Exploring the Use of "Honorary Transition Metals" To Push the Boundaries of Planar Hypercoordinate Alkaline-Earth Metals.

The quest for planar hypercoordinate atoms (phA) beyond six has predominantly focused on transition metals, with dodecacoordination being the highest reported thus far. Extending this bonding scenario to main-group elements, which typically lack d orbitals despite their larger atomic radius, has posed significant challenges. Intrigued by the potentiality of covalent bonding formation using the d orbitals of the heavier alkaline-earth metals (Ae = Ca, Sr, Ba), the so-called "honorary transition metals", we aim to push the boundaries of planar hypercoordination. By including rings formed by 12-15 atoms of boron-carbon and Ae centers, we propose a design scheme of 180 candidates with a phA. Further systematic screening, structural examination, and stability assessments identified 10 potential clusters with a planar hypercoordinate alkaline-earth metal (phAe) as the lowest-energy form. These unconventional structures embody planar dodeca-, trideca-, tetradeca-, and pentadecacoordinate atoms. Chemical bonding analyses reveal the important role of Ae d orbitals in facilitating covalent interactions between the central Ae atom and the surrounding boron-carbon rings, thereby establishing a new record for coordination numbers in the two-dimensional realm.

InnTl4-nH+ (n = 0∼4): Tetracoordinate Hydrogen in a Planar Fashion?

The recent report of planar tetracoordinate hydrogen (ptH) in In4H+ is very intriguing in planar hypercoordinate chemistry. Our high-level CCSD(T) calculations revealed that the proposed D4h-symmetric ptH In4H+ is a first-order saddle point with an imaginary frequency in the out-of-plane mode of the hydrogen atom. In fact, at the CCSD(T)/aug-cc-pV5Z/aug-cc-pV5Z-PP level, the C4v isomer, with the H atom located 0.70 Å above the In4 plane, is 0.5 kcal/mol more stable than the D4h isomer. However, given the small perturbation from planarity and essentially barrierless C4v ↔ D4h ↔ C4v transition, the vibrationally averaged structure can still be considered as a planar. Extending our exploration to the InnTl4-nH+ (n = 0-3) systems, we found all these ptH structures, except for In2Tl2H+, to be the putative global minimum. The single σ-delocalized interaction between the central hydrogen atom and InnTl4-n ligand rings proves pivotal in establishing planarity and aromaticity and conferring substantial stability upon these rule-breaking ptH species.

BeM(CO)3- (M = Co, Rh, Ir) and BeM(CO)3 (M = Ni, Pd, Pt): Triply bonded terminal beryllium in zero oxidation state.

We perform detailed potential energy surface explorations of BeM(CO)3- (M = Co, Rh, Ir) and BeM(CO)3 (M = Ni, Pd, Pt) using both single-reference and multireference-based methods. The present results at the CASPT2(12,12)/def2-QZVPD//M06-D3/def2-TZVPPD level reveal that the global minimum of BeM(CO)3- (M = Co, Rh, Ir) and BePt(CO)3 is a C3v symmetric structure with an 1A1 electronic state, where Be is located in a terminal position bonded to M along the center axis. For other cases, the C3v symmetric structure is a low-lying local minimum. Although the present complexes are isoelectronic with the recently reported BFe(CO)3- complex having a B-Fe quadruple bond, radial orbital-energy slope (ROS) analysis reveals that the highest occupied molecular orbital (HOMO) in the title complexes is slightly antibonding in nature, which bars a quadruple bonding assignment. Similar weak antibonding nature of HOMO in the previously reported BeM(CO)4 (M = Ru, Os) complexes is also noted in ROS analysis. The bonding analysis through energy decomposition analysis in combination with the natural orbital for chemical valence shows that the bonding between Be and M(CO)3q (q = -1 for M = Co, Rh, Ir and q = 0 for M = Ni, Pd, Pt) can be best described as Be in the ground state (1S) interacting with M(CO)30/- via dative bonds. The Be(spσ) → M(CO)3q σ-donation and the complementary Be(spσ) ← M(CO)3q σ-back donation make the overall σ bond, which is accompanied by two weak Be(pπ) ← M(CO)3q π-bonds. These complexes represent triply bonded terminal beryllium in an unusual zero oxidation state.

[Tetrahydropalmatine inhibiting mitophagy through ULK1/FUNDC1 pathway to alleviate hypoxia/reoxygenation injury in H9c2 cells].

