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BackgroundIgG4-related kidney disease (IgG4-RKD) can affect multiple organs, which was first reported as a complication or extra-organ manifestation of autoimmune pancreatitis in 2004. It is characterized by abundant IgG4-positive plasma cells infiltration in tissues involved.Case presentationA 69-year-old man presented with cough and renal dysfunction with medical history of hypertension and diabetes. Pathological findings revealed interstitial nephritis and he was initially diagnosed with IgG4-RKD. Prednisone helped the patient to get a remission of cough and an obvious decrease of IgG4 level. However, he developed invasive pulmonary fungal infection while steroid theatment. Anti-fungal therapy was initiated after lung puncture (around cavitary lung lesion). Hemodialysis had been conducted because of renal failure and he got rid of it 2 months later. Methylprednisolone was decreased to 8 mg/day for maintenance therapy. Anti-fungal infection continued for 4 months after discharge home. On the 4th month of follow-up, Chest CT revealed no progression of lung lesions.ConclusionsThe corticosteroids are the first-line therapy of IgG4-RD and a rapid response helps to confirm the diagnosis. This case should inspire clinicians to identify IgG4-related lung disease and secondary pulmonary infection, pay attention to the complications during immunosuppressive therapy for primary disease control.

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Recently, the Klotho protein (Klotho) has received substantial attention as protective factor against cardiovascular complications of chronic kidney disease (CKD). However, the direct effect and mechanism of Klotho on endothelial cells injury are not well‐known. In this study, we incubated human vein umbilical endothelial cells (HUVECs) with uremic toxin indoxyl sulfate (IS) to mimic CKD internal environment and investigated the direct effect of Klotho on the HUVECs injury induced by IS and to explore the mechanism in this process. We found IS inhibited cell viability, increased endoplasmic reticulum stress, and mediated apoptosis of HUVECs. Treatment with Klotho significantly attenuated IS‐induced above effects. Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP‐activated protein kinase (AMPK) α1 phosphorylation instead of directly upregulating AMPKα1, which could be partly blocked by AMPK pathway inhibitor‐Compound C. In addition, Klotho also inhibited intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) expression induced by IS. Altogether, these results indicated that Klotho can protect HUVECs from IS‐induced injury by alleviating AMPKα1‐mediated endoplasmic reticulum stress., Indoxyl sulfate (IS) injured human vein umbilical endothelial cells (HUVECs) and increased endoplasmic reticulum stress and mediated apoptosis of HUVECs. Klotho attenuated IS‐induced above effects via promoting AMP‐activated protein kinase (AMPK) α1 phosphorylation instead of directly upregulating AMPKα1.

Objectives: As accumulating data supporting the potential role of the complement system in the pathogenesis of diabetic kidney disease (DKD), the present study aimed to explore the association of glomerular complement C4c deposition with the baseline clinicopathological characteristics and the prognosis of DKD in type 2 diabetes (T2DM) patients. Methods: A total of 79 T2DM patients with biopsy-proven DKD were enrolled. Clinicopathological features and renal outcomes were compared between groups divided by the glomerular C4c deposition patterns and median values of serum C4. Renal outcomes were defined by doubling of serum creatinine level or progression to end-stage renal disease (ESRD). A Cox proportional hazards model was employed to identify the risk factors associated with renal events. Results: Patients with glomerular C4c deposition had worse renal insufficiency than those without C4c deposits, along with higher 24-h urinary protein, triglyceride, but lower serum albumin and higher interstitial inflammation score. Besides, serum C4 levels positively correlated with urinary protein and serum C3 levels. During 21.85 ± 16.32 months of follow-up, Kaplan-Meier curve analysis showed significantly faster deterioration of renal function for patients with positive glomerular C4c deposition as well as higher levels of serum C4. More specifically, more than 50% of the patients with glomerular C4c had co-deposition of C3c or C1q, and patients with glomerular complement complex of C4c and one or two of C3/C1q deposition had more severe proteinuria and a higher rate of DKD progression than those with negative C4c deposits. The univariate Cox regression indicated that factors of combined serum and glomerular C4, urinary protein, serum creatinine, serum C3, combined glomerular C4c and IgM and interstitial inflammation were associated with an increased risk of DKD, but only glomerular C4c intensity (HR 1.584, 95% CI [1.001, 2.508], p = 0.0497), as well as baseline age and diabetic neuropathy, were independent risk factors for renal survival by the multivariate Cox analysis. Conclusions: Glomerular C4c deposition was associated with deteriorated renal function and outcomes in patients with T2DKD. Glomerular C4c deposition was an independent risk factor for DKD progression.

