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OBJECTIVE@#To explore the expression of Exosome Component 4（EXOSC4） in the tissues of newly diagnosed patients with diffuse large B-cell lymphoma (DLBCL) and its clinical significance.@*METHODS@#The expression of EXOSC4 protein in the tissues of 181 newly diagnosed DLBCL patients was analyzed by immunohistochemical staining. Clinical data were collected. The correlation between EXOSC4 protein expression in the tissues of newly diagnosed DLBCL patients and clinical features were analyzed and its prognostic significance.@*RESULTS@#The positive rate of EXOSC4 protein expression was 68.51% in the tissues of 181 newly diagnosed DLBCL patients. These patients were divided into two groups, with 44 cases in high expression group and 137 cases in low expression group. There were no significant differences in age, gender, B symptoms, serum lactate dehydrogenase (LDH) level, Eastern Cooperative Oncology Group (ECOG) score, Ann Arbor stage, extranodal disease, International Prognostic Index (IPI) score, National Comprehensive Cancer Network IPI (NCCN-IPI) score, and cell origin between the two groups (P>0.05). Cox multivariate regression analysis showed that high EXOSC4 protein expression in tissues was an independent poor prognostic factor for OS and PFS in newly diagnosed DLBCL patients (all P<0.05). K-M survival analysis showed that newly diagnosed DLBCL patients with high EXOSC4 protein expression had significantly shorter overall survival (OS) and progression free survival (PFS) than those patients with low EXOSC4 protein expression (all P<0.05).@*CONCLUSION@#High EXOSC4 protein expression in tissues of newly diagnosed DLBCL patients is an independent poor prognostic factor for survival.
Subject(s)
Humans , Clinical Relevance , Lymphoma, Large B-Cell, Diffuse/pathology , Prognosis , Retrospective Studies , Exosome Multienzyme Ribonuclease Complex/geneticsABSTRACT
Objective: To investigate the feasibility of endoscopic lateral neck dissection via the breast and transoral approaches (ELNDBTOA) for papillary thyroid carcinoma (PTC). Methods: From February 2015 to April 2019, 10 patients with PTC (cN1b) including 1 male and 9 females aged from 22 to 53 years old received ELNDBTOA in the General Surgery Department of Zhongshan Hospital, Xiamen University. Total thyroidectomy, the central lymph node dissection and the selective neck dissection (levels Ⅱ, Ⅲ and Ⅳ) were performed endoscopically via the breast approach, and then the residual lymph nodes were dissected via transoral approach. The medical records, operation time, blood loss, complications and postoperative follow-up outcomes were analyzed retrospectively. SPSS 22.0 software package was used for statistical processing of clinical data of patients. Results: All cases were successfully treated with ELNDBTOA without transfer to open surgery. The average operative time was (362.5±79.7) min, the blood loss was (23.0±14.9) ml, and the postoperative hospital stay was (5.1±1.3) days. The mean number of harvested cervical lymph nodes were (34.2±25.8), and the mean number of positive lymph nodes were (6.5±4.9). Lymph nodes were dissected by the further dissection via oral approach in 6 patients and a total of 9 lateral lymph nodes were havested from 2 of the 6 patients, with 3 positive lymph nodes. Two patients had transient skin numbness in the mandibular area and recovered within two weeks. One patient developed transient hypoparathyroidism and recovered within two months. No secondary bleeding, recurrent laryngeal nerve paralysis, chylous leakage, neck infection, permanent hypoparathyroidism or other complications were observed. The follow-up time was from 16 to 66 months with a median of 42.5 months, no tumor recurrence or metastasis occurred, and also no obvious deformity, abnormal sensation or movement in the chest, neck and mouth was observed. Conclusions: ELNBTOA is safe and feasible, with good cosmetic outcome.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , Lymph Nodes , Neck Dissection , Retrospective Studies , Thyroid Cancer, Papillary/surgery , Thyroid Neoplasms/surgery , ThyroidectomyABSTRACT
Netrin-1, an axon guidance factor, and its receptor UNC5B play important roles in axonal development and angiogenesis. This study examined netrin-1 and UNC5B expression in kidneys with diabetic kidney disease (DKD) and investigated their roles in angiogenesis. Netrin-1 and UNC5B were upregulated in streptozotocininduced DKD Wistar rats, and their expression was compared with that in healthy controls. However, exogenous netrin-1 in UNC5B-depleted human renal glomerular endothelial cells (HRGECs) inhibited cell migration and tubulogenesis. This effect was likely associated with SRC pathway deactivation. Netrin-1 treatment also eliminated the pro-angiogenic effects of exogenous VEGF-165 on UNC5B-silenced HRGECs. These results indicate that UNC5B antagonizes netrin-1 and that UNC5B upregulation contributes partly to enhancing angiogenesis in DKD. Therefore, introducing exogenous netrin-1 and depleting endogenous UNC5B are potential strategies for reducing the incidence of early angiogenesis and mitigating kidney injury in DKD.
