Network Canvas: Key decisions in the design of an interviewer assisted network data collection software suite.

Self-reported social network analysis studies are often complex and burdensome, both during the interview process itself, and when conducting data management following the interview. Through funding obtained from the National Institute on Drug Abuse (NIDA/NIH), our team developed the Network Canvas suite of software - a set of complementary tools that are designed to simplify the collection and storage of complex social network data, with an emphasis on usability and accessibility across platforms and devices, and guided by the practical needs of researchers. The suite consists of three applications: Architect: an application for researchers to design and export interview protocols; Interviewer: a touch-optimized application for loading and administering interview protocols to study participants; and Server: an application for researchers to manage the interview deployment process and export their data for analysis. Together, they enable researchers with minimal technological expertise to access a complete research workflow, by building their own network interview protocols, deploying these protocols widely within a variety of contexts, and immediately attaining the resulting data from a secure central location. In this paper, we outline the critical decisions taken in developing this suite of tools for the network research community. We also describe the work which guides our decision-making, including prior experiences and key discovery events. We focus on key design choices, taken for theoretical, philosophical, and pragmatic reasons, and outline their strengths and limitations.

Quantitation of HLA antigens on red cells by immunoradiometric assay.

Immunoradiometric assay was employed to quantitate HLA antigens on red cells. Using this technique HLA-B7, HLA-B17 and HLA-A28 were detected on the red cells of all individuals studied irrespective of the serological status of the Bennett-Goodspeed (Bg) antigens. However, HLA antigenic sites for serologically Bg positive red cells were significantly more than that for Bg negative red cells (P less than 0.001). Bga positive red cells possessed maximum number of antigenic sites as compared to Bgb and Bgc positive red cells.

HLA and complement C4 studies in psoriasis vulgaris.

BACKGROUND: Psoriasis vulgaris is known to be associated with the presence of certain HLA antigens and complement factors but only studies of Western populations have been reported. We investigated the HLA and complement profile in Indian patients with psoriasis vulgaris. METHODS: Sixty-seven patients and 132 normal subjects were typed for class I antigens using 262 sera, and 55 patients and 104 normal subjects were typed for class II antigens using 174 sera. The sera from patients and normals were sent to Japanese laboratories for the study of class III antigens. RESULTS: The study revealed that patients had an increased frequency of A1 (p < 0.0025), B17 (p < 0.0025), Cw6 (p < 0.001) DR7 (p < 0.05) and DQw3 (p < 0.005) when compared to normal controls. Analysis of two and three antigen haplotypes revealed a significant increase in the incidence of all haplotypes involving those antigens which showed a high frequency among patients. A significant association was also found with complement factors C4A6.3 and C4A6,X. However, the relative risk was high for C4BQO (10.73). CONCLUSIONS: Psoriasis in Indians is associated with the A1, B17 and Cw6 but not with B13 antigens and the complement allotypes mentioned above. The strong association with C4 factors may be as a result of a close linkage between the class III region and Ir genes.

An epidemiological study of febrile seizures with special reference to family history and HLA linkage.

One hundred and forty four cases of febrile seizures, 95 simple (typical) and 49 complex (atypical); were studied and compared for clinical and epidemiological data and family history of febrile and afebrile seizures. Major results were: maximum age of onset below three years (75%) in both simple and complex groups, male preponderance, respiratory infection as the commonest etiology (69.4%) and maximum seizure onset within 24 hours of fever (73%). The familial prevalence of all seizures was 29.1%, 23.2% in the simple and 40.8% in the complex group (p < 0.01). The familial prevalence of febrile seizures was 20%; similar in both groups. The familial prevalence of afebrile seizures was 13.9%; 6.3% in simple and 28.6% in complex group (p < 0.01). The commonest relative was a sibling (13.2%). The prevalence in parents was 4%. Families with two additional members with history of seizures revealed complex seizure patterns in two-thirds of index cases. There was no correlation between family history of seizures and age at onset or sex. No clear inheritance pattern emerged and polygenic inheritance is likely. One third of eighteen families had siblings with identical segregation of parental HLA-A and B haplotypes. Five families showed the presence of HLA All. This small though adequate sample size did not reveal an HLA marker for febrile seizures.

Characteristics of the positive ion source at reduced gas feed.

The neutral beam injector of steady state superconducting tokamak (SST1-NBI) at IPR is designed for injecting upto 1.7 MW of neutral beam (Hº, 30-55 keV) power to the tokamak plasma for heating and current drive. Operations of the positive ion source (PINI or Plug-In-Neutral-Injector) of SST1-NBI were carried out on the NBI test stand. The PINI was operated at reduced gas feed rate of 2-3 Torr l/s, without using the high speed cryo pumps. Experiments were conducted to achieve a stable beam extraction by optimizing operational parameters namely, the arc current (120-300 A), acceleration voltage (16-40 kV), and a suitable control sequence. The beam divergence, power density profiles, and species fractions (H(+):H2(+):H3(+)) were measured by using the diagnostics such as thermal calorimetry, infrared thermography, and Doppler shift spectroscopy. The maximum extracted beam current was about 18 A. A further increase of beam current was found to be limited by the amount of gas feed rate to the ion source.

HLA antigens and E-rosettes in tetanus patients.

