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Gestational diabetes mellitus (GDM) increases the risk of fetal heart malformations, though little is known about the mechanism of hyperglycemia-induced heart malformations. Thus, we aimed to reveal the global landscape of miRNAs and mRNAs in GDM-exposed fetoplacental arterial endothelial cells (dAECs) and establish regulatory networks for exploring the pathophysiological mechanism of fetal heart malformations in maternal hyperglycemia. Gene Expression Omnibus (GEO) datasets were used, and identification of differentially expressed miRNAs (DEMs) and genes (DEGs) in GDM was based on a previous sequencing analysis of dAECs. A miRNA-mRNA network containing 20 DEMs and 65 DEGs was established using DEMs altered in opposite directions to DEGs. In an in vivo study, we established a streptozotocin-induced pregestational diabetes mellitus (PGDM) mouse model and found the fetal cardiac wall thickness in different regions to be dramatically increased in the PGDM grouValidation of DEMs and DEGs in the fetal heart showed significantly upregulated expression of let-7e-5p, miR-139-5p and miR-195-5p and downregulated expression of SGOL1, RRM2, RGS5, CDK1 and CENPA. In summary, we reveal the miRNA-mRNA regulatory network related to fetal cardiac development disorders in offspring, which may shed light on the potential molecular mechanisms of fetal cardiac development disorders during maternal hyperglycemia., graphic abstract

Renal injury in lupus nephritis (LN) does not manifest as one uniform entity. The clinical presentation, management, and prognosis of membranous LN (MLN) differ from that of the proliferative LN (PLN). Differentiating the molecular mechanisms involved in MLN and PLN and discovering the reliable biomarkers for early diagnosis and target therapy are important. We compared the kidney protein expression patterns of 11 pure MLN and 12 pure PLN patients on formalin-fixed paraffin-embedded (FFPE) kidney tissues using label-free liquid chromatography-mass spectrometry (LC-MS) for quantitative proteomics analysis. FunRich software was used to identify proteins in differentially expressed pathways. Quantitative comparisons of differentially expressed proteins in each patient were further analyzed based on protein intensity levels determined by LC-MS. The protein–protein interaction (PPI) network of the differentially expressed genes (DEGs) was established through Search Tool for the Retrieval of Interacting Genes database (STRING) website, visualized by Cytoscape. A total of 5112 proteins were identified. In total, 12 significantly upregulated (fold change ≥2, p < 0.05) proteins were identified in the MLN group and 220 proteins (fold change ≥2, p < 0.05) were upregulated in the PLN group. Further analysis showed that the most significant upregulated pathway involved in MLN was histone deacetylase (HDAC) class I pathway, and the three most significant upregulated pathways in PLN were interferon signaling, interferon gamma signaling, and the immune system. Next, we selected sirtuin-2 (SIRT2) in MLN, and vascular cell adhesion protein 1 (VCAM1) and Bcl-xl in PLN for further mass spectrometry (MS) intensity and PPI analysis. SIRT2 expression was significantly increased in the MLN group compared with the PLN group, and VCAM1, Bcl-xl expression was significantly increased in the PLN group compared with the MLN group, based on MS intensity. These results may help to improve our understanding of the underlying molecular mechanisms of MLN and PLN and provide potential targets for the diagnosis and treatment of different subclasses of LN.

OBJECTIVE: To investigate the clinical treatment outcomes and the changes of the outcomes over time in extremely preterm twins in Guangdong Province, China. METHODS: A retrospective analysis was performed for 269 pairs of extremely preterm twins with a gestational age of

