Endoscopic retrograde cholangiopancreatography for diagnosing and treating pediatric biliary and pancreatic diseases.

BACKGROUND: This study evaluated the safety and effectiveness of endoscopic retrograde cholangiopancreatography (ERCP) in pediatric patients with biliary and pancreatic diseases. A retrospective analysis was conducted on 57 ERCP procedures performed in 41 children, primarily for treating pancreatic diseases. The overall success rate was 91.2%, with no major complications observed. Post-ERCP pancreatitis (PEP) occurred in 8.8% of cases. Follow-up examinations over one year showed no recurrence of biliary or pancreatic diseases. Notably, endoscopic treatment led to a significant increase in body mass index (BMI). These findings demonstrate the valuable role of ERCP in managing such conditions. AIM: To evaluate the safety and efficacy of ERCP for the management of biliary and pancreatic diseases in pediatric patients. METHODS: We conducted a retrospective analysis of data from children aged 1-18 years who underwent ERCP for biliary and pancreatic diseases at Beijing Children's Hospital between January 2021 and December 2022. The collected data included procedure time, endoscopic treatment, success rate, and postoperative complications. RESULTS: Forty-one children underwent 57 ERCP procedures, including 14 with biliary duct disease and 27 with pancreatic disease. The mean age of the patients was 7.48 ± 3.48 years. Biliary duct-related treatments were performed 18 times, and pancreatic disease treatments were performed 39 times. ERCP was primarily used to treat pediatric pancreatic diseases [68.4% (39/57) of the procedures]. The overall success rate was 91.2% (52/57 patients). PEP was noted in five patients (8.8%, 5/57), and no instances of bleeding, perforation, or cholangitis were observed. The patients were followed up for over one year, and no recurrence of biliary or pancreatic diseases was detected. Importantly, BMI significantly increased after endoscopic treatment compared to that before treatment (P = 0.001). CONCLUSION: The high success rate and lack of major complications support the valuable role of ERCP in the management of pediatric biliary and pancreatic diseases in the pediatric population.

Liquid nitrogen frozen cells for chemotherapy drug delivery and vaccination of melanoma.

PURPOSE: Cancer vaccine (CV) has thrived as a promising tool for cancer prevention and treatment. However, how to maintain the integrity and diversity of individualized vaccine antigens and activate the adaptive immune system is still challenging. METHODS: Herein, a preventive and therapeutic vaccine platform for in situ effective multi-model synergistic therapy is developed. In our study, we process B16F10 cells by liquid nitrogen frozen (LNF) to obtain LNF cells, the characterization of LNF cells were conducted. Moreover,  the anti-tumor effect and immune activation ability were studied, and the role as a CV were investigated. RESULTS: The LNF cells preserve intact cellular structure and tumor-associated self-antigen gp100. Moreover, LNF cells have the ability of loading and releasing doxorubicin (DOX). Except for the anti-tumor effect of chemotherapy brought by DOX, the LNF cells can promote the maturation of dendritic cells (DCs) and induce immune response by activating CD4+ and CD8+ T cells, particularly with the existence of adjuvant, R848. Specifically, the CD8+ T cells of mice in LNF-DOX/R848 group are 6 times of that in PBS group in tumor microenvironment, and twice in spleen. Therefore, LNF cells can also be utilized as a CV. Vaccination with LNF/R848 cells effectively suppress the tumor growth in mice by fivefold as compared to the control group. CONCLUSION: In this work, we obtain the LNF cells with a simple procedure. The LNF cells not only provides a tumor cells-based multi-modal system for cancer therapy but inspires new insights into future development of individualized CVs strategies. This study processes live B16F10 cells by liquid nitrogen frozen to obtain LNF cells, which preserve cell integrity and homologous targeting ability. The LNF cells can load and deliver drug and can serve as tumor vaccine. Results demonstrated the LNF cells have effective prophylactic ability, and ideal anti-tumor ability with the loaded drug and adjuvant.

Prognostic significance of age on superficial spreading melanoma after resection: lessons from SEER database involving 12 536 patients.

