Objectiye To investigate the expression of regulated on activation, normal T-cell expressed and secreted (RANTES) and occluding in brain, and investigate the role of expression of RANTES in the change of blood-brain barrier permeability of rats with acute pancreatitis. Methods 49 Sprague-Dawley rats were randomly divided into 7 groups according to random number table, including sham-operated group (SO) , acute edematous pancreatitis (AEP) 3, 6 h group and acute necrotizing pancreatitis (ANP) 3, 6, 12 and 24 h group. AEP and ANP were induced by retrograde injection of 0. 5% and 5% sodium taurocholate, respectively. RT-PCR, Western blot, and immunohistochemistry methods were performed to assess the expression of RANTES and occludin mRNA and protein in brain tissue. Results The RANTES mRNA expressions in SO, AEP 3, 6 h, ANP 3, 6, 12, 24 h group were 0, 0, 0, 0.36±0.05, 0.47±0.04, 0.65±0.05, 0.83±0.07, respectively; The RANTES protein expressions were 0, 0, 0, 0.42±0. 03, 0. 57±0.04,0.78±0.08, 1.05±0.08, respectively; the values in ANP group were significantly lower than those in SO group and AEP group (P<0.01). The occludin mRNA expressions were 1.21±0.07,1.17±0.07, 1.15±0.08,0.84±0.07,0.77±0.05,0.64±0.09,0.56±0.09, respectively, the occludin protein expressions were 1.18 ±0.08, 1. 16 ±0. 10, 1. 11 ±0. 10, 0. 90 ±0. 03, 0. 65 ±0."05, 0.57 ±0.05, 0.48 ±0.05, respectively, the values in ANP group were significantly lower than those in SO group and AEP group (P< 0.01). The expression of RANTES was positively related to the pancreatic pathologic score (r = 0. 936,P< 0. 001) ; the expression of occluding was negatively related to the pancreatic pathologic score (r = - 0. 943, P < 0.001). The expression of RANTES was negatively related to the expression of occluding (r = -0. 943, P <0. 001). Conclusions The expression of RANTES was progressively increased in the brain tissue in rats with ANP, while the expression of occluding was progressively decreased; RANTES may play an important role in the change of blood-brain barrier permeability via down-regulating the expression of occluding.

Objective To investigate the effects of abdominal breathing training on sleep disorders in elderly patients with chronic heart failure. Methods Total of 100 patients with chronic heart failure complain of sleeping disorders and Pittsburgh Sleep Quality Index (PSQI)>7 points were assigned into two groups by random digits table method, 50 cases in each group. The observation group and the control group were nursed in the same way except that abdominal breathing was adapted to the observation group. Sleep status, heart rate, blood pressure, SpO2 and brain natriuretic peptide (BNP) were evaluated before training, one week and eight weeks after training respectively. Statistics was used to analyze the differences between two groups. Results After training one week, the sleep status of the observation group was ameliorated, but without significant difference compared to the control group (P>0.05). And after training eight weeks, the PSQI, BNP and heart rate were (9.21 ± 6.38) points, (193.78 ± 152.16) μg/L, (63.5 ± 10.8) times/min in the observation group, and (12.92 ± 0.33) points, (417.55 ± 262.47) μg/L, (70.7 ± 8.5) times/min in the control group, and there was significant differences between 2 groups (t=3.627, 2.041, 2.767, all P < 0.05), while the blood pressure, SpO2 did not change obviously(P>0.05). Conclusions Abdominal breathing training could ameliorate sleep status in elderly patients with chronic heart failure.