This study explored the specific mechanism by which tetrahydropalmatine(THP) inhibited mitophagy through the UNC-51-like kinase 1(ULK1)/FUN14 domain containing 1(FUNDC1) pathway to reduce hypoxia/reoxygenation(H/R) injury in H9c2 cells. This study used H9c2 cells as the research object to construct a cardiomyocyte H/R injury model. First, a cell viability detection kit was used to detect cell viability, and a micro-method was used to detect lactate dehydrogenase(LDH) leakage to evaluate the protective effect of THP on H/R injury of H9c2 cells. In order to evaluate the protective effect of THP on mitochondria, the chemical fluorescence method was used to detect intracellular reactive oxygen species, intramitochondrial reactive oxygen species, mitochondrial membrane potential, and autophagosomes, and the luciferin method was used to detect intracellular adenosine 5'-triphosphate(ATP) content. Western blot was further used to detect the ratio of microtubule-associated protein 1 light chain 3(LC3) membrane type(LC3-Ⅱ) and slurry type(LC3-Ⅰ) and activated cleaved caspase-3 expression level. In addition, ULK1 expression level and its phosphorylation degree at Ser555 site, as well as the FUNDC1 expression level and its phosphorylation degree of Ser17 site were detected to explore its specific mechanism. The results showed that THP effectively reduced mitochondrial damage in H9c2 cells after H/R. THP protected mitochondria by reducing the level of reactive oxygen species in cells and mitochondria, increasing mitochondrial membrane potential, thereby increasing cellular ATP production, enhancing cellular activity, reducing cellular LDH leakage, and finally alleviating H/R damage in H9c2 cells. Further studies have found that THP could reduce the production of autophagosomes, reduce the LC3-Ⅱ/LC3-Ⅰ ratio, and lower the expression of the apoptosis-related protein, namely cleaved caspase-3, indicating that THP could reduce apoptosis by inhibiting autophagy. In-depth studies have found that THP could inhibit the activation of the ULK1/FUNDC1 pathway of mitophagy and the occurrence of mitophagy by reducing the phosphorylation degree of ULK1 at Ser555 and FUNDC1 at Ser17. The application of ULK1 agonist BL-918 reversely verified the effect of THP on reducing the phosphorylation of ULK1 and FUNDC1. In summary, THP inhibited mitophagy through the ULK1/FUNDC1 pathway to reduce H/R injury in H9c2 cells.

[Ginsenoside Re regulates mitochondrial biogenesis through Nrf2/HO-1/PGC-1α pathway to reduce hypoxia/reoxygenation injury in H9c2 cells].

This article explored the mechanism by which ginsenoside Re reduces hypoxia/reoxygenation(H/R) injury in H9c2 cells by regulating mitochondrial biogenesis through nuclear factor E2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)/peroxisome prolife-rator-activated receptor gamma coactivator-1α(PGC-1α) pathway. In this study, H9c2 cells were cultured in hypoxia for 4 hours and then reoxygenated for 2 hours to construct a cardiomyocyte H/R injury model. After ginsenoside Re pre-administration intervention, cell activity, superoxide dismutase(SOD) activity, malondialdehyde(MDA) content, intracellular reactive oxygen species(Cyto-ROS), and intramitochondrial reactive oxygen species(Mito-ROS) levels were detected to evaluate the protective effect of ginsenoside Re on H/R injury of H9c2 cells by resisting oxidative stress. Secondly, fluorescent probes were used to detect changes in mitochondrial membrane potential(ΔΨ_m) and mitochondrial membrane permeability open pore(mPTP), and immunofluorescence was used to detect the expression level of TOM20 to study the protective effect of ginsenoside Re on mitochondria. Western blot was further used to detect the protein expression levels of caspase-3, cleaved caspase-3, Cyto C, Nrf2, HO-1, and PGC-1α to explore the specific mechanism by which ginsenoside Re protected mitochondria against oxidative stress and reduced H/R injury. Compared with the model group, ginse-noside Re effectively reduced the H/R injury oxidative stress response of H9c2 cells, increased SOD activity, reduced MDA content, and decreased Cyto-ROS and Mito-ROS levels in cells. Ginsenoside Re showed a good protective effect on mitochondria by increasing ΔΨ_m, reducing mPTP, and increasing TOM20 expression. Further studies showed that ginsenoside Re promoted the expression of Nrf2, HO-1, and PGC-1α proteins, and reduced the activation of the apoptosis-related regulatory factor caspase-3 to cleaved caspase-3 and the expression of Cyto C protein. In summary, ginsenoside Re can significantly reduce I/R injury in H9c2 cells. The specific mechanism is related to the promotion of mitochondrial biogenesis through the Nrf2/HO-1/PGC-1α pathway, thereby increasing the number of mitochondria, improving mitochondrial function, enhancing the ability of cells to resist oxidative stress, and alleviating cell apoptosis.

