Malic enzyme 1 is important for uterine decidualization in response to progesterone/cAMP/PKA/HB-EGF pathway.

Malic enzyme 1 (Me1), a member of the malic enzymes involving in glycolytic pathway and citric acid cycle, is essential for the energy metabolism and maintenance of intracellular redox balance state, but its physiological role and regulatory mechanism in the uterine decidualization are still unknown. Current study showed that Me1 was strongly expressed in decidual cells, and could promote the proliferation and differentiation of stromal cells followed by an accelerated cell cycle transition, indicating an importance of Me1 in the uterine decidualization. Silencing of Me1 attenuated NADPH generation and reduced GR activity, while addition of NADPH improved the defect of GR activity elicited by Me1 depletion. Further analysis found that Me1 modulated intracellular GSH content via GR. Meanwhile, Me1 played a role in maintaining mitochondrial function as indicated by these observations that blockadge of Me1 led to the accumulation of mitochondrial O2- level and decreased ATP production and mtDNA copy numbers accompanied with defective mitochondrial membrane potential. In uterine stromal cells, progesterone induced Me1 expression through PR-cAMP-PKA pathway. Knockdown of HB-EGF might impede the regulation of progesterone and cAMP on Me1. Collectively, Me1 is essential for uterine decidualization in response to progesterone/cAMP/PKA/HB-EGF pathway and plays an important role in preventing mitochondrial dysfunction.

Removal characteristics of dissolved organic matter and membrane fouling in ultrafiltration and reverse osmosis membrane combined processes treating the secondary effluent of wastewater treatment plant.

The widespread implementation of municipal wastewater treatment and reuse must first ensure the safety of reused wastewater. The effluent of the municipal wastewater treatment plant contains a large amount of dissolved organic matter (DOM), which adversely affects the reuse of wastewater. In this study, the ultrafiltration (UF) + reverse osmosis (RO) process was used to treat the secondary effluent from wastewater treatment plants. The relationship between the removal performance, membrane fouling of the UF + RO process, and DOM removal characteristics of influent were studied. The results show that DOM can be removed effectively by UF + RO process. The UF mainly removes DOM with a molecular weight greater than 10 kDa, while RO has a significant removal effect on low-molecular-weight DOM, which mainly causes UF and RO membrane fouling. The UF + RO process has a significant removal rate on fulvic acid, humic acid, tyrosine, and tryptophan, and the order is humic acid > fulvic acid > tyrosine > tryptophan. Fulvic acid contributed the most to the UF membrane fouling, while fulvic acid and protein-like proteins contributed mainly to the RO membrane fouling.

Risk Factors for Stillbirth among Pregnant Women Infected with Syphilis in the Zhejiang Province of China, 2010-2016.

BACKGROUND: The World Health Organization estimated that about 1.36 million pregnant women suffered from syphilis in 2008, and nearly 66% of adverse effects occurred in those who were not tested or treated. Syphilis infection is one of the most common maternal factors associated with stillbirth. OBJECTIVE: This study aimed to determine the risk factors for stillbirth among pregnant women infected with syphilis. METHODS: In this retrospective study, data on stillbirth and gestational syphilis from 2010 to 2016 were extracted from the prevention of mother-to-child transmission (PMTCT) program database in the Zhejiang province. A total of 8,724 pregnant women infected with syphilis were included. Multiple logistic regression analysis was performed to determine the degree of association between gestational syphilis and stillbirth. RESULTS: We found that the stillbirth percentage among pregnant women infected with syphilis was 1.7% (152/8,724). Compared with live births, stillbirth was significantly associated with lower maternal age, not being married, lower gravidity, the history of syphilis, nonlatent syphilis stage, higher maternal serum titer for syphilis, inadequate treatment for syphilis, and later first antenatal care visit. In multiple logistic analysis, nonlatent syphilis (adjusted odds ratio (AOR) = 2.03; 95% CI = 1.17, 3.53) and maternal titers over 1 : 4 (AOR = 1.78; 95% CI = 1.25, 2.53) were risk factors for stillbirth, and adequate treatment was the only protective factor for stillbirth (AOR = 0.16; 95% CI = 0.10, 0.25). CONCLUSIONS: Nonlatent syphilis and maternal titers over 1 : 4 were risk factors for stillbirth, and adequate treatment was the only protective factor for stillbirth.

