Growth-promoting effect of antimicrobial peptide Scy-hepc on mariculture large yellow croaker Larimichthys crocea and the underlying mechanism.

With the antibiotics prohibition in feedstuffs worldwide, antimicrobial peptides (AMPs) are considered a more promising substitute for antibiotics to be used as feed additives, and positive results have been reported in livestock feeding studies. However, whether dietary supplementation of AMPs could promote the growth of mariculture animals such as fish and the underlying mechanism has not been elucidated yet. In the study, a recombinant AMP product of Scy-hepc was used as a dietary supplement (10 mg/kg) to feed mariculture juvenile large yellow croaker (Larimichthys crocea) with an average initial body weight (BW) of 52.9 g for 150 days. During the feeding trial, the fish fed with Scy-hepc showed a significant growth-promoting performance. Especially at 60 days after feeding, fish fed with Scy-hepc weighed approximately 23% more than the control group. It was further confirmed that the growth-related signaling pathways such as the GH-Jak2-STAT5-IGF1 growth axis, the PI3K-Akt and Erk/MAPK pathways were all activated in the liver after Scy-hepc feeding. Furthermore, a second repeated feeding trial was scheduled for 30 days using much smaller juvenile L. crocea with an average initial BW of 6.3 g, and similar positive results were observed. Further investigation revealed that the downstream effectors of the PI3K-Akt pathway, such as p70S6K and 4EBP1, were significantly phosphorylated, suggesting that Scy-hepc feeding might promote translation initiation and protein synthesis processes in the liver. Taken together, as an effector of innate immunity, AMP Scy-hepc played a role in promoting the growth of L. crocea and the underlying mechanism was associated with the activation of the GH-Jak2-STAT5-IGF1 axis, as well as the PI3K-Akt and Erk/MAPK signaling pathways.

Tracking registration of optical see-through augmented reality based on the Riemannian manifold constraint.

Two three-dimensional tracking registration methods combined with Riemannian manifold object constraints are proposed to solve problems of low accuracy and instability of three-dimensional tracking registration in sparse and complex scenes. A deep convolution neural network is used to extract three-dimensional instance objects from the location by analyzing reasons that affect registration accuracy in sparse and complex scenes. The three-dimensional tracking registration model is established according to the Riemannian manifold constraint relationship of instance objects in different states. The stability of the three-dimensional tracking registration algorithm is improved by combining inertial sensors, and cumulative error is optimized using instance object labels to improve algorithm robustness. The proposed algorithm can effectively improve the accuracy of three-dimensional tracking registration. It can improve the performance of augmented reality systems and be applied to power system navigation, medical, and other fields.

Dysregulation of the Urothelial Cancer Associated 1 Long Noncoding RNA Promotes Proliferation of Vascular Smooth Muscle Cells by Modulating Expression of P27KIP1/CDK2.

Background: Atherosclerosis is one of the leading causes of morbidity and mortality worldwide. A variety of long noncoding RNAs (lncRNAs) have been reported to be significantly involved in vascular smooth muscle cell (VSMC) proliferation, which is an essential process for atherosclerotic plaque formation. The aim of this study was to investigate the mechanism of lncRNA urothelial cancer associated 1 (UCA1) involvement in atherosclerosis. Method: The effects of oxidized low-density lipoprotein (oxLDL) and UCA1 on VSMC proliferation and colony-forming ability was measured by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyl-2H-tetrazolium bromide (MTT) assays, real-time polymerase chain reaction (PCR), and western blots, as well as to determine the effect that oxLDL has on UCA1 expression, and the effect of oxLDL and UCA1 on the expression of cyclin-dependent kinase 2 (CDK2). Results: oxLDL treatment increased the proliferation rate of VSMCs in a concentration-dependent manner. Importantly, UCA1 apparently increased the viability of VSMCs as the VSMCs exhibited a significantly reduced growth rate when UCA1 expression was knocked down by specific small interfering RNAs (siRNAs). In conjunction with increasing cell viability, oxLDL also enhanced the colony-forming ability of VSMCs while UCA1 siRNA decreased the colony-forming ability of VSMCs. Furthermore, UCA1 significantly decreased the percentage of VSMCs in G1 phase, while increasing their percentage in S phase. In contract siRNA knockdown of UCA1 caused an increased percentage of cell in G1 phase, and a reduction in the percentage of cells in S phase. Using real-time PCR and western blot assays, we showed that oxLDL significantly increased the expression levels of UCA1 and CDK2. Furthermore, UCA1 siRNA and CDK2 siRNA almost abolished the positive effect of oxLDL on CDK2 expression. Finally, overexpression of UCA1 induced an increase in CDK2 levels, and knockdown of UCA1 caused inhibition of CDK2 expression. Conclusion: Upregulation of UCA1 enhances abnormal proliferation of VSMC by promoting G1/S transition through modulating the expression of CDK2.