Background With the increase in extremely low birth weight (ELBW) infants, their outcomes received special attention. However, in China, studies of the outcomes of ELBW infants are rare. Methods The hospitalized records of ELBW infants discharged from twenty-six neonatal intensive care units were reviewed and analyzed. Results A total of 2575 ELBW infants were enrolled and the overall survival rate was 55.11%. From 2008 to 2017, the number of ELBW infants increased rapidly from 91 to 466, and the survival rate improved steadily from 41.76–62.02%. The survival rate rose with increasing BW, the ascending level of regional economic development and specialist hospitals. The incidence of complications was neonatal respiratory distress syndrome (85.2%), bronchopulmonary dysplasia (63.7%), retinopathy of prematurity (39.3%), intraventricular hemorrhage (29.4%), necrotizing enterocolitis (12.0%), and periventricular leukomalacia (8.0%). Among the 1156 nonsurvivors, 90.0% of infants died during the neonatal period (≤ 28 days), and the other died after the neonatal period. A total of 768 ELBW infants died after medical care withdrawal, with economic factors and expected outcome being important causes. Conclusion The number of ELBW infants is increasing in China, and the overall survival rate is still low but is improving steadily.

Xanthoceras sorbifolia, an excellent oil-rich woody species, has high comprehensive economic value in edible, medicinal, and ornamental fields. The chemical composition, pharmacological effect, and quality control of X. sorbifolia were introduced, and its development and application were reviewed in this study. As revealed by the previous research, the main chemical constituents of X. sorbifolia were triterpenoids, flavonoids, fatty acids, phenylpropanoids, steroids, phenolic acids, organic acids, etc. It possesses pharmacological effects, such as neuroprotection, bacteriostasis, anti-oxidation, anti-tumor, anti-inflammation, analgesia, anti-HIV, and anti-coagulation. X. sorbifolia is widely applied in medical, food, chemical industry, and other fields, and deserves in-depth research and development.

Summary There is high risk of fetal neurodevelopmental defects in pregestational diabetes mellitus (PGDM). However, the effective mechanism of hyperglycemia-induced neurodevelopmental negative effects, including neural stem cell self-renewal and differentiation, still remains obscure. Neuropoietic cytokines have been shown to play a vital part during nervous system development and in the coordination of neurons and gliocytes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) dysfunction might be related to a reduction of self-protective response in brain malformation induced by hyperglycemia. We therefore evaluated the role of Nrf2 and neuropoietic cytokines in fetal neurodevelopmental defects induced by PGDM and determined the mechanisms involved. Our data reveal that PGDM dramatically impairs the developmental switch of neural stem cells from neurogenesis to gliogenesis, principally under the cooperative mediation of neuropoietic cytokine CNTF and Nrf2 antioxidative signaling. This indicates that CNTF and Nrf2 could be potentially used in the prevention or therapy of neurodevelopmental defects of PGDM offspring., Graphical Abstract, Highlights • Hyperglycemia affects self-renewal ability of neural progenitor cells • Hyperglycemia twists the developmental switch from neurogenesis into gliogenesis • CNTF regulates hyperglycemia-induced imbalance between neurogenesis and gliogenesis • CNTF and Nrf2 co-ordinately regulate neural development through p-STAT3, Molecular Neuroscience; Developmental Neuroscience; Diabetology

Considering the instability and low photoluminescence quantum yield (PLQY) of blue-emitting perovskites, it is still challenging and attractive to construct single crystalline hybrid lead halides with highly stable and efficient blue light emission. Herein, by rationally introducing d10 transition metal into single lead halide as new structural building unit and optical emitting center, we prepared a bimetallic halide of [(NH4 )2 ]CuPbBr5 with new type of three-dimensional (3D) anionic framework. [(NH4 )2 ]CuPbBr5 exhibits strong band-edge blue emission (441 nm) with a high PLQY of 32 % upon excitation with UV light. Detailed photophysical studies indicate [(NH4 )2 ]CuPbBr5 also displays broadband red light emissions derived from self-trapped states. Furthermore, the 3D framework features high structural and optical stabilities at extreme environments during at least three years. To our best knowledge, this work represents the first 3D non-perovskite bimetallic halide with highly efficient and stable blue light emission.

