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Background/Objectives: Eosinophilic esophagitis (EoE) and achalasia are two chronic esophageal disorders, characterized by inflammatory and neuromotor dysfunction, respectively, that share overlapping immune-inflammatory features. Emerging evidence suggests that dysbiosis of the oral and esophageal microbiota may represent a common determinant in their pathophysiology. This review aims to provide a comparative and integrated overview of microbial and immune alterations in EoE and Achalasia, with potential diagnostic and therapeutic implications. Methods: A bibliographic search was conducted on PubMed and Scopus including clinical studies, experimental research, and review articles published between 2015 and 2025. The keywords Eosinophilic Esophagitis, Achalasia, Microbiota, and Dysbiosis were used for article selection. Results: In EoE, several studies demonstrated increased bacterial diversity with predominance of Prevotella and reduction of Streptococcus, findings associated with greater inflammatory severity and epithelial barrier dysfunction. Conversely, Achalasia is characterized by reduced microbial diversity and a shift from Gram-positive commensals to Gram-negative taxa capable of activating pro-inflammatory pathways (TLR4-MYD88-NF-κB), leading to neuronal loss and impaired peristalsis. Conclusions: Both EoE and Achalasia share the hallmark of dysbiosis, although with distinct immune profiles (Th2 vs. Th17). The identification of specific microbial "signatures" suggests promising perspectives for non-invasive biomarkers and microbiota-targeted therapies, including probiotics and glycan-modulating strategies. Further prospective studies are needed to clarify causal mechanisms and validate microbiota manipulation as a complementary therapeutic approach in esophageal diseases.
Sensory processing requires selectivity to salient sensory input. Many autistic individuals report different sensory processing, which has been associated with altered sensory selectivity. The locus-coeruleus norepinephrine (LC-NE) system modulates the neuronal gain of sensory input, which represents a neurophysiological mechanism of sensory selectivity. In autistic individuals, we hypothesized that LC-NE tonic upregulation reduces sensory selectivity and underlies different sensory processing. Autistic (n = 139) and non-autistic (n = 98) individuals were assessed during a passive auditory oddball task with pupillometry and electroencephalography. For every trial, a baseline pupil size (BPS) assessed LC-NE tonic activity that coincides with current arousal, while a stimulus-evoked pupillary response (SEPR) assessed LC-NE phasic activity that estimated sensory selectivity. Electroencephalography assessed amplitudes of mismatch negativity (MMN-amp) that estimated pre-attentive change detection as a brain-activity readout of sensory selectivity. Measures were modeled between groups within the task by combining Frequentist and Bayesian approaches. Across groups, higher BPS was associated with more negative MMN-amp to standards and oddballs. A more negative MMN-amp to standards was associated with a higher SEPR to standards. Controlling for these associations, autistic versus non-autistic individuals showed a higher SEPR in response to standards. In addition, a positive association of BPS and SEPR to standards was specific to autistic individuals. With task progression, autistic versus non-autistic individuals showed a higher initial increase and subsequently steeper decrease of BPS. This was supported by Bayesian posterior distribution estimates. A short trial duration required concatenating trials to epochs and applying a linear-time invariant filter to capture the slow pupil changes. Without an LC-NE manipulation, we cannot rule out that pupil changes are evoked by other cortical pathways than the LC-NE. Across groups, LC-NE tonic upregulation is emphasized as a general mechanism that un-specifically increases pre-attentive change detection to all sensory stimuli, which then increases sensory selectivity to frequent stimuli. In autistic individuals, different sensory processing is characterized by increased sensory selectivity to frequent stimuli. This is likely caused by an LC-NE tonic upregulation. It associates autistic sensory processing with increased arousal upregulation that increases sensory selectivity to inconspicuous auditory information.
