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Remote endoscopy can improve diagnostic efficiency of gastrointestinal (GI) diseases for patients in remote areas. A novel remote magnetically controlled capsule endoscopy (MCE) system based on a 5G network was developed for real-time remote GI examinations. We aimed to evaluate the feasibility and safety of the 5G-based remote MCE for examination of the stomach and small bowel.This was a prospective, nonrandomized, comparative study. Consecutive participants enrolled in the First People's Hospital of Yinchuan underwent remote MCE examinations performed by an endoscopist located in Changhai Hospital. Consecutive participants enrolled in Changhai Hospital underwent conventional MCE examinations performed by the same endoscopist. The main outcomes included the complete visualization rate of the stomach and small bowel, safety assessment and network latency time of remote MCE examinations.From March 2021 to June 2021, 20 participants in each group were enrolled. The complete visualization rate of the stomach and small bowel was 100% in both groups (p 0.999) without any adverse event. The median network latency time of remote MCE group was 19.948 ms. Gastric examination time (8.96 vs. 8.92 min, p = 0.234), maneuverability (15.00 vs. 15.00, p = 0.317), image quality (1.00 vs. 1.00, p 0.999) and diagnostic yields in the stomach and small bowel (55% vs. 30%, 5% vs. 0%, both p 0.05) were comparable between remote and conventional MCE groups. All participants in remote MCE group considered remote MCE acceptable and necessary.5G-based remote MCE was a feasible and safe method for viewing the stomach and small bowel.

Background Chronic hepatitis B is a highly heterogeneous disease that can be divided into four phases: Immune tolerant (IT), immune active (IA), inactive carrier (IC) and hepatitis B envelope antigen (HBeAg)-negative hepatitis (ENEG). Aim To investigate the immune status of natural killer (NK) and T cells in different phases of chronic hepatitis B. Methods The frequency, phenotype and function of circulating NK cells, as well as nonantigen-specific and hepatitis B virus (HBV)-specific T cell responses were detected by flow cytometry in healthy and HBV-infected subjects. Results The ability of NK cells to produce IFN-γ was markedly attenuated in HBV-infected patients overall but was less compromised in IC patients. Patients in the IT and IA phases also displayed significantly lower TNF-α production compared to healthy subjects. NK cells were phenotypically activated in the IA and ENEG phases, as evidenced by the upregulation of NKp44 in CD56bright NK cells and CD69 in CD56dim NK cells. Furthermore, global T-cells from the ENEG phase displayed a proinflammatory cytokine profile with upregulated IFN-γ and TNF-α expression, while this profile was suppressed in IT and IA patients. Finally, core and S antigen-specific T cell responses were significantly stronger after in vitro expansion in the IC phase compared to other phases. Conclusion Our findings demonstrate the changes in immune response pattern during the natural history of HBV infection. Both NK and T cells are functionally impaired in the IT and IA phases. With the spontaneous clearance of HBeAg and hepatitis B surface antigen decline, NK cell cytokine production and HBV-specific T responses are partially restored in IC phase, and the ENEG phase is dominated by nonantigen-specific T cell responses.

Four starburst molecules with a triphenylamine (TPA) core through the amide group linked to the terminal triphenylamine or (N-phenyl)carbazole (NPC) unit, coded as T-3(NHCO-TPA), T-3(NHCO-NPC), T-3(CONH-TPA), and T-3(CONH-NPC), were synthesized and their electrochemistry and electropolymerization were investigated. The oxidation potential and the stability of the oxidized forms of the starbursts are affected by the orientation of amide linkage and the structure of terminal triarylamine unit. Robust polymeric films could be built onto ITO/glass surface by repetitive cyclic voltammetry (CV) of the T-3(NHCO-TPA) solution containing an electrolyte. The electrodeposited films exhibited reversible electrochemical processes and strong color changes upon electro-oxidation, which can be switched by potential modulation. The electrochromic behavior of the film was clearly interpreted on the basis of spectroelectrochemical studies. T-3(CONH-TPA) did not undergo electropolymerization effectively. T-3(CONH-NPC) also could electrochemically polymerize to polymer films upon repeated CV scans. However, their electrochromic switching stability is less than that of the polymer film from T-3(NHCO-TPA).

