An empowerment model of workplace support following disclosure, for people with MS.

BACKGROUND: Vocational interventions aimed at increasing job retention for people with multiple sclerosis (MS) are reliant upon a partnership with a supportive work environment. A better understanding of the types of psychosocial support that are most conducive to retaining employees' sense of work-efficacy will enhance the success of interventions aimed at reducing workplace barriers to job maintenance. OBJECTIVE: The objective of this study is to identify the types of psychosocial support that people with MS require post-disclosure, in order to maintain their employment status. In particular, we examined the roles of psychological safety and work-efficacy. METHODS: We interviewed 40 employees with MS either individually (n = 25) or within three focus groups (n = 15). These interviews were audio-taped and the content analysed, using an inductive thematic approach. RESULTS: Themes to emerge in organisational responses to disclosure were: a focus on ability (leading to enhanced perceptions of psychological safety and higher work-efficacy) and on disability (leading to diminished psychological safety and reduced perceptions of work-efficacy). CONCLUSION: Organisational responses to disclosure demonstrating trust and inclusive decision making, and focussing on employee abilities, enhance perceptions of psychological safety at work. This increases the likelihood that employees with MS will retain their sense of work-efficacy and reduce their intentions to leave.

Disclosure of diagnosis of multiple sclerosis in the workplace positively affects employment status and job tenure.

BACKGROUND: For many employees with multiple sclerosis (MS), disclosure of their diagnosis at work is seen as a high-risk strategy that might lead to diminished perceptions of their capabilities by supervisors and colleagues, if not outright discrimination. The consequence of this mistrust surrounding the disclosure process is that employees with MS may leave it until too late to effectively manage symptoms at work. OBJECTIVE: The objective of this paper is to statistically evaluate the relationship between disclosure of diagnosis at work and maintenance of employment. METHODS: Three annual, large-sample self-report surveys of MS patients prospectively examined the relationship between disclosure of diagnosis at work and employment status. A total of 1438 people responded to all three surveys. Of employed persons in 2010 (n = 946), 673 also responded to the 2012 survey. Of these 673 respondents 564 were still employed. RESULTS: People who had disclosed their MS status to an employer were more likely to remain in employment in Year 3. The effect of disclosure in predicting employment status remained after controlling for age, gender, hours worked and level of disability. CONCLUSION: This study provides the first empirical support for the positive role of disclosure in maintaining employment status, measured both as job retention and tenure in current employment.

Non-viral chimeric antigen receptor (CAR) T cells going viral.

Chimeric antigen receptor (CAR) T cell therapy has made significant strides in the treatment of B-cell malignancies, but its application in treating solid tumors still poses significant challenges. Particularly, the widespread use of viral vectors to deliver CAR transgenes into T cells comes with limitations, including high costs and regulatory restrictions, which hinder the translation of novel genetic engineering concepts into clinical applications. Non-viral methods, such as transposon/transposase and clustered regularly interspaced short palindromic repeats (CRISPR)/Cas systems, offer promising alternatives for stable transgene insertion in CAR-T cells. These methods offer the potential to increase accessibility and efficiency in the development and delivery of CAR-T cell therapies. The main challenge in using non-viral methods, however, is their low knock-in efficiency, which leads to low transgene expression levels. In this review, we discuss recent developments in non-viral approaches for CAR-T cell production, the manufacturing requirements for clinical-grade production of non-viral CAR-T cells, and the adjustments needed in quality control for proper characterization of genomic features and evaluation of potential genotoxicity.

Exercise therapy and recovery after SCI: evidence that shows early intervention improves recovery of function.

STUDY DESIGN: This was designed as an experimental study. OBJECTIVES: Locomotor training is one of the most effective strategies currently available for facilitating recovery of function after an incomplete spinal cord injury (SCI). However, there is still controversy regarding the timing of treatment initiation for maximal recovery benefits. To address this issue, the present study compares the effects of exercise initiated in the acute and secondary phase of SCI. SETTING: Texas A&M University, College Station, TX, USA. METHODS: Rats received a moderate spinal contusion injury and began an exercise program 1 (D1-EX) or 8 days (D8-EX) later. They were individually placed into transparent exercise balls for 60 min per day, for 14 consecutive days. Control rats were placed in exercise balls that were rendered immobile. Motor and sensory recovery was assessed for 28 days after injury. RESULTS: The D1-EX rats recovered significantly more locomotor function (BBB scale) than controls and D8-EX rats. Moreover, analyses revealed that rats in the D8-EX group had significantly lower tactile reactivity thresholds compared with control and D1-EX rats, and symptoms of allodynia were not reversed by exercise. Rats in the D8-EX group also had significantly larger areas of damage across spinal sections caudal to the injury center compared with the D1-EX group. CONCLUSION: These results indicate that implementing an exercise regimen in the acute phase of SCI maximizes the potential for recovery of function.