C3 glomerulopathy (C3G) is a rare renal disease characterized by predominant glomerular C3 staining. Complement alternative pathway dysregulation due to inherited complement defects is associated with C3G. To identify novel C3G-related genes, we screened 86 genes in the complement, coagulation and endothelial systems in 35 C3G patients by targeted genomic enrichment and massively parallel sequencing. Surprisingly, the most frequently mutated gene was VWF. Patients with VWF variants had significantly higher proteinuria levels, higher crescent formation and lower factor H (FH) levels. We further selected two VWF variants to transiently express the von Willebrand factor (vWF) protein, we found that vWF expression from the c.1519A > G variant was significantly reduced. In vitro results further indicated that vWF could regulate complement activation, as it could bind to FH and C3b, act as a cofactor for factor I-mediated cleavage of C3b. Thus, we speculated that vWF might be involved in the pathogenesis of C3G.

Malignant peripheral nerve sheath tumor (MPNST) is a rare tumor that can develop on the lining of nerves and within the network of nerve fibers in different organs, and it is commonly found in the head and neck, limbs, and trunk. These tumors can occur in patients of any age. They most commonly occur in adults aged 20 to 50 years; however, fewer cases of this tumor in children have been reported. To date, no neonatal case of MPNST in the nasal cavity has been reported. Here, we report the case of a 4-day-old female newborn who presented with a nasal mass that re-enlarged after surgery and was diagnosed as MPNST of the nasal cavity on the basis of pathological results. This is the first report of MPNST in the nasal cavity of a neonate. Differential diagnosis and treatment of nasal masses have been proposed in the related literature.

In recent years, organic-inorganic hybrid metal halides have emerged as a highly promising class of semiconducting light emitting diodes (LEDs) due to their fascinating photoluminescence properties. Here, by specifically selecting different organic cations as templates, a series of new hybrid cuprous halides have been solvothermally prepared, namely [Me-Py]CuI2 (1), [(Me)2-DABCO]Cu2I4 (2), [Me-MePy]Cu2I3 (3), and [H2DABCO]Cu3X5 (X = I (4) and Br (5)). These hybrid cuprous halides feature one-dimensional (1D) [CuI2]-, [Cu2I3]- and [Cu3X5]2- (X = Br, I) chains surrounded and charge-balanced by organic cations. Under UV photoexcitation, these hybrid cuprous halides exhibit strong tunable photoluminescence from cyan (480 nm) to red (675 nm) emissions with large Stokes shifts (345 nm). The intrinsic nature of PL emissions is also investigated based on temperature-dependent PL emission, lifetime, photoluminescence quantum efficiencies, etc.

There is high risk of fetal neurodevelopmental defects in pregestational diabetes mellitus (PGDM). However, the effective mechanism of hyperglycemia-induced neurodevelopmental negative effects, including neural stem cell self-renewal and differentiation, still remains obscure. Neuropoietic cytokines have been shown to play a vital part during nervous system development and in the coordination of neurons, gliocytes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) dysfunction might be related to a reduction of self-protective response in brain malformation induced by hyperglycemia. We therefore evaluated the role of Nrf2 and neuropoietic cytokines in fetal neurodevelopmental defects induced by PGDM and determined the mechanisms involved. Our data reveal that PGDM dramatically impairs the developmental switch of neural stem cells from neurogenesis to gliogenesis, principally under the cooperative mediation of neuropoietic cytokine CNTF and Nrf2 antioxidative signaling. This indicates that CNTF and Nrf2 could be potentially used in the prevention or therapy of neurodevelopmental defects of PGDM offspring.