BACKGROUND: This study sought to analyse the impact of elderly age on long-term prognosis of superficial spreading melanoma (SSM) after surgery. METHODS: A population-based cohort of patients undergoing resection for SSM from 2004 to 2015 was collected, using data from National Cancer Institute' Surveillance, Epidemiology, and End Results (SEER)* Stat software. Patients were divided into the non-elderly group (≤70 years) and elderly group (>70 years). Baseline characteristics and long-term survivals were compared between the two groups. A 1:1 propensity score matching (PSM) was used to reduce the risk of bias. The impact of the elderly age on overall survival (OS) and cause-specific mortality (CSM) was estimated by Cox-regression and competing-risk regression models. RESULTS: Among 12 536 patients with SSM after resection included into the cohort, 8664 patients were ≤70 years, and 3872 were >70 years. Patients in the elderly group had higher incidences of multiple tumours, worse tumour stage and infiltration degree, lymphatic metastasis, and larger size of primary lesions. Using PSM, 3581 pairs of patients were created. On matched analysis, the elderly group was associated with worse OS and CSM. On multivariable Cox-regression and competing-risk regression analyses, elderly age was identified as an independent risk factor of OS and CSM after adjusting for other prognostic variables. CONCLUSIONS: The elderly age of patients was independently associated with worse OS and CSM after resection of SSM when baseline and tumour characteristics were balanced. Adjuvant therapy and individualized strategy on follow-up should be made for elderly patients after resection of SSM.

Sintilimab-Induced Diabetic Ketoacidosis in a Patient with Radiation and Multichemorefractory Penile Cancer: A Case Report and Literature Review.

Penile squamous cell carcinoma (PSCC) is a rare disease. The treatment options for advanced penile cancer are often limited, and the prognosis remains poor. We reported a 52-year-old male recurrent and metastatic PSCC patient with high PD-L1 expression (90%) and TMB (14.4 muts/Mb). He had undergone penectomy, bilateral inguinal lymph node dissection, and excision of the abdominal wall mass. Despite cisplatin-based concurrent chemoradiotherapy and sequential chemotherapy with docetaxel plus cisplatin then being carried out, the carcinoma still progressed. The patient then obtained progression-free survival with continuous sintilimab, although he experienced the new onset of ICI-induced diabetes after 24 cycles of sintilimab and required sustained insulin treatment. He had negative type 1 diabetes-associated autoantibodies and the susceptible HLA genotype DR3-DQ2 haplotype. This is the first patient with radiation and multichemorefractory PSCC who has obtained the remarkable anti-tumor effect of partial regression exceeding 32 months during continuous sintilimab and anlotinib treatment.

Two-step artificial intelligence system for endoscopic gastric biopsy improves the diagnostic accuracy of pathologists.

Background: Endoscopic biopsy is the pivotal procedure for the diagnosis of gastric cancer. In this study, we applied whole-slide images (WSIs) of endoscopic gastric biopsy specimens to develop an endoscopic gastric biopsy assistant system (EGBAS). Methods: The EGBAS was trained using 2373 WSIs expertly annotated and internally validated on 245 WSIs. A large-scale, multicenter test dataset of 2003 WSIs was used to externally evaluate EGBAS. Eight pathologists were compared with the EGBAS using a man-machine comparison test dataset. The fully manual performance of the pathologists was also compared with semi-manual performance using EGBAS assistance. Results: The average area under the curve of the EGBAS was 0·979 (0·958-0·990). For the diagnosis of all four categories, the overall accuracy of EGBAS was 86·95%, which was significantly higher than pathologists (P< 0·05). The EGBAS achieved a higher κ score (0·880, very good κ) than junior and senior pathologists (0·641 ± 0·088 and 0·729 ± 0·056). With EGBAS assistance, the overall accuracy (four-tier classification) of the pathologists increased from 66·49 ± 7·73% to 73·83 ± 5·73% (P< 0·05). The length of time for pathologists to manually complete the dataset was 461·44 ± 117·96 minutes; this time was reduced to 305·71 ± 82·43 minutes with EGBAS assistance (P = 0·00). Conclusions: The EGBAS is a promising system for improving the diagnosis ability and reducing the workload of pathologists.

Adipose-Derived Stem Cells Exosomes Improve Fat Graft Survival by Promoting Prolipogenetic Abilities through Wnt/ß-Catenin Pathway.