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OBJECTIVE@#Small ubiquitin-related modifiers (SUMOs) are a group of post-translational modification proteins extensively expressed in eukaryotes. Abnormal SUMOylation can lead to the development of various diseases. This article summarizes the progress on research of the role of SUMOs in various types of kidney diseases to further increase the understanding of the regulatory functions of SUMOylation in the pathogenesis of kidney diseases.@*DATA SOURCES@#This review was based on articles published in the PubMed databases up to January 2018, using the keywords including "SUMOs," "SUMOylation," and "kidney diseases."@*STUDY SELECTION@#Original articles and critical reviews about SUMOs and kidney disease were selected for this review. A total of 50 studies were in English.@*RESULTS@#SUMO participates in the activation of NF-κB inflammatory signaling pathway, playing a central regulatory role in the inflammation and progression of DN, and the secretion of various chemokines in AKI. SUMO involves in the regulation of TG2 and Nrf2 antioxidant stress, affecting renal tubular injury in AKI. SUMO affects the MAPK/ERK pathway, regulating intracellular signal transduction, modulating the transcription and expression of effector molecules in DN. SUMO contributes to the TGF-β/Smad pathway, leading to fibrosis of the kidney. The conjugate combination of SUMO and p53 regulates cell proliferation and apoptosis, and participates in the regulation of tumorigenesis. In addition, SUMOylation of MITF modulates renal tumors secondary to melanoma, Similarly, SUMOylation of tumor suppressor gene VHL regulates the occurrence of renal cell carcinoma in VHL syndrome.@*CONCLUSIONS@#Tissue injury, inflammatory responses, fibrosis, apoptosis, and tumor proliferation in kidney diseases all involve SUMOs. Further research of the substrate SUMOylation and regulatory mechanisms of SUMO in kidney diseases will improve and develop new treatment measures and strategies targeting kidney diseases.
Subject(s)
Humans , Acute Kidney Injury , Carcinoma, Renal Cell , Diabetic Nephropathies , Fibrosis , Kidney , Pathology , Kidney Diseases , Metabolism , Kidney Neoplasms , SUMO-1 Protein , Physiology , SumoylationABSTRACT
Purpose To investigate the effect of specific long-chain non-coding RNA AP000344. 3 on the proliferation and invasion of bladder cancer cells and its mechanism. Methods qRT-PCR was used to detect the expression of AP000344. 3 in bladder cancer cells and normal bladder epithelial cells. The cancer cells with the lowest expression rate were selected for subsequent experiments. The AP000344. 3 plasmid or the negative control plasmid was transferred into bladder cancer cells by Lipofectamine 2000, and the transfection efficiency of AP000344. 3 was detected by qRT-PCR. Cell proliferation activity was measured by MTT method,and cell invasion ability was detected by Transwell assay. Bioinformatics was used to predict downstream miRNA and downstream genes of AP000344. 3. qRT-PCR and Western blot were used to detect the expression of downstream genes. Results The expression of AP000344. 3 in bladder cancer cells was significantly lower than that in normal bladder epithelial cells (P < 0. 01) ,and the expression of AP000344. 3 was the lowest in BIU87 cells (P < 0. 01) . The expression of AP000344. 3 in BIU87 cells was up-regulated at 48 h after transfection with AP000344. 3 (P < 0. 01) . The proliferation activity of BIU87 cells was decreased (P < 0. 05) ,and the cell invasion ability was decreased (P < 0. 05) . AP000344. 3 can target and bind to miR-135a-5p,and miR-135a-5p to human chemokine-like factor superfamily member 3 (CMTM3) . After up-regulation of AP000344. 3,miR-135a-5p expression was down-regulated (P < 0. 01) ,and CMTM3 was up-regulated in mRNA and protein expression (P < 0. 01) . Conclusion AP000344. 3 is significantly down-regulated in bladder cancer cells,and up-regulation of AP000344. 3 can inhibit the proliferation and invasion of bladder cancer cells. The mechanism may be to inhibit the expression of miR-135a-5p and up-regulate the expression of CMTM3 protein,providing a theoretical basis for finding new therapeutic targets for bladder cancer.