Pregestational diabetes mellitus (PGDM) enhances the risk of fetal neurodevelopmental defects. However, the mechanism of hyperglycaemia-induced neurodevelopmental defects is not fully understood. In this study, several typical neurodevelopmental defects were identified in the streptozotocin-induced diabetes mouse model. The neuron-specific class III beta-tubulin/forkhead box P1-labelled neuronal differentiation was suppressed and glial fibrillary acidic protein-labelled glial cell lineage differentiation was slightly promoted in pregestational diabetes mellitus (PGDM) mice. Various concentrations of glucose did not change the U87 cell viability, but glial cell line-derived neurotrophic factor expression was altered with varying glucose concentrations. Mouse maternal hyperglycaemia significantly increased Tunel(+) apoptosis but did not dramatically affect PCNA(+) cell proliferation in the process. To determine the cause of increased apoptosis, we determined the SOD activity, the expression of Nrf2 as well as its downstream anti-oxidative factors NQO1 and HO1, and found that all of them significantly increased in PGDM fetal brains compared with controls. However, Nrf2 expression in U87 cells was not significantly changed by different glucose concentrations. In mouse telencephalon, we observed the co-localization of Tuj-1 and Nrf2 expression in neurons, and down-regulating of Nrf2 in SH-SY5Y cells altered the viability of SH-SY5Y cells exposed to high glucose concentrations. Taken together, the data suggest that Nrf2-modulated antioxidant stress plays a crucial role in maternal hyperglycaemia-induced neurodevelopmental defects.

Corneal diseases are currently the second main cause of blindness in China. Although most of the corneal blindness could be treated by corneal transplantation, only about 10 000 operations were carried out each year owing to the severe shortage of corneal donors and limited eye bank programs. A feasible cornea donation program was established through the organization of the Red Cross, and in situ corneal removal techniques were developed to avoid conflicts with Chinese traditions of keeping the deceased intact. The number of donated corneas, which had a safe and secure quality, increased significantly year by year.

Diabetes mellitus in pregnancy has been known to affect the embryonic development of various systems, including cardiovascular and nervous systems. However, whether this disease could have a negative impact on embryonic respiratory system remains controversial. In this study, we demonstrated that pregestational diabetes mellitus (PGDM)-induced defects in lung development in mice are mainly characterized by the changes in the morphological structure of the lung. Immunostaining and Western blotting showed that proliferation increased and apoptosis decreased in PGDM. Hyperglycaemia caused pulmonary tissue fibrationas manifested by an increase in Masson staining and decorin expression in PGDM lungs, and the immunofluorescent pro-SPC+ type II pulmonary epithelial cell number was decreased. The alteration of pulmonary epithelial cell differentiation might be due to hyperglycaemia-activated Wnt signalling and suppressed GATA6 expression in PGDM mouse lung tissues and MLE-12 cells. The treatment of MLE-12 cells with high glucose in the presence/absence of XAV939 or su5402 further proved that hyperglycaemia suppressed the expression of GATA6 and pro-SPC by activating Wnt signalling and induced the expression of decorin, α-SMA and TGF-β by activating Fgf signalling. Therefore, in this study, we revealed that hyperglycemia induced dysfunctional pulmonary cell apoptosis and proliferation, as well as pulmonary myofibroblast hyperplasia, which contributed to the formation of aberrant structure of alveolar walls. Furthermore, the hyperglycaemia also inhibited the differentiation of pulmonary epithelial cells through the canonical Wnt and Fgf signalling, and the alteration of Fgf and Wnt signalling activated TGF-β, which would promote the AECII EMT process.