Background: There has been considerable interest in whether old age is associated with IgA nephropathy (IgAN) progression, which is still controversial. Methods: We searched multiple databases for studies published from 1980 to 2012. The inclusion criteria were case-control, cohort studies published in any language. The included studies needed to have an older group. IgAN was proven by biopsy. Results: We included 9 studies with a total of 6,543 patients. The meta-analyses of other risk factors between the older group (>50 years old) and the non-older group (15-50 years old) found significant differences in the presence of hypertension, proteinuria, serum cholesterol levels and baseline renal function. In the overall analysis, compared to the non-older group, older age significantly increased the incidence of developing end-stage renal disease [ESRD; relative risk (RR) random model 1.95; 95% CI: 1.27-3.01]. In the subgroup analyses, we found the age limit and traditional risk factors of IgAN may be the sources of heterogeneity between studies. Moreover, the RR (2.56) of the Asian countries was much higher than the RR (1.11) of the European countries. Conclusions: This comprehensive review revealed that old age is a real risk factor for IgAN progression to ESRD. The incidence of ESRD in the older IgAN patients was 1.95 times higher than that in the non-older IgAN patients. Moreover, the risk of IgAN progression to ESRD of the older patients in Asia was higher than that of the older patients in Europe.

Objective Numerous Chinese patients with IgA nephropathy (IgAN) have benefited from Tripterygium wilfordii Hook F (TwHF) from two decades ago. However, to date there is no systematic evaluation of this remedy for IgAN. Methods We conducted a meta-analysis of all eligible randomized clinical trials (RCTs) to assess the effect of TwHF on IgAN for the first time. In August 2009 a systematic search was performed among eight electronic databases. Review Manager (RevMan) version 5.0 was used. Results (i) Four eligible RCTs with 188 participants were included; (ii) The validities of included RCTs were generally acceptable; (iii) TwHF brought about a favorable increase in complete remission (CR) (RR 1.53, 95%CI 1.09 to 2.16, I2=12%) and total remission (TR) (RR 1.27, 95%CI 1.08 to 1.48, I2=0%) compared with non-TwHF treatment; and this result was further confirmed by intention-to-treat analysis; (iv) Exploiting subgroup meta-analysis, TwHF led to significantly greater improvements of IgAN with non-nephrotic proteinuria with regard to the increase of CR (RR 1.80, 95%CI 1.21 to 2.68, I2=0%) and TR (RR 1.32, 95%CI 1.11 to 1.57, I2=0%), and decrease of urinary proteinuria excretion (UPE) (MD -467.41 mg/24h, 95%CI -633.99 to -300.82, I2=0%). Meanwhile, the renal function was well preserved (MD -2.66 μmol/L, 95%CI -9.26 to 3.94, I2=0%). Conclusion Although the results of this meta-analysis should be interpreted with caution and warrant further investigation, TwHF was certainly a valuable and promising immunosuppressive remedy for IgAN, which was in accordance with the accruing evidence from numerous large clinical and experimental studies.

Concurrent glomeruli and liver involvement in patients with Sjögren's syndrome (SS) has seldom been reported. Meanwhile, IgA nephropathy (IgAN) associated with SS is not as common as other types of glomerulonephritis, such as membranoproliferative glomerulonephritis (MPGN) and membranous nephropathy (MN). Two patients with SS and IgAN are presented. Case 1 was diagnosed as SS complicated with IgAN (Haas subclass III) and severe AIH, while case 2 was diagnosed as SS and IgAN (Haas subclass I) with serious tubulointerstitial lesions. The true prevalence of IgAN secondary to SS is certainly underestimated and the crucial pathogenetic factors may be polyclonal hypergammaglobulinemia and hypocomplementemia (especially C4). The frequent presence of multiple immunoglobulin and complement deposition in glomeruli, especially weak deposits of C4 and (or) C1q, is an immunofluorescence staining feature of IgAN secondary to SS and may be associated with disease severity and activity.

The aims of the present study were to validate the differential diagnostic model of diabetic nephropathy (DN) and non-diabetic renal diseases (NDRD) established in 2003 and to establish a new diagnostic model suitable for the current clinical characteristics of DN.We examined 200 patients with Type 2 diabetes who underwent kidney biopsy from 2004 to 2012. The 2003 differential diagnostic model based on the data collected from 1993 to 2003 was evaluated by the diagnostic test and changes in the clinical differentiation parameters of DN and NDRD were analyzed. Logistic regression, receiver operating characteristics (ROC) curve, net reclassification improvement (NRI), and integrated discrimination improvement (IDI) analysis were applied.The 2003 diagnostic model showed an accuracy of 77.5%. A significantly elevated incidence of hematuria, longer history of diabetes, and reduced level of glycated hemoglobin (HbA1c) were observed in the DN group from 2004 to 2012 compared with DN group from 1993 to 2003. Histories of diabetes mellitus (Dm), systolic blood pressure (Bp), HbA1c (Gh), hematuria (Hu), diabetic retinopathy (Dr), and hemoglobin (Hb) are independently related to DN. Thus, a new diagnostic model was constructed as follows: PDN = exp (0.846 + 0.022 Dm + 0.033Bp + 2.050 Gh-2.664 Hu-0.078 Hb + 2.942Dr)/[1 + exp (0.846 + 0.022 Dm + 0.033 Bp + 2.050 Gh-2.664 Hu-0.078 Hb + 2.942 Dr)].Validation tests determined that the accuracy of the new model were 90.9%.Changes in people with DN, clinical characteristics have reduced the diagnostic efficacy of the 2003 diagnostic model. The newly established model can provide a better, more current differentiation between DN and NDRD.

