Effects of NAD+ booster NMN on ovarian function and late-life bone health

Ovarian ageing is a major health concern with socioeconomic consequences, manifesting at the comparatively young age of around 35 years. In cancer patients who have undergone chemotherapy, this process is greatly accelerated and can lead to premature ovarian insufficiency, infertility and early menopause, which severely impact the quality of life of cancer survivors. Options for preserving fertility may be limited by the urgency of cancer treatment or by patient age. Recently, repletion with the nicotinamide adenine dinucleotide (NAD+ ) precursor nicotinamide mononucleotide (NMN) was shown to maintain reproductive function during ageing. Here, we sought to test whether NMN treatment might protect against chemotherapy-induced infertility and whether this could extend beyond fertility to other aspects of late-life health. We found that co-treatment of NMN with doxorubicin (Dox) maintains primordial follicle health, however, this did not reach statistical significance. This finding was in line with previous findings regarding the ability of NMN to maintain breeding performance during Dox. We also tested whether NMN could maintain the ovarian reserve when delivered following early-life cisplatin (CDDP) treatment, which modelled pediatric cancer treatment. While there was no impact of NMN on CDDP-induced follicle loss, this treatment did improve aspects of late-life health, with drastic improvements in bone function as measured by CT structural imaging, mechanical testing, and histological analysis. In line with the absence of an effect on ovarian reserve, there was no effect of NMN on estrogen (E2) levels, suggesting that the rescue in bone function was unrelated to ovarian effects. These promising effects may be important to maintaining the late-life health of female cancer survivors, but further work will be required to elucidate the mechanisms of action

Precarity and identity in the ivory tower: exploring the effects of performative pressures in UK and French business schools

Recent marketization trends in Higher Education trigger concerns about growing precarity of the academic profession. Global pressures from reputational mechanisms such as international rankings and accreditations underpin the risk of institutional isomorphism and a possible convergence of academic career paths. This thesis draws from a comparative empirical study of academic careers in UK and French Business Schools and focuses on two areas of inquiry. The first study demonstrates how context-bound career scripts, their validation mechanisms, and the margins they allow for individual agency variously shape permeable and impermeable career boundaries and mechanisms for precarity, and condition the agentic behaviour of academics. I argue that the particular ways in which performance incentives and punishments are balanced in each country under supranational competitive pressures produce different results in terms of segregation and casualization of academics. The second study explores identity responses of female faculty to performative pressures in the two countries and the strategies they adopt to reconcile compliance with managerialist requirements and their own need for recognition and meaningful work in what is traditionally seen as a gendered professional environment. My contributions deepen the understanding of contextual responses to international challenges and highlight the implications for academics and institutions

A case of non-compaction cardiomyopathy

The aim of this case report was to present a rare myocardial disease, the so-called isolated non-compaction cardiomyopathy (NCCM). This disorder, a primary genetic cardiomyopathy, attracts increasing attention. A woman with a sudden onset of shortness of breath and isolated NCCM is described. Criteria for diagnosis as well as echocardiographic findings and magnetic resonance imaging of the heart are presented. Although rare, a new option of myocardial disease with various modes of clinical presentation but, most commonly, with acute or chronic heart failure should be taken into consideration. Multiple imaging modalities are available and should be used for proper diagnosis.Scripta Scientifica Medica 2013; 45(3): 86-89

