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Supercomputing centers are unique resources that aim to enable scientific knowledge discovery by employing large computational resources-the "Big Iron." Design, acquisition, installation, and management of the Big Iron are carefully planned and monitored. Because these Big Iron systems produce a tsunami of data, it's natural to colocate the visualization and analysis infrastructure. This infrastructure consists of hardware (Little Iron) and staff (Skinny Guys). Our collective experience suggests that design, acquisition, installation, and management of the Little Iron and Skinny Guys doesn't receive the same level of treatment as that of the Big Iron. This article explores the following questions about the Little Iron: How should we size the Little Iron to adequately support visualization and analysis of data coming off the Big Iron? What sort of capabilities must it have? Related questions concern the size of visualization support staff: How big should a visualization program be-that is, how many Skinny Guys should it have? What should the staff do? How much of the visualization should be provided as a support service, and how much should applications scientists be expected to do on their own?

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This study was designed to investigate the effects of maternal diabetes on glucose transporter expression and glucose transport activity in the human placenta. Syncytiotrophoblast microvillous and basal membranes were prepared from placental tissue obtained at term from pregestational diabetics (White class B) and gestational diabetics controlled either by diet alone (class A1) or by diet and insulin (class A2). These membranes were used to measure GLUT1 glucose transporter expression and D-glucose transport activity. Diabetic groups showed no differences in placental weights or neonatal birth weights compared to controls, although 8 of 25 diabetic fetuses were macrosomic. Glycemic control in the diabetics at term, as assessed by maternal glycosylated hemoglobin, was within normal limits. Basal membrane GLUT1 density was about 2-fold higher in all diabetic groups compared to that in controls, as measured by immunoblotting, whereas no changes were found for the microvillous membranes. D-Glucose uptake across the basal membrane was increased by 40% in the diabetic groups; no changes were observed for the microvillous membrane. These results demonstrate that diabetes causes an increase in basal membrane GLUT1 expression and activity that persists despite a lack of evidence for current or recent maternal hyperglycemia. This suggests the potential for an extended increase in transplacental glucose flux in the absence of maternal hyperglycemia, which may contribute to fetal macrosomia and the other consequences of diabetic pregnancy.

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Autoimmune polyglandular syndrome may complicate pregnancy and be confused with hyperemesis gravidarum as a cause of hypoglycemia and electrolyte imbalance in the first trimester of pregnancy. Autoimmune polyglandular syndromes are uncommon disorders characterized by the development and presentation of multiple endocrine and organ dysfunction. To our knowledge, we present the first case of an autoimmune polyglandular syndrome complicating pregnancy. A 26-year-old woman, gravida 5 para 3 at 12 weeks gestation, presented with hyperemesis and signs and symptoms consistent with adrenal insufficiency and hypothyroidism. Evaluation revealed autoimmune polyglandular syndrome type II. Autoimmune polyglandular syndromes are a myriad group of diseases characterized by polyglandular dysfunction. These syndromes should be kept in mind when dealing with pregnant patients presenting with hyperemesis and an electrolyte imbalance who do not improve with the usual treatment for hyperemesis. An endocrine dysfunction such as polyglandular syndrome may exist.

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Tuberculosis (TB) during pregnancy and in the perinatal period was once considered to be an infrequent event in the United States. After a decade of steady decline, however, the disease has begun a resurgence. According to the CDC, a 20% increase in the number of reported cases occurred between 1985 and 1992. The factors associated with this increase are the emergence of human immunodeficiency virus (HIV) infection, the development of drug-resistant organisms, substance abuse, homelessness, and immigration. Environmental factors promoting transmission can be found in overcrowded areas such as correctional facilities, nursing homes, hospitals, and migrant-worker camps. For a large number of medically underserved women, the obstetrician is the only interface with medical care, as most of these patients do not have primary-care providers. It is important, therefore, that health-care providers recognize the clinical symptoms of TB and follow the recognized guidelines for antenatal screening for TB because the omission of these steps can lead to potentially disastrous sequelae in the fetus and neonate.

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Though spinal and femoral measurements are typically preferred for evaluating skeletal density, an abundance of forearm data exists, primarily from single photon absorptiometry (SPA) devices. Most dual X-ray absorptiometry (DXA) scanners are capable of scanning the forearm and provide analysis tools to duplicate conventional SPA measurements. In this study, we have compared the radius density measurements from three commonly available densitometers: a Norland 278 SPA, a Lunar DPX-L, and a Hologic 1000/W. Radius bone mineral density (BMD) on the nondominant forearm was measured in 28 volunteers (21 women and 7 men) aged 24-78, with an average age of 51 +/- 17 years. Values were compared and regression relationships derived at corresponding measurement sites. SPA and DXA BMD values were found to be highly correlated (r = 0.99) with small standard errors (0.014 g/cm2-0.021 g/cm2), though significant absolute differences were observed at most measurement regions. Correlation slopes ranged from 0.85 to 1.04, with intercepts from 0.01 to 0.08 g/cm2. Using the resultant regression equations, SPA BMD values can be converted to DXA values with an expected error of roughly 3%. DXA BMD can also be interconverted between Lunar and Hologic with a similar expected error. In situations where this level of imprecision is acceptable, patient forearm measurements obtained on different systems can be interconverted.

