Diagnosis of infections in newborns using a new particle-mediated immunoassay for serum C-reactive protein

C-reactive protein (CRP) levels were measured using a new particle-mediated immunoassay. Tests for precision and linearity of this method gave satisfactory results. The minimum sensitivity of the assay was 1 ng/ml. Interference by bilirubin (<220mg/l) and haemoglobin (<20g/l) was not observed. Using this method, CRP was assayed as a means of monitoring for infection in newborns up to 72 h after delivery. The pattern of time course elevation curves was similar for both groups (10 healthy subjects and 26 patients), but the serum CRP (ng/ml) of infected newborns rose significantly higher than in healthy subjects at 24 h after birth. The rate of increase of CRP (∆CRP; ng/ml/h) may be a more useful parameter to detect infection, since a significant change in ∆CRP was apparent only 12 h after birth. The reported method was reliable and the parameters obtained were considered clinically useful for early detection of infection

Succinyl-CoA:3-ketoacid coenzyme A transferase (SCOT): development of an antibody to human SCOT and diagnostic use in hereditary SCOT deficiency

AbstractSuccinyl-CoA:3-ketoacid CoA transferase (SCOT) is a key enzyme for ketone body utilization. Hereditary SCOT deficiency in humans (McKusick catalogue number 245050) is characterized by intermittent ketoacidotic attacks and permanent hyperketonemia. Since previously-available antibody to rat SCOT did not crossreact with human SCOT, we developed an antibody against recombinant human SCOT expressed in a bacterial system. The recombinant SCOT was insoluble except under denaturing conditions. Antibody raised to this polypeptide recognized denatured SCOT and proved useful for immunoblot analysis. On immunoblots, SCOT was easily detectable in control fibroblasts and lymphocytes but was detected neither in fibroblast extracts from four SCOT-deficient patients, nor in lymphocytes from two SCOT-deficient patients. These data indicate that immunoblot analysis is useful for diagnosis of SCOT deficiency in combination with enzyme assay

Oncocytic carcinoma of parotid gland: a case report with clinical, immunohistochemical and ultrastructural features

BACKGROUND: Oncocytic carcinoma is an extremely rare neoplasm of the salivary glands. We report a case of oncocytic carcinoma arising in a parotid gland in a 66-year-old female. METHOD: An excisional biopsy of the parotid tumor was performed. The specimen was submitted for histology and after fixation in formalin solution and inclusion in paraffin, 3–5 μm sections were stained with hematoxylin and eosin for conventional evaluation and Periodic acid Schiff stain. Immunohistochemical studies were performed using antibodies against mitochondrial antigen, keratin, S-100, alpha-actin, vimentin, alpha-1-antichymotrypsin as well as an ultrastructural analysis was performed. RESULTS: Frozen sections revealed an infiltrative growth pattern and the diagnosis of a malignant epithelial lesion was made. Permanent sections stained with haematoxylin and eosin revealed a neoplasm that had replaced a wide area of the parotid gland and had invaded subcutaneous adipose tissue. Perineural invasion was evident, but vascular invasion was not found. Neoplastic elements were large, round or polyhedral cells and were arranged in solid sheets, islands and cords. The cytoplasm was abundant, eosinophilic and finely granular. The nuclei were large and located centrally or peripherally. The nucleoli were distinct and large. Periodic acid Schiff stain demonstrated a granular cytoplasm. Immunohistochemistry demonstrated mithochondrial antigen, keratin, and chymotrypsin immunoreactivity in the neoplastic cells. Ultrastructural analysis revealed numerous mitochondria packed into the cytoplasm of the neoplastic cells. Thus, the final diagnosis was that of oncocytic carcinoma of parotid gland. CONCLUSION: This neoplasm shows clinical, microscopical, histological and ultrastructural features of oncocytic carcinoma and this must be considered in the differential diagnosis of other proliferations in the parotid gland with abundant granular cytoplasm and metastatic oncocytic carcinomas

Observation of isotropic giant magnetoresistance in paramagnetic Au80 Fe20

Magnetization and magnetoresistance were measured at room temperature and above on Au80Fe20 platelets and ribbons obtained by solid-state quenching and melt spinning. The as-quenched samples contain a solid solution of Fe in Au and exhibit a paramagnetic (Curie-Weiss) behavior in the considered temperature range; magnetic data indicate very short-ranged magnetic correlation among adjacent spins, enhanced by local composition fluctuations. The solid solution is very stable. Only a very limited fraction (never exceeding 1%) of nanometer-sized, bcc Fe particles appears after long-time isothermal anneals at suitable temperatures. A negative magnetoresistance was observed at room temperature in all examined samples. The observed effect is anhysteretic, isotropic, and quadratically dependent on magnetic field H and magnetization M. The signal scales with M rather than with H, indicating that it depends on the field-induced magnetic order of the Fe moments, as it does for conventional giant magnetoresistance in granular magnetic systems. This effect derives from spin-dependent scattering of conduction electrons from single Fe spins or very small Fe clusters. The scattering centers are almost uncorrelated at a distance of the order of the electronic mean free path (of the order of 1.5 nm, or a few atomic spacings, at RT

Nf-κb Inhibition Rescues Cardiac Function By Remodeling Calcium Genes In A Duchenne Muscular Dystrophy Model

Duchenne muscular dystrophy (DMD) is a neuromuscular disorder causing progressive muscle degeneration. Although cardiomyopathy is a leading mortality cause in DMD patients, the mechanisms underlying heart failure are not well understood. Previously, we showed that NF-κB exacerbates DMD skeletal muscle pathology by promoting inflammation and impairing new muscle growth. Here, we show that NF-κB is activated in murine dystrophic (mdx) hearts, and that cardiomyocyte ablation of NF-κB rescues cardiac function. This physiological improvement is associated with a signature of upregulated calcium genes, coinciding with global enrichment of permissive H3K27 acetylation chromatin marks and depletion of the transcriptional repressors CCCTC-binding factor, SIN3 transcription regulator family member A, and histone deacetylase 1. In this respect, in DMD hearts, NF-κB acts differently from its established role as a transcriptional activator, instead promoting global changes in the chromatin landscape to regulate calcium genes and cardiac function

Identification of Novel SNPs in Glioblastoma Using Targeted Resequencing

High-throughput sequencing opens avenues to find genetic variations that may be indicative of an increased risk for certain diseases. Linking these genomic data to other “omics” approaches bears the potential to deepen our understanding of pathogenic processes at the molecular level. To detect novel single nucleotide polymorphisms (SNPs) for glioblastoma multiforme (GBM), we used a combination of specific target selection and next generation sequencing (NGS). We generated a microarray covering the exonic regions of 132 GBM associated genes to enrich target sequences in two GBM tissues and corresponding leukocytes of the patients. Enriched target genes were sequenced with Illumina and the resulting reads were mapped to the human genome. With this approach we identified over 6000 SNPs, including over 1300 SNPs located in the targeted genes. Integrating the genome-wide association study (GWAS) catalog and known disease associated SNPs, we found that several of the detected SNPs were previously associated with smoking behavior, body mass index, breast cancer and high-grade glioma. Particularly, the breast cancer associated allele of rs660118 SNP in the gene SART1 showed a near doubled frequency in glioblastoma patients, as verified in an independent control cohort by Sanger sequencing. In addition, we identified SNPs in 20 of 21 GBM associated antigens providing further evidence that genetic variations are significantly associated with the immunogenicity of antigens