Novel insights into Dhh signaling in antler chondrocyte proliferation and differentiation: Involvement of Foxa.

The desert hedgehog (Dhh) is crucial for spermatogenesis and Leydig cell differentiation, but little is known regarding its physiological function in cartilage. In this study, Dhh mRNA was abundant in antler chondrocytes, where it advanced cell proliferation concomitant with accelerated transition from the G1 to the S phase and induced elevation of the hypertrophic chondrocyte markers, Col X and Runx2. Silencing of Ptch1 resulted in appreciable Smo accumulation and enhanced rDhh stimulation of Smo, whose impediment by cyclopamine obscured the proliferative function of Dhh and alleviated its guidance of chondrocyte differentiation. Further analysis evidenced the noteworthy positive action of Smo in the bridging between Dhh and Gli transcription factors. Obstruction of Gli1 by GANT58 caused the failed stimulation of Col X and Runx2 by rDhh. Analogously, siRNA against Gli1-3 hindered chondrocyte differentiation in the context of rDhh. Simultaneously, Gli transcription factors mediated the regulation of Dhh on Foxa1, Foxa2, and Foxa3, whose knockdown impaired chondrocyte differentiation. Attenuation of Foxa antagonized the augmentation of Col X and Runx2 generated by rDhh. Collectively, Dhh signaling through its target Foxa appears to induce antler chondrocyte proliferation and differentiation.

[Value of galactose-deficient IgA1 in the early diagnosis of Henoch-Schönlein purpura nephritis in children].

OBJECTIVE: To explore the value of galactose-deficient IgA1 (Gd-IgA1) in the early diagnosis of Henoch-Schönlein purpura nephritis (HSPN) in children. METHODS: A total of 67 hospitalized children who were definitely diagnosed with HSPN between January and April 2018 and 58 hospitalized children with Henoch-Schönlein purpura (HSP) were enrolled in the study. Twenty children undergoing routine physical examinations served as controls. The levels of serum and urine Gd-IgA1 were determined using ELISA. The receiver operating characteristic curve was used to analyze the value of serum Gd-IgA1 and urine Gd-IgA1/urine creatinine ratio in the diagnosis of HSPN. RESULTS: The level of serum Gd-IgA1 and urine Gd-IgA1/urine creatinine ratio in children with HSP or HSPN were significantly higher than those in healthy control group (P<0.01), with a significantly greater increase observed in children with HSPN (P<0.01). Serum Gd-IgA1 ≥1 485.57 U/mL and/or urine Gd-IgA1/urine creatinine ratio ≥105.74 were of favorable value in the diagnosis of HSPN. During the six-month follow-up of the 49 children with HSP, the incidence of HSPN was 47% (23/49), which included a 100% incidence in children with serum Gd-IgA1 ≥1 485.57 U/mL and a 73% incidence in children with urine Gd-IgA1/urine creatinine ratio ≥105.74. CONCLUSIONS: Serum and urine Gd-IgA1 is of favorable clinical value in the early diagnosis of HSPN.

WNT4 acts downstream of BMP2 to mediate the regulation of ATRA signaling on RUNX1 expression: Implications for terminal differentiation of antler chondrocytes.

Although ATRA is involved in regulating the proliferation and differentiation of chondrocytes, its underlying mechanism remains unknown. Here we showed that ATRA could stimulate the proliferation of antler chondrocytes and expression of COL X and MMP13 which were two well-known markers for hypertrophic chondrocytes. Silencing of CRABP2 prevented the induction of ATRA on chondrocyte terminal differentiation, while overexpression of CRABP2 exhibited the opposite effects. CYP26A1 and CYP26B1 weakened the sensitivity of antler chondrocytes to ATRA. Further analysis evidenced that ATRA might induce chondrocyte terminal differentiation and modulate the expression of BMP2, WNT4, and RUNX1 through RARα/RXRα. Knockdown of BMP2 enhanced the induction of ATRA on the expression of COL X and MMP13, whereas overexpression of BMP2 abrogated this effectiveness. WNT4 might mediate the effects of ATRA and BMP2 on chondrocyte terminal differentiation. Dysregulation of BMP2 impaired the regulation of ATRA on WNT4 expression. Administration of ATRA to antler chondrocytes transfected with RUNX1 siRNA failed to induce the differentiation. Conversely, rRUNX1 strengthened the stimulation of ATRA on the expression of COL X and MMP13. Simultaneously, RUNX1 was a downstream effector of BMP2 and WNT4 in chondrocyte terminal differentiation. Moreover, WNT4 might play an important role in the crosstalk between BMP2 and RUNX1. Attenuation of BMP2 or WNT4 enhanced the interaction between ATRA and RUNX1, while constitutive expression of BMP2 or WNT4 reversed the regulation of ATRA on RUNX1. Collectively, WNT4 may act downstream of BMP2 to mediate the effects of ATRA on the terminal differentiation of antler chondrocytes through targeting RUNX1.

