The role of smoking status on postoperative complications and survival in lung cancer patients presenting to M.D. Anderson Cancer Center

It is estimated that 50% of all lung cancer patients continue to smoke after diagnosis. Many of these lung cancer patients who are current smokers often experience tremendous guilt and responsibility for their disease, and feel it might be too late for them to quit smoking. In addition, many oncologists may be heard to say that it is 'too late', 'it doesn't matter', 'it is too difficult', 'it is too stressful' for their patients to stop smoking, or they never identify the smoking status of the patient. Many oncologists feel unprepared to address smoking cessation as part of their clinical practice. In reality, physicians can have tremendous effects on motivating patients, particularly when patients are initially being diagnosed with cancer. More information is needed to convince patients to quit smoking and to encourage clinicians to assist patients with their smoking cessation. ^ In this current study, smoking status at time of lung cancer diagnosis was assessed to examine its impact on complications and survival, after exploring the reliability of smoking data that is self-reported. Logistic Regression was used to determine the risks of smoking prior to lung resection. In addition, survival analysis was performed to examine the impact of smoking on survival. ^ The reliability of how patients report their smoking status was high, but there was some discordance between current smokers and recent quitters. In addition, we found that cigarette pack-year history and duration of smoking cessation were directly related to the rate of a pulmonary complication. In regards to survival, we found that current smoking at time of lung cancer diagnosis was an independent predictor of early stage lung cancer. This evidence supports the idea that it is "never too late" for patients to quit smoking and health care providers should incorporate smoking status regularly into their clinical practice.^

The role of cardiorespiratory fitness and weight status on 24-hr ambulatory blood pressure among adolescents

BACKGROUND: This observational research study investigated the association of cardiorespiratory fitness and weight status with repeated measures of 24-hr ambulatory blood pressure (24-hr ABP). Little is known about these associations and few data exist examining the interaction between cardiorespiratory fitness and weight status and the contributions of each on 24-hr ABP in youth. ^ METHODS: This research study used secondary analysis data from the "Adolescent Blood Pressure and Anger: Ethnic Differences" study. This current study sample included 374 African-American, Anglo-American, and Mexican-American adolescents 11-16 years of age. Mixed-effects models were used for testing the relationship between weight status and cardiorespiratory fitness and repeated measures of ambulatory blood pressure over 24 hours (24-hr ABP). Weight status was categorized into "normal weight" (BMI<85th percentile), "overweight" (85th≤BMI<95th), and "obese" (BMI≥95th). Cardiorespiratory fitness, determined by heart rate recovery (HRR), was defined as the difference between heart rate at peak exercise and heart rate at two minutes post-exercise, as measured by a height-adjusted step test and stratified into two groups: low and high fitness, using a median split. Ambulatory blood pressure (ABP) was monitored for a 24-hr period on a school day using the Spacelabs ambulatory monitor (Model 90207). Blood pressure and heart rate were recorded at 30 minute intervals throughout the day of recording and at 60 minute intervals during sleep. ^ RESULTS: No significant associations were found between weight status and mean 24-hr systolic blood pressure (SBP) or mean arterial pressure (MAP). A significant and inverse association between weight status and mean 24-hr diastolic blood pressure (DBP) was revealed. Cardiorespiratory fitness was significantly and inversely associated with mean 24-hr ABP. High fitness adolescents had significantly lower mean 24-hr SPB, DBP, and MAP measurements than low fitness adolescents. Compared to low fitness adolescents, high fitness adolescents had 1.90 mmHg, 1.16 mmHg, and 1.68 mmHg lower mean 24-hr SBP, DBP, and MAP, respectively. Additionally, high fitness appeared to afford protection from higher mean 24-hr SBP and MAP, irrespective of weight status. Among normal weight adolescents, low fitness resulted in higher mean 24-hr SBP and MAP, compared to their fit counterparts. Among adolescents categorized as high fitness, increasing weight status did not appear to result in higher mean 24-hr SBP or MAP. Cardiorespiratory fitness, rather than weight status, appeared to be a more dominant predictor of mean 24-hr SBP and MAP. ^ CONCLUSIONS: To our knowledge, this research is the first study to investigate the independent and combined contributions of cardiorespiratory fitness and weight status on 24-hr ABP, all objectively measured. The results of this study may potentially guide and inform future research. It appears that early cardiovascular disease (CVD) prevention should focus on improving cardiorespiratory fitness levels among all adolescents, particularly those adolescents least fit, regardless of their weight status, while obesity prevention efforts continue.^

