Researching peers and disaster vulnerable communities: an insider perspective

Conducting research among peers and communities that a researcher also serves may be both daunting and rewarding. Researching peers may make the researcher feel uncomfortable raising certain questions that are sensitive or that could be construed to be testing their competencies. This paper is inclined more towards showing that it is advantageous to be an insider, whose position can facilitate collection of information that could not have been accessed, or revealed to an outsider. The paper reports on fieldwork conducted in a low-income country in Sub-Sahara Africa as part of a doctoral study with communities affected by disasters and those that work with such communities. The paper demonstrates the complexities of conducting such research and provides some insights that may be useful to insiders, outsiders or “in-betweeners” embarking on fieldwork in low-income countries and among vulnerable population struggling with manifold stresses and shocks

Image_2_Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model.pdf

<p>Hypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysfunction is induced without loss of cortical neurons are currently unclear. To reveal the mechanisms underlying mild motor dysfunction in neonatal H-I model, electrical responsiveness and dendrite morphology in the sensorimotor cortex were investigated at 10 weeks of age. Responses to intracortical microstimulation (ICMS) revealed that the cortical motor map was significantly changed in this model. The cortical area related to hip joint movement was reduced, and the area related to trunk movement was increased. Sholl analysis in Golgi staining revealed that layer I–III neurons on the H-I side had more dendrite branches compared with the contralateral side. To investigate whether changes in the motor map and morphology appeared at earlier stages, ICMS and Sholl analysis were also performed at 5 weeks of age. The minimal ICMS current to evoke twitches of the hip area was higher on the H-I side, while the motor map was unchanged. Golgi staining revealed more dendrite branches in layer I–III neurons on the H-I side. These results revealed that alterations of both dendrite morphology and ICMS threshold of the hip area occurred before the rearrangement of the motor map in the neonatal H-I model. They also suggest that altered dendritic morphology and altered ICMS responsiveness may be related to mild motor dysfunction in this model.</p

Table_1_Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model.docx

<p>Hypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysfunction is induced without loss of cortical neurons are currently unclear. To reveal the mechanisms underlying mild motor dysfunction in neonatal H-I model, electrical responsiveness and dendrite morphology in the sensorimotor cortex were investigated at 10 weeks of age. Responses to intracortical microstimulation (ICMS) revealed that the cortical motor map was significantly changed in this model. The cortical area related to hip joint movement was reduced, and the area related to trunk movement was increased. Sholl analysis in Golgi staining revealed that layer I–III neurons on the H-I side had more dendrite branches compared with the contralateral side. To investigate whether changes in the motor map and morphology appeared at earlier stages, ICMS and Sholl analysis were also performed at 5 weeks of age. The minimal ICMS current to evoke twitches of the hip area was higher on the H-I side, while the motor map was unchanged. Golgi staining revealed more dendrite branches in layer I–III neurons on the H-I side. These results revealed that alterations of both dendrite morphology and ICMS threshold of the hip area occurred before the rearrangement of the motor map in the neonatal H-I model. They also suggest that altered dendritic morphology and altered ICMS responsiveness may be related to mild motor dysfunction in this model.</p

Image_1_Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model.pdf

<p>Hypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysfunction is induced without loss of cortical neurons are currently unclear. To reveal the mechanisms underlying mild motor dysfunction in neonatal H-I model, electrical responsiveness and dendrite morphology in the sensorimotor cortex were investigated at 10 weeks of age. Responses to intracortical microstimulation (ICMS) revealed that the cortical motor map was significantly changed in this model. The cortical area related to hip joint movement was reduced, and the area related to trunk movement was increased. Sholl analysis in Golgi staining revealed that layer I–III neurons on the H-I side had more dendrite branches compared with the contralateral side. To investigate whether changes in the motor map and morphology appeared at earlier stages, ICMS and Sholl analysis were also performed at 5 weeks of age. The minimal ICMS current to evoke twitches of the hip area was higher on the H-I side, while the motor map was unchanged. Golgi staining revealed more dendrite branches in layer I–III neurons on the H-I side. These results revealed that alterations of both dendrite morphology and ICMS threshold of the hip area occurred before the rearrangement of the motor map in the neonatal H-I model. They also suggest that altered dendritic morphology and altered ICMS responsiveness may be related to mild motor dysfunction in this model.</p

Demographic details of post-mortem brain specimens from controls and Creutzfeldt-Jakob disease patients.