ATRA Signaling Regulates the Expression of COL9A1 through BMP2-WNT4-RUNX1 Pathway in Antler Chondrocytes.

Although all-trans retinoic acid (ATRA) is involved in the regulation of cartilage growth and development, its regulatory mechanisms remain unknown. Here, we showed that ATRA could induce the expression of COL9A1 in antler chondrocytes. Silencing of cellular retinoic acid binding protein 2 (CRABP2) could impede the ATRA-induced upregulation of COL9A1, whereas overexpression of CRABP2 presented the opposite effect. RARα agonist Am80 induced the expression of COL9A1, whereas treatment with RARα antagonist Ro 41-5253 or RXRα small-interfering RNA (siRNA) caused an obvious blockage of ATRA on COL9A1. In antler chondrocytes, CYP26A1 and CYP26B1 weakened the sensitivity of ATRA to COL9A1. Simultaneously, Bone morphogenetic protein 2 (BMP2) and WNT4 mediated the regulation of ATRA on COL9A1 expression. Knockdown of WNT4 could abrogate the inhibitory effect of BMP2 overexpression on COL9A1. Conversely, constitutive expression of WNT4 reversed the upregulation of COL9A1 elicited by BMP2 siRNA. Together these data indicated that WNT4 might act downstream of BMP2 to mediate the effect of ATRA on COL9A1 expression. Further analysis evidenced that attenuation of runt-related transcription factor 1 (RUNX1) could prevent the stimulation of ATRA on COL9A1 expression, while exogenous rRUNX1 further enhanced this effectiveness. Moreover, RUNX1 might serve as an intermediate to mediate the regulation of BMP2 and WNT4 on COL9A1 expression. Collectively, ATRA signaling might regulate the expression of COL9A1 through BMP2-WNT4-RUNX1 pathway.

[Comparison of therapeutic effects of prednisone combined with mycophenolate mofetil versus cyclosporin A in children with steroid-resistant nephrotic syndrome].

OBJECTIVE: To compare the therapeutic effects of prednisone combined with mycophenolate mofetil (MMF) versus cyclosporin A (CsA) in children with steroid-resistant nephrotic syndrome (SRNS). METHODS: The clinical data of 164 SRNS children who were treated with prednisone combined with MMF or CsA between January 2004 and December 2013 were collected, and the clinical effect of prednisone combined with MMF (MMF group, 112 children) or CsA (CsA group, 52 children) was analyzed retrospectively. RESULTS: At 1 month after treatment, the CsA group had a significantly higher remission rate than the MMF group (67.3% vs 42.9%; P<0.05). At 3 months after treatment, the CsA group also had a significantly higher remission rate than the MMF group (78.8% vs 63.3%; P<0.05). The 24-hour urinary protein excretion in both groups changed significantly with time (P<0.05) and differed significantly between the two groups (P<0.05). There were no serious adverse events in the two groups. CONCLUSIONS: Prednisone combined with MMF or CsA is effective and safe for the treatment of SRNS in children, and within 3 months of treatment, CsA has a better effect than MMF.

[Significance of trace deposition of immunoglobulin M in glomerular mesangium in children with minimal change nephrotic syndrome].