Fibroblastic growth factor 23 (FGF23) is a hormone secreted primarily by bone. FGF23 is elevated in the serum of chronic kidney disease (CKD) patients, but the exact mechanism is not well known. Klotho is identified as an aging suppressor, which is mainly expressed in the kidney, and the level of soluble Klotho is negatively associated with FGF23 in CKD. The aim of this study was to investigate the effect and possible mechanism of Klotho on FGF23 synthesis in osteoblast-like UMR-106 cells. UMR-106 cells were divided into five groups: (i) control group; (ii) β-glycerophosphate (β-GP) group; (iii) β-GP + Klotho group; (iv) β-GP+ lithium chloride (LiCl, a Wnt/β-catenin pathway agonist) group; and (v) β-GP + Klotho + LiCl group. Subsequently, UMR-106 cells were cultured for 72 h, and the expression of FGF23, P-glycogen synthase kinase-3β (P-GSK-3β), and glycogen synthase kinase-3β(GSK-3β) were measured with Western blot analysis. The mRNA levels of FGF23 and the Wnt/β-catenin pathway target gene c-myc were determined with RT-qPCR. The results showed that β-GP induced increased expression of FGF23 mRNA and protein. Compared with the β-GP group, expression of FGF23 mRNA and protein expression were downregulated in the β-GP + Klotho group. In addition, β-GP induced increased expression of P-GSK-3β/GSK-3β and c-myc, which were all downregulated in the β-GP + Klotho group. Moreover, the expression of FGF23, P-GSK-3β/GSK-3β, and c-myc mRNA were upregulated when treated with LiCl. These results demonstrate that soluble Klotho suppresses FGF23 synthesis in osteoblast-like UMR-106 cells. The mechanism of this suppression may be partially through the inhibition of the Wnt/β-catenin pathway.

Glucocorticoids (GCs) are commonly used in the treatment of nephrotic syndrome. However, high doses and long periods of GC therapy can result in severe side effects. The present study aimed to selectively deliver albumin‑methylprednisolone (MP) nanoparticles towards glomerular podocytes, which highly express the specific neonatal Fc receptor (FcRn) of albumin. Bovine serum albumin (BSA) was labeled with a fluorescent dye and linked with modified MP via an amide bond. The outcome nanoparticle named BSA633‑MP showed a uniform size with a diameter of approximately 10 nm and contained 12 drug molecules on average. The nanoconjugates were found to be stable at pH 7.4 and acid‑sensitive at pH 4.0, with approximately 72% release of the MP drug after 48 h of incubation. The nanoparticle demonstrated a 36‑fold uptake in receptor‑specific cellular delivery in the FcRn‑expressing human podocytes compared to the uptake in the non-FcRn-expressing control cells. Co‑localization further confirmed that uptake of the nanoconjugates involved receptor‑mediated endocytosis followed by lysosome associated transportation. In vitro cellular experiments indicated that the BSA633‑MP ameliorated puromycin aminonucleoside‑induced podocyte apoptosis. Moreover, in vivo fluorescence molecular imaging showed that BSA633-MP was mainly accumulated in the liver and kidney after intravenous dosing for 24 h. Collectively, this study may provide an approach for the effective and safe therapy of nephrotic syndrome.

Paraoxonase (PON) enzymes possess antioxidant properties and protect against cardiovascular diseases. As a member of PON family, PON3 is primarily synthesized in the liver and poorly investigated. This study aimed to examine the expression of PON3 in human hepatocellular carcinoma (HCC) and investigate the clinical significance and biological function of PON3 in HCC patients. We first analyzed PON3 expression in 50 paired HCC samples (HCC tissues vs matched para-cancerous tissues) and 160 clinical HCC specimens by using immunohistochemistry (IHC). Our results showed that the expression of PON3 was downregulated in HCC and significantly associated with tumor-node-metastasis (TNM) stage, tumor size, and tumor number. Kaplan-Meier survival and Cox regression analyses showed that PON3 was an independent prognostic factor for overall survival (OS) and time to recurrence (TTR). Finally, we aimed to reveal the biological function of PON3 in HCC growth and metastasis, and our results showed that overexpression of PON3 potently inhibited growth and metastasis of HCC. Collectively, our study demonstrated that PON3 exhibited tumor-suppressive effects toward HCC and it might serve as a novel prognostic marker in HCC.

