scholarly journals Dreaming of Freedom: Palestinian Child Prisoners Speak

2017 ◽  
Vol 4 (1) ◽  
pp. 195-195
Author(s):  
Yousef M. Aljamal
Keyword(s):  
Palestinian Child

The Existential Underpinnings of Intergroup Helping: When Normative and Defensive Motivations Collide

2017 ◽  
Vol 43 (10) ◽  
pp. 1469-1484
Author(s):  
Gilad Hirschberger ◽  
Jenna Hayes ◽  
Adi Shtrul ◽  
Tsachi Ein-Dor
Keyword(s):  
Medical Treatment ◽  
Child Study ◽  
Group Members ◽  
To Receive ◽  
Palestinian Child

Five studies examined defensive intergroup helping—when responsibility for an out-group victim’s injury decreases helping, whereas lack of responsibility increases helping when death is salient. In Study 1 ( N = 350), implicit death primes increased petition signings to allow a Palestinian child to receive medical treatment in Israel, when the child was a victim of Palestinian fire. When the child was a victim of Israeli fire, however, death primes decreased petition signings. Study 2 ( N = 200) partially replicated these effects on commitment to donate blood to an injured Palestinian child. Study 3 ( N = 162) found that moral affirmation primes moderate defensive helping effects. Study 4 ( N = 372) replicated defensive helping, but failed to replicate the moral affirmation effect found in Study 3. Study 5 ( N = 243) partially replicated defensive helping and found that different framings of existential threat moderate the effect. Overall, results indicate that self-protective concerns underlie prosocial responses to out-group members in need.

Combined mineralocorticoid and glucocorticoid deficiency is caused by a novel founder nicotinamide nucleotide transhydrogenase mutation that alters mitochondrial morphology and increases oxidative stress

2015 ◽  
Vol 52 (9) ◽  
pp. 636-641 ◽  
Author(s):  
Ariella Weinberg-Shukron ◽  
Abdulsalam Abu-Libdeh ◽  
Fouad Zhadeh ◽  
Liran Carmel ◽  
Aviram Kogot-Levin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Morphology ◽  
Atp Content ◽  
Nicotinamide Nucleotide Transhydrogenase ◽  
Whole Exome ◽  
Acth Receptor ◽  
Mitochondrial Defects ◽  
Glucocorticoid Deficiency ◽  
Glucocorticoid Production ◽  
Palestinian Child

BackgroundFamilial glucocorticoid deficiency (FGD) reflects specific failure of adrenocortical glucocorticoid production in response to adrenocorticotropic hormone (ACTH). Most cases are caused by mutations encoding ACTH-receptor components (MC2R, MRAP) or the general steroidogenesis protein (StAR). Recently, nicotinamide nucleotide transhydrogenase (NNT) mutations were found to cause FGD through a postulated mechanism resulting from decreased detoxification of reactive oxygen species (ROS) in adrenocortical cells.Methods and resultsIn a consanguineous Palestinian family with combined mineralocorticoid and glucocorticoid deficiency, whole-exome sequencing revealed a novel homozygous NNT_c.598 G>A, p.G200S, mutation. Another affected, unrelated Palestinian child was also homozygous for NNT_p.G200S. Haplotype analysis showed this mutation is ancestral; carrier frequency in ethnically matched controls is 1/200. Assessment of patient fibroblasts for ROS production, ATP content and mitochondrial morphology showed that biallelic NNT mutations result in increased levels of ROS, lower ATP content and morphological mitochondrial defects.ConclusionsThis report of a novel NNT mutation, p.G200S, expands the phenotype of NNT mutations to include mineralocorticoid deficiency. We provide the first patient-based evidence that NNT mutations can cause oxidative stress and both phenotypic and functional mitochondrial defects. These results directly demonstrate the importance of NNT to mitochondrial function in the setting of adrenocortical insufficiency.

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