Dichlorido[N,N-diethyl-N′-(2-pyridyl­methyl­ene)ethane-1,2-diamine]mercury(II)

The Hg atom in the title compound, [HgCl2(C12H19N3)], adopts a distorted trigonal-bipyramidal geometry, being ligated by two Cl atoms and three N atoms of the N,N-diethyl-N′-(2-pyridylmethyl­ene)ethane-1,2-diamine ligand. The dihedral angle between the HgN3 and HgCl2 least-squares planes is 88.6 (1)°. The Hg—N distances including the pyridine N and the ammonium N atom are about 0.20 Å longer than the Hg—N distance including the imino N atom

The effect of low-dose intravenous bisphosphonate treatment on osteoporosis in children with quadriplegic cerebral palsy

PurposeQuadriplegic children with cerebral palsy are more susceptible to osteoporosis because of various risk factors that interfere with bone metabolism. Pamidronate is effective for pediatric osteoporosis, but there are no guidelines for optimal dosage or duration of treatment in quadriplegic children with osteoporosis. We aimed to evaluate the efficacy of low-dose pamidronate treatment in these patients.MethodsTen quadriplegic patients on antiepileptic drugs (6 male, 4 female patients; mean age, 10.9±5.76 years), with osteoporosis and gross motor function classification system level V, were treated with pamidronate (0.5–1.0 mg/kg/day, 2 consecutive days) every 3–4 months in a single institution. The patients received oral supplements of calcium and vitamin D before and during treatment. The lumbar spine bone mineral density (BMD) z score and biochemical markers of bone metabolism were measured regularly during treatment.ResultsThe main underlying disorder was perinatal hypoxic brain damage (40%, 4 of 10). The mean cumulative dose of pamidronate was 4.49±2.22 mg/kg/yr, and the mean treatment period was 10.8±3.32 months. The BMD z score of the lumbar spine showed a significant increase from −4.22±1.24 before treatment to −2.61±1.69 during treatment (P=0.008). Alkaline phosphatase decreased during treatmentn (P=0.037). Significant adverse drug reactions and new fractures were not reported.ConclusionLow-dose pamidronate treatment for quadriplegic children with cerebral palsy increased lumbar BMD and reduced the incidence of fracture

Occlusion of Traumatic Carotid Cavernous Fistula by Incidentally Formed Thrombus During the Interventional Procedure: A Case Report

In this report, we present a rare case of traumatic carotid cavernous fistula that was occluded during the interventional procedure by incidentally formed blood clot. Sudden occlusion of the fistula and the resolution process of the precarious blood clot can be clearly seen on the serial angiogram

High resolution crystal structure of PedB: a structural basis for the classification of pediocin-like immunity proteins

<p>Abstract</p> <p>Background</p> <p>Pediocin-like bacteriocins, ribosomally-synthesized antimicrobial peptides, are generally coexpressed with cognate immunity proteins in order to protect the bacteriocin-producer from its own bacteriocin. As a step for understanding the mode of action of immunity proteins, we determined the crystal structure of PedB, a pediocin-like immunity protein conferring immunity to pediocin PP-1.</p> <p>Results</p> <p>The 1.6 Å crystal structure of PedB reveals that PedB consists of an antiparallel four-helix bundle with a flexible C-terminal end. PedB shows structural similarity to an immunity protein against enterocin A (EntA-im) but some disparity to an immunity protein against carnobacteriocin B2 (ImB2) in both the C-terminal conformation and the local structure constructed by α3, α4, and their connecting loop. Structure-inspired mutational studies reveal that deletion of the last seven residues of the C-terminus of PedB almost abolished its immunity activity.</p> <p>Conclusion</p> <p>The fact that PedB, EntA-im, and ImB2 share a four-helix bundle structure strongly suggests the structural conservation of this motif in the pediocin-like immunity proteins. The significant difference in the core structure and the C-terminal conformation provides a structural basis for the classification of pediocin-like immunity proteins. Our mutational study using C-terminal-shortened PedBs and the investigation of primary sequence of the C-terminal region, propose that several polar or charged residues in the extreme C-terminus of PedB which is crucial for the immunity are involved in the specific recognition of pediocin PP-1.</p

