Trump,Freud, the Puzzle of Femininity—and #MeToo

Abstract

Beneath Donald Trump’s repudiation of democratic values and practically all vestiges of Obama’s legacy (which has spurred a clamor to repudiate Trump) lies a repudiation of the feminine. It underwrites Trump’s cult of hypermasculinity and enables his exploitation of masculine insecurity, along with the gutting of climate protections and reproductive rights. Freud believed the repudiation of femininity was “psychological bedrock” (for both sexes); this article argues that, on the contrary, we have no fundamental need to repudiate the feminine. In fact, to embrace the feminine, in both material and symbolic ways, would be to open an important space for a more democratic polity. But claiming the feminine is so threatening that some, perhaps most, would prefer to lock it up and deny its vast and elemental erotic power and democratizing possibility. #MeToo unleashes the feminine potential for an emancipatory politics beyond patriarchy.     

To what ends? Psychotherapy goals and outcomes, the good life, and the principle of beneficence

Psychotherapists aim to benefit others, especially clients. The corresponding ethical principle, beneficence, is found in the aspirational, not enforceable, section of the American Psychological Association (2002) ethics code, is central to the idea of a professional, and is a crucial component of ethical excellence. Beneficence and related controversies (e.g., varying ideas about what it means to benefit others) are described, then linked to psychotherapy's goals and outcomes (which are, in part, the ethical ends toward which therapy aims and by which it is evaluated), especially through ideas about the good life. I conclude by discussing ways in which therapists can--through careful reflection and action aimed at benefiting others--move toward ethical excellence regarding beneficence. (PsycINFO Database Record (c) 2010 APA, all rights reserved).     

Preliminary investigations on melatonin and 5-methoxytryptophol synthesis in the pineal,retina, and Harderian gland of the mole rat and in the pineal of the mouse “eyeless”

Summary Hydroxyindole-O-methyltransferase (HIOMT) activity for the synthesis of melatonin and 5-methoxytryptophol, both 5-methoxyindoles, was measured in the pineal, the Harderian gland and the retina of the mole rat and in the pineal of the mouse eyeless. In the pineal and the Harderian gland of the mole rat a larger amount of 5-methoxytryptophol than of melatonin is synthesized. 5-Methoxyindole synthesis is extremely high in the Harderian gland, whereas in the retina HIOMT activity is low and variable. In the pineal of the mouse eyeless, a low 5-methoxyindole synthesis showing no circadian rhythm is demonstrated. It is concluded that, besides the generally accepted regulation of the indole metabolism by light, in species with atrophied eyes having Harderian glands (mole rat) and in species without eyes other factors than light might be responsible for the indole metabolism in the pineal gland.     

On the history of lacunes, etat criblé, and the white matter lesions of vascular dementia

The history of lesions associated with vascular dementia (17th to 19th century) is reviewed. Recognition of ischemic and hemorrhagic stroke types dates back to the 17th century; however, at that time a third type ('cerebral congestion') emerged as the most common form of apoplexy. This entity vanished as arterial hypertension became established with the introduction of the sphygmomanometer (1905). Before the 19th century, apoplexy was considered a uniformly fatal disease, although Willis first recognized post-stroke dementia in 1672. Dechambre (1838) first reported 'lacunes' in stroke survivors with small cerebral softenings. Durand-Fardel (1842) described interstitial atrophy of the brain (leukoaraiosis) and état criblé (cribriform state) reflecting chronic cerebral congestion. In 1894, Alzheimer and Binswanger identified 'arteriosclerotic brain atrophy,' a form of vascular dementia characterized by 'miliary apoplexies' (lacunes). Also in 1894, Binswanger described the disease that now bears his name. In 1901, Pierre Marie coined the name état lacunaire (lacunar state) for the clinical syndrome of elderly patients with multiple lacunes.     

What are the computations of the cerebellum,the basal ganglia and the cerebral cortex?

