Biomedical subjects

Christopher A Loffredo

Publications and source records attributed to Christopher A Loffredo.

17 recordsLinked to original sources

PubMed2022

Insights on the pathogenesis of type 2 diabetes as revealed by signature genomic classifiers in an African American population in the Washington, DC area.

AIMS: African Americans (AA) in the United States have a high risk of type 2 diabetes mellitus (T2DM) and suffer from disparities in the prevalence, mortality, and comorbidities of the disease compared to other Americans. The present study aimed to shed light on the molecular mechanisms of disease pathogenesis of T2DM among AA in the Washington, DC region. METHODS: We performed TaqMan Low Density Arrays (TLDA) on 24 genes of interest that belong to three categories: metabolic disease and disorders, cancer-related genes, and neurobehavioural disorders genes. The 18 genes, viz. ARNT, CYP2D6, IL6, INSR, RRAD, SLC2A2 (metabolic disease and disorders), APC, BCL2, CSNK1D, MYC, SOD2, TP53 (Cancer-related), APBA1, APBB2, APOC1, APOE, GSK3B, and NAE1 (neurobehavioural disorders), were differentially expressed in T2DM participants compared to controls. RESULTS: Our results suggest that factors including gender, smoking habits, and the severity or lack of control of T2DM (as indicated by HbA1c levels) were significantly associated with differential gene expression. APBA1 was significantly (p-value <0.05) downregulated in all diabetes participants. Upregulation of APOE and CYP2D6 genes and downregulation of the INSR gene were observed in the majority of diabetes patients. CONCLUSIONS: Tobacco smoking and gender were significantly associated with case-control differences in expression of the APBA1 and APOE genes (connected with Alzheimer's disease) and the INSR and CYP2D6 (associated with metabolic disorders). The results highlight the need for more effective management of T2DM and for tobacco smoking cessation interventions in this community, and further research on the associations of T2DM with other disease processes, including cancer and neurobehavioral pathways.

Humans↗

PubMed2007

Behavioral risk factors among Black and White women newly diagnosed with breast cancer.

BACKGROUND: To determine the rates of three behavioral risk factors (depression symptoms, smoking, and drinking) among women newly diagnosed with breast cancer and to examine if the rates under investigation differed between Black and White women. METHOD: Subjects were 147 women (47% Black, 53% White) newly diagnosed with breast cancer and participating in an epidemiologic interview study conducted at two metropolitan area cancer centers in the same city. The epidemiologic interview included women's tobacco, alcohol, and drug use history, medical and family history, and depression symptoms. RESULTS: Among all women in the sample, 33% reported clinically significant depression symptoms, 10% currently smoked cigarettes, and 57% currently drank alcohol. Seventy percent of women reported experiencing one or more behavioral risk factors, and White women were more likely than Black women to do so. After controlling for other demographic variables, White women were 50% more likely to report clinical symptoms of depression (odds ratio=1.55, 95% confidence interval=1.03, 2.30) and over two times more likely to report being current drinkers (odds ratio=2.19, 95% confidence interval=1.45, 3.30) than were Black women (p<0.05). CONCLUSIONS: The results suggest that certain behaviors of Black women may be associated with lower levels of self-reported distress. These findings also suggest the need for further research to examine behavioral comorbidity among women with breast cancer, and the roles that race, ethnicity, and culture may play in their expression.

Adult↗

PubMed2006

Enrichment of low molecular weight fraction of serum for MS analysis of peptides associated with hepatocellular carcinoma.

A challenging aspect of biomarker discovery in serum is the interference of abundant proteins with identification of disease-related proteins and peptides. This study describes enrichment of serum by denaturing ultrafiltration, which enables an efficient profiling and identification of peptides up to 5 kDa. We consistently detect several hundred peptide-peaks in MALDI-TOF and SELDI-TOF spectra of enriched serum. The sample preparation is fast and reproducible with an average CV for all 276 peaks in the MALDI-TOF spectrum of 11%. Compared to unenriched serum, the number of peaks in enriched spectra is 4 times higher at an S/N ratio of 5 and 20 times higher at an S/N ratio of 10. To demonstrate utility of the methods, we compared 20 enriched sera of patients with hepatocellular carcinoma (HCC) and 20 age-matched controls using MALDI-TOF. The comparison of 332 peaks at p < 0.001 identified 45 differentially abundant peaks that classified HCC with 90% accuracy in this small pilot study. Direct TOF/TOF sequencing of the most abundant peptide matches with high probability des-Ala-fibrinopeptide A. This study shows that enrichment of the low molecular weight fraction of serum facilitates an efficient discovery of peptides that could serve as biomarkers for detection of HCC as well as other diseases.