MicroRNA-34c suppresses proliferation of vascular smooth muscle cell via modulating high mobility group box protein 1.

BACKGROUND: Atherosclerosis is the most frequent pathological process that causes cardiovascular diseases. OBJECTIVE: The present study aimed to confirm miRNAs associated with atherosclerosis and explore the molecular mechanism of miR-34c and its target high mobility group box protein 1 (HMGB1) in the control of growth of smooth muscle cells in the development of atherosclerosis. METHODS: Real-time PCR was firstly performed to confirm miRNA correlation with atherosclerosis, and computational analysis and luciferase assay were performed to explore the target of miR-34c, Western blot, and real-time PCR were also utilized to reveal the effect of whether high glucose (HG) and miR-34c affect miR-34c, HMGB1 levels, NF-κB p65 and TNF-α levels, and the role of miR-34c on vascular smooth muscle cells (VSMCs) viability induced by HG. Students' unpaired t test was performed to compare data between two groups. RESULTS: MiR-34c level was associated with atherosclerosis with different expression between VSMCs treated with high glucose or normal VSMCs. Then, HMGB1 is a virtual target of miR-34c with predicted binding site resided in HMGB1 3'UTR and further verified by that miR-34c remarkably reduced luciferase activity of wild HMGB1 3'UTR under a concentration-dependent fashion, and miR-34c cannot influence luciferase activity of mutant HMGB1 3'UTR. CONCLUSIONS: The results suggested miR-34c might be a novel therapeutic strategy in the management of atherosclerosis by suppressing the expression of HGMB1 and its downstream effectors.

Seawater quality criteria derivation and ecological risk assessment for oil pollution in China.

The establishment of water quality criteria (WQC) for oil pollutants is the basis for ecological risk assessment of marine oil pollution. Ecotoxicity data of oil pollutants to marine organisms in China were collected and toxicity test of oil to nine Chinese marine organisms were performed. Based on the WQC guidelines of the United States, the sea WQC of oil pollutants in China were studied. Then, the ecological risk of oil in 7 sea areas of China was assessed. Results showed that the long-term and short-term criteria of oil pollutants in China are 7.3 µg/L and 36 µg/L, respectively. Except for Qinhuangdao and Xiamen sea areas, the highest oil concentration in the other five sea areas exceeded the long-term WQC by >10 times, and the highest oil concentration in the Pearl River Estuary exceeded the long-term WQC by >100 times, indicating serious ecological risk.

LncRNA H19-elevated LIN28B promotes lung cancer progression through sequestering miR-196b.

LncRNA H19 is involved in the development of multiple cancers. Here, we firstly provide new evidence that H19 can induce LIN28B, a conserved RNA binding protein, to accelerate lung cancer growth through sponging miR-196b. Abundance in LIN28B was observed in clinical lung cancer samples. A positive link was observed between H19 and LIN28B in clinical lung cancer samples. In lung cancer cells, H19 was capable of increasing LIN28B expression. Mechanistically, miR-196b directly targeted LIN28B to inhibit LIN28B expression. H19 was capable of promoting LIN28B expression through sequestering miR-196b. Functionally, H19-increased LIN28B conferred the cell proliferation of lung cancer. Our finding indicates that H19 depresses miR-196b to elevate LIN28B, resulting in accelerating cell proliferation in lung cancer.

Author Correction: Expression of both poly r(C) binding protein 1 (PCBP1) and miRNA-3978 is suppressed in peritoneal gastric cancer metastasis.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.

Is Unsedated Colonoscopy Gaining Ground Over Sedated Colonoscopy?

Colorectal cancer (CRC) is a prevalent cancer with high global incidence and a leading cause of cancer death worldwide. CRC screening is important for early cancer detection and prevention. Most premalignant adenomas can be identified and removed before they become malignant. Colonoscopy plays a vital role in reducing the risk for developing CRC. Although screening programs with colonoscopy have been implemented in many countries and considered beneficial for a number of people, this technique is generally associated with anxiety, embarrassment, pain, and discomfort, resulting in lack of adherence to the recommended screening guidelines. In the US, colonoscopy is mostly performed under sedation, thereby causing amnesia and analgesia. In contrast to sedated colonoscopy, which has been associated with some disadvantages, unsedated colonoscopy exhibits advantages and has been preferred over sedated colonoscopy in numerous cancer centers worldwide. This review enumerates the features of sedated and unsedated colonoscopy with the use of the current relevant evidence-based literature. Unsedated colonoscopy can be a reasonable option for routine and unscheduled CRC screening.