The effect of group-based exercise on cognitive performance and mood in seniors residing in intermediate care and self-care retirement facilities: a randomised controlled trial.

OBJECTIVE: To determine the effect of a general group-based exercise programme on cognitive performance and mood among seniors without dementia living in retirement villages. DESIGN: Randomised controlled trial. SETTING: Four intermediate care and four self-care retirement village sites in Sydney, Australia. PARTICIPANTS: 154 seniors (19 men, 135 women; age range 62 to 95 years), who were residents of intermediate care and self-care retirement facilities. INTERVENTION: Participants were randomised to one of three experimental groups: (1) a general group-based exercise (GE) programme composed of resistance training and balance training exercises; (2) a flexibility exercise and relaxation technique (FR) programme; or (3) no-exercise control (NEC). The intervention groups (GE and FR) participated in 1-hour exercise classes twice a week for a total period of 6 months. MAIN OUTCOME MEASURES: Using standard neuropsychological tests, we assessed cognitive performance at baseline and at 6-month re-test in three domains: (1) fluid intelligence; (2) visual, verbal and working memory; and (3) executive functioning. We also assessed mood using the Geriatric Depression Scale (GDS) and the Positive and Negative Affect Schedule (PANAS). RESULTS: The GE programme significantly improved cognitive performance of fluid intelligence compared with FR or NEC. There were also significant improvements in the positive PANAS scale within both the GE and FR groups and an indication that the two exercise programmes reduced depression in those with initially high GDS scores. CONCLUSIONS: Our GE programme significantly improved cognitive performance of fluid intelligence in seniors residing in retirement villages compared with our FR programme and the NEC group. Furthermore, both group-based exercise programmes were beneficial for certain aspects of mood within the 6-month intervention period.

Abnormal T cell differentiation persists in patients with rheumatoid arthritis in clinical remission and predicts relapse.

OBJECTIVES: An abnormal CD4+ T cell subset related to inflammation exposure (inflammation-related cells, IRC) has been identified in rheumatoid arthritis (RA). Patients with inflammatory and non-inflammatory diseases were used to examine the relationship between inflammation and this T cell subset in vivo. METHODS: Blood was collected from healthy controls and patients with RA (active disease or in clinical remission), Crohn's disease and osteoarthritis. IRC and chemokine receptors were quantified by flow cytometry. Thymic activity and apoptotic factors were measured by real-time polymerase chain reaction. Circulating cytokines were measured by enzyme-linked immunosorbent assay. CXCR4 and SDF1 in synovial biopsies were measured using immunohistochemistry. RESULTS: IRC were identified in patients with RA (p<0.0001) and Crohn's disease (p = 0.005), but not in those with osteoarthritis. In RA in remission, IRC persisted (p<0.001). In remission, hyperproliferation of IRC was lost, chemokine receptor expression was significantly lowered (p<0.007), Bax expression dropped significantly (p<0.001) and was inversely correlated with IRC (rho = -0.755, p = 0.03). High IRC frequency in remission was associated with relapse within 18 months (OR = 6.4, p<0.001) and a regression model predicted 72% of relapse. CONCLUSIONS: These results suggest a model in which, despite the lack of systemic inflammation, IRC persist in remission, indicating that IRC are an acquired feature of RA. They have, however, lost their hyper-responsiveness, acquired a potential for survival, and no longer express chemokine receptors. IRC persistence in remission confirms their important role in chronic inflammation as circulating precursors of pathogenic cells. This was further demonstrated by much higher incidence of relapse in patients with high IRC frequency in remission.

Hemoglobin Savannah (B6(24) beta-glycine is greater than valine): an unstable variant causing anemia with inclusion bodies.

