Measuring female intrasexual competition by the scale for intrasexual competition: a validation of the German version

Competitive behaviour amongst members of the same sex is termed intrasexual competition. The tendency to engage in such competition appears to be strongly related to stable individual characteristics such as personality traits. Additionally, recent studies have revealed transient fluctuations in competitiveness according to the female menstrual cycle. To date, no German questionnaire exists to measure intrasexual competition. Our first study aimed to translate and validate the Intrasexual Competition Scale (ICS) by Buunk and Fisher (J Evol Psychol 7:37–48, 2009) in a population of healthy Swiss females (n = 241). Our second study applied the validated German ICS in a group of healthy, regularly cycling females (n = 49) in order to examine possible associations between the menstrual cycle phase and ICS scores. The psychometric properties suggest that the German ICS is a reliable and valid tool to assess individual differences in female intrasexual competition. Furthermore, our second study demonstrated that on average, women showed higher intrasexual competition scores when tested in the late follicular phase (M = 35.77 ± SD = 12.03) compared to the mid-luteal phase (M = 30.93 ± SD = 10.20). Our studies support previous findings of an association between ICS scores and relatively stable individual characteristics such as personality traits. Furthermore, our research endorses the assumption of cycle-dependent fluctuations in intrasexual competition. Future research should clarify the precise mechanisms underlying these findings and include biomarkers such as oestrogen and testosterone.

     

The Relationship between AKI and CKD in Patients with Type 2 Diabetes: An Observational Cohort Study

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Migraine and the Risk for Stroke and Cardiovascular Disease

Numerous data have pointed to an association between migraine and cardiovascular diseases. The majority of the available data have indicated that migraine with aura can be considered a risk factor for ischemic stroke, whereas migraine without aura cannot be reliably considered as such. High frequency of attacks and a recent onset of migraine have been related to an increased ischemic stroke risk. In addition, in young subjects with ischemic stroke migraine with aura represents an independent risk factor of overall recurrent vascular events and of recurrent ischemic stroke. Also the risk of transient ischemic attack seems to be increased in migraineurs, although this issue has not been extensively investigated. Several studies have also addressed the possible association between migraine and hemorrhagic stroke. Although the results of these individual studies were conflicting, their meta-analysis showed that migraine is associated with a 1.5-fold increase in the risk of hemorrhagic stroke (including intracerebral and subarachnoid hemorrhage). Some studies have identified migraine also as a possible risk factor for cardiac vascular events while others have yielded negative results. A meta-analysis did not show an increased risk of myocardial infarction in subjects with any migraine vs no migraine but subsequently, data has pointed to an association between any migraine with cardiac ischemic disease. Migraine has also been associated by some studies with vascular mortality and with vascular diseases in regions other than the brain and the heart. Several studies have also indicated that compared with nonmigraineurs, migraineurs have a higher burden of asymptomatic white matter brain lesions and, according to some studies, also infarct-like lesions at brain magnetic resonance. The mechanisms underlying the relationship between migraine and cardiovascular disease are still unclear. The possible explanation may rely on a peculiar vascular vulnerability of migraineurs that may contribute to the pathogenesis of migraine and, in the presence of some other unknown factors may also contribute, over time, to the development of cardiovascular disease. At the moment, there are no reliable features that may indicate which subjects, across the overall migraine population, will develop vascular events and so far, no drugs are recommended for the vascular prevention in migraineurs unless other clear indications are present. In general, the acute treatment and the secondary prevention measures of a patient with stroke who has a history of migraine do not differ from that of other stroke patients. There is currently no direct evidence to support that a migraine prophylactic treatment will reduce future stroke risk in secondary prevention.     

Melatonin down‐regulates MDM2 gene expression and enhances p53 acetylation in MCF‐7 cells

Compelling evidence demonstrated that melatonin increases p53 activity in cancer cells. p53 undergoes acetylation to be stabilized and activated for driving cells destined for apoptosis/growth inhibition. Over‐expression of p300 induces p53 acetylation, leading to cell growth arrest by increasing p21 expression. In turn, p53 activation is mainly regulated in the nucleus by MDM2. MDM2 also acts as E3 ubiquitin ligase, promoting the proteasome‐dependent p53 degradation. MDM2 entry into the nucleus is finely tuned by two different modulations: the ribosomal protein L11, acts by sequestering MDM2 in the cytosol, whereas the PI3K‐AkT‐dependent MDM2 phosphorylation is mandatory for MDM2 translocation across the nuclear membrane. In addition, MDM2‐dependent targeting of p53 is regulated in a nonlinear fashion by MDM2/MDMX interplay. Melatonin induces both cell growth inhibition and apoptosis in MCF7 breast cancer cells. We previously reported that this effect is associated with reduced MDM2 levels and increased p53 activity. Herein, we demonstrated that melatonin drastically down‐regulates MDM2 gene expression and inhibits MDM2 shuttling into the nucleus, given that melatonin increases L11 and inhibits Akt‐PI3K‐dependent MDM2 phosphorylation. Melatonin induces a 3‐fold increase in both MDMX and p300 levels, decreasing simultaneously Sirt1, a specific inhibitor of p300 activity. Consequently, melatonin‐treated cells display significantly higher values of both p53 and acetylated p53. Thus, a 15‐fold increase in p21 levels was observed in melatonin‐treated cancer cells. Our results provide evidence that melatonin enhances p53 acetylation by modulating the MDM2/MDMX/p300 pathway, disclosing new insights for understanding its anticancer effect.     

Effectiveness of primary percutaneous coronary intervention for acute ST-elevation myocardial infarction from a 5-year single-center experience

Primary percutaneous coronary intervention (PCI) is currently viewed as the preferred reperfusion strategy in patients with ST-elevation acute myocardial infarction (STEMI). This method was introduced in our hospital in 2000. From January 1, 2000, to December 31, 2004, a total of 2,393 consecutive patients with STEMI were admitted (27% transferred from 9 non-PCI hospitals and 31 prehospital emergency units/outpatient clinics). Of these patients, 1,666 (70%) underwent urgent coronary angiography and primary PCI. Platelet glycoprotein llb/llla inhibitors were used in 40% and stent placement, in 78%. Postprocedural Thrombolysis In Myocardial Infarction (TIMI) 3 flow was documented in 86%. Intra-aortic balloon counterpulsation was used in 6%; mechanical ventilation, in 8.6%; and inotropic drugs/vasopressors, in 15.8%. Mortality rates in patients with Killip's class I or II ranged from 1% to 4.9% without negative influence of ischemic time. In patients with Killip's class III or IV, mortality rates increased from 18% to 54% with increasing ischemic delay up to 6 hours (p = 0.06) and remained at around 40% afterward. Independent predictors of mortality were age (odds ratio [OR] 1.29, 95% confidence interval [CI] 1.01 to 1.64, p = 0.04), resuscitated cardiac arrest (OR 2.44, 95% CI 1.18 to 5.05, p = 0.02), and postprocedural TIMI flow (OR 0.31, 95% CI 0.16 to 0.59). Overall mortality rates of patients who underwent a primary PCI strategy from 2000 to 2004 were significantly lower than in the control group of 152 consecutive patients who underwent thrombolysis from 1995 to 1996 (6.2% vs 16.4%; p <0.001). In conclusion, introduction of a primary PCI strategy significantly decreased hospital mortality in our unselected group of patients with STEMI compared with the thrombolytic era. Our study further emphasized the importance of shortening myocardial ischemic time, particularly in the presence of severe heart failure on admission.