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Malnutrition during childhood precedes growth failure and affects the child’s well-being later in life. This study aims to investigate the potency of iron-fortified klutuk banana (Musa balbisiana Colla) flour on growth parameters and fibroblast growth factor 21 (FGF21) expression in malnourished rat model.

Rats were allocated into normal control (NC), untreated malnutrition (MC), malnutrition + iron-fortified klutuk banana flour (IBF) and malnutrition + Indonesian Government-issued biscuit (GB). Malnutrition was induced by an isoenergetic low-protein diet for five weeks. The IBF and GB groups were supplemented with IBF 1.2 g/200 gBW and GB 1.2 g/200 gBW, respectively, via gavage daily for three weeks. The body weight and length, the levels of plasma and liver FGF21 and red blood cell indices were analyzed.

After three weeks of supplementation, the IBF group showed higher body weight (245 ± 13.6 g vs 201.8 ± 16.3 g; p = 0.0004) and length (20.9 ± 0.5 cm vs 19.8 ± 0.5 cm; p = 0.021) compared with the untreated group. The plasma FGF21 level decreased in the IBF group (p = 0.034). The IBF group altered mean corpuscular volume and mean corpuscular hemoglobin, suggesting the IBF might attenuate malnutrition-induced anemia. Overall, the IBF prevented growth failure in malnourished condition. This might be mediated by the suppression of FGF21 expression, along with the prevention of malnutrition and anemia.

This study provides preliminary information about the potential use of rarely consumed banana, klutuk banana, as a supplement to treat malnutrition. This study might help the developing countries to eliminate the widespread malnutrition in economically challenged communities.

Traumatic brain injuries (TBIs) are a significant public health problem that affect an estimated 1.7 million US residents yearly. TBI patients experience a variety of symptoms related to physical functioning, sensory processing, cognition, communication, behavior, and mental health, all of which differ in severity by individual. Recent evidence suggests that hypothalamic pituitary dysfunction may be impacting recovery. The purpose of this paper is to increase awareness about the frequency of hypothalamic pituitary dysfunction following a TBI and its effect on functional recovery.

The paper reviews the literature regarding hypothalamic pituitary dysfunction following TBI and discusses the potential benefits of hormone replacement therapy for individuals with hormone deficiencies.

The rate of hypothalamic pituitary dysfunction following TBI has been reported as anywhere between 25 and 80 percent. Specifically, abnormal hormone levels, both chronic and acute, are generally estimated to be approximately 5-22 percent for thyroid hormones, 15-33 percent for growth hormone (GH), and 25-80 percent for testosterone. The effect of hypopituitarism has been reported on several aspects cognitive and physical function as well as overall quality of life. In these studies, GH and testosterone deficiencies appear to underlie the observed impairments.

The paper suggests the importance of understanding and screening for hypothalamic pituitary dysfunction as hormone replacement therapy may be a beneficial intervention to promote physical and cognitive rehabilitation.

The paper's purpose is to examine evidence for the benefits of exercise in relation to cancer development, progression and prevention.

The reviewed literature was divided into categories according to the role exercise plays in cancer prevention and progression, during treatment, and in relapse prevention.

There is now persuasive evidence that exercise improves the physical and psychological function of patients with cancer, reduces the risk of recurrence and possibly improves survival.

Previous research highlights the importance of exercise in cancer prevention and throughout the cancer experience. However, current knowledge of the mechanisms by which physical activity may positively influence the activity of cancers is poorly understood; these mechanisms are explored in this paper.

Agonistic antagonistic system theory and praxis were born in the medical field, but may be defined now from an epistemological and biomathematical point of view. Describes new developments in agonistic antagonistic (AA) theory and presents new applications. These include new mathematical approaches that involve variable parameters and partial derivatives in models for the regulation of AA couples (MRAAC). Gives new biomedical applications and, in explanation, a mechanism called “pathological homeostasis” (PH) is introduced. Also provides details of therapeutical trials. Suggests systems science or cybernetical strategies which are likely to have a broad field of application, particularly among decision makers in general.

It has been suggested that there is a link between the dietary intake of certain nutrients and the risk of prostate cancer. The aim of this study is to examine the associations between dietary intakes of all nutrients and the risk of prostate cancer in Kermanshah.

This case-control study was conducted in Kermanshah, a province in the west of Iran in November of 2016. The sample consisted of 50 patients with confirmed prostate cancer, and 150 healthy men who matched in age with these cases and did not have any symptoms of prostate disorder were chosen as controls. Dietary intakes were collected by a semi-quantitative food frequency questionnaire that contained 147 food items and were then analyzed by Nutritionist 4 software.

After adjustment for potential confounding factor, highest tertile compared to lowest tertile of dietary vitamin E intake [odds ratio (OR) = 0.21; 95% confidence interval (CI) = 0.05-0.89], lycopene intake (OR = 0.11; 95% CI = 0.01-0.86) and magnesium intake (OR = 0.02; 95% CI = 0.01-0.55) had a protective effect on the incidence of prostate cancer. However, there were no associations between dietary intakes of fiber, vitamin A, vitamin D, vitamin B₁₂, folate and calcium with prostate cancer.