The aim of the present study was to investigate the effect of the serum of patients with secondary hyperparathyroidism (SHPT) on endothelial cells and to examine the protective effect and the possible mechanism of Klotho. A total of three types of mixed serum from 15 patients with SHPT scheduled for parathyroidectomy, 10 chronic kidney disease (CKD) patients at stage 5 without SHPT and 15 healthy volunteers were collected. Initially, human umbilical vein endothelial cells (HUVECs) were incubated in vitro with the three types of serum and levels of proliferation were compared by assessing viable cell numbers with cell counting kit-8 (CCK-8). Subsequently, HUVECs were divided into three groups: Control group (healthy serum medium), SHPT group (SHPT serum) and Klotho treatment group (SHPT serum and Klotho). The proliferative and apoptotic levels of endothelial cells were evaluated by CCK-8 and flow cytometry, respectively. The levels of extracellular signal-regulated kinase (ERK1/2) and phosphorylated forms of ERK1/2 (p-ERK1/2) were detected using western blotting (with or without ERK1/2 inhibitor PD98059). The synthesis of nitric oxide (NO) was measured using the nitrate reduction method. The proliferation of HUVECs was inhibited by the serum from SHPT patients and CKD-5 patients without SHPT and the inhibitory effects of the SHPT serum were the most marked (P

Fibroblastic growth factor 23 (FGF23) is a hormone secreted primarily by bone. FGF23 is elevated in the serum of chronic kidney disease (CKD) patients, but the exact mechanism is not well known. Klotho is identified as an aging suppressor, which is mainly expressed in the kidney, and the level of soluble Klotho is negatively associated with FGF23 in CKD. The aim of this study was to investigate the effect and possible mechanism of Klotho on FGF23 synthesis in osteoblast-like UMR-106 cells. UMR-106 cells were divided into five groups: (i) control group; (ii) β-glycerophosphate (β-GP) group; (iii) β-GP + Klotho group; (iv) β-GP+ lithium chloride (LiCl, a Wnt/β-catenin pathway agonist) group; and (v) β-GP + Klotho + LiCl group. Subsequently, UMR-106 cells were cultured for 72 h, and the expression of FGF23, P-glycogen synthase kinase-3β (P-GSK-3β), and glycogen synthase kinase-3β(GSK-3β) were measured with Western blot analysis. The mRNA levels of FGF23 and the Wnt/β-catenin pathway target gene c-myc were determined with RT-qPCR. The results showed that β-GP induced increased expression of FGF23 mRNA and protein. Compared with the β-GP group, expression of FGF23 mRNA and protein expression were downregulated in the β-GP + Klotho group. In addition, β-GP induced increased expression of P-GSK-3β/GSK-3β and c-myc, which were all downregulated in the β-GP + Klotho group. Moreover, the expression of FGF23, P-GSK-3β/GSK-3β, and c-myc mRNA were upregulated when treated with LiCl. These results demonstrate that soluble Klotho suppresses FGF23 synthesis in osteoblast-like UMR-106 cells. The mechanism of this suppression may be partially through the inhibition of the Wnt/β-catenin pathway.

We looked for differentially expressed MicroRNAs (miRNAs) in Immunoglobulin A nephropathy (IgAN). Forty-eight miRNAs were identified through the initial screening phase (2 IgAN pools vs. 1 normal control (NC) pool) using quantitative reverse transcription polymerase chain reaction (qRT-PCR) based Exiqon panel (miRCURY-Ready-to-Use-PCR-Human-panel-I + II-V1.M). By qRT-PCR, these miRNAs were further assessed in the training (32 IgAN VS. 31 NCs) and testing stages (51 IgAN VS. 51 NCs). The renal pathological lesions of patients with IgAN were evaluated according to Lee's grading system. We discovered a plasma miRNA signature including four up-regulated miRNAs (miR-148a-3p, miR-150-5p, miR-20a-5p and miR-425-3p) and the areas under the receiver operating characteristic (ROC) curve (AUC) were 0.80 and 0.76 for the training and testing stage, respectively. The expression of the four miRNAs in IgAN grade I–II subgroups (according to Lee's grading system) was obviously higher than that in IgAN grade III-V (P