OBJECTIVE: To study the significance of trace immunoglobulin M (IgM) deposits in glomerular mesangium in children with minimal change primary nephrotic syndrome (PNS). METHODS: One hundred and six children who were clinically diagnosed with PNS and pathologically diagnosed with minimal change disease (MCD) and trace deposition of IgM in renal tissues were enrolled as subjects. Eighty-one PNS children with MCD but no deposition of immune complexes were used as the control group. The clinical characteristics and efficacies of glucocorticoids and immunosuppressants were retrospectively analyzed in the two groups. All patients were given full-dose prednisone by oral administration, and patients with glucocorticoid resistance or frequent relapses were additionally given immunosuppressants. RESULTS: The incidence of glucocorticoid resistance in the IgM deposit group was significantly higher than that in the control group (27.2% vs 12.3%; P<0.05). The incidence of frequent relapses in the IgM deposit group was also significantly higher than that in the control group (48.1% vs 10.4%; P<0.05). The complete remission rate for glucocorticoid-resistant patients treated with prednisone combined with mycophenolate mofetil (MMF) was 68% and 62% respectively in the IgM deposit and control groups (P>0.05). The relapse frequency in patients with frequent relapses was significantly reduced in both groups after treatment with prednisone and MMF in combination (P<0.05). CONCLUSIONS: Trace deposition of IgM in renal tissues may be an important factor for glucocorticoid resistance and frequent relapses in PNS children with MCD. Prednisone combined with MMF may be a better choice in the treatment of patients with glucocorticoid resistance or frequent relapses.

[Clinical characteristics of children with an initial onset of IgA nephropathy with nephrotic syndrome].

OBJECTIVE: To study the clinical characteristics of children with an initial onset of IgA nephropathy with nephrotic syndrome and compare them with children with primary nephrotic syndrome, in order to provide a theoretical basis for the differential diagnosis of the two diseases. METHODS: Fifty children diagnosed with an initial onset of IgA nephropathy with nephrotic syndrome were included in this study. Seventy-two children diagnosed with an initial onset of primary nephrotic syndrome served as the control group. The clinical and laboratory examination characteristics were compared between the two groups. RESULTS: The IgA nephropathy group had significantly higher incidence rates of gross haematuria, microscopic haematuria, hypertension, acute kidney injury, low serum high-density lipoprotein cholesterol, anemia, low serum complement C4, steroid resistance, and nephritis-type nephrotic syndrome and a significantly lower incidence of elevated serum IgE compared with the control group (P<0.05). There were significant differences in serum creatinine, serum uric acid, serum total cholesterol, serum high-density lipoprotein cholesterol, serum IgE, serum complement C4, and hemoglobin levels between the IgA nephropathy and the control groups (P<0.05). The thresholds of serum IgE (<131.2 IU/mL) and high-density lipoprotein cholesterol (<1.35 mmol/L) were reference parameters in the differential diagnosis of IgA nephropathy with nephrotic syndrome and primary nephrotic syndrome. CONCLUSIONS: Children with IgA nephropathy presenting nephrotic syndrome manifest mainly as nephritis type and steroid-resistant type in the clinical classification. Cinical manifestations accompanied by serum levels of high-density lipoprotein cholesterol and IgE are helpful for differential diagnosis of IgA nephropathy presenting nephrotic syndrome and primary nephrotic syndrome.

Effects of PTHrP on chondrocytes of sika deer antler.

Parathyroid-hormone-related peptide (PTHrP) is an important regulator of chondrocyte differentiation in growth plates but little is known about its role in deer antler cartilage. The aim of the present study was to use the deer antler as a model to determine the possible role of PTHrP in regulating chondrocyte differentiation of deer antler. PTHrP and its receptor PTH1R mRNA were highly expressed in the perichondrium and cartilage of sika deer antler, as shown by in situ hybridization. Chondrocytes of deer antler were identified by toluidine blue staining of glycosaminoglycan and immunocytochemical staining of type II collagen (Col II). Treatment with PTHrP (1-34) reduced the expression of prehypertrophic chondrocyte marker Col IX and hypertrophic chondrocyte marker Col X. In order to confirm the mechanism of action of PTHrP, we initially examined the expression of cyclin D1, Bcl-2 and runt-related transcription factor 2 (Runx2) in sika deer antler by in situ hybridization and found that cyclin D1, Runx2 and Bcl-2 mRNA were also expressed in antler chondrocytes. Exogenous PTHrP induced the expression of cyclin D1 and Bcl-2 mRNA by various signalling pathways, whereas it inhibited Runx2 expression through PKA, p38MAPK, MEK and PI3K signalling pathways. Thus, PTHrP might promote the proliferation of antler chondrocytes and prevent their differentiation; it might furthermore influence the growth and development of sika deer antler.

Effects of PTHrP on expression of MMP9 and MMP13 in sika deer antler chondrocytes.