An abnormal hemoglobin, termed Hb Savannah, was found in red cell hemolysate of a young Caucasian girl with severe hemolytic anemia. The presence of this unstable variant became evident when inclusion bodies appeared rapidly upon exposure of red cells to redox dyes and a large percentage of hemoglobin in hemolysate precipitated on warming to 65 degrees C. Treatment of the hemoglobin with p-hydroxymercuribenzoate (PMB) caused a rapid dissociation into monomers; starch-gel electrophoresis of PMB-treated hemoglobin showed the presence of abnormal beta-chains. Data from structural studies of isolated beta-chains indicated substitution of a valyl residue for the normally occurring glycyl residue at position 24, which corresponds to helical residue B6. A similar substitution but with an arginine replacing the glycyl residue has been observed in Hb Riverdale-Bronx. The glycine to valine substitution will change the relationship of the B and the E helices which results in extensive conformational changes in the beta-chain. This change presumably causes an increased dissociation of the hemoglobin molecule into dimers and probably monomers, and a decreased stability of the alphabeta-dimers. The hemoglobin abnormality may be the result of a fresh mutation because the abnormality is not present in the parents nor in any of the seven siblings.

Shigatoxin encoding Bacteriophage ϕ24B modulates bacterial metabolism to raise antimicrobial tolerance.

How temperate bacteriophages play a role in microbial infection and disease progression is not fully understood. They do this in part by carrying genes that promote positive evolutionary selection for the lysogen. Using Biolog phenotype microarrays and comparative metabolite profiling we demonstrate the impact of the well-characterised Shiga toxin-prophage ϕ24B on its Escherichia coli host MC1061. As a lysogen, the prophage alters the bacterial physiology by increasing the rates of respiration and cell proliferation. This is the first reported study detailing phage-mediated control of the E. coli biotin and fatty acid synthesis that is rate limiting to cell growth. Through ϕ24B conversion the lysogen also gains increased antimicrobial tolerance to chloroxylenol and 8-hydroxyquinoline. Distinct metabolite profiles discriminate between MC1061 and the ϕ24B lysogen in standard culture, and when treated with 2 antimicrobials. This is also the first reported use of metabolite profiling to characterise the physiological impact of lysogeny under antimicrobial pressure. We propose that temperate phages do not need to carry antimicrobial resistance genes to play a significant role in tolerance to antimicrobials.

Accumulation and salvage of adenosine and inosine by isolated mature cardiac myocytes.

Reoxygenation of ischaemic, energy-depleted heart does not result in sufficiently rapid regeneration of normal adenine nucleotide concentrations for preservation of cardiac function and structure. Salvage of nucleoside as a mechanism for restoration of ATP in the post-ischaemic myocardium is limited by efflux of adenosine during ischaemia. Isolated cardiac myocytes have been used to establish the kinetics of uptake and salvage of adenosine and inosine, measuring the distribution of radioactive nucleoside incorporated into ATP, ADP and AMP. Maximum rates of catalysis of reactions on the salvage pathway, and of enzymes competing for substrates on the pathway, have been established in myocyte extracts. Myocytes have little capacity to salvage or catabolise inosine. Enzyme measurements indicate that salvage of adenosine should proceed at 7-8-times the rate exhibited by intact myocytes dependent upon extracellular adenosine as substrate. The data indicate that the rate of transport of adenosine is not determined by its metabolic utilization, but is the rate-limiting step in the salvage of adenosine.

5'-Nucleotidase activity of isolated mature rat cardiac myocytes.

Specific location of 5'-nucleotidase in the heart has been uncertain, some authors citing evidence for an exclusively non-myocyte location, while other data point to the existence of cytoplasmic and membrane-bound fractions. Single myocytes isolated from mature rat heart, and free of endothelial or interstitial cells, have been used to establish that muscle cells of the myocardium are rich in 5'-nucleotidase, exhibiting activity sufficient to account for the total myocardial content of this enzyme. All 5'-nucleotidase is accessible to extracellular AMP. Inhibitors of 5'-nucleotidase and adenosine transport have been used to establish that only the adenosine component of adenine nucleotides is taken up by myocytes, but hydrolysis of AMP by 5'-nucleotidase does not commit the adenosine formed to transport across the sarcolemmal membrane. Myocytes also have ecto-phosphatases which hydrolyse ADP and ATP.

Metabolism and salvage of adenine and hypoxanthine by myocytes isolated from mature rat heart.

