This is the Nut You Should be Eating for Better Gut Health

The consumption of dried fruit is a dietary habit that is growing year by year. Nutrition specialists and others have carried out numerous studies confirming that the introduction of a controlled daily intake in the diet can bring benefits both in the prevention of major metabolic and cardiovascular diseases and in the well-being of the microbiome. The intake of dried fruit plays an important role in improving the quality and quantity of the microbial families of our intestine, leading to an increased production of short-chain fatty acids, which participate in numerous pathophysiological mechanisms and in the prevention of numerous diseases. The present review chapter compares numerous articles focusing on the characteristics and behavior of fibers and other main components of nuts

Negative Pressure Wound Therapy applied to a cholecystoparietal fistula: How to treat a rare complication of a common condition - a case report

A cholecystoparietal fistula is an uncommon complication of gallstone disease as a result of neglected gallbladder disease).The subcutaneous abdominal wall abscess, derived from this condition, might be wide and hard to treat, especially in elderly and debilitated patients. The best management of cholecystoparietal fistula depends on its etiology and may require medical, surgical, or endoscopic treatment. Negative Pressure Wound Therapy (NPWT) is a valuable support therapy that can improve the prognosis of the disease and the patient’s outcome. We report the case of an 89-year-old female patient affected by a spontaneous cholecystoparietal fistula with a wide abdominal wall abscess treated by a one-stage surgical approach combined with NPWT over the resulting skin loss

Role of nutraceuticals in cancer therapy.

Nutraceuticals are natural bioactive products with food value and promising therapeutic properties in several diseases. Current cancer treatments, such as chemotherapy, radiotherapy and surgery, induce unintended side effects compromising also health and well-being of patients. Emerging studies suggest that some plant-based agents may impact cellular and molecular processes underlying tumor progression. However, some of these molecules might also play an antagonistic activity against classic therapeutic agents. The aim of this article is to review the current knowledge underpinning the use of nutraceuticals in cancer prevention and therapy.</p

Major postoperative complications and survival for colon cancer elderly patients

BACKGROUND: Increased life expectancy has led to elevating the mean age of the patients at the time of diagnosis of colon cancer and subsequent treatment. Differences in complication rates and outcome between elderly and younger patients have been investigated. METHODS: We retrospectively analysed a database containing the information of patients who underwent surgery for stage I-III colorectal cancer from January 2004 to January 2012 at our institution and compared demographic, cancer-related, and outcomes data of 235 elderly patients with 211 patients ≤65 years old. RESULTS: Intraoperative complications did not differ between young and old patients whereas some differences have been found in postoperative and late complications: elderly patients suffered more by ileus (P = 0.024), peritonitis or septic shock (P = 0.017), pelvic abscess (P = 0.028), wound infection (P = 0.031), and incisional/port herniation (P = 0.012) compared with younger patients. Moreover, elderly patients suffered by systemic complications such as cardiovascular (4.7% vs. 1.4%, P = 0.049), renal (4.7% vs. 0.5%, P = 0.006), and respiratory (10.6% vs. 5.2%, P = 0.036). The multivariate analysis assessing the odds of having a complication revealed that older age (Odd Ratio [OR] 2.75, 95% Confidential Interval [CI]: 1.67-4.52) and open surgery (OR 1.63, 95% CI: 1.01-2.62) are significantly and independently associated with having a complication. CONCLUSIONS: In our series, elderly patients have presented a slight higher incidence of comorbidities that may affect the incidence rates of postoperative complications. These results have implications in increasing the hospital stay as well as a higher rate of death

Stress-Induced Changes of Hippocampal NMDA Receptors: Modulation by Duloxetine Treatment

It is now well established that the glutamatergic system contributes to the pathophysiology of depression. Exposure to stress, a major precipitating factor for depression, enhances glutamate release that can contribute to structural abnormalities observed in the brain of depressed subjects. On the other hand, it has been demonstrated that NMDA antagonists, like ketamine, exert an antidepressant effect at preclinical and clinical levels. On these bases, the purpose of our study was to investigate whether chronic mild stress is associated with specific alterations of the NMDA receptor complex, in adult rats, and to establish whether concomitant antidepressant treatment could normalize such deficits. We found that chronic stress increases the expression of the obligatory GluN1 subunit, as well as of the accessory subunits GluN2A and GluN2B at transcriptional and translational levels, particularly in the ventral hippocampus. Concomitant treatment with the antidepressant duloxetine was able to normalize the increase of glutamatergic receptor subunit expression, and correct the changes in receptor phosphorylation produced by stress exposure. Our data suggest that prolonged stress, a condition that has etiologic relevance for depression, may enhance glutamate activity through post-synaptic mechanisms, by regulating NMDA receptors, and that antidepressants may in part normalize such changes. Our results provide support to the notion that antidepressants may exert their activity in the long-term also via modulation of the glutamatergic synapse

Prolonged abstinence from developmental cocaine exposure dysregulates BDNF and its signaling network in the medial prefrontal cortex of adult rats.

