Feeding associated neonatal necrotizing enterocolitis (Primary NEC) is an inflammatory bowel disease

Neonatal necrotizing enterocolitis which develops after feeding preterm infants is characterized by severe intestinal inflammation and profound systemic metabolic acidosis. The fermentation of undigested dietary carbohydrate by colonic flora yields gases (CO₂ and H₂) and short chain organic acids. These organic acids can disrupt the intestinal mucosa and initiate inflammation driven predominantly by resident mast cells and by granulocytes which are recruited from blood. A systemic acidosis ensues derived from intestinal acids, not classic lactic acidosis produced from anaerobic metabolism. The systemic acidosis further compromises inflamed bowel leading to bowel necrosis.     

Genomic profiling of inflammatory breast cancer: A review

Inflammatory breast cancer (IBC) is a rare but aggressive form of breast cancer. Despite efforts in the past decade to delineate the molecular biology of IBC by applying high-throughput molecular profiling technologies to clinical samples, IBC remains insufficiently characterized. The reasons for that include limited sizes of the study population, heterogeneity with respect to the composition of the IBC and non-IBC control groups and technological differences across studies. In 2008, the World IBC Consortium was founded to foster collaboration between research groups focusing on IBC. One of the initial projects was to redefine the molecular profile of IBC using an unprecedented number of samples and search for gene signatures associated with survival and response to neo-adjuvant chemotherapy. Here, we provide an overview of all the molecular profiling studies that have been performed on IBC clinical samples to date.     

牙周炎和慢性阻塞性肺疾病间共同危险因素及相关机制研究进展

慢性阻塞性肺疾病和牙周病两者都是感染引起的慢性炎症反应性疾病，两者的临床表现均涉及结缔组织的破坏。该文就两者的流行病学情况、共同危险因素、相关的生物学机制的研究进展进行综述。文献复习结果表明牙周炎与慢性阻塞性肺疾病两者之间可相互影响，感染细菌同源性，炎症因子和中性粒细胞都参与了两种疾病的过程，两者的共同危险因素有年龄增长、社会经济状况差、吸烟等，但仍需进一步研究来明确牙周炎和慢性阻塞性肺疾病之间相互作用的具体机制。     

上颌窦炎性肌纤维母细胞瘤病例报告及文献回顾

摘要：目的探讨上颌窦炎性肌纤维母细胞瘤的临床表现，病理学特征、诊断、治疗及预后，旨在提高耳鼻咽喉科医生对该病的认识和治疗水平，并减少漏诊误诊。方法报告1例上颌窦炎性肌纤维母细胞瘤，并复习相关的国内外文献。结果CT扫描示窦腔可见低密度肿块影且突入眼眶，邻近窦壁明显受压、变薄，增强明显不均匀强化。MRI示类圆形稍高/等T2、T1信号肿块影，边界不清。病理示瘤组织主要由梭形肌纤维母细胞及大量炎性细胞组成。免疫组化中SMA、VIM等呈阳性，CK呈阴性。术后随访9个月，复查CT示左上颌窦窦腔未见明显新生物，呈术后改变。结论上颌窦炎性肌纤维母细胞瘤是非常罕见的，其诊断主要依靠病理及免疫组化检测。根治性手术切除仍为目前首选治疗方法，对于体积过大的血供占位病变，术前可辅助介入栓塞治疗。     

干细胞疗法治疗炎症性肠病的应用

炎症性肠病是一种慢性炎症性疾病,主要包括克罗恩病和溃疡性结肠炎,其发病原因尚不清楚。干细胞疗法在治疗炎症性肠病方面可能是非常有价值的,近年来,干细胞疗法的研究也更加突出而显著,本文就干细胞疗法治疗炎症性肠病的应用作一概述。     

Tofacitinib for the treatment of ulcerative colitis

ABSTRACT

Introduction: New generations of small molecules are being developed for the treatment of ulcerative colitis. Among them, tofatinib (a Janus kinase (JAK) inhibitor) has demonstrated efficacy for inducing and maintaining remission and achieving mucosal healing with a reasonable safety profile. Oral administration is attractive for patients and lack of immunogenicity represents an advantage over biologic drugs.

