Surgical treatment for prostatic utricle cyst in children: A single-center report of 15 patients.

OBJECTIVES: To report our single-center experience of the management of children with prostatic utricle cysts. METHODS: We retrospectively analyzed 15 children who were incidentally found to have a prostatic utricle cyst and were admitted to our department between October 2013 and August 2020. Clinical characteristics and management were collected and catalogued. RESULTS: Recurrent genitourinary tract infections were the most frequent complaint, and two-thirds of patients also had hypospadias. A connection between the posterior urethra and the prostatic utricle cyst was found in all cases. Two patients directly had their progressively enlarging prostatic utricle cyst resected laparoscopically. Endoscopic techniques were used in 13 patients, two of whom underwent laparoscopic excision for repeated symptoms. The mean (range) follow-up period was 34.9 (2-82) months. No recurrences were observed in four patients who underwent prostatic utricle cyst excision and eight patients who received endoscopic treatment. Three patients had recurrent symptoms after endoscopic treatment and were managed by nonsurgical treatment. CONCLUSIONS: Prostatic utricle cyst is a rare disease which can cause recurrent genitourinary tract infections. Extra attention should be paid to evaluation for prostatic utricle cyst in children with external genital anomalies. Retrograde urethrogram and magnetic resonance imaging are useful tools with which to distinguish prostatic utricle cyst from other cystic lesions that are located in the midline pelvis in male patients. Individualized treatment is appropriate when considering fertility preservation, recurrences and malignancy. Laparoscopic excision is feasible for symptomatic and large prostatic utricle cyst. Regular long-term monitoring is recommended for all patients with prostatic utricle cyst.

CELF1/p53 axis: a sustained antiproliferative signal leading to villus atrophy under total parenteral nutrition.

Intestinal villus atrophy is a major complication of total parenteral nutrition (TPN). Our previous study revealed that TPN-induced villus atrophy is accompanied by elevated expression of CUGBP, Elav-like family member 1 (CELF1); however, its mechanism of action has not been fully understood. Herein, we report a pivotal role of CELF1/p53 axis, which induces a sustained antiproliferative signal, leading to suppressed proliferation of intestinal epithelial cells (IECs). By using a rat model of TPN, we found synchronous upregulation of CELF1 and p53 in jejunum mucosa, accompanied by a 51% decrease in crypt cell proliferation rate. By using HCT-116 cells as an IEC model in vitro, we found that the expression of CELF1 altered dynamically in parallel to proliferation rate, suggesting a self-adaptive expression pattern in IECs in vitro. Furthermore, ectopic overexpression of CELF1 elicited a significant antiproliferative effect in HCT-116, Caco-2, and IEC-6 cells, whereas knockdown of CELF1 elicited a significant proproliferative effect. Moreover, cell-cycle assay revealed that ectopic overexpression of CELF1 induced sustained G2 arrest and G1 arrest in HCT-116 and IEC-6 cells, respectively, which could be abolished by p53 silencing. Mechanistically, polysomal profiling and nascent protein analysis revealed that regulation of p53 by CELF1 was mediated through accelerating its protein translation in polysomes. Taken together, our findings revealed a sustained suppression of IEC proliferation evoked by CELF1/p53 axis, which may be a potential therapeutic target for the treatment of TPN-induced villus atrophy.-Yan, J.-K., Zhang, T., Dai, L.-N., Gu, B.-L., Zhu, J., Yan, W.-H., Cai, W., Wang, Y. CELF1/p53 axis: a sustained antiproliferative signal leading to villus atrophy under total parenteral nutrition.

Butyrate stimulates the growth of human intestinal smooth muscle cells by activation of yes-associated protein.

Intestinal smooth muscle cells play a critical role in the remodeling of intestinal structure and functional adaptation after bowel resection. Recent studies have shown that supplementation of butyrate (Bu) contributes to the compensatory expansion of a muscular layer of the residual intestine in a rodent model of short-bowel syndrome (SBS). However, the underlying mechanism remains elusive. In this study, we found that the growth of human intestinal smooth muscle cells (HISMCs) was significantly stimulated by Bu via activation of Yes-Associated Protein (YAP). Incubation with 0.5 mM Bu induced a distinct proliferative effect on HISMCs, as indicated by the promotion of cell cycle progression and increased DNA replication. Notably, YAP silencing by RNA interference or its specific inhibitor significantly abolished the proliferative effect of Bu on HISMCs. Furthermore, Bu induced YAP expression and enhanced the translocation of YAP from the cytoplasm to the nucleus, which led to changes in the expression of mitogenesis genes, including TEAD1, TEAD4, CTGF, and Cyr61. These results provide evidence that Bu stimulates the growth of human intestinal muscle cells by activation of YAP, which may be a potential treatment for improving intestinal adaptation.

