Allergic rhinitis, allergic contact dermatitis and disease comorbidity belong to separate entities with distinct composition of T-cell subsets, cytokines, immunoglobulins and autoantibodies.

BACKGROUND: Allergic rhinitis (AR) and allergic contact dermatitis (ACD) are prevalent allergic diseases and have significant impacts on patients' daily life. Despite many studies on AR or ACD have been conducted separately, little is known about the immune responses in patients of AR combined with ACD and the interplay between AR and ACD. Our study compared various aspects of immune elements in patients with AR or/and ACD, aiming to characterize the immune responses in AR, ACD, and AR combined with ACD. METHODS: A total of 57 patients diagnosed with AR or/and ACD and 28 healthy volunteers were included. AR patients were further divided into seasonal AR (SAR) and perennial AR (PAR). All subjects' blood samples were taken to assess the concentration of immunoglobulins, complement C3, C4, autoantibodies and cytokines in serum by immunoturbidimetry, ELISA or Luminex200 platform. Peripheral blood mononuclear cells (PBMCs) were subjected to the analysis of lymphocyte subpopulations by flow cytometry. RESULTS: It indicated that AR disease caused elevated levels of IgE, IgA, IgG, IgG4, as well as IL-4, IL-15, IL-8 and IL-6 in serum. AR patients possessed a decreased CD4/CD8 ratio and an increased proportion of memory CD4 + T-cell subset, with a skewed Th2 response and an enhanced CD8 + T-cell activation. Compared with patients with sole AR or ACD condition, AR + ACD patients presented with a significantly increased proportion of memory CD8 + T-cell subset and were prone to autoimmune disorders as indicated by the increased autoantibodies. The immune elements in patients with ACD only were least affected compared with those in other conditions. Additionally, seasonal or perennial AR patients exhibited different cytokine profiles and proportions of memory T-cell subsets. CONCLUSIONS: In this study, we illuminated the respective characteristics of immune responses in AR, ACD, and AR combined with ACD. Meanwhile, we discovered that the PAR and SAR patients possessed different cytokine profiles and T-cell compartments. It suggested that these allergic conditions belong to different disease entities. Characterizing the detailed immune changes in these allergic diseases would help to develop proper treatments targeting particular immune elements in different allergic diseases.

[Electroacupuncture in the prevention and treatment of sore throat and nausea and vomiting after gastrointestinal surgery: a randomized controlled trial].

OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention on postoperative sore throat (POST) and postoperative nausea and vomiting (PONV) after endotracheal intubation and general anesthesia. METHODS: According to the random number table, 60 patients of gastrointestinal surgery under general anesthesia with tracheal intubation were randomly divided into EA group (30 cases) and control group (30 cases). Patients in the EA group were given acupuncture at Shaoshang (LU11) 30 minutes before general anesthesia, and EA at Chize (LU5) and Hegu (LI4) continued until the operation was completed. The incidence and severity of POST and visual analogue scale (VAS) score at 12, 24, and 48 h after surgery, and the incidence and severity of PONV at 12, 24 h after surgery were analyzed, respectively. RESULTS: The incidence and severity of POST and PONV, and VAS score in the EA group were significantly lower than those in the control group 12 h and 24 h after surgery (P<0.05). Both groups had significant reductions in VAS score at 24 h and 48 h after surgery compared with that at 12 h (P<0.05). CONCLUSION: EA can significantly improve the prognosis of patients on sore throat and reduce the incidence of PONV.

Ursolic Acid Reverses the Chemoresistance of Breast Cancer Cells to Paclitaxel by Targeting MiRNA-149-5p/MyD88.

Paclitaxel (PTX) is widely used as a front-line chemotherapy for breast cancer treatment. However, its clinical applications are limited by the development of chemoresistance. The objective of this study was to investigate the reversal effects of ursolic acid (UA) on PTX resistance and the possible mechanisms in breast cancer. The role of miRNA-149-5p/MyD88 in the regulation of PTX resistance was investigated by the transfection of breast cancer cells with MDA-MB-231 (231) and MDA-MB-231/PTX-resistance (231/PTX) with lentiviruses carrying the MyD88 gene, shRNA specific for MyD88, the miR-149-5p gene, and shRNA specific for miR-149-5p. The PTX sensitivity was assessed by a CCK-8 assay. qRT-PCR and Western blot analyses were used to detect changes in the mRNA and protein levels. Flow cytometry was used to measure the rate of cell apoptosis. A luciferase activity assay was used to detect the binding site of miR-149-5p on the 3'UTR of MyD88. 231/PTX cells were injected into the flanks of female athymic nude mice, and the mice were randomly divided into the five following groups: PBS, PTX (low), PTX (high), UA, and PTX+UA. Our data show that UA reversed the resistance of breast cancer 231/PTX cells to PTX in vitro and in vivo. UA treatment significantly increased the expression of miR-149-5p, which was lower in 231/PTX cells than in 231 cells. Furthermore, the overexpression of miR-149-5p increased the sensitivity of 231/PTX cells to PTX treatment, whereas the knockdown of the miR-149-5p gene attenuated the effects of UA on the regulation of PTX sensitivity. A luciferase assay demonstrated that miR-149-5p could directly regulate the transcriptional activity of MyD88, a known PTX-resistance gene, by targeting the 3'UTR of MyD88. Meanwhile, the downregulation of MyD88 through the overexpression of miR-149-5p or UA treatment inhibited the activation of the Akt signaling pathway in 231/PTX cells. Thus, our data indicate that UA can reverse PTX resistance by targeting the miRNA-149-5p/MyD88 axis in breast cancer cells.