Exosomal microRNAs in tubal fluid may be involved in damage to tubal reproductive function associated with tubal endometriosis.

RESEARCH QUESTION: What is the effect of tubal endometriosis on tubal epithelial ultrastructure and is there a differential expression of exosomal microRNAs (miRNAs) in tubal fluid which may affect tubal infertility? DESIGN: Human fallopian tube epithelium and tubal fluid samples were obtained from patients with and without tubal endometriosis. Scanning electron microscopy and transmission electron microscopy were used to assess ultrastructural changes. Exosomal miRNAs in tubal fluid were extracted for microarray. RESULTS: Epithelial damage was visualized in the tubal endometriosis group using electron microscopy. The number of organelles decreased (P = 0.0314), and organelle structure was destroyed. A total of 14 differentially expressed exosomal miRNAs were detected in tubal fluid (fold change >2 and P < 0.05). Four miRNAs (miR-1273f, miR-5699-5p, miR-6087 and miR-6747-5p) were validated by quantitative real-time polymerase chain reaction. Bioinformatic analysis showed that most of the target genes participated in embryo transport, regulation of cell communication, anatomical structure morphogenesis and immune system processes. CONCLUSIONS: Tubal endometriosis results in damage to the tubal epithelial ultrastructure in human specimens and the presence of differentially expressed exosomal miRNAs in tubal liquid. These findings help to clarify the pathogenesis of tubal endometriosis-associated infertility and the mechanisms driving tubal epithelial ultrastructure damage in tubal endometriosis.

Source apportionment and risk assessment of heavy metals in typical greenhouse vegetable soils in Shenyang, China.

In this study, the concentrations of Cr, Cu, Ni, Pb, Zn, Cd, As, and Hg in the typical greenhouse vegetable soils in Shenyang, Northeast of China, were determined, and the pollution characteristics and primary sources of heavy mental pollution in soil were analyzed. Results showed that the sum of the mean values of eight typical heavy metals in the soil of the greenhouse soils was 219.79 mg/kg. According to the "Chinese Environmental Quality Evaluation Standard for Farmland of Greenhouse Vegetables Production" (HJ/T 333-2006), the concentrations of Cu (33.50 ± 11.99 mg/kg), Cd (0.246 ± 0.156 mg/kg), and Hg (0.214 ± 0.177 mg/kg) exceeded the limit values in 14.29%, 39.29%, and 39.29% of sampling points, respectively. The single factor pollution index and the Nemerow comprehensive pollution index of heavy metal elements showed that most greenhouse soils were at safety, alert, or light pollution levels. The potential ecological risk index (RI = 505.19) showed that 42.86% of the samples were at high or very high risk and Cd and Hg were the main ecological risk factors. Based on the result of correlation analysis, the Positive Matrix Factorization (PMF) differentiated sources of heavy metal pollution in the study area into four components, including fertilizer input, soil parent material, pesticide spraying and raw coal combustion, and plastic film mulching, which accounted for 36.76%, 22.64%, 20.89%, and 19.71%, respectively, of the total sources of heavy metals.

E3 ubiquitin ligase Triad1 promotes neuronal apoptosis by regulating the p53-caspase3 pathway after spinal cord injury.