Defining the role of IL-15 trans-presentation by distinct cell-types during the development and homeostasis of Natural Killer and invariant Natural Killer T cells

The immuno-regulatory functions displayed by NK and iNKT cells have highlighted their importance as key lymphocytes involved in innate and adaptive immunity. Therefore, understanding the dynamics influencing the generation of NK and iNKT cells is extremely important. IL-15 has been shown to provide a critical signal throughout the development and homeostasis of NK and iNKT cells; however, the cellular source of IL-15 has remained unclear. In this investigation, I provide evidence that the cell-type providing IL-15 to NK and iNKT cells via trans-presentation is determined by the tissue site and the maturation status of NK and iNKT cells. For NK cells, I revealed the non-hematopoietic compartment provides IL-15 to NK cells in the early stages of development while hematopoietic cells were crucial for the generation and maintenance of mature NK cells. Regarding iNKT cells in the thymus, IL-15 trans-presentation by non-hematopoietic cells was crucial for the survival of mature iNKT cells. In the liver, both hematopoietic and non-hematopoietic compartments provided IL-15 to both immature and mature iNKT cells. This IL-15 signal helped mediate the survival and proliferation of both NK and iNKT cells as well as induce the functional maturation of mature iNKT cells via enhanced T-bet expression. In conclusion, my work illustrates an important notion that the immunological niche of NK and iNKT cells is tightly regulated and that this regulation is meticulously influenced by the tissue microenvironment.

Human Trafficking: What is the Role of the Health Care Provider?

The article will address the global and local issue of human trafficking. An estimated 20,000 people are trafficked within the U.S. each year. Trafficked people are forced, defrauded and coerced into labor and sexual service for profit of others. Traffickers use individual vulnerabilities and immigration status, language ability and poor understanding of U.S. laws to identify future victims. One case in 2005 in Texas resulted in 100 victims being identified, none of whom revealed themselves to health care professionals. Health care professionals need contemporary and updated information and resources about health risks, screening methods, and identification of trafficked persons. Readers will learn about common medical problems experienced by individuals who are leaving trafficking situations. Legal and health care intersections will be explored. Implementation of a response protocol to assist those who may currently be enslaved will be introduced. Real case examples from trafficking survivors will be presented and discussed. Participants will learn how to reach out, look beneath the surface, provide assistance, and access resources to help victims, and gain a better understanding of the health challenges faced by trafficked victims.

ROLE OF GSH METABOLISM IN MEDIATING STROMAL-LEUKEMIA INTERACTION AND PROMOTING CELL SURVIVAL AND DRUG RESISTANCE IN CHRONIC LYMPHOCYTIC LEUKEMIA

