Yiwei Xiaoyu granules for treatment of chronic atrophic gastritis with deficiency syndrome of the spleen and stomach.

BACKGROUND: The Correa sequence, initiated by Helicobacter pylori (H. pylori), commonly progresses to gastric cancer through the stage of chronic atrophic gastritis (CAG). Although eradication of H. pylori only reduces the risk of gastric cancer, it does not eliminate the risk for neoplastic progression. Yiwei Xiaoyu granules (YWXY) are a commonly used composite preparation in Chinese clinics. However, the pursuit of excellence in clinical trials and the establishment of standardized animal experiments are still needed to contribute to full understanding and application of traditional Chinese medicine in the treatment of CAG. AIM: To demonstrate the effectiveness of YWXY in patients with CAG and spleen-stomach deficiency syndrome (DSSS), by alleviating histological scores, improving response rates for pathological lesions, and achieving clinical efficacy in relieving DSSS symptoms. METHODS: We designed a double-blind, randomized, controlled trial. The study enrolled seventy-two H. pylori-negative patients (mean age, 52.3 years; 38 men) who were randomly allocated to either the treatment group or control group in a 1:1 ratio, and treated with 15 g YWXY or 0.36 g Weifuchun (WFC) tablet combined with the respective dummy for 24 wk. The pre-randomization phase resulted in the exclusion of 72 patients: 50 participants did not meet the inclusion criteria, 12 participants declined to participate, and 10 participants were excluded for various other reasons. Seven visits were conducted during the study, and histopathological examination with target endoscopic biopsy of narrow-band imaging was requested before the first and seventh visits. We also evaluated endoscopic performance scores, total symptom scores, serum pepsinogen and gastrin-17. RESULTS: Six patients did not complete the trial procedures. Treatment with YWXY improved the Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) stage, compared with WFC (P < 0.05). YWXY provided better relief from symptoms of DSSS and better improvement in serum gastric function, compared with WFC (P < 0.05). CONCLUSION: YWXY compared with WFC significantly reduced the risk of mild or moderate atrophic disease, according to OLGIM stage, significantly relieved symptoms of DSSS, and improved serum gastric function.

[Risk factors of melamine-contaminated milk powder related urolithiasis: a multicenter nested case-control study].

OBJECTIVE: To further confirm and clarify the risk factors of melamine associated urolithiasis. METHODS: Case control research was performed in 6 centers from 5 provinces/cities in China. Children less than 36 months old were screened for urolithiasis and recruited in the study. The children with urolithiasis were included as cases and those without urolithiasis as controls. The children with congenital abnormality of urinary tract were excluded. According to the case:control ratios of 1:1, we sampled the controls from healthy children screened randomly. Due to the complete missing data on factors of vomiting/diarrhea/fever in control group of Center 4, we analyzed the data from 6 centers and 5 centers respectively. The possible influencing factors for urolithiasis including melamine concentration, birth type, age, feeding style and history of vomiting or diarrhea or fever were analyzed by Logistic analysis. RESULTS: There were 1 329 cases and 1 317 controls with a mean age of 18.4 months. The analysis of data from 6 centers showed the children fed with high melamine formula were 6.26 times more likely to have stones (P<0.01) than those with non melamine formula. Preterm infants were 2.03 times (P<0.01) more likely to have urolithiasis than term infants. The children aged less than 0.5 year, 0.5 to 1 year, 1 to 2 year, 2 to 2.4 year were 2.78 (P<0.01), 2.61 (P<0.01), 2.09 (P<0.01), 1.57 (P<0.01), 1.44 (P<0.05) times more likely to have stones than those more than 2.5 year. Boys were 1.19 times more likely to have stones than girls. Children fed with formula alone were 1.94 times (P<0.01) more likely to have stones than those with formula and breast milk. The analysis of data from 5 centers showed that children fed with high melamine formula were 4.38 times (P<0.01) more likely to have stones compared with those with non melamine formula. Children aged less than 1 year and 1 to 1.9 year were 2.24 (P<0.01) and 1.31 (P<0.05) times more likely to have stones than those more than 2 year. The children fed with formula alone were 1.67 times (P<0.01) more likely to have stones compared to those with formula and breast milk. The children with any two symptoms of vomiting, diarrhea and fever were 15.21 times (P<0.05) more likely to have urolithiasis. The multiple logistic regression model confirmed that above risk factors were independent risk factors for urolithiasis. CONCLUSION: We confirm that the children fed with high melamine infant formula, preterm infant, boy, children fed with formula alone, and the children with symptoms of vomiting or diarrhea or fever are more likely to have urolithiasis. We also found the risk for urolithiasis decreased with age.

[Establishment of a podocyte cell injury model induced by puromycin aminonucleoside].

