Impact of Nanoplastic Particles on Macrophage Inflammation and Intestinal Health in a Mouse Model of Inflammatory Bowel Disease.

Background: The increasing presence of plastics in the human diet is raising public concern about the potential risks posed by nanoplastic (NP) particles, which can emerge from the degradation of plastic debris. NP ingestion poses particular risks to individuals with inflammatory bowel disease (IBD), as compromised epithelial barriers may facilitate NP translocation.

Methods: In vitro, bone-marrow-derived macrophages (BMDMs) were exposed to 25 nm polymethacrylate (PMMA) or 50 nm polystyrene (PS) particles to assess morphological changes and alterations in pro- and anti-inflammatory gene expression.

TiO nanoparticles abrogate the protective effect of the Crohn's disease-associated variation within the PTPN22 gene locus.

Objective: Inflammatory bowel disease (IBD) is a multifactorial condition driven by genetic and environmental risk factors. A genetic variation in the protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene has been associated with autoimmune disorders while protecting from the IBD subtype Crohn's disease. Mice expressing the murine orthologous PTPN22-R619W variant are protected from intestinal inflammation in the model of acute dextran sodium sulfate (DSS)-induced colitis.

Ingested nano- and microsized polystyrene particles surpass the intestinal barrier and accumulate in the body.

Plastic pollution is a major global challenge of our times, baring a potential threat for the environment and the human health. The increasing abundance of nanoplastic (NP) and microplastic (MP) particles in the human diet might negatively affect human health since they - particularly in patients suffering from inflammatory bowel disease (IBD) - might surpass the intestinal barrier. To investigate whether ingested plastic particles cross the intestinal epithelium and promote bowel inflammation, mice were supplemented with NP or MP polystyrene (PS) particles for 24 or 12 weeks before inducing acute or chronic dextran sodium sulfate (DSS) colitis with continuous plastic administration.

Combination of Vedolizumab With Tacrolimus Is More Efficient Than Vedolizumab Alone in the Treatment of Experimental Colitis.

Background: Vedolizumab is a widely used and safe therapy in inflammatory bowel disease, particularly in ulcerative colitis (UC), making it a promising candidate for enhanced efficacy by combining it with additional immunomodulatory medications. In this study, we studied the impact of vedolizumab monotreatment vs vedolizumab coadministration with other immunomodulatory drugs on intestinal inflammation and intestinal immune cells in vivo.

Methods: Colon tissue from human patients with UC with active disease or in remission with or without vedolizumab treatment was stained by immunohistochemistry.

Energy Drink Administration Ameliorates Intestinal Epithelial Barrier Defects and Reduces Acute DSS Colitis.

Background: The rise in the prevalence of inflammatory bowel diseases in the past decades coincides with changes in nutritional habits, such as adaptation of a Western diet. However, it is largely unknown how certain nutritional habits, such as energy drink consumption, affect intestinal inflammation. Here, we assessed the effect of energy drink supplementation on the development of intestinal inflammation in vitro and in vivo.

Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells.

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 () and their role in the development of intestinal inflammation.

Protein tyrosine phosphatase nonreceptor type 2 controls colorectal cancer development.

Protein tyrosine phosphatase nonreceptor type 2 (PTPN2) recently emerged as a promising cancer immunotherapy target. We set out to investigate the functional role of PTPN2 in the pathogenesis of human colorectal carcinoma (CRC), as its role in immune-silent solid tumors is poorly understood. We demonstrate that in human CRC, increased PTPN2 expression and activity correlated with disease progression and decreased immune responses in tumor tissues.

Solute carrier family 12 member 2 as a proteomic and histological biomarker of dysplasia and neoplasia in ulcerative colitis.

Background And Aims: Ulcerative colitis (UC) patients have a greater risk of developing colorectal cancer through inflammation-dysplasia-carcinoma sequence of transformation. The histopathological diagnosis of dysplasia is therefore of critical clinical relevance, but dysplasia may be difficult to distinguish from inflammatory changes.

Methods: A proteomic pilot study on 5 UC colorectal dysplastic patients highlighted proteins differentially distributed between paired dysplastic, inflammatory and normal tissues.

Deletion of Protein Tyrosine Phosphatase Nonreceptor Type 2 in Intestinal Epithelial Cells Results in Upregulation of the Related Phosphatase Protein Tyrosine Phosphatase Nonreceptor Type 23.

Background/aims: Knockdown of protein tyrosine phosphatase nonreceptor type 2 () exaggerates IFN-γ-induced intestinal barrier defects, but mice constitutively lacking in epithelial cells (PTPN2xVilCre mice) do not show changes in epithelial function or enhanced susceptibility to experimental colitis. Here, we investigated whether PTPN2 modulates the expression of related tyrosine phosphatases.

Methods: PTPN2 knockdown in HT-29 cells was induced using siRNA constructs.

Cell migration inhibition activity of a non-RGD disintegrin from venom.

Background: In recent decades, snake venom disintegrins have received special attention due to their potential use in anticancer therapy. Disintegrins are small and cysteine-rich proteins present in snake venoms and can interact with specific integrins to inhibit their activities in cell-cell and cell-ECM interactions. These molecules, known to inhibit platelet aggregation, are also capable of interacting with certain cancer-related integrins, and may interfere in important processes involved in carcinogenesis.

PTPN2 Regulates Inflammasome Activation and Controls Onset of Intestinal Inflammation and Colon Cancer.

Variants in the gene locus encoding protein tyrosine phosphatase non-receptor type 2 (PTPN2) are associated with inflammatory disorders, including inflammatory bowel diseases, rheumatoid arthritis, and type 1 diabetes. The anti-inflammatory role of PTPN2 is highlighted by the fact that PTPN2-deficient mice die a few weeks after birth because of systemic inflammation and severe colitis. However, the tissues, cells, and molecular mechanisms that contribute to this phenotype remain unclear.

TECHNOLOGY ASSESSMENT IN HOSPITALS: LESSONS LEARNED FROM AN EMPIRICAL EXPERIMENT.

Objectives: Hospital Based Health Technology Assessment (HBHTA) practices, to inform decision making at the hospital level, emerged as urgent priority for policy makers, hospital managers, and professionals. The present study crystallized the results achieved by the testing of an original framework for HBHTA, developed within Lombardy Region: the IMPlementation of A Quick hospital-based HTA (IMPAQHTA). The study tested: (i) the HBHTA framework efficiency, (ii) feasibility, (iii) the tool utility and completeness, considering dimensions and sub-dimensions.

[The surgical treatment of strangulated inguinal-crural hernias in geriatric patients].

The authors describe their own experience relative to 79 patients, aged 70 years or older, who underwent, during three years, emergency surgical intervention for inguinal or crural strangulated hernia. They report a postoperative mortality rate of 8.8% and a postoperative morbidity rate of 40%.

[Autotransfusion: its use in a case of spontaneous splenic rupture in non-Hodgkin's lymphoma].

The article refers to autotransfusion experience in a patient affected by lymphoma (not Hodgkin type), who reached surgery for haemoperitoneum caused by the spontaneous rupture of the spleen. Considering the pathology, this method brought unpredictable variations in the hemochrome thus leading to a deep reflection on the limitations of the use of autotransfusion.

[Anti H2 receptors and perforated peptic ulcer. Review of 442 cases].

H2 blockers have accelerated the reduction in elective peptic ulcer surgery but appear to have had no equivalent effect on the incidence of perforated ulcer success. A 13 year (1975-1987) review of perforated peptic ulcer is presented. The mean annual number of operations for perforation fell from 8.