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To investigate the effect and mechanism of miR-498 on Th17 cell differentiation of peripheral blood mononuclear cells (PMBCs) in rheumatoid arthritis (RA) patients, peripheral blood samples were collected from RA patients and healthy controls, respectively. The proportion of CD4IL-17 T cells (Th17 cells) or CD4FOXP3 T cells (Tregs) in T cells and the Th17/Treg ratio were identified by the flow cytometer. The STAT3 and miR-498 expression were measured by Western blot and real-time PCR, respectively. ELISA was used to detect IL-17 concentrations. Luciferase assay was performed to confirm that miR-498 directly targeted the 3' untranslated region (3'UTR) of STAT3 in CD4 T cells. The effect of miR-498 on Th17 cell differentiation was explored by transfection of miR-498 mimic and/or pcDNA-STAT3 into CD4 T cells. In PMBCs of RA patients, the Th17/CD4 T cell ratio was significantly increased, while the Tregs/CD4 T cell ratio was obviously decreased, leading to a higher Th17/Treg ratio. The results showed a reduced miR-498 expression and an increased STAT3 protein expression in PMBCs, and an increased IL-17 concentration in serum of RA patients. In cells transfected with wild-type-STAT3-LU, miR-498 mimic significantly reduced the luciferase activity, STAT3 gene and protein expression, and miR-498 inhibitor had an opposite function. While the miR-498 mimic/inhibitor had no effect on the luciferase activity and STAT3 expression in cells transfected with mutant-STAT3-LU. CD4 T cells transfected with miR-498 mimic had a lower Th17/CD4 T cell ratio and IL-17 concentration, however, transfection of pcDNA-STAT3 reversed the effect of miR-498 mimic on Th17/CD4 T cell ratio and IL-17 concentration. These results suggest that overexpression of miR-498 suppresses Th17 cell differentiation by targeting STAT3 in RA patients.
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Background@#Focal segmental glomerulosclerosis (FSGS) is a kidney disease that is commonly associated with proteinuria and the progressive loss of renal function, which is characterized by podocyte injury and the depletion and collapse of glomerular capillary segments. The pathogenesis of FSGS has not been completely elucidated; however, recent advances in molecular genetics have provided increasing evidence that podocyte structural and functional disruption is central to FSGS pathogenesis. Here, we identified a patient with FSGS and aimed to characterize the pathogenic gene and verify its mechanism.@*Methods@#Using next-generation sequencing and Sanger sequencing, we screened the causative gene that was linked to FSGS in this study. The patient's total blood RNA was extracted to validate the messenger RNA (mRNA) expression of coenzyme Q monooxygenase 6 (COQ6) and validated it by immunohistochemistry. COQ6 knockdown in podocytes was performed in vitro with small interfering RNA, and then, F-actin was determined using immunofluorescence staining. Cell apoptosis was evaluated by flow cytometry, the expression of active caspase-3 was determined by Western blot, and mitochondrial function was detected by MitoSOX.@*Results@#Using whole-exome sequencing and Sanger sequencing, we screened a new causative gene, COQ6, NM_182480: exon1: c.G41A: p.W14X. The mRNA expression of COQ6 in the proband showed decreased. Moreover, the expression of COQ6, which was validated by immunohistochemistry, also had the same change in the proband. Finally, we focused on the COQ6 gene to clarify the mechanism of podocyte injury. Flow cytometry showed significantly increased in apoptotic podocytes, and Western blotting showed increases in active caspase-3 in si-COQ6 podocytes. Meanwhile, reactive oxygen species (ROS) levels were increased and F-actin immunofluorescence was irregularly distributed in the si-COQ6 group.@*Conclusions@#This study reported a possible mechanism for FSGS and suggested that a new mutation in COQ6, which could cause respiratory chain defect, increase the generation of ROS, destroy the podocyte cytoskeleton, and induce apoptosis. It provides basic theoretical basis for the screening of FSGS in the future.
