FDK-Type Algorithms with No Backprojection Weight for Circular and Helical Scan CT

We develop two Feldkamp-type reconstruction algorithms with no backprojection weight for circular and helical trajectory with planar detector geometry. Advances in solid-state electronic detector technologies lend importance to CT systems with the equispaced linear array, the planar (flat panel) detectors, and the corresponding algorithms. We derive two exact Hilbert filtered backprojection (FBP) reconstruction algorithms with no backprojection weight for 2D fan-beam equispace linear array detector geometry (complement of the equi-angular curved array detector). Based on these algorithms, the Feldkamp-type algorithms with no backprojection weight for 3D reconstruction are developed using the standard heuristic extension of the divergent beam FBP algorithm. The simulation results show that the axial intensity drop in the reconstructed image using the FDK algorithms with no backprojection weight with circular trajectory is similar to that obtained by using Hu's and T-FDK, algorithms. Further, we present efficient algorithms to reduce the axial intensity drop encountered in the standard FDK reconstructions in circular cone-beam CT. The proposed algorithms consist of mainly two steps: reconstruction of the object using FDK algorithm with no backprojection weight and estimation of the missing term. The efficient algorithms are compared with the FDK algorithm, Hu's algorithm, T-FDK, and Zhu et al.'s algorithm in terms of axial intensity drop and noise. Simulation shows that the efficient algorithms give similar performance in axial intensity drop as that of Zhu et al.'s algorithm while one of the efficient algorithms outperforms Zhu et al.'s algorithm in terms of computational complexity

Beneficiation of Manganese Ore Fines for the Production of Battery Grade MnO2

Though India is a leading producer of manganese ore, it is important battery grade manganese dioxide to meet the domestic requirements. The total consumption of manganese dioxide by 10 to 12 units of battery industry for the production of 1,214 million pieces of batteries per annum was around 21,521 tonnes in 1981-82, In 1980, the import of battery grade MnO2 was more than 50% of the total requirements of the industry

COLORECTAL CANCER AND ITS RISK FACTORS AMONG PATIENTS ATTENDING A TERTIARY CARE HOSPITAL IN SOUTHERN KARNATAKA, INDIA

Objective: To determine the association between certain socio-demographic and life style factors with colorectal cancer.Methods: This case-control study was conducted using a pre-designed questionnaire among 100 incident colorectal cancer patients and 200 unmatched controls attending a tertiary care hospital in southern Karnataka. Cases and the controls were interviewed and details regarding their socio-demographic factors were collected. Information on lifestyle factors such as dietary habits, physical activity levels and substance use were documented. They were also assessed for presence of existing co-morbidities and family history of colorectal and other cancers. Multivariable logistic regression was performed to determine the association between various risk factors and colorectal cancer.Results: In the present hospital based study, mean age of the participants was less than 55 years. Sixty three percent of the cases and 54.5% of the controls were males. On multivariable analysis age ≥50years (OR=1.87; 95%CI=1.02-3.45), low physical activity (OR=5.66; 95%CI=3.10-10.34) and low frequency of fruits consumption (OR=4.10; 95%CI=2.21-7.50) and hypertension (OR= 4.65; 95% CI=1.32-16.44) showed a positive association with colorectal cancer.Conclusion: Promoting healthy dietary practices and physical activity among the middle aged population appears to be significant in the context of colorectal cancer prevention in the Indian subcontinent.Keywords: Colorectal cancer, Case–control, Risk factors, Lifestyle, Comorbidities

Homozygosity for a missense mutation in the 67 kDa isoform of glutamate decarboxylase in a family with autosomal recessive spastic cerebral palsy: parallels with Stiff-Person Syndrome and other movement disorders

Background Cerebral palsy (CP) is an heterogeneous group of neurological disorders of movement and/or posture, with an estimated incidence of 1 in 1000 live births. Non-progressive forms of symmetrical, spastic CP have been identified, which show a Mendelian autosomal recessive pattern of inheritance. We recently described the mapping of a recessive spastic CP locus to a 5 cM chromosomal region located at 2q24-31.1, in rare consanguineous families. Methods Here we present data that refine this locus to a 0.5 cM region, flanked by the microsatellite markers D2S2345 and D2S326. The minimal region contains the candidate gene GAD1, which encodes a glutamate decarboxylase isoform (GAD67), involved in conversion of the amino acid and excitatory neurotransmitter glutamate to the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Results A novel amino acid mis-sense mutation in GAD67 was detected, which segregated with CP in affected individuals. Conclusions This result is interesting because auto-antibodies to GAD67 and the more widely studied GAD65 homologue encoded by the GAD2 gene, are described in patients with Stiff-Person Syndrome (SPS), epilepsy, cerebellar ataxia and Batten disease. Further investigation seems merited of the possibility that variation in the GAD1 sequence, potentially affecting glutamate/GABA ratios, may underlie this form of spastic CP, given the presence of anti-GAD antibodies in SPS and the recognised excitotoxicity of glutamate in various contexts

A wide spectrum of clinical and brain MRI findings in patients with SLC19A3 mutations