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Idiotypes and antiidiotypes are thought to be important immune regulators and have provided clues for the origin and pathogenicity of autoantibodies. Many lupus and Sjögren's syndrome patients, as well as most neonatal lupus infants with congenital heart block or dermatitis, have antibodies to the ribonucleoprotein Ro/SSA, which is one of a group of RNA-protein autoantigens commonly found in human lupus sera. To characterize the fine specificity of anti-Ro/SSA antibodies, a rabbit antidiotypic serum was prepared against polyclonal affinity purified anti-Ro/SSA F(ab')2. The resulting antiidiotype, anti-Id-Rol, is specific for the F(ab')2 fraction of the anti-Ro/SSA immunogen and its binding to anti-Ro/SSA is inhibited by purified Ro/SSA. These data indicate that the Id-Rol epitope on anti-Ro/SSA is associated with the antigen binding site of these same antibodies. The Id-Rol idiotype was present by ELISA in 3 of 12 additional anti-Ro/SSA preparations from precipitin-positive donor sera and in anti-Ro/SSA from one normal donor with low level antibody. This is the first shared idiotype to be found in the human autoantibodies binding to this RNA-protein antigen. Idiotypic differences between anti-Ro/SSA autoantibodies have the potential to explain the variation in pathologic associations found in individuals who develop this autoantibody specificity.

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Subacute cutaneous lupus and neonatal lupus are closely associated with the presence of anti-Ro (SSA) autoantibodies, but there is no direct evidence establishing a role for anti-Ro (SSA) in these diseases. After parental injection into mice, IgG from sera containing anti-Ro (SSA) will bind human skin grafted onto the mice. To determine whether the antibody binding is due to anti-Ro (SSA), affinity-purified anti-Ro (SSA) and serum depleted of anti-Ro (SSA) were prepared. After injection into human skin-grafted mice, purified anti-Ro (SSA) antibodies bound an antigen in the human skin graft, while preabsorbing anti-Ro (SSA) serum with Ro (SSA) virtually abolished binding to the human skin graft. Moreover, the pattern of IgG deposition was primarily epidermal and was identical in the human skin-grafted mice injected with purified anti-Ro (SSA) when compared with that found in five patients with subacute lupus (four adults, one neonate). These data directly show that anti-Ro (SSA) antibodies bind to the skin, and support the hypothesis that anti-Ro (SSA) autoantibodies are involved in the disease process that produces subacute cutaneous lupus and neonatal lupus.

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The diagnosis of SLE is associated with an enlarging assortment of autoantibodies. The presence or absence of particular antibodies influences the confidence with which this diagnosis is made. It is the presence of autoantibodies and the deposit of immunoglobulin that has led to the general conclusion that lupus is an autoimmune disease.

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Available data support the idea that the neonatal lupus erythematosus syndrome results from an autoantibody produced in the mother and passed across the placenta to the fetus. Despite the evidence for the presence of the Ro(SSA) autoantigen both in the skin and heart and the almost universal presence of the Ro(SSA) autoantibody in mothers of infants with neonatal lupus, there are emerging data to suggest that La(SSB) and, rarely, nRNP antibodies play an important pathologic role in some cases of the neonatal lupus syndrome.

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We have applied a sensitive assay to analyze lupus and Sjögren's syndrome autoantibodies in 40 normal sera. Seven of these bound Ro/Sjögren's syndrome A antigen (SSA). Although this binding was 1,000-fold lower than the highest anti-Ro/SSA level measured from patients, it was inhibited by human Ro/SSA. Positive normal serum-bound Ro/SSA in Western immunoblots and binding activity was demonstrated in the F(ab')2 fragment of IgG. Affinity purification of normal anti-Ro/SSA IgG increased the specific anti-Ro/SSA binding by greater than 17-fold. This purified antibody formed a Ro/SSA precipitin and had a relative affinity for Ro/SSA identical to that of Ro/SSA precipitin-positive patients. These data demonstrate that the anti-Ro/SSA present in healthy normal donors is true autoantibody. Anti-La/Sjögren's syndrome B antigen (SSB) autoantibodies were found in 3 of the 40 normal sera, while none bound nuclear ribonucleoprotein (Sm). Finding low levels of anti-Ro/SSA and anti-La/SSB among normals may indicate that anti-Ro/SSA and anti-La/SSB occur in disease by enhancement of a preexisting immune response.

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