The incidence rate of allergic rhinitis(AR)is high and difficult to cure,which seriously affects the quality of life of patients.The theory of"deficient qi inducing stagnation"is highly consistent with the occurrence and development of this disease.This article believed that the"deficient qi"state of the deficiency of the lungs,spleen and kidney was the fundamental factor of the onset of AR,and the external pathogenic factors,cold,dampness and endogenous phlegm,stasis and turbidity caused by"deficient qi"were the inducing and aggravating factors of AR.It proposed to cultivate the earth to produce gold,gold and water to"replenish the deficient qi",to dispel the wind,to dissipate cold and dampness,to dispel phlegm and dampness,and to reducing stasis and promoting circulation,and to use the two-way regulation of strengthening the healthy qi and dispelling the pathogens,so that the healthy qi could be filled and the pathogen stagnation could be dispelled,in order to provide ideas for the TCM treatment of this disease.

The incidence rate of allergic rhinitis(AR)is high and difficult to cure,which seriously affects the quality of life of patients.The theory of"deficient qi inducing stagnation"is highly consistent with the occurrence and development of this disease.This article believed that the"deficient qi"state of the deficiency of the lungs,spleen and kidney was the fundamental factor of the onset of AR,and the external pathogenic factors,cold,dampness and endogenous phlegm,stasis and turbidity caused by"deficient qi"were the inducing and aggravating factors of AR.It proposed to cultivate the earth to produce gold,gold and water to"replenish the deficient qi",to dispel the wind,to dissipate cold and dampness,to dispel phlegm and dampness,and to reducing stasis and promoting circulation,and to use the two-way regulation of strengthening the healthy qi and dispelling the pathogens,so that the healthy qi could be filled and the pathogen stagnation could be dispelled,in order to provide ideas for the TCM treatment of this disease.

The occurrence and development of laryngopharyngeal reflux(LPR)are closely related to the changes in the qi movement of the spleen,stomach,liver and lungs.The authors believed that"earth stagnation and wood depression"is the key to the onset of LPR.Based on this,the disease could be treated in three stages.In the early stage,the main symptoms are spleen clearing but not rising,difficulty in reducing gastric turbidity and abnormal rise and fall.Treatment should focus on regulating the spleen and stomach,promoting clearing and reducing turbidity,and commonly using modified Liujunzi Decoction;at the beginning of the middle stage,the main symptoms are earth stagnation,stagnation of qi and reflux of the throat.The treatment is suitable for using herbs clearing wood and promoting earth,regulating qi movement,and commonly using Sini Powder combined with modified Banxia Houpo Decoction or Chaihu Shugan Powder;at the end of the middle stage,the main treatment methods are wood stagnation turning into fire,horizontal rebellion invading the earth and upper inflammation punishing the metal.The treatment is suitable for using herbs acid in flavour for dispersing and herbs bitter in flavour foe descending,clearing the liver and stomach,and commonly using modified Banxia Xiexin Decoction and Zuojin Pills;in the later stage,the main symptoms are spleen and stomach deficiency,failure of earth to produce gold and failure of gold to break through without making a sound.The treatment is suitable for using herbs cultivating earth to produce gold,nourishing the throat and benefiting the throat,and commonly using modified Maimendong Decoction or Shenling Baizhu Powder,in order to provide theoretical basis for the treatment of LPR with TCM,broaden the thinking of diagnosis and treatment,and better improve clinical efficacy.

The occurrence and development of laryngopharyngeal reflux(LPR)are closely related to the changes in the qi movement of the spleen,stomach,liver and lungs.The authors believed that"earth stagnation and wood depression"is the key to the onset of LPR.Based on this,the disease could be treated in three stages.In the early stage,the main symptoms are spleen clearing but not rising,difficulty in reducing gastric turbidity and abnormal rise and fall.Treatment should focus on regulating the spleen and stomach,promoting clearing and reducing turbidity,and commonly using modified Liujunzi Decoction;at the beginning of the middle stage,the main symptoms are earth stagnation,stagnation of qi and reflux of the throat.The treatment is suitable for using herbs clearing wood and promoting earth,regulating qi movement,and commonly using Sini Powder combined with modified Banxia Houpo Decoction or Chaihu Shugan Powder;at the end of the middle stage,the main treatment methods are wood stagnation turning into fire,horizontal rebellion invading the earth and upper inflammation punishing the metal.The treatment is suitable for using herbs acid in flavour for dispersing and herbs bitter in flavour foe descending,clearing the liver and stomach,and commonly using modified Banxia Xiexin Decoction and Zuojin Pills;in the later stage,the main symptoms are spleen and stomach deficiency,failure of earth to produce gold and failure of gold to break through without making a sound.The treatment is suitable for using herbs cultivating earth to produce gold,nourishing the throat and benefiting the throat,and commonly using modified Maimendong Decoction or Shenling Baizhu Powder,in order to provide theoretical basis for the treatment of LPR with TCM,broaden the thinking of diagnosis and treatment,and better improve clinical efficacy.

