Zhujimenez2691

Artificial intelligence (AI) is currently transforming all aspects of our daily life, including the practice of medicine. Paxalisib in vitro Artificial neural networks are a key method of AI. They can very effectively detect subtle patterns in imaging data and speech or text data. This is highly relevant for the practice of gastroenterology. Here, we summarize the state of the art in AI in gastroenterology and outline major clinical applications. Our focus is on AI-based analysis of endoscopy images, non-invasive imaging and histology images. In these applications, AI can support human pattern recognition. Beyond detection and classification of pathological findings, AI can predict clinical outcome from subtle image features.Pituitary tumors are frequent (estimated prevalence in adults up to 10 %). However, diagnostic work-up and therapeutic concepts are not well standardized; especially for non-functioning tumors. In the beginning of 2020, the first German interdisciplinary guideline on these topics was published. Here, we present shortly the most important aspects of this guideline. One key message is that all patients with pituitary tumors should be managed by an interdisciplinary team (consisting at least of an endocrinologist, a neurosurgeon, and a (neuro-)radiologist). At first presentation, detailed morphological characterization (with magnet resonance imaging) and endocrine work-up to exclude (or prove) hormonal excess or deficiency states is required. An ophthalmological examination is needed only in presence of symptoms or large tumors affecting the visual system. In asymptomatic, hormonally inactive tumors a 'wait and scan' strategy is standard of care. In case of an (impending) visual impairment, surgical treatment shall be performed by an experienced pituitary surgeon. If the surgical resection was incomplete or if tumors are recurrent, therapeutic modalities (e. g. re-operation, radiotherapy, observation) should be interdisciplinary considered. In all patients with or without therapeutic intervention, long-term follow-up is required. Patient with larger pituitary tumors or former surgery/radiotherapy should be regularly counseled regarding potential symptoms of hormonal insufficiency.Peripheral arterial disease (PAD) of the upper extremity is much less frequent and aetiologically more heterogeneous than lower extremity PAD. The clinical approach to patients with upper extremity PAD must consider a range of distinctive features regarding symptoms, physical findings and diagnostic strategies. This review focusses on these specific characteristics of upper extremity PAD and the new developments in this field. Arteriosclerotic subclavian artery obstruction, large vessel vasculitis, thoracic outlet syndrome and secondary Raynaud's phenomenon are four pivotal causes and manifestations of upper extremity PAD. These four entities are exemplarily discussed.Glucagon-like peptide-2 (GLP-2) is a peptide hormone that belongs to the glucagon-derived peptide family. We have previously shown that analogues of the sister hormone Glucagon-like peptide-1 (GLP-1) showed neuroprotective effects. Here we investigated the effect of a GLP-2 agonist in a cell model of Parkinson's disease (PD) created by treating SH-SY5Y or Neuro-2a cells with 1-Methyl-4-phenyl-pyridine ion (MPP+). Cell viability and cell cytotoxicity was detected by MTT and LDH assays, respectively. The protein expression levels of mitochondrial, autophagy and apoptotic biomarkers including PGC-1α, Mfn2, IRE1, ATG7, LC3B, Beclin1 and Bcl-2 were detected by western blot. Mitochondrial superoxide was detected by MitoSOX Red. In addition, mitochondrial morphology, autophagosome and apoptotic corpuscles were observed by transmission electron microscope (TEM). We found that the GLP-1 and the GLP-2 agonists both protect cells against mitochondrial damage, autophagy impairments and apoptosis induced by MPP+both in SH-SY5Y and Neuro-2a cells. Cell signaling for mitogenesis was enhanced, and oxidative stress levels much reduced by the drugs. This demonstrates for the first time the neuroprotective effects of a GLP-2 analogue in PD cellular models, in which oxidative stress, autophagy and apoptosis play crucial roles. The protective effects were comparable to those seen with the GLP-1 analogue liraglutide. The results suggest that not only GLP-1, but also GLP-2 has neuroprotective properties and may be useful as a novel treatment of PD.

Malignant melanoma is a common form of skin cancer that contains different cell types recognized by various cell surface markers. Dacarbazine-based combination chemotherapy is frequently used for the treatment of melanoma. Despite its potent anticancer properties, resistance to dacarbazine develops in malignant melanoma. Here, we aim to improve response to dacarbazine therapy by pretreatment with all-trans retinoic acid (ATRA) in CD117

melanoma cells.

The CD117

melanoma cells were sorted from A375 malignant melanoma cell line using magnetic-activated cell sorting (MACS). The cell viability was examined by cell proliferation assay (MTT). Apoptosis was determined by acridine orange/ ethidium bromide staining. Indeed, we performed flow cytometry to evaluate the cell cycle arrest.

Here, the CD117

melanoma cells were incubated with various concentrations of ATRA, dacarbazine, and their combination to determine IC

values. We found that 20 µM ATRA treatment followed by dacarbazine was found to be more effective than dacarbazine alone. There was an indication that the combination of ATRA with dacarbazine (ATRA/dacarbazine) caused more apoptosis and necrosis in the melanoma cells (P<0.05). Furthermore, ATRA/dacarbazine treatment inhibited the cell at the G0/G1 phase, while dacarbazine alone inhibited the cells at S phase.

Collectively, combined treatment with ATRA and dacarbazine induced more apoptosis and enhanced the cell cycle arrest of CD117

melanoma cells. These results suggested that ATRA increased the sensitivity of melanoma cells to the effect of dacarbazine.

Collectively, combined treatment with ATRA and dacarbazine induced more apoptosis and enhanced the cell cycle arrest of CD117+ melanoma cells. These results suggested that ATRA increased the sensitivity of melanoma cells to the effect of dacarbazine.