Deer antlers are the only mammalian appendages to display an annual cycle of full regeneration. However, little is known about the molecular mechanisms of antler regeneration. Our previous study has demonstrated that parathyroid hormone-related peptide (PTHrP) can promote proliferation of antler chondrocytes and inhibit its differentiation, but the mechanism underlying such regulation is not fully understood. We have determined the role of PTHrP on the mRNA expression of matrix metalloproteinase-9 (MMP9) and MMP13 in the antler chondrocytes. The possible pathways that transduce PTHrP effects were examined. In situ hybridization showed that MMP9 and MMP13 were mainly localized in the dermal fibroblasts, perichondrium, and cartilage in the sika deer antler, of which MMP9 and MMP13 were highly expressed in the chondrocytes. Exogenous PTHrP could inhibit the expression of MMP9 and MMP13 in the antler chondrocytes. The inhibitory effect of PTHrP on MMP9 was abolished by JNK inhibitor, SP600125, while P38MAPK inhibitor SB203850 and PKC inhibitor GF109203X could rescue the inhibitory effect of PTHrP on MMP13. The results suggest that PTHrP can inhibit MMP9 expression by JNK signaling pathway and MMP13 expression by p38MAPK and PKC signaling pathways in the antler chondrocytes. Thus PTHrP is involved in the control of antler chondrocytes maturation and cartilage matrix degradation.

Suppressive effects of oral administration of heat-killed Lactobacillus acidophilus on T helper-17 immune responses in a bovine ß-lactoglobulin-sensitized mice model.

The present study was planned to explore the effect of Lactobacillus (L.) acidophilus on the T helper-17 (Th17) immune response in a mouse model of ß-lactoglobulin (ß-lg) allergy. Bovine ß-lg sensitised BALB/c mice were orally administered with different doses of heat-killed L. acidophilus (low, 5×10(7) colony forming unit (CFU); medium, 5×10(8) CFU; high, 5×10(9) CFU) in 200 µL of phosphate buffered saline (PBS) three times a week, starting from 1 week before ß-lg sensitisation for 4 weeks. After the allergen challenge, the numbers of blood eosinophils and neutrophils were examined by light microscope; the levels of cytokine (interleukin (IL)-12, IL-4, tumor growth factor (TGF)-ß, IL-10, IL-6 and IL-17A), total immunoglobulin E (IgE) and ß-lg-specific IgE contents in the serum were measured with enzyme-linked immunosorbent assay (ELISA); The mRNA expression levels of TGF-ß, IL-17A,CD25, Foxp3, retinoic acid-related orphan receptor γt (RORγt) and IL-10 were analyzed using real-time polymerase chain reaction (PCR). The results showed that oral administration of L. acidophilus suppressed hypersensitivity responses, attenuated the numbers of inflammatory cells and inhibited IgE production. We found up-regulation of TGF-ß and down-regulation of IL-17A in the serum of L. acidophilus-treated group, along with IL-6 levels was significantly decreased than that of the allergy group (p<0.05). Moreover, the mRNA expression levels of CD25, forkhead box P3 and TGF-ß were significantly higher in the spleen of L. acidophilus-treated group, while the mRNA expression levels of IL-17A, RORγt and IL-10 were significantly lower than that in the allergy group (p<0.05). In conclusion, the suppression of major allergic symptoms by oral administration of L.acidophilus was probably due to improve the regulatory T (Treg)/Th17 balance and inhibit the IL-6 production.

RCCS enhances EOE cell proliferation and their differentiation into ameloblasts.

In this article we report on the culturing of dental enamel organ epithelia (EOE) using a rotary cell culture system (RCCS) bioreactor associated with a cytodex-3 microcarrier. This culture system enhanced the proliferation and differentiation of the EOE into ameloblasts. Primary dental EOE trypsinized from 4-day old post-natal rat pups were cultured in the RCCS associated with Cytodex-3. The results were analyzed in comparison to a conventional plate system (control). Cells grown in RCCS have shown higher viabilities (above 90%) and final cell densities in terms of cells/ml than in the control system. In the case of RCCS, 46±2 manifold increases were obtained, while significantly lower yields of 10.8±2.5 manifod were obtained for control plates. Throughout the experiments, glucose levels were maintained within the accepted physiological range. In this case, LDH levels are kept low (below 150 mmol/ml), which is in accordance with the low cell death observed in the RCCS. Scanning electron microscopy revealed cells that were spread and forming three dimensional aggregates on the surface of cytodex-3. Cells cultured in the RCCS exhibited a stronger positive immunofluorescence staining for ameloblastin than those in control plates. RT-PCR results revealed that cells cultured in RCCS have higher amelogenin mRNA levels compared to controls. We have done an exploratory study on biological characteristics and self-assembling of epithelium cellula intersitialis, which demonstrated that the special 3D environment enhanced the rat dental EOE cell proliferation and differentiation into ameloblasts. The study has revealed that RCCS could be used to study the reaction of the EOE cells, tooth enamel organ cells and mesenchymal cells under the spacial 3D culture system, which will also provide a novel hypothesis for dental regeneration.

HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-Ca2+-FOXO1 pathway.

Polycystic ovarian syndrome (PCOS) is one of the most prevalent endocrinopathies and the leading cause of anovulatory infertility, but its pathogenesis remains elusive. Although HB-EGF is involved in ovarian cancer progression, there is still no clarity about its relevance with PCOS. The present study exhibited that abundant HB-EGF was noted in follicular fluid from PCOS women, where it might induce the granulosa cells (GCs) production of more estrogen via the elevation of CYP19A1 expression after binding to EGFR. Furthermore, HB-EGF transduced intracellular downstream cAMP-PKA signaling to promote the phosphorylation of JNK and ERK whose blockage impeded the induction of HB-EGF on estrogen secretion. Meanwhile, HB-EGF enhanced the accumulation of intracellular Ca2+ whose chelation by BAPTA-AM abrogated the stimulation of HB-EGF on FOXO1 along with an obvious diminishment for estrogen production. cAMP-PKA-JNK/ERK-Ca2+ pathway played an important role in the crosstalk between HB-EGF and FOXO1. Treatment of GCs with HB-EGF resulted in mitochondrial dysfunction as evinced by the reduction of ATP content, mtDNA copy number and mitochondrial membrane potential. Additionally, HB-EGF facilitated the opening of mitochondrial permeability transition pore via targeting BAX and raised the release of cytochrome C from mitochondria into the cytosol to trigger the apoptosis of GCs, but this effectiveness was counteracted by estrogen receptor antagonist. Collectively, HB-EGF might induce mitochondrial dysfunction and GCs apoptosis through advancing estrogen hypersecretion dependent on cAMP-PKA-JNK/ERK-Ca2+-FOXO1 pathway and act as a promising therapeutic target for PCOS.

The reconstruction of lung alveolus-like structure in collagen-matrigel/microcapsules scaffolds in vitro.

This study attempted to use collagen-Matrigel as extracellular matrix (ECM) to supply cells with three-dimensional (3D) culture condition and employ alginate-poly-l-lysine-alginate (APA) microcapsules to control the formation of alveolus-like structure in vitro. We tested mice foetal pulmonary cells (FPCs) by immunohistochemistry after 2D culture. The alveolus-like structure was reconstructed by seeding FPCs in collagen-Matrigel mixed with APA microcapsules 1.5 ml. A self-made mould was used to keep the structure from contraction. Meanwhile, it provided static stretch to the structure. After 7, 14 and 21 days of culture, the alveolus-like structure was analysed histologically and immunohistochemically, or by scanning transmission electron microscopy (TEM). We also observed these structures under inverted phase contrast microscope. The expression of pro-surfactant protein C (SpC) was detected by reverse transcription-polymerase chain reaction (RT-PCR). We obtained fibroblasts, epithelial cells and alveolar type II (AE2) cells in FPCs. In the reconstructed structure, seeding cells surrounding the APA microcapsules constructed alveolus-like structures, the size of them ranges from 200 to 300 µm. In each reconstructed lung tissue sheet, microcapsules had integrity. Pan-cytokeratin, vimentin and SpC positive cells were observed in 7- and 14-day cultured structures. TEM showed lamellar bodies of AE2 cells in the reconstructed tissues whereas RT-PCR expressed SpC gene. Primary mice FPCs could form alveolus-like structures in collagen-Matrigel/APA microcapsules engineered scaffolds, which could maintain a differentiated state of AE2 cells.

Parachute mitral valve associated with reticular chordae tendineae in an adult: case report.

