Basement membrane components are key players in specialized extracellular matrices

More than three decades ago, basement membranes (BMs) were described as membrane-like structures capable of isolating a cell from and connecting a cell to its environment. Since this time, it has been revealed that BMs are specialized extracellular matrices (sECMs) with unique components that support important functions including differentiation, proliferation, migration, and chemotaxis of cells during development. The composition of these sECM is as unique as the tissues to which they are localized, opening the possibility that such matrices can fulfill distinct functions. Changes in BM composition play significant roles in facilitating the development of various diseases. Furthermore, tissues have to provide sECM for their stem cells during development and for their adult life. Here, we briefly review the latest research on these unique sECM and their components with a special emphasis on embryonic and adult stem cells and their niches

Single strand conformation polymorphisms analysis of the glucose transporter gene GLUT1 in maturity-onset diabetes of the young

Maturity-onset diabetes of the young, (MODY), an autosomal dominant, early-onset form of type-2 diabetes, is caused by mutations in five different genes all leading, to defect(s) in the pancreatic beta cell. However, some patients with this form of diabetes do not bear a mutation in any of the known (MODY1 - MODY5) loci, a notion prompting the search for new MODY genes. Clinical and genetic data point toward a defect in cell function in the majority of patients with MODY, and partners of the glucose-sensing device are reasonable functional candidates. The high-capacity glucose transporter GLUT2 has the ideal kinetic features for performing this task. However, complete GLUT2 deficiency in humans leads to hepato-renal glycogenosis (Fanconi-Bickel syndrome), and heterozygous GLUT2 mutations apparently behave in a recessive manner. Furthermore, in the human beta cell GLUT1 mRNA is predominant when compared to GLUT2 and glucose influx appears to be largely mediated by this low-Km transporter. Thus, we looked for the presence of sequence variants by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP) within the GLUT] gene in 90 Italian pedigrees negative at the search for mutations in glucokinase (MODY2) and hepatocyte nuclear factor-1 alpha (MODY3), the two genes responsible for about 60% of MODY cases in Italian children. We found three already described silent Mutations and a new single base deletion in position -173 of the 5' regulatory region. The -173delA variant, which was detected in the heterozygous or homozygous state in 30.8% of MODY patients examined and is located in a Nuclear Factor Y binding, sequence, is not associated with hyperglycemia in affected relatives of MODY probands. In conclusion, it appears from these results that the glucose transporter gene GLUT] is unlikely to play a major role in the etiology of MODY diabetes

A NEW METHOD FOR THE DETECTION OF HUMAN IGG1 AND IGG4 IN SERA AND URINE - AN INDEX FOR CHARGE PERMSELECTIVITY MODIFICATIONS IN DIABETIC-PATIENTS

IgG subclass excretion in diabetic nephropath

EARLY DETECTION OF NEUROLOGICAL INVOLVEMENT IN IDDM AND NIDDM - MULTIMODAL EVOKED-POTENTIALS VERSUS METABOLIC CONTROL

Clarification of the extent and mechanisms of damage to the central nervous system in diabetes is a frontier of current neurological research. Our aim was to obtain ample electrophysiological documentation of possible neurological abnormalities in both insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients with a short duration of disease and without overt complications, taking into account metabolic control. Group 1 comprised 11 IDDM patients, and group 2 included 14 NIDDM patients treated with diet alone; the duration of disease was less than 4 yr, and no concomitant clinical complications were present. Age- and sex-matched normal subjects formed groups 3 and 4. Pattern visual evoked potentials (VEP), brain stem auditory evoked potentials (BAEP), and somatosensory evoked potentials (SEP; after the stimulation of both median and tibial nerves) were recorded in all subjects, and metabolic control was evaluated in terms of glycemia and glycosylated hemoglobin. In group 1, significant abnormalities were found in the latency values of VEP, median SEP, and tibial SEP compared with control subjects. Similar latency abnormalities were shown in group 2 for VEP, median SEP, and tibial SEP values and for wave I latency of BAEP. Glycosylated hemoglobin values were correlated with BAEP and SEP abnormalities in many patients in both groups. Furthermore, in group 2, glycemic values correlated with SEP abnormalities. We therefore conclude that neurophysiological abnormalities are present at different levels in IDDM and NIDDM patients only a few years after clinical diagnosis and before the appearance of overt complications, and these abnormalities seem to be correlated with metabolic control status

REGRESSION OF NEUROPHYSIOLOGICAL ABNORMALITIES IN EXPERIMENTAL DIABETES AFTER ISLET TRANSPLANTATION

Regression of neurophysiological abnormalities in experimental diabetes after islet transplantation Autori F Purrello, V Caltabiano, M Vetri, C DEGANO, E VALLE, G POZZESSERE, S MORANO, G PUGLIESE, M SENSI, U DIMARIO Data pubblicazione 1994/8/1 Conferenza Diabetologia Volume 37 Pagine A217-A21

GLOMERULAR PERMSELECTIVITY CHANGES INDUCED BY DOPAMINE INFUSION IN NORMOALBUMINURIC TYPE-1 (INSULIN-DEPENDENT) DIABETIC-PATIENTS

Dopamine infusion and proteinuria in Type 1 diabetic patient

FUNCTIONAL, MORPHOLOGICAL AND BIOCHEMICAL-ALTERATIONS OF CENTRAL-NERVOUS-SYSTEM IN EXPERIENTIAL DIABETES

In experimental diabetic neuropathy functional, morphological and biochemical alterations have been evidence