Subject(s)
Adolescent , Animals , Female , Humans , Mice , Apoptosis , Genetics , Physiology , Cell Line , Flow Cytometry , Glomerulosclerosis, Focal Segmental , Genetics , Immunohistochemistry , Mutation , Genetics , Podocytes , Metabolism , Pathology , RNA, Messenger , Genetics , RNA, Small Interfering , Genetics , Metabolism , Ubiquinone , Genetics , MetabolismABSTRACT
Objective To investigate the expression of calcineurin 1 (RCAN1) regulator and calcineurin A (Ca-NA) in brain tissue of temporal lobe (TLE) epilepsy patients and pentylenetetrazol (PTZ)-induced rat model. Methods Cortical samples from 18 patients with temporal lobe epilepsy were collected as epilepsy group and corti-cal samples from 11 patients with brain trauma were used as control group. 30 SD rats were randomly divided into model control group (MC) and PTZ group. The expression of RCAN1 and CaNA in human brain cortex,rat cortex and rat hippocampus were detected by Western blot and Immunohistochemistry assay. The location analysis of RCAN1 was detected by immunofluorescence. Moreover,co-immunoprecipitation was used to test whether there was an interaction between RCAN1 and CaNA. Results RCAN1 mainly located in neuronal cytomembrane.The expres-sion of RCAN1 was down-regulated and expression of CaNA was up-regulated both in the epileptic patients and epi-leptic rats (P<0.01). RCAN1 interacted with CaNA. Conclusions Decreased expression of RCAN1 and increased expression of CaNA indicate that RCAN1 may be involved in the epileptogenesis by regulating CaNA.
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Purpose To observe the effect of specific miR-448 inhibitor on the proliferation and migration of prostate cancer cells and its molecular mechanism. Methods Real-time fluo-rescent quantitative polymerase chain reaction ( qRT-PCR) was used to detect the expression of miR-448 in normal prostate epi-thelial cells and cancer cells. The cells with the highest expres-sion of miR-448 were selected for follow-up experiment. The miR-448 inhibitor or miR-NC was transferred into prostate canc-er cells using liposome transfection reagent. The expression of miR-448 and CMTM3 mRNA were detected by qRT-PCR. The expression of related proteins were detected by Western blotting. MTT assay was used to detect the cell proliferation activity. Tr-answell assay was used to detect the cell migration ability. Re-sults The expression of miR-448 in normal prostate epithelial cells was significantly lower than that in cancer cells ( P ＜0. 01), and the expression of miR-448 was the highest in DU- 145 cells ( P ＜0. 01). The expression of miR-448 in DU-145 cells was down-regulated 48 h after transfection with miR-448 in-hibitor (P＜0. 01). The expression of CMTM3 mRNA was up-regulated (P＜0. 01). The expression of CMTM3, E-cadherin and β-catenin proteins were up-regulated. The expression of N-cadherin and Snail proteins were down-regulated. Cell prolifera-tion was decreased (P＜0. 05). Cell migration ability decreased (P ＜ 0. 01 ). Conclusion miR-448 is highly expressed in prostate cancer cells. miR-448 inhibitor can down-regulate the expression of miR-448 in DU-145 cells, up-regulate the expres-sion of CMTM3 protein, inhibit the proliferation and migration of prostate cancer cells, which showing a potential function in mo-lecular therapy of prostate cancer.