Adenine and hypoxanthine can be utilised by cardiac muscle cells as substrates for the synthesis of ATP. A possible therapeutic advantage of these compounds as high-energy precursors is their lack of vasoactive properties. Myocytes isolated from mature rat heart have been used to establish in kinetic detail the capacity of the heart to incorporate adenine, hypoxanthine and ribose into cellular nucleotides. Maximum rates of catalysis by enzymes on the salvage pathways have been established. Whilst the rate of incorporation of adenine into the ATP pool appears to depend upon intracellular concentrations of adenine and phosphoribosylpyrophosphate, for hypoxanthine the pattern is more complex. Hypoxanthine is salvaged at a slow rate compared with adenine, and is incorporated into GTP and IMP as well as into adenine nucleotides. The rate of incorporation of hypoxanthine into both IMP and ATP is accelerated in myocytes incubated with ribose. However, the rate-limiting reaction appears to be that catalysed by adenylosuccinate synthetase, for the rate of ATP synthesis is not accelerated when hypoxanthine concentration is increased from 10 to 50 microM, while the rate of IMP synthesis is more than doubled. Adenine and hypoxanthine phosphoribosyl transferases are present in equal catalytic amounts, but rat cardiac myocytes have very little adenylosuccinate synthetase activity. Exogenous ribose is incorporated into adenine nucleotides in amounts equimolar with adenine or hypoxanthine.

Salvage mechanisms for regeneration of adenosine triphosphate in rat cardiac myocytes.

Since mitochondrial oxidative phosphorylation does not produce sufficient adenosine triphosphate for rapid restoration of contractile function in myocardium reoxygenated after ischaemia alternative non-oxidative routes by which purine nucleosides or bases may be used to increase the cytoplasmic adenine nucleotide pool were studied. Comparative rates of uptake and salvage of adenosine, adenine, and hypoxanthine were determined using myocytes isolated from adult rat heart. For each precursor reactions limiting the overall rate at which substrate in the extracellular fluid is incorporated into the intracellular adenosine triphosphate pool were identified. Adenosine was salvaged at twice the rate seen with adenine in the presence of ribose, whereas the rate of salvage of hypoxanthine, in the presence of ribose, was only 5% of that for adenosine. Adenine may be an advantageous substrate since high concentrations of adenine are not inhibitory to salvage and do not influence cardiac haemodynamics. Salvage of hypoxanthine appeared to be limited by the rate of adenylosuccinate synthetase, which was present at less than 1% of the adenylosuccinase rate in rat, rabbit, and beef heart. In addition, since salvage of bases is dependent on the availability of phosphoribosylpyrophosphate rates of synthesis of phosphoribosylpyrophosphate were measured in whole myocytes from ribose and in cytoplasmic extracts from ribose and from ribose-5-phosphate. Metabolic sites were identified at which interventions designed to accelerate salvage rates might best be directed.

Lack of predictive indices in kernicterus: a comparison of clinical and pathologic factors in infants with or without kernicterus.

A review of 398 neonatal autopsies at Downstate Medical Center revealed 27 cases of kernicterus during the seven-year period from 1971 through 1977. With the current intensive care of the sick newborn, kernicterus continues to occur, mainly in premature infants with relatively low levels of serum bilirubin (mean of 11.5 mg/100 ml). To understand the factors contributing to the development of kernicterus, clinical and pathologic findings in 27 infants with kernicterus were compared to 103 "control" infants with retrospectively. Birth weight, gestational age, sex, and Apgar scores were comparable in both groups. The duration of survival was significantly shorter in infants with kernicterus than in the control infants. The clinical signs and symptoms of kernicterus were nonspecific and the premortem diagnosis of kernicterus was not suspected in most of the cases. There were no significant differences in the peak serum bilirubin values, incidence of hypothermia, hypoglycemia, convulsions, anemia, infection, use of phototherapy, transfusion and exchange transfusion in the two groups. Serum albumin values and bilirubin binding capacity measured by 2-(4-hydroxybenzeneazo)benzoic acid were significantly lower in the kernicteric group although the bilirubin-albumin molar ratio was equal in both groups. The incidences of severe acidosis and hypoxic encephalopathy were significantly higher in the kernicteric infants. In this study, acidosis, hypoxia, hypoalbuminemia, and low bilirubin binding capacity were seen more often in kernicteric infants than in control infants. However, analysis of previously suggested risk factors failed to identify any single factor or combination of factors which could be predictive to the development of kernicterus.