The classical notion that the cerebellum and the basal ganglia are dedicated to motor control is under dispute given increasing evidence of their involvement in non-motor functions. Is it then impossible to characterize the functions of the cerebellum, the basal ganglia and the cerebral cortex in a simplistic manner? This paper presents a novel view that their computational roles can be characterized not by asking what are the “goals” of their computation, such as motor or sensory, but by asking what are the “methods” of their computation, specifically, their learning algorithms. There is currently enough anatomical, physiological, and theoretical evidence to support the hypotheses that the cerebellum is a specialized organism for supervised learning, the basal ganglia are for reinforcement learning, and the cerebral cortex is for unsupervised learning.This paper investigates how the learning modules specialized for these three kinds of learning can be assembled into goal-oriented behaving systems. In general, supervised learning modules in the cerebellum can be utilized as “internal models” of the environment. Reinforcement learning modules in the basal ganglia enable action selection by an “evaluation” of environmental states. Unsupervised learning modules in the cerebral cortex can provide statistically efficient representation of the states of the environment and the behaving system. Two basic action selection architectures are shown, namely, reactive action selection and predictive action selection. They can be implemented within the anatomical constraint of the network linking these structures. Furthermore, the use of the cerebellar supervised learning modules for state estimation, behavioral simulation, and encapsulation of learned skill is considered. Finally, the usefulness of such theoretical frameworks in interpreting brain imaging data is demonstrated in the paradigm of procedural learning.     

Levodopa, vitamins, ageing and the neuropathy of Parkinson’s disease

Higher prevalence of neuropathy has been described in patients with Parkinson’s disease (PD) in comparison with age and gender-matched controls. The cause of neuropathy may be levodopa-induced impairment of vitamin B₁₂ metabolism, suggesting levodopa-naïve subjects should be unaffected. There may, however, be other yet unidentified determinants of neuropathy in PD. We screened 33 consecutive levodopa-naïve PD patients for neuropathy. Demographics, vitamin B₁₂ and folate levels were studied. Findings were analyzed in the light of our previous available data on levodopa-treated PD patients. Four of 33 (12.1 %) levodopa-naïve PD patients were diagnosed with neuropathy. This compared to 13/36 (36.1 %) previously evaluated levodopa-treated patients (p = 0.027) and 3/37 controls (p = 0.7). Analysis of our whole PD cohort consisting of a total of 70 subjects, including levodopa-naïve and levodopa-treated patients, revealed that neuropathy correlated with use of levodopa (p = 0.041), cumulative levodopa exposure (p = 0.046), age at time of study (p = 0.005) and serum folate levels <10 μg/L (p = 0.003). There was no association of neuropathy with PD duration. Multivariate regression analysis showed that neuropathy was only independently associated with age (p = 0.016) and serum folate levels <10 μg/L (p = 0.012). We conclude that this study confirms the roles of levodopa usage and cumulative levodopa exposure in the neuropathy of PD. However, the effects of levodopa only appear contributory and are surpassed by age and lower folate levels. In view of the independent implication of lower folate levels, the need for preventative/protective supplementation including folate in addition to vitamin B₁₂, probably irrespective of levodopa use, may deserve consideration in patients with PD.     

General practitioners’ knowledge,practices, and obstacles in the diagnosis and management of dementia

Objectives: To identify general practitioners’ (GPs) knowledge, practices, and obstacles with regard to the diagnosis and management of dementia.

Methods: Standardized questionnaires covering knowledge, practices, and obstacles were distributed among a purposive sample of GPs in Kathmandu, Nepal. Three hundred and eighty GPs responded (response rate = 89%).

Results: Knowledge of practitioners’ with regard to the diagnosis and management of dementia was unsatisfactory (<50%). Diagnosis and management barriers are presented with regard to GP, patient, and carer factors. Specifically, the results address the following issues: communicating the diagnosis, negative views of dementia, difficulty diagnosing early-stage dementia, acceptability of specialists, responsibility for extra issues, knowledge of dementia and aging, less awareness of declining abilities, diminished resources to handle care, lack of specific guidelines, and poor awareness of epidemiology.

Conclusions: Demographic changes mean that dementia will represent a significant problem in the future. The following paper outlines the problems and solutions that the Nepalese medical community needs to adopt to deal effectively with diagnosis, care, and management of dementia.     

The Effects of Fibrillar Forms of α-Synuclein Protein on Neurogenesis in the Hippocampus,Dopaminergic Neurons of the Substantia Nigra,and the Behavior of Ageing Mice