<p>Abstract</p> <p>Background</p> <p>SLC19A3 (solute carrier family 19, member 3) is a thiamin transporter with 12 transmembrane domains. Homozygous or compound heterozygous mutations in <it>SLC19A3 </it>cause two distinct clinical phenotypes, biotin-responsive basal ganglia disease and Wernicke's-like encephalopathy. Biotin and/or thiamin are effective therapies for both diseases.</p> <p>Methods</p> <p>We conducted on the detailed clinical, brain MRI and molecular genetic analysis of four Japanese patients in a Japanese pedigree who presented with epileptic spasms in early infancy, severe psychomotor retardation, and characteristic brain MRI findings of progressive brain atrophy and bilateral thalami and basal ganglia lesions.</p> <p>Results</p> <p>Genome-wide linkage analysis revealed a disease locus at chromosome 2q35-37, which enabled identification of the causative mutation in the gene <it>SLC19A3</it>. A pathogenic homozygous mutation (c.958G > C, [p.E320Q]) in <it>SLC19A3 </it>was identified in all four patients and their parents were heterozygous for the mutation. Administration of a high dose of biotin for one year improved neither the neurological symptoms nor the brain MRI findings in one patient.</p> <p>Conclusion</p> <p>Our cases broaden the phenotypic spectrum of disorders associated with <it>SLC19A3 </it>mutations and highlight the potential benefit of biotin and/or thiamin treatments and the need to assess the clinical efficacy of these treatments.</p

Quantitative Analysis and Diagnostic Significance of Methylated SLC19A3 DNA in the Plasma of Breast and Gastric Cancer Patients

Background: Previously, we have examined the methylation status of SLC19A3 (solute carrier family 19, member 3) promoter and found that SLC19A3 was epigenetically down-regulated in gastric cancer. Here, we aim to develop a new biomarker for cancer diagnosis using methylated SLC19A3 DNA in plasma. Methodology/Principal Findings: SLC19A3 gene expression was examined by RT-qPCR. Methylation status of SLC19A3 promoter was evaluated by methylation-specific qPCR. SLC19A3 expression was significantly down-regulated in 80% (12/15) of breast tumors (P<0.005). Breast tumors had significant increase in methylation percentage when compared to adjacent non-tumor tissues (P<0.005). A robust and simple methylation-sensitive restriction enzyme digestion and real-time quantitative PCR (MSRED-qPCR) was developed to quantify SLC19A3 DNA methylation in plasma. We validated this biomarker in an independent validation cohort of 165 case-control plasma including 60 breast cancer, 45 gastric cancer patients and 60 healthy subjects. Plasma SLC19A3 methylated DNA level was effective in differentiating both breast and gastric cancer from healthy subjects. We further validated this biomarker in another independent blinded cohort of 78 plasma including 38 breast cancer, 20 gastric cancer patients and 20 healthy subjects. The positive predictive values for breast and gastric cancer were 90% and 85%, respectively. The negative predictive value of this biomarker was 85%. Elevated level in plasma has been detected not only in advanced stages but also early stages of tumors. The positive predictive value for ductal carcinoma in situ (DCIS) cases was 100%. Conclusions: These results suggested that aberrant SLC19A3 promoter hypermethylation in plasma may be a novel biomarker for breast and gastric cancer diagnosis. © 2011 Ng et al.published_or_final_versio

A Mild Form of SLC29A3 Disorder: A Frameshift Deletion Leads to the Paradoxical Translation of an Otherwise Noncoding mRNA Splice Variant

We investigated two siblings with granulomatous histiocytosis prominent in the nasal area, mimicking rhinoscleroma and Rosai-Dorfman syndrome. Genome-wide linkage analysis and whole-exome sequencing identified a homozygous frameshift deletion in SLC29A3, which encodes human equilibrative nucleoside transporter-3 (hENT3). Germline mutations in SLC29A3 have been reported in rare patients with a wide range of overlapping clinical features and inherited disorders including H syndrome, pigmented hypertrichosis with insulin-dependent diabetes, and Faisalabad histiocytosis. With the exception of insulin-dependent diabetes and mild finger and toe contractures in one sibling, the two patients with nasal granulomatous histiocytosis studied here displayed none of the many SLC29A3-associated phenotypes. This mild clinical phenotype probably results from a remarkable genetic mechanism. The SLC29A3 frameshift deletion prevents the expression of the normally coding transcripts. It instead leads to the translation, expression, and function of an otherwise noncoding, out-of-frame mRNA splice variant lacking exon 3 that is eliminated by nonsense-mediated mRNA decay (NMD) in healthy individuals. The mutated isoform differs from the wild-type hENT3 by the modification of 20 residues in exon 2 and the removal of another 28 amino acids in exon 3, which include the second transmembrane domain. As a result, this new isoform displays some functional activity. This mechanism probably accounts for the narrow and mild clinical phenotype of the patients. This study highlights the ‘rescue’ role played by a normally noncoding mRNA splice variant of SLC29A3, uncovering a new mechanism by which frameshift mutations can be hypomorphic

Industry/University Collaboration at the University of Michigan-Dearborn: A Focus on Relevant Technology

https://deepblue.lib.umich.edu/bitstream/2027.42/154106/1/kampfner1998.pd

Proteoglycans and osteolysis.

Osteolysis is a complex mechanism resulting from an exacerbated activity of osteoclasts associated or not with a dysregulation of osteoblast metabolism leading to bone loss. This bone defect is not compensated by bone apposition or by apposition of bone matrix with poor mechanical quality. Osteolytic process is regulated by mechanical constraints, by polypeptides including cytokines and hormones, and by extracellular matrix components such as proteoglycans (PGs) and glycosaminoglycans (GAGs). Several studies revealed that GAGs may influence osteoclastogenesis, but data are very controversial: some studies showed a repressive effect of GAGs on osteoclastic differentiation, whereas others described a stimulatory effect. The controversy also affects osteoblasts which appear sometimes inhibited by polysaccharides and sometimes stimulated by these compounds. Furthermore, long-term treatment with heparin leads to the development of osteoporosis fueling the controversy. After a brief description of the principal osteoclastogenesis assays, the present chapter summarizes the main data published on the effect of PGs/GAGs on bone cells and their functional incidence on osteolysis