Prostate cancer is one of the most common cancers in adult men. Heat shock proteins (HSPs),as molecular chaperones widely involved in the pathogenesis,diagnosis,treatment and prognosis of various cancers,play crucial biological functions in prostate cancer and it can be considered as valuable biomarkers for cancer therapy, such as prostate-specific membrane antigen. As a member of the heat shock protein family, HSP27 is related to prostate cancer castration resistance,and its expression can promote tumor resistance,invasion and bone metastasis,making prostate cancer more invulnerable to treatments. Therefore,targeting HSP27 in prostate cancer can be perceived as one promising cancer treatment strategy. This article reviews the structure and function of HSP27,and its potential role on castration resistance and targeted therapy in order to provide a new theoretical basis for the clinical treatment of prostate cancer.

Objective:To investigate the effect of recombinant insulin-like growth factor-1 (IGF-1) on ovarian development in MEX3C knockout mice. Methods:Mice were randomly divided into four groups (6 mice in each group): wild type group, homozygous group, homozygous+IGF-1 treatment group, and treatment control group. The weight and wet ovarian weight of mice in each group was compared before and after IGF-1 injection. The serum levels of estradiol was determined using enzyme linked immunosorbent assay (ELISA). The morphological structure of the ovary was observed by HE staining. The expression of MEX3C, IGF-1 receptor (IGF-1R), and the phosphorylation of AKT (Ser473)(p-AKT) were detected by immunohistochemistry and Western blotting.Results:Before IGF-1 injection, the body weight of homozygote group [(6.33±0.31) g] was significantly lighter than that in wild type group [(15.20±0.35) g, P<0.001]. Serum estradiol level was significantly higher in homozygous+IGF-1 treatment group [(17.245 3±0.073 1) ng/L] than in treatment control group [(8.124 8±0.847 7) ng/L, P=0.001]. HE staining results showed that compared with the treatment control group, the primitive follicles (19.83±2.94) and primary follicles (15.50±2.69) were increased in homozygous+IGF-1 treatment group, while the atretic follicles (7.17±1.42) were decreased (all P<0.05). Western blotting results further confirmed that compared with the treatment control group, IGF-1R and p-AKT protein expressions were significantly decreased in homozygous+IGF-1 treatment group ( P=0.014 1, P=0.002 5). Conclusion:IGF-1 promotes ovarian follicular development in MEX3C knockout mice. The mechanism is related to the up-regulation of IGF-1R and P-AKT protein expression. IGF-1 can increase serum estrogen and promote follicular development.

Objective:To investigate the effect of recombinant insulin-like growth factor-1 (IGF-1) on ovarian development in MEX3C knockout mice. Methods:Mice were randomly divided into four groups (6 mice in each group): wild type group, homozygous group, homozygous+IGF-1 treatment group, and treatment control group. The weight and wet ovarian weight of mice in each group was compared before and after IGF-1 injection. The serum levels of estradiol was determined using enzyme linked immunosorbent assay (ELISA). The morphological structure of the ovary was observed by HE staining. The expression of MEX3C, IGF-1 receptor (IGF-1R), and the phosphorylation of AKT (Ser473)(p-AKT) were detected by immunohistochemistry and Western blotting.Results:Before IGF-1 injection, the body weight of homozygote group [(6.33±0.31) g] was significantly lighter than that in wild type group [(15.20±0.35) g, P<0.001]. Serum estradiol level was significantly higher in homozygous+IGF-1 treatment group [(17.245 3±0.073 1) ng/L] than in treatment control group [(8.124 8±0.847 7) ng/L, P=0.001]. HE staining results showed that compared with the treatment control group, the primitive follicles (19.83±2.94) and primary follicles (15.50±2.69) were increased in homozygous+IGF-1 treatment group, while the atretic follicles (7.17±1.42) were decreased (all P<0.05). Western blotting results further confirmed that compared with the treatment control group, IGF-1R and p-AKT protein expressions were significantly decreased in homozygous+IGF-1 treatment group ( P=0.014 1, P=0.002 5). Conclusion:IGF-1 promotes ovarian follicular development in MEX3C knockout mice. The mechanism is related to the up-regulation of IGF-1R and P-AKT protein expression. IGF-1 can increase serum estrogen and promote follicular development.