Hyperproduction and disturbance of the protein conformation of α-synuclein that are associated with the formation of aggregated forms, which have a neurotoxic effect, are the key link in the mechanisms of the pathogenesis of synucleinopathies, which are chronic progressive neurodegenerative diseases. We studied the effects of chronic intranasal administration of fibrillar forms of α-synuclein on the processes of neurogenesis in the hippocampus, the content of dopaminergic neurons in the substantia nigra, motor and exploratory activity, short- and long-term memory, and anxiety in ageing animals. The experiments were performed with 12-month-old male C57Bl/6 mice, which were administered intranasally once a day with a solution of α-synuclein fibrils or physiological solution for 14 days. Behavioral experiments included the Open field, novel object recognition, passive avoidance, and elevated plus maze tests. We used antibodies against bromodeoxyuridine, doublecortin, and tyrosine hydroxylase to stain proliferating cells, immature neurons, and dopaminergic nerve cells. We found that α-synuclein fibrils do not cause significant changes in indices of neurogenesis, the number of proliferating cells and immature neurons in the hippocampal dentate gyrus; nor do they have a significant effect on exploratory behavior, short- and long-term memory, and anxiety in mice. However, animals that were treated with fibrils of α-synuclein had a significant increase in the number of dopaminergic neurons in the substantia nigra pars compacta and an increase in some indices of general motor activity. We compared the data on the effects of α-synuclein fibrils and the results of a previous study of the action of α-synuclein oligomers under the conditions of a similar experimental protocol. We discuss possible mechanism of the revealed effect of α-synuclein fibrils on dopaminergic neurons of the substantia nigra of ageing mice.     

How can studies of memory and language enhance the authenticity,validity and reliability of interviews?

Gathering reliable and valid information is the cornerstone of applicable research. Interviews provide a basis for collecting information about an individual's experiences, attitudes and beliefs. Yet interviews place significant demands on an individual's cognitive and linguistic skills. Such demands have implications for interviews with children and people with specific and general learning disabilities. In order to provide a range of views in research and practice specific attention must be paid to the mechanisms that limit participation or result in unreliable reports. This paper examines the ways in which studies of memory and language can provide relevant data to help interpret interviews and support the development of techniques to enhance the reliability and validity of the information provided.     

Do knowledge of, perception of, and attitudes toward epilepsy affect the quality of life of Turkish children with epilepsy and their parents?

The main goal of this study was to evaluate knowledge of, perceptions of, and attitudes toward epilepsy and then to correlate knowledge with quality of life and stigmatization of children with epilepsy and their families. Specific questionnaires were administered to children aged 8 to 17 with epilepsy (n=220) and their parents (n=313). Poor school performance, less social support, less self-esteem, higher anxiety, greater stigmatization, and more depressive symptoms were documented in children who were less knowledgeable (P<0.05). Parents were found to be more knowledgeable about the antiepileptic drugs used, understanding both the effects and the side effects of the medications (P<0.05). Family activities were less restricted if they were more knowledgeable and these parents reported worrying less about their children (P<0.05). Knowledge about epilepsy is associated with less perceived stigmatization and social isolation, as well as fewer depressive symptoms and misperceptions.     

Postnatal profiles of myogenic regulatory factors and the receptors of TGF-β2, LIF and IGF-I in the gastrocnemius and rectus femoris muscles of dy mouse

The dystrophin-deficient mdx mouse presents muscle fiber necrosis but active muscle regeneration, probably due to an extensive recruitment of myogenic regulatory factors (MRF), several growth factors and cytokines, and favorable interaction of satellite cells. In contrast, the laminin α2 (merosin)-deficient dy mouse shows progressive muscle fiber necrosis and ineffective muscle regeneration. Using Western blot and immunohistochemical analyses, we investigated the adaptive changes in MRF, growth factors and cytokines and their receptors in the muscles of dy mice during postnatal growth. The relative volume of MyoD, myogenin and Myf-5 proteins was markedly lower in the gastrocnemius and rectus femoris muscles of dy mice. Transforming growth factor-β2, leukemia inhibitory factor (LIF) and basic fibroblast growth factor were not up-regulated in the muscles of dy mice. The levels of the LIF receptor and insulin-like growth factor-I receptor levels were markedly decreased in the muscles of dy mice during the entire postnatal period observed in this study. Therefore, unlike the situation in mdx mice, the milieu of regeneration following repetitive damage seems to be degraded in the muscles of dy mice. Received: 10 December 1998 / Revised: 7 April/27 May 1999 / Accepted: 27 May 1999     

Are the effects of the antidepressants amitriptyline, maprotiline, and fluoxetine on inhibitory avoidance state-dependent?