PURPOSE To evaluate the outcomes of femtosecond laser-assisted deep lamellar keratoplasty (FDLK) in treating advanced keratoconus. METHODS In the management of keratoconus in advanced stages, 89 patients (94 eyes) received FDLK, and 100 patients (100 eyes) underwent vacuum trephine-assisted deep anterior lamellar keratoplasty (DALK). Visual acuity, corneal curvature, and central corneal thickness were measured. The follow-up duration was 1 year. RESULTS The best-corrected visual acuity (logMAR) was 0.23 ± 0.15 at 6 months and 0.08 ± 0.07 at 1 year in the FDLK group, which was significantly better than that in the vacuum trephination group (0.30 ± 0.10 and 0.13 ± 0.08, respectively). The mean curvature was 43.24 ± 5.25 D in the eyes treated by FDLK and 48.31 ± 3.68 D in the eyes treated by vacuum trephine-assisted DALK at 1 year. The mean astigmatism in the FDLK group was lower as compared with the vacuum trephination group. In the FDLK group, the graft adhered well with the recipient, which was 72 ± 17 μm in thickness. In the vacuum trephination group, the remaining peripheral corneal thickness was 153 ± 25 μm. The epithelium healed at 3 ± 2 days and 6 ± 2 days in both groups, respectively. CONCLUSIONS The vacuum trephine remains as a major surgical tool for deep lamellar keratoplasty. The precise control of side cut in the diameter and depth in the FDLK procedure can help to accelerate the healing of epithelium and the improvement of visual acuity early after surgery for advanced keratoconus, compared with vacuum trephine-assisted DALK.

Juvenile trees of Malus xiaojinensis produce leaves with three to five lobes; however, adult trees do not. Thus, M. xiaojinensis serves as a model plant for studies on rejuvenation of woody perennials. To better understand effects of in vitro culture, number of passages, and plant growth regulators on observed somaclonal variations in leaf morphology, total levels of DNA methylation and expression of associated genes, including DRM2 and MET1, of apical shoot meristems of M. xiaojinensis, were evaluated. Following 17 passages of nodal stem segment culture and four passages of callus culture, levels of DNA methylation and expression of DRM2 and MET1 were determined, and found to decrease from the 11th passage of nodal stem segment culture or adventitious bud culture and from the first passage of callus culture. Levels of DNA methylation increased with increasing 2,4-dichlorophenoxyacetic acid concentrations, but decreased significantly with increasing 6-benzyladenine (BA) concentrations. Expression of DRM2 and MET1 in regenerated plantlets were negatively correlated with BA concentrations in the culture medium. Overall, less than 11 passages of nodal stem segment or adventitious bud culture did not contribute to incidence of somaclonal variation, even in the presence of low concentrations of BA (

Objective The aim of this study was to evaluate renal arteriosclerotic lesions in patients with lupus nephritis and investigate their associations with clinical and pathological characteristics, especially cardio-vascular features. Design A retrospective cohort study. Participants Seventy-nine patients with renal biopsy-proven lupus nephritis, diagnosed between January 2000 and June 2008 from Peking University First Hospital. Results In clinico-pathological data, patients with arteriosclerosis had higher ratio of hypertension and more severe renal injury indices compared with patients with no renal vascular lesions. More importantly, patients with renal arteriosclerosis had worse cardiac structure and function under transthoracic echocardiographic examination. Patients with renal arteriosclerosis tend to have higher ratios of combined endpoints compared with those of no renal vascular lesions, although the difference didn’t reach statistical meanings (P = 0.104). Conclusion Renal arteriosclerotic lesion was common and associated with vascular immune complex deposits in lupus nephritis. It might have a certain degree of association with poor outcomes and cardiovascular events, which needs further explorations.

Rationale C3 glomerulonephritis (C3GN) and complement-mediated hemolytic uremic syndrome (HUS) both result from the abnormal regulation of the complement system. A significant number of patients with C3GN or complement-mediated HUS have mutations of more than 1 complement protein. This discovery has had a major impact on identifying the underlying cause of familial C3GN or complement-mediated HUS. Patient concerns We report the cases of 2 brothers (herein referred to as patient II-1 and patient II-9), both with complement disorders that differed in their clinical and genetic features. Diagnoses Patient II-1 clinically presented with nephrotic syndrome and acute kidney injury and pathologically presented with C3GN combined with thrombotic microangiopathy (TMA) and subacute tubulointerstitial nephritis. Meanwhile, patient II-9 clinically presented with HUS and pathologically presented with TMA combined with acute severe tubular injury. Interventions Screenings for genetic mutations contributed to complement system dysregulation were performed on patient II-1. Outcomes The genome sequencing identified that patient II-1 had a heterozygous mutation in the C3 gene (c.C1774T/p.R592W). Nine other relatives of the brothers were checked for this C3 mutation and only the daughter of patient II-1 (herein referred to as patient III-2) carried it, but so far, she does not have any clinical manifestations of kidney disease. Lessions Family members with a dysregulation of the complement alternative pathway may differ in its clinical and genetic features.

