ObjectiveTo observe the clinical efficacy and safety of Modified Guomin Decoction （加味过敏煎， MGD） in patients with mild to moderate atopic dermatitis （AD） of the traditional Chinese medicine （TCM） pattern of heart fire and spleen deficiency， and to explore its possible mechanisms. MethodsIn this randomized， double-blind， placebo-controlled study， 72 patients with mild to moderate AD and the TCM pattern of heart fire and spleen deficiency were randomly divided into a treatment group and a control group， with 36 cases in each group. The treatment group received oral MGD granules combined with topical vitamin E emulsion， while the control group received oral placebo granules combined with topical vitamin E treatment. Both groups were treated twice daily for 4 weeks. Clinical efficacy， TCM syndrome scores， Visual Analogue Scale （VAS） for pruritus， Dermatology Life Quality Index （DLQI） scores， Scoring Atopic Dermatitis （SCORAD） and serum biomarkers， including interleukin-33 （IL-33）， interleukin-1β （IL-1β）， immunoglobulin E （IgE）， and tumor necrosis factor-α （TNF-α） were compared before and after treatment. Safety indexes was also assessed. ResultsThe total clinical effective rates were 77.78% （28/36） in the treatment group and 38.89% （14/36） in the control group， with cure rates of 19.44% （7/36） and 2.78% （1/36）， respectively. The treatment group showed significantly better clinical outcomes compared to the control group （P＜0.05）. The treatment group exhibited significant reductions in total TCM syndrome scores， including erythema， edema， papules， scaling， lichenification， pruritus， irritability， insomnia， abdominal distension， and fatigue scores， as well as reductions in VAS， DLQI， SCORAD， and serum IgE and IL-33 levels （P＜0.05 or P＜0.01）. Compared to the control group， the treatment group had significantly better improvements in all indicators except for insomnia （P＜0.05）. No adverse events occurred in either group. ConclusionMGD is effective and safe in treating mild to moderate AD patients with heart fire and spleen deficiency pattern. It significantly alleviates pruritus， improves TCM syndromes and quality of life， and enhances clinical efficacy， possibly through modulation of immune responses.

Objective:To investigate the effects of propionic acid produced by Akkermansia muciniphila on the radiosensitivity of colorectal cancer and the underlying mechanism. Methods:Normal human colon mucosal epithelial cells (NCM460) were used to determine the appropriate concentration of propionic acid. Human colorectal cancer cells (HCT-8) were treated with A. muciniphila-conditioned medium or propionic acid, followed by exposure to 6 Gy γ-ray irradiation, and cell survival and proliferation were measured by clone formation assay and Cell Counting Kit-8 (CCK-8) assay, respectively. A mouse model of colorectal cancer was established using azoxymethane/dextran sodium sulfate. The mice were divided into control model group, irradiation group, and irradiation+ propionic acid group. Their body weight, colorectal length, tumor count, and tumor area were recorded. The radiosensitizing effect of propionic acid was assessed with HE staining, immunohistochemical staining, and enzyme-linked immunosorbent assay. The mechanism was explored by using RT-PCR and flow cytometry. Results:CCK-8 assay showed that 1-mmol/L propionic acid had no significant effect on the proliferation of NCM460 cells ( P>0.05), which was used for subsequent experiments. Pretreated with A. muciniphila-conditioned medium or propionic acid, the survival and proliferation abilities of irradiated HCT cells were significantly decreased ( t=3.14-34.98, P<0.05). Compared with the irradiation group, the colorectal cancer mice in the irradiation+ propionic acid group showed a significantly longer colorectal length ( t=3.50, P<0.05) and a significantly smaller number of tumors ( t=3.48, P<0.05); the two groups had significantly smaller tumor areas than the control model group ( t=5.97, 7.30, P<0.05). HE staining and immunohistochemical staining showed that propionic acid restored colorectal structure, and decreased Ki67 expression in colorectal tissue ( t=14.50, 3.40, P<0.05). Propionic acid treatment significantly reduced the levels of the inflammatory factors interleukin-6 and tumor necrosis factor-α, as compared with the mice receiving irradiation alone ( t=4.86, 5.06, P<0.05). Irradiation plus propionic acid treatment significantly increased p53 expression and significantly aggravated G 2/M phase block and cell apoptosis ( t=20.35, 13.05, P<0.05). Conclusions:The A. muciniphila metabolite propionic acid plays a sensitizing role in radiation therapy for colorectal cancer by promoting G 2/M phase block and apoptosis in colorectal cancer cells.