Chronic lymphocytic leukemia (CLL) is the most common adult leukemia in the western countries. The interaction between CLL cells and the bone marrow stromal environment is thought to play a major role in promoting the leukemia cell survival and drug resistance. My dissertation works proved a novel biochemical mechanism by which the bone marrow stromal cells exert a profound influence on the redox status of primary CLL cells and enhance their ability to sustain oxidative stress and drug treatment. Fresh leukemia cells isolated from the peripheral blood of CLL patients exhibited two major redox alterations when they were cultured alone: a significant decrease in cellular glutathione (GSH) and an increase in basal ROS levels. However, when cultured in the presence of bone marrow stromal cells, CLL cells restored their redox balance with an increased synthesis of GSH, a decrease in spontaneous apoptosis, and an improved cell survival. Further study showed that CLL cells were under intrinsic ROS stress and highly dependent on GSH for survival, and that the bone marrow stromal cells promoted GSH synthesis in CLL cells through a novel biochemical mechanism. Cysteine is a limiting substrate for GSH synthesis and is chemically unstable. Cells normally obtain cysteine by uptaking the more stable and abundant precursor cystine from the tissue environment and convert it to cysteine intracellularly. I showed that CLL cells had limited ability to take up extracellular cystine for GSH synthesis due to their low expression of the transporter Xc-, but had normal ability to uptake cysteine. In the co-culture system, the bone marrow stromal cells effectively took up cystine and reduced it to cysteine for secretion into the tissue microenvironment to be taken up by CLL cells for GSH synthesis. The elevated GSH in CLL cells in the presence of bone marrow stromal cells significantly protected the leukemia cells from stress-induced apoptosis, and rendered them resistant to standard therapeutic agents such as fludarabine and oxaliplatin. Importantly, disabling of this protective mechanism by depletion of cellular GSH using a pharmacological approach potently sensitized CLL cells to drug treatment, and effectively enhanced the cytotoxic action of fludarabine and oxaliplatin against CLL in the presence of stromal cells. This study reveals a key biochemical mechanism of leukemia-stromal cells interaction, and identifies a new therapeutic strategy to overcome drug resistance in vivo.

THE ROLE OF E2F1 IN THE RESPONSE TO DNA DOUBLE STRAND BREAKS

The importance of E2F transcription factors in the processes of proliferation and apoptosis are well established. E2F1, but not other E2F family members, is also phosphorylated and stabilized in response to various forms of DNA damage to regulate the expression of cell cycle and pro-apoptotic genes. E2F1 also relocalizes and forms foci at sites of DNA double-strand breaks but the function of E2F1 at sites of damage is still unknown. Here I reveal that E2F1 deficiency leads to increased spontaneous DNA break and impaired recovery following exposure to ionizing radiation. In response to DNA double-strand breaks, NBS1 phosphorylation and foci formation are defective in cells lacking E2F1, but NBS1 expression levels are unaffected. Moreover, it was observed that an association between NBS1 and E2F1 is increased in response to DNA damage, suggesting that E2F1 may promote NBS1 foci formation through a direct or indirect interaction at sites of DNA breaks. E2F1 deficient cells also display impaired foci formation of RPA and Rad51, which suggests a defect in DNA end resection and formation of single-stranded DNA at DNA double-strand breaks. I also found E2F1 status affects foci formation of the histone acetyltransferase GCN5 in response to DNA double-strand breaks. E2F1 is phosphorylated at serine 31 (serine 29 in mouse) by the ATM kinase as part of the DNA damage response. To investigate the importance of this event, our lab developed an E2F1 serine 29 mutant mouse model. I find that E2F1 serine 29 mutant cells show loss of E2F1 foci formation in response to DNA double-strand breaks. Furthermore, DNA repair and NBS1 foci formation are impaired in E2f1S29A/S29A cells. Taken together, my results indicate novel roles for E2F1 in the DNA damage response, which may directly promote DNA repair and genome maintenance.

Familial aggregation, candidate genes and genome scans: Analyzing the role of genetics in stroke