PURPOSE: Spinal cord injury entails a high risk of major disability, but there is still no effective treatment for this condition. This study aims to explore the neuronal apoptosis after spinal cord injury, which is a key component of secondary injury processes, and plays a critical role in the development of neurological dysfunction. MATERIALS AND METHODS: We studied the expression of the E3 ubiquitin ligase Triad1 and its interaction with p53 in the spinal cord after a spinal cord contusion injury in rats. We explored the regulation function of Triad1 to the neuronal apoptosis through p53-caspase3 pathway in primary neurons. RESULTS: Triad1 was markedly up-regulated in the grey matter one day after injury, and the distribution and time point of Triad1 expression correlated with the presence of apoptotic neurons. Co-immunoprecipitation experiments further demonstrated that Triad1 interacted with p53 after spinal cord injury. Specific siRNA and overexpression plasmids for Triad1 were transfected into primary neurons, and the expression of both p53 and caspase3 was altered following the change of Triad1. CONCLUSIONS: These findings indicate that Triad1 is involved in regulating the pathological process of neuronal apoptosis mediated by p53-caspase3 pathway after spinal cord injury.

Effects of ER-resident and secreted AGR2 on cell proliferation, migration, invasion, and survival in PANC-1 pancreatic cancer cells.

BACKGROUND: Anterior gradient-2 (AGR2) is a proto-oncogene involved in tumorigenesis and cancer progression. AGR2, predominantly localized in the endoplasmic reticulum (ER), is also a secreted protein detected in the extracellular compartment in multiple cancers. However, the biological functions of intracellular and extracellular AGR2 remain to be elucidated. METHODS: Based on the biochemical structure of AGR2 protein, PANC-1 pancreatic cancer cells stably expressing ER-resident or secreted AGR2 were generated by a lentivirus-mediated stable overexpression system. The capacities of cell proliferation, migration, invasion and survival were assessed in PANC-1 stable cells. Moreover, EGFR expression and activation were determined to explore the possible mechanism of AGR2 roles in pancreatic cancer tumorigenesis. RESULTS: It was discovered that secreted AGR2, but not ER-resident AGR2, promotes cell proliferation, migration and invasion of PANC-1 cells. Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment. However, EGFR expression and activation were not found to be involved in AGR2-dependent oncogenic phenotypes in PANC-1 cells. CONCLUSIONS: Secreted AGR2 is predominantly involved in cell proliferation, migration and invasion in PANC-1 pancreatic cancer cells. Both secreted and ER-resident AGR2 contribute to the survival of PANC-1 cells under the challenging conditions. These findings provide insight into how different localizations of AGR2 have contributed to pancreatic cancer growth, metastasis, and drug sensitivity.

milRNApredictor: Genome-free prediction of fungi milRNAs by incorporating k-mer scheme and distance-dependent pair potential.

MicroRNA-like small RNAs (milRNAs) with length of 21-22 nucleotides are a type of small non-coding RNAs that are firstly found in Neurospora crassa in 2010. Identifying milRNAs of species without genomic information is a difficult problem. Here, knowledge-based energy features are developed to identify milRNAs by tactfully incorporating k-mer scheme and distance-dependent pair potential. Compared with k-mer scheme, features developed here can alleviate the inherent curse of dimensionality in k-scheme once k becomes large. In addition, milRNApredictor built on novel features performs comparably to k-mer scheme, and achieves sensitivity of 74.21%, and specificity of 75.72% based on 10-fold cross-validation. Furthermore, for novel miRNA prediction, there exists high overlap of results from milRNApredictor and state-of-the-art mirnovo. However, milRNApredictor is simpler to use with reduced requirements of input data and dependencies. Taken together, milRNApredictor can be used to de novo identify fungi milRNAs and other very short small RNAs of non-model organisms.

Integrated analysis of mRNA and protein expression profiling in tubal endometriosis.

Tubal endometriosis (tubal EM) is a subtype of endometriosis (EM) associated with fallopian tube impairments and infertility. Since the molecular mechanism underlying tubal EM is not clear, we assume that an aberrant transcriptome of fallopian tube epithelium and microenvironment changes caused by cytokines in tubal fluid are possible causes. The aim of this study was to identify potential hub mRNAs/proteins of tubal EM through integrated transcriptomic and proteomic analyses and to elucidate significant pathways, cellular functions, and interaction networks during the initiation and progression of tubal EM. We obtained human fallopian tube epithelium and tubal fluid samples from patients with and without tubal EM. Tubal epithelia were analyzed using microarray, and tubal fluid was analyzed using quantitative label-free LC-MS/MS. We identified differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) and determined common mRNAs/protein. We observed 35 commonly deregulated mRNAs/proteins, and IPA indicated that cellular movement, inflammatory response, and immune cell trafficking were significantly activated during the pathogenesis of tubal EM. We also identified acute phase response signaling pathway activation as a unique pathogenesis signature of tubal EM. Our results demonstrate that an integrated analysis of the transcriptome and proteome has the potential to reveal novel disease mechanisms at a molecular level.

