scholarly journals Toward a Developmental Taxonomy of Adult Sexual Aggressors of Women: Antisocial Trajectories in Youth, Mating Effort, and Sexual Criminal Activity in Adulthood

2011 ◽  
Vol 26 (1) ◽  
pp. 16-32 ◽  
Author(s):  
Jesse Cale ◽  
Patrick Lussier

Recent studies suggest that sexual aggressors of women are characterized by early- and late-onset antisocial trajectories. However, these studies have not examined the role of mating effort and its role on sexual offending in adulthood. This study examined differences in the level of mating effort of early- and late-onset offenders and the association between mating effort and sexual offending in adulthood. Factor analysis identified two latent constructs of sexuality: mating effort and high sexual drive. Early-onset offenders exhibited significantly higher levels of mating effort and sexual drive. Furthermore, high mating effort and high sexual drive were more strongly associated with an earlier onset and a higher frequency of sexual crimes in adulthood than group membership. This study provided empirical evidence that a developmental taxonomy of early and late onset distinguishes the sexual activity and sexual criminal activity of adult sexual aggressors. The findings are discussed in light of a developmental taxonomy of sexual aggressors of women.

Author(s):  
Karen Holt ◽  
James Kissinger ◽  
Corey Spickler ◽  
Vicki Roush

Despite no definitive relationship between pornography and sexual offenses, there exists an assumption that use plays a role in the commission of sexual crimes and may increase risk of recidivism. This has led to the development of post-release restrictions on adult media for those convicted of a sexual offense. We conducted semi-structured interviews with 101 incarcerated individuals convicted of a sexual offense to explore the central research questions: (1) What are the common themes among individual’s experiences regarding pornography and how do they construct the role of pornography in their offending? (2) How do they frame pornography use post-release and understand pornography use as related to risk of re-offense? A qualitative analysis revealed common themes regarding how individuals constructed pornography use and notions of risk. Strategic and targeted monitoring and supervision of those who perceive their pornography use as consuming and facilitating may be a more effective practice than abstinence-only blanket restrictions.


2011 ◽  
Vol 38 (8) ◽  
pp. 854-873 ◽  
Author(s):  
Julie Carpentier ◽  
Benoit Leclerc ◽  
Jean Proulx

The aim of the study was to identify the factors associated with age of onset of sexual aggression, and variety and desistance of criminal activity, among adolescent sexual aggressors. The sample consisted of 351 adolescents ( M age = 15.8 years, SD = 1.8) who were assessed in an outpatient psychiatric clinic between 1992 and 2002. Recidivism data were collected after a mean follow-up period of 8 years. Hierarchical logistic regression analyses demonstrated that some variables related to childhood and adolescent development discriminated among participants who went on to follow different criminal activity trajectories. Indices of early antisocial behaviors (aggressive behavior, antisocial traits) were associated with early activation of a pattern of sexual offending as well as a polymorphic criminal career in adolescence. Findings supported previous research indicating that most adolescent sexual offenders who persist in a criminal career commit a variety of offenses and do not specialize in sexual crimes.


2016 ◽  
Vol 17 (3) ◽  
pp. 266-283 ◽  
Author(s):  
Anne-Marie McAlinden ◽  
Mark Farmer ◽  
Shadd Maruna

The literature on desistance from crime has become well established in recent years with strong bodies of evidence supporting the role of factors such as employment, relationships and identity change in this process. However, the relevance of this literature to individuals convicted of sexual crimes is not known as such individuals are almost always excluded from this research. This article presents the results from one of the first empirical studies on desistance from sexual offending based on 32 in-depth life story interviews with adult males previously convicted of child sex offences. In this analysis we explore the significance of work, the role of relationships and changes in imagined selves in the self-identities of individuals successfully desisting from sexual offending. The findings provide support for all three factors in helping to sustain desistance from sex offending, but also suggest clear differences between desistance from sex offending and other types of crime in these regards.


2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.