Changes in the intestinal expression of drug metabolism-related genes in a piglet model of parenteral nutrition.

BACKGROUND: Parenteral nutrition (PN) may serve as a nutritional supportive therapy accompanied by oral medication, but the effect of PN on intestinal expression of drug metabolism-related genes remains unknown. METHODS: Twelve Bama piglets receiving PN for 14 days were used as in vivo model. Changes in intestinal drug metabolism-related genes were examined by proteomic analysis. Serum levels of fibroblast growth factor 19 (FGF19) were determined by ELISA, and the effect of FGF19 on the expression of drug metabolism-related genes was examined using murine ileum organoids. RESULTS: A total of 1063 differentially expressed proteins were identified in PN group. Of note, two drug transporters (Abcb1 and Abcc2) were significantly decreased in PN group, along with two glutathione-related drug-metabolizing enzymes, glutathione peroxidase (Gpx2) and glutathione S-transferase (Gsta1). Serum FGF19 levels were dramatically reduced in PN group. Treatment with recombinant FGF19 in vitro dose-dependently up-regulated the expression of Abcb1, Abcc2, Gpx2 and Gsta1 in organoids. CONCLUSION: Our data indicated that intestinal drug metabolism-related genes were significantly dysregulated under PN, and some of the changed genes were attributed to gut-derived FGF19.

Three-dimensional digital measurement of the facet joint in normal individual and lumbar intervertebral disc herniation patients aged 13 - 18 years.

BACKGROUND: Lumbar facet joint is an important element of spinal "three-joint complex". Whether there is a relationship between strange structure of facet joint and adolescent lumbar disc herniation (ALDH) is nonetheless controversial, and the current research is mainly centered on adults. OBJECTIVE: To find out the normal lumbar facet joints between 13 and 18 years old to provide anatomical basis for early diagnosis and therapy of lumbar disc herniation. METHODS: CT imaging information of 32 sufferers with lumbar disc herniation aged from 13 to 18 years old in Inner Mongolia have been collected as the ALDH group, and 62 wholesome subjects in the equal period had been chosen as the normal group. Uncooked records of continuous scanning lumbar tomography pix were imported into MIMICS 21.0 for evaluation and size in DICOM format. The parameters include facet joint height, facet joint width, et al. RESULTS: 1. The left and right transverse angle of L5S1 segment in the ALDH group were (52.41 ± 9.2) ° and (55.99 ± 10.91) ° (P < 0.05), and the differences were statistically significant. The right side is larger than the left side. 2. Facet joint thickness in L3-L5 segment of the normal group was significantly higher than that of male (1.63 ± 0.32) mm than that of female (1.38 ± 0.25) mm; In 16-18 years old group, comparison of facet joint cross-sectional area was statistically significant (22.1 ± 3.04) mm2 in male than (18.92 ± 3.71) mm2 in female. 3. In comparison between normal and ALDH group, there was significant difference in L3-4 transverse angle (P < 0.05), L4-5 facet joint height and facet joint thickness (P < 0.05), L5S1 facet joint thickness and transverse angle (P < 0.05). CONCLUSION: When ALDH occurs in the L5S1 segment, there is a substantial difference between the left and right sides of the transverse angle, and there is a difference in the thickness and the facet joint cross-sectional area between males and females, which is generally larger in males than in females. Facet joint height is larger, transverse angle of left and right is asymmetric, inferior articular process is larger, and facet joint thickness is smaller can indicate that lumbar disc herniation is effortless to occur.

[Preparation and identification of a monoclonal antibody against human PD-L1].

