Documenting Mass Rape: Medical Evidence Collection Techniques as Humanitarian Technology
Keywordsmedical evidence; rape kits; sexual assault medical forensic exam; medical certificate; mass rape; sexual violence in conflict
Bioethics and Medical Ethics
Forensic Science and Technology
Gender and Sexuality
Law and Society
Medicine and Health
Science and Technology Studies
Sociology of Culture
Theory, Knowledge and Science
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AbstractAim: Emerging global networks of human rights activists, doctors, and nurses have advocated for increased collection of medical evidence in conflict-affected countries to corroborate allegations of sexual violence and facilitate prosecution in international and domestic courts. Such initiatives are part of broader shifts in human rights advocacy to document human rights violations using rigorous, standardized methodologies. In this paper, I consider three principal forms of medical evidence to document sexual violence and their use in these settings: the patient medical record, the medical certificate, and the sexual assault medical forensic exam (commonly known as the “rape kit”). Methods: Combining archival research with interviews of activists, healthcare practitioners, lawyers, investigators, and other experts, I trace the collection and use of medical evidence to document mass rape since the establishment of the International Criminal Tribunals for Rwanda and the former Yugoslavia. Results: The use of medical evidence collection techniques to document sexual violence during and shortly after armed conflict or mass violence against civilians is still relatively new and not well institutionalized. When available, medical evidence has been used to document patient disclosures, describe patterns of crime, prompt investigation, issue indictments, and provide context evidence to establish international crimes occurred. Conclusions: Drawing on approaches in science and technology studies, law and society, and cultural sociology, I argue that medical evidence collection techniques represent an emerging humanitarian technology that may influence what comes to count as sexual violence, which crimes are deemed justiciable, and ultimately how events come to be remembered, within and beyond courts.
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Aggravation of chronic stress effects on hippocampal neurogenesis and spatial memory in LPA₁ receptor knockout mice.Castilla-Ortega, Estela; Hoyo-Becerra, Carolina; Pedraza, Carmen; Chun, Jerold; Rodríguez De Fonseca, Fernando; Estivill-Torrús, Guillermo; Santín, Luis J (Public Library of Science, 2012-12-10)BACKGROUND The lysophosphatidic acid LPA₁ receptor regulates plasticity and neurogenesis in the adult hippocampus. Here, we studied whether absence of the LPA₁ receptor modulated the detrimental effects of chronic stress on hippocampal neurogenesis and spatial memory. METHODOLOGY/PRINCIPAL FINDINGS Male LPA₁-null (NULL) and wild-type (WT) mice were assigned to control or chronic stress conditions (21 days of restraint, 3 h/day). Immunohistochemistry for bromodeoxyuridine and endogenous markers was performed to examine hippocampal cell proliferation, survival, number and maturation of young neurons, hippocampal structure and apoptosis in the hippocampus. Corticosterone levels were measured in another a separate cohort of mice. Finally, the hole-board test assessed spatial reference and working memory. Under control conditions, NULL mice showed reduced cell proliferation, a defective population of young neurons, reduced hippocampal volume and moderate spatial memory deficits. However, the primary result is that chronic stress impaired hippocampal neurogenesis in NULLs more severely than in WT mice in terms of cell proliferation; apoptosis; the number and maturation of young neurons; and both the volume and neuronal density in the granular zone. Only stressed NULLs presented hypocortisolemia. Moreover, a dramatic deficit in spatial reference memory consolidation was observed in chronically stressed NULL mice, which was in contrast to the minor effect observed in stressed WT mice. CONCLUSIONS/SIGNIFICANCE These results reveal that the absence of the LPA₁ receptor aggravates the chronic stress-induced impairment to hippocampal neurogenesis and its dependent functions. Thus, modulation of the LPA₁ receptor pathway may be of interest with respect to the treatment of stress-induced hippocampal pathology.
A comparative study of dyslipidaemia in men and woman with androgenic alopeciaArias-Santiago, Salvador; Gutierrez-Salmeron, Maria Teresa; Buendia-Eisman, Agustin; Giron-Prieto, Maria Sierra; Naranjo-Sintes, Ramon (Society for the Publication of Acta Dermato-Venereologica, 2011-12-21)Several studies have analyzed the relationship between androgenetic alopecia and cardiovascular disease (mainly heart disease). However few studies have analyzed lipid values in men and women separately. This case-control study included 300 patients consecutively admitted to an outpatient clinic, 150 with early onset androgenetic alopecia (80 males and 70 females) and 150 controls (80 males and 70 females) with other skin diseases. Female patients with androgenic alopecia showed significant higher triglycerides values (123.8 vs 89.43 mg/dl, p = 0.006), total cholesterol values (196.1 vs 182.3 mg/dl, p = 0.014), LDL-C values (114.1 vs 98.8 mg/dl, p = 0.0006) and lower HDL-C values (56.8 vs 67.7 mg/dl, p <0.0001) versus controls respectively. Men with androgenic alopecia showed significant higher triglycerides values (159.7 vs 128.7 mg/dl, p = 0.04) total cholesterol values (198.3 vs 181.4 mg/dl, p = 0.006) and LDL-C values (124.3 vs 106.2, p = 0.0013) versus non-alopecic men. A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia.
Life-long environmental enrichment counteracts spatial learning, reference and working memory deficits in middle-aged rats subjected to perinatal asphyxia.Galeano, Pablo; Blanco, Eduardo; Logica Tornatore, Tamara M A; Romero, Juan I; Holubiec, Mariana I; Rodríguez de Fonseca, Fernando; Capani, Francisco (Frontiers Media, 2016-08-09)Continuous environmental stimulation induced by exposure to enriched environment (EE) has yielded cognitive benefits in different models of brain injury. Perinatal asphyxia results from a lack of oxygen supply to the fetus and is associated with long-lasting neurological deficits. However, the effects of EE in middle-aged rats suffering perinatal asphyxia are unknown. Therefore, the aim of the present study was to assess whether life-long exposure to EE could counteract the cognitive and behavioral alterations in middle-aged asphyctic rats. Experimental groups consisted of rats born vaginally (CTL), by cesarean section (C+), or by C+ following 19 min of asphyxia at birth (PA). At weaning, rats were assigned to standard (SE) or enriched environment (EE) for 18 months. During the last month of housing, animals were submitted to a behavioral test battery including Elevated Plus Maze, Open Field, Novel Object Recognition and Morris water maze (MWM). Results showed that middle-aged asphyctic rats, reared in SE, exhibited an impaired performance in the spatial reference and working memory versions of the MWM. EE was able to counteract these cognitive impairments. Moreover, EE improved the spatial learning performance of middle-aged CTL and C+ rats. On the other hand, all groups reared in SE did not differ in locomotor activity and anxiety levels, while EE reduced locomotion and anxiety, regardless of birth condition. Recognition memory was altered neither by birth condition nor by housing environment. These results support the importance of environmental stimulation across the lifespan to prevent cognitive deficits induced by perinatal asphyxia.