2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Ahmed Ayuna ◽  
Nik Abidin

Abstract Background Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Our article aims to focus on the role of neurohormonal blockers in the primary prevention of anthracycline-induced cardiotoxicity, whether it is acute, early, or late onset. Main body of the abstract PubMed and Google Scholar database were searched for the relevant articles; we reviewed and appraised 15 RCTs, and we found that angiotensin-converting enzyme inhibitors (ACEI) and B-blockers were the most commonly used agents. Angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were used in a few other trials. The follow-up period was on the range of 1–156 weeks (mode 26 weeks). Left ventricular ejection fraction (LVEF), left ventricular diameters, and diastolic function were assessed by either echocardiogram or occasionally by cardiac magnetic resonance imaging (MRI). The occurrence of myocardial injury was assessed by troponin I. It was obvious that neurohormonal blockers reduced the occurrence of LVEF and myocardial injury in 14/15 RCTs. Short conclusion Beta-blockers, especially carvedilol and ACEI, especially enalapril, should be considered for the primary prevention of acute- and early-onset cardiotoxicity. ARB and MRA are suitable alternatives when patients are intolerant to ACE-I and B-blockers. We recommend further studies to explore and establish the role of neurohormonal blockers in the primary prevention of the acute-, early-, and late-onset cardiotoxicity.


2021 ◽  
Vol 79 (3) ◽  
pp. 961-968
Author(s):  
Wolfgang J. Streit ◽  
Habibeh Khoshbouei ◽  
Ingo Bechmann

Microglia constitute the brain’s immune system and their involvement in Alzheimer’s disease has been discussed. Commonly, and in line with the amyloid/neuroinflammation cascade hypothesis, microglia have been portrayed as potentially dangerous immune effector cells thought to be overactivated by amyloid and producing neurotoxic inflammatory mediators that lead to neurofibrillary degeneration. We disagree with this theory and offer as an alternative the microglial dysfunction theory stating that microglia become impaired in their normally neuroprotective roles because of aging, i.e., they become senescent and aging neurons degenerate because they lack the needed microglial support for their survival. Thus, while the amyloid cascade theory relies primarily on genetic data, the dysfunction theory incorporates aging as a critical etiological factor. Aging is the greatest risk factor for the sporadic (late-onset) and most common form of Alzheimer’s disease, where fully penetrant genetic mutations are absent. In this review, we lay out and discuss the human evidence that supports senescent microglial dysfunction and conflicts with the amyloid/neuroinflammation idea.


Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 139-145
Author(s):  
Jelena Vucic ◽  
Miodrag Vucic ◽  
Tatjana Stankovic ◽  
Hristina Stamenkovic ◽  
Sandra Stankovic ◽  
...  

Abstract Not fully maturated immune system in preterm neonates may contribute to the increased susceptibility to infection. The levels of some cytokines can be useful in the prediction and diagnosis of sepsis in premature neonates. In the present study, we evaluated the potential predictive role of IFN-γ and IL-5 in cord and venous blood, together with the determination of C-reactive protein and procalcitonin (PCT) for sepsis development in premature neonates. A total of 80 participants were included. The laboratory results and clinical histories showed that 21 participants had sepsis. Early onset sepsis was detected in 3 patients while late onset sepsis was observed in 18 participants. The venous plasma levels of IFN-γ and PCT was markedly increased in sepsis groups when compared to the participants without sepsis. On the other hand, levels of IL-5 did not significantly change in the evaluated groups of sepsis and in the control group of participants. Simultaneously, plasma venous levels were not altered in any of the evaluated groups. Obtained findings suggest that venous plasma levels of IFN-γ, rather than levels of IFN-γ in cord blood plasma, and PCT may have predictive potential for sepsis development in preterm neonates. Further studies are necessary to get more comprehension of the complex function of cytokines for sepsis development in preterm neonates.


2007 ◽  
Vol 144B (2) ◽  
pp. 159-164 ◽  
Author(s):  
Rickard L. Sjöberg ◽  
Kent W. Nilsson ◽  
Hanna-Linn Wargelius ◽  
Jerzy Leppert ◽  
Leif Lindström ◽  
...  

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2072 ◽  
Author(s):  
Heather T Whittaker ◽  
Yichen Qui ◽  
Conceição Bettencourt ◽  
Henry Houlden

Multiple system atrophy (MSA) is one of the few neurodegenerative disorders where we have a significant understanding of the clinical and pathological manifestations but where the aetiology remains almost completely unknown. Research to overcome this hurdle is gaining momentum through international research collaboration and a series of genetic and molecular discoveries in the last few years, which have advanced our knowledge of this rare synucleinopathy. In MSA, the discovery of α-synuclein pathology and glial cytoplasmic inclusions remain the most significant findings. Families with certain types of α-synuclein mutations develop diseases that mimic MSA, and the spectrum of clinical and pathological features in these families suggests a spectrum of severity, from late-onset Parkinson’s disease to MSA. Nonetheless, controversies persist, such as the role of common α-synuclein variants in MSA and whether this disorder shares a common mechanism of spreading pathology with other protein misfolding neurodegenerative diseases. Here, we review these issues, specifically focusing on α-synuclein mutations.


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