Areas covered: This review discusses the molecular aspects of the JAK-STAT pathway; the mechanism of action of tofacitinib pertinent to ulcerative colitis and the evidence on the efficacy of tofacitinib for achieving clinically relevant outcomes, including clinical remission, mucosal healing, and normalization of quality of life, as well as safety aspects with special attention to adverse events related to the mode of action of the drug.

Expert commentary: Tofacitinib will be the first drug on the class of JAK inhibitors to be available for treatment of ulcerative colitis. The efficacy of the drug, with a rapid onset of action even in cases of severe colitis, oral administration, and possibility to use the drug intermittently without generating immunogenicity, will bring about a redesign of current treatment paradigms for ulcerative colitis.     

Molecular and pathogenic effects of endoplasmic reticulum aminopeptidases ERAP1 and ERAP2 in MHC-I-associated inflammatory disorders: Towards a unifying view

The inflammatory diseases that are most strongly associated with major histocompatibility Complex class I (MHC-I) alleles are also influenced by endoplasmic reticulum aminopeptidase (ERAP) 1 and/or 2, often in epistasis with the susceptibility MHC-I allele. This review will focus on the four major MHC-I-associated inflammatory disorders: ankylosing spondylitis, birdshot chorioretinopathy, Behçet’s disease and psoriasis. The genetics of ERAP1/ERAP2 association and the alterations induced by polymorphism of these enzymes on the risk MHC-I allotypes will be examined. A pattern emerges of analogous effects on peptide length, sequence and affinity of disparate peptidomes, suggesting that similar peptide-mediated mechanisms underlie the pathogenesis and the joint contribution of ERAP1/ERAP2 and MHC-I to distinct inflammatory diseases. Processing of specific antigens, peptide-dependent changes in global properties of the MHC-I molecules, such as folding and stability, or both may be pathogenic.     

Persistent Enhancement on Contrast-Enhanced Ultrasound Studies of Severe Crohn's Disease: Stuck Bubbles?

A small population of patients with severe Crohn's disease (CD) exhibit atypical lack of intensity decline on intestinal contrast-enhanced ultrasound. From a retrospective CD cohort examined with contrast-enhanced ultrasound, 104 patients were identified. Twenty study patients with severe active disease exhibited high peak enhancement (>23 dB) and minimal decline. From the same cohort, 84 control patients also exhibited high peak enhancement >23dB, but with typical intensity decline. Patient outcomes were assessed. Time–intensity curve analysis revealed a significantly higher (p < 0.0001) area under the curve (44.7 ± 1.5 dB·s), washout time and intensities at 60s and 120s in the study population compared with controls (40.0 ± 1.1 dB·s). Study patients had a worse overall outcome with surgery in 30% versus 10% (p?=?0.027) during follow-up. Heightened enhancement with lack of decline on contrast-enhanced ultrasound suggests microbubbles are stuck within the inflamed bowel wall for an extended period. This observation occurs in patients with severe disease and a bad outcome.     

How will insights from genetics translate to clinical practice in inflammatory bowel disease?

Inflammatory bowel disease, consisting of Crohn's disease and ulcerative colitis, is a chronic inflammatory disease of the gut, which arises through an excessive immune response to the normal gut flora in a genetically susceptible host. The disease affects predominantly young adults and due to its chronic and relapsing nature gives rise to a high disease burden both financially, physically and psychologically. Current therapy still cannot prevent the need for surgical intervention in more than half of IBD patients. Consequently, advances in IBD therapy are of high importance. Recently, several new forms of targeted therapy have been introduced, which should improve surgery-free prognosis of IBD patients. Recent identification of genetic risk variants for IBD has led to new insights into the biological mechanisms of the disease, which will, in the future, lead to new targeted therapy. In the meantime repositioning of drugs from biologically similar diseases towards IBD might lead to new IBD therapies.