To observe the clinical effects of 10%, 30% lactate clearance rate and early goal-directed therapy (EGDT) as 6-hour resuscitation goals directing treatment in septic shock patients with severe pneumonia.In this randomized, perspective study, septic shock patients with severe pneumonia were divided into control group and experimental group, which included 10% lactate clearance rate group and 30% lactate clearance rate group, adopting random number method. The control group was treated with 6-hour EGDT strategy, and the experimental groups were treated with 10% lactate clearance rate protocol and 30% lactate clearance rate protocol respectively, beside the EGDT.There were 19 patients in control group, and 43 patients in experimental group, which included 22 patients in 10% lactate clearance rate group and 21 patients in 30% lactate clearance rate group. Patients were well matched by basic features. After 48 hours, the acute physiology and chronic health evaluation II (APACHE II ) score of both 10% lactate clearance rate group (13.76 ± 6.00, P0.05) and 30% lactate clearance rate group (13.60 ± 6.18, P0.05) were lower than that of control group (18.15 ± 6.62). There were no differences in time of mechanical ventilation (hours) between control group and experimental group (10% group 136.90 ± 100.02, 30% group 97.00 ± 75.20, control group 152.32 ± 96.51, P0.05). The length in intensive care unit (ICU, days) of 10% and 30% lactate clearance rate groups were significantly shorter than control group (10% group 7.94 ± 6.00, 30% group 7.51 ± 3.99, control group 11.31 ± 5.97, both P0.05). The three groups had no differences in 7-day mortality rate (10% group 18.18%, 30% group 14.29%, control group 21.05%, all P0.05), but the 28-day mortality of 10% and 30% lactate clearance rate groups were significantly lower than control group (10% group 36.36%, 30% group 28.57%, control group 63.16%), especially in 30% lactate clearance rate group (P0.05).For the septic shock patients with severe pneumonia, prompt archiving EGDT strategy and 6-hour lactate clearance more than 30% were associated with an optimal outcome.

To investigate the effect of continuous blood purification (CBP) in patients with severe sepsis, and to evaluate the change in endothelial cell function in patients with severe sepsis during CBP therapy.According to random principle, 45 patients were divided into control group (n=22) and CBP group (n=23). All patients of both groups received routine treatment according to international guidelines 2008 for management of severe sepsis, but the patients in the CBP group also received continuous veno-venous hemofiltration (CVVH) for 72 hours, the ultrafiltrate volume was 40 ml×kg(-1)×h(-1). Blood gas analysis was done before and 24 hours and 72 hours after CVVH therapy. The activated protein C (APC), soluble intercellular adhesion molecule-1 (sICAM-1) and von Willebrand factor (vWF) were measured. Also the length of stay in intensive care unit (ICU), time of mechanical ventilation, and death rate of patients in 28 days were observed.Compared with control group, the length of stay in ICU (days) and length of use of ventilator (days) in CBP group were shorter (9.12±3.07 vs. 11.64±4.82, 5.52±3.48 vs. 8.02±5.25, both P0.05), and the death rate in 28 days was lower [13.0% (3/23) vs. 40.9% (9/22), P0.05]. After therapy, patients in CBP group showed more reduction in the APACHEII score compared with control group (3.96±4.07 vs. 1.68±2.43, P0.05). Patients in control group showed less change in APC, sICAM-1 and vWF. APC in CBP group increased at 72 hours, and sICAM-1 and vWF of CBP group respectively decreased at 24 hours or 72 hours, while the APC (μg/L) and vWF (mg/L) at 72 hours showed significant change compared with that of the control group (15.12±7.57 vs. 10.01±5.83, 1.58±0.73 vs. 2.64±1.34, P0.05 and P0.01). In patients who died in 28 days (12 patients) there were little changes in APC, sICAM-1 and vWF, while patients who lived for 28 days (33 patients), showed significantly more reduction in sICAM-1 (μg/L) and vWF (mg/L, 61.03±45.58 vs. 104.64±71.08, 1.88±1.21 vs. 2.70±0.95,both P0.05). The APC value (μg/L) was increased after treatment in patients who survived for 28 days (13.55±7.11 vs. 10.37±7.60, P0.01).CBP therapy can protect endothelial cell function and ameliorate dysfunction, and it reduces the severity of the severe sepsis as well as improves the outcome of patients with severe sepsis.