Background and Aim: Neutropenia is a serious adverse event for patients who are treated with cetuximab, an inhibitor of endothelial growth factor receptor. However, there is no consistent result of the relationship between cetuximab and neutropenia in randomized controlled trials (RCTs). We did a systematic review and meta-analysis of published RCTs to assess the overall risk of neutropenia associated with cetuximab. Methods: PubMed, Cochrane Central Register of Controlled Trials, EMBASE, and American Society of Clinical Oncology conferences were searched for relevant RCTs. Quantitative and qualitative analyses were carried out to evaluate the association between neutropenia and cetuximab. Both the fixed-effect model and random-effects model were used. Results: A total of 7186 patients with a variety of advanced cancers from 14 trials were included in our analysis. The overall incidence of neutropenia in patients receiving cetuximab was 33% (95% CI 26, 43). Patients treated with cetuximab had a significantly increased risk of neutropenia compared with patients treated with control medication, with a relative risk (RR) of 1.12 (95% CI 1.05, 1.19; fixed-effect model). Risk varied with tumor type. Higher risks were observed in patients with colorectal carcinoma (RR 1.17; 95% CI 1.04, 1.32; fixed-effect model) and non-small cell lung cancer (RR 1.07; 95% CI 0.99, 1.16; fixed-effect model). Conclusion: Cetuximab is associated with a significant risk of neutropenia in patients with advanced cancer receiving concurrent chemotherapy.

There is a paucity of published works that systematically evaluate gene anomalies or clinical features of patients with renal cysts and diabetes syndrome (RCAD)/maturity onset diabetes of the young type 5 (MODY5). The purpose of this review was to systematically assess the detection rate, genetic and phenotypic implications of heterozygous autosomal dominant TCF2 anomalies.MEDLINE database was searched to select articles recorded in English from 1997 to 2008. The focus was monoallelic germline TCF2 gene mutations/deletions. Biallelic inactivation, polymorphisms, DNA modification (hypomethylation and hypermethylation), loci associated with cancer risk, and somatic TCF2 anomalies were all excluded.After searching the literature, 50 articles were selected.The detection rate of TCF2 anomalies was 9.7% and varied considerably among MODY (1.4%), renal structure anomalies (RSA) (21.4%) and RSA with MODY (41.2%) subgroups. Mutations were strikingly located within the DNA binding domain and varied among exons of the DNA binding domain: exons 2 and 4 were the hottest spots, while mutations were sporadically distributed in exon 3. The consistent phenotypes were RSA (89.6%) and diabetes mellitus (DM) (45.0%). However, the concurrence of RSA and DM was relatively low (27.5%), which hinders the optimal performance of genetic testing and obtainment of timely diagnosis. Other organ involvements were complementary and necessary for the early identification of patients with TCF2 anomalies. Analysis of phenotypes of TCF2 point mutations showed significant differences in the detection rates of RSA, impaired renal function (IRF) and DM according to mutation type but not mutation location.These valuable features of TCF2 anomalies that previously did not receive sufficient attention should not be neglected.

This study first investigates the anti-metastatic effect of alpha-tomatine in the human lung adenocarcinoma cell line: A549. In this study, we first noted alpha-tomatine inhibited A549 cells invasion and migration by wound-healing assay and Boyden chamber assay. The data also showed alpha-tomatine could inhibit phosphorylation of Akt and extracellular signal-regulated kinase 1 and 2 (ERK1/2), which is involved in the up-regulating matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) or urokinase-type plasminogen activator (u-PA), whereas it did not affect phosphorylation of c-Jun N-terminal kinase (JNK) and p38. Next, alpha-tomatine significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun. Also, treating A549 cells with alpha-tomatine also leads to a dose-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1). Further, the treatment of inhibitors specific for PI3K (Wortmannin) or ERK (U0126) to A549 cells could cause reduced activities of MMP-2, MMP-9, and u-PA. These results showed alpha-tomatine could inhibit the metastatic ability of A549 cells by reducing MMP-2, MMP-9, and u-PA activities through suppressing phosphoinositide 3-kinase/Akt (PI3K/Akt) or ERK1/2 signaling pathway and inhibition NF-kappaB or AP-1 binding activities. These findings proved alpha-tomatine might be an anti-metastatic agent against human lung adenocarcinoma.