Although evidence exists that chronic cocaine exposure during adulthood is associated with changes in BDNF expression, whether and how cocaine exposure during adolescence modulates BDNF is still unknown. To address this issue, we exposed rats to repeated cocaine injections from post-natal day (PD) 28 to PD 42, a period that roughly approximates adolescence in humans, and we carried out a detailed analysis of the BDNF system in the medial prefrontal cortex (mPFC) of rats sacrificed 3 d (PD 45) and 48 d (PD 90) after the last cocaine treatment. We found that developmental exposure to cocaine altered transcriptional and translational mechanisms governing neurotrophin expression. Total BDNF mRNA levels, in fact, were enhanced in the mPFC of PD 90 rats exposed to cocaine in adolescence, an effect sustained by changes in BDNF exon IV through the transcription factors CaRF and NF-kB. While a profound reduction of specific BDNF-related miRNAs (let7d, miR124 and miR132) may contribute to explaining the increased proBDNF levels, the up-regulation of the extracellular proteases tPA is indicative of increased processing leading to higher levels of released mBDNF. These changes were associated with increased activation of the trkB-Akt pathway resulting in enhanced pmTOR and pS6 kinase, which ultimately produced an up-regulation of Arc and a consequent reduction of GluA1 expression in the mPFC of PD 90 cocaine-treated rats. These findings demonstrate that developmental exposure to cocaine dynamically dysregulates BDNF and its signaling network in the mPFC of adult rats, providing novel mechanisms that may contribute to cocaine-induced changes in synaptic plasticity

Modeling the Distribution of New MRI Cortical Lesions in Multiple Sclerosis Longitudinal Studies

Objective: Recent studies have shown the relevance of the cerebral grey matter involvement in multiple sclerosis (MS). The number of new cortical lesions (CLs), detected by specific MRI sequences, has the potential to become a new research outcome in longitudinal MS studies. Aim of this study is to define the statistical model better describing the distribution of new CLs developed over 12 and 24 months in patients with relapsing-remitting (RR) MS. Methods: Four different models were tested (the Poisson, the Negative Binomial, the zero-inflated Poisson and the zeroinflated Negative Binomial) on a group of 191 RRMS patients untreated or treated with 3 different disease modifying therapies. Sample size for clinical trials based on this new outcome measure were estimated by a bootstrap resampling technique. Results: The zero-inflated Poisson model gave the best fit, according to the Akaike criterion to the observed distribution of new CLs developed over 12 and 24 months both in each treatment group and in the whole RRMS patients group adjusting for treatment effect. Conclusions: The sample size calculations based on the zero-inflated Poisson model indicate that randomized clinical trials using this new MRI marker as an outcome are feasible

Chronic treatment with fluoxetine up-regulates cellular BDNF mRNA expression in rat dopaminergic regions.

During the last few years several studies have highlighted the possibility that major depression can be characterized by a general reduction in brain plasticity and an increased vulnerability under challenging situations. Such dysfunction may be the consequence of reduced expression and function of proteins important for neuroplasticity such as brain-derived neurotrophic factor (BDNF). On this basis, by using a sensitive non-radioactive in-situ hybridization, we evaluated the effects of a chronic treatment with fluoxetine on BDNF expression within rat dopaminergic regions. In fact, besides the well-established role of the hippocampus, increasing evidence indicates that other brain regions may be involved in the pathophysiology of depression and consequently be relevant for the therapeutic action of antidepressant drugs. Our results indicate that 3 wk of fluoxetine administration up-regulates BDNF mRNA levels selectively within structures belonging to the meso-cortico-limbic pathway. The expression of the neurotrophin is significantly increased in the ventral tegmental area, prefrontal cortex, and shell region of the nucleus accumbens, whereas no changes were detected in the substantia nigra and striatum. Moreover, in agreement with previous studies, fluoxetine increased BDNF mRNA levels in the hippocampus, an effect that was limited to the cell bodies without any change in its dendritic targeting. These data show that chronic treatment with fluoxetine increases BDNF gene expression not only in limbic areas but also in dopaminergic regions, suggesting that such an effect may contribute to improve the function of the dopaminergic system in depressed subjects

Modulation of BDNF expression by repeated treatment with the novel antipsychotic lurasidone under basal condition and in response to acute stress

Abstract It is known that long-term treatment with antipsychotic drugs (APDs) produces neuroadaptive changes through the modulation of different proteins that, by enhancing neuronal plasticity and cellular resiliency, may improve core disease symptoms. The aim of this study was to investigate the ability of chronic treatment with the novel antipsychotic lurasidone to modulate BDNF expression in hippocampus and prefrontal cortex, under basal conditions or in response to an acute stress, a major precipitating element in psychiatric disorders. By means of real-time PCR, we found that (1) chronic lurasidone treatment increases total BDNF mRNA levels in rat prefrontal cortex and, to less extent, in hippocampus ; (2) the modulation of BDNF mRNA levels in response to acute swim stress in lurasidone-treated rats was markedly potentiated in hippocampus, and to less extent in prefrontal cortex, through the selective regulation of different neurotrophin isoforms. The increase of BDNF mRNA levels in prefrontal cortex was paralleled by an enhancement of mature BDNF protein levels. In conclusion, repeated exposure to lurasidone regulates BDNF expression, through a finely tuned modulation of its transcripts. This effect may contribute to the amelioration of functions, such as cognition, closely associated with neuronal plasticity, which are deteriorated in schizophrenia patients