Enhancement of seawater corrosion resistance in copper using acetone-derived graphene coating

We show that acetone-derived graphene coating can effectively enhance the corrosion efficiency of copper (Cu) in a seawater environment (0.5-0.6 M (???3.0-3.5%) sodium chloride). By applying a drop of acetone (???20 ??l cm-2) on Cu surfaces, rapid thermal annealing allows the facile and rapid synthesis of graphene films on Cu surfaces with a monolayer coverage of almost close to ???100%. Under optimal growth conditions, acetone-derived graphene is found to have a relatively high crystallinity, comparable to common graphene grown by chemical vapor deposition. The resulting graphene-coated Cu surface exhibits 37.5 times higher corrosion resistance as compared to that of mechanically polished Cu. Further, investigation on the role of graphene coating on Cu surfaces suggests that the outstanding corrosion inhibition efficiency (IE) of 97.4% is obtained by protecting the underlying Cu against the penetration of both dissolved oxygen and chlorine ions, thanks to the closely spaced atomic structure of the graphene sheets. The increase of graphene coating thickness results in the enhancement of the overall corrosion IE up to ???99%, which can be attributed to the effective blocking of the ionic diffusion process via grain boundaries. Overall, our results suggest that the acetone-derived graphene film can effectively serve as a corrosion-inhibiting coating in the seawater level and that it may have a promising role to play for potential offshore coating.close0

Spontaneous Tonsillar Hemorrhage and Post-Tonsillectomy Hemorrhage

Spontaneous tonsillar hemorrhage from infectious causes is extremely rare and post-tonsillectomy hemorrhage, although also relatively rare, is an unavoidable complication of the procedure. Hemorrhage in association with tonsillitis or tonsillectomy is potentially dangerous and can be life threatening. We report here the presentation and management of a 42-yr-old man with severe spontaneous hemorrhage from infected tonsils and post-tonsillectomy hemorrhage. We suggest that if attempts to control the bleeding are not successful or if severe spontaneous tonsillar hemorrhage occurs repeatedly or a malignancy is suspected, tonsillectomy and close postoperative follow up is recommended

Aerosol delivery of kinase-deficient Akt1 attenuates Clara cell injury induced by naphthalene in the lungs of dual luciferase mice

Conventional lung cancer therapies are associated with poor survival rates; therefore, new approaches such as gene therapy are required for treating cancer. Gene therapies for treating lung cancer patients can involve several approaches. Among these, aerosol gene delivery is a potentially more effective approach. In this study, Akt1 kinase-deficient (KD) and wild-type (WT) Akt1 were delivered to the lungs of CMV-LucR-cMyc-IRES-LucF dual reporter mice through a nose only inhalation system using glucosylated polyethylenimine and naphthalene was administrated to the mice via intraperitoneal injection. Aerosol delivery of Akt1 WT and naphthalene treatment increased protein levels of downstream substrates of Akt signaling pathway while aerosol delivery of Akt1 KD did not. Our results showed that naphthalene affected extracellular signal-regulated kinase (ERK) protein levels, ERK-related signaling, and induced Clara cell injury. However, Clara cell injury induced by naphthalene was considerably attenuated in mice exposed to Akt1 KD. Furthermore, a dual luciferase activity assay showed that aerosol delivery of Akt1 WT and naphthalene treatment enhanced cap-dependent protein translation, while reduced cap-dependent protein translation was observed after delivering Akt1 KD. These studies demonstrated that our aerosol delivery is compatible for in vivo gene delivery