TRPV4 is involved in levonorgestrel-induced reduction in oviduct ciliary beating.

Previous studies revealed the increasing risk of tubal pregnancy following failure of levonorgestrel (LNG)-induced emergency contraception, which was attributed to the reduced ciliary motility in response to LNG. However, understanding of the mechanism of LNG-induced reduction in the ciliary beat frequency (CBF) is limited. The transient receptor potential vanilloid (TRPV) 4 channel is located widely in the female reproductive tract and generates an influx of Ca2+ following its activation under normal physiological conditions, which regulates the CBF. The present study aimed to explore whether LNG reduced the CBF in the Fallopian tubes by modulating TRPV4 channels, leading to embryo retention in the Fallopian tubes and subsequent tubal pregnancy. The study provided evidence that the expression of TRPV4 was downregulated in the Fallopian tubes among patients with tubal pregnancy and negatively correlated with the serum level of progesterone. LNG downregulated the expression of TRPV4, limiting the calcium influx to reduce the CBF in mouse oviducts. Furthermore, the distribution of ciliated cells and the morphology of cilia did not change following the administration of LNG. LNG-induced reduction in the CBF and embryo retention in the Fallopian tubes and in mouse oviducts were partially reversed by the progesterone receptor antagonist RU486 or the TRPV4 agonist 4α-phorbol 12,13-didecanoate (4α-PDD). The results indicated that LNG could downregulate the expression of TRPV4 to reduce the CBF in both humans and mice, suggesting the possible mechanism of tubal pregnancy. © 2019 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Fasudil reduces ß-amyloid levels and neuronal apoptosis in APP/PS1 transgenic mice via inhibition of the Nogo-A/NgR/RhoA signaling axis.

Recent studies have shown that Nogo-A and the Nogo-A receptor affect ß-amyloid metabolism and the downstream Rho GTP enzyme signaling pathway, which may affect the levels of ß-amyloid and tau. Nogo-A may play a key role in the pathogenesis of Alzheimer's disease. However, the underlying molecular mechanisms of Fasudil treatment in Alzheimer's disease are not yet clear. Our results have found that Fasudil treatment for two months substantially ameliorated behavioral deficits, diminished ß-amyloid plaque and tau protein pathology, and alleviated neuronal apoptosis in APP/PS1 transgenic mice. More importantly, two well-established markers for synaptic function, growth-associated protein 43 and synaptophysin, were upregulated after Fasudil treatment. Finally, the levels of Nogo-A, Nogo-A receptor complex NgR/p75NTR/LINGO-1 and the downstream Rho/Rho kinase signaling pathway were significantly reduced. These findings suggest that Fasudil exerts its neuroprotective function in Alzheimer's disease by inhibiting the Nogo-A/NgR1/RhoA signaling pathway.

Set-reset latch logic operation in a bistable system under suprathreshold and subthreshold signals.

A set-reset latch is a basic building block of computers and can be used to store state information. Here, by testing the influence of the two logical input signals on the reliable set-reset latch logic operation in the bistable system, we found that there are two types of input signals, namely, suprathreshold and subthreshold signals. For the suprathreshold signals, reliable set-reset logic operation can be achieved without any driving forces and exhibits certain anti-interference ability; for the subthreshold signals, a single harmonic could induce correct set-reset latch logic operation but with a narrow optimal parameter region. The introduction of biharmonic-induced set-reset latch logic operation (logical vibrational resonance) could greatly expand the parameter region. Explanations for the above results were provided by taking the logical inputs as the dynamic bias to analyze the dynamic changes in the system. Finally, the results were further verified by circuit simulation and actual hardware circuit.

Left-Right Asymmetry of Tubal Pregnancy: A 12-Year Retrospective Hospital-Based Study.