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Hypoxia leads to increased red blood cells and blood viscosity at high altitude while moderate trauma increases coagulation in blood. Under the above-mentioned conditions, venous sinus thrombosis is more likely to occur. A patient suffering bilateral acetabular fractures together with the gradual disturbance of consciousness was admitted to our hospital. Though computed tomography arteriogram (CTA) of the brain displayed normal blood vessels; bilateral thalamus and brainstem infarction were found on head computed tomography (CT) and Galen vein thrombosis on cerebral computed tomography venography (CTV). Dehydration and tracheotomy were immediately conducted with antiplatelet, anticoagulant and neurotrophic medicine administered to the patient. After three days' treatment, the patient's consciousness gradually improved and eventually became clear enough to leave the hospital. On follow-up, no dysfunction was documented.
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BACKGROUND: The preliminary study found that domestic porous tantalum is conducive to the early adhesion and proliferation of MG63 cells, which can be used as a scaffold material for bone tissue engineering. As an optimized product of platelet-rich plasma, platelet lysate is more suitable for bone induction in the bone repair. OBJECTIVE: To further investigate the effect of platelet lysate and domestic porous tantalum scaffold constructs on the proliferation of MG63 cells and expression of integrin β1 (ITGβ1)/Vinculin/F-actin signaling pathway based on our previous findings. METHODS: MG3 cells were cultured and inoculated onto domestic porous tantalum scaffolds with the addition of 3%, 5%, 7% and 10% platelet lysates. Then, 7% as the best volume fraction of platelet lysate was screened by cell counting kit-8 method. There were four experimental groups including blank group (normally cultured MG63 cells), platelet lysate group (MG63 cells were cultured in 7% platelet lysate), porous tantalum scaffold group (MG63 cells were cultured on the domestic porous tantalum scaffold), and combined group (MG63 cells were cultured with 7% platelet lysate and porous tantalum scaffold. Scanning electron microscope was used to observe the surface morphology of domestic porous tantalum and platelet lysate-porous tantalum scaffold-MG63 cell complex. Cell counting kit-8 method was used to detect the proliferation of MG63 cells. Real-time fluorescence quantitative PCR (qPCR), immunocytochemical staining and western blot were used to detect the expression of ITGβ1, Vinculin, F-actin in MG63 cells at mRNA and protein levels. RESULTS AND CONCLUSION: Under the scanning electron microscope, MG63 cells adhered well to the scaffold surface. Compared with the blank group, the proliferation of MG63 cells could be significantly promoted by either platelet lysate or porous tantalum scaffold (P < 0.05). Moreover, the proliferation of MG63 cells was significantly improved in the combined group compared with the other three groups (P < 0.05). Findings from qPCR, immunocytochemical staining and western blot showed the highest expression of ITGβ1, Vinculin, F-actin mRNA and protein in the combined group (P < 0.05). These results indicate that platelet lysate and the domestic porous tantalum scaffold can synergistically promote the proliferation of MG63 cells, and up-regulate the expression of ITGβ1, Vinculin and F-actin mRNA and protein. Activation of the ITGβ1/Vinculin/F-actin signaling pathway may contribute to the proliferation, adhesion and differentiation of MG63 cells.
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Objective To explore and optimize the processes for synthesis of key intermediates of phosphorodiamidate morpholino oligonucleotides-7'-hydroxy-N-trityl morpholino nucleoside monomer in order to contribute to the research of phosphorodiamidate morpholino oligonucleotides antisense nucleotides.Methods With N-benzoylcytidine,guanosine and 5-methyluridine as starting materials,the ribose was modified to morpholino and the key chemical groups were protected to obtain 7'-hydroxy-N-trityl morpholino nucleoside monomer.Results Compounds N4-benzoyl-7'-hydroxy-N-trityl morpholinocytidine,N2-benzoyl-7'-hydroxy-N-trityl morpholinoguanosine and 7'-hydroxy-N-trityl morpholinothymidine were synthesized.The synthetic processes were optimized as well.The structures of all the intermediates and title compounds were characterized.Conclusion The synthetic processes of 7'-hydroxy-N-trityl morpholino nucleoside monomers have been optimized,which can be employed to prepare title compounds on a large scale.