Renal fibrosis is a hallmark feature of chronic kidney disease, which is reflected by proliferation and migration of interstitial fibroblasts and extracellular matrix (ECM) accumulation. β-Aminoisobutyric acid (BAIBA) is recently demonstrated to exert a protective role from metabolic diseases. However, whether and how BAIBA on fibroblast activation and renal fibrosis response to angiotensin II (Ang II) remains largely obscure. Herein, we showed that BAIBA significantly depressed the proliferation and migration of NRK-49F cells in vitro. Treatment with Ang II remarkably up-regulated the expressions of fibronectin (FN), collagen 1 (COL 1), α-smooth muscle actin (α-SMA), interleukin-17 (IL-17) and nicotinamide adenine dinucleotide phosphate oxidase (NOX2)-derived reactive oxygen species (ROS) production in cultured NRK-49F cells. Pretreatment with BAIBA almost blocked Ang II-induced ECM production and IL-17-mediated oxidative stress in NRK-49F cells. BAIBA treatment ameliorates fibroblasts activation and renal fibrosis in rat obstructed kidneys involving inhibition of Ang II/IL-17/ROS signaling transduction, which may be considered as a therapeutic candidate for fibrosis-related diseases.

Podocyte injury may contribute to the pathogenesis of diabetic nephropathy (DN), but the underlying mechanism of hyperglycemia induced podocyte damage is not fully understood. The Ras GTPase-activating-like protein IQGAP1 is associated to the slit diaphragm proteins and the actin cytoskeleton in podocyte. Here, we studied IQGAP1 expression alterations in human DN biopsies and extracellular signal-regulated kinase (ERK)-dependent pathways of IQGAP1 expression in podocyte under high glucose (HG) media. In vivo, analysis of renal biopsies from patients with DN revealed a significant reduction in IQGAP1 expression compared to controls. In vitro, IQGAP1 mRNA and protein expression were observed to decline under HG media at 48 h. But phosphorylation of ERK1/2 was activated under HG media at 24 h and 48 h. However, HG-induced downregulation of IQGAP1 protein was attenuated by specific ERK1/2 activation inhibitor PD98059. Taken together, these results highlight the importance of IQGAP1 in DN, and suggest that IQGAP1 expression in podocyte under HG media is modulated by the ERK1/2 pathway, which may lead to the future development of therapies targeting IQGAP1 dysfunction in podocytes in DN.

BACKGROUND Hyperphosphatemia is associated with up-regulation of the extracellular matrix formation in vascular smooth muscle cells (VSMCs) and increased risk of cardiovascular disease. In the present study, the role of transforming growth factor-β1 (TGF-β1) in the production of fibronectin (FN) in vascular smooth muscle cells in high-phosphate environments was evaluated. METHODS Rat VSMCs were stimulated by high levels of phosphate or TGF-β1 in vitro. Levels of FN, TGF-β1, and TGF-β1 type I receptor (TβRI) proteins were measured by Western blot and immunostaining. Levels of active TGF-β1 in the supernatant of the culture medium were detected by ELISA. RESULTS Production of FN was increased after VSMCs were incubated under high-phosphate conditions (2.5 mmol/L) for 12 hours. TGF-β1 (1 ng/mL) increased FN levels in cells as early as 3 hours after the start of treatment. Both TGF-β1 and TβRI were significantly up-regulated after 3-6 hours of stimulation with high phosphate. When VSMCs were pretreated with TGF-β1 neutralization antibody (10 µg/mL) for 30 minutes, induction of FN stimulated by high levels of phosphate was largely attenuated. CONCLUSION TGF-β1 plays a critical role in the pathogenesis of high-phosphate-induced FN production in VSMCs in vitro.