The finding suggests that the dietary intakes of vitamin E, lycopene and magnesium could decrease the risk of prostate cancer. Nevertheless, dietary intake of other nutrients such as fiber, calcium, vitamins D, A, B₁₂ and folate was not associated with prostate cancer.

The ageing process is often discussed as though it is unique to humans. However, it can be observed throughout the plant and animal kingdoms. In every species in which it occurs, the ageing process has common traits. It is a progressive, intrinsic, cumulative and deleterious process that eventually gives rise to physiological frailty, morbidity and death. Historically, biogerontology had a slow start but the last 10 years have seen exceptional progress in understanding both why and how ageing changes occur. As a result of this new knowledge, interventions that could produce longer, healthier human lives are close to becoming clinical realities. Unfortunately, the speed and scale of these advances is not well understood outside the relatively small community of biological gerontologists. This article reviews some of these advances for a non‐specialist audience, speculates on their potential impact and identifies current barriers to future progress.

Although first rank symptoms focus on positive symptoms of psychosis they are shared by a number of psychiatric conditions. The difficulty in differentiating bipolar disorder from schizophrenia with affective features has led to a third category of patients often loosely labeled as schizoaffective. Research in schizophrenia has attempted to render the presence or absence of negative symptoms and their relation to etiology and prognosis more explicit. A dichotomous population is a recurring theme in experimental paradigms. Thus, schizophrenia is defined as process or reactive, deficit or non-deficit and by the presence or absence of affective symptoms. Laboratory tests confirm the clinical impression showing conflicting responses to dexamethasone suppression and clearly defined differences in autonomic responsiveness, but their patho-physiological significance eludes mainstream theory. Added to this is the difficulty in agreeing to what exactly constitutes useful clinical features differentiating, for example, negative symptoms of a true deficit syndrome from features of depression. Two recent papers proposed that the general and specific cognitive features of schizophrenia and major depression result from a monoamine-cholinergic imbalance, the former due to a relative muscarinic receptor hypofunction and the latter, in contrast, to a muscarinic hypersensitivity exacerbated by monoamine depletion. Further development of these ideas will provide pharmacological principles for what is currently an incomplete and largely, descriptive nosology of psychosis. It will propose a dimensional view of affective and negative symptoms based on relative muscarinic integrity and is supported by several exciting intracellular signaling and gene expression studies. Bipolar disorder manifests both muscarinic and dopaminergic hypersensitivity. The greater the imbalance between these two receptor signaling systems, the more the clinical picture will resemble schizophrenia with bizarre, incongruent delusions and increasingly disorganized thought. The capacity for affective expression, by definition a non-deficit syndrome, will remain contingent on the degree of preservation of muscarinic signaling, which itself may be unstable and vary between trait and state examinations. At the extreme end of muscarinic impairment, a deficit schizophrenia subpopulation is proposed with a primary and fixed muscarinic receptor hypofunction.

The genomic profile of bipolar disorder and schizophrenia overlap and both have a common dopaminergic intracellular signaling which is hypersensitive to various stressors. It is proposed that the concomitant muscarinic receptor upregulation differentiates the syndromes, being marked in bipolar disorder and rather less so in schizophrenia. From a behavioral point of view non-deficit syndromes and bipolar disorder appear most proximate and could be reclassified as a spectrum of affective psychosis or schizoaffective disorders. Because of a profound malfunction of the muscarinic receptor, the deficit subgroup cannot express a comparable stress response. None -theless, a convergent principle of psychotic features across psychiatric disorders is a relative monoaminergic-muscarinic imbalance in signal transduction.

One limitation of research that assesses the effectiveness of physical activity interventions for people with dementia is that most do not describe the intervention in sufficient detail to ascertain a theoretical basis or mechanism of action that determines the effective components. This paper aims to identify studies which evaluate the mechanisms of action of physical activity interventions for people with dementia, to further inform effective intervention development.

Papers were screened for evidence of evaluation of specific forms of physical activity, using pre-defined inclusion criteria. Analysis was conducted to ascertain if mechanisms of action were corroborated by data within and between studies.

The authors identified 26 studies with a measured mechanism of action; these related to the effects of physical activity on either neurological structure or endocrinal markers, including hormones. Physical activity had potential to reduce hippocampal atrophy, increase neural recruitment, activate the noradrenergic system and improve anti-inflammatory responses. While individual studies were hampered by small sample sizes, the body of evidence indicated that physical activity may have potential to delay cognitive decline.

Mechanisms of action in relation to dementia and physical activity are likely to be multifaceted, and physical activity may be protective against progression in the early stages of cognitive decline. Physical activity may be of greatest benefit if incorporated into on-going lifestyle, rather than engaged in for short periods, and combined with social interaction.

This paper is unique in its focus on the mechanisms of action of physical activity interventions for people with dementia.