OBJECTIVE To determine the feasibility of clindamycin-loaded calcium phosphate cement(CLCPC) as a local antibiotic delivery system.METHODS The initial setting time(tI) and the final setting time(tF) were measured for 0%,2% and 5% CLCPC according to ASTM C266-89 method.Clindamycin concentrations eluting from the samples of 2% and 5% CLCPC in PBS were analyzed by HPLC at different times.The bacteriostasis tests were done by plate diffusion method for 2% and 5% CLCPC and 2% Palacos R-40 bone cement(PMMP) samples,and the diameters of the bacteriostasis ring and bacteriostasis duration were observed.The setting product and crystal size of 0%,2% and 5% CLCPC were analyzed and observed by X-ray diffraction(XRD) and scanning electron microscopy(SEM).RESULTS The setting time could be shortened by adding clindamycin(tI,tF) of 2% and 5% CLCPC.Clindamycin was with burst-release from CLCPC within the intial 6-hour period and the release rate slowed down on 4th day.Clindamycin could still release until to the 42th day.The ring of 2% Palacos R-40 bone cement(PMMP) bacteriostasis was smaller than that of 2% CLCPC,and the ring of 2% CLCPC bacteriostasis was smaller than that of 5%CLCPC.The bacteriostasis still existed to the 42th day of test for 2% and 5%CLCPC and 2% Clindamycin-loaded Palacos R-40 bone cement(CLPMMP).From the 30th day,many bacterial colonies were seen in the culture media laying 2%CLPMMP sample.On the contrary,bacterial colony was not found in the media putting 2% and 5%CLCPC.XRD and SEM showed that clindamycin did′t have an influence on setting product,crystal size and structure of CPC.CONCLUSIONS Clindamycin-loaded calcium phosphate cement can be used as a local antibiotic delivery system.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

OBJECTIVE: To analyze Th1 and Th2 immune balance related cytokines and clinical significance in obstructive sleep apnea hypopnea syndrome children without allergic rhinitis and asthma. METHOD: Collected 91 cases of obstructive sleep apnea hypopnea syndrome children with obstructive level data, and measured the serum Th1 cytokine TNF-beta and IFN-gamma, Th2 cytokines IL-4 and IL-5 levels. One hundred and five normal children were enrolled for the same detection of serum cytokines. RESULT: Non-allergic rhinitis and asthma children serum levels of IFN-gamma was lower than control group children, the difference was statistically significant (P < 0. 01). Other cytokines (TNF-beta, IL-4 and IL-5) were no significant difference with the control group. CONCLUSION Th1 and Th2 immune response was imbalance in non-allergic rhinitis and asthma obstructive sleep apnea hypopnea syndrome children. The decline in Th1 cell-mediated protective immune response cells may cause disease.
Asthma ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Interferon-gamma ; blood ; Interleukin-4 ; blood ; Interleukin-5 ; blood ; Lymphotoxin-alpha ; blood ; Male ; Rhinitis, Allergic ; Rhinitis, Allergic, Perennial ; Sleep Apnea, Obstructive ; blood ; Th1 Cells ; metabolism ; Th2 Cells ; metabolism

OBJECTIVE: To explore application of endoscope assisting in retrosigmoid approach vestibular schwannoma resection and its signification. METHOD: Through retrosigmoid approach with endoscope assisting, vestibular schwannoma in the cerebellopontine angle was removed in 12 cases. Assessment of function of facial nerve and auditory was made for all patients preoperative and postoperative. RESULT: Vestibular schwannoma in 12 patients were removed completely, then the facial nerve and the acoustic nerve were preserved after tumor removal. No complication was found in six months. We observed the hearing loss in postoperative patients, and there is no difference in facial nerve function between preoperative and postoperative. The alteration of auditory and facial nerves functions is no difference between two retrosigmoid approach groups with or without endoscope assisting. CONCLUSION Application of endoscope assisting in retrosigmoid approach can be helpful for totally resection of vestibular schwannoma in inner acoustic meatus without lesion of canalis semicircularis and glomus jugulare. Application of the endoscope assisting in retrosigmoid approach is helpful to provide the precise information of CPA anatomic structure and decrease the incidence rate of complication.
Adult ; Aged ; Cerebellopontine Angle ; surgery ; Endoscopy ; methods ; Female ; Humans ; Male ; Middle Aged ; Neuroma, Acoustic ; surgery