Amino Acid Sequence↗

PubMed2006

On using a cancer center cancer registry to identify newly affected women eligible for hereditary breast cancer syndrome testing: practical considerations.

The goals of this research were to describe the process of identifying and recruiting individuals registered with a cancer center's cancer registry who were eligible to participate in cancer genetic research. This study specifically focused on younger women with personal and family cancer histories strongly suggestive of hereditary breast cancer syndromes, as determined by genetic counselor review. Of special interest was to determine the proportion of women from minority backgrounds who were (a) identifiable in this manner and (b) interested in genetic testing for hereditary breast cancer through a family cancer clinical research program. An initial query of the 292 cases of women newly affected with breast cancer and contained within the registry indicated that 124 met demographic eligibility criteria. The personal and family cancer histories of each of these women were then reviewed by a genetic counselor and the remaining, eligible patients (n = 31) were subsequently contacted by mail and telephone: approximately three-fifths (18/31) of these patients were White and two-fifths (13/31) were Black or of another racial background. Of the women who were sent one or more study-related mailings, 10% (3/31) were unreachable by telephone due to incorrect contact information, 32% (10/31) were reachable by telephone but unresponsive to messages left, 26% (8/31) had already participated in the family cancer program (i.e., were positive controls), 6% (2/31) were interested in participating in the program, 23% (7/31) were uninterested in participating in the program, and 3% (1/31) were later determined to be ineligible. Comparing the racial backgrounds of women who were either positive controls or interested in participating (i.e., "tester" category) to women who were either unreachable, nonresponsive, uninterested, or ineligible (i.e., "nontester" category), there was a nonsignificant trend for more non-White women to fall into the nontester than tester category, Fisher's Exact Test = .09. This work underscores practical steps in planning and carrying-out cancer genetic testing research among women newly affected with breast cancer and members of special populations. It also underscores the role that genetic counseling professionals play in this process.

Adult↗

PubMed2005

Less efficient g2-m checkpoint is associated with an increased risk of lung cancer in African Americans.

Cell cycle checkpoints play critical roles in the maintenance of genomic integrity. The inactivation of checkpoint genes by genetic and epigenetic mechanisms is frequent in all cancer types, as a less-efficient cell cycle control can lead to genetic instability and tumorigenesis. In an on-going case-control study consisting of 216 patients with non-small cell lung cancer, 226 population-based controls, and 114 hospital-based controls, we investigated the relationship of gamma-radiation-induced G2-M arrest and lung cancer risk. Peripheral blood lymphocytes were cultured for 90 hours, exposed to 1.0 Gy gamma-radiation, and harvested at 3 hours after gamma-radiation treatment. gamma-Radiation-induced G2-M arrest was measured as the percentage of mitotic cells in untreated cultures minus the percentage of mitotic cells in gamma-radiation-treated cultures from the same subject. The mean percentage of gamma-radiation-induced G2-M arrest was significantly lower in cases than in population controls (1.18 versus 1.44, P < 0.01) and hospital controls (1.18 versus 1.40, P = 0.01). When dichotomized at the 50th percentile value in combined controls (population and hospital controls), a lower level of gamma-radiation-induced G2-M arrest was associated with an increased risk of lung cancer among African Americans after adjusting for baseline mitotic index, age, gender, and pack-years of smoking [adjusted odd ratio (OR), 2.25; 95% confidence interval (95% CI), 0.97-5.20]. A significant trend of an increased risk of lung cancer with a decreased level of G2-M arrest was observed (P(trend) = 0.02) among African Americans, with a lowest-versus-highest quartile adjusted OR of 3.74 (95% CI, 0.98-14.3). This trend was most apparent among African American females (P(trend) < 0.01), with a lowest-versus-highest quartile adjusted OR of 11.75 (95% CI, 1.47-94.04). The results suggest that a less-efficient DNA damage-induced G2-M checkpoint is associated with an increased risk of lung cancer among African Americans. Interestingly, we observed a stronger association of DNA damage-induced G2-M arrest and lung cancer among African Americans when compared with Caucasians. If replicated, these results may provide clues to the exceedingly high lung cancer incidence experienced by African Americans.

Black or African American↗

PubMed2005

Analysis of mass spectral serum profiles for biomarker selection.

