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Malnutrition poses a critical challenge in inflammatory bowel disease, with the potential to detrimentally impact medical treatment, surgical outcomes, and general well-being. Parenteral nutrition is crucial in certain clinical scenarios, such as with patients suffering from short bowel syndrome, intestinal insufficiency, high-yielding gastrointestinal fistula, or complete small bowel obstruction, to effectively manage malnutrition. Nevertheless, research over the years has attempted to define the potential effects of parenteral nutrition on the intestinal barrier and the composition of the gut microbiota. In this narrative review, we have gathered and analyzed findings from both preclinical and clinical studies on this topic. Based on existing evidence, there is a clear correlation between short- and long-term parenteral nutrition and negative effects on the intestinal system. These include mucosal atrophic damage and immunological and neuroendocrine dysregulation, as well as alterations in gut barrier permeability and microbiota composition. However, the mechanistic role of these changes in inflammatory bowel disease remains unclear. Therefore, further research is necessary to effectively address the numerous gaps and unanswered questions pertaining to these issues.

Inflammatory bowel diseases (IBDs) are intricate systemic conditions that can extend beyond the gastrointestinal tract through both direct and indirect mechanisms. Sarcopenia, characterized by a reduction in muscle mass and strength, often emerges as a consequence of the clinical course of IBDs. Indeed, sarcopenia exhibits a high prevalence in Crohn's disease (52%) and ulcerative colitis (37%). While computed tomography and magnetic resonance imaging remain gold-standard methods for assessing muscle mass, ultrasound is gaining traction as a reliable, cost-effective, and widely available diagnostic method. Muscle strength serves as a key indicator of muscle function, with grip strength test emerging nowadays as the most reliable assessment method. In IBDs, sarcopenia may arise from factors such as inflammation, malnutrition, and gut dysbiosis, leading to the formulation of the 'gut-muscle axis' hypothesis. This condition determines an increased need for surgery with poorer post-surgical outcomes and a reduced response to biological treatments. Sarcopenia and its consequences lead to reduced quality of life (QoL), in addition to the already impaired QoL. Of emerging concern is sarcopenic obesity in IBDs, a challenging condition whose pathogenesis and management are still poorly understood. Resistance exercise and nutritional interventions, particularly those aimed at augmenting protein intake, have demonstrated efficacy in addressing sarcopenia in IBDs. Furthermore, anti-TNF biological therapies showed interesting outcomes in managing this condition. This review seeks to furnish a comprehensive overview of sarcopenia in IBDs, elucidating diagnostic methodologies, pathophysiological mechanisms, and clinical implications and management. Attention will also be paid to sarcopenic obesity, exploring the pathophysiology and possible treatment modalities of this condition.

Microplastics and nanoplastics (MNPs) are becoming an increasingly severe global problem due to their widespread distribution and complex impact on living organisms. Apart from their environmental impact, the effects of MNPs on living organisms have also continued to attract attention. The harmful impact of MNPs has been extensively documented in marine invertebrates and larger marine vertebrates like fish. However, the research on the toxicity of these particles on mammals is still limited, and their possible effects on humans are poorly understood. Considering that MNPs are commonly found in food or food packaging, humans are primarily exposed to them through ingestion. It would be valuable to investigate the potential harmful effects of these particles on gut health. This review focuses on recent research exploring the toxicological impacts of micro- and nanoplastics on the gut, as observed in human cell lines and mammalian models. Available data from various studies indicate that the accumulation of MNPs in mammalian models and human cells may result in adverse consequences, in terms of epithelial toxicity, immune toxicity, and the disruption of the gut microbiota. The paper also discusses the current research limitations and prospects in this field, aiming to provide a scientific basis and reference for further studies on the toxic mechanisms of micro- and nanoplastics.

There is an increasing interest in using popular diets to manage inflammatory bowel diseases (IBDs), such as ulcerative colitis and Crohn disease. These conditions are often associated with nutritional deficiencies, protein‑energy malnutrition, micronutrient malnutrition, altered body composition, and sarcopenia. While dietary interventions can be supportive in treating intestinal symptoms of adult IBD patients, it is important to note that current guidelines from major scientific societies do not recommend any specific dietary interventions in this field. This review aims to provide a summary of the current evidence on dietary‑nutritional management for patients with IBD, specifically when the disease appears to be in remission, but the patient continues to experience irritable bowel syndrome (IBS) symptoms or functional gastrointestinal symptoms. We focus on vital aspects, such as malnutrition and sarcopenia definitions, screening, and nutritional assessment. We then discuss in detail the most popular diets used for IBD management over the years, characterizing each one in terms of effects on gut inflammation, IBS‑like symptoms, and potential risk of malnutrition. These diets include a low‑fermentable oligosaccharides, disaccharides, monosaccharides, and polyols diet, a gluten‑free diet, a Mediterranean diet, and a plant‑based diet. To date, current evidence does not conclusively establish the optimal diet for patients with IBS, suggesting that personalized dietary approaches may be the best strategy.