Diagnostic Value of Serum hsa-mir-92a in Patients with Cervical Cancer.

BACKGROUND: Hsa-mir-92a acts as an onco-miRNA and may contribute to the progression and invasion of cervical cancer, which is a common malignant tumor in women worldwide. The objective of the present study was to evaluate whether serum hsa-mir-92a could serve as a diagnostic biomarker for cervical cancer patients. METHODS: The expression levels of hsa-mir-92a were analyzed in the serum of patients with CIN I, CIN II, CIN III, cervical cancer Ia - IIa and compared with those of the control group samples. The receiver operating characteristic (ROC) curve was used to evaluate the diagnostic significance of cervical cancer. RESULTS: It was found that the expression of hsa-miR-92a in the serum of individuals with CIN or cervical cancer was significantly higher than that in healthy volunteers (p < 0.01). The expression of hsa-miR-92a was higher in the serum of patients with advanced stage and cervical cancer than those with early stage. ROC analysis revealed that the cutoff value of hsa-mir-92a was 1.52 for the diagnosis of CIN and cervical cancer. The sensitivity and specificity were 69.6% and 80.4%, respectively, and an area under the curve (AUC) was 0.83. CONCLUSIONS: hsa-mir-92a up-regulation was associated with cervical cancer and the serum level of hsa-mir-92a could be used as an independent marker for the diagnosis of cervical cancer.

Biphasic effect of androgens on prostate cancer cells and its correlation with androgen receptor coactivator dopa decarboxylase.

The aim of this study was to explore the mechanism underlying the dual effect of androgen on prostate cancer cells and further explore its correlation with dopa decarboxylase (DDC), an androgen receptor (AR) coactivator and a traditional neuroendocrine differentiation (NED) marker. Cell proliferation and cycling after treatment with synthetic nonmetabolizable androgen R1881 was determined by the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) method and flow cytometry. Differential gene expression was analyzed by cDNA microarrays. DDC expression during the dual effect of R1881 was further explored with microarray, quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot, and enzyme activity assays. Proliferation of LNCaP cells was inhibited by 1 nM R1881 but stimulated by 0.1 nM R1881. Compared with the untreated cells, 320 (2.26%; 170 up-regulated, 150 down-regulated) and 4608 (32.65%; 2046 up-regulated, 2562 down-regulated) genes were found to be expressed differentially in the 1 nM and 0.1 nM R1881-treated cells, respectively. The results were partially confirmed by RT-PCR and Western blot. The DDC gene was down-regulated in the 1 nM R1881-treated cells and up-regulated in 0.1 nM R1881- and 30 nM hydroxyflutamide-treated cells. The enzymatic activity of DDC in the latter 2 groups was also strengthened. Meanwhile, the NED markers CgA and synaptophysin were not affected by these AR activators. R1881 had a dose-dependent biphasic effect on LNCaP cell proliferation. AR coactivator DDC was respectively down- and up-regulated in high and low concentrations of R1881. DDC up-regulation by exogenous AR activators is not accompanied by up-regulation of definitive NED markers.

Change of the cell cycle after flutamide treatment in prostate cancer cells and its molecular mechanism.

AIM: To explore the effect of androgen receptor (AR) on the expression of the cell cycle-related genes, such as CDKN1A and BTG1, in prostate cancer cell line LNCaP. METHODS: After AR antagonist flutamide treatment and confirmation of its effect by phase contrast microscope and flow cytometry, the differential expression of the cell cycle-related genes was analyzed by a cDNA microarray. The flutamide treated cells were set as the experimental group and the LNCaP cells as the control. We labeled cDNA probes of the experimental group and control group with Cy5 and Cy3 dyes, respectively, through reverse transcription. Then we hybridized the cDNA probes with cDNA microarrays, which contained 8 126 unique human cDNA sequences and the chip was scanned to get the fluorescent values of Cy5 and Cy3 on each spot. After primary analysis, reverse transcription polymerase chain reaction (RT-PCR) tests were carried out to confirm the results of the chips. RESULTS: After AR antagonist flutamide treatment, three hundred and twenty-six genes (3.93%) expressed differentially, 97 down-regulated and 219 up-regulated. Among them, eight up-regulated genes might be cell cycle-related, namely CDC10, NRAS, BTG1, Wee1, CLK3, DKFZP564A122, CDKN1A and BTG2. The CDKN1A and BTG1 gene mRNA expression was confirmed to be higher in the experimental group by RT-PCR, while p53 mRNA expression had no significant changes. CONCLUSION: Flutamide treatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells. The protein expressions of CDKN1A and BTG1 play an important role in inhibiting the proliferation of cancer cells. CDKN1A has a great impact on the cell cycle of prostate cancer cells and may play a role in the cancer cells in a p53-independent pathway. The prostate cancer cells might affect the cell cycle-related genes by activating AR and thus break the cell cycle control.