Chfr is linked to tumour metastasis through the downregulation of HDAC1

Chfr is a ubiquitin ligase that functions in the mitotic checkpoint by delaying entry into metaphase in response to mitotic stress. It has been suggested that Chfr is a tumour suppressor as Chfr is frequently silenced in human cancers. To better understand how Chfr activity relates to cell-cycle progression and tumorigenesis, we sought to identify Chfr-interacting proteins using affinity purification combined with mass spectrometry. Histone deacetylase 1 (HDAC1), which represses transcription by deacetylating histones, was newly isolated as a Chfr-interacting protein. Chfr binds and downregulates HDAC1 by inducing its polyubiquitylation, both in vitro and in vivo. Ectopic expression of Chfr in cancer cells that normally do not express it results in downregulation of HDAC1, leading to upregulation of the Cdk inhibitor p21^(CIP1/WAF1) and the metastasis suppressors KAI1 and E-cadherin. Coincident with these changes, cells arrest in the G1 phase of the cell cycle and become less invasive. Collectively, our data suggest that Chfr functions as a tumour suppressor by regulating HDAC1

Changes in intravenous hydration frequency and emergency department length of stay after implementation of oral ondansetron therapy in children with dehydration due to acute gastroenteritis

Purpose Oral ondansetron is a safe and effective antiemetic drug to facilitate oral rehydration therapy in acute gastroenteritis (AGE) with mild dehydration. We investigated the effect of oral ondansetron therapy on intravenous (IV) hydration frequency and emergency department length of stay (EDLOS) in dehydrated children with AGE. Methods We reviewed 15,813 children aged 12-60 months with primary diagnosis of AGE who visited a tertiary care university-affiliated hospital emergency department. The enrolled children were divided into the pre- (from January 2009 to June 2011) and post- (from January 2016 to June 2018) ondansetron groups according to the implementation of oral ondansetron therapy in the emergency department. As primary outcomes, IV hydration frequency, EDLOS, and hospitalization rate were compared between the 2 groups. As secondary outcomes, EDLOS and hospitalization rate were compared between the children in the post-ondansetron group who underwent the therapy, and those who did not. Results Of 7,990 enrolled children, 3,300 (41.3%) were designated as the post-ondansetron group, and among them 1,093 (33.1%) underwent oral ondansetron therapy. This group showed a lower IV hydration frequency, a shorter median EDLOS compared to the other group (61.9% vs. 55.8%, P < 0.001; 223.0 minutes vs. 175.0 minutes, P < 0.001, respectively), and a higher hospitalization rate (7.9% vs. 9.9%, P < 0.001). The children in the post-ondansetron group who underwent the therapy showed a shorter median EDLOS and a lower hospitalization rate compared to those who did not (142.0 vs 205.0 minutes, P < 0.001; 2.9% vs. 13.4%, P < 0.001, respectively). Conclusion Oral ondansetron therapy may reduce IV hydration frequency and EDLOS in dehydrated children with AGE, and can be considered in those having severe vomiting

Activation of AMP-activated protein kinase stimulates the nuclear localization of glyceraldehyde 3-phosphate dehydrogenase in human diploid fibroblasts