A rapid fluorometric method for determining bilirubin levels and binding in the blood of neonates: comparisons with a diazo method and with 2-(4'-hydroxybenzene)azobenzoic acid dye binding.

A simple, rapid fluorometric method for determining the albumin-bound bilirubin concentration, total blood bilirubin concentration, and the bilirubin reserve-binding capacity of albumin was clinically evaluated using blood specimens from 79 neonates. This study showed that these bilirubin determinations, made by means of the Bell Laboratories hematofluorometer, correlated well with plasma bilirubin levels obtained by a diazotization (Jendrassik-Grof) method. Hematofluorometer reserve-binding capacities correlated very well with 2-(4'-hydroxybenzene)azobenzoic acid (HABA) dye reserve-binding capacities for specimens of artificially jaundiced adult blood. For specimens of neonatal blood the HABA dye reserve capacity was, on the average, higher than the hematofluorometer reserve-binding capacity, particularly for specimens from low-birth-weight babies (less than 2,000 gm). Comparison of HABA reserve capacity and hematofluorometer reserve capacity for high-birth-weight babies (greater than 2,000 gm) gave data very similar to those for adult blood specimens. The specific bilirubin-binding capacity of albumin was found to be greater for infants whose birth weight exceeded 2,000 gm than for the lower birth weight group. The total blood bilirubin concentration obtained by the hematofluorometer is shown to be significantly higher than the concentration of bilirubin bound to albumin, an indication of other important compartments of bilirubin in blood.

Oesophageal atresia, related malformations, and medical problems: a family study.

Oesophageal atresia (OA) and tracheo-oesophageal fistula (TOF) are life-threatening malformations of generally undefined cause. Previous reports of familial cases suggest a genetic contribution. The pattern of inheritance appears non-Mendelian, i.e., multifactorial. Individuals with OA/TOF often have other malformations and medical problems. The aim of this study was to determine the association in OA/TOF cases and healthy control subjects of associated malformations, midline defects, and medical conditions. We also investigate the relationships of these conditions in the relatives of the cases and controls. The results show that infants with OA/TOF frequently have VACTERL anomalies (vertebral, 17%; anal, 12%; cardiac, 20%; renal, 16%; limb, 10%) and other midline defects (cleft lip and palate, 2%; sacral dysgenesis, 2%; urogenital anomalies, 5%). The following medical problems were also reported: oesophageal dysmotility, 21%; gastro-oesophageal reflux, 22%; chest infections, 6%; and autonomic dysfunction, 0.5%. The first-degree relatives of children with OA are much more likely to have one of the aforementioned malformations or medical conditions when compared with the control group: one or more VACTERL anomalies (P < 0.01), gastro-oesophageal reflux (P < 0.05), recurrent respiratory infections (P < 0.05), and autonomic dysfunction (P < 0.001). The more distant relatives also show an increased incidence of such problems although in this case the data must be viewed with caution. The results confirm that the associated malformations and related medical problems occur significantly more frequently in the relatives of individuals with OA/TOF. These families may prove valuable for linkage analysis in an attempt to determine the genetics of OA/TOF.

The influence of infant and maternal sickle cell disease on birth outcome and neonatal course.

OBJECTIVE: To compare the influence of maternal hemoglobin phenotype as well as that of the infant on birth outcome and neonatal complications. RESEARCH DESIGN: Prospective, natural history study with retrospective chart review for neonatal complications. SETTING: Nineteen pediatric sickle cell centers across the United States. PATIENTS: Four hundred eighty infants with sickle cell disease (SCD) who were enrolled in the Cooperative Study of Sickle Cell Disease at less than 6 months of age, as well as a comparison cohort of 118 infants with sickle cell trait born to women with sickle cell anemia in the Cooperative Study. RESULTS: In the SCD cohort, overall rates of preterm (< 37 weeks), low-birth-weight (< 2500 g), and small-for-gestational age births were 9%, 10%, and 8%, respectively; no significant differences were found according to infant hemoglobin phenotype. Term births accounted for 59% of the infants with low birth weight, significantly higher than the 41% US rate for black low-birth-weight infants (P = .014). Expectant mothers with sickle cell anemia are 2.5 times more likely to bear newborns who are small for gestational age than are women with other types of sickle cell disease, sickle trait, or C-trait. The most common prepartum and neonatal complications in infants with SCD were jaundice (25%), fetal distress (13%), anemia (10%), and respiratory distress (6%). Complication rates did not differ significantly by hemoglobin phenotype in the infants with SCD, but infants born to women with sickle cell anemia had higher rates of jaundice (P < .0001). CONCLUSIONS: Rates of adverse birth outcomes and neonatal complications in infants with SCD are similar to the rates for normal infants, although preterm birth accounts for fewer of the low-birth-weight outcomes among newborns with SCD relative to US black newborns. The hemoglobin phenotype of infants with SCD does not influence birth outcome and neonatal course, but infants born to women with sickle cell anemia are at greater risk of preterm birth, low birth weight, being small for gestational age, and neonatal jaundice.