MOTIVATION: Mass spectrometric profiles of peptides and proteins obtained by current technologies are characterized by complex spectra, high dimensionality and substantial noise. These characteristics generate challenges in the discovery of proteins and protein-profiles that distinguish disease states, e.g. cancer patients from healthy individuals. We present low-level methods for the processing of mass spectral data and a machine learning method that combines support vector machines, with particle swarm optimization for biomarker selection. RESULTS: The proposed method identified mass points that achieved high prediction accuracy in distinguishing liver cancer patients from healthy individuals in SELDI-QqTOF profiles of serum. AVAILABILITY: MATLAB scripts to implement the methods described in this paper are available from the HWR's lab website http://lombardi.georgetown.edu/labpage

Algorithms↗

PubMed2005

Associations of pesticides, HCV, HBV, and hepatocellular carcinoma in Egypt.

The rate of hepatocellular carcinoma (HCC) is increasing in Egypt where the major risk factors are chronic infections with hepatitis B and C viruses (HBV and HCV). A major segment of the population is employed in agriculture, raising the possibility that exposure to pesticides is an additional risk factor for HCC. The objective of this study is to investigate pesticides as environmental risk factors for HCC while taking into account viral risk factors. We conducted a case-control study of 236 subjects with confirmed HCC recruited from the National Cancer Institute, Cairo University, Egypt, and 236 controls matched on sex, age group and urban-rural status recruited from orthopedic department, Cairo University Hospital, Egypt. Patients who agreed to participate signed a consent form, answered a questionnaire and gave a blood sample for hepatitis virus testing. The manuals of the Ministry of Agriculture for approved use and type of pesticides since 1965 were linked to the questionnaire data for types of crops and pests that the subject had to combat, to attribute specific pesticides that were used by each subject. Subjects also reported duration of the exposure (years). Case-control comparisons in these data were stratified by sex, age group, and urban vs. rural residence. Data were analyzed using unconditional logistic regression models adjusting for age, HCV RNA, and current hepatitis B infection. Among rural males, the adjusted odds ratio (OR) for organophosphorus compounds was 2.7 (95% CI = 1.3-5.3) and for carbamates it was 2.9 (95% CI = 1.4-5.8). No statistically significant associations between HCC and pesticides were observed for urban males or for females. As expected, the strongest risk factors for HCC in this study were HCV RNA (OR = 16-17) and current HBV infection (OR = 27-28). This study therefore suggests that exposures to organophophorus and carbamate pesticides are additive risk factors to current HCV and HBV infection among rural males. Future investigation should address the possible hepatocarcinogenicity of pesticides using biomarkers of exposure and other techniques to better estimate dose-response relationships.

Adult↗

PubMed2005

The role of the tumor necrosis factor (TNF)--Fas L and HCV in the development of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a major public health problem in Egypt due to the high prevalence of hepatitis C viral (HCV) infection. The mechanism by which HCV exerts its carcinogenic effect on the liver is not yet understood. Previous research has suggested that perturbations of the Fas-Fas L tumor necrosis system could result in uncontrolled cancerous cell growth in the liver. This study aims to assess the relationship of Fas ligand (Fas L) to HCC. A total of 28 cases (HCC) and 56 controls (28 cirrhosis and 28 chronic hepatitis) were included in the study. Sera and tissue biopsies were tested for HCV antibody and HCV-RNA. Fas ligand expression in tissue was examined immunohistochemically using a rabbit purified polyclonal antibody. Levels of soluble Fas L were determined in serum by ELISA. The HCC cases were graded as: 17.9% Grade I, 32.1% Grade II, 35.7% Grade III and 14.3% were Grade IV. Among the cases, 81% had evidence of cirrhosis. All the cases and controls were positive for HCV-RNA. Tissue and serum PCR results were identical within the same subjects. Fas ligand cytoplasmic expression was more pronounced in HCC than in cirrhosis, and in cirrhosis more than in chronic hepatitis. This expression was higher with increasing grades of malignancy and in tissues adjacent to the tumor, than in those without nearby tumor. Soluble Fas L levels were higher in cases than in controls, with similar results as that of immunohistochemical expression. These results suggest that HCV and Fas ligand play a key role in hepatocarcinogenesis, consistent with the hypothesis that HCV induces overexpression of Fas ligand in the liver cells, resulting in escape from killing by the immune system cells, with subsequent uncontrolled growth of tissue and the development of malignancy.

Adult↗

PubMed2005

Genetic and environmental influences on malformations of the cardiac outflow tract.

