Biomedical subjects

A Marotta

Publications and source records attributed to A Marotta.

14 recordsLinked to original sources

PubMed1995

Developmental induction of Golgi structure and function in the primitive eukaryote Giardia lamblia.

A fundamental characteristic of eukaryotic cells is the presence of membrane-bound compartments and membrane transport pathways in which the Golgi complex plays a central role in the selective processing, sorting, and secretion of proteins. The parasitic protozoan Giardia lamblia belongs to the earliest identified lineage among eukaryotes and therefore offers unique insight into the progression from primitive to more complex eukaryotic cells. Here, we report that Giardia trophozoites undergo a developmental induction of Golgi enzyme activities, which correlates with the appearance of a morphologically identifiable Golgi complex, as they differentiate to cysts. Prior to this induction, no morphologically or biochemically identifiable Golgi complex exists within nonencysting cells. Remarkably, protein secretion in both nonencysting and encysting trophozoites is inhibited by brefeldin A, and brefeldin A-sensitive membrane association of ADP-ribosylation factor and beta-COP is observed. These results suggest that the secretory machinery of Giardia resembles that of higher eukaryotes despite the absence of a Golgi complex in nonencysting trophozoites. These findings have implications both for defining the minimal machinery for protein secretion in eukaryotes and for examining the biogenesis of Golgi structure and function.

4-Chloro-7-nitrobenzofurazan↗

PubMed1995

Total anomalous left pulmonary venous connection with intact atrial septum: surgical treatment of a rare case.

Total anomalous left pulmonary venous connection with intact atrial septum is an extremely rare form of congenital heart disease. We describe a case never reported before in which the left pulmonary veins drained directly into the right atrium through a common vein. Surgical correction was successfully obtained by redirecting the blood flow through a newly created atrial septal defect into the left atrium using a gluteraldehyde-treated autologous pericardial patch. Follow-up at 6 months shows no signs of any complication.

Child↗

PubMed1995

Kinesin is the motor for microtubule-mediated Golgi-to-ER membrane traffic.

The distribution and dynamics of both the ER and Golgi complex in animal cells are known to be dependent on microtubules; in many cell types the ER extends toward the plus ends of microtubules at the cell periphery and the Golgi clusters at the minus ends of microtubules near the centrosome. In this study we provide evidence that the microtubule motor, kinesin, is present on membranes cycling between the ER and Golgi and powers peripherally directed movements of membrane within this system. Immunolocalization of kinesin at both the light and electron microscopy levels in NRK cells using the H1 monoclonal antibody to kinesin heavy chain, revealed kinesin to be associated with all membranes of the ER/Golgi system. At steady-state at 37 degrees C, however, kinesin was most concentrated on peripherally distributed, pre-Golgi structures containing beta COP and vesicular stomatitis virus glycoprotein newly released from the ER. Upon temperature reduction or nocodazole treatment, kinesin's distribution shifted onto the Golgi, while with brefeldin A (BFA)-treatment, kinesin could be found in both Golgi-derived tubules and in the ER. This suggested that kinesin associates with membranes that constitutively cycle between the ER and Golgi. Kinesin's role on these membranes was examined by microinjecting kinesin antibody. Golgi-to-ER but not ER-to-Golgi membrane transport was found to be inhibited by the microinjected anti-kinesin, suggesting kinesin powers the microtubule plus end-directed recycling of membrane to the ER, and remains inactive on pre-Golgi intermediates that move toward the Golgi complex.

Animals↗

PubMed1995

Reduced bone mineral content and normal serum osteocalcin in non-steroid-treated patients with juvenile rheumatoid arthritis.

OBJECTIVES: To distinguish the effects of juvenile rheumatoid arthritis (JRA) on bone mineralisation from those possibly caused by steroid therapy. METHODS: Bone mineral status was evaluated in 20 children (five boys and 15 girls) with active JRA who never received steroids. Seven had oligoarticular, nine had polyarticular, and four had systemic JRA. Bone mineral content (BMC) was assessed by single beam photon absorptiometry and expressed as a Z score relative to normal values in healthy children. Serum calcium, phosphate, and alkaline phosphatase were measured by colorimetric methods. Whole parathyroid hormone was assayed by Immuno Radiometric Assay. Serum osteocalcin was measured by specific radioimmunoassay. Nutrient intake was assessed by a 24 hours dietary recall. BMC and nutrient intake were also assessed in an age and sex matched control group. RESULTS: BMC was -1.5 (SEM 0.8) Z scores in patients and 0.4 (0.3) in the control group (p = 0.02). BMC averaged -4.9 (2) Z scores in the systemic JRA group, -1 (0.6) in the polyarticular group and 0.3 (0.7) in oligoarticular JRA patients. Serum calcium, phosphate and osteocalcin values were normal in all patients. No significant difference was found between JRA patients and controls in calcium, phosphate, energy, and protein intake. CONCLUSION: JRA subjects have significantly reduced BMC even in the absence of any steroid therapy. Bone demineralisation appears to depend more on disease activity and on reduced motility than on reduced nutrient intake.

Adolescent↗

PubMed1991

Cerebrospinal fluid beta-2-microglobulin in HIV-1 infection, as a marker of neurological involvement.

Cerebrospinal fluid (CSF) and serum concentration of beta-2-microglobulin (beta-2-m) were evaluated in 30 patients in various stages of HIV-1 infection. CSF beta-2-m and CSF/serum ratio were significantly higher in patients with neurological complications respect to asymptomatic subjects. These findings indicate that CSF beta-2-m and CSF/serum ratio may be a useful marker of neurological involvement in HIV-1 infection.

Acquired Immunodeficiency Syndrome↗

PubMed1965