This article examines ways in which slaves and missionaries used public declarations before witnesses to carve out a distinctive space of legal proceedings in pursuit of emancipation in western ...Tanzania. This way of pursuing emancipation shows slaves deploying their intellectual creativity and cultural knowledge to shape the German and British colonial legal systems. Interviews provide evidence that these public declarations drew on long-standing practices of oathing in western Tanzanian societies, while administrative sources indicate that oaths had been used in Islamic legal practice. Both mission and administrative sources show that these public declarations became a fairly routine means to facilitate slave emancipation between about 1907 and the 1920s. They were seen as legitimate by both (ex)owners and (ex)slaves, and were welcomed by officials as they mitigated tensions between owners and slaves, and between slave owners and missions. This legal practice was not codified in either the gradualist German-era laws on slavery or the more proactive abolitionist laws enacted by the British. It was a bottom-up innovation, developed in a context in which effective emancipation depended on drawn-out struggles and negotiations over personal autonomy and malleable social norms.
...his book is absorbing, insightful and thought-provoking. ...Gissibl shows that this continuity extends to what he calls ‘ecoracial’ assumptions about the need for a non-African (formerly colonial, ...now international) agency to protect African wildlife from African humans. ...it is worth mentioning that the author and editors caught most Germanisms in the text and the book is beautifully produced.
In recent years, anthropologists, historians, and others have
been drawn to study the profuse and creative usages of digital
media by religious movements. At the same time, scholars of
Christian ...Africa have long been concerned with the history of
textual culture, the politics of Bible translation, and the status
of the vernacular in Christianity. Students of Islam in Africa have
similarly examined politics of knowledge, the transmission of
learning in written form, and the influence of new media. Until
now, however, these arenas-Christianity and Islam, digital media
and "old" media-have been studied separately.
Religion, Media, and Marginality in Modern Africa is
one of the first volumes to put new media and old media into
significant conversation with one another, and also offers a rare
comparison between Christianity and Islam in Africa. The
contributors find many previously unacknowledged correspondences
among different media and between the two faiths. In the process
they challenge the technological determinism-the notion that
certain types of media generate particular forms of religious
expression-that haunts many studies. In evaluating how media usage
and religious commitment intersect in the social, cultural, and
political landscapes of modern Africa, this collection will
contribute to the development of new paradigms for media and
religious studies.
Contributors: Heike Behrend, Andre Chappatte, Maria Frahm-Arp,
David Gordon, Liz Gunner, Bruce S. Hall, Sean Hanretta, Jorg
Haustein, Katrien Pype, and Asonzeh Ukah.
Objective
Benign familial infantile seizures (BFIS), paroxysmal kinesigenic dyskinesia (PKD), and their combination—known as infantile convulsions and paroxysmal choreoathetosis (ICCA)—are related ...autosomal dominant diseases. PRRT2 (proline‐rich transmembrane protein 2 gene) has been identified as the major gene in all 3 conditions, found to be mutated in 80 to 90% of familial and 30 to 35% of sporadic cases.
Methods
We searched for the genetic defect in PRRT2‐negative, unrelated families with BFIS or ICCA using whole exome or targeted gene panel sequencing, and performed a detailed cliniconeurophysiological workup.
Results
In 3 families with a total of 16 affected members, we identified the same, cosegregating heterozygous missense mutation (c.4447G>A; p.E1483K) in SCN8A, encoding a voltage‐gated sodium channel. A founder effect was excluded by linkage analysis. All individuals except 1 had normal cognitive and motor milestones, neuroimaging, and interictal neurological status. Fifteen affected members presented with afebrile focal or generalized tonic–clonic seizures during the first to second year of life; 5 of them experienced single unprovoked seizures later on. One patient had seizures only at school age. All patients stayed otherwise seizure‐free, most without medication. Interictal electroencephalogram (EEG) was normal in all cases but 2. Five of 16 patients developed additional brief paroxysmal episodes in puberty, either dystonic/dyskinetic or “shivering” attacks, triggered by stretching, motor initiation, or emotional stimuli. In 1 case, we recorded typical PKD spells by video‐EEG‐polygraphy, documenting a cortical involvement.
