Publications by authors named "Goodman Y"

Drawing on interviews with Jewish Orthodox psychotherapists in Israel and on sources that represent the social, political, and cultural milieu within which these therapists work, we analyze the practices they use when working with religious gay men. Given debates and prohibitions on homosexuality in Jewish law, the therapists deploy three practices: reproducing religious norms, allowing homosexuality to be privately acknowledged while advocating its concealment from the public eye, or adopting religious distinctions that enable two men to live together while abstaining from sexual intercourse. These interventions express therapists' pragmatic cultural work, sorting out opposing therapeutic discourses, like the liberal-professional and the religious, and engaging with contestations beyond the clinic's boundaries.

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According to psychiatry, Attention-Deficit/Hyperactivity Disorder (ADHD) is a chronic condition beginning in early life. Psychiatry advocates for early diagnosis to prevent comorbidities that may emerge in untreated cases. "Late"-diagnosis is associated with various hazards that might harm patients' lives and society.

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Following the growing critique of the use of Post-Traumatic Stress Disorder in post-disaster interventions, a new type of intervention aimed at building resilience in the face of traumatic events has been making its first steps in the social field. Drawing on fieldwork of a resilience-building program for pre-clinical populations in Israel, we analyze the paradoxes and ambiguities entailed in three inter-related aspects of this therapeutic project: The proposed clinical ideology aimed at immunizing against traumas; the discursive and non-discursive practices used by the mental-health professionals; and, participants' difficulties to inhabit the new resilient subject. These contradictions revolve around the injunction to rationally handle emotions in response to disruptive traumatic events.

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This article traces a critical change in the professional therapy of posttraumatic stress disorder (PTSD): from treatment of a disorder borne by individuals to treatment of an anticipated disorder to be prevented by fortifying the entire population. A community resilience program in the city of Sderot in southern Israel, which has been subjected to Qassam rockets by its Palestinian neighbors across the border, serves as our case study. Drawing on an ethnographic study of this new therapeutic program, we analyze how the social body that the professionals attempt to immunize against trauma was treated.

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Rather than viewing therapeutic interventions as either compliance or resistance to the social order, I analyze them as mimesis of cultural ideal selves. In particular, I examine the new mediations of the social order constituted in mimetic therapeutic practices and their entailed creativity and ambivalence. Drawing on participant observation in a Jewish ultra-Orthodox (Haredi) rehabilitation site I explore how, given the ruptures brought about in mental disorders, caretakers offer their clients new ways to inhabit the normal self through its imitation.

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This paper explores the meaning and social functions of referral letters sent to a mental health clinic in Israel by Haredi (ultra-orthodox) rabbis. The letters exemplify social mechanisms by which various institutions and individuals (careproviders, therapists, and other social actors) negotiate different therapies, advice, and interventions in cross-cultural encounters. We argue that beyond the practical functions of the letters, the rabbis-representatives of a "popular" and religious social sphere-use them to negotiate their position in relation to the psychiatric clinic as a representative of a professional and secular sphere.

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By comparing versions of mental illness narratives - told by Haredi (Utraorthodox Jews) male patients of a mental health clinic in Israel and by their rabbis - this paper relates to two distinct, yet interrelated, theoretical questions: the place and agency of narrators, and the tension between experience and representation. A pair of narratives exemplifies a pattern in which the patients (Talmudic students) tell a narrative of a sudden breakdown related to a dramatic meeting with a non-human figure (often, a woman) or force. Their rabbis, by contrast, tell a narrative that emphasizes their students' mundane symptoms, "abnormal" and "immoral" behavior, and use a local adaptation of a Western psychological explanatory model.

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Uric acid is a well-known natural antioxidant present in fluids and tissues throughout the body. Oxyradical production and cellular calcium overload are believed to contribute to the damage and death of neurons that occurs following cerebral ischemia in victims of stroke. We now report that uric acid protects cultured rat hippocampal neurons against cell death induced by insults relevant to the pathogenesis of cerebral ischemia, including exposure to the excitatory amino acid glutamate and the metabolic poison cyanide.

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The transcription factor NF-kappaB is expressed in neurons wherein it is activated in response to a variety of stress- and injury-related stimuli including exposure to cytokines such as tumor necrosis factor-alpha (TNFalpha), and excitotoxic and oxidative insults. NF-kappaB may play a role in the anti-death actions of TNFalpha in cultured hippocampal neurons exposed to metabolic and oxidative insults. We now report that pretreatment of hippocampal cell cultures with agents that activate NF-kappaB (TNFalpha and C2-ceramide) confers resistance of neurons to apoptosis induced by the oxidative insults FeSO4 and amyloid beta-peptide (Abeta25-35).

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Studies of human patients with temporal lobe epilepsy and animal models of epilepsy have established relationships between seizures, excitotoxic hippocampal damage, and memory impairment. We report that bacterial alkaloids, recently shown to mimic actions of neurotrophic factors in cell culture, attenuate seizure-induced damage to hippocampal neurons and memory impairment in adult rats when administered subcutaneously. Intrahippocampal administration of convulsant doses of kainic acid (KA) to adult rats resulted in degeneration of neurons in CA3, CA1, and hilus.

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Steroid hormones, particularly estrogens and glucocorticoids, may play roles in the pathogenesis of neurodegenerative disorders, but their mechanisms of action are not known. We report that estrogens protect cultured hippocampal neurons against glutamate toxicity, glucose deprivation, FeSO4 toxicity, and amyloid beta-peptide (A beta) toxicity. The toxicity of each insult was significantly attenuated in cultures pretreated for 2 h with 100 nM-10 microM 17 beta-estradiol, estriol, or progesterone.