OBJECTIVE: To establish a podocyte cell injury model induced by puromycin aminonucleoside (PAN), an in vitro model for studying the role of podocytes, especial the slit diaphragm molecules in proteinuria at the cellular and molecular levels. METHODS: MPC5 were treated for 24 and 48 hours by 15, 45 and 75 mg/L PAN, respectively. The podocyte molecular behavior during podocyte injury was evaluated: the apoptotic podocyte cells were revealed with FITC-Annexin V and Propidium Iodide (PI) assay and the proliferative podocyte cells detected with MTT assay after PAN treatment. The distribution of Nephrin and Podocin was revealed with indirect-immunofluorescent staining under confocal microscope. The distribution of F-actin was revealed with direct-immunofluorescent staining under microscope. RESULTS: The percentage of apoptotic podocyte cells was increased in a dose- and time-dependent manner after PAN treatment. In PAN-treated group, the apoptosis was obviously increased at hour 48, the PAN-45 treated group was 33.48% +/- 14.55% and PAN-75 treated group 38.01% +/- 12.13% vs the control group 6.38% +/- 0.50% (P<0.01). CONCLUSION: We set up an in vitro podocyte injury model treated with PAN for the first time. This reliable cell model is a good basis for further studies on podocyte injury.

[Clinical characteristics and WT1 genetic analysis of patients with steroid-resistant nephrotic syndrome accompanied with genitourinary malformations].

OBJECTIVE: To analyze the clinical features and WT1 gene mutations in patients with steroid-resistant nephrotic syndrome (SRNS) accompanied with genitourinary malformations. The expression of podocyte molecules was also investigated in renal specimen of these WT1 mutated patients. METHODS: From January 2005 to May 2007, 3 cases of SRNS accompanied with genitourinary malformations were involved in this study. The expression of podocyte molecules (nephrin, podocin, alpha-actinin 4, WT1 and CD2AP) in 2 cases was analyzed by immunofluorescence and immunohistochemistry; using PCR to amplify genomic DNA and RT-PCR to amplify WT1 cDNA. GeneScan and GeneScan software were used to quantify the ratio of +KTS/-KTS isoforms. RESULTS: The age of onset of the 3 cases were 6 months, 1 year and 10 years, respectively. The age at diagnosis was 7 months, 9 years and 15 years, respectively. The phenotype of case 1 and case 3 was male accompanied with genitourinary malformations. Case 2 was phenotypic female. Karyotype analysis of the 3 cases revealed 46, XY. Each case was diagnosed as SRNS. Focal segmental glomerulosclerosis (FSGS) was confirmed in 2 cases. Podocyte molecular expression altered in renal tissues of 2 cases. WT1 staining was negative in case 1. WT1 expression in case 2 showed a diffuse nuclear staining with less obvious speckles compared with controls. WT1 IVS 9 + 5 G > A mutation was detected in case 2 and WT1 exon 9 1186 G > A mutation was detected in case 3. No WT1 mutation was detected in case 1. CONCLUSIONS: Karyotype analysis and WT1 genetic analyzing should be performed for all female patients with early onset SRNS and in male patients with SRNS accompanied with genitourinary malformations. The abnormal ratio of +KTS/-KTS isoforms caused by WT1 mutations along with abnormal expression of podocyte molecules were involved in the pathogenesis of proteinuria.

Clinical characteristics and WT1 genetic analysis of patients with steroid resistant nephrotic syndrome accompanied with genitourinary malformations.

OBJECTIVE: To understand WT1 mutations in patients with steroid resistant nephrotic syndrome (SRNS) accompanied with genitourinary malformations. METHODS: Three cases of SRNS accompanied with genitourinary malformations were enrolled. The expression of podocyte molecules (nephrin, podocin, alpha-actinin-4, WT1, and CD2AP) in 2 cases was analyzed with the immunofluorescence and immunohistochemistry techniques. The genomic DNA and cDNA of WT1 were analyzed by using PCR and RT-PCR, respectively. GeneScan and GeneScan software were used to quantify the ratio of +KTS/-KTS isoforms. RESULTS: The onset ages of 3 cases were 6 months, 1 year, and 10 years old, respectively. The diagnosis age was 7 months, 9 years, and 15 years old, respectively. The phenotype of Case 1 and Case 3 was male accompanied with genitourinary malformations. Case 2 was phenotypic female. Karyotype analysis of 3 cases revealed 46, XY. Three cases were diagnosed as SRNS. Focal segmental glomerulosclerosis (FSGS) was confirmed in 2 cases. Podocyte molecular expression altered in renal tissues of 2 cases. In addition, WT1 staining was negative in Case 1. WT1 expression in Case 2 showed diffuse nuclear staining with less obvious speckles compared with controls. WT1 IVS 9 +5 G>A mutation was detected in Case 2 and WT1 Exon 9 1186 G>A mutation was detected in Case 3. No WT1 mutation was detected in Case 1. CONCLUSION: Karyotype analysis and WT1 genetic testing should be done in all female patients with early onset steroid resistant FSGS and in male patients with SRNS accompanied with genitourinary malformations. Abnormal podocyte molecular expression suggests that more podocyte molecules might be involved in the pathogenesis of proteinuria in WT1 mutational patients.