<p>Demographic details of post-mortem brain specimens from controls and Creutzfeldt-Jakob disease patients.</p

Demographic details of post-mortem brain specimens from controls and Alzheimer’s disease patients.

<p>Demographic details of post-mortem brain specimens from controls and Alzheimer’s disease patients.</p

A decrease in GPI-PLD expression was observed in the caveolin-enriched membrane (CEM) fraction.

<p>Gradient fractions from control and from scrapie-infected brain lysates were assayed for GPI-PLD and PrP^Sc as described in the <i>Materials and Methods</i> section. Equal sucrose gradient fractions (1 ml each following centrifugation) were analyzed by Western blotting with the anti-GPI-PLD and anti-PrP 10E4 antibodies. Each experiment was repeated at least three times, and similar results were obtained in each experiment. An anti-caveolin-1 antibody was used as the positive control for the CEM fractions. Note lanes 5, 8 and 9, in which PrP^Sc and caveolin-1 are abundant. * Significance <i>p</i> < 0.05 compared with control levels; ** Significance <i>P</i> < 0.01 compared with control levels.</p

GPI-PLD is down-regulated in the scrapie-infected brains.

<p>(<b>A</b>) RT-PCR analysis of GPI-PLD expression levels using total RNA samples extracted from the whole brains of mice injected with either ME7 or normal brain homogenates at 160 dpi. The GPI-PLD mRNA levels were quantified using a densitometer analysis. Each value represents the mean ± SD of three samples. *Significance <i>P</i> < 0.05 compared with control levels. Actin was used as the control. (<b>B</b>) Western blot analysis of GPI-PLD protein levels in whole brain at 150 dpi from mice injected with either ME7 or normal brain homogenates. Total brain lysates of control and scrapie-infected mice were prepared as described in the <i>Materials and Methods</i> section and analyzed by western blotting with the GPI-PLD antibody. Each value represents the mean ± SD of three samples. **Significance <i>P</i> < 0.01 compared with control levels. Each experiment was repeated at least three times, and similar results were obtained in each experiment. β-actin was detected by anti-β-actin antibody and it served as the control. (<b>C-D</b>), GPI-PLD begins to be reduced at the time PrP^Sc is detected. Total lysates, which were prepared as described in the <i>Materials and Methods</i> section, were analyzed by Western blotting with the anti-GPI-PLD (C) and anti-PrP 10E4 antibodies; the latter experiment is done following PK treatment (D). Each experiment was repeated at least three times, and similar results were obtained in each experiment. β-actin was detected by anti-β-actin antibody and was used as the control. * Significance <i>p</i> < 0.05 compared to control 60 days after scrapie infection; ** Significance <i>p</i> < 0.01 compared to control 140 and 160 days after scrapie infection.</p

Additional file 1: Figure S1. of A diagnostic marker for superficial urothelial bladder carcinoma: lack of nuclear ATBF1 (ZFHX3) by immunohistochemistry suggests malignant progression

Specificity and sensitivity of the seven anti-ATBF1 antibodies. Western blot analysis of ATBF1 in HEK293T cells using the seven anti-ATBF1 antibodies (Fig. 5a MB33, MB34, MB39, D1-120, MB44, MB47 and MB49). Lanes 1, 3, 5, 7, 9, 11, and 13 represent HEK293T cells with an HA-tag expression vector (pCI-HA). Lanes 2, 4, 6, 8, 10, 12, and 14 represent HEK293T cells containing an HA-tagged ATBF1 expression vector (pCI-HA-ATBF1). HEK293T cells were grown in DMEM supplemented with 10 % fetal bovine serum at 37 °C and 5 % CO2. HEK293T cells were transfected with the HA-tagged expression vector or the HA-tagged ATBF1 expression vector (HA-ATBF1) using transIT-293 reagent. (PPTX 215 kb