Power and Privilege

Digital open source information — including the videos and photographs that people post to social media and other publicly accessible platforms — is increasingly valued as a critical source of evidence. While investigators have repeatedly established the value of open source information for researching a range of crimes, there is a subset of crimes that investigators have struggled to address with digital open sources — namely, sexual violence. In this article, we report on findings pulled from our interviews with international investigators and gender experts with regards to the perceived strengths and weaknesses of integrating digital open source information into international criminal investigations of sexual violence. More specifically, we elaborate on three insights into how open source investigations may be refined to better respect and protect the interests of survivors: by considering contextual issues related to ethics, power, and privilege, including the identity of the investigator and of the victims; by integrating a gender analysis and an intersectional analysis into online investigation planning; and by being thoughtful about consent, privacy, trauma and control — including who determines what happens with open source information and how such information is used in courts. We conclude with a discussion of what is needed to strengthen the efficacy and ethics of sexual violence investigations through the use of digital open sources

Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2

Deficiency of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney. To examine this further, we produced mice with targeted disruption of the 11β-HSD2 gene. Homozygous mutant mice (11β-HSD2(–/–)) appear normal at birth, but ∼50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11β-HSD2(–/–) mice are markedly hypertensive, with a mean arterial blood pressure of 146 ± 2 mmHg, compared with 121 ± 2 mmHg in wild-type controls and 114 ± 4 mmHg in heterozygotes. The epithelium of the distal tubule of the nephron shows striking hypertrophy and hyperplasia. These histological changes do not readily reverse with mineralocorticoid receptor antagonism in adulthood. Thus, 11β-HSD2(–/–) mice demonstrate the major features of SAME, providing a unique rodent model to study the molecular mechanisms of kidney resetting leading to hypertension. J. Clin. Invest. 103:683–689 (1999

Lack of Renal 11 Beta-Hydroxysteroid Dehydrogenase Type 2 at Birth, a Targeted Temporal Window for Neonatal Glucocorticoid Action in Human and Mice

International audienceBackground Glucocorticoid hormones play a major role in fetal organ maturation. Yet, excessive glucocorticoid exposure in utero can result in a variety of detrimental effects, such as growth retardation and increased susceptibility to the development of hypertension. To protect the fetus, maternal glucocorticoids are metabolized into inactive compounds by placental 11beta-hydroxysteroid dehydrogenase type2 (11βHSD2). This enzyme is also expressed in the kidney, where it prevents illicit occupation of the mineralocorticoid receptor by glucocorticoids. We investigated the role of renal 11βHSD2 in the control of neonatal glucocorticoid metabolism in the human and mouse. Methods Cortisol (F) and cortisone (E) concentrations were measured in maternal plasma, umbilical cord blood and human newborn urine using HPLC. 11βHSD2 activity was indirectly assessed by comparing the F/E ratio between maternal and neonatal plasma (placental activity) and between plasma and urine in newborns (renal activity). Direct measurement of renal 11βHSD2 activity was subsequently evaluated in mice at various developmental stages. Renal 11βHSD2 mRNA and protein expression were analyzed by quantitative RT-PCR and immunohistochemistry during the perinatal period in both species. Results We demonstrate that, at variance with placental 11βHSD2 activity, renal 11βHSD2 activity is weak in newborn human and mouse and correlates with low renal mRNA levels and absence of detectable 11βHSD2 protein. Conclusions We provide evidence for a weak or absent expression of neonatal renal 11βHSD2 that is conserved among species. This temporal and tissue-specific 11βHSD2 expression could represent a physiological window for glucocorticoid action yet may constitute an important predictive factor for adverse outcomes of glucocorticoid excess through fetal programming

Spironolactone-induced inhibition of aldosterone biosynthesis in primary aldosteronism: Morphological and functional studies

Twenty-five patients harboring aldosterone-producing adenomas were treated with spironolactone for 2-170 days immediately preoperatively. In the early period of administration of the drug (up to 27 days), plasma and urinary aldosterone decreased sharply while plasma renin activity (PRA) and serum potassium were rising. During this period of time, spironolactone bodies (SB), which form exclusively in cells actively producing aldosterone, were forming rapidly in the tumor cells but not in the inactive glomerulosa cells proper. The SB appear to be a morphological expression of a block in aldosterone biosynthesis. Since SB do not occur in normal fasciculata cells, which, like glomerulosa cells, also synthesize corticosterone, it is concluded that spironolactone inhibition of aldosterone biosynthesis occurs between corticosterone and aldosterone. Recent studies in vitro by others have suggested that the inhibition occurs at the corticosterone-methyl oxidase step, I (Ulick's nomenclature). The great diuresis of sodium and retention of potassium resulting from continued administration of the drug sharply activates aldosterone stimulatory factors. Aldosterone production may return to baseline levels in several weeks but it is inappropriately low in relation to the levels of PRA and serum potassium. With the further passage of time (average 4-6 wk), aldosterone production may increase 50%-100% above baseline levels, suggesting that the block has disappeared or is receding. At this time SB are diminishing in number and by 170 days of the drug they have virtually disappeared. We have hypothesized, among other possibilities, that recovery of the ability to convert corticosterone to aldosterone occurs by virtue of a mechanism activated by sodium deficiency, independent of angiotensin, which stimulates step 1 of the corticosterone-methyl oxidase system. As the block in the final step(s) of the biosynthetic pathway recedes, the existing elevated levels of angiotensin become much more effective in stimulating the production of aldosterone.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22806/1/0000363.pd