Breastfeedilzg Support Services in the Neonutd Intensive-Care Unit

Objective: To describe a model for providing breastfeeding support in the neonatal intensive-care unit (NICU).
Design: Naturalistic, participant observation.
Setting: Suburban Level III NICU.
Patients: One hundred thirty-two mother-infant pairs over 1 year. Infants were hospitalized In the NICU, and mothers had initiated lactation efforts.
Interventions: Investigators provided breastfeeding interventions for the mother-infant pairs, based on identified problems, the research literature, or both.
Main Outcome Measures: Percentage of mothers who were breastfeeding at the time of discharge from the NICU.
Results: Interventions were classified into jive categories: expression and collection of mothers' milk, gavage feeding of expressed mothers' milk, in-hospital breastfeeding sessions, postdischarge breastfeeding management, and additional consultation.
Conclusions: This model was effective In preventing breastfeeding failure for this population. The model can provide the basis for NICU breastfeeding standards of care, protocols, and chart records, or for reimbursement purposes. The model also provides a framework for studying a specific category or breastfeeding intervention.     

The Encapsulation of Squid Diisopropylphosphorofluoridate-Hydrolyzing Enzyme within Mouse Erythrocytes

This study describes the entrapment of squid-type diisopropylphosphorofluoridate-hydrolyzingenzyme (DFPase) within mouse red blood cells. These erythrocytesthereby gain the ability to rapidly hydrolyze alkylphosphatecholinesterase (ChE) inhibitors such as diisopropyl fluorophosphate(DFP). DFPase rapidly hydrolyzes DFP to diisopropyl phosphate.Resealed erythrocytes provide a stable carrier system that canpreserve the activity of encapsulated enzymes against otherwiserapid in vivo degradation; thus, ChE inhibitors can be degradedto relatively nontoxic metabolites by these erythrocyte carriers.Squid DFPase was purified from the hepatopancreas of Atlanticsquid and DFPase activity was determined by measuring changesin fluoride ion concentration using a fluoride ion selectiveelectrode. Mouse erythrocytes in suspension with excess squidDFPase were dialyzed against hypotonic buffer to allow the encapsulationof the enzyme to occur. Cells were then resealed by returningthe suspension to isosmotic with saline. Rate of DFP hydrolysisobserved with these cells was much greater than the rate ofnonenzymatic hydrolysis and was directly proportional to theamount of the erythrocyte suspension added to the assay solution.The rate of hydrolysis was first order in substrate. Erythrocytecontrols showed no endogenous DFPase activity. These resultssuggest that enzyme entrapment may be developed as a methodto prevent and antagonize organophosphate poisoning.     

Addiction versus stages of change models in predicting smoking cessation

Prospective data from the California Tobacco Surveys (n=2066) were used to perform a critical test of the Prochaska et al. (1991) stages of change model. When the stages of change model was used as a stand alone predictor, smokers in preparation at baseline were more likely to be in cessation at follow-up than smokers in pre-contemplation at baseline (OR adj="1.9)" When stage membership was combined with baseline measures of addiction including smoking behaviors and quitting history, it was not a significant predictor of future cessation. A prediction equation that combined daily vs. occasional smoking, cigarettes per day smoked, life-time quits of at least a year, and quits of more than 5 days in the previous year discriminated smokers in cessation at follow-up of 1 to 2 years better than did the stages of change model. The area under the ROC curve for the equation based on addiction measures was 69.3% vs. 55.1% for the stages of change. Cessation rates ranged from 7.7% to 35.7% for the four-category addiction equation compared with 15.1% to 24.9% for stages of change model.     

Polychlorinated Biphenyl Congeners in Adipose Tissue Lipid and Serum of Past and Present Transformer Repair Workers and a Comparison Group

Polychlorinated Biphenyl Congeners in Adipose Tissue Lipid andSerum of Past and Present Transformer Repair Workers and a ComparisonGroup. FAIT, A., GROSSMAN, E., SELF, S., JEFFRIES, J., PELLIZZARI,E. D., AND EMMETT, E. A. (1989). Fundam. Appl. Toxicol 12, 42-55. The concentrations of individual PCB's were determined inboth serum and adipose tissue lipid from 35 transformer repairworkers currently exposed to PCBs, mainly Aroclor 1260, 17 previoustransformer repair workers, and 56 comparison workers neveroccupationally exposed to PCBs. The analysis used fused-silicacapillary gas chromatography with electron capture detector(FSCGC/ECD) and FSCGC with negative ion chemical ionizationmass spectrometry to verify PCB congener levels. Eighty-ninePCB peaks were identified and confirmed. More congeners weredetected in adipose tissue. In serum approximately 50% of peakswere below the level of detection. Statistical techniques toaccount for left and interval censoring allowed comparison ofconcentration distributions even where data were incomplete.We found that unquantifiable levels were unlikely to contributesubstantially to the true values for total [PCBs] over and beyondthe contribution of the measured values. However, the totalserum [PCBs] determined by FSCGC/ECD greatly exceeded that fromstandard packed cell gas chromatography (PCGC/ECD). The underestimationwas less marked for adipose samples. In serum the total [PCBs]was highest in currently exposed workers and lowest in unexposedworkers, with past-exposed workers clearly intermediate. Inadipose tissue [PCBs] in the currently exposed group was muchhigher than in the other two groups, in whom the distributionof results was broadly similar. In all worker groups hexachlorinatedand heptachlorinated species predominated followed by octachlorinatedand pentachlorinated. The relative distribution of individualPCB congeners in the three groups was similar although the amountsvaried. The seven major peaks in serum and adipose tissue were2,3,5,6,3',4',5'/2,3,4,5,2',4',5' hepta-CB; 2,3,4,2',3',5' hexa-CB;2,4,6,3',4',5'/ 2,4,5,2',4',5'/2,3,4,5,2',5' hexa-CB; 2,3,4,5,2',3',4'hepta-CB; 2,3,4,5,2',3',5',6'/2,3,4,5,6,2',3',5', octa-CB; 2,4,5,3',4',/3,4,5,2',3'penta-CB; and 2,3,4,2',3',4'/2,3,5,6,2',4',5'/2,3,4,5,2',4',6'multi-CB. The distribution of PCB peaks in our populations differsfrom that in capacitor workers (exposed to less highly chlorinatedPCBs) and from Yu-Cheng patients suggesting differing toxicpotentials from PCBs in these three circumstances.     

