-Stressand anxiety-related disorders are on the rise in both military and general populations. Over the next decade, it is predicted that treatment of these conditions, in particular, posttraumatic stress disorder (PTSD), along with its associated longterm comorbidities, will challenge the health care system. Multiple organ systems are adversely affected by PTSD, and PTSD is linked to cancer, arthritis, digestive disease, and cardiovascular disease. Evidence for a strong link between PTSD and cardiovascular disease is compelling, and this review describes current clinical data linking PTSD to cardiovascular disease, via inflammation, autonomic dysfunction, and the renin-angiotensin system. Recent clinical and preclinical evidence regarding the role of the renin-angiotensin system in the extinction of fear memory and relevance in PTSD-related immune and autonomic dysfunction is also addressed. posttraumatic stress disorder; cardiovascular disease; renin-angiotensin system POSTTRAUMATIC STRESS DISORDER (PTSD) is a psychiatric illness characterized by persistent emotional and mental stress following a traumatic event. Symptoms of PTSD include hyperarousal, flashbacks, intrusive thoughts, or nightmares, and avoidance of activities that trigger memories of the traumatic event. The health consequences of PTSD are substantial, affecting multiple organ systems, with evidence linking PTSD to diseases such as cancer, arthritis, digestive disease, and cardiovascular disease (CVD) (13,14,112). The evidence demonstrating increased risk for CVD in PTSD (9,15,19,49,57,58) is compelling, and several excellent recent review articles have highlighted this association (20,23,52,63,112). While this association could certainly be due, in part, to related unhealthy behaviors, such as increased prevalence of smoking, poor diet, and physical inactivity (46,119). Yet even after adjustments for lifestyle, comorbid conditions, and combat engagements in multivariate models, PTSD remains a significant and independent risk factor for the development of CVD and CVD-related mortality (15).Increased CVD risk in PTSD has been demonstrated in both military (21) and civilian populations (44,82). A co-twin study design (monozygotic and dizygotic), which controlled for genetic and familial confounders, demonstrated that the incidence of coronary heart disease was more than double in Vietnam War veteran twins with PTSD (22.6%) compared with those without PTSD (8.9%) (106). Most recently, one of the largest longitudinal studies examining the association between PTSD and heart failure was completed, and veterans with PTSD were shown to be nearly 50% more likely to develop heart failure than veterans without PTSD (91). This remained significant after adjustments for age, sex, diabetes, hyperlipidemia, hypertension, body mass index, combat, and military service. Civilian PTSD populations are also at greater risk for CVD. Following life-threatening traumatic events such as earthquakes (82), the 9 -11 World Trade Center attack (45), and living in urban dis...

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One of the most distinct features of middle ear cholesteatoma is bone destruction. Aetiology of cholesteatoma is thought to be multifactorial. Endotoxins produced by bacteria are thought to initiate the inflammation process in the middle ear leading to cholesteatoma. There are physiological differences in bone metabolism between men and women. The aim of our study was the immunohistochemical evaluation of the contents of two key components of the OPG/RANK/RANKL triad-RANKL and OPG in cholesteatoma, to analyse if there are any differences between the sexes and to evaluate the bacteria species isolated from cholesteatoma just before surgical treatment and to evaluate their plausible influence on the expression of OPG and RANKL in cholesteatoma. Twenty-one adult patients with acquired cholesteatoma who underwent surgery were analysed. There were no statistically significant differences in the expression of both regulators of osteoclastogenesis between the sexes. In 38.1 % patients cholesteatoma was not infected, whereas in 61.9 % patients various bacterial infections or mycosis were found. The most frequently isolated species was Pseudomonas aeruginosa (14.29 % infections) followed by Staphylococcus aureus (9.52 % infections). There were no statistically significant differences in expression of both OPG and RANKL between uninfected and infected cholesteatomas.

Since the last review paper published in Cerebellum in 2002 [1], there has been a substantial increase in the number of experiments utilizing transgenic manipulations in murine cerebellar Purkinje cells. Most of these approaches were made possible with the use of the Cre/loxP methodology and pcp2/L7 based Cre recombinase expressing transgenic mouse strains. This review aims to summarize all studies which used Purkinje cell specific transgenesis since the first use of mouse strain with Purkinje cell specific Cre expression in 2002.

The high-fat and low-carbohydrate ketogenic diet (HFKD) is extensively studied within the fields of numerous diseases, including cancer and neurological disorders. Since most studies incorporate animal models, ensuring the quality of ketogenic rodent diets is important, both in the context of laboratory animal welfare as well as for the accuracy of the obtained results. In this study we implemented a modification to a commonly used ketogenic rodent chow by replacing non-resorbable cellulose with wheat bran. We assessed the effects of month-long treatment with either the unmodified or the modified HFKD on the growth and development of young male rats. Daily body weight, functional performance, and brain morphometric parameters were assessed to evaluate the influence of both applied diets on rodent development. Our results revealed that the unmodified ketogenic chow induced strong side effects that included weakness, emaciation, and brain undergrowth concomitant to growth inhibition. However, application of the ketogenic chow supplemented with wheat bran suppressed these adverse side effects, which was associated with the restoration of insulin-like growth factor 1 and a decrease in corticosterone levels. We have also shown that the advantageous results of the modified HFKD are not species- or sex-specific. Our data indicate that the proposed HFKD modification even allows for its application in young animals, without causing detrimental side effects.