[Different rapid maxillary expansion methods in the treatment of adult patients with obstructive sleep apnea hypopnea syndrome].

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a common sleep respiratory disorder characterized by upper respiratory collapse during sleep, with a high prevalence and potentially fatal complications. Currently, maxillary transverse deficiency are considered to be an important pathogenic factor of OSAHS. For patients with poor compliance with positive airway pressure therapy, rapid maxillary expansion can increase the volume and ventilation of the upper respiratory tract, which is an alternative treatment. This paper reviewed the current research on surgically assisted rapid palatal expansion, miniscrew assisted rapid palatal expansion, and distraction osteogenesis maxillary expansion in the treatment of adult OSAHS. By comparing the indications, contraindications, complications, efficacy and long-term stability of the three treatment methods, it provided reference for treatment of patients with OSAHS.

Correction: Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance.

Cancer stem cells (CSCs) are inherently resistant to chemotherapy, and CSCs in chemotherapy-failed recurrent tumors are enriched; however, the cellular origin of chemotherapy-induced CSC enrichment remains unclear. Communication with stromal fibroblasts may induce cancer cell dedifferentiation into CSCs through secreted factors. We recently demonstrated that fibroblast-derived exosomes promote chemoresistance in colorectal cancer (CRC). Here, we report that fibroblasts confer CRC chemoresistance via exosome-induced reprogramming (dedifferentiation) of bulk CRC cells to phenotypic and functional CSCs. At the molecular level, we provided evidence that the major reprogramming regulators in fibroblast-exosomes are Wnts. Exosomal Wnts were found to increase Wnt activity and drug resistance in differentiated CRC cells, and inhibiting Wnt release diminished this effect in vitro and in vivo. Together, our results indicate that exosomal Wnts derived from fibroblasts could induce the dedifferentiation of cancer cells to promote chemoresistance in CRC, and suggest that interfering with exosomal Wnt signaling may help to improve chemosensitivity and the therapeutic window.

Culture and characterization of chicken small intestinal crypts.

The integrity and normal function of the small intestinal epithelium depends critically on the rapid renewal of epithelial cells from basal stem cells. The intensive proliferation that fuels this self-renewal process is confined to the intestinal crypts. Establishment of suitable protocols for crypt isolation and culture is pivotal for the studies of intestinal self-renewal mechanisms. In this study, chicken small intestinal crypts were isolated, purified, and further cultured in a Matrigel 3-D culture system. The growth factor concentration assay on the fourth d of culture showed that Group C (50 ng/mL epidermal growth factor (EGF), 100 ng/mL Noggin, and 500 ng/mL R-spondin 1) supplement in culture medium could significantly enlarge the diameter of organoids when compared with Group A (5 ng/mL EGF, 10 ng/mL Noggin, 50 ng/mL, and R-spondin 1) and Group B (10 ng/mL EGF, 20 ng/mL Noggin, and 100 ng/mL R-spondin 1) by 188.4% (P = 0.026) and 176.9% (P = 0.034), respectively. Transmission electron microscopy, neutral red staining, and 5-ethynyl-2΄-deoxyuridine incorporation demonstrated the integrated structure, high viability, and proliferative activity in cultured chicken intestinal organoids. In addition, intestinal stem cell marker genes (Olfm4, Znrf3, Hopx, and Lgr5) also could be detected in cultured intestinal organoids. Furthermore, CHIR99021 (a glycogen synthase kinase 3ß inhibitor) could enhance the expression of Olfm4, Znrf3, Hopx, and Lgr5 by 750% (P = 0.001), 467% (P < 0.001), 450% (P < 0.001), and 333% (P = 0.008), respectively, indicating the responsiveness of the cultured chicken intestinal organoids to exogenous stimulus. This study modified a murine culture model and optimized it to provide a chicken intestinal organoid model for use as a physiological or pathological research platform in vitro.

Attenuating effect of melatonin on lipopolysaccharide-induced chicken small intestine inflammation.

