Pesticide and non-dioxin-like polychlorinated biphenyls (NDL-PCBs) residues in foodstuffs from Ismailia city, Egypt.

Samples of vegetables and cereals from Egypt were screened for 113 pesticides, of which 68 were quantified, using gas chromatography-mass spectrometry (GC/MS) with limits of detection (LODs) ranging from 0.02 to 1.9 µg kg⁻¹. In addition, the residues of 17 non-dioxin-like polychlorinated biphenyls (NDL-PCBs) were measured in samples of animal origin (meat, dairy products and seafood) using high-resolution gas chromatography (HRGC)/high-resolution mass spectroscopy (HRMS). None of the cereal samples and 72.7% of the vegetables contained any detectable levels of the pesticides. Detectable residues, not exceeding the current European Union maximum residue limits (MRLs) were found in 27.3% of vegetables. The estimated daily intake for detected pesticides was well below their corresponding acceptable daily intake (ADI), with exposure ranges between 0.002% of the ADI for profenofos and 0.2% of the ADI for lambda-cyhalothrin. The sum concentration of 17 PCBs congeners varied between 2.5 and 322 ng g⁻¹ fat, corresponding to 1.7-216 ng g⁻¹ fat for the seven indicator PCBs. The highest values were measured in seafood, the lowest in dairy products. Hexa-CB 153, 138 and hepta-CB180 were the congeners with the highest contribution. PCBs congener profiles found in most of the samples were consistent with the expected profile for Aroclor 1260 and 1262. PCBs' contamination levels reported in this paper were many times lower than in developed countries, except for chicken samples. Also, the dietary intake of seven indicator PCBs due to the consumption of food of animal origin (4.84 ng kg⁻¹ body weight day⁻¹) from Ismailia city, Egypt, is several times lower than the intake in European Union countries.

Assessment of medial olivocochlear system function in pre-term and full-term newborns using a rapid test of transient otoacoustic emissions.

This study was conducted to investigate maturation of the medial olivocochlear efferent system (MOCS) in pre- and full-term neonates using Quickscreen (Otodynamics Ltd) and to confirm previous findings on transient otoacoustic emission (TEOAE) suppression in neonates. MOCS maturation was investigated in 46 neonates born at the Chaim Sheba Medical Center, Tel Hashomer, Israel, using Quickscreen. All neonates were normal with no family history of general or auditory disease and no risk factors for hearing impairment. MOCS function appears gradually in human pre-term neonates and is considered to reach maturity shortly after term birth. The clinical value of MOCS testing in specific populations of newborns at risk for hearing and/or brainstem function can be legitimately raised as activation of the MOCS clearly alters cochlear output. The present results can be interpreted to support the testing of infants at risk of developing abnormal MOCS function using a commercially available rapid TEOAE measurement system.

Prospective assessment of microsatellite instability in gastrointestinal neoplasia in Ashkenazi and non-Ashkenazi Jews.

BACKGROUND: Microsatellite instability (MSI) is a useful marker of replication errors in neoplasia, resulting from mutations in the mismatch repair (MMR) genes. Nearly all hereditary non-polyposis colorectal cancer (HNPCC) and about 15% of sporadic colorectal cancers (CRC) exhibit high MSI (MSI-H). The use of the Amsterdam criteria for HNPCC diagnosis may fail to identify many HNPCC cases. Genetic screening of mutations in the MMR genes is laborious, time-consuming, expensive and limited by a low detection rate. Hence, MSI testing is a feasible and cost-effective method to select suspected HNPCC patients for genetic analysis. MSI has not been used routinely or prospectively in the assessment of newly diagnosed CRC. AIMS: To prospectively evaluate MSI status in a cohort of patients seen at the Gastrointestinal Oncology Unit of the Tel Aviv Medical Center. METHODS: Ninety-eight consecutive patients with colonic or gastric neoplasia were included. Samples from neoplastic and normal mucosa were obtained at the time of diagnostic endoscopy. MSI was determined based on five Bethesda markers using standard polymerase chain reaction procedures. RESULTS: The overall incidence of MSI was 20.4%. MSI-H was detected in 22.2% of CRC, 20% of colonic adenomas and 18.2% of gastric neoplasia. MSI-positive neoplasia tended to display multiple colonic sites, moderate-well differentiated tumors, and a higher rate of familial gastrointestinal neoplasia. CONCLUSIONS: MSI may be involved in the early stages of some colorectal tumorigenesis pathways since it may be detected in adenomas. MSI may serve as a cost-effective, reliable and important tool in the selection of HNPCC-suspected families for genetic testing. A small study population, referral bias or ethnic variation might explain the higher MSI rate. It is suggested that, similar to familial adenomatous polyposis, a state of attenuated HNPCC may exist. Hence, the clinical approach in positive patients, and their family members, should be conducted as for families with genetically proven HNPCC.

Care guidelines: journey through the managed care maze.

Home health care agencies face significant challenges as they respond to the changes in reimbursement for health care services. In this era of "out of control" increases in costs for health services, health care managers must ensure the prudent allocation of health care dollars while maintaining adequate quality of services delivered. One method advocated to accomplish this goal is a change from a fee-for-service reimbursement system to a managed care model. The patient care pathway, a formatted time line for interventions and anticipated outcomes, is an important tool for health care agencies in responding to the demands of the managed care model. This article describes the development of a patient care pathway in one home health agency.

Isolation of a cDNA that encodes the peptide core of the secretory granule proteoglycan of rat basophilic leukemia-1 cells and assessment of its homology to the human analogue.

It has been previously shown that a single gene is used to encode the peptide core of the extracellular proteoglycan of rat L2 yolk sac tumor cells and the intracellular proteoglycan of rat basophilic leukemia (RBL)-1 cells. In order to determine if the predicted amino acid sequences of these proteoglycans are identical as well as to isolate a full length cDNA encoding a rat secretory granule proteoglycan, a cDNA library was prepared from RBL-1 cells and screened with the 165-base pair 5'----XmnI fragment of pPG-1, a partial cDNA which encodes the rat L2 cell proteoglycan peptide core. Based on the consensus nucleotide sequence of two full length RBL-1 cell-derived cDNAs, the 5' untranslated region of the mRNA that is expressed in RBL-1 cells is shorter than that expressed in the rat L2 cells although the coding regions of the mRNAs from the two cell types are identical. These findings indicate that the targeting of proteoglycans to an intracellular or extracellular compartment is a cell-specific event which is independent of the translated peptide core. Since the RBL-1 cell and the rat L2 cell proteoglycans have different types of glycosaminoglycans bound to them, it can also be concluded that the selection of the type of glycosaminoglycan that will be synthesized onto a peptide core is a cell-specific event which is not exclusively dependent on the translated peptide core. When the predicted amino acid sequence of the RBL-1 cell proteoglycan peptide core was compared to the predicted sequence of the homologous human molecule from HL-60 cells, 48% of the amino acids were identical. The N terminus was the most highly conserved area of the molecule. This region of the peptide core, which precedes the serine-glycine repeat region, is likely to be of critical importance for the biosynthesis and/or function of these proteoglycans. Analysis of 10 different mouse/hamster somatic cell hybrid lines with a SspI----3' fragment of the rat L2 cell cDNA revealed that, as in the human, the gene that encodes the mouse analogue of this peptide core resides on chromosome 10.