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<p><b>OBJECTIVE</b>To investigate the effect of vildagliptin on pentamethazol (PTZ)-induced epilepsy in rats and explore the molecular mechanism.</p><p><b>METHODS</b>Samples of temporal cortex from 23 patients with temporal lobe epilepsy were collected as epilepsy group and samples of temporal cortex from 14 patients with brain trauma were used as control group. Ninety male SD rats were randomly divided into control group (group A), PTZ-induced epilepsy group (group B), saline 2 mL/kg group (group C), vildagliptin 2.5 mg/kg group (group D), vildagliptin 5mg/kg group (group D) and vildagliptin 10 mg/kg group (group F). Use chronic model of epilepsy induced by PTZ (35 mg/kg) intraperitoneal injection for 3 consecutive weeks, and changes of behavior were observed. The expression of GLP-1R was detected by Western blotting and immunohistochemical (IHC) staining, and the expression of GLP-1 was detected by enzyme-linked immunosorbent assay (ELISA). The location of GLP-1R was detected by immunofluorescent staining.</p><p><b>RESULTS</b>Immunofluorescent staining showed that the GLP-1R located in the neurons, and GLP-1R expression was obviously decreased both in patients with TLE and in rats with epilepsy. The latency time was prolonged and epilepsy attack time was decreased after vildagliptin treatment (P<0.05). GLP-1R expression was increased after vildagliptin treatment (P<0.05). ELISA showed the change of GLP-1 expression was the same as GLP-1R.</p><p><b>CONCLUSION</b>Vildagliptin can suppress temporal lobe epilepsy in rats by up-regulating GLP-1 and GLP-1R expressions.</p>
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<p><b>BACKGROUND</b>The mechanisms of pathological retinal neovascularization (RNV) remain unknown. Several microRNAs were reported to be involved in the process of RNV. Oxygen-induced retinopathy (OIR) is a useful model to investigate RNV. Our present work explored the expression and the role of microRNA-128 (miR-218) in oxygen-induced RNV.</p><p><b>METHODS</b>OIR was used to establish RNV model. The expression level of miR-218 in the retina from OIR mice was assessed by quantitative real-time reverse transcriptase polymerase chain reaction. Fluorescein angiography was performed in retinae of OIR mice, and RNV was quantified by hematoxylin and eosin staining to evaluate the effect of pCDH-CMV-miR-218 intravitreal injection on RNV in OIR mice. Roundabout 1 (Robo1) expression was detected by Western blotting in mouse retinal vascular endothelial cells expressing a high or low level of miR-218 and retinal tissues from OIR mice. Cell migration was evaluated by scratch wound assay.</p><p><b>RESULTS</b>In OIR mice, the expression level of miR-218 was significantly down-regulated (P = 0.006). Retinal Robo1 expression was significantly increased at both mRNA and protein levels (P = 0.001, 0.008; respectively). miR-218 intravitreal injection inhibited retinal angiogenesis in OIR mice, and the restoration of miR-218 in retina led to down-regulation of Robo1.</p><p><b>CONCLUSIONS</b>Our experiments showed that restoration of miR-218 inhibited retinal angiogenesis via targeting Robo1. MiR-218 contributed to the inhibition of retinal angiogenesis and miR-218 might be a new therapeutic target for preventing RNV.</p>
Subject(s)
Animals , Mice , Cell Movement , Cells, Cultured , Mice, Inbred C57BL , MicroRNAs , Physiology , Nerve Tissue Proteins , Physiology , Oxygen , Pharmacology , Receptors, Immunologic , Physiology , Retinal NeovascularizationABSTRACT
<p><b>BACKGROUND</b>Chronic kidney disease (CKD) has become a public health problem. New interventions to slow or prevent disease progression are urgently needed. In this setting, cell therapies associated with regenerative effects are attracting increasing interest. We evaluated the effect of embryonic stem cells (ESCs) on the progression of CKD.</p><p><b>METHODS</b>Adult male Sprague-Dawley rats were subjected to 5/6 nephrectomy. We used pedicled greater omentum flaps packing ESC-loaded gelatin microcryogels (GMs) on the 5/6 nephrectomized kidney. The viability of ESCs within the GMs was detected using in vitro two-photon fluorescence confocal imaging. Rats were sacrificed after 12 weeks. Renal injury was evaluated using serum creatinine, urea nitrogen, 24 h protein, renal pathology, and tubular injury score results. Structural damage was evaluated by periodic acid-Schiff and Masson trichrome staining.