Congenital cardiovascular malformations are the most common form of birth defect recorded. Specific malformations of the outflow portions of the heart are termed conotruncal malformations and arise from the septation of the common conotruncus of the heart. There are multiple lines of evidence that point towards genetic-environmental interactions in the genesis of conotruncal congenital cardiovascular malformations. In particular, environmental exposures that involve vitamin A, retinol, folic acid or retinol receptors are identified as cardiac teratogens. Other environmental agents for which there is evidence of cardiac teratogenicity for outflow tract malformations include nitrofen, ambient air pollution, chlorinated hydrocarbons and pesticides. Genetic polymorphisms of xenobiotic metabolism are clearly differentiating in the effect of potential teratogens. Work in this field is at a new cusp, with the ability to measure xenobiotic exposure, document xenobiotic metabolizing genetic polymorphisms and integrate these data into models of cardiac teratogenesis.

Animals↗

PubMed2004

Case-control study of non-Hodgkin's lymphoma and hepatitis C virus infection in Egypt.

BACKGROUND: Chronic infection with hepatitis C virus (HCV) has been associated in some studies with increased risk for B-cell non-Hodgkin's lymphoma (NHL). To assess this further, we conducted a case-control study in Egypt, where HCV prevalence is extremely high. METHODS: Cases with B-cell NHL (N = 227) were recruited from the National Cancer Institute of Cairo University, a major referral centre. Controls (N = 227) were patients with fractures being treated at the Kasr El-Aini Orthopaedic Hospital, from the same referral base as the cases, and were frequency-matched by gender, rural versus urban birthplace, and age. Subjects were interviewed about their medical history and possible risk factors, and blood samples were collected for HCV diagnostic tests. Anti-HCV and HCV RNA were determined by enzyme-linked immunoassay and reverse transcription-polymerase chain reaction, respectively. Odds ratios (OR) and 95% CI were calculated from logistic regression models. RESULTS: Overall, 42% of subjects were anti-HCV positive and 33% had HCV RNA. There was a statistically significant unadjusted association of HCV RNA with NHL (OR = 2.3, 95% CI: 1.5, 3.5), which differed slightly by gender (males: OR = 2.1, 95% CI: 1.2, 3.7 versus females: OR = 2.5, 95% CI: 1.3, 4.8). Anti-HCV without HCV RNA was not associated with case status (OR = 0.9, 95% CI: 0.5, 1.6). After adjustment for age, gender, rural versus urban birthplace, and rural versus urban current residence, the association of HCV RNA with the risk of NHL remained statistically significant (OR = 2.9, 95% CI: 1.9, 4.5). CONCLUSIONS: These data support the hypothesis that NHL is a malignant outcome of chronic HCV infection.

Adult↗

PubMed2004

Prevalence of congenital cardiovascular malformations among relatives of infants with hypoplastic left heart, coarctation of the aorta, and d-transposition of the great arteries.

Cardiovascular malformations (CVM) are the most common birth defects and carry significant and lifelong personal and societal costs. Research into genetic and environmental risk factors is therefore critical in identifying clues to causation and prevention. The purpose of this study was to investigate patterns of familial aggregation in CVM, specifically among infants with left-sided obstructive heart defects. We ascertained families of probands with hypoplastic left heart (HLH: N = 38), coarctation of the aorta (CoA: N = 46), and d-transposition of the great arteries (dTGA: N = 22). First degree relatives had clinical examinations and echocardiograms; all other relatives had detailed reviews of medical records. A total of 2,694 relatives were included in the study: 379 1st degree, 986 2nd degree, and 1,329 3rd degree. Mean nuclear family size and sibship size were similar among the groups. CVM were detected more frequently in 1st degree relatives of probands with HLH (19.3%) or CoA (9.4%) than among dTGA families (2.7%). The proportions of affected 2nd degree relatives were similar across groups (</=1%). In 3rd degree relatives, CVM was detected in 1.8% of the HLH families compared to 1.2% in CoA and 0.4% in dTGA families. The predominant types of CVM among relatives of HLH and CoA probands were left-sided obstructive lesions, in 72% (21 of 29) and 67% (25 of 37) of the affected relatives, respectively. Familial aggregation of these types of CVM is therefore confirmed in this study, potentially facilitating the search for specific genetic and other risk factors in recurrent CVM.

Aortic Coarctation↗

PubMed2003

Population-based study of l-transposition of the great arteries: possible associations with environmental factors.