Enriched melatonin (MEL) has been found in the mammalian intestine and has been recently demonstrated to alleviate rodent colitis. In this study, the effect of MEL on lipopolysaccharide (LPS)-induced intestinal inflammations was investigated in new chicken hatchlings. The chicks were fed with a diet supplemented with MEL (12.5 mg/day) from D1 to D10. Meanwhile, the chicks in the LPS or MEL + LPS groups were injected with LPS (10 mg/kg BW, i.p.) at D10. LPS treatment for 6 h increased the expression of IL-6, IL-4, caspase-3 mRNAs and TUNEL-positive cell populations, but decreased populations of the goblet and PCNA+ cells, IgA production and the expression of MUC2 mRNA in the duodenum. Compared with the LPS group, MEL pre-feeding alleviated duodenal inflammation and decreased the expression of TNF-α mRNAs by 23.6% (P = 0.004), IL-6 mRNAs by 69.4% (P = 0.001), IL-4 mRNAs by 4.1% (P = 0.824) and caspase-3 mRNAs by 45.8% (P < 0.001). Conversely, MEL pre-feeding attenuated the LPS-induced changes of IgA production by 161.6% (P = 0.013) and PCNA+ cell populations by 172.1% (P < 0.001) in the duodenum. TLR4 mRNA was also up-regulated by LPS treatment but down-regulated by MEL pre-feeding. In conclusion, dietary MEL could attenuate LPS-induced chick duodenal inflammation by down-regulating the expression of inflammatory cytokines, promoting epithelial cell proliferation, improving the immunological barrier and inhibiting epithelial apoptosis via the mediation of TLR4.

Effect of melatonin on renewal of chicken small intestinal mucosa.

A higher concentration of melatonin (MEL) in the intestine - even more than that in the plasma and pineal gland - implies its putative important role in the gastrointestinal structural or functional regulation. However, little evidence has shown that MEL can regulate the physiological functions of the intestinal mucosa. In this study, fertilized chicken eggs were treated with MEL (0.1 to 10 µg/d) from embryonic d 12 (E12) to post-hatching d 6 (D6), and the small intestine samples were collected at D6 to determine the changes in mucosal construction and function. Results of HE staining showed that the enterocyte number was not changed after MEL treatment. Alcian blue - periodic acid Schiff reaction (AB-PAS) staining and qRT-PCR showed that the goblet cells populations and mucins gene (MUC2) expression in the small intestine were significantly increased after MEL treatment. Meanwhile, 5-ethynyl-2'-deoxyuridine staining showed that both the proliferation and migration rates of the small intestine mucosal epithelium were promoted by MEL treatment. Importantly, MEL significantly increased the activities of the digestive enzymes (maltase, sucrose, and lactase) and expression of the nutrient transporter genes such as GLUT5, BOAT, and EAAT3 mRNAs in the duodenum or jejunum. Meanwhile, the expression of Notch receptors (Notch1 and Notch2) and their ligands (Dll1 and Dll4) were remarkably decreased after MEL treatment. In conclusion, MEL treatment increased the goblet cell populations, MUC2 expression, epithelium migration, and digestive and absorptive function of the chicken small intestine involving repressed Notch signaling.

Identification of the Paneth cells in chicken small intestine.

The Paneth cells are highly specialized cells in the epithelium of the small intestine of many vertebrate species. These cells reside at the base of crypts of the Lieberkühn and contain abundant secretory granules. Previous studies suggesting the existence of Paneth cells in the chicken (Gallus gallus) remained controversial. Here we seek to identify the Paneth cells in the chicken small intestine through morphological examination and specific gene expression. Histological staining and transmission electron microscope confirmed the presence of granulated secretory cells at the base of the crypts in the chicken small intestine. Western blotting experiment also manifested the expression of lysozyme protein, which is specifically secreted by the Paneth cells in the small intestine. Moreover, lysozyme c and lysozyme g mRNAs were expressed in the small intestine of chickens at different ages. Lysozyme c mRNA, in particular, was located at the base of the small intestinal crypts as displayed by in situ hybridization. Collectively, we provide evidences that the Paneth cells indeed exist in the small intestine of the chicken.

Individualized treatment of NSCLC: from research to clinical practice.