</p><p><b>RESULTS</b>In vitro, ESCs could be automatically loaded into the GMs. Uniform cell distribution, good cell attachment, and viability were achieved from day 1 to 7 in vitro. After 12 weeks, in the pedicled greater omentum flaps packing ESC-loaded GMs on 5/6 nephrectomized rats group, the plasma urea nitrogen levels were 26% lower than in the right nephrectomy group, glomerulosclerosis index was 62% lower and tubular injury index was 40% lower than in the 5/6 nephrectomized rats group without GMs.</p><p><b>CONCLUSIONS</b>In a rat model of established CKD, we demonstrated that the pedicled greater omentum flaps packing ESC-loaded GMs on the 5/6 nephrectomized kidney have a long-lasting therapeutic rescue function, as shown by the decreased progression of CKD and reduced glomerular injury.</p>
Subject(s)
Animals , Male , Mice , Rats , Cell Proliferation , Cryogels , Disease Progression , Embryonic Stem Cells , Transplantation , Gelatin , Kidney , Pathology , Mice, Inbred C57BL , Rats, Sprague-Dawley , Renal Insufficiency, Chronic , Pathology , TherapeuticsABSTRACT
Objective To investigate the management and prevention of the complications of sigmoid rectal pouch for urinary division after radical cystectomy. Methods The clinical data of 34 patients who underwent a sigmoid rectal pouch procedure were analyzed retrospectively, and the clinical experience was summarized in the management and prevention of the complications of sigmoid rectal pouch for diversion. Results Twenty-six patients were followed up for 2 months to 11 years, and 10 patients lost in follow-up. The early follow-up results were as follows:3 patients had postoperative high fever with unilateral the kidney water, 1 patient had retropubic bleeding and need to stop bleeding, 3 patients suffered from wound split open and were performed relaxation suture, and 1 patient had sigmoid colon rectum bladder fistula 10d after operation. The late follow-up results were as follows:1 patient had urethral neoplasms recurrence, 5 patients developed distance metastases, and 5 patients developed nocturnal incontinence and worn safety pad. There were no hyperchloremic acidosis requiring clinical treatment, hydronephrosis as well as retrograde pelvis infection. Conclusions The operation of sigmoid rectal pouch for urinary division is fairly simple, with no serious complication. It is a better alternative diversion procedure, and should be accepted gradually by patients and surgeons.
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<p><b>OBJECTIVE</b>To investigate the effects of Biejia Ruangan Tablet ([symbol in text], BRT)-containing serum on the expression of matrix metalloproteinase (MMP-9) and tissue inhibitor of metalloproteinase (TIMP-1) in cultured renal interstitial fibroblasts.</p><p><b>METHODS</b>Different BRT-containing sera were prepared by gastric gavages to rats with the high-dose (7 g/kg), mid-dose (3.5 g/kg), and low-dose (1.75 g/kg) BRT respectively. The expression of extracellular matrix in NRK-49F cells was induced by treatment with human transforming growth factor-β1 (recombined human TGF-β1), and BRT-containing serum. Western blotting and Northern blotting were used to measure type I and III procollagen, MMP-9, and TIMP-1.</p><p><b>RESULTS</b>The high dose BRT-containing serum could decrease the type I and III procollagen gene expression which boosted by TGF-β1, at the same time cut down TIMP-1 protein and gene expression which increased by TGF-β1 (P <0.05). Treatment of cells with recombined human TGF-β1 had no significant effect on MMP-9 expression and BRT-containing serum also had no effect on MMP-9 expression.</p><p><b>CONCLUSIONS</b>High dose BRT has anti-fibrosis effects in NRK-49F cells, as indicated by its inhibition of type I and III procollagen and TIMP-1 expression.</p>
Subject(s)