MicroRNA-106b overexpression alleviates inflammation injury of cardiac endothelial cells by targeting BLNK via the NF-κB signaling pathway.

We aim to investigate whether microRNA-106b (miR-106b) affects the inflammation injury of cardiac endothelial cells (ECs) by targeting B-cell linker (BLNK) via the NF-κB signaling pathway. Human cardiac microvascular endothelial cells (HCMECs) were assigned into the control, hypoxia/reoxygenation (H/R), negative control (NC), pyrrolidine dithiocarbamate (PDTC), miR-106b mimic, miR-106b inhibitor, and si-BLNK, and miR-106b inhibitor+si-BLNK groups. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were conducted for miR-106b expression and expressions of BLNK, interleukin (IL)-6, IL-1ß, tumor necrosis factor (TNF)-α, NF-κB, pIκBα, BTK, and PLC-γ2. Enzyme-linked immunosorbent assay was applied for levels of IL-6, IL-10, and TNF-α; cell counting Kit-8 assay for cell proliferation; and flow cytometry for cell cycle and ensuing apoptosis. In-vitro tube formation assay was performed for tube formation ability. Dual-luciferase reporter assay revealed that BLNK was verified as the target gene of miR-106b. Compared with the H/R and NC groups, the PDTC, miR-106b mimic, and si-BLNK groups had declined expressions of IL-6, IL-1ß, TNF-α, BTK, PLC-γ2, NF-κB p105/p50, and pIκBα as well as levels of L-6 and TNF-α, but contrarily elevated levels of NF-κB p105/p50 and IL-10. The PDTC, miR-106b mimic, and si-BLNK groups had less cell number in G0 /G1 phase but higher cell count in both S and G2 phases, decreased cell apoptosis but increased proliferation and tube formation ability, while opposite trends were observed in the miR-106b inhibitor group. Our findings indicated that the overexpression of miR-106b alleviated the inflammation injury of cardiac ECs by targeting BLNK via the NF-κB signaling pathway.

Expression of both poly r(C) binding protein 1 (PCBP1) and miRNA-3978 is suppressed in peritoneal gastric cancer metastasis.

The expression of legumain which has been shown overexpressed in patients with metastatic gastric cancer is positively correlated to both disease progression and outcome, and negatively correlated to microRNA (miR)-3978 expression. The RNA-binding protein, poly r(C) binding protein 1 (PCBP1) was the most downregulated protein in the metastatic tissue specimens. Quantitative real-time PCR showed that PCBP1 expression is transcriptionally downregulated in peritoneal metastasis tissues. RNA immunoprecipitation experiments showed that PCBP1 and miR-3978 are sequestered in normal peritoneal tissue, but the complex is disrupted following metastatic progression. PCBP1 expression mimicked miR-3978 expression across gastric cancer patients. Finally, replenishment of PCBP1 or miR-3978 expression in the peritoneal metastasis cell line MKN45 decreased legumain protein expression and chemosensitized the cells to treatment with docetaxel. However, replenishment of one and concomitant depletion of the other failed to induce chemosensitivity to docetaxel. Replenishment of miR-3978 also resulted in induction of PCBP1 protein expression, potentially indicating that miR-3978 expression might downregulate a negative regulator targeting PCBP1. Our current study reveals PCBP1 as an additional biomarker in peritoneal metastasis. PCBP1 and miR-3978 expression were correlated and suggests a potential interplay of differential miRNA biogenesis and RNA binding protein during metastatic progression.

A single nucleotide polymorphism located in microRNA-499a causes loss of function resulting in increased expression of osbpl1a and reduced serum HDL level.

