Evaluation of a new semi-automated high-performance liquid chromatography method for glycosylated haemoglobins

The authors report data on the evaluation of a new ion-exchange high performance liquid chromatographic system (HLC-723GHb Glycopack-Dyamat), recently introduced by Bio-Rad Laboratories (Segrate, Milano, Italy) to measure the glycosylated haemoglobins in blood samples. The system operates on haemolysates, which have to be performed separately, by diluting 5 \u3bcl of blood with 1 ml of haemolysing reagent. Each analysis takes about 8 min and the results are printed-out, together with a chromatogram. Precision and accuracy (comparison with the minicolumn ion-exchange method) were found to be excellent. The analysis if not affected by the presence of the so-called 'labile fractions', as demonstrated by experiments of incubation with glucose or saline solutions at 37\ub0 C. Some haemolysates containing abnormal haemoglobins (HbS, HbE, HbJ Paris and Hb Lepore) were also analysed. The effects of the different mutants on the glycated haemoglobins assay are discussed. The HbF content is also measured by this system, but the accuracy, concerning this particular determination, at the lower concentrations (HbF <2%) is not satisfactory, and needs further improvement

Potential of 3'-fluoro-3' deoxythymidine as a cellular proliferation marker in PET oncology examination

Development of the positron emission tomography (PET) diagnostic radiopharmaceutical (18F) fluoro-2-deoxy-D-glucose (18F-FDG) subsequently facilitated the discovery and clinical evaluation of several new tracers as imaging markers for cancer. While 18F-FDG is a widely employed marker forenhanced intracellular glycolysis and metabolic function, one of the newer tracers, (18F)-3'-fluoro-3'deoxythymidine (18F-FLT), has been developed as a biomarker for cell proliferation. In this review, the potential of 18F-FLT as a biomarker for cancer imaging is discussed

An evaluation of the Diamat HPLC analyser for simultaneous determination of haemoglobins A2 and F

The authors describe a modification of the instrumental parameters of the Diamat fully automated HPLC system for Hb A2 assay (Bio-Rad Laboratories, Milan, Italy) in order to obtain simultaneous determination of Hb A2 and Hb F

Preparation and Control of Ethylene Glycol-Stabilized Haemolysates for Glycated Haemoglobin Assay

Peer Reviewe

Early upregulation of 18-kDa translocator protein in response to acute neurodegenerative damage in TREM2-deficient mice

Mutations in the TREM2 gene confer risk for Alzheimer's disease and susceptibility for Parkinson's disease (PD). We evaluated the effect of TREM2 deletion in a 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP)–induced PD mouse model, measuring neurodegeneration and microglia activation using a combined in vivo imaging and postmortem molecular approach. In wild-type mice, MPTP administration induced a progressive decrease of [11C]FECIT uptake, culminating at day 7. Neuronal loss was accompanied by an increase of TREM2, IL-1β, and translocator protein (TSPO) transcript levels, [11C]PK11195 binding and GFAP staining (from day 2), and an early and transient increase of TNF-α, Galectin-3, and Iba-1 (from day 1). In TREM2 null (TREM2−/−) mice, MPTP similarly affected neuron viability and microglial cells, as shown by the lower level of Iba-1 staining in basal condition, and reduced increment of Iba-1, TNF-α, and IL-1β in response to MPTP. Likely to compensate for TREM2 absence, TREM2−/− mice showed an earlier increment of [11C]PK11195 binding and a significant increase of IL-4. Taken together, our data demonstrate a central role of TREM2 in the regulation of microglia response to acute neurotoxic insults and suggest a potential modulatory role of TSPO in response to immune system deficit

KIDNEY TRANSPLANTATION AND BONE MASS: A CONTROLLED STUDY SIX AND EIGHTEEN MONTHS AFTER SURGERY

The introduction of cyclosporine has allowed a reduction of cumulative dose of steroids and then an improvement of bone loss in the post-transplant period was expected. In a previous cross-sectional study performed in 24 patients during the early phase after kidney transplantation (Tx) we found a mild to moderate bone mineral density (BMD) loss that was not associated to steroid treatment and seemed to be related to the preexisting condition of secondary hyperparathyroidism . Then, in order to better evaluate the behaviour of bone mineralization after Tx, we studied the BMD 6 and 18 months after surgery in a selected group of patients who underwent their first kidney Tx. We studied 13 patients (12 males, 1 females), aged 39.7 ± 7.3 years, with duration of dialysis treatment of 50.1 ± 40.0 months, a good renal function recovery (mean serum creatinine 1.33 ± 0.2 mg/dl), treated with the conventional steroid and immunosuppressive therapy. We evaluated plasma levels of calcium, phosphorus, total alkaline phosphatase activity (ALP), serum intact parathyroid hormone (PTH), using standard techniques both 6 and 18 months after Tx. BMD was evaluated by DEXA (dual energy x-ray absorptiometry; Hologic QDR 1000) at lumbar spine (L1-L4) and proximal femur (neck), and osteosonography (DBM Sonic BP) at the phalanges of non dominant hand, measuring amplitude-dependent speed of sound (Ad-SoS). 6 months after Tx both clinical and biochemical parameters showed almost normal values and did not change throughout the study (PTH 102±60 pg/ml, phosphorus 2.81±.0.74 mg/dl, ALP 226.3±119.1 U/L, Calcium 10.1±0.58 mg/dl). 18 months after Tx lumbar spine BMD averaged values significantly lower as compared to control (6 months) both when evaluated as g/cm² (0.87± 0.11 vs 0.91± 0.13, p=0.01) and as Z-score (-1.87± 0.97 vs -1.47± 1.17, p=0.01). Femoral neck BMD averaged lower values as compared to control (6 months) both when evaluated as g/cm² (0.72± 0.18 vs 0.76± 0.18, p=0.07) and as Z-score (-1.60± 1.15 vs -1.23± 1.51, p=0.09) despite the differences were not statistically significant. Notwithstanding this, according to WHO criteria, all the patients showed a worsening in BMD at this site when evaluated as T-score. Furthermore 18 months after Tx the phalanges BMD averaged values significantly lower as compared to control both when evaluated as Ad-SoS (2031± 55 m/s vs 2059± 72, p<0.05) and as Z-score (-1.08± 0.73 vs -0.70± 0.93, p<0.05). Multivariate analysis were performed at each skeleton site using ΔBMD as dipendent variable and BMI, age, corticosteroid cumulative dose, Δcorticosteroid cumulative dose, ΔPTH and cyclosporine A cumulative dose as covariates. Our data show that bone mass loss is still an important and worsening complication at least in the first two years after kidney Tx. Moreover, despite the significant cumulative dose reduction, steroid treatment seems to be the most relevant factor in inducing BMD loss in these patients. Keywords: transplant: complications; bone diseases; cyclosporine; steroid