OBJECTIVE: To prepare mouse anti-human PD-L1 monoclonal antibodies (mAbs) and identify their biological characteristics. METHODS: BALB/c mice were immunized with recombinant GST-PDL1 protein,and the strain of hybridoma cell secreting anti-PD-L1 mAb was obtained. The specificity of anti-PD-L1 mAb was checked and evaluated with ELISA and Western blot. Its titer, immunoglobulin subtype were also measured. The combining capacity of anti-PD-L1 mAb with PD-L1 on MDA-MB-231 cells, which had been induced with IFN-gamma for 72 hours, was identified through immunohistochemistry and flow cytometry. The peripheral blood mononuclear cell was labeled with CFSE, and the effect of anti-PD-L1 mAb on the activation and proliferation of the lymphocyte induced with antigens was evaluated by flow cytometry analysis. RESULTS: A strain of hybridoma cell secreting anti-PD-L1 mAb was successfully obtained and identified belong to IgG1 subtype. Its titers in cultural supernatant and ascetic fluid were 1:6400 and 1:102400, respectively, by ELISA. The purified mAbs showed good affinity and specificity against GST-PDL1 protein in Western blot, also could block the PD-1/PD-L1 pathway and promote the proliferation of lymphocyte induced with antigens. CONCLUSION: Hyperactivity mouse anti-human PD-L1 hybridoma cell lines and their secreted monoclonal antibodies have been successfully obtained and identified.

[Effects of different feeding patterns on body weight of perinatal women in rural area].

OBJECTIVE: To study the relations between different feeding patterns and the body weight retention of the perinatal women living in rural areas of China. METHODS: A cluster sampling method was used to investigate 409 women, who are currently living in rural areas of Tianjin, at pregnant and perinatal status. While, their body weights and heights before pregnancy, antepartum and postpartum were measured, respectively. Body weight retention was the difference of the measured data after postpartum minus pre-pregnant weight. Variance analysis was used for statistic comparison. RESULTS: The rate of exclusive breastfeeding was 70.9% (290/409) within four months. The net body weight retention of women (5.8 kg) using the exclusive breastfeeding was lower than that of the women (7.0 kg) using artificial feeding within 4 - 6 months, but there was no significantly statistic difference (F = 1.45, P = 0.236). However, there was the opposite result within 7 - 9 months, the data showed that the body weight retention in the women using the exclusive breastfeeding was 4.9 kg, which was significantly higher than that the women (2.9 kg) with artificial feeding (F = 3.17, P = 0.043). The food consumption of the women (901 g) using exclusive breastfeeding was the highest, followed by those (877 g) using mixed feeding and the women (750 g) using artificial feeding. CONCLUSION: The body weight retention after postpartum should be related to infant feeding patterns. After postpartum, the weight loss of women using the exclusive breastfeeding is relatively low. While, for the women using the exclusive breastfeeding, the net weight retention during pregnancy and after postpartum were lower than those with artificial feeding. Therefore, it is necessary to enhance health education and guidance on promoting exclusive breast-feeding as well as increasing awareness on pre-pregnant health.

Butyrate promotes the adaptation of intestinal smooth muscle cells through the yes-associated protein (YAP) pathway in a rat model of short bowel syndrome.

Our previous study demonstrated that the proliferation of human intestinal smooth muscle (ISM) cells was stimulated by butyrate through the yes-associated protein (YAP) pathway in vitro, suggesting a valuable approach for intestinal adaption of short bowel syndrome (SBS). This study was conducted to confirm these findings in vivo. Three-week-old Sprague-Dawley rats were randomly divided into the following groups: Sham group (bowel transection and reanastomosis), SB W group (80% small bowel resection/water ad libitum), and SB Bu group (80% small bowel resection/50 mM sodium butyrate ad libitum). Morphological changes were determined by hematoxylin and eosin staining; the proliferation rate of ISM cells was examined by Ki67 staining, and apoptosis was determined in the TUNEL assay. Changes in the expression of YAP and its downstream genes were evaluated by quantitative-polymerase chain reaction and western blotting. Fourteen days post-operation, a significant increase in ISM thickness was observed in the SB Bu group compared to the SB W group, accompanied by enhanced proliferation of ISM cells and suppression of apoptosis. Notably, YAP expression was also significantly increased in the SB Bu group, with a 6.5-fold increase in the proportion of YAP-positive ISM cells, 2.2-fold increase in YAP mRNA expression, and 3.4-fold increase in protein expression. In conclusion, our results suggest that butyrate promotes ISM adaption through YAP in vivo, which may be a potential therapeutic approach for SBS patients.

Hereditary pancreatitis of 3 Chinese children: Case report and literature review.