Objective:To investigate the effects of propionic acid produced by Akkermansia muciniphila on the radiosensitivity of colorectal cancer and the underlying mechanism. Methods:Normal human colon mucosal epithelial cells (NCM460) were used to determine the appropriate concentration of propionic acid. Human colorectal cancer cells (HCT-8) were treated with A. muciniphila-conditioned medium or propionic acid, followed by exposure to 6 Gy γ-ray irradiation, and cell survival and proliferation were measured by clone formation assay and Cell Counting Kit-8 (CCK-8) assay, respectively. A mouse model of colorectal cancer was established using azoxymethane/dextran sodium sulfate. The mice were divided into control model group, irradiation group, and irradiation+ propionic acid group. Their body weight, colorectal length, tumor count, and tumor area were recorded. The radiosensitizing effect of propionic acid was assessed with HE staining, immunohistochemical staining, and enzyme-linked immunosorbent assay. The mechanism was explored by using RT-PCR and flow cytometry. Results:CCK-8 assay showed that 1-mmol/L propionic acid had no significant effect on the proliferation of NCM460 cells ( P>0.05), which was used for subsequent experiments. Pretreated with A. muciniphila-conditioned medium or propionic acid, the survival and proliferation abilities of irradiated HCT cells were significantly decreased ( t=3.14-34.98, P<0.05). Compared with the irradiation group, the colorectal cancer mice in the irradiation+ propionic acid group showed a significantly longer colorectal length ( t=3.50, P<0.05) and a significantly smaller number of tumors ( t=3.48, P<0.05); the two groups had significantly smaller tumor areas than the control model group ( t=5.97, 7.30, P<0.05). HE staining and immunohistochemical staining showed that propionic acid restored colorectal structure, and decreased Ki67 expression in colorectal tissue ( t=14.50, 3.40, P<0.05). Propionic acid treatment significantly reduced the levels of the inflammatory factors interleukin-6 and tumor necrosis factor-α, as compared with the mice receiving irradiation alone ( t=4.86, 5.06, P<0.05). Irradiation plus propionic acid treatment significantly increased p53 expression and significantly aggravated G 2/M phase block and cell apoptosis ( t=20.35, 13.05, P<0.05). Conclusions:The A. muciniphila metabolite propionic acid plays a sensitizing role in radiation therapy for colorectal cancer by promoting G 2/M phase block and apoptosis in colorectal cancer cells.

Gut microbiota constitute a complicated but manifold ecosystem, in which specific symbiotic relationships are formed among various bacteria. To maintain a steady state, the gastrointestinal tract and the liver form a close anatomical and functional two-way, interconnected network through the portal circulation. "Gut-liver axis" plays a key role in the pathogenesis of liver diseases. Accumulating evidence indicates that gut microbiota can influence the liver pathophysiology directly or indirectly via a variety of signal pathways. In a pathological state where an ecological imbalance occurs at the compositional and functional levels, gut microbes would interact with the host immune system and other type of cells to cause liver steatosis, inflammation and fibrosis, which in turn give rise to the development of such liver diseases as alcoholic liver disease, nonalcoholic fatty liver disease, primary sclerosing cholangitis, and acute liver failure, to name a few. Studies have shown that microorganisms, such as prebiotics and probiotics, can improve the prognosis of certain diseases, which open a new era of treating liver diseases with bacteria. There are many unknowns and hidden values in the gut microbiome. To explore the pathophysiological mechanism of various complex diseases and develop scientific and effective clinical treatment strategies, efforts should be made to obtain insights into how certain intestinal microbiota participates in the occurrence and progression of liver diseases. As the connection between gut microbiota and liver diseases at both the acute and chronic phases was not elaborated in previously published review articles, herein we discuss the association between gut microbiota and both acute and chronic liver injury. The anatomical structure of the liver enables it to form a close network with the gut microbiota, which is an important mediator in the regulation of the hepatic physiological and pathological functions.
Ecosystem ; Gastrointestinal Microbiome ; Humans ; Intestines ; Liver ; Liver Diseases ; Probiotics

Isolation rearing (IR) enhances aggressive behavior, and the central serotonin (5-hydroxytryptamine, 5-HT) system has been linked to IR-induced aggression. However, whether the alteration of central serotonin is the cause or consequence of enhanced aggression is still unknown. In the present study, using mice deficient in central serotonin Tph2 and Lmx1b, we examined the association between central serotonin and aggression with or without social isolation. We demonstrated that central serotonergic neurons are critical for the enhanced aggression after IR. 5-HT depletion in wild-type mice increased aggression. On the other hand, application of 5-HT in Lmx1b mice inhibited the enhancement of aggression under social isolation conditions. Dopamine was downregulated in Lmx1b mice. Similar to 5-HT, L-DOPA decreased aggression in Lmx1b mice. Our results link the serotoninergic system directly to aggression and this may have clinical implications for aggression-related human conditions.

