9 research outputs found
Crosstalk between intestine and kidney. Revival of an ancient link
Chronic kidney disease (CKD) is associated with systemic inflammation. The latter accelerates comorbidities that
are associated with CKD (cardiovascular disease, anemia, infections, cachexia and several other conditions),
shortens life span and greatly impairs the quality of life.
Recently the attention has been focused intestine and intestinal microbiota as sources of systemic inflammation.
On one hand, the microbiota promotes the production of uraemic solute with a biological impact on the progression
of kidney failure and vascular diseases. On the other hand, the uraemic status alters the composition of the
intestinal microbiota and the structure of the epithelial barrier, causing the translocation of both microbiota and
uraemic toxins into the blood stream.
Several approaches have recently been tested, including dietary measures, prebiotics, synbiotics and intestinal
sorbents in order to reduce the generation and serum concentration of uraemic toxins
An inducible cell line (Natasha), from a neuroblastoma patient with circulating HSR-positive blasts, expressing neurohormones
A cell line, established from a neuroblastoma patient, expresses NCAM and L1 cell adhesion molecules. Two chromosomal abnormalities were present in bone marrow (10%) and cell line (82%) metaphases: (i) a homogeneously staining region (HSR) at the distal part of chromosome 14, and (ii) an insertion of unidentified dark G-banding material in 1 p36. The identification in the patient of chr 14-HSR-positive tumour cells, before the in vitro adaptation, suggests a direct HSR formation without preceding double minutes (dms; or a very early in vivo dms----HSR transformation). N-myc was amplified in the HSR. Cells expressed proopiomelanocortin and corticotropin releasing factor mRNAs. Untreated cells were relatively differentiated; nevertheless they dramatically responded to retinoic acid, forming extensive neurites, growth-cones, cell-cell and cell-neurite junctions. Neurofilaments and synaptic figures containing many dense core granules were identified. This differentiation was irreversible. This cell line is therefore useful for the study of differentiation and in particular for the involvement of neurohormones in the differentiation process
Characterisation of a human glioblastoma cell line (LI) expressing hypothalamic and pituitary hormones
The human glioblastoma cell line LI showed morphological features typical of its neuroectodermal origin. Cells were positive by immunofluorescence to GFAP, MHC class II, and L1 determinants. Cytogenetic analysis showed the presence of a modal chromosome number of 63, ranging from 58 to 69 chromosomes (DNA index was 1.6). Northern blot analysis demonstrated the presence of mRNA transcripts specific for transglutaminase C (type II or "tissue"), growth-hormone releasing-hormone (GHRH), insulin-like growth factor II (IGF-II), and proopiomelanocortin (POMC). The GHRH mRNA was present in two different sizes, one similar to the normal hypothalamic species of 0.75 kb, whilst the second species was a large transcript of approximately 10 kb size. Treatment with 5 microM retinoic acid or 5 mM alpha-difluoromethylornithine for 5 days sharply reduced the growth rate and also induced modulation of the ultrastructure and antigenic profile. This cell line may be useful to study glial differentiation and the relationship of GHRH, IGF-II and POMC expression with differentiation in neuroectodermal tumours
Parapelvic cysts, a distinguishing feature of renal Fabry disease
Background Fabry's disease (FD) is a rare, multi-organ lysosomal disease, caused by the deficiency of the enzyme \u3b1-galactosidase A, and is difficult to diagnose. Although parapelvic cysts (PC) were previously associated with FD, their prevalence and significance are unclear. Methods The present study aimed to: (i) evaluate, by renal ultrasound, the real prevalence of PC and of their determinants in a multicentre, nationwide cohort of FD patients (n = 173, Study 1) and (ii) ascertain whether a greater accuracy of PC detection improved their identification, in FD patients from a single centre (n = 67, Study 2). In both studies, for each FD patient, an age-and renal function-matched subject was selected for comparison (1:1). Results In Study 1, PC were detected in 28.9% of FD subjects and in only 1.1% of control subjects (P < 0.001). The presence of other renal abnormalities did not differ between the groups, nor differences exist in the main demographic and laboratory parameters between the groups. In Study 2, the greater accuracy of ultrasound increased PC prevalence from 29.8% to 43.3% in the same subjects (P < 0.05). In both studies, no correlation was detected between PC and the main demographic, clinical and biochemical parameters, including use of enzyme replacement therapy (P < 0.1, minimum value). Finally, no difference existed between FD patients with and without PC. Conclusions The present study suggests that the presence of PC in renal patients should alert physicians to consider the diagnosis of FD, primarily in subjects with an unclear family history of renal disease and in the presence of other stigmata of the disease