Industrial toxic pollution of marine waters - the Minamata Case

Industrial toxic pollution of seawater poses a risk to the lives and health of the local population. Accumulation of toxic chemicals in the food chain can seriously harm not only people in the area but also their generations. Minamata disease is a typical example of harm caused to people by environmental pollution.Literature on industrial toxic pollution of marine waters and the subsequent health problems has been collected and analyzed. Monographs, articles in Bulgarian and foreign scientific journals, and other literature sources on methylmercury pollution found out in Minamata Bay, Kumamoto Prefecture, Japan, have been investigated and summarized.Minamata disease is a methylmercury poisoning with neurological symptoms due to the daily consumption of fish, seafood and seaweed obtained fromJapan`s highly toxic, polluted area. Two outbreaks of the disease have been observed. Conclusions have been drawn that methylmercury (a by-product of the production of acetaldehyde discharged by the wastewater of chemical plants) accumulates in the marine inhabitants` food chain causing Minamata disease. It has not only a medical aspect but also a social and economic one. Identifying the cause of the disease leads to serious measures being taken in Japan to protect the environment and the health of the population. Chemical enterprises are closed and the victims are paid benefits. Millions of dollars have been invested to eradicate the accumulated methylmercury in the sediments of the Shiranui Sea. Establishing the link between the consumption of mercury-contaminated foods and Minamata disease lead to significant legislative changes in Japan and later in the whole world

Susceptibility to Neurodegenerative Disorders: Insights from Paleogenomic Data

Ancient human genome data that has accumulated in recent years can be employed to establish the spatiotemporal trajectories of genetic variants associated with human diseases. Such knowledge might illuminate if and how past adaptations impact contemporary human health and medicine. Scarcely any studies have yet been attempted to evaluate the genetic susceptibility to neurodegenerative disorders in ancient human communities. Using publicly available ancient human genome-wide data the present study evaluates the molecular predisposition to neurodegenerative disorders in ancient human communities. To this end we screened the ancient genome-wide data for the presence of variants unequivocally associated with neurodegenerative disorders in modern populations, and their historical and geographic prevalence was assessed. These variants are two rare variants in the LRRK2 gene associated with Mendelian Parkinson\u27s disease, a pathogenic variant in the CRH gene, associated with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), and a rare variant in the TREM2 gene, a possible risk modifier associated with Alzheimer\u27s disease. Our assessment of the historical and geographic prevalence indicates differing spatiotemporal frequency dynamics for these clinically significant variants. Neurodegenerative disorders are often with poorly understood pathogenesis that might be elucidated by studying the interaction of past genetic variability with ecological and evolutionary factors such as adverse environmental conditions, specific selective pressures, periods of population isolation and admixture processes. Data on molecular predisposition to neurodegenerative disorders in ancient genomes is instructive to modern medical diagnostic and therapeutic practices

Levels of carboxylated and undercarboxylated osteocalcin in patients with type 2 diabetes

Introduction: Osteocalcin (OC) is a bone-derived protein that undergoes vitamin K-dependent carboxylation. The undercarboxylated form of the protein (ucOC) is released in the circulation during the process of bone resorption. Experimental studies on mice and rats have revealed that ucOC is involved in the regulation of energy homeostasis, linking in this way the bone, pancreas, and adipose tissue metabolism. Experimental studies suggest no hormonal role for the carboxylated form (cOC) of the protein.Aim: In the current study we aimed to examine the levels of OC in its carboxylated and undercarboxylated form in patients with type 2 diabetes and control subjects, and to compare the vitamin K status between the two groups. Materials and Methods: The present cross-sectional study involved a sample of 46 adults type 2 diabetes patients and a control group of 19 individuals. The carboxylated and undercarboxylated forms of OC were measured in serum by using highly sensitive sandwich-type enzyme immunoassay kits. Vitamin K status was evaluated by the ratio ucOC/cOC. Student’s two-tailed unpaired t-test was used to compare the groups.Results: UcOC and cOC serum levels were significantly lower in patients with type 2 diabetes compared to controls. We found no difference in the vitamin K status between the groups.Conclusion: Our results show that OC might be involved in the regulation of carbohydrate metabolism. In humans, it appears that the carboxylation state might not be essential for the hormonal role of the protein as in mice and rats

Towards Better Understanding of Ancient Civilizations by Storytelling and Gaming

The new strategies for teaching and learning point to the investigation and the deployment of workable learning methods and scenarios for better understanding of the learning content and engagement learners in more active participation during the perception of knowledge. This paper presents a new learning approach for studying the ancient history and civilization and the Thracian civilization in particular, by storytelling and serious game combination