Risk of Cancer in Patients with Iron Deficiency Anemia: A Nationwide Population-Based Study

ObjectiveThis study evaluated the risk of cancer among patients with iron deficiency anemia (IDA) by using a nationwide population-based data set.MethodPatients newly diagnosed with IDA and without antecedent cancer between 2000 and 2010 were recruited from the Taiwan National Health Insurance Research Database. The standardized incidence ratios (SIRs) of cancer types among patients with IDA were calculated.ResultsPatients with IDA exhibited an increased overall cancer risk (SIR: 2.15). Subgroup analysis showed that patients of both sexes and in all age groups had an increased SIR. After we excluded patients diagnosed with cancer within the first and first 5 years of IDA diagnosis, the SIRs remained significantly elevated at 1.43 and 1.30, respectively. In addition, the risks of pancreatic (SIR: 2.31), kidney (SIR: 2.23), liver (SIR: 1.94), and bladder cancers (SIR: 1.74) remained significantly increased after exclusion of patients diagnosed with cancer within 5 years after IDA diagnosis.ConclusionThe overall cancer risk was significantly elevated among patients with IDA. After we excluded patients diagnosed with IDA and cancer within 1 and 5 years, the SIRs remained significantly elevated compared with those of the general population. The increased risk of cancer was not confined to gastrointestinal cancer when the SIRs of pancreatic, kidney, liver, and bladder cancers significantly increased after exclusion of patients diagnosed with IDA and cancer within the first 5 years. This finding may be caused by immune activities altered by IDA. Further study is necessary to determine the association between IDA and cancer risk.     

Regional,Layer, and Cell-Type-Specific Connectivity of the Mouse Default Mode Network

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Production of a monoclonal antibody that recognizes the lipopolysaccharide of a Campylobacter-like organism.

A monoclonal antibody was produced to a Campylobacter-like organism (RMIT 32A) which was isolated from the terminal ileum of a pig with proliferative enteritis. Isotyping of the antibody revealed that it was an IgG2a with kappa light chains. Immunoblots using the antibody against proteinase-K-treated whole cell lysates of RMIT 32A, a selection of Campylobacter species and other enteric bacteria showed that the antibody was specific for RMIT 32A and was directed against the lipopolysaccharide. This antibody can be used for the specific detection of RMIT 32A.     

Chemical modification of mitochondria: I. Specific labeling by 2,4-dinitro-5-(bromo-[2-14C]acetoxyethoxy) phenol

The uncoupler dinitrobromoacetoxyethoxyphenol (DNBP) has been synthesized and found to label rapidly and specifically a small number of cysteine residues in rat liver mitochondria. The labeling reaction was essentially complete in a few minutes. Only eight of the mitochondrial polypeptide bands, of MW 97, 58, 52, 43, 30, 26, 22, 13 × 10³, respectively, as separated by SDS gel electrophoresis, were found to carry the radioactive label. In each case, the label which survived acid hydrolysis was covalently bound to cysteine residues through alkylation reaction. Under the present experimental conditions, only 0.45 mole of the label was covalently bound to mitochondrial protein per mole of cytochrome aa₃ and only 1 out of about 650 sulfhydryl groups was so labeled. Consideration of the specificity of the labeling and the observed time-dependence of DNBP-stimulated respiration suggests that the labeled protein molecules are either at or very close to the mitochondrial coupling sites and probably play an important role in the primary energy transduction process.     

Evaluation of an enrichment programme for a colony of long-tailed macaques (Macaca fascicularis) in a rescue centre

Primates - Long-tailed macaques are highly social primates that are commonly used in biomedical research as animal models. The aim of this study was to evaluate the effects of different kinds of...     

Time‐to‐event continual reassessment method incorporating treatment cycle information with application to an oncology phase I trial

Delayed dose limiting toxicities (i.e. beyond first cycle of treatment) is a challenge for phase I trials. The time‐to‐event continual reassessment method (TITE‐CRM) is a Bayesian dose‐finding design to address the issue of long observation time and early patient drop‐out. It uses a weighted binomial likelihood with weights assigned to observations by the unknown time‐to‐toxicity distribution, and is open to accrual continually. To avoid dosing at overly toxic levels while retaining accuracy and efficiency for DLT evaluation that involves multiple cycles, we propose an adaptive weight function by incorporating cyclical data of the experimental treatment with parameters updated continually. This provides a reasonable estimate for the time‐to‐toxicity distribution by accounting for inter‐cycle variability and maintains the statistical properties of consistency and coherence. A case study of a First‐in‐Human trial in cancer for an experimental biologic is presented using the proposed design. Design calibrations for the clinical and statistical parameters are conducted to ensure good operating characteristics. Simulation results show that the proposed TITE‐CRM design with adaptive weight function yields significantly shorter trial duration, does not expose patients to additional risk, is competitive against the existing weighting methods, and possesses some desirable properties.     

Synthesis of the allo-analogue of trehalose

Selective benzoylation of HO-2 and HO-2′ of 4,6-O-benzylidene-α-D-glucopyranosyl 4,6-O-benzylidene-α-D-glucopyranoside with N-benzoylimidazole led to the exclusive formation of 2-O-benzoyl-4,6-O-benzylidene-α-D-glucopyranosyl 2-O-benzoyl-4,6-O-benzylidene-α-D-glucopyranoside. Oxidation of either the dibenzoate or the corresponding ditosylate with methyl sulphoxide-phosphorus pentaoxide gave the 3,3′-diulose, and subsequent reduction with borohydride gave the 3,3′diepimers having the allo-allo configuration. De-esterification and hydrolysis of the benzylidene substituents gave α-D-allopyranosyl α-D-allopyranoside.