Indicators of domestic/intimate partner violence are structured by genetic and nonshared environmental influences

One of the most consistent findings to emerge from domestic/intimate partner violence (IPV) research is that IPV tends to “run in the family.” Social learning theories appear to be consistent with empirical data, but almost no attention has been given to alternative explanations, including that genetic factors explain intergenerational transmission of IPV. Data for this study were drawn from wave 4 of the National Longitudinal Study of Adolescent Health (Add Health). Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance. These findings point to the importance of genetic factors in the etiology of IPV.     

Early partial reperfusion in a new rat model of focal cerebral ischaemia

The influence of early partial reperfusion in a new rat model of focal cerebral ischaemia was investigated. Two groups, each of 30 adult male rats, were subjected to permanent occlusion of the right middle cerebral artery. The former, (group A) had an additional permanent occlusion of both common carotid arteries; the latter (group B) had a temporary carotid occlusion lasting for two hours. Mortality rate, evaluated within three days, was 70% ingroup A and 20% in group B. The mean size of cerebral infarcts was 63% in group A whereas it was 21% in group B. These data suggest that, in this animal model, early partial reperfusion is effective in reducing the mortality rate, and the size of the cerebral infarcts. Furthermore, this experimental model appears suitable for studies elucidating the role of reperfusion andlor other efforts in focal cerebral ischaemia.     

Experimental intracerebral hemorrhage: Description of a double injection model in rats

Abstract

For experimental purposes, f/ie mosf common technique of producing an intracerebral hematoma in rats is the injection of unclotted autologous blood. All modifications of this model share the problem that size and extension of the hematoma are not reproducible, because the injected blood either ruptures into the ventricular system or it extends to the subarachnoid or subdural space. Therefore a double injection model of experimental intracerebral hemorrhage in rats has been developed using 19 male Sprague-Dawley rats. After inducing anesthesia a cannula was stereotactically placed into the caudate nucleus and an intracerebral hematoma was produced with the double injection method in which first a small amount of fresh autologous blood is injected which is allowed to clot (preclotting) in order to block the way back along the needle track; the actual hematoma is produced in a second step of the injection. The clot volume was measured on stained serial sections. A total injection volume of 50 \i! of autologous blood produced intracerebral hematomas of 41.1 ± 10.0 \i\ and of similar shapes. The double injection method allows to generate reproducible hematomas in rats. This new model of intracerebral hemorrhage will allow further investigation of fibrinolytic and cytoprotective therapies. [Neurol Res 1996; 18: 475-477]     

Clinical analysis of factors predisposing the recurrence of primary intracerebral hemorrhage in patients taking anti-hypertensive drugs: A prospective cohort study

Objective

The study examined differences in the recurrence rate of primary intracerebral hemorrhage (P-ICH) according to anti-hypertensive drug (AHD) use by patients with hypertension.

Methods

This prospective, longitudinal cohort study was performed on 2384 patients diagnosed with supratentorial P-ICH and hypertension in the stroke unit of a single-center. During follow-up (mean, 44.9 ± 31.5 months), investigators interviewed subjects or caregivers by telephone or examined patients every 3–6 months. Target blood pressure was <140/90 mmHg in the P-ICH cohort with hypertension.

Results

Of 1317 P-ICH patients defined to be taking AHDs, P-ICH recurrence occurred in 129 (9.8%). 1211 patients (92.0%) reached target blood pressure. In multivariate regression analysis, advanced age (≥70 years), poor functional outcome after first P-ICH, lobar location of P-ICH, previous history of cerebral ischemia, diuretic monotherapy and α- or β-blocker monotherapy were associated with risk of recurrence.

Conclusions

Although hypertension is the most important factor for preventing P-ICH recurrence, we found that, even in the presence of optimal anti-hypertensive medication, recurrent P-ICH attack can occur. Therefore, management of other risk factors of recurrent P-ICH, such as modification of lifestyle, must be considered in treating the P-ICH patients.     