STUDY OBJECTIVE: To investigate whether there are left-right asymmetries, factors affecting lateral dominance, and clinical feature differences in the left and right sides of tubal pregnancy (TP). DESIGN: Retrospective study (Canadian Task Force classification II-2). SETTING: International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University. PATIENTS: Patients (n = 6186) with TP treated surgically. INTERVENTIONS: We used data from the digital medical records system of the hospital. Women diagnosed with ectopic pregnancy(EP) between January 2005 and December 2016 in the inpatient department of gynecology were included. All data from the medical files were obtained retrospectively, including demographic characteristics; reproductive, gynecologic, and surgical history; clinical features; and treatment. Patients who were previously treated by salpingectomy or nonsurgical management and those with unknown-site EP or non-TPs were excluded. MEASUREMENTS AND MAIN RESULTS: The overall frequency of right-sided TP was 54.48% (3370/6186), which is significantly higher than 50% (p < .001, binominal test). The proportion of right-sided TPs decreased with age (p for trend = .007) and from the proximal (interstitial) end to the distal (fimbrial) end of the tube (p for trend = .017). Of the TP patients with a corpus luteum, we found the corpus luteum was more frequently located in the right ovary (p < .001) and in the contralateral ovary to the TP side in 41.38% of cases. However, tubal rupture was more frequent in left TP than the in right TP (p = .005). CONCLUSION: The left-right asymmetries of TP include right-side dominance and the clinical feature differences between the 2sides of TP.

Therapeutic potentials of the Rho kinase inhibitor Fasudil in experimental autoimmune encephalomyelitis and the related mechanisms.

Multiple sclerosis (MS), Parkinson's disease (PD), Alzheimer's disease (AD), and other neurodegenerative diseases of central nervous system (CNS) disorders are serious human health problems. Rho-kinase (ROCK) is emerging as a potentially important therapeutic target relevant to inflammatory neurodegeneration diseases. This is supported by studies showing the beneficial effects of fasudil, a ROCK inhibitor, in inflammatory neurodegeneration diseases. MS is an autoimmune disease resulting from inflammation and demyelination in the white matter of the CNS. It has been postulated that activation of Rho/ROCK causes neuropathological changes accompanied with related clinical symptoms, which are improved by treatment with ROCK inhibitors. Therefore, inhibition of abnormal activation of the Rho/ROCK signaling pathway appears to be a new mechanism for treating CNS diseases. In this review, we extensively discussed the role of ROCK inhibitors, summarized the efficacy of fasudil in the MS conventional animal model of experimental autoimmune encephalomyelitis (EAE), both in vivo and in vitro, and highlighted the mechanism involved. Overall, the findings collected in this review support the role of the ROCK signaling pathway in neurodegenerative diseases. Hence, ROCK inhibitors such as fasudil can be novel, and efficacious treatment for inflammatory neurodegenerative diseases.

Effects of pelvic endometriosis and adenomyosis on ciliary beat frequency and muscular contractions in the human fallopian tube.

BACKGROUND: Pelvic endometriosis (EM) and adenomyosis (AM) have different effects on the fallopian tube. This study aimed to assess the transport capability of the fallopian tube in women with pelvic EM or AM. METHODS: Twenty women with uterine leiomyoma (control group), 20 with adenomyosis without pelvic EM (AM group) and 35 with pelvic EM without AM (EM group) were included. EM cases were further divided into the tubal EM and non-tubal EM subgroups. Ciliary beat frequency (CBF), percentage of ciliated cells, and smooth muscle contraction were measured. RESULTS: CBFs of the ampulla in EM cases were significantly lower than those of control and AM cases; CBFs of the ampulla and isthmus in tubal EM cases were significantly lower than those of the control group and non-tubal EM subgroup. In both the ampulla and isthmus segment, percentages of ciliated cells in EM patients were significantly lower than those of AM and control patients; the tubal EM subgroup showed significantly lower values than the control group and non-tubal EM subgroup. Amplitude-to-weight ratios of longitudinal muscular contractility in EM cases were significantly lower than control values; tubal EM cases showed significantly lower values than controls and the non-tubal EM subgroup. Contraction frequencies in EM cases were significantly lower than those of control and AM cases, in both longitudinal and circular muscles; tubal EM cases showed significantly lower values than controls and the non-tubal EM subgroup. CONCLUSION: EM with tubal EM damaged transport function of the fallopian tube, to varying degrees, whereas tubal function in EM without tubal EM and in AM is not altered.

Effects of Levonorgestrel and progesterone on Oviductal physiology in mammals.