Autologous fat grafting has been widely used in plastic surgery in recent years, but the unstable retention of fat graft has always been a key clinical problem. Adipose tissue has poor tolerant to ischemia, so the transplanted adipose tissue needs to rebuild blood supply at an early stage in order to survive stably. Our previous study has found that comparing to human foreskin fibroblast exosome (HFF-Exo), human adipose-derived stem cells exosome (hADSC-Exo) can significantly improve the proliferation of vascular endothelial cells and the angiogenic effect of artificial dermal preconstructed flaps. Therefore, the ability of hADSC-Exo to improve the retention of adipose grafts and its potential regenerative mechanism aroused our strong interest. In this study, we applied hADSC-Exo and HFF-Exo to adipose grafts and explored the potential regeneration mechanism through various means such as bioinformatics, immunofluorescence, immunohistochemistry, and adipogenic differentiation. The results showed that hADSC-Exo can significantly promote grafts angiogenesis and adipogenic differentiation of ADSC to improve the retention of fat grafts and may downregulate the Wnt/ß-catenin signaling pathway to promote the adipogenic differentiation. In summary, our results provide a theoretical basis for the clinical translation of hADSC-Exo in fat grafting.

Targeting RAS phosphorylation in cancer therapy: Mechanisms and modulators.

RAS, a member of the small GTPase family, functions as a binary switch by shifting between inactive GDP-loaded and active GTP-loaded state. RAS gain-of-function mutations are one of the leading causes in human oncogenesis, accounting for ∼19% of the global cancer burden. As a well-recognized target in malignancy, RAS has been intensively studied in the past decades. Despite the sustained efforts, many failures occurred in the earlier exploration and resulted in an 'undruggable' feature of RAS proteins. Phosphorylation at several residues has been recently determined as regulators for wild-type and mutated RAS proteins. Therefore, the development of RAS inhibitors directly targeting the RAS mutants or towards upstream regulatory kinases supplies a novel direction for tackling the anti-RAS difficulties. A better understanding of RAS phosphorylation can contribute to future therapeutic strategies. In this review, we comprehensively summarized the current advances in RAS phosphorylation and provided mechanistic insights into the signaling transduction of associated pathways. Importantly, the preclinical and clinical success in developing anti-RAS drugs targeting the upstream kinases and potential directions of harnessing allostery to target RAS phosphorylation sites were also discussed.

An innovative technique of hydrosurgery in the treatment of osmidrosis.

BACKGROUND: We aimed at evaluating the effects of hydrosurgery and traditional surgical approach with two parallel incisions in the treatment of osmidrosis. METHODS: This prospective study enrolled patients with axillary osmidrosis between January 2015 and November 2016. For hydrosurgery, a 1-cm-long incision was made in the middle of the posterior long axis. The hand piece was turned upside down and processed in a 'W-O' way. For traditional method, two 3-cm-long parallel incisions were made transversely. Patient demographics, complications, duration of procedures and the outcomes were collected and compared. All patients had a follow-up period of 24-36 months. RESULTS: A total of 93 patients were included: 41 patients in hydrosurgery group and 52 patients in traditional method group. No severe complications occurred in the hydrosurgery group, while necrosis occurred in six sides of axillae of traditional surgical group. No recurrence occurred in both groups. Both groups showed similar odor and hair growth reduction rate. Only one in 82 sides occurred slight scar formation, while in traditional group, 22 sides of axillae formed scars (p < .001). CONCLUSIONS: The application of hydrosurgery in the treatment of osmidrosis is efficient and effective. Moreover, it has less postoperative complications, and high patient satisfaction rates.

VASH-1 Regulates Oxidative Stress and Fibrosis in Diabetic Kidney Disease via SIRT1/HIF1α and TGFß1/Smad3 Signaling Pathways.

