressing affection or requesting interactions (Carr & Kologinsky, 1983). This paper provides a review of the communicative topographies used to ameliorate spontaneous communication functions in individuals with autism and addresses the behavioral interventions that are used to induce such spontaneity.     

A dyadic analysis of the effects of setting and communication partner on elicited and spontaneous communication of children with Autism Spectrum Disorder and typically developing children

The study examined the effects of condition and communication partner on spontaneous and elicited communication in children with Autism Spectrum Disorder (ASD) in comparison to age matched typically developing children. Eighteen children participated in the study (nine children diagnosed with ASD and nine typically developing children). Each participant was video recorded for 2 h 15 min periods across two conditions (academic activity and free-time). The two conditions represented a naturalistic view of the children's environment. Spontaneous and elicited communication were further analysed in terms of verbal behavior functions including requests, mands for information, mands for attention, greetings, terminating an activity, comments/tacts, language of negotiation, specifying using autoclitics and reject. Communication partner was further analysed at two levels, peer and adult. There was no difference between the frequency of functions of communication emitted and diagnosis of the participant. There was a significant difference for communication partner, whereby the main communicative partner for children with ASD was an adult in contrast to typically developing children who spoke more to their peers. Typically developing children engaged in more spontaneous communication than children diagnosed with ASD.