Hyperglycemia in diabetic mothers enhances the risk of fetal cardiac hypertrophy during gestation. However, the mechanism of high-glucose-induced cardiac hypertrophy is not largely understood. In this study, we first demonstrated that the incidence rate of cardiac hypertrophy dramatically increased in fetuses of diabetic mothers using color ultrasound examination. In addition, human fetal cardiac hypertrophy was successfully mimicked in a streptozotocin (STZ)-induced diabetes mouse model, in which mouse cardiac hypertrophy was diagnosed using type-M ultrasound and a histological assay. PH3 immunofluorescent staining of mouse fetal hearts and in vitro-cultured H9c2 cells indicated that cell proliferation decreased in E18.5, E15.5 and E13.5 mice, and cell apoptosis in H9c2 cells increased in the presence of high glucose in a dose-dependent manner. Next, we found that the individual cardiomyocyte size increased in pre-gestational diabetes mellitus mice and in response to high glucose exposure. Meanwhile, the expression of β-MHC and BMP-10 was up-regulated. Nkx2.5 immunofluorescent staining showed that the expression of Nkx2.5, a crucial cardiac transcription factor, was suppressed in the ventricular septum, left ventricular wall and right ventricular wall of E18.5, E15.5 and E13.5 mouse hearts. However, cardiac hypertrophy did not morphologically occur in E13.5 mouse hearts. In cultured H9c2 cells exposed to high glucose, Nkx2.5 expression decreased, as detected by both immunostaining and western blotting, and the expression of KCNE1 and Cx43 was also restricted. Taken together, alterations in cell size rather than cell proliferation or apoptosis are responsible for hyperglycemia-induced fetal cardiac hypertrophy. The aberrant expression of Nkx2.5 and its regulatory target genes in the presence of high glucose could be a principal component of pathogenesis in the development of fetal cardiac hypertrophy.

We investigate 750 nm and 532 nm dual-wavelength laser for applications in the internet of things. A kind of optical maser is developed, in which the semiconductor module outputs the 808 nm pump light and then it goes into a double-clad Nd3+ :YAG monocrystal optical fiber through the intermediate coupler and forms a 1064 nm laser. The laser outputs come from both left and right terminals. In the right branch, the laser goes into the right cycle polarization LinNbO3 (PPLN) crystal through the right coupler, produces the optical parametric oscillation and forms the signal light λ1 (1500 nm), the idle frequency light λ2 (3660.55 nm), and the second-harmonic of the signal light λ3 (750 nm). These three kinds of light and the pump light λ4 together form the frequency matching and the quasi-phase matching, then the four-wave mixing occurs to create the high-gain light at wavelength 750 nm. Meanwhile, in the left branch, the laser goes into the left PPLN crystal through the left coupler, engenders frequency doubling and forms the light at wavelength 532 nm. That is to say, the optical maser provides 750 nm and 532 nm dual-wavelength laser outputting from two terminals, which is workable.