Acute pancreatitis (AP) is an acute inflammation of the pancreas caused by the activation of digestive enzymes in the pancreatic tissue. The main causes of AP are cholelithiasis and alcohol abuse; less commonly, it can be caused by drugs, with a prevalence of up to 5%. Causal associations between drugs and pancreatitis are largely based on case reports or case series with limited evidence. We reviewed the available data on drug-induced AP, focusing on antimicrobial drugs and antivirals, and discussed the current evidence in relation to the classification systems available in the literature. We found 51 suspected associations between antimicrobial and antiviral drugs and AP. The drugs with the most evidence of correlation are didanosine, protease inhibitors, and metronidazole. In addition, other drugs have been described in case reports demonstrating positive rechallenge. However, there are major differences between the various classifications available, where the same drug being assigned to different probability classes. It is likely that the presence in multiple case reports of an association between acute pancreatitis and a drug should serve as a basis for conducting prospective randomized controlled trials to improve the quality of the evidence.

Quantitative analysis of biochemical parameters is crucial for a correct diagnosis and prognosis of patients subject to acute myocardial infarction (AMI). In order to achieve a quantitative understanding of the dynamics of cardiac biomarkers, we have developed a mathematical model that can be exploited to extrapolate the release curve of cardiac troponin T (cTnT) into the plasma from few experimental acquisitions. The present work introduces a novel approach, based on the cTnT-release model, aimed at the identification of the infarct onset time. Indeed, in spite of the clinical importance of such information, in many cases, it is not easy to establish the exact time of occurrence of the ischemic event. We show that using a model-based optimization approach, the infarct onset time can be reliably estimated using the cTnT concentration acquisitions taken in the first few hours post-AMI. The assessment of the proposed approach is conducted on an experimental dataset, in which the infarct has been artificially induced and, therefore, the onset time is exactly known. In particular, the effectiveness of the devised estimation algorithm has been tested under several scenarios, with the first cTnT acquisition taken up to 12 h after AMI. Altogether, the proposed model-based approach provides a useful tool to help the clinicians in the quantitative estimation of important clinical parameters from the release curves of the cardiac biomarkers.

In the present work, we introduce a novel technique to identify the infarct time from time-series meaurements of the cardiac troponin T (cTnT) into plasma. Although this information is extremely valuable from a clinical standpoint, it is not always possible to establish with certainty the exact infarct time. Here, we show how the infarct time can be reliably estimated from the cTnT release data in the first few hours after AMI, by using an optimization-based procedure and a model-based approach. To validate the present approach, we have used a clinical dataset of patients in whom the infarct has been induced and, therefore, the infarct time is certain.

Endothelial dysfunction, wall thickening and plaque are progressive manifestations of atherosclerosis. Delayed or absent brachial artery dilation after ischemic stimulus has been associated with severity of extracoronary and coronary atherosclerosis. In the current study, we aimed to verify if delayed or absent dilation associates with critical coronary stenosis. We also evaluated the association between coronary stenosis, carotid artery wall thickness and peripheral artery disease. Endothelial function was investigated by flow-mediated dilation of the brachial artery up to 3 min after ischemia, and patients classified as early, late or no dilators. Coronary angiography was performed through transradial or femoral artery approach. Computerized quantitative angiography was used to obtain percent stenosis of all lesions, while the Gensini score was used to evaluate the severity of coronary atherosclerosis. Seventy-four patients were enrolled. Carotid wall thickness and plaque, and peripheral artery disease were detected by ultrasound. Subjects with critical coronary stenosis showed a higher prevalence of delayed or absent dilation (coronary stenosis ≥70 per cent: late dilators 50 per cent, no dilators 35 per cent; coronary stenosis ≤70 per cent : late dilators 27 per cent, no dilators 6 per cent). The Gensini score was progressively higher in late dilators and no dilators compared with early dilators (early: 4.5±13.5; late 17.5±27.1; no 39.7±55.0; P<0.02). Carotid atherosclerosis and peripheral artery disease were more prevalent in subjects with critical coronary stenosis. Delayed or absent dilation associates with coronary stenosis and different degree of coronary atherosclerosis. The kinetic of arterial dilation seems to be relevant as the magnitude of dilation., Competing Interests: Competing interests: None declared., (© American Federation for Medical Research (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Authors studied the effects of thyroid hormones and their diasteroisomers and 3,5-diiodothyronine (LT2) on the fluidity properties of inner mitochondrial membrane (IMM) by specifical fluorescent probe for the internal zone of biological membranes, the 1,6-diphenyl-1,3,5-hexatriene (DPH). The studied parameters are Arrhenius and Perrin plots. The DPH shows a decreased fluorescence quenching in the presence of both T3 and T4. The maximum effect is observed with 2 nM LT2. LT2 is more effective than LT3 in the central zone. The data confirm the selective action of LT3 and LT4 on IMM fluidity.