BACKGROUND: Our previous study indicated that emergency contraception, including levonorgestrel and progesterone, could lead to ectopic pregnancy following contraception failure. However, our understanding of the effects of levonorgestrel and progesterone on oviductal physiology is limited. METHODS: The receptivity of the fallopian tubal epithelium after levonorgestrel and progesterone treatment was examined through western blots for receptivity markers and JAr-spheroid-fallopian tubal epithelial cell attachment assays. The ciliary beat frequency was analyzed using an inverted bright-field microscope. Furthermore, an in vivo animal model of embryo-tubal transplantation was also studied to determine the effects of levonorgestrel- and progesterone-induced ciliary beat reduction. RESULTS: Our results showed that levonorgestrel and progesterone did not change the levels of fallopian tubal epithelial cell receptive markers, including LIF, STAT3, IGFBP1, ITGB3, MUC1, and ACVR1B, or affect JAr-spheroid implantation. However, levonorgestrel and progesterone reduced the ciliary beat frequency in fallopian tubes in a dose-dependent manner. An in vivo model also showed that levonorgestrel and progesterone could lead to embryo retention in the oviducts. CONCLUSIONS: These findings show that levonorgestrel and progesterone can reduce the ciliary beat frequency without altering receptivity, indicating a possible mechanism for progesterone- or levonorgestrel-induced tubal pregnancy.

Micro-RNA-137 Inhibits Tau Hyperphosphorylation in Alzheimer's Disease and Targets the CACNA1C Gene in Transgenic Mice and Human Neuroblastoma SH-SY5Y Cells.

BACKGROUND Alzheimer's disease (AD) results in cognitive impairment. The calcium voltage-gated channel subunit alpha-1 C CACNA1C gene encodes an alpha-1 C subunit of L-type calcium channel (LTCC). The aim of this study was to investigate the role of micro-RNA-137 (miR-137) and the CACNA1C gene in APPswe/PS1ΔE9 (APP/PS1) double-transgenic AD mice and in human neuroblastoma SH-SY5Y cells. MATERIAL AND METHODS Six-month-old APP/PS1 double-transgenic AD mice (N=6) and age-matched normal C57BL/6 mice (N=6) underwent a Morris water maze (MWM) test, expression levels of amyloid-ß (Aß), LTCC, the CACNA1C gene, and miR-137 were measured in the rat hippocampus and cerebral cortex in both groups of mice. A luciferase assay was used to evaluate the effect of miR-137 on the expression of CACNA1C in SH-SY5Y human neuroblastoma SH-SY5Y cells. Western blotting was used to detect the CACNA1C, phosphorylated-tau (p-tau), and Aß proteins. RESULTS In APP/PS1 transgenic AD mice, spatial learning and memory was significantly reduced, levels of Aß1-40 and Aß1-42 were increased in the serum, hippocampus, and cerebral cortex, expression levels of miR-137 were reduced, expression of CACNA1C protein was increased in the hippocampus and cerebral cortex, compared with normal control mice. miR-137 regulated the expression of the CACNA1C gene. Increased expression levels of p-tau (Ser202, Ser396, and Ser404) induced by Aß1-42 were inhibited by miR-137 mimics in SH-SY5Y human neuroblastoma cells in vitro. CONCLUSIONS In a transgenic mouse model of AD, miR-137 and expression of the CACNA1C gene inhibited the hyperphosphorylation of tau protein.

Charge carrier kinetics of carbon nitride colloid: a femtosecond transient absorption spectroscopy study.

Carbon nitrides (CN) have been widely used in photocatalytic applications. However, the charge carrier kinetics of CN after light excitation remains unclear. Herein, we prepared a stable and transparent CN colloid in an aqueous tetraethylammonium hydroxide solution and investigated its carrier kinetics using both femtosecond transient absorption and picosecond time-resolved fluorescence spectroscopy. We found that a new and positive absorption band appears in the femtosecond transient absorption spectrum of the CN colloid, which could be attributed to the absorption of the photogenerated electron/hole pairs (or the electronic excited state) of the CN colloid after light excitation. Moreover, we found that the charge carrier kinetics obtained from the femtosecond transient absorption measurements is dramatically different from that obtained from the picosecond time-resolved fluorescence measurements, indicating that the photophysical process of the CN colloid after light excitation is complicated. With the results obtained from both the femtosecond transient absorption and picosecond time-resolved fluorescence measurements, we proposed a schematic to understand the photophysics and charge carrier kinetics of the CN colloid. We believe that the current study is also significant for researchers to understand the photophysics and charge carrier kinetics of bulk CN.