One-hundred-and-fifty-four tetanus patients and 118 normal persons were typed for 27 HLA antigens of A and B loci. There was no significant difference in the frequency of any of these antigens between the normal controls and the tetanus patients. Classification of the patients into mild, moderate and severe also did not show any significant deviation in the frequency of HLA antigens from the controls. Percentage E-rosettes in normal individuals showed lower values among a low socioeconomic group. The values for E-rosettes among tetanus patients were similar to those observed in low socioeconomic normal individuals. The distribution of ABO and Rho (D) groups among the tetanus patients were not significantly different from the frequencies in the normal population.

Abnormal myelocytic cell development in interleukin-2 (IL-2)-deficient mice: evidence for the involvement of IL-2 in myelopoiesis.

Mice lacking interleukin-2 (IL-2) developed a severe hematopoietic disorder characterized by the abnormal development of myeloid cells and neutropenia. Analysis of the bone marrow of IL-2-deficient (IL-2(-/-)) mice showed that the number of mature polymorphonuclear cells was decreased by 65% to 75%, and granulocyte/macrophage precursor cells were reduced by 50%. Bone marrow cells from IL-2(-/-) mice were unable to sustain myelopoiesis in lethally irradiated mice and in long-term bone marrow cultures (LTBMC). The addition of exogenous IL-2 to LTBMC of IL-2(-/-) cells partially restored hematopoietic progenitor activity. In the bone marrow of wild-type mice, immature (Mac-1(lo)) myeloid cells, including myeloblasts and promyelocytes, constitutively expressed the beta-chain of the IL-2R, and the number of Mac-1(lo)IL-2Rbeta+ cells was increased by twofold to threefold in IL-2(-/-) mice. During culture in the presence of IL-2 and the absence of stromal cells, Mac-1(lo)IL-2Rbeta+ immature myeloid cells proliferated and gave rise to mature granulocytes and macrophages. Collectively, these observations indicate that defective myelopoiesis in IL-2(-/-) mice is at least in part a consequence of their direct dependency on IL-2, and by regulating the growth of immature myeloid cells, IL-2 plays an important role in the homeostatic regulation of myelocytic cell generation.

Induction by herpes simplex virus of free and heteromeric forms of E2F transcription factor.

We have determined that HSV causes rapid and large increases in cell-cycle-regulated free E2F and S-phase p107/E2F DNA binding activities in asynchronous cultures of C33A cells. Induction occurred by 4 hr postinfection and coincided with the appearance of viral encoded immediate-early and delayed-early proteins, i.e., when viral DNA replication normally commences. No increase in E2F activities occurred when cells were infected with viruses expressing mutant regulatory proteins ICP4 or ICP27, or mutant replication proteins ICP8, pol or helicase, or when cells were infected with wild-type virus in the presence of inhibitors of DNA synthesis. In contrast, ICP8 mutant-infected cells contained elevated amounts of NF kappa B activity equivalent to WT virus, no induction of Sp1 relative to WT virus, and reduced ATF/CREB activity relative to WT virus. Results of transient expression assays with E2F-responsive reporters indicated that the net effect of induction of both active (free E2F) and repressive (p107/E2F) complexes was a decrease in AdE2 promoter activity and an increase in c-myc promoter activity. Taken together these results suggest that HSV can cause unscheduled changes in the amount and functional status of a cell-cycle-regulated transcription factor. These results are discussed in light of possible roles for viral-induced alterations in E2F, especially as related to imposing or overriding cell-cycle checkpoints.

Lymphoid hyperplasia, autoimmunity, and compromised intestinal intraepithelial lymphocyte development in colitis-free gnotobiotic IL-2-deficient mice.

IL-2-deficient (IL-2(-/-)) mice develop disorders of the hemopoietic and immune systems characterized by anemia, lymphocytic hyperplasia, and colitis. The mechanisms responsible for these abnormalities remain unclear. To investigate the underlying basis of autoimmunity, the particular role of commensal gut flora in the initiation of colitis, and the role of IL-2 in the development of intestinal intraepithelial lymphocytes (iIEL), we evaluated IL-2(-/-) mice reared and maintained under gnotobiotic (germfree) conditions. By 8 wk of age, 80% (20 of 25) of germfree IL-2(-/-) mice show signs of disease, including anemia, disturbances in bone marrow hemopoietic cells, lymphocytic hyperplasia, and generalized autoimmunity, similar to those seen in specific pathogen-free (SPF) IL-2(-/-) mice. In striking contrast to SPF IL-2(-/-) mice, germfree IL-2(-/-) mice do not develop colitis. However, the numbers of gammadelta+ and TCR alphabeta+ CD8 alphaalpha+ iIELs are reduced, and in lethally irradiated SPF IL-2(+/+) mice, reconstituted with IL-2(-/-) bone marrow TCR gammadelta+ iIELs fail to develop, consistent with an important role of IL-2/IL-2R signaling in the development of gammadelta iIELs. Consequently, our findings demonstrate that the colitis seen in SPF IL-2(-/-) mice depends upon the presence of intestinal bacterial flora and that environmental Ags are not responsible for the anemia and extraintestinal lymphoid hyperplasia that occur in IL-2(-/-) mice. Thus, germfree IL-2(-/-) mice represent a unique system in which the role of IL-2 deficiency in hemopoietic and immune system disorders can be investigated in dissociation from complications that may arise due to colitis.