BACKGROUND: Parachute mitral valve with reticular chordae tendineae is an extremely rare anomaly. CASE PRESENTATION: We present a case of parachute mitral valve associated with distinctive reticular chordae tendineae in an adult. It was diagnosed from the echocardiogram. The patient was referred for surgery. Valve analysis showed thickened mitral valve leaflets and commissures. The chordae tendinae were lengthy and thick. All the chordae tendinae merged into a solitary papillary muscle. A distinctive reticular fibrous tissue was found on mitral valve apparatus as the chordae tendinae intermixed each other. The only functional communication between the left atrium and the left ventricle was through the reticular spaces. This anomaly was considered to be unrepairable and was replaced with a mechanical valve. CONCLUSIONS: An extremely rare and unique case of parachute mitral valve associated with reticular chordae tendineae was reported. Mitral valve replacement is a reasonable choice in patients with parachute mitral valve with reticular chordae tendineae.

Conservative treatment of left ventricular pseudoaneurysm after mitral valve replacement due to early left ventricular rupture: a case report.

BACKGROUND: Left ventricular pseudoaneurysm due to early left ventricle rupture is a serious complication after cardiac surgery. Urgent surgery is recommended in most cases with a high mortality rate. Conservative treatment of a left ventricular pseudoaneurysm due to early left ventricle rupture is very rare. CASE PRESENTATION: We present a 61-year-old woman with left ventricular pseudoaneurysm after mitral valve replacement due to early left ventricle rupture. This patient was treated in a conservative approach. This patient had an uneventful recovery. She was in good condition and remained asymptomatic 3.5 years after mitral valve surgery. CONCLUSION: This case suggests that medical treatment left ventricular pseudoaneurysm patients has a limited but acceptable role in selected and unusual circumstances.

Predictive value of circulating sex hormone-binding globulin for gestational diabetes: a meta-analysis.

Aim: To detect predictive value of preconception or early pregnancy sex hormone-binding globulin (SHBG) for subsequent gestational diabetes mellitus (GDM). Materials & methods: We searched Embase, Medline, PubMed, Web of Science and Cochrane library up to January 2020. Studies assessing diagnostic performance of SHBG for GDM diagnosed by well-defined diagnostic criteria using oral glucose tolerance test. Results: Totally seven studies with 1947 women were included and 247 were diagnosed as GDM. SHBG had a combined diagnostic odds ratio of 6.68 (95% CI: 4.58-9.74), sensitivity of 0.70 (95% CI: 0.51-0.84), specificity of 0.74 (95% CI: 0.52-0.88), positive likelihood ratio of 2.49 (95% CI: 1.73-3.57) and negative likelihood ratio of 0.37 (95% CI: 0.23-0.61). The area under the summary receiver operating characteristic curve was 0.78 (95% CI: 0.74-0.82). Conclusion: SHBG had a predictive value for GDM and might improve GDM screening. However, heterogeneity between studies warrants more research into this topic.

[Relationship between integrin-linked kinase expression and renal glomerular damage in children with Henoch-Schnlein purpura nephritis].

OBJECTIVE: Recent studies have shown that integrin linked kinase (ILK) plays an important role in the pathogenesis and development of some kidney diseases. This study aimed to investigate the relationship between ILK and renal glomerular damage in children with Henoch schonlein purpura nephritis (HSPN). METHODS: One hundred and eighty eight HSPN children (aged 3 to 17 years) were assigned to five groups according to the classification of the International Study of Kidney Disease in Children (ISKDC): grade < or = IIa (n = 62), grade IIb (n = 42), grade IIIa (n = 29), grade IIIb (n = 40) and grade > or = IV (n = 15). Fifteen children with basement membrane nephropathy served as the control group. ILK expression on glomeruli was ascertained by immunohistochemical staining. The relationships of ILK expression on glomeruli with glomerular histopathologic lesions and urinary protein excretions were examined. RESULTS: The positive areas of ILK expression on glomeruli in the control, grade < or = IIa, grade IIb, grade IIIa, grade IIIb and grade > or = IV groups were (3.35 + or - 1.01)%, (4.88 + or - 1.13)%, (9.64 + or - 1.36)%, (11.27 + or - 1.68)%, (17.42 + or -3.0)% and (20.62 + or - 2.32%), respectively. There were significant differences in the ILK expression between groups (p<0.01). ILK expression on glomeruli increased with increased urinary protein excretions. There were significant differences in the ILK expression in children with different urinary protein excretions (p<0.01). CONCLUSIONS: ILK might be involved in the process of renal glomerular histopathologic damage and the production of proteinuria in children with HSPN.