The exact clinical significance of EGFR mutation status in NSCLC at the time of initial diagnosis remains disputable. The gene expression module in NSCLC for chemotherapy outcome prediction needs to be developed. We analyzed 56 patients with NSCLC received chemotherapy either with (n=20) or without EGFR-TKIs (n=36) between 2008 and 2012 in China. EGFR mutation test and gene expression profiling were performed in samples obtained before medication treatment by liquidchip platform. Significant association (P = 0.028) was seen between EGFR mutation status before first-line chemotherapy and EGFR-TKIs treatment outcomes, which even can be found from the status before second- or third-line treatment. A14-gene expression profiling had been studied. Patients with low mRNA expression of ERCC1 or TYMS preferred higher DCR to cisplatin and pemetrexed than those with high expression (P = 0.39 and P= 0.11). Highly co-expression of TUBB3 and STMN1 gene has associated with the resistance to antimicrotubule drugs (P = 0.03). Our data suggest the EGFR mutations status, even at the time of initial diagnosis, is predictive of outcomes of TKIs treatment after chemotherapy. The mRNA expression profiling investigated in this study has a predictive value in NSCLC treatment, but further research with expanded samples is still required.

The isoflavonoid daidzein attenuates the oxidative damage induced by polychlorinated biphenyls on cultured chicken testicular cells.

The soy isoflavonoid daidzein (DAI) is one of the most abundant phenolic compounds in the human diet and in animal feedstuffs. Daidzein possesses a wide spectrum of physiological and pharmacological functions related to human health. The aim of this study was to evaluate the effect of DAI on oxidative damage induced by a potential carcinogen, polychlorinated biphenyl. Testicular cells were dispersed from 18-d-old chicken embryos and exposed to DAI alone or in combination with a mixture of polychlorinated biphenyls, Aroclor 1254 (A1254), in culture. Oxidative damage was estimated by measuring the lipid peroxidation and superoxide dismutase activities and glutathione content. Results showed that DAI (10 microg/mL) increased germ cell numbers, which were inhibited by cotreatment with the estrogen receptor antagonist tamoxifen at 0.1 microg/mL. Exposure to A1254 (10 microg/mL) reduced superoxide dismutase activity and glutathione content but increased lipid peroxidation significantly. However, simultaneous supplementation with 10 microg/mL of DAI restored these parameters. The above results indicated that DAI may exert weak estrogenic activity, and more important, that DAI may display an antioxidant effect to prevent oxidative damage induced by the oxidant A1254.

Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms.

We investigated 10 naturally ventilated schools in Shanghai, in winter. Pupils (13-14 years) in 30 classes received a questionnaire, 1414 participated (99%). Classroom temperatures were 13-21 degrees C (mean 17 degrees C), relative air humidity was 36-82% (mean 56%). The air exchange rate was 2.9-29.4 ac/h (mean 9.1), because of window opening. Mean CO2 exceeded 1000 ppm in 45% of the classrooms. NO2 levels were 33-85 microg/m3 indoors, and 45-80 microg/m3 outdoors. Ozone were 1-9 microg/m3 indoors and 17-28 microg/m3 outdoors. In total, 8.9% had doctors' diagnosed asthma, 3.1% wheeze, 23.0% daytime breathlessness, 2.4% current asthma, and 2.3% asthma medication. Multiple logistic regression was applied. Observed indoor molds was associated with asthma attacks [odds ratio (OR) = 2.40: P < 0.05]. Indoor temperature was associated with daytime breathlessness (OR = 1.26 for 1 C; P < 0.001), and indoor CO2 with current asthma (OR = 1.18 for 100 ppm; P < 0.01) and asthma medication (OR = 1.15 for 100 ppm; P < 0.05). Indoor NO2 was associated with current asthma (OR = 1.51 for 10 microg/m3; P < 0.01) and asthma medication (OR = 1.45 for 10 microg/m3; P < 0.01). Outdoor NO2 was associated with current asthma (OR = 1.44 for 10 microg/m3; P < 0.05). Indoor and outdoor ozone was negatively associated with daytime breathlessness. In conclusion, asthma symptoms among pupils in Shanghai can be influenced by lack of ventilation and outdoor air pollution from traffic. Practical Implications Most urban schools in Asia are naturally ventilated buildings, often situated in areas with heavy ambient air pollution from industry or traffic. The classes are large, and window opening is the only way to remove indoor pollutants, but this results in increased exposure to outdoor air pollution. There is a clear need to improve the indoor environment in these schools. Building dampness and indoor mold growth should be avoided, and the concept of mechanical ventilation should be introduced. City planning aiming to situate new schools away from roads with heavy traffic should be considered.