BACKGROUND: L-transposition of the great arteries (l-tga) is an uncommon congenital cardiovascular malformation that occurs from abnormal looping of the primitive cardiac tube. Little is known about risk factors for the development of l-tga. METHODS: This study is a case-control study of 36 cases of l-tga compared to 3,495 population-based live born infant controls in the Baltimore Washington Infant Study (1981-1989 births). Extensive personal and occupational exposure data from parental interviews were available for all subjects. A geographic information system was used to identify potential environmental exposures, for example, hazardous waste sites prioritized for cleanup (National Priority List sites). Adjusted odds ratios (OR) and 95% confidence intervals (CI) were calculated using exact parameter estimates from logistic regression. RESULTS: Most infants with l-tga had multiple cardiovascular anomalies, with single ventricle in 47%. Over 75% of all cases of l-tga occur in two regions of contiguous cases. Within these regions, the case control OR of l-tga are 13.4 (95% CI, 4.7-37.8) Both areas are characterized by release of toxic chemicals into air and by hazardous waste sites. Parental exposures to hair dye, smoking and laboratory chemicals are also associated with case status. CONCLUSIONS: L-tga, a congenital cardiovascular malformation due to very early abnormalities in embryogenesis, is associated strongly with residency in two small regions of Maryland and District of Columbia (DC), and with other parental personal or occupational exposures. Additional research is needed to identify the components of spatial and other associations that constitute etiologic risk factors.

Case-Control Studies↗

PubMed2003

Variability in human metabolism of arsenic.

Estimating the nature and extent of human cancer risks due to arsenic (As) in drinking water is currently of great concern, since millions of persons worldwide are exposed to arsenic, primarily through natural enrichment of drinking water drawn from deep wells. Humans metabolize and eliminate As through oxidative methylation and subsequent urinary excretion. While there is debate as to the role of methylation in activation/detoxification, variations in arsenic metabolism may affect individual risks of toxicity and carcinogenesis. Using data from three populations, from Mexico, China, and Chile, we have analyzed the distribution in urine of total arsenic and arsenic species (inorganic arsenic (InAs), monomethyl arsenic (MMA), and dimethyl arsenic (DMA). Data were analyzed in terms of the concentration of each species and by evaluating MMA:DMA and (MMA+DMA):InAs ratios. In all persons most urinary As was present as DMA. Male:female differences were discernible in both high- and low-exposure groups from all three populations, but the gender differences varied by populations. The data also indicated bimodal distributions in the ratios of DMA to InAs and to MMA. While the gene or genes responsible for arsenic methylation are still unknown, the results of our studies among the ethnic groups in this study are consistent with the presence of functional genetic polymorphisms in arsenic methylation leading to measurable differences in toxicity. This analysis highlights the need for continuing research on the health effects of As in humans using molecular epidemiologic methods.

Arsenic↗

PubMed2003

Bleomycin-induced chromosome breaks as a risk marker for lung cancer: a case-control study with population and hospital controls.

Environmental exposure to carcinogens and individual susceptibility play significant roles in cancer risk. Suboptimal DNA repair capability, measured by quantifying mutagen-induced chromosome breaks, might explain variable host susceptibility to environmental carcinogens. In an ongoing lung cancer case-control study, we compared individual sensitivity to bleomycin-induced chromosome breaks in 152 non-small cell lung cancer patients with 94 population controls and 85 hospital controls with no history of cancer. Mutagen sensitivity was measured by mean number of chromatid breaks per cell in cultured peripheral blood lymphocytes treated with bleomycin. Non-parametric tests and chi(2) tests were used to determine the statistical significance of the crude case-control comparisons, followed by logistic regression to adjust for important covariates. The mean number of bleomycin-induced breaks per cell was 1.01 for the cases compared with 0.86 for hospital controls (P < 0.01) and 0.89 for population controls (P < 0.01). The mean number of breaks per cell was 1.01 for those >65 years old and 0.81 for those < or = 65 years old (P < 0.01) among population controls. Defining bleomycin sensitive as >0.84 break/cell (the median level in population controls), 67% of the cases were bleomycin sensitive compared with 49% of the hospital controls [adjusted odds ratio (OR) = 2.69, 95% confidence interval (CI) = 1.44, 5.04], and 51% of the population controls (adjusted OR = 2.18, 95% CI = 1.13, 4.21). Our data indicate that the increased number of bleomycin-induced chromosome breaks was significantly associated with an increased risk of lung cancer in the first 331 subjects.

Aged↗

PubMed2002

Infants with single ventricle: a population-based epidemiological study.