Differences between human and mouse alpha‐fetoprotein expression during early development

Alpha‐fetoprotein (AFP) is the major serum protein during development. AFP is one of the earliest proteins to be synthesised by the embryonic liver. The synthesis of AFP decreases dramatically after birth and only trace amounts are expressed in the adult liver. The tissue distribution of AFP in early human embryogenesis has not been defined. We have studied the expression pattern of AFP mRNA in human and mouse embryos by in situ hybridisation. In humans, AFP is expressed in the hepatic diverticulum at 26 d postovulation as it differentiates from the foregut endoderm (i.e. in the most primitive hepatocytes). It is also expressed in the endoderm of the gastrointestinal tract and in the yolk sac at this age. AFP is subsequently expressed in the mesonephros and transiently in the developing pancreas. In the mouse, no expression of AFP was observed in the mesonephros but other sites of expression were similar. Thus AFP has a distinct temporospatial expression pattern during the embryonic period and this differs between human and mouse species. It is interesting that AFP is expressed by tumours such as primitive gastrointestinal, renal cell and pancreatic tumours as well as those of hepatocyte origin. This distribution reflects the sites of AFP expression during development.     

Linkage relationships between the three phosphoglucomutase loci PGM1, PGM2 and PGM3

1. Phosphoglucomutase phenotypes have been studied in several generations of the family of an individual heterozygous at each of the three loci, PGM₁, PGM₂, and PGM₃. 2. PGM₁ and PGM₂ phenotypes were determined using red cells. Fibroblasts grown in tissue culture were used for PGM₃ phenotyping. 3. The family results support the genetical hypothesis based on the analysis of dizygotic twin pairs that the PGM₃ isozyme patterns found in the placenta are determined by two alleles, PGM¹₃ and PGM²₃. 4. Locus PGM₃ is not closely linked to locus PGM₂ 5. The data also support the previous findings that locus PGM₁ is not closely linked to PGM₂ or PGM₃.     

Separation of the Toxic and Glutathione-Enhancing Effects of the Naturally Occuring Nitrile, Cyanohydroxybutene

Cyanohydroxybutene (CHB) is reported to be hepatotoxic in maleFischer 344 rats at an oral dose of 300 mg/kg and, while nolonger hepatotoxic, pancreatotoxic at 200 mg/kg. In addition,the 200 mg/kg dose causes a persistent elevation in hepaticand pancreatic glutathione (GSH). This study was conducted tode termine if smaller doses of CHB could cause GSH elevationin the absence of toxicity. A single oral dose of 100 mg/kgor multiple lower doses (50 mg/kg daily for 3 days or 30 mg/kgfor 6 days) caused a significant and persistent increase inpancreatic GSH, although hepatic levels were unchanged. Tenmilligrams per kilogram, even daily for 24 days, was withouteffect on hepatic or pancreatic GSH. Neither a single oral doseof 100 mg/kg nor multiple lower doses were associated with toxicity.However, when either 100 or 50 mg/kg were administered intravenously,pancreatic apoptosis was observed. In animals dosed with 100mg/kg iv, mixed histiocytic and suppurative inflammation andfrank pancreatic necrosis also developed and were associatedwith elevated plasma lipase and amylase. The animals receivingCHB intravenously also exhibited elevated GSH levels in bothpancreas and liver. This study shows that oral doses between30 and 100 mg CHB/kg can be used to elevate GSH levels withoutany pancreatotoxicity. However, a single 50 mg CHB/kg dose givenintravenously causes apoptosis, while 100 mg/kg causes severepancreatotoxicity with necrosis.     

Molecular detection of t(8;21)/AML1-ETO in AML M1/M2: correlation with cytogenetics,morphology and immunophenotype

The t(8;21) identifies a subgroup of acute myeloid leukaemia (AML) with a relatively good prognosis which may merit different treatment. It is associated predominantly, but not exclusively, with AML M2, and corresponds to rearrangements involving the AML1 and ETO genes. AML1-ETO positive, t(8;21) negative cases are well recognized but their incidence is unknown. In order to determine optimal prospective AML1-ETO RT-PCR screening strategies, we analysed 64 unselected AML M1 and M2 cases and correlated the results with other biological parameters. Molecular screening increased the overall detection rate from 8% to 14%. AML1-ETO was found in 3% (1/32) of AML M1 and 25% (8/32) of M2, including three patients without a classic t(8;21) but with chromosome 8 abnormalities. It was more common in younger patients. Correlation with morphology enabled development of a scoring system which detected all nine AML1-ETO-positive cases with a false positive rate of 7% (4/55). Although certain AML1-ETO-positive cases demonstrated characteristic immunological features (CD19 and CD34 expression, CD33 negativity), each of these markers was insufficiently specific to permit prediction in an individual case. We conclude that initial routine prospective molecular screening for AML1-ETO in all AMLs, combined with standardized morphological and immunological analysis, is desirable in order to produce improved prognostic stratification and to determine whether screening can ultimately be restricted to appropriate subgroups.