The genetic etiology of stroke likely reflects the influence of multiple loci with small effects, each modulating different pathophysiological processes. This research project utilized three analytical strategies to address the paucity of information related to the identification and characterization of genetic variation associated with stroke in the general population. ^ First, the general contribution of familial factors to stroke susceptibility was evaluated in a population-based sample of unrelated individuals. Increased risk of subclinical cerebral infarction was observed among individuals with a positive parental history of stroke. This association did not appear to be mediated by established stroke risk factors, specifically blood pressure levels or hypertension status. ^ The need to identify specific gene variation associated with stroke in the general population was addressed by evaluating seven candidate gene polymorphisms in a population-based sample of unrelated individuals. Three polymorphisms were significantly associated with increased subclinical cerebral infarction or incident clinical ischemic stroke risk. These relationships include the G-protein β3 subunit 825C/T polymorphism and clinical stroke in Whites, the lipoprotein lipase S/X447 polymorphism and subclinical and clinical stroke in men, and the angiotensin I-converting enzyme Ins/Del polymorphism and subclinical stroke in White men. These associations did not appear to be obfuscated by the stroke risk factors adjusted for in the analysis models specifically blood pressure levels or anti-hypertensive medication use. ^ The final research strategy considered, on a genome-wide scale, the idea that genetic variation may contribute to the occurrence of hypertension or stroke through a common etiologic pathway. Genomic regions were identified for which significant evidence of heterogeneity was observed among hypertensive sibpairs stratified by family history of stroke information. Regions identified on chromosome 15 in African Americans, and chromosome 13 in Whites and African Americans, suggest the presence of genes influencing hypertension and stroke susceptibility. ^ Insight into the role of genetics in stroke is useful for the potential early identification of individuals at increased risk for stroke and improved understanding of the etiology of the disease. The ultimate goal of these endeavors is to guide the development of therapeutic intervention and informed prevention to provide a lasting and positive impact on public health. ^

Pathways linking socioeconomic position and diabetes: The role of psychosocial factors

Despite increasing interest in the relationship between socioeconomic position (SEP) and health, there remains little understanding of the mechanisms through which SEP is related to chronic disease. This dissertation utilized data from 2,592 U.S. households in the 1995 telephone survey of the Aging, Status, and the Sense of Control study to: (1) investigate potential mediating factors in the association between educational level and prevalence of diabetes and (2) to investigate the association between the three major measures of SEP—income, education, and occupation—and the prevalence of diabetes. Regression analyses were conducted to examine the degree to which sense of personal control and social support mediate the association between level of educational attainment and diabetes and to examine the contribution of each of the SEP measures to diabetes. After adjusting for age, obesity, sex, and race, respondents with less than a high school education had greater odds of having diabetes than those with a college degree or higher level of educational attainment, although the corresponding confidence interval contained the null value (OR = 1.2, 95% CI: 0.7, 2.0). Neither sense of control nor social support significantly mediated the association between education and diabetes. However, sense of control was associated with diabetes status (OR = 0.7, 95% CI: 0.5, 1.0). Compared with income and education, employment status was the most strongly associated measure of SEP with diabetes prevalence. After adjusting for age, obesity, sex, and race, respondents who were unable to work due to disability had fourfold greater odds of having diabetes than those who were employed full time (OR = 4.0; 95% CI: 1.9, 8.3). Adding income and/or education to the model did not improve the fit. Understanding the impact of socioeconomic factors on diabetes requires consideration of multiple measures of SEP as well as the psychosocial pathways through which SEP may influence diabetes. ^

The association of area socioeconomic status and cancer screening: A systematic review and multilevel study

Background. The gap between actual and ideal rates of routine cancer screening in the U.S., particularly for colorectal cancer screening (CRCS) (1;2), is responsible for an unnecessary burden of morbidity and mortality, particularly for disadvantaged groups. Knowledge about the effects of individual and area influences is being advanced by a growing body of research that has examined the association of area socioeconomic status (SES) and cancer screening after controlling for individual SES. The findings from this emerging and heterogeneous research in the cancer screening literature have been mixed. Moreover, multilevel studies in this area have not yet adequately explored the possibility of differential associations by population subgroup, despite some evidence suggesting gender-specific effects. ^ Objectives and methods. This dissertation reports on a systematic review of studies on the association of area SES and cancer screening and a multilevel study of the association between area SES and CRCS. The specific aims of the systematic review are to: (1) describe the study designs, constructs, methods, and measures; (2) describe the association of area SES and cancer screening; and (3) identify neglected areas of research. ^ The empiric study linked a pooled sample of respondents aged ≥50 years without a personal history of colorectal cancer from the 2003 and 2005 California Health Interview Surveys with a comprehensive set of census-tract level area SES measures from the 2000 U.S. Census. Two-level random intercept models were used to test 2 hypotheses: (1) area SES will be associated with adherence to two modalities of CRCS after controlling for individual SES; and (2) gender will moderate the relationship between area socioeconomic status and adherence to both modalities of CRCS. ^ Results. The systematic review identified 19 eligible studies that demonstrated variability in study designs, methods, constructs, and measures. The majority of tested associations were either not statistically significant or significant and in the positive direction, indicating that as area SES increased, the odds of CRCS increased. The multilevel study demonstrated that while multiple aspects of area SES were associated with CRCS after controlling for individual SES, associations differed by screening modality and in the case of endoscopy, they also differed by gender. ^ Conclusions. Conceptual and methodologic heterogeneity and weaknesses in the literature to date limit definitive conclusions about the underlying relationships between area SES and cancer screening. The multilevel study provided partial support for both hypotheses. Future research should continue to explore the role of gender as a moderating influence with the aim of identifying the mechanisms linking area SES and cancer prevention behaviors. ^