Objective: To observe the process of nasal mucosa injury and repair induced by nasal decongestants in guinea pigs Methods: Sixty-five male guinea pigs were randomly divided into 4groups by digital random method.The guinea pigs in Group A (20 guinea pigs)were treated with 2 sprays of 0.1% Naphazoline 6 times a day for 2 weeks; Group B (20 guinea pigs)with 2 drops of 1% Ephedrine 6 times a day for 2 weeks; Group C(20 guinea pigs) with 2 sprays of Naphazolin hydrochloride and Chlorphenamine Maleate Nasal Spray 8 times a day for 2 weeks.Group D (5guinea pigs)did not do any intervention as a control group.At the end of first and second weekend, 6 guinea pigs randomly selected from each group were observed the morphological changes of the nasal cavity with nasal endoscope and pathological microscope.Two weeks after stopping use of decongestant, 24 animals were grouped.Three guinea pigs were selected randomly from each group to form Group E (n=9) and Group F (n=9)respectively. The 6 remaining guinea pigs falled into Group G. Group E received 2 sprays of Mometasone Furoate Nasal Spray once a day for 2 weeks; Group F received 1 ml 2.3% saline to wash the nasal cavities once a day for 2 weeks.Group F was used to show the natural progess without any treatment.At the end of the third and fourth weekend, nasal endoscopic and pathological microscopes were used to observe the nasal cavity structure and the pathological changes of nasal mucosa. Results: Nasal mocusa congestion and edema were observed with nasal endoscopy after 2 weeks of using nasal decongestant. Cell edema, blood vessel expansion, acute and chronic inflammatory cell infiltration, cilium lodging or loss were observed under the pathological microscope in GroupA, B, C. After using MometasoneFuroate Nasal Spray and 2.3% saline for 2 weeks, the above changes were all recovered in Group E and F. No recovery was found in Group G. Conclusions Short-term and over dose of nasal decongestant can result in the injury of nasal mucosa in guinea pigs, and the injury is much severe as using decongestant last longer.MometasoneFuroate nasal spray and 2.3% saline can repair the injury.

Objective: To evaluate the effects of extended nursing mode on the asthmatic children with allergic rhinitis (AR). Methods: Totally116 children aged 6-14 years old with asthma and AR were enrolled to this study from November 2015 to October 2016 in our hospital. They were divided into the regular nursing group and the extended nursing group according to the voluntary principle. The patients in regular nursing group were received routine nursing care in or out of hospital, while the patients in extended nursing group received extended care besides routine nursing. The children were required to record diary about asthma and AR And participate in asthma action projects. Before and after intervention we observed the quantitative score of symptoms and signs, the times of acute attack, the times of oblivion medication, the average days of stay in hospital, the days of fail to School or kindergarten, the lung function and the fractional exhaled nitric oxide (FeNO) in children with asthma and AR within 1 year. These above marks were assessed five times respectively at starting (baseline) , 3 months, 6 months, 9 months and 12 months (1 year) The differences between two groups were compared with appropriate statistical methods. Results: 1 year later, out of 58 cases in extended nursing group, 40 patients (68.97%)were in good control and 18 cases (31.03%) in partial control. Out of 58 cases in regular nursing group, 22 cases (37.93%) were in good control and 36 patients (62.07%) in partial control. There were significant differences between two groups in the effect of disease (χ²=11.23, all P<0.01), the experimental group was significantly better than the control group. The symptoms and signs of allergic rhinitis average scores in regular nursing group were 1.88 ± 0.72, extended nursing group were 0.79 ± 0.71, the difference was statistically significant (t=8.080, P<0.01) with the extended nursing group much better that the regular nursing group. The symptoms and signs of asthma average scores in regular nursing group were1.83 ± 0.75, extended nursing group were 0.88 ± 0.67, the difference was also statistically significant (t=7.133, P<0.01) with the extended nursing group much better that the regular nursing group. In extended nursing groups within 1 year the numbers of acute attack (0.60±0.59), the times of oblivion medication (11.05±7.40), the average days of stay in hospital (8.83±2.79) days,the average days of failing to school or kindergarten (8.69±5.46) days, while in regular nursing group within 1 year the numbers of acute attack(2.94±1.52), the times of oblivion medication (35.28±8.84), the average days of stay in hospital(20.95±5.46 days), the average days of fail to school or kindergarten(24.72±5.92) days, the differences were also statistically significant (t=10.50-15.87, P<0.01). The lung function in extended nursing group (PEF: 82.02±6.04, FEVI: 88.19±5.10, FEV25: 80.67±4.88, FEV50: 80.07±3.73, FEV75: 81.52±3.85) and in regular nursing group (PEF: 79.02±6.12,, FEV1: 80.52±4.72, FEV25: 75.05±7.79, FEV50: 77.59±4.60, FEV75: 78.41±4.19) . The differences were also statistically significant (t=2.90-6.15, P<0.01).The FeNO(13.66±2.87) ppb in extended nursing group and (14.95±3.12) ppb in regular nursing group. There were statistical significant differences between the two groups (t=2.30, P<0.05) with extended nursing group much better than regular nursing group. Conclusion The effect of extended care group is better than that of regular nursing group, and extended care is much more benefit to control asthma and allergic rhinitis in children.