Aims: To investigate the role of Vasohibin-1 (VASH-1), silence information adjustment factor 2-related enzyme 1 (SIRT1)/hypoxic-inducible factor 1α (HIF1α) and transforming growth factor-ß1 (TGFß1) /Smad3 signaling pathways in oxidative stress and fibrosis of diabetic kidney disease (DKD). Materials and Methods: A diabetic rat model was established in vivo and rat mesangial cells (RMCs) were cultured in vitro with high glucose via transfection with Vash1 small interfering RNA (siRNA), Hif1a siRNA, Sirt1 siRNA and TGFß1/Smad3 pathway inhibitor (SB431542). Renal histology was used to detect renal changes. Real-time PCR and western blot were used to analyze the expression of VASH-1, SIRT1, HIF1α, TGFß1, Smad3, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and fibronectin (FN). Expression levels of tumor necrosis factor-α (TNFα), TGFß1, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) in rat tissues and cell culture supernatant were detected by ELISA and chemiluminescence assay, while cell proliferation was detected by CCK-8. Results: The level of VASH-1 in renal tissues of diabetic rats was decreased, while both high glucose and Vash1 siRNA inhibited the expression of VASH-1 and SIRT1, increased the levels of HIF1α, TGFß1, and Smad3 in RMCs, thus up-regulating oxidative stress and fibrosis factors, and abnormally increasing cell proliferation activity (P < 0.05). However, inhibition of SIRT1/HIF1α signaling pathway only reduced TGFß1 and Smad3 (P < 0.05), while VASH-1 remained unchanged (P > 0.05). Conclusion: VASH-1 was under-expressed in renal tissues of diabetic rats and regulated the pathological process of oxidative stress and fibrosis in DKD via downstream SIRT1/HIF1α and TGFß1/Smad3 signaling pathways.

Vaginoplasty With Mesh Autologous Buccal Mucosa in Vaginal Agenesis: A Multidisciplinary Approach and Literature Review.

BACKGROUND: Vaginal agenesis, a rare condition, is treated by various surgical techniques to achieve neovaginal reconstruction. The main difference between the approaches lies in the graft material used to cover the newly formed cavity. OBJECTIVES: The purpose of this retrospective study was to describe the surgical procedure and outcomes of autologous buccal mucosal grafting in neovaginal reconstruction. METHODS: Sixteen patients with vaginal agenesis admitted to our department between January 2016 and January 2019 were included in our study. A reconstruction procedure, described in detail here, involving autologous buccal mucosa as graft material was successfully conducted in all of the patients. Long-term anatomic and functional outcomes were evaluated. RESULTS: The blood loss during operation was estimated to be 15 to 20 mL in all cases. No rectal or bladder injury occurred. The buccal mucosal wound completely healed 10 to 14 days after the operation. All patients had a well-formed neovagina 8 to 10 cm in length, with a mean diameter of >3 finger-breadths. CONCLUSIONS: The application of autologous buccal mucosa in neovaginal construction is a simple procedure. Autologous buccal mucosa is an ideal material to achieve excellent cosmetic and functional results in patients with vaginal agenesis.

Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154.

Renal carcinoma (RCC) is widely accepted as a malignant tumour of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. To examine cellular viability of ACHN and CAKI-1 cells, cell counting kit-8 (CCK-8) assay was exploited here. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/ß-catenin/Notch. LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that overexpressed LINC01939 inactivated Wnt/ß-catenin and Notch through suppressing miR-154. Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.

Metformin alleviates oxidative stress and enhances autophagy in diabetic kidney disease via AMPK/SIRT1-FoxO1 pathway.

Metformin, as the basic pharmacological therapy and the first preventive drug in type 2 diabetes mellitus (T2DM), is proved to have potential protection in diabetic kidney disease (DKD). Here, we established a diabetic rat model induced by high-fat diet and low dose streptozotocin, and high glucose cultured rat mesangial cells (RMCs) pre-treated with metformin or transfected with AMPK, SIRT1 and FoxO1 small interfering RNA, and detected oxidative stress and autophagy related factors to explore the molecular mechanisms of metformin on DKD via adenosine monophosphate-activated protein kinase (AMPK)/silent mating type information regulation 2 homolog-1 (sirtuin-1, SIRT1)-Forkhead box protein O1 (FoxO1) pathway. We found that metformin effectively alleviated the disorders of glycolipid metabolism, renal function injury in diabetic rats, and relieved oxidative stress, enhanced autophagy and slowed down abnormal cell proliferation in high glucose cultured RMCs through AMPK/SIRT1-FoxO1 pathway, indicating the protective role of metformin against the pathological process of DKD.