The socioeconomic status of families of hyperglycemic versus non-hyperglycemic children: A descriptive analysis

The proportion of children and adolescents living with type 2 diabetes mellitus (DM) is rising at an alarming rate. Studies have shown that poor dietary choices and sedentary behaviors account for progression of some of the most prevalent diseases in America, including obesity, heart disease and diabetes. Other studies have shown that genetics plays a role in the diabetic determination of an individual, although not very common. What are some of the differentiating factors between elevated and non-elevated fasting capillary glucose (FCG) levels in children of similar ages, knowing they spend a majority of their lives at home or at school? Why are some children acquiring diabetes while others are not? This study utilized an IRB-approved Family Demographic Survey to determine gender, family income, parent education levels, sedentary practices, and household size. Only those families who gave consent to take part in the study received a questionnaire. The statistical results were used to test the hypothesis that children living with elevated FCG levels are more likely to descend from families with lower incomes, and lower levels of education.^ With regard to household income and FCG status of non-hyperglycemic and hyperglycemic children (Table 4b), there are 10.4% more hyperglycemic children in the lower income bracket than non-hyperglycemic children in the same income bracket.^ With regard to maternal education and FCG status (Table 5b), there are 7.0% more hyperglycemic children in the high school or less maternal educational attainment level than non-hyperglycemic children in the same maternal educational level. The Pearson correlation of maternal education and FCG status showed a negative correlation value of -.035 (Table 5d). The higher the occurrence of hyperglycemia in a child, the lower the maternal educational status is. Household size ranges and averages are nearly identical in families of both hyperglycemic and non-hyperglycemic children. ^

Role of telomere dysfunction, DNA damage response and p53 mutations in tumorigenesis and aging

The ends of eukaryotic chromosomes are protected by specialized ribonucleoprotein structures termed telomeres. Telomeres protect chromosomes from end-to-end fusions, inappropriate repair and degradation. Disruption of this complex activates an ATM/ATR DNA damage response (DDR) pathway. One component of the complex is the Protection Of Telomeres 1 (POT1) protein, an evolutionarily conserved protein which binds single-stranded 3' overhang and is required for both chromosomal end protection and telomere length regulation. The mouse contains two POT1 orthologs, Pot1a and Pot1b. Here we show that both proteins colocalize with telomeres through interaction with the adapter protein TPP1. In addition, compared to Pot1a, the OB-folds of Pot1b possess less sequence specificity for telomeres. Disruption of POT1 proteins result in telomere dysfunction and activation of an ATR-dependent DDR at telomeres, suggesting that this response is normally suppressed by POT1 binding to the single-stranded G-overhang. ^ Telomeres are maintained by telomerase, and its absence in somatic cells results in telomere progressive loss that triggers the activation of p53. Telomere dysfunction initiates genomic instability and induces both p53-dependent replicative senescence and apoptosis to suppress tumorigenesis. In the absence of functional p53, this genomic instability promotes cancer. It was previously not known which aspect of the p53 dependent DNA damage response is important to suppress tumorigenesis initiated by dysfunctional telomeres. The p53R172P knock-in mouse, which is unable to induce apoptosis but retains intact cell cycle arrest/cellular senescence pathways, allowed us to examine whether p53-dependent apoptosis is a major tumor suppression pathway initiated in the setting of telomere dysfunction. Spontaneous tumorigenesis remains potently suppressed in late generation telomerase null mice possessing the p53P/P mutation. These results suggest that suppression of spontaneous tumorigenesis initiated by dysfunctional telomeres requires activation of a p53-dependent senescence pathway. In addition, we used another knock-in mouse model with a p53R172H (p53H) point mutation to test the hypothesis that telomere dysfunction promotes chromosomal instability and accelerates the onset of tumorigenesis in vivo in the setting of this most common gain-of-function mutation in the human Li Fraumeni cancer syndrome. We unexpectedly observed that telomerase null mice possessing dysfunctional telomeres in the setting of the p53H/+ mutation develop significantly fewer tumors, die prematurely and exhibit higher level of cellular senescence, apoptosis and elevated genomic instability compared to telomerase intact p53H/+ and telomerase null p53+/+ mice. These contrasting results thus link cancer and aging to the functional status of telomeres and the integrity of the p53 pathway. ^