To investigate the effects of phosphonoformic acid (PFA) and sevelamer hydrochloride (Renagel) on renal type IIa sodium-dependent phosphate cotransporter (NaPi-2) mRNA expression in hyperphosphatemia rats.Thirty rats were randomly divided into five groups based on the diet for 2 weeks after 5/6 nephrectomy (Nx): Nx + high-phosphate (HP; 1.2% P) diet; Nx + low-phosphate (LP; 0.2% P) diet; HP + PFA (injected with 0.15 g/kg PFA daily); HP + Saline (injected with the same amount of saline daily); and HP + Renagel (2%) group. Another 12 rats were sham operated and divided into Sham + HP and Sham + LP groups. Serum ionized calcium, phosphorus (P), and intact parathyroid hormone (iPTH) were measured on days 2, 7, and 14. Serum 1,25(OH)2D3 was measured on day 14 and NaPi-2 mRNA levels were assayed by RT-PCR.PFA decreased iPTH level but had no effect on NaPi-2 mRNA expression. Renagel decreased serum P and iPTH levels, but upregulated renal NaPi-2 mRNA expression.Both PFA and Renagel are effective drugs to decrease iPTH level and they might be potential candidates for treatment of clinical secondary hyperparathyroidism. Renagel can also decrease serum P and upregulate renal NaPi-2 mRNA expression.

SUMMARY: Aim: Vascular access is the lifeline of haemodialysis patients and radial-cephalic fistula is the preferred type of access. We investigated vascular calcification in uraemia radial arteries and compared it with clinical parameters. Methods: Artery specimens from 30 end-stage renal disease patients were collected, examined calcification by von Kossa and Alizarin red staining. Expression of α-smooth muscle actin (α-SMA) and the main component of bone matrix, osteopontin (OP) were detected by immunohistochemistry. Results: In uraemia vessels, calcification was mainly located in the medial layer. Nineteen (63.33%) patients had no evidence of calcification, six (20%) had mild/moderate calcification and five (16.66%) had severe calcification. Upregulation of OP and diminished expression of α-SMA occurred in the medial layer, especially in the area of severe calcification. The calcification score, decreased expression of α-SMA and upregulation of OP were positively correlated with older age, serum calcium, serum phosphorus and calcium × phosphorus product (P

Renal thrombotic microangiopathy (TMA) is an uncommon vascular complication of severe hypertension. Until now, its clinical-pathological characteristics and renal survival have been unclear. Twenty-one patients with biopsy-proven renal TMA and with severe or malignant hypertension were retrospectively studied. All the patients exhibited severe hypertension, with systolic blood pressure at 200-280 mmHg and diastolic pressure at 110-180 mmHg. No patients had hemorrhagic manifestations. Elevated lactate dehydrogenase and thrombocytopenia were found in 6 and 5 patients, respectively. Significant proteinuria (3 g/day) was present in 2 patients and microscopic hematuria in 18 patients. All patients presented with renal insufficiency (creatinine 3.1+/-2.1 mg/dL). The level of von Willebrand factor:antigen (vWF:Ag) in patients was not significantly higher than that in the healthy subjects, while the ADAMTS13 (a disintegrin and metalloprotease, with thrombospondin-1-like domains) activity was not significantly lower than that in the healthy subjects. Renal histology showed a TMA involving preglomerular arterioles and/or interlobular arteries characterized by fibrin deposits and vascular wall sclerosis. Fibrin glomerular microthrombi were not observed in these patients. Four patients required hemodialysis upon admission for severe acute renal failure. On follow-up, 3 patients had recovered normal renal function and 14 had mild renal insufficiency (creatinine 1.8+/-0.3 mg/dL), while 4 patients still required persistent hemodialysis. In conclusion, compared with patients having hemolytic uremic syndrome/thrombocytopenic purpura, our patients showed a low incidence of thrombocytopenia and better renal outcome.

Objective To evaluate the effects of different concentrations of phosphate on calcium deposition and osteocalcin level in cultured bovine aortic smooth muscle cell, investigate the mechanism of hyperphosphatemia to evoke calcification of vascular smooth muscle cell and observe the effects of phosphonoformic acid(PFA) in different concentrations on vascular calcification. Methods The bovine aortic smooth muscle cells (BASMC) were cultured. Calcium deposition and the expression of osteocalcin of BASMC in different concentrations of phosphate (1.5 mmol/L and 2.0 mmol/L) and PFA were determined by o-cresolphthalein complexone and radioimmunity methods, respectively. Osteocalcin mRNA expressions were determined by RT-PCR. Results After six or nine days of BASMC cultured, the calcium deposition in Pi 2.0 mmol/L group was more than that in Pi 1.5 mmol/L group[(77.187 ±11.692)μg/(mg•protein) vs(25.768 ±1.750)μg/(mg•protein), P Conclusion Hyperphosphate may directly promote calcium deposition and the osteocalcin expression of BASMCs. It may be a new explanation for the phenomenon of vascular calcification in hyperphosphatemic conditions. Hyperphosphatemia is an independent factor to stimulate vascular calcification. PFA can inhibit calcium deposition and osteocalcin expression induced by elevated phosphate. PFA may be a new medicine to treat vascular calcification induced by elevated phosphate.