BACKGROUND: Single ventricle, a rare congenital cardiac defect, often occurs as part of a complex group of cardiovascular abnormalities. Little is known of its epidemiologic associations. METHODS: Using data from the Baltimore-Washington Infant Study [BWIS], (1981-89), a population based case-control study of cardiovascular malformations, infants with single ventricle were evaluated with respect to infant and family characteristics and maternal and paternal exposures. The cases were analyzed according to presence/absence of abnormal cardio-visceral situs. Controls were 3,572 infants without heart defects randomly selected from the regional cohort of live births. Odds ratios and 95% confidence intervals were used as measures of association. RESULTS: Single ventricle occurred in 1.25% of infants with congenital cardiovascular defects in the BWIS. Fifty-five infants had single ventricle. In 48 families (87.3%) the parents were interviewed. Thirty-three infants had normal situs and 15 had abnormal situs. Paternal alcohol consumption (OR = 2.0, 95% CI 1.1-3.9) and paternal cigarette smoking (OR = 2.4, 95% CI 1.1-5.1) were associated with all cases of single ventricle. These associations were even stronger in the subset of infants with abnormal situs. Maternal history of a previous induced abortion was also associated with infants born with abnormal situs (OR = 3.2, 95% CI 1.1-11.5). Paternal marijuana use was associated with cases of single ventricle in normal situs (OR = 2.2, 95% CI 1.0-5.2). CONCLUSIONS: Potential risk factors included paternal smoking and alcohol consumption, highlighting the need for future studies to consider environmental factors in the pathogenesis of this cardiac defect.

Adult↗

PubMedDate not supplied

Fetal ADH2*3, maternal alcohol consumption, and fetal growth.

There is some evidence suggesting the allele for alcohol dehydrogenase 2*3 (ADH2*3) is associated with a protective effect against alcohol-related intrauterine growth retardation (IUGR). This study was conducted to explore the affect of the ADH2*3 allele on fetal growth. Bloodspots (n = 1016) belonging to individual infants of a subgroup of the Baltimore-Washington Infant Study (BWIS) were assayed for the presence of the ADH2*3 allele by a polymerase chain reaction (PCR)-based method. Infants genotyped for ADH2*3 were those for whom bloodspots were identified and obtained from the Maryland Newborn Screening Program. The effect of ADH2*3 and maternal alcohol consumption on intrauterine growth was explored by multivariable linear regression analysis. Twenty-six percent of the 306 blood spots belonging to African-American infants were positive for ADH2*3 (4% were homozygous and 22% were heterozygous). Only a small percentage of bloodspots for Caucasian (1.3%) were positive for the ADH2*3 allele. Consequently, further analysis concentrated on gene-exposure interactions for African-American infants. It was found that the incidence of being small-for-gestation-age (SGA) was lower for ADH2*3-positive infants (2.5% versus 8.8%; p = .08). SGA infants had elevated odds for being ADH2*3 negative (OR: 3.15, 95% C.I.: 0.70-14.26) and for being born to mothers that consumed alcohol during pregnancy (OR: 2.31, 95% C.I.: 0.77-6.91). A negative trend between maternal alcohol consumption and mean offspring birthweight was found; however, ADH2*3 did not have a significant impact on mean birthweight for infants born to mothers that drank during pregnancy. These results could be interpreted as possible support for the hypothesis that ADH2 genotype in the infant may impact risk for alcohol-related IUGR. However, this study has limitations in that it is a "nested study of convenience" and involves a relatively small number of infants born to mothers reporting moderate to heavy alcohol use during pregnancy.

Adult↗

PubMedDate not supplied

Evaluation of Papanicolaou stain for studying micronuclei in buccal cells under field conditions.

OBJECTIVE: To compare Papanicolaou (Pap) and May-Grünwald Giemsa (MGG) stain as 2 techniques for staining for buccal mucosal cells to detect micronuclei (MN) infield studies. STUDY DESIGN: Eighty cytologic smears (2 per individual) were taken from the buccal mucosa of 40 cigarette smokers recruited at a rural village in Egypt. Forty smears were stained with Pap stain and 40 with MGG stain. All were assessed for cellularity and scored for MN. RESULTS: Pap stain was faster and easier to process and transport in the field study than was MGG stain. Regarding MGG smears, bacteria and cell debris masked the MN as compared to Pap smears, in which the fixative destroyed the bacteria and made the cell boundaries clearly demarcated. Using Pap stain, MN were seen easily in transparent cytoplasm. CONCLUSION: Pap stain is the preferred method infield studies for scoring and detecting MN in cells of buccal mucosa.

Azure Stains↗