The aim of any oncological treatment is not just to eliminate the tumour, but to maximise patient survival and quality of life. Since the liver has a vital function, any radical treatment that severely compromises liver function will result in a shortening of life expectancy, rather than a prolongation. Furthermore, even non-severe liver damage may prevent the delivery of further effective therapies. This is particularly important in the case of hepatocellular carcinoma (HCC), as it is associated with underlying cirrhosis in most patients - cirrhosis itself is not only a potentially lethal disease and independent prognostic factor in HCC, but it also makes liver function fragile. Accordingly, some information about liver dysfunction is included in most staging systems for HCC and can be used to guide the selection of treatments that the functional liver reserve can tolerate. Unfortunately, the prediction of functional damage to the liver in the case of antitumor treatments is very challenging and still suboptimal in any given patient. Moreover, while the assessment of functional reserve can now be used to avoid postoperative liver failure in the surgical setting, its use has been less well clarified for non-surgical therapies, which is of particular relevance today, as several lines of effective non-surgical treatments, including systemic therapies, have become available. The present article will a) critically review the implications of the assessment of liver functional reserve in patients with HCC, b) illustrate the available tools to assess liver functional reserve and c) discuss the role of functional assessment for each type of non-surgical therapy for HCC.
Diabetes mellitus (DM) is one of the most common comorbid conditions in persons with COVID-19 and a risk factor for poor prognosis. The reasons why COVID-19 is more severe in persons with DM are currently unknown although the scarce data available on patients with DM hospitalized because of COVID-19 show that glycemic control is inadequate. The fact that patients with COVID-19 are usually cared for by health professionals with limited experience in the management of diabetes and the need to prevent exposure to the virus may also be obstacles to glycemic control in patients with COVID-19. Effective clinical care should consider various aspects, including screening for the disease in at-risk persons, education, and monitoring of control and complications. We examine the effect of COVID-19 on DM in terms of glycemic control and the restrictions arising from the pandemic and assess management of diabetes and drug therapy in various scenarios, taking into account factors such as physical exercise, diet, blood glucose monitoring, and pharmacological treatment. Specific attention is given to patients who have been admitted to hospital and critically ill patients. Finally, we consider the role of telemedicine in the management of DM patients with COVID-19 during the pandemic and in the future.
The objective was to prospectively determine CT density changes in bone metastases, before and after intravenous zoledronic acid for a maximum period of 12 months. Twenty-three consecutive patients presented with bone metastases and underwent therapy with zoledronic acid from December 2004. All patients underwent CT of the chest, abdomen, and pelvis. Bone density, measured in Hounsfield units (HU), was determined by segmenting lesions in the same anatomical area of the metastasis sites on the axial images of the sequential series of CT examinations. The effects of zoledronic acid were evaluated by calculating absolute and relative increases in bone density. The patients presented with multiple metastases in 65% of the cases. When compared with the baseline, all groups demonstrated a significant increase in bone density, which significantly (p < 0.01) correlated with the number of zoledronic acid administrations. There was increased bone density of at least 100% in 57%, and an increase of at least 50% in 87% of the patients. This increase was significant in both lytic and sclerotic metastases after 3 months of therapy. No significant bone density difference was found in normal-appearing bone. Bone density measured by CT increases at metastatic sites after zoledronic acid treatment, regardless of the type of metastasis, in contrast to apparently normal bone.
Urinary tract infections caused by enterobacteriaceae secreting extended-spectrum beta-lactamase (EESBL) is an issue for most family physicians. The aim of our study was to evaluate their practice in case of EESBL discovered after urinalysis and culture (U/C). This epidemiological and retrospective study was conducted from the January 1, to December 31, 2012, in 5 laboratories of Savoie and Isere. Results of U/C prescribed by family physicians and positive for EESBL were collected. The data collected with questionnaires, concerned characteristics of the infection, antibiotic treatment adequateness, the implementation of specific hygiene measures, and risk factors for EESBL infection. One hundred and three U/C out of 19,494 were considered, and 56 questionnaires were collected. The rate of EESBL positive U/C was 0.60%. The antibiotic treatment was adequate for 35 patients (62.5%). Specific hygiene measures were implemented for 22 patients (32.3%). Both antibiotic treatment and specific hygiene measures were initiated for 13 patients (23.2%). Fourteen cases of community-acquired infections (25%) were reported. Five patients (8.9%) had traveled to an endemic zone in the previous 6 months. The concomitant initiation of both antibiotic treatment and specific hygiene measures in case of U/C positive for EESBL is insufficient when managed by family physicians. It could be improved by offering tools for the management of these infections, by developing EESBL networks between hospital and family physicians, and epidemiological surveillance in community settings.