Objective. To investigate the role and possible mechanism ofα-Klotho in the calcification and the osteogenic transition of cultured VSMCs.Methods. VSMCs were culturedin vitroand divided into 5 groups, each using a different medium: (1) control; (2)β-GP; (3)β-GP + Klotho; (4)β-GP + LiCl; (5)β-GP + Klotho + LiCl. Calcium deposits were visualized using Alizarin Red S staining. The calcium concentrations were determined by the o-cresolphthalein complexone method. BMP2, Runx2 andβ-catenin levels were estimated by western blotting, and the level ofα-SMA was determined by using immunofluorescence at day 12.Results.β-GP induced an increase in the expression of BMP2, Runx2, andβ-catenin. The calcium content increased, and the expression ofα-SMA decreased. Alizarin Red S staining was positive under the high phosphorus conditions. BMP2, Runx2, andβ-catenin levels and the calcium content decreased when the cells were cultured with rmKlotho; however, the levels of each were upregulated after treatment with the LiCl.Conclusions. Klotho can ameliorate the calcification and osteogenic transition of VSMCs induced byβ-GP. The mechanism of Klotho in preventing calcification in VSMCs may be partially mediated by the inhibition of the Wnt/β-catenin signaling pathway.

Functionally graded materials (FGM) open the promising approach for bone tissue repair. In this study, a novel functionally graded hydroxyapatite (HA) bioceramic with micrograin and nanograin structure was fabricated. Its mechanical properties were tailored by composition of micrograin and nanograin. The dynamic mechanical analysis (DMA) indicated that the graded HA ceramics had similar mechanical property compared to natural bones. Their cytocompatibility was evaluated via fluorescent microscopy and MTT colorimetric assay. The viability and proliferation of rabbit bone marrow mesenchymal stem cells (BMSCs) on ceramics indicated that this functionally graded HA ceramic had better cytocompatibility than conventional HA ceramic. This study demonstrated that functionally graded HA ceramics create suitable structures to satisfy both the mechanical and biological requirements of bone tissues.

Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosis of liver, lung and kidney by regulating the expression of many profibrogenic cytokines and extracellular matrix (e.g., fibronectin). However, few available reports elucidated whether the SGK1 is involved in the pathogenesis of peritoneal fibrosis (PF) in patients with peritoneal dialysis (PD). So far, there is no study about the interaction between the statins and SGK1 in PMC. The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway. Cultured HPMC were divided into groups of control, high-glucose peritoneal dialysis solution (HGPDS), HGPDS with fluvastatin (10−8 mol/L ~ 10−6 mol/L) or GSK650394 10−5 mol/L (the competitive inhibitor of SGK1), fluvastatin 10−6 mol/L or GSK650394 10−5 mol/L alone. The expression of SGK1 and FN was detected by RT-PCR, western immunoblotting or ELISA. Compared with the control, the mRNA and protein expression of SGK1 and FN increased significantly in HPMC treated with HGPDS (p

At present, the small diameter thin-walled steel tube has been widely used as pipeline in aerospace, military, nuclear industry and other important fields. In order to guarantee the steel tube without leakage in service, so it is necessary to inspect the defect accurately. Many experts and scholars have done a lot of research on this issue. As we know, ultrasonic testing is commonly used to detect a workpiece before, during and after testing. This paper surveys the ultrasonic inspection technology for small diameter thin-walled tube, including some theories of ultrasonic testing, algorithms be used in this subject, the components of the testing system. And then, the development trends and some suggestion of the ultrasonic inspection technology for small diameter thin-walled tube will be discussed.

The aim of the paper is to discuss the method for lightning early warning. The methods involve a few ways. Firstly, the signals of electric field before lightning are detected by atmospheric electric apparatus. Then, the signals of electric field before lightning are decomposed with the algorithm of Empirical Mode Decomposition (EMD). Compared with the signals in sunny days, the frequency and energy features of each mode are proposed. The results show that the algorithm of Empirical Mode Decomposition is able to distinguish the activity of electric field before lightning. The method could be used for lightning early warning about 30 minutes.