State-dependent learning (SDL) is a phenomenon in which the retrieval of newly acquired information is possible if the subject is in the same physiological state as during the encoding phase. SDL makes it possible to separate the effects of drugs per se on learning from the effects due to changes in drug state during the task. The present work was designed to investigate whether the antidepressants amitriptyline (30 mg/kg), maprotiline (25 mg/kg), and fluoxetine (15 mg/kg) produce SDL of the inhibitory avoidance conditioning in male and female CD1 mice. In three separate experiments, independent groups were used for each pharmacological treatment and for each sex using a 2 x 2 experimental design. The results do not show SDL in any of the drugs. In the case of amitriptilyline, the data can be attributed to a memorization deficit, while the maprotiline results are interpreted as simultaneously influenced by memorization deficit and performance facilitation due to motor impairment. Fluoxetine treatment did not produce any deteriorating effect on the conditioning. Drugs had some different effects on the performance of males and females, males showing a slightly higher deterioration than females with administration of amitriptyline and maprotiline. This study shows that these antidepressants affect the acquisition/consolidation but not the retrieval process in the inhibitory avoidance learning.     

Monoamine oxidases — activities,genotypes and the shaping of behaviour

Summary The importance of an interaction between environment and biological factors for the expression for a particular behaviour is illustrated by results from a series of adolescents in which effects of platelet MAO activity and psychosocial environment on criminality was investigated. In a favourable environment platelet MAO-B activity was not associated with criminality, while a very strong association was found in adolescents from a bad psychosocial environment. Essentially similar findings were obtained when a MAO-A promoter polymorphism was analysed instead of platelet MAO-B activity. In boys, presence of the low functioning allele seemed to be protective against criminal activity in combination with a good environment, while it predisposed for criminality in a bad psycho-social environment. In girls, instead, homozygosity for the high activity MAO-A allele interacted with environment to predict criminality. Possible mechanisms underlying the role of monoamine oxidases for behaviour are discussed.     

Dose-related biphasic effect of the Parkinson’s disease neurotoxin MPTP,on the spread,accumulation, and toxicity of α-synuclein

BackgroundParkinson’s disease (PD), the second most common progressive neurodegenerative disorder, is characterized by the abnormal accumulation of intraneuronal inclusions enriched in aggregated α-synuclein (α-syn), known as Lewy bodies (LBs) and Lewy neurites (LNs), and significant loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the brain. Recent evidence suggests that the intrastriatal inoculation of α-syn preformed fibrils (PFF) in mice brain triggers endogenous α-syn in interconnected brain regions. 1-methyl, 4-phenyl, 1,2,3,6 tetrahydropyridine (MPTP), a mitochondrial neurotoxin, has been used previously to generate a PD mouse model. However, the common methods of MPTP exposure do not induce LB or α-syn aggregation in mice. In the present study, we evaluated the effect of different doses of MPTP (10 mg/kg.b.wt and/or 25 mg/kg.b.wt) on the spread, accumulation, and toxicity of endogenous α-syn in mice administered an intrastriatal injection of human α-syn PFF.MethodsWe inoculated human WT α-syn PFF in mouse striatum. At 6 weeks post PFF injection, we challenged the animal with two different doses of MPTP (10 mg/kg.b.wt and 25 mg/kg.b.wt) once daily for five consecutive days. At 2 weeks from the start of the MPTP regimen, we collected the mice brain and performed immunohistochemical analysis, and Rotarod test to assess motor coordination and muscle strength before and after MPTP injection.ResultsA single injection of human WT α-syn PFF in the mice striatum induced the propagation of α-syn, occurring as phosphorylated α-synuclein (pS129), towards the SNpc, within a very short time. Injection of a low dose of MPTP (10 mg/kg.b.wt) at 6 weeks post α-syn PFF inoculation further enhanced the spread, whereas a high dose of MPTP (25 mg/kg.b.wt.) reduced the spread. Majority of the accumulated α-syn were proteinase K resistant, as recognized using a conformation-specific α-syn antibody. Injection of α-syn PFF alone caused 12 % reduction in the number of tyrosine hydroxylase positive neurons while α-syn PFF + a low dose of MPTP caused 33 % reduction (loss), compared to the control mice injected with saline. This combination also reduced the motor coordination. Interestingly, a low dose of MPTP alone did not cause any significant reduction in the number of tyrosine hydroxylase positive neurons compared to saline treatment. Animals that received α-syn PFF and a high dose of MPTP showed massive activation of glial cells and decreased spread of α-syn, majority of which were detected in the nucleus.ConclusionOur results suggest that a combination of human WT α-syn PFF and a low dose of MPTP increases the pathological conversion and propagation of endogenous α-syn, and neurodegeneration, within a very short time. Our model can be used to study the mechanisms of α-syn propagation and screen for potential drugs against PD.