Animals , Humans , Male , Cells, Cultured , Collagen Type I , Genetics , Metabolism , Collagen Type III , Genetics , Metabolism , Drugs, Chinese Herbal , Pharmacology , Fibroblasts , Metabolism , Gene Expression Regulation , Kidney , Cell Biology , Matrix Metalloproteinase 9 , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Rats, Sprague-Dawley , Serum , Metabolism , Tablets , Tissue Inhibitor of Metalloproteinase-1 , Genetics , Metabolism , Transforming Growth Factor beta1 , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of storage time on arginase level, and the possible source of arginase in suspended red blood cells (RBC).</p><p><b>METHODS</b>The arginase and myeloperoxidase (MPO) levels in suspended RBC and control plasma were detected by ELISA. The free hemoglobin level in suspended RBC and control plasma were detected by colorimetric method. The relationship between arginase level, MPO level and free hemoglobin level in suspended RBC was analyzed by the related methods.</p><p><b>RESULTS</b>The arginase and free hemoglobin levels in suspended RBC were higher than those in control plasma. Otherwise, MPO level was not significantly different between suspended RBC and control plasma. All of them did not increase along with prolonging of storage time. There was not a significant correlation between arginase level and free hemoglobin level in suspended RBC of different storage time (r = 0.03), but arginase level positively correlated with MPO level in the suspended RBC of different storage time (r = 0.76).</p><p><b>CONCLUSION</b>The arginase level in suspended RBC storaged for different time increases significantly, but not along with prolonging of storage time. The main possible source of arginase in the suspended RBC is the residual white blood cell, especially neutrophils.</p>
Subject(s)
Humans , Arginase , Chemistry , Blood Preservation , Erythrocytes , Peroxidase , Chemistry , Plasma , Time FactorsABSTRACT
To compare the diagnostic accuracy of stroke volume variation [SVV] and pulse pressure variation [PPV] in studies that examined both parameters in the same patient population. Literature search was conducted in PubMed, EMBASE, CINAHL, and Google Scholar. Receiver operator characteristic [ROC] curves were examined, and summary ROC curves were plotted. The study was conducted from January to July 2013 in The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China. The meta-analysis of 19 studies published during the years 2005 and 2013 revealed a high degree of diagnostic accuracy of both SVV and PPV in predicting fluid responsiveness. The sensitivity and specificity of both the parameters were observed above 80% in a heterogeneous group of over 850 patients of which 55% responded to fluid challenge. The following values along with 95% confidence interval were noticed: SVV - sensitivity 82 [59-93%] and specificity 84 [62-95%], PPV - sensitivity 84 [62-95%] and specificity 83 [58-94%]. Area under the curve values obtained in the pooled analysis were 0.84 [0.79-0.89] for SVV, and 0.88 [0.84-0.92] for PPV. Both SVV and PPV exhibit a high degree of diagnostic accuracy in predicting the success or failure of a fluid challenge in hemodynamically unstable critically ill patients under controlled mechanical ventilation
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To investigate risk factors and efficacy of reoperation for neovascular glaucoma ( NVG) secondary to vitrectomy in proliferative diabetic retinopathy (PDR). ●METHODS:Seven cases (7 eyes) from October, 2009 to December, 2012 were analyzed retrospectively. All the patients had NVG after the primary vitrectomy for PDR and were performed secondary vitrectomy combined with laser photocoagulation . ●RESULTS: The mean intraocular pressure ( lOP) was (11. 21±4. 22)mmHg before primary surgery. The number of laser spots ranged from 622 to 1124 during the first vitrectomy. Cataract extraction was performed in all 7 cases and intraocular lens was implanted in 5 cases. The mean lOP was (10. 11± 3. 62) mmHg during 2mo after the primary surgery. During follow- up, all the patients had significantly progressive intraocular inflammation. Vitreous hemorrhage was not absorbed completely in 2 cases and recurrent vitreous hemorrhage occurred in the other 5 cases. Five cases had poor glycemic control and the other 2 cases had bad blood pressure control. NVG occurred in all 7cases. The mean lOP was (41. 13 ± 7. 76) mmHg before the secondary surgery. After the secondary surgery, the lOP were under control in 5 cases. For the other 2 cases, the lOP was controlled in one case by transscleral cyclophotocoagulation, another one was lost in follow-up with uncontrolled lOP. ●CONCLUSlON: Primary vitrectomy combined with lens extraction, insufficient laser speckle, unabsorbed and recurrent vitreous hemorrhage, intraocular inflammation and systemic condition may be the risk factors associated with the occurrent of NVG after vitrectomy in PDR. Secondary vitrectomy combined with sufficient retinal photocoagulation is efficiency for NVG after vitrectomy for the PDR.