Reference values and hematologic changes from birth to 5 years in patients with sickle cell disease. Cooperative Study of Sickle Cell Disease.

OBJECTIVE: To examine hematologic changes from birth to 5 years of age and establish hematologic reference values for infants and children with sickle cell disease. RESEARCH DESIGN: Prospective natural history study. SETTING: Nineteen pediatric sickle cell centers across the United States. PATIENTS: Six hundred ninety-four infants with sickle cell disease (sickle cell anemia, sickle cell-hemoglobin C disease, and sickle-beta-thalassemia) who were enrolled in the Cooperative Study of Sickle Cell Disease at younger than 6 months of age. Median follow-up time through 5 years of age was 4.1 years. MEASUREMENTS AND RESULTS: We present longitudinal analyses of total hemoglobin concentration, percent fetal hemoglobin values, mean corpuscular volumes, total bilirubin concentration, and red blood cell (RBC), "pocked" RBC, white blood cell, platelet, and reticulocyte counts. Anemia was apparent by 10 weeks of life in infants with sickle cell anemia (SS infants). This anemia was associated with a rising reticulocyte count consistent with a hemolytic process. The reticulocyte count of SS infants increased steadily, exceeding 12% at 5 years of age. The fetal hemoglobin concentration of SS infants declined more slowly than that of infants with sickle cell hemoglobin C disease (SC infants). Pocked RBC counts rose sharply after 6 months of age, and by 1 year, 28% of SS infants had abnormal counts, above 3.5%, indicating poor splenic function. At 3 years of age, 78% of SS patients and 32% of SC patients had abnormal pocked RBC counts. The SS patients with concurrent alpha-thalassemia had, after 6 months of age and throughout early childhood, a slightly higher mean total hemoglobin concentration and lower mean pocked RBC and reticulocyte counts than SS patients without alpha-thalassemia. The hematologic profile of SC infants more closely resembled that of normal black infants, but there was mild anemia (10.5 g/dL) and slightly elevated mean values for reticulocytes (3%) and fetal hemoglobin (3%) during early childhood.

Pregnancy in sickle cell disease: experience of the Cooperative Study of Sickle Cell Disease.

OBJECTIVE: To determine the maternal and fetal outcomes of pregnancy in women with sickle cell disease. METHODS: The subjects were part of a cohort recruited from 19 centers for a prospective study of the clinical course of sickle cell disease. Each participant was evaluated using a structured protocol in which steady-state data and information on both sickle- and non-sickle-related events were collected. The rates of antepartum and intrapartum complications were tallied for pregnancies carried to delivery. Fetal outcome was assessed according to gestational age, birth weight, and Apgar score. Differences among genotypes in event rates were assessed using Fisher exact test. Differences in gestational age and birth weight, and predictors of these outcomes, were assessed using analyses of covariance. RESULTS: Two hundred eighty-six of the 445 reported pregnancies proceeded to delivery. Non-sickle-related antepartum and intrapartum complication rates were comparable with those of African-American women who did not have sickle cell disease. One of the two deaths observed during this study was directly related to the presence of sickle cell disease. Rates of maternal morbidity from sickle cell disease were the same during pregnancy as during the nonpregnant state. Ninety-nine percent of those pregnancies carried to delivery resulted in a live birth. Twenty-one percent of the infants born to women of the SS genotype were small for gestational age (SGA). Preeclampsia and acute anemic events were identified as risk factors for SGA infants. CONCLUSIONS: Those caring for women with sickle cell disease should support them if they desire to have children.