Objective To observe the clinical effect of treating diabetic nephropathy with Shengqidihuang decoction combined with metformin. Methods 54 cases with diabetic nephropathy were randomly divided into two groups by means of random number table. Both groups were given diabetic routine treatment. The control group was treated with metformin, 0.25 mg each time, three times a day, based on the diabetic routine treatment for 8 weeks, and the treatment group was treated with Shengqidihuang decoction, once a day, 4 weeks as a course, continuously treated for 2 courses based on the control group. 24 h urinary protein (24hUAE) , serum creatinine (SCr) , blood urea nitrogen (BUN) and fasting blood glucose (FBG) were detected before and after the treatment. The clinical effect was observed between the two groups after the treatment. Results The total effective rate of the treatment group and the control group was 85.2% and 66.7% respectively, showing a significant difference (λ2=3.376, P<0.05). Compared with the control group, 24 hUA ,SCr, BUN and FBG in the treatment group decreased significantly (λ2=4.231, P<0.05) after the treatment.24hUAE, SCr, BUN and FBG decreased significantly after the treatment, especially in the treatment group, also showing a significant difference (λ2= 3.754, P<0.05). Conclusion The therapy of mefformin combined with Shengqidihuang decoction on diabetic nephropathy was better than metformin only.

Objective To study a fingerprint of raw material of Rhizoma Polygoni Cuspidati from(various) habitats by RP-HPLC. Methods Kromasil C_(18) column(150 mm?4.6 mm,5 ?m) was used,with mixtures of acetonitrile and water as mobile phase in a gradient mode.The flow rate was 1 mL/min and wavelength was 303 nm.Results According to the optimum chromatographic conditions,a good fingerprint of Rhizoma Polygoni Cuspidati has been described.Conclusion The method is simple and accurate with good reproducibility.It may be practical value for the quality control of sample for Rhizoma Polygoni Cuspidati from various habitats.

AIM: To investigate the changes of oxidative stress in the kidneys and their roles in nephropathy in diabetic rats. METHODS: Diabetic rats were induced by streptozotocin (STZ). 36 rats were divided into three groups randomly: (1) NC group, normal control rats; (2) DM group, diabetic rats received protamine zinc insulin (PZI) 2U-4U/2 d; (3) DT group, diabetic rats received PZI 9-12 U/kg body weigh/day. 12 weeks later, rats were killed, blood glucose, blood cholesterol, serum creatinine, blood urea nitrogen, HbA1c, urinary creatinine, and urinary protein for 24 h were measured. The activities of antioxidant enzymes in renal cortex, including total superoxide dismutase (TSOD), Cu-Zn superoxide dismutase (Cu-Zn SOD), Mn superoxide dismutase (Mn SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and maleic dialdehyde (MDA) were measured by chromatometry. RT-PCR was performed to detect the expression of different antioxidant enzymes mRNA. RESULTS: For all the targets we measured, there was no significant difference between NC and DT groups. Compared with the other two groups, the levels of blood glucose, cholesterol, trigalloyl glycerol, HbA1c in DM group increased significantly. The activities of TSOD, Cu-Zn SOD and CAT decreased significantly. The activity of GSH-Px increased significantly. There was no significant difference among the activities of Mn SOD in all three groups. The level of MDA in DM group was much higher than that in NC or DT group. The relative expression levels of GSH-Px and Cu-Zn SOD mRNA in DM group were higher than those in other two groups, while the relative expression level of CAT decreased. Mn SOD mRNA was expressed without significant difference in all groups. Compared with NC or DT group, urinary protein in DM group increased significantly, while creatinine clearance rate decreased. CONCLUSIONS: Hyperglycemia affected the expression of antioxidant enzymes. Oxidative stress was caused by hyperglycemia in diabetic rats and may be an important factor in the etiology of diabetic nephropathy.