The HPLC method here described allows to separate CNBr collagen peptides within 2.5 h by reversed phase and gradient elution. The method is useful to determine both peptide bond and pyridinoline groups by absorbance spectophotometry. The fractions can be recovered and then submitted to other characterization techniques.

The authors studied the effect of graded concentrations of papaverine on membrane potential in isolated synaptosomes from pig brain by fluorescence. The indicator dye for membrane potential is rhodamine 6G (Rh6G). The membrane voltage is determined at both high (127.2) and low (30 mM) final sodium (Na+) concentrations. The results demonstrate a hyperpolarizing action of papaverine directly proportional to papaverine concentration.

In this research we have investigated the effects of mitochondrial peptide fraction bound to DNA on stationary rat hepatocyte cultures. The treatment with this peptide was responsible of cellular lysis, followed by significant proliferation after 46th day until 51st in which it is reestablished. In the present study it seems that peptides bound to hepatocyte mitochondrial DNA are involved in longer term cultural stabilization properties. Our results demonstrate that the peptide is a lysing factor activity at short terms.

A peptide fraction from the mitochondrial DNA of calf's liver was isolated using Drouin's method (1). This peptide fraction, which was extracted at pH 9.5 from an extensively purified mitochondrial DNA (2), has been shown to exert an in vitro regulatory role on the transcription and duplication activity of DNA (3). The same fraction also binds with mitochondrial DNA with a high affinity constant and stabilizes DNA from calf's thymus against thermal denaturation. The peptides from mitochondrial DNA have been subfractionated by fingerprinting-like techniques and one of them has been sequenced.

In this research the amino acidic composition of a peptide fraction from mitochondrial DNA has been determined, using HPLC and the fingerprinting technique. This peptide fraction has been shown to be composed of two sub-fractions with different reactivity to ninhydrin, and thus supplied with several N-substitute groups. The composition of the first fraction is Gln, Glu, Pro, Leu. The second fraction composition is Pro, Glu or Gln, Asp or Asn, Ser.

Authors tested "in vitro" action of a low molecular weight peptide fraction extracted by mitochondrial DNA from calf liver. The fraction acts upon duplication performed by E. Coli DNA polymerase I on poli dAT dAT template inhibiting chain elongation. The authors hypothesize that a similar role is exerted by this fraction "in vitro" on mitochondrial DNA template.

The authors verified the effect of a peptidic fraction from mitochondrial DNA on liver cell cultures. Primary cultures treated with the mitochondrial peptidic fraction (final concentration 0.025 O.D./ml) showed a higher viability after 48 hours with respect to cultures without mitochondrial peptidic fraction (p < 0.05). The results indicate a probable action of the mitochondrial peptidic fraction on liver cell viability.

In this paper the authors studied the effects of thyroid hormones and their structural analogues on the mitochondrial calcium transport activities. The thyroid hormones, 3,5,3' L-triiodothyronine (LT3) and 3,5,3'5' L-tetraiodothyronine (LT4) at physiological intracellular concentrations between 7.2 and 9 nM, decouple total Ca++ transport, as well as inhibit the passive transport of Ca++, either due to oxidation of pyruvate, malate or succinate or after inhibition with rotenone. The optical isomers 3,5,3' D-triiodothyronine (DT3) and 3,5,3',5' D-tetraiodothyronine (DT4) are less effective at all the used concentrations. Furthermore the structural analogues 3,3',5' L-triiodothyronine (LrT3), 3,5-dicloro, 3',5' L-diiodothyronine (LDiClT2) and 3,5 L-diiodothyronine (LT2) furnished even less effects on the same activities. The effect of the thyroid hormones and of their structural analogues has revealed that the mitochondrial calcium transport may be influenced both by a stereospecific interaction between hormones and protein ligands and by a lipophilic chaotropic action on the mitochondrial membranes lipids. In this context it is interesting to consider that both thyroid hormones and Ca++ transport activity are interacting with the energetic metabolism by means of phosphorylation and substrate oxidation mechanism.

The Authors demonstrate that the in vitro stimulation of mitochondrial RNA synthesis produced by thyroid hormones takes place also at physiological levels, equal to those held in the liver cells of experimental animals. Two groups of male rats have been used: normal control animals (N) and animals surgically thyroidectomized on the 25th day of life (T). The animals were fed and kept in standard conditions and killed on the 85th day of life. The purification of mitochondrial samples and the determination of the mitochondrial RNA synthesis were carried out as previously described. The results suggest that the in vitro stimulation of mitocondrial RNA synthesis is already significant at the concentration of lnM. The trends are qualitatively comparable for either N or T animals. The structural analogues TRIAC (3,5,3'-triiodothyroacetic acid) and TRIPROP (3,5,3'-triiodothyropropionica acid) exhibit a clearly stimulatory effect on samples of N animals, while on samples of T animals is significant only for the first analogue. Similar trends are also observed on ADP/O ratio.