Indirect comparison between immune checkpoint inhibitors and targeted therapies for the treatment of melanoma.

Background: This systematic review and meta-analysis aims to provide comparative and quantitative data about immune checkpoint inhibitor (IMM) and targeted therapy (TAR) in this work. Methods: A literature search was performed with PubMed, Embase, PMC database, and Web of Science databases to identify relevant studies. Hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS), and odds ratios (ORs) for overall response rate (ORR) were estimated. Results: Eighteen manuscripts were ultimately utilized for indirect comparisons. In general, both TAR and IMM can prolong the PFS either by monotherapy, combination therapy with chemotherapy or adjuvant therapy. BRAF inhibitor monotherapy showed superiority over anti-CTLA-4 in OS (HR: 1.28, 95%CI: 0.93-1.75) and best ORR (OR: 12.57, 95%CI: 6.63-23.82), as well as longer PFS (HR: 1.63, 95%CI: 1.00-2.67) and higher best ORR (OR: 3.29, 95%CI: 1.94-5.55) compared with anti-PD-1. However, MEK inhibitor monotherapy showed no priority. When combined with chemotherapy, anti-CTLA-4 showed marginally advantages over MEK inhibitor in OS (HR: 0.68, 95%CI: 0.44-1.03), however no advantage in PFS (HR: 1.12, 95%CI: 0.76-1.64), or ORR (OR: 1.78, 95%CI: 0.70-4.49). For post-operational melanoma patient, adjuvant TAR and adjuvant IMM showed no difference in OS (HR: 1.14, 95%CI: 0.82-1.58) or PFS (HR: 1.20, 95%CI: 0.79-1.83). Moreover, the high-rate adverse events and underlying diseases should be considered during the application of those agents. Conclusions: For the unresectable late-stage melanoma, IMM may be a better choice for the combined treatment with chemotherapy. If the chemotherapy is not tolerable for patients, BRAFi involved TAR can be considered.

Critical role for non­GAP function of Gαs in RGS1­mediated promotion of melanoma progression through AKT and ERK phosphorylation.

Regulator of G­protein signaling 1 (RGS1) has been found to be a critical factor in melanoma and other malignancies. However, the mechanism involved in the RGS1­mediated promotion of melanoma progression is not clear. We based our study on samples collected from pathological specimens of melanoma patients. We found by immunohistochemistry that RGS1 expression was significantly higher in melanoma than that noted in nevus tissue (P<0.05). Kaplan­Meier analysis demonstrated a significant correlation between increased RGS1 expression and reduced disease­specific survival (P<0.05). RGS1 expression was also found to be related to the proliferation and migration of melanoma cells. RGS1 was able to bind to the Gαs in immunoprecipitation, but this interaction did not accelerate GTP hydrolysis in our experiment. Furthermore, we found that RGS1 may promote melanoma progression through the downstream effects of Gαs signaling, such as the increased phosphorylation of AKT and ERK by western blotting. Our results demonstrated that RGS1 promotes melanoma progression through regulation of Gαs­mediated inactivation of AKT and ERK. Therefore, RGS1 is a novel therapeutic target for melanoma treatment.

Melanocyte-specific gene 1 promotes melanoma progression by enhancing the expression of Bcl-2.

Malignant melanoma is a class of highly malignant tumors derived from melanocytes. At present, the dysregulated gene expression involved in the progression of melanoma has attracted much attention. In the present study, the gene expression profile of human melanoma tissue was screened using a cDNA microarray, and it was identified that melanocyte-specific gene 1 (MSG1) was significantly overexpressed in melanoma tissue compared with paired nevus tissues. The overexpression of MSG1 in melanoma was subsequently confirmed using immunohistochemistry in a set of melanoma tissues. It was additionally identified that the overexpression of MSG1 may promote cell viability and inhibit cell apoptosis in human melanoma A375 cells, thus promoting melanoma progression. Mechanistically, following screening of the expression of apoptosis-associated proteins, MSG1 was demonstrated to enhance the expression of the apoptosis inhibitor B-cell lymphoma 2 (Bcl-2) to inhibit melanoma cell apoptosis. Therefore, it was concluded that the overexpression of MSG1 inhibits apoptosis by enhancing Bcl-2 expression in malignant melanoma, thus promoting melanoma progression.