Interpretation
Our study establishes SCN8A as a novel gene in which a recurrent mutation causes BFIS/ICCA, expanding the clinical–genetic spectrum of combined epileptic and dyskinetic syndromes. ANN NEUROL 2016;79:428–436
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Recent studies reported DEPDC5 loss‐of‐function mutations in different focal epilepsy syndromes. Here we identified 1 predicted truncation and 2 missense mutations in 3 children with rolandic ...epilepsy (3 of 207). In addition, we identified 3 families with unclassified focal childhood epilepsies carrying predicted truncating DEPDC5 mutations (3 of 82). The detected variants were all novel, inherited, and present in all tested affected (n = 11) and in 7 unaffected family members, indicating low penetrance. Our findings extend the phenotypic spectrum associated with mutations in DEPDC5 and suggest that rolandic epilepsy, albeit rarely, and other nonlesional childhood epilepsies are among the associated syndromes. Ann Neurol 2014;75:788–792
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Recent studies reported mutations in the gene encoding the proline-rich transmembrane protein 2 (PRRT2) to be causative for paroxysmal kinesigenic dyskinesia (PKD), PKD combined with infantile ...seizures (ICCA), and benign familial infantile seizures (BFIS). PRRT2 is a presynaptic protein which seems to play an important role in exocytosis and neurotransmitter release. PKD is the most common form of paroxysmal movement disorder characterized by recurrent brief involuntary hyperkinesias triggered by sudden movements. Here, we sequenced
PRRT2
in 14 sporadic and 8 familial PKD and ICCA cases of Caucasian origin and identified three novel mutations (c.919C>T/p.Gln307*, c.388delG/p.Ala130Profs*46, c.884G>A/p.Arg295Gln) predicting two truncated proteins and one probably damaging point mutation. A review of all published cases is also included.
PRRT2
mutations occur more frequently in familial forms of PRRT2-related syndromes (80–100 %) than in sporadic cases (33-46 %) suggesting further heterogeneity in the latter.
PRRT2
mutations were rarely described in other forms of paroxysmal dyskinesias deviating from classical PKD, as we report here in one ICCA family without kinesigenic triggers. Mutations are exclusively found in two exons of the
PRRT2
gene at a high rate across all syndromes and with one major mutation (c.649dupC) in a mutational hotspot of nine cytosines, which is responsible for 57 % of all cases in all phenotypes. We therefore propose that genetic analysis rapidly performed in early stages of the disease is highly cost-effective and can help to avoid further unnecessary diagnostic and therapeutic interventions.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Mutations in
SLC2A1
, encoding the glucose transporter type 1 (Glut1), cause a wide range of neurological disorders: (1) classical Glut1 deficiency syndrome (Glut1-DS) with an early onset epileptic ...encephalopathy including a severe epilepsy, psychomotor delay, ataxia and microcephaly, (2) paroxysmal exercise-induced dyskinesia (PED) and (3) various forms of idiopathic/genetic generalized epilepsies such as different forms of absence epilepsies. Up to now, focal epilepsy was not associated with
SLC2A1
mutations. Here, we describe four cases in which focal seizures present the main or at least initial category of seizures. Two patients suffered from a classical Glut1-DS, whereas two individuals presented with focal epilepsy related to PED. We identified three novel
SLC2A1
mutations in these unrelated individuals. Our study underscores that focal epilepsy can be caused by
SLC2A1
mutations or that focal seizures may present the main type of seizures. Patients with focal epilepsy and PED should undergo genetic testing and can benefit from a ketogenic diet. But also individuals with pharmaco-resistant focal epilepsy and cognitive impairment might be candidates for genetic testing in
SLC2A1
.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
This article traces the history of slavery and of post-slavery struggles for livelihood and status in the layout, the physical structures, and the social lives of three towns on the southern Swahili ...Coast: Kilwa, Mikindani, and Lindi. These towns were long surrounded by plantations that relied on the labor of enslaved people. In the first decades of the twentieth century, slave populations dissipated quickly. In towns, the colonial cash crop economy, voluntary rural-urban migration, and the decline of slave-owning elites combined to allow former slaves to assimilate and adopt new urbanite identities. Sufi orders played a central role in affording ex-slaves a respectable presence in town. Nevertheless, former slave owners and former slaves lived in different parts of these towns, former slaves' livelihoods were more precarious, and the imputation of slave origins remains offensive, even today. Indeed, the era of slavery still divides people and still engages the social imagination.
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