In addition to its well-known glycolytic activity, GAPDH displays multiple functions, such as nuclear RNA export, DNA replication and repair, and apoptotic cell death. This functional diversity depends on its intracellular localization. In this study, we explored the signal transduction pathways involved in the nuclear translocation of GAPDH using confocal laser scanning microscopy of immunostained human diploid fibroblasts (HDFs). GAPDH was present mainly in the cytoplasm when cultured with 10% FBS. Serum depletion by culturing cells in a serum-free medium (SFM) led to a gradual accumulation of GAPDH in the nucleus, and this nuclear accumulation was reversed by the re-addition of serum or growth factors, such as PDGF and lysophosphatidic acid. The nuclear export induced by the re-addition of serum or growth factors was prevented by LY 294002 and SH-5, inhibitors of phosphoinositide 3-kinase (PI3K) and Akt/protein kinase B, respectively, suggesting an involvement of the PI3K signaling pathway in the nuclear export of GAPDH. In addition, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), an activator of AMP-activated protein kinase (AMPK), stimulated the nuclear translocation of GAPDH and prevented serum- and growth factor-induced GAPDH export. AMPK inhibition by compound C or AMPK depletion by siRNA treatment partially prevented SFM- and AICAR-induced nuclear translocation of GAPDH. Our data suggest that the nuclear translocation of GAPDH might be regulated by the PI3K signaling pathway acting mainly as a nuclear export signal and the AMPK signaling pathway acting as a nuclear import signal.Peairs A, 2009, CLIN EXP IMMUNOL, V156, P542, DOI 10.1111/j.1365-2249.2009.03924.xChen Z, 2009, CIRC RES, V104, P496, DOI 10.1161/CIRCRESAHA.108.187567Cao C, 2008, J BIOL CHEM, V283, P28897, DOI 10.1074/jbc.M804144200Li XX, 2008, ARTERIOSCL THROM VAS, V28, P1789, DOI 10.1161/ATVBAHA.108.172452Lombardi M, 2008, J CELL BIOL, V182, P327Sen N, 2008, NAT CELL BIOL, V10, P866, DOI 10.1038/ncb1747Kim HS, 2008, J BIOL CHEM, V283, P3731, DOI 10.1074/jbc.M704432200Du ZX, 2007, ENDOCRINOLOGY, V148, P4352, DOI 10.1210/en.2006-1511Harada N, 2007, J BIOL CHEM, V282, P22651, DOI 10.1074/jbc.M610724200Goirand F, 2007, J PHYSIOL-LONDON, V581, P1163, DOI 10.1113/jphysiol.2007.132589Barbini L, 2007, MOL CELL BIOCHEM, V300, P19, DOI 10.1007/s11010-006-9341-1Hurley RL, 2006, J BIOL CHEM, V281, P36662, DOI 10.1074/jbc.M606676200Hara MR, 2006, CELL MOL NEUROBIOL, V26, P527, DOI 10.1007/s10571-006-9011-6Tisdale EJ, 2006, J BIOL CHEM, V281, P8436, DOI 10.1074/jbc.M513031200Rattan R, 2005, J BIOL CHEM, V280, P39582, DOI 10.1074/jbc.M507443200Hara MR, 2005, NAT CELL BIOL, V7, P665, DOI 10.1038/ncb1268Sirover MA, 2005, J CELL BIOCHEM, V95, P45, DOI 10.1002/jcb.20399Jones RG, 2005, MOL CELL, V18, P283, DOI 10.1016/j.molcel.2005.03.027Tisdale EJ, 2004, J BIOL CHEM, V279, P54046, DOI 10.1074/jbc.M409472200Hardie DG, 2004, J CELL SCI, V117, P5479, DOI 10.1242/jcs.01540Li J, 2004, AM J PHYSIOL-ENDOC M, V287, pE834, DOI 10.1152/ajpendo.00234.2004Cooray S, 2004, J GEN VIROL, V85, P1065, DOI 10.1099/vir.0.1977-0Brown VM, 2004, J BIOL CHEM, V279, P5984, DOI 10.1074/jbc.M307071200Tisdale EJ, 2003, J BIOL CHEM, V278, P52524, DOI 10.1074/jbc.M309343200HAWLEY SA, 2003, J BIOL, V2, P28Schmitz HD, 2003, CELL BIOL INT, V27, P511, DOI 10.1011/S1065-6995(03)00096-9Tisdale EJ, 2002, J BIOL CHEM, V277, P3334, DOI 10.1074/jbc.M109744200Schmitz HD, 2001, EUR J CELL BIOL, V80, P419Dastoor Z, 2001, J CELL SCI, V114, P1643Yeo EJ, 2000, MOL CELLS, V10, P415Stein SC, 2000, BIOCHEM J, V345, P437Sirover MA, 1999, BBA-PROTEIN STRUCT M, V1432, P159Shashidharan P, 1999, NEUROREPORT, V10, P1149Rameh LE, 1999, J BIOL CHEM, V274, P8347Sawa A, 1997, P NATL ACAD SCI USA, V94, P11669Vincent MF, 1996, BIOCHEM PHARMACOL, V52, P999Reiss N, 1996, BIOCHEM MOL BIOL INT, V38, P711CORTON JM, 1995, EUR J BIOCHEM, V229, P558KAWAMOTO RM, 1986, BIOCHEMISTRY-US, V25, P657BOYCE ST, 1983, J INVEST DERMATOL S, V81, P33