Mesenchymal stem cells induce epithelial mesenchymal transition in melanoma by paracrine secretion of transforming growth factor-ß.

Mesenchymal stem cells (MSCs) are considered for potential use as an ideal vehicle to efficiently deliver therapeutic agents in treatment against cancers including melanoma. However, emerging evidence indicates that MSCs promote tumor growth and progression. Therefore, a comprehensive understanding of the role of MSCs is very important to evaluate the MSCs-based therapy in melanoma. B16 melanoma cells treated by MSC conditioned medium (CM), showed significantly enhanced migration and invasion, which was also confirmed in a lung metastasis mice model in vivo. Later, it was found that MSC CM induced an epithelial mesenchymal transition (EMT) in B16 cells. The ELISA assay showed that transforming growth factor-ß (TGF-ß) was secreted by MSCs and EMT was also induced by recombinant TGF-ß in B16 melanoma cells, which suggests the important role of TGF-ß in mediating EMT caused by MSC CM. When TGF-ß signaling was inhibited by SB431542, the EMT process was significantly eliminated in vitro and in xenograft tumors in vivo. Snail, as a downstream target of TGF-ß signaling and an EMT regulator, was upregulated by MSC CM and inhibited by SB431542, which confirms the key role of TGF-ß signaling in EMT induced by MSC CM in B16 cells. Taken together, this study shows that MSC induces EMT in melanoma cells in a paracrine manner, which might be mediated by the TGF-ß/Snail signaling pathway. Thus, caution should be exercised when considering MSCs-based therapy in melanoma and also in other cancers. Targeting TGF-ß signaling and Snail could be further investigated as potential therapeutic approaches for melanoma.

Changes of serum Mir-217 and the correlation with the severity in type 2 diabetes patients with different stages of diabetic kidney disease.

The aim of this study is to investigate the correlation between serum microRNA-217 and the severity of diabetic kidney disease determined by albuminuria. Four hundred ninety five type 2 diabetes patients were divided into three groups: normoalbuminuric group, microalbuminuric group, and macroalbuminuric group. Serum microRNA-217 levels were validated by real-time polymerase chain reaction. Serum silent information regulator 1, Hypoxia-inducible factor-1α and vascular endothelial growth factor were determined by enzyme-linked immunosorbent assay. Compared with control, serum microRNA-217 levels were significantly increased in type 2 diabetes patients and gradually increased in patients of normoalbuminuric, microalbuminuric, and macroalbuminuric groups (P < 0.01). Moreover, increased levels of serum microRNA-217, hypoxia-inducible factor-1α, vascular endothelial growth factor, diabetes mellitus duration, fasting blood glucose, fasting insulin, homeostasis model assessment for insulin resistance, glycated hemoglobin, low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, and decreased levels of serum silent information regulator 1 and high-density lipoprotein were significantly correlated with Ln(ACR) (P < 0.05). In addition, serum microRNA-217 was positively correlated with diabetes mellitus duration, homeostasis model assessment for insulin resistance, glycated hemoglobin, Ln(ACR), low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, hypoxia-inducible factor-1α, vascular endothelial growth factor (P < 0.05), and negatively correlated with serum silent information regulator 1 (P = 0.002). Our findings suggest that microRNA-217 may have an association with the development of proteinuria in type 2 diabetes patients. Serum microRNA-217 may be involved in the development of diabetic kidney disease by promoting chronic inflammation, renal fibrosis, and angiogenesis.

Reconstruction of auricular conchal defects with local flaps.

Reconstruction of the auricular conchal cavity is relatively difficult because of its unique structure, shape, and location. We compared different methods of repair of the auricular concha to determine the method that would cause the least injury to the donor site.The method selected was based on the location and size of the defect. If the defect was located in the upper part of the concha, or if the defect was >15 mm in diameter, we used a post-auricular subcutaneous pedicle island flap that was pulled through a post-auricular sulcus tunnel to cover the wound. If the defect was located in the lower part of the concha and was <15 mm in diameter, we used a pre-auricular translocation flap that was passed through the intertragic notch to cover the wound. The donor site was closed primarily. All flaps survived well and any scars associated with the surgery were unnoticeable. No tumor relapse or metastasis was observed over a mean follow-up period of 35 months. All patients were satisfied with the outcome.The periauricular flap technique chosen for reconstruction of skin defects in the auricular concha depends on the size and location of the defect. With appropriate flap selection, excellent functional, and aesthetic outcomes are achieved.