Household risk factors and the health and nutritional status of children in rural Honduras

During this cross-sectional study, both quantitative and qualitative research methods were used to elucidate the role that household environment and sanitation play in the nutritional status of children in a rural Honduran community. Anthropometric measurements were taken as measures of nutritional status among children under five years of age, while interviews regarding the household environment were conducted with their primary caregivers. Community participatory activities were conducted with primary caregivers, and results from water quality testing were analyzed for E. coli contamination. Anthropometric results were compared using the 1977 NCHS Growth Charts and the 2006 WHO Child Growth Standard to examine the implications of using the new WHO standard. The references showed generally good or excellent agreement between z-score categories, except among height-for-age classifications for males 24-35.9 months and weight-for-age classifications for males older than 24 months. Comparing the proportion of stunted, underweight, and wasted children, using the WHO standard generally resulted in higher proportions of stunting, lower underweight proportions, and higher overweight proportions. Logistic regression was used to determine which household and sanitation factors most influenced the growth of children. Results suggest only having water from a spring, stream, or other type of surface water as the primary source of drinking water is a significant risk factor for stunting. A protective association was seen between the household wealth index and stunting. Through participatory activities, the community provided insight on health issues important for improving child health. These activities yielded findings to be harnessed as a powerful resource to unify efforts for change. The qualitative findings were triangulated with the quantitative interview and water testing results to provide intervention recommendations for the community and its primary health care clinic. Recommendations include educating the community on best water consumption practices and encouraging the completion of at least some primary education for primary caregivers to improve child health. It is recommended that a community health worker program be developed to support and implement community interventions to improve water use and household sanitation behaviors and to encourage the involvement of the community in targeting and guiding successful interventions. ^

Social support, health status and health services utilization among the noninstitutionalized elderly: An analysis of the Supplement on Aging to the 1984 national health interview survey

The association between Social Support, Health Status, and Health Services Utilization of the elderly, was explored based on the analysis of data from the Supplement on Aging to the National Health Interview Survey, 1984 (N = 11,497) using a modified framework of Aday and Andersen's Expanded Behavioral Model. The results suggested that Social Support as operationalized in this study was an independent determinant of the use of health services. The quantity of social activities and the use of community services were the two most consistent determinants across different types of health services use.^ The effects of social support on the use of health services were broken down into three components to facilitate explanations of the mechanisms through which social support operated. The Predisposing and Enabling component of Social Support had independent, although not uniform, effects on the use of health services. Only slight substitute effects of social support were detected. These included the substitution of the use of senior centers for longer stay in the hospital and the substitution of help with IADL problems for the use of formal home care services.^ The effect of financial support on the use of health services was found to be different for middle and low income populations. This differential effect was also found for the presence of intimate networks, the frequencies of interaction with children and the perceived availability of support among urban/rural, male/female and white/non-white subgroups.^ The study also suggested that the selection of appropriate Health Status measures should be based on the type of Health Services Utilization in which a researcher is interested. The level of physical function limitation and role activity limitation were the two most consistent predictors of the volume of physician visits, number of hospital days, and average length of stay in the hospital during the past year.^ Some alternative hypotheses were also raised and evaluated, when possible. The impacts of the complex sample design, the reliability and validity of the measures and other limitations of this analysis were also discussed. Finally, a revised framework was proposed and discussed based on the analysis. Some policy implications and suggestions for future study were also presented. ^