Adenosine A2A receptor deficiency alleviates blast-induced cognitive dysfunction

Traumatic brain injury (TBI), particularly explosive blast-induced TBI (bTBI), has become the most prevalent injury among military personnel. The disruption of cognitive function is one of the most serious consequences of bTBI because its long-lasting effects prevent survivors fulfilling their active duty and resuming normal civilian life. However, the mechanisms are poorly understood and there is no treatment available. This study investigated the effects of adenosine A2A receptor (A2AR) on bTBI-induced cognitive deficit, and explored the underlying mechanisms. After being subjected to moderate whole-body blast injury, mice lacking the A2AR (A2AR knockout (KO)) showed less severity and shorter duration of impaired spatial reference memory and working memory than wild-type mice did. In addition, bTBI-induced cortical and hippocampal lesions, as well as proinflammatory cytokine expression, glutamate release, edema, cell loss, and gliosis in both early and prolonged phases of the injury, were significantly attenuated in A2AR KO mice. The results suggest that early injury and chronic neuropathological damages are important mechanisms of bTBI-induced cognitive impairment, and that the impairment can be attenuated by preventing A2AR activation. These findings suggest that A2AR antagonism is a potential therapeutic strategy for mild-to-moderate bTBI and consequent cognitive impairment.     

Self-reported experiences as predictors for onset of psychotropic medication. A prospective study of healthy draftees

Abstract

Background: Psychosis and other psychiatric disorders are often preceded by prodromal symptoms. There are few community-based studies on symptom predictors of severe mental problems in healthy people. Aims: We aimed to study how a new self-reported screen for prodromal symptoms (PROD) predicts onset of all psychotropic and antipsychotic medication in healthy draftees. Methods: In a prospective follow-up study, 2330 18-year-old Finnish draftees who at call-up in 1999 completed the PROD comprising 21 symptom items divided into positive, negative and general symptom categories were prospectively followed for 6 years. First purchases of any psychotropic and antipsychotic drugs separately between 2000 and 2005 were used as an indicator of the onset of psychiatric disorder and predicted by PROD symptoms in Cox regression analysis. Results: A majority of the PROD items significantly predicted the first purchases of any psychotropic and of antipsychotic drugs, separately. Positive, negative and general symptoms predicted purchases of any psychotropic medication, while negative and general symptoms predicted purchases of antipsychotic drugs. General symptoms, in particular anxiety, had a strong independent association with onset of psychotropic medication. Conclusions: In young healthy men, self-reported sub-clinical psychic symptoms predict onset of psychiatric disorders requiring psychotropic, including antipsychotic, medication.     

Attachment-Based Family Therapy for Adolescent Self-Injury

There is growing awareness in the popular media and in clinical reports of the increasing prevalence of self-injury, especially among adolescents. Self-injury affects the entire family and is, in turn, affected by the family system. Thus, family therapy is an important component when working with adolescents who are still dependent on their families. However, available treatments, for the most part, do not address the relational-systemic aspects of self-harm, and treat only the individual. This article situates self-harm within the relational framework of adolescent attachment theory and presents a case study demonstrating the treatment of adolescent self-injury with attachment-based family therapy.     

Minocycline suppresses experimental autoimmune encephalomyelitis by increasing tissue inhibitors of metalloproteinases

Matrix metalloproteinases (MMPs) that are secreted by activated T cells play a significant role in degradation of the extracellular matrix around the blood vessels and facilitate autoimmune neuroinflammation; however, it remains unclear how MMPs act in lesion formation and whether MMP‐targeted therapies are effective in disease suppression. In the present study, we attempted to treat experimental autoimmune encephalomyelitis (EAE) by administration of small interfering RNAs (siRNAs) for MMP‐2, MMP‐9, and minocycline, all of which have MMP‐inhibiting functions. Minocycline, but not siRNAs, significantly suppressed disease development. In situ zymography revealed that gelatinase activities were almost completely suppressed in the spinal cords of minocycline‐treated animals, while significant gelatinase activities were measured in the EAE lesions of control animals. However, MMP‐2 and MMP‐9 mRNAs and proteins in the spinal cords of treated rats were unexpectedly upregulated. At the same time, mRNA for tissue inhibitors of MMPs (TIMP)‐1 and ‐2 were also upregulated. The EnzChek Gelatinase/Collagenase assay using tissue containing native MMPs and TIMPs demonstrated that gelatinase activity levels in the spinal cords of treated rats were suppressed to the same level as those in normal spinal cord tissues. Finally, double immunofluorescent staining demonstrated that MMP‐9 immunoreactivities of treated rats were almost the same as those of control rats and that MMP‐9 and TIMP‐1 immunoreactivities were colocalized in the spinal cord. These findings suggest that minocycline administration does not suppress MMPs at mRNA and protein levels but that it suppresses gelatinase activities by upregulating TIMPs. Thus, MMP‐targeted therapies should be designed after the mechanisms of candidate drugs have been considered.