A subset of patients with systemic lupus erythematosus has autoantibodies to acidic phospholipids. Since lipids are poor immunogens, the mechanism responsible for the induction of these antibodies is unclear. Immunization of a normal rabbit and normal mice with purified human g62-glycoprotein I (apolipoprotein H) resulted in the production of high levels of two non-cross-reactive antibody populations, anti-apolipoprotein H, and antiphospholipid. The antiphospholipid antibodies had binding specificities indistinguishable from autoantibodies obtained from human and murine lupus. These findings suggest a novel mechanism for the induction ofantiphospholipid autoantibodies. (J. Clin. Invest. 1992. 90:1105-1109

The PALM-COEIN classification for causes of abnormal uterine bleeding (AUB) was proposed by the International Federation of Gynecology and Obstetrics (FIGO) in 2011, which has been gradually applied in the diagnosis of AUB in the past 2 years in China. However, there are no reports yet on the causes of chronic AUB among Chinese women with this new classification system.The purpose of this study was to describe the prevalence of the causes of chronic AUB among Chinese women of reproductive age using the PALM-COIEN classification system.This is a cross-sectional study. Beijing Shijitan Hospital, Capital Medical University.A total of 1053 women aged 15 to 55 years with chronic AUB were evaluated between November 2016 and May 2017.Prevalence of the causes of chronic AUB using the PALM-COEIN classification. AUB-O was the most frequent finding in women with chronic AUB, accounting for 608 (57.7%) cases. AUB-P was found in 171 (16.2%) women, AUB-L in 130 (12%) women, AUB-A in 52 (4.94%) women, AUB-E in 28 (2%) women, AUB-I in 23 (2%) women, AUB-M in 20 (1.9%) women, AUB-C in 10 (1%) women, and AUB-N in 10 (0.9%) women.Ovulatory dysfunction (AUB-O) is the most common cause of AUB among the nonstructural causes. Endometrial polyps (AUB-P) are the most common among the structural causes, followed by uterine fibroids (AUB-L) and uterine adenomyosis (AUB-A).

Heat stressed pigs show typical characteristics of inflammatory bowel disease (IBD). However, little is known about the pathogenesis of heat stress (HS)-induced IBD in pigs. In this study, we determined the effects of HS on colon morphology, intestinal microbiota diversity, transcriptome genes (transcripts), and short chain fatty acids (SCFAs) metabolism in pigs. In addition, the correlation among these parameters was analyzed by weighted gene co-expression network analysis. Results showed that the liver and kidney functions related to blood biochemical indexes were partially changed in pigs under HS. Furthermore, the levels of diamine oxidase and D-lactic acid were significantly increased, whereas the levels of secretory immunoglobulin A were decreased. The integrity of colonic tissue was damaged under HS, as bleeding, lymphatic infiltration, and villi injury were observed. The concentrations of SCFAs in the colon, such as acetic acid and butyric acid, were decreased significantly. In addition, the composition of colon microbiota, such as decrease in Lactobacillus johnsonii, Lactobacillus reuteri and increase in Clostridium sensu stricto 1 of day 7 and 14 while under HS. These changes were associated with changes in the concentration of SCFAs and biochemical indexes above mentioned. Differentially expressed genes were enriched in the nucleotide-binding oligomerization domain-like receptor signaling pathway, Th17 cell differentiation, and IBD pathway, which were also associated with the changes in SCFAs. Thus, the structure, diversity of intestinal microorganisms, and changes in the levels of SCFAs in colon of heat stressed pigs changed significantly, contributing to the activation of immune response and inflammatory signal pathways and causing abnormal physiological and biochemical indexes and intestinal mucosal damage. These results highlight the interconnections between intestinal microbiota, SCFAs, and immune response and their role in the pathogenesis of stress induced IBD therapy.

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Heat stress can significantly affect the immune function of the animal body. Heat stress stimulates oxidative stress in intestinal tissue and suppresses the immune responses of mice. The protecting effects of chitosan on heat stress induced colitis have not been reported. Therefore, the aim of this study was to investigate the protective effects of chitosan on immune function in heat stressed mice. Mice were exposed to heat stress (40 °C per day for 4 h) for 14 consecutive days. The mice (C57BL/6J), were randomly divided into three groups including: control group, heat stress, Chitosan group (LD: group 300 mg/kg/day, MD: 600 mg/kg/day, HD: 1000 mg/kg/day). The results showed that tissue histology was improved in chitosan groups than heat stress group. The current study showed that the mice with oral administration of chitosan groups had improved body performance as compared with the heat stress group. The results also showed that in chitosan treated groups the production of HSP70, TLR4, p65, TNF-α, and IL-10 was suppressed on day 1, 7, and 14 as compared to the heat stress group. In addition Claudin-2, and Occludin mRNA levels were upregulated in mice receiving chitosan on day 1, 7, and 14 of heat stress. Furthermore, the IL-6, IL-10, and TNF-α plasma levels were down-regulated on day 1, 7, and 14 of heat stress in mice receiving the oral administration of chitosan. In conclusion, the results showed that chitosan has an anti-inflammatory ability to tolerate hot environmental conditions.