Role of {\it Mycobacterium avium-intracellulare\/} complex infection in AIDS mortality

Disseminated MAC (dMAC) is the third most prevalent opportunistic infection in AIDS patients. In order to understand the role MAC infection plays in affecting survival of AIDS patients, a cohort of 203 suspected dMAC veterans seen at the Houston Veterans Affairs Medical Center between August 14, 1987 and December 31, 1991 were analyzed. The criteria for suspected dMAC infection was HIV+ men having a CD4+ level $\le$200 cells/mm$\sp3,$ on zidovudine treatment $\ge$1 month and who had any of the following: (a) a confirmed respiratory MAC infection, (b) fever $\ge$101$\sp\circ\rm F$ for $\ge$48 hours, (c) unexplained weight loss of 10 lbs or $\ge$10% BW over 3 months or (d) Hgb $\le$7.5 g/dl or decrease in Hgb $\ge$3.0 g/dl, while on 500-600 mg/day AZT. The study was conducted before the commencement of an effective MAC anti-mycobacterial therapy, so the true course of MAC infection was seen without the confounder of a therapeutic regimen. Kaplan-Meier and Cox regression survival analysis was used to compare 45 MAC culture positive and 118 MAC culture negative veterans. The 1 year survival rate of veterans with documented dMAC infection was 0.37 compared to 0.50 for veterans not acquiring dMAC infection. Significant differences between subgroups were also seen with the variables: PCP prophylaxis, the AIDS indicator disease Candida esophagitis, CD4+ lymphocyte level, CD4 percent lymphocyte level, WBC level, Hgb and Hct levels. Using multivariate modeling, it was determined that PCP prophylaxis (RR = 6.12, CI 2.24-16.68) was a predictor of survival and both CD4% lymphocytes $\le$6.0% (RR = 0.33, CI 0.17-0.68) and WBC level $\le$3000 cells/mm$\sp3$ (RR = 0.60, CI 0.39-0.93) were predictors of mortality. CD4+ level $\le$50 cells/mm$\sp3$ was not a significant predictor of mortality. Although MAC culture status was a significant predictor of mortality in the univariate model, a positive dMAC culture was not a significant predictor of AIDS mortality in the multivariate model. A positive dMAC culture, however, did affect mortality in a stratified analysis when baseline laboratory values were: CD8+ lymphocytes $>$600 cells/mm$\sp3,$ Hgb $>$11.0 g/dl, Hct $>$31.0% and WBC level $>$3000 cells/mm$\sp3.$ ^

Health status of Saudi women, the case of Yanbu al-Sinaiya

Detailed data on the health status of Saudi women are lacking. This cross sectional study attempts to provide a comprehensive description of the health status of Saudi females between the ages of 15-45 residing in Yanbu Al-Siniyah. The purpose is to assess women's needs for health services. The health status indicators are chronic tracer conditions, reported symptoms and multidimensional functioning levels. The generic functioning instrument of the Medical Outcome Study was used to estimate physical, social, and role functioning; degree of pain and health perceptions. The information was obtained by interviewing subjects and abstracting facts from their medical records. The results show functioning scores are in the "well health" range for physical, social, role and pain. Crowding and education have an equal or stronger effect of reducing functioning levels than the diagnosed tracer conditions. The highest prevalence conditions having a definite functional impact and diagnosed adequately in primary care are anemia, urinary tract infection, hemorrhoids, rheumatoid arthritis, caries and gingivitis. Reported symptoms strongly reducing function levels in this study are dyspnea, heart pain, incontinence, eye and skin problems, and joint ache. The impact of the reliability and validity of the measures used and other limitations of the results are discussed. Finally, some policy implications and suggestions for future study are presented. ^