Rhinitis medicamentosa (RM) refers to nonallergic inflammation in the nasal mucosa which is caused by the abuse of nasal decongestant and it often occurs in patients with allergic/nonallergic rhinitis along with nasal congestion. RM is characterized by nasal congestion based on long-term use of nasal decongestant, without rhinorrhoea or sneezing. The signs of RM include nasal swelling, thickening, loss of elasticity, and loss of sensitivity to the decongestant. The histological changes of RM are loss of nasal mucosa cilia, squamous epithelium metaplasia, edema of epithelium cell, hyperplasia of goblet cell, increased expression of epidermal growth factor receptor and infiltration of inflammatory cells, etc. There is no precise diagnosis standard for RM, making it even harder for its objective diagnosis. Patients with RM should immediately stop using nasal decongestant, in stead of using nasal glucocorticoid spray for the recovery of the nasal mucosa′s function.

Objective To observe the effects of Wendan decoction (WD) on depression-like behavior in a rat model of Parkinson's disease (PD) and explore the related mechanism.Methods Rodent model of PD was established by unilaterally lesioning medial forebrain bundle with 6-hydrodopamine.After intragastric administration with WD,the rats's behavior changes were detected by the open field test,sucrose preference test and forced swimming test;the contents of monoamine neurotransmitters in the rat brain were assessed by high-performance liquid chromatography with electrochemical detection.Results Compared with those of sham-operated rats,the horizontal and vertical activities of the PD model rats decreased significantly,and sucrose consumption decreased significantly,but immobility time during forced swimming was significantly prolonged.The contents of dopamine (DA),5-hydroxytryptamine (5-HT) and noradrenaline (NA) in the medial prefrontal cortex (mPFC) and DA in the striatum decreased significantly.After administration of WD for 2 weeks,the immobility time of the PD model rats was significantly decreased,sucrose consumption increased significantly;DA,5-HT and NA levels in the mPFC increased significantly.Conclusion WD improves the depression-like behavior in PD model rats,and the mechanisms may involve the regulation of monoamine neurotransmitters in mPFC.

OBJECTIVETo investigate the expression of full-length spleen tyrosine kinase [SYK (L)] mRNA and protein in human oral squamous cell carcinoma (OSCC) as well as its possible effects on the invasion and metastasis of OSCC.

METHODSThe expression of SYK (L) was detected in 27 cases of OSCC tissues and its matched adjacent non-cancerous tissues by real-time quantitative polymerase chain reaction (RT-qPCR), Western blot, and immunohistochemistry. Fourteen cases of normal oral gingival tissues were also analyzed as a normal control.

RESULTSReduced mRNA and protein expression of SYK (L) in OSCC tissues was observed compared with that in normal oral gingival tissues (P<0.01) and adjacent non-cancerous tissues (P<0.05). SYK(L) expression was significantly associated with lymph-node metastasis (P<0.05).

CONCLUSIONSYK(L) is a candidate tumor suppressor for OSCC tissues, and has an inhibitive effect on the initiation, proliferation, and lymph-node metastasis of human OSCC.

Blotting, Western ; Carcinoma, Squamous Cell ; metabolism ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Mouth Neoplasms ; metabolism ; RNA, Messenger ; Syk Kinase ; metabolism