IBS is one of the most common types of functional bowel disorder. Increasing attention has been paid to the causative role of food in IBS. Food ingestion precipitates or exacerbates symptoms, such as abdominal pain and bloating in patients with IBS through different hypothesised mechanisms including immune and mast cell activation, mechanoreceptor stimulation and chemosensory activation. Wheat is regarded as one of the most relevant IBS triggers, although which component(s) of this cereal is/are involved remain(s) unknown. Gluten, other wheat proteins, for example, amylase-trypsin inhibitors, and fructans (the latter belonging to fermentable oligo-di-mono-saccharides and polyols (FODMAPs)), have been identified as possible factors for symptom generation/exacerbation. This uncertainty on the true culprit(s) opened a scenario of semantic definitions favoured by the discordant results of double-blind placebo-controlled trials, which have generated various terms ranging from non-coeliac gluten sensitivity to the broader one of non-coeliac wheat or wheat protein sensitivity or, even, FODMAP sensitivity. The role of FODMAPs in eliciting the clinical picture of IBS goes further since these short-chain carbohydrates are found in many other dietary components, including vegetables and fruits. In this review, we assessed current literature in order to unravel whether gluten/wheat/FODMAP sensitivity represent 'facts' and not 'fiction' in IBS symptoms. This knowledge is expected to promote standardisation in dietary strategies (gluten/wheat-free and low FODMAP) as effective measures for the management of IBS symptoms.
It is well known that bone metastases from breast cancer usually show osteolytic changes. We retrospectively analysed the computed tomography (CT) appearance of bone metastases to quantify the distribution of lytic, mixed and sclerotic changes in a series of patients presenting with neoplastic bone involvement from breast cancer. Between 1996 and 2005, 468 women with a diagnosis of breast cancer were referred to our department for staging or follow-up CT examinations. Staging CT examinations detected systemic metastases in 142/468 patients, 60 of which had bone involvement. Patients with a second primary tumour or bone metabolic disorders were excluded from this retrospective analysis. In patients with bone metastases, CT identified 18 with osteolytic lesions (30%), 32 with osteosclerotic lesions (53.3%) and ten with mixed lesions (16.7%). Analysis of the cases observed for the first time during the 1996-2000 period showed osteolytic lesions in 53.6% (15/28), osteosclerotic lesions in 32.1% (9/28) and mixed lesions in 14.3% (4/28). Results were 9.4% (3/32), 71.9% (23/32) and 18.7% (6/32), respectively, for the same groups in the 2001-2005 period. Histological analysis of all cases included 81.9% of infiltrative ductal carcinoma, 11.2% of infiltrative lobular carcinoma, 3.7% of ductal lobular mixed carcinoma and 3% of medullar carcinoma. We found no statistically significant correlation between histological type of breast cancer and radiological appearance of bone metastasis. A significant difference between patients treated with or without zoledronic acid was observed, with a higher prevalence of osteosclerotic lesions in the former group of patients (p<0.05). We observed an increasing prevalence of osteosclerotic bone metastasis when comparing the 1996-2000 period with the 2001-2005 period. The significance of these distribution changes is not clear. However, we found a significant correlation of osteosclerotic lesions with zoledronic acid treatment. The advent of third generation bisphosphonates may have changed the CT appearance of bone metastasis from breast cancer.
C:\ArsGames takes a look at the time Chris Roberts more or less made a whole movie
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