Effect of partial splenic embolization on the immune function of cirrhosis patients with hypersplenism.

OBJECTIVE: To discover the effect of partial splenic embolization on the immune function of cirrhotic patients with hypersplenism. METHODS: Patients involved in the study were enrolled and divided into three groups, including control group, experimental group, and complication group. Numbers of CD3(+), CD4(+) and CD8(+) T cells and CD4(+)CD25(+)CDl27(low/-) Treg cells in the peripheral blood of patients before surgery, 1 month, 6 months, 1 year, and 2 years after surgery were analyzed by fluorescence active cell sorting (FACS). Contents of immunoglobulins (IgA, IgG and IgM) were analyzed by auto immunoassay analyzer. RESULTS: In the peripheral blood of patients from experimental group, numbers of CD3(+), CD4(+) and CD8(+) T cells initially declined, but afterwards increased to normal level; in the peripheral blood of patients from complication group, CD3(+) and CD8(+) T cells showed the same trend, but the number of CD4(+) T cells was below normal level at all detection times. Furthermore, CD3(+), CD4(+) and CD8(+) T cells in the peripheral blood of patients from complication group were initially less than those in experimental group, and afterwards were comparable between two groups. In patients from both experimental group and complication group, the number of CD4(+) CD25(+) CDl27(low/-)Treg cells increased 1 month and 6 months after surgery, and gradually restored to normal level. CD4(+)CD25(+)CDl27(low/-) Treg cell counts in patients from complication group were initially more than those in patients from experimental group 1 month and 6 months after surgery, but then they were comparable. Furthermore, contents of immunoglobulins (IgA, IgG and IgM) were comparable in three groups at all detection times. CONCLUSION: Partial splenic embolization influenced the immune function of cirrhotic patients with hypersplenism in the short term but the immune function could afterwards gradually restore to normal. Our results implicated that measures that prevent infection and improve immune function were necessary in early stage after undergoing PSE in order to reduce complications.

Levels of Serum 25(OH)VD3, HIF-1α, VEGF, vWf, and IGF-1 and Their Correlation in Type 2 Diabetes Patients with Different Urine Albumin Creatinine Ratio.

OBJECTIVE: To investigate changes in serum 25(OH)VD3, HIF-1α, VEGF, vWf, IGF-1, and their correlation in type 2 diabetes patients at different stages of diabetic kidney disease (DKD). METHODS: 502 type 2 diabetes patients were divided into three groups: Normoalbuminuric group (201 patients), Microalbuminuric group (171 patients), and Macroalbuminuric group (130 patients). Serum 25-hydroxyvitamin D3 [25(OH)VD3] was measured by chemiluminescence. Serum hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), von Willebrand factor (vWf), and insulin-like growth factor-1 (IGF-1) were determined by enzyme-linked immunosorbent assay. We detected the aforementioned serum factors in all cases and 224 control subjects. RESULTS: Serum HIF-1α, VEGF, vWf, and IGF-1 in type 2 diabetes patients were significantly higher than those in the control group and increased with the increase of Ln(ACR), respectively (P < 0.001). Serum 25(OH)VD3 was significantly lower in type 2 diabetes patients and decreased with the increase of Ln(ACR) (P < 0.001). Ln(ACR) was positively correlated with duration, HbA1c, Scr, BUN, TC, LDL, TG, UA, HIF-1α, VEGF, IGF-1, vWf, and Fg and negatively correlated with 25(OH)VD3 and eGFR. CONCLUSION: Serum HIF-1α, VEGF, vWf, and IGF-1 may be involved in DKD process through inflammation, angiogenesis, and endothelial injury. Serum 25(OH)VD3 may have protective effects on DKD partly by inhibiting inflammation, abnormal angiogenesis, and vascular endothelial dysfunction.