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The transcription factor NF kappa B is activated by various signals associated with brain injury, including tumor necrosis factor (TNF), oxidative insults, and amyloid beta-peptide (A beta). We recently reported that TNFs activate NF kappa B in neurons and protect them against excitotoxic and oxidative insults, including A beta toxicity. We now report that C2-ceramide (C2), a membrane-permeant activator of NF kappa B, protects cultured rat hippocampal neurons against death induced by glutamate, FeSO4, and A beta.

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Potassium channel openers (KCOs) such as diazoxide and levochromakalim can protect cardiac myocytes against ischemic injury and neurons against excitotoxic injury, presumably because of their ability to hyperpolarize the plasma membrane and reduce calcium influx. We now report that diazoxide, levocromakalim (LCC), and to a lesser extent pinacidil, protect cultured rat hippocampal neurons against oxidative injury induced by exposure to FeSO4 and amyloid beta-peptide (A beta). Imaging studies of intracellular peroxide levels revealed that KCOs suppressed the generation of peroxides induced by FeSO4 and A beta.

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The excitatory neurotransmitter glutamate is believed to play important roles in development, synaptic plasticity, and neurodegenerative conditions. Recent studies have shown that neurotrophic factors can modulate neuronal excitability and survival and neurite outgrowth responses to glutamate, but the mechanisms are unknown. The present study tested the hypothesis that neurotrophic factors modulate responses to glutamate by affecting the expression of specific glutamate-receptor proteins.

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In Alzheimer disease (AD) the amyloid beta-peptide (A beta) accumulates in plaques in the brain. A beta can be neurotoxic by a mechanism involving induction of reactive oxygen species (ROS) and elevation of intracellular free calcium levels ([Ca2+]i). In light of evidence for an inflammatory response in the brain in AD and reports of increased levels of tumor necrosis factor (TNF) in AD brain we tested the hypothesis that TNFs affect neuronal vulnerability to A beta.

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The amyloid beta-peptide (A beta) that accumulates as insoluble plaques in the brains of Alzheimer's victims can be neurotoxic, by a mechanism that may involve generation of reactive oxygen species (ROS) and destabilization of cellular calcium homeostasis. We now provide evidence that the mechanism of neurotoxicity of two other amyloidogenic peptides (APs), human amylin and beta 2-microglobulin, also involves induction of ROS and elevation of [Ca2+]i. Human amylin, beta 2-microglobulin and A beta 1-40 all caused significant death of neurons in rat hippocampal cell cultures during 24-48 h exposure periods.

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Increasing evidence supports the involvement of amyloid beta-peptide (A beta) and an excitotoxic mechanism of neuronal injury in the pathogenesis of Alzheimer's disease. However, approaches aimed at preventing A beta toxicity and neurofibrillary degeneration are undeveloped. We now report that anticonvulsants (carbamazepine, phenytoin, and valproic acid) can protect cultured rat hippocampal neurons against A beta- and glutamate-induced injury.

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Recent findings indicate that amyloid beta-peptide (A beta) can be neurotoxic by a mechanism involving an increase in the concentration of intracellular free Ca2+ ([Ca2+]i) and the generation of free radicals. In the present study, the lipoxygenase inhibitor/antioxidant nordihydroguaiaretic acid (NDGA) protected cultured rat hippocampal neurons against the toxicity of A beta in a concentration-dependent manner. Measurements of cellular oxidation (using the oxidation-sensitive dye 2,7-dichlorofluorescin) and intracellular free Ca2+ levels (using the Ca2+ indicator dye fura-2), showed that NDGA suppressed A beta-induced accumulation of reactive oxygen species (ROS) and Ca2+; Ca2+ responses to glutamate were also suppressed by NDGA.

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Neurotrophin-4/5 (NT-4/5) is a recently discovered member of the neurotrophin family of neurotrophic factors which includes NGF, BDNF and NT-3. NT-4/5 is expressed in the brain where its function is unknown. We have found that NT-4/5 can protect cultured embryonic rat hippocampal and cortical neurons against glucose deprivation-induced injury.

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Recent studies have shown that amyloid beta-peptide (A beta) can be directly neurotoxic by a mechanism related to secondary structure of the peptide, and mediated by free radical production and an increase in the concentration of intracellular free calcium ([Ca2+]i). We now report that staurosporine and K-252 compounds, low molecular weight alkaloids of bacterial origin, can protect cultured rat hippocampal neurons against the toxicity of A beta in a concentration-dependent manner. The alkaloids also protected neurons against iron-induced (free radical-mediated) injury.

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Alternative processing of the beta-amyloid precursor protein (beta APP) can result in liberation of either secreted forms of beta APP (APPSs), which may play roles in neuronal plasticity and survival, or amyloid beta-peptide (A beta), which can be neurotoxic. In rat hippocampal cell cultures A beta 1-40 caused a time- and concentration-dependent reduction in neuronal survival. APPS695 and APPS751 significantly reduced A beta-induced injury in a concentration-dependent manner.

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When a child is sent home on peritoneal dialysis, the family is faced with enormous challenges. Despite the coordination of community resources, there are few opportunities for relief from the many tasks required to keep a child home on dialysis. The intensity and duration of the home care required for children awaiting renal transplantation have often led to overwhelming parental stress, marital discord and burn-out.

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The peritoneal equilibration test (PET) has been recommended in adults as a standardized means of estimating solute transport. Based on results of the PET, adult peritoneal permeability has been classified as high, high average, low average, and low. We performed a PET on 32 children aged 0.

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An enzyme-linked immunosorbent assay was developed for detection of immunoglobulin A (IgA) antibody to Bordetella pertussis (PsIgA) in nasopharyngeal secretions as an indicator of recent infection. Secretion specimens submitted for pertussis culture were examined for PsIgA by this technique. Of 348 specimens tested, B.

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