BACKGROUND: Hereditary pancreatitis (HP) is quite rare and is distinguished by incomplete penetrance presentation as early-onset relapsing pancreatitis, usually beginning in childhood. HP is now known to be commonly relevant to mutations in the PRSS1 (gene-encoding cationic trypsinogen), SPINK1 (serine protease inhibitor, Kazal type 1), CFTR (cystic fibrosis), carboxypeptidase A1 (CPA1), and chymotrypsin C (CTRC) genes as reported in some Caucasian studies. HP has a variable spectrum of severity and may develop complications. METHODS & RESULTS: We describe the clinical course of 3 preschool children, hospitalized with postprandial abdominal pain, whose laboratory tests showed high serum amylase. Similar episodes of abdominal pain led to readmission, and the patients recovered quickly after using symptomatic therapy. The condition of the first boy, who developed a pancreatic tail pseudocyst and splenic infarction, was especially complicated. The boy underwent 2 endoscopic retrograde cholangiopancreatographies and stenting, along with a surgical procedure that completely relieved his symptoms for 3 months. The 3 patients and their parents were given genetic testing. All of the patients carried 1 or more gene mutations inherited from their mothers, fathers, or both parents; however, none of the parents were affected. CONCLUSION: For children with repeated pancreatitis, clinicians should consider HP in the differential diagnosis. It is reliable to perform gene sequencing on suspicious patients and their parents. Multidisciplinary and comprehensive treatment should be recommended to manage HP and its complications. Cholangiopancreatography and stenting is a relatively minimally invasive approach when compared with surgery and can be tried as an early intervention. Surgical procedures should be reserved for patients with complications.

3D nanostructured Ni(OH)2 microspheres as an efficient immobilization matrix of Ru(bpy)3(2+) for high-performance electrochemiluminescence sensor.

The electrochemistry and electrochemiluminescence (ECL) of novel three-dimensional nanostructured Ru(bpy)(3)(2+)/Ni(OH)(2) microspheres were investigated for the first time. The negatively charged porous Ni(OH)(2) microspheres composed of Ni(OH)(2) nanowires were specifically designed to interact with Ru(bpy)(3)(2+). The large surface area and porous structure of Ni(OH)(2) microspheres enhance loading of Ru(bpy)(3)(2+) and mass transport of the model analyte, tripropylamine (TPA). Excellent ECL performance of the presented sensor was achieved including good stability and wide linear range from 7.7x10(-10) to 3.8x10(-3)M with the detection limit of 2.6x10(-10)M to TPA.

[The effect of ginkgolic acids on multidrug resistance in oral squamous cell carcinoma].

OBJECTIVE: Carboplatin (CBP)-resistant cell line (Tca8113/CBP) and pingyangmycin (PYM)-resistant cell line (Tca8113/PYM) were established in vitro. Ginkgolic acids' influence over multidrug resistance (MDR) of drug-resistant cells was discussed by ginkgolic acids coupled with chemotherapy drugs. METHODS: The expression of P-glycoprotein (P-gp) was detected by immunohistochemistry. MTT assay was applied to ascertain the resistance index of drug-resistant cells. The effect of different concentrations of ginkgolic acids on the proliferation of drug-resistant cells and parental cell was measured by MTT assay. Making sure the non-toxic concentration of ginkgolic acids and observing the reversal effect of ginkgolic acids on drug-resistant cells. Resistance index was redetermined by MTT assay after ginkgolic acids coupled with chemotherapy drugs induced the cell lines for some time. RESULTS: Immunohistochemistry showed that P-gp positive expression rate of drug-resistant cells was significantly higher than parental cells. The non-toxic concentration of ginkgolic acids which was determined by MTT assay was 10 microg x mL(-1). The reversal folds of Tca8113/CBP cell line to CBP and Tca8113/PYM cell line to PYM were 2.94 and 2.43 respectively. Before coupled with ginkgolic acids, the resistance indices of Tca8113/CBP and Tca8113/PYM cell lines were 3.24 and 11.9 respectively. When ginkgolic acids was added with chemotherapy drugs for some time, the resistance indices of Tca8113/CBP and Tca8113/PYM cell lines were 2.18 and 4.43 respectively. CONCLUSION: This experiment successfully induced the drug-resistant cell lines of Tca8113/CBP and Tca8113/PYM. The method of chemotherapy drugs coupled with ginkgolic acids further confirmed the effect on proliferation of Tca8113/CBP and Tca8113/PYM cell lines was reducing. Non-toxic concentration of ginkgolic acids can partially reverse the drug resistance of Tca8113/ CBP and Tca8113/PYM cell lines. Furthermore, MDR level of drug-resistant cells decreased somewhat when they were induced by ginkgolic acids coupled with chemotherapy drugs for some time.