Atherosclerosis is the main pathological process that induces CVD (cardiovascular diseases), and the objective of our study was explore whether miR­499a rs3746444 polymorphism was associated with the HDL level, one of the risk factors of atherosclerosis. Online public miRNA database was utilized to predict the miR­499a target, and luciferase assay was conducted to confirm that miR­499a targeted osbpl1a, then western blot analysis and real-time PCR were performed to verify miRNA-mRNA regulatory relationship between miR­499a and osbpl1a. Based on results of bioinformatics algorithms, osbpl1a was predicted as a candidate target gene of miR­499a, luciferase reporter was generated, and it was found that the luciferase activity of cells was substantial downregulated following co-transfection with wild osbpl1a 3'UTR and miR­499a compared to that in scramble control, while the inhibitory effect of miR­499a was abolished after transfection of mutant osbpl1a 3'UTR. Then, miRNA-mRNA regulatory relationship between miR­499a and osbpl1a was detected, a concentration-dependent effect of miR­499a on the miR­499a expression was observed, and both osbpl1a mRNA and protein levels of cells transfected with miR­449a (30 and 60 nM) or osbpl1a siRNA were markedly reduced, while notably improved subsequent to transfect with anti­miR­449a (30 and 60 nM) in comparison with NC groups, moreover, the inhibitory effect among 30 or 60 nM miR­499a, osbpl1a siRNA was similar, the improved effect of 30 or 60 nM anti­miR­499a showed no significant change. The influence of rs3746444 A allele on expression level of miR­499a represented a recessive pattern in high-grade group with a higher level of miR­499a in AA group, and HDL level in AA group was significantly reduced related to those in AG and GG groups. This study validated that rs3746444 polymorphism influenced the expression of miR­499a, its target gene, osbpl1a, and thereby associated with the HDL level, which makes it a potential factor involved in the mechanism of atherosclerosis.

Role of microRNA-130a in the pathogeneses of obstructive sleep apnea hypopnea syndrome-associated pulmonary hypertension by targeting the GAX gene.

OBJECTIVE: The purpose of this study was to elucidate the role of microRNA-130a (miR-130a) in obstructive sleep apnea hypopnea syndrome (OSAHS)-associated pulmonary hypertension (PHT) by targeting the growth arrest-specific homeobox (GAX) gene. METHODS: A total of 108 patients with OSAHS-associated PHT were recruited as the OSAHS-associated PHT group and 110 healthy individuals were randomly selected as the normal control group. Human umbilical vein endothelial cells (HUVECs) were selected and divided into the control, miR-130a mimic, mimic negative control (NC), miR-130a inhibitor, and inhibitor-NC groups. The dual luciferase reporter gene assay was used to identify the relationship between miR-130a and the GAX gene. The quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were applied for the relative expressions of miR-130a and the mRNA and protein expressions of GAX. Serum levels of endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), nitric oxide (NO), and super oxide dismutase (SOD) were detected. Cell apoptosis and angiogenic activity were analyzed by flow cytometry and cell tube formation assay. RESULTS: GAX was a target gene of miR-130a. Compared with the normal control group, the relative expression of miR-130a and the serum levels of ET-1 and VEGF were increased, whereas the mRNA expression of GAX and the serum levels of NO and SOD were decreased in the OSAHS-associated PHT group. Compared with the control, mimic-NC, and inhibitor-NC groups, the relative expressions of miR-130a in the miR-130a mimic group were enhanced, whereas the expression of miR-130a in the miR-130a inhibitor group was reduced. However, the mRNA and protein expressions of GAX showed an opposite trend in the miR-130a mimic and miR-130a inhibitor groups. In comparison to the control, mimic-NC, and inhibitor-NC groups, the miR-130a mimic group had an increase of ET-1 and VEGF expressions, whereas the expressions of NO and SOD were reduced. However, the miR-130a inhibitor group exhibited an opposite trend. The apoptosis rate and tube formation number in the miR-130a mimic group were obviously increased, whereas the miR-130a inhibitor group showed an obvious decrease. CONCLUSION: These data provided strong evidence that miR-130a may be involved in the progression of OSAHS-associated PHT by down-regulating GAX gene.

Crystal structures of [Mn(bdc)(Hspar)2(H2O)0.25]·2H2O containing MnO6+1 capped trigonal prisms and [Cu(Hspar)2](bdc)·2H2O containing CuO4 squares (Hspar = sparfloxacin and bdc = benzene-1,4-di-carboxyl-ate).

The syntheses and crystal structures of 0.25-aqua-(benzene-1,4-di-carboxyl-ato-κ(2) O,O')bis-(sparfloxacin-κ(2) O,O')manganese(II) dihydrate, [Mn(C8H4O4)(C19H22F2N4O3)2(H2O)0.25]·2H2O or [Mn(bdc)(Hspar)2(H2O)0.25]·2H2O, (I), and bis-(sparfloxacin-κ(2) O,O')copper(II) benzene-1,4-di-carboxyl-ate dihydrate, [Cu(C19H22F2N4O3)2](C8H4O4)·2H2O or [Cu(Hspar)2](bdc)·2H2O, (II), are reported (Hspar = sparfloxacin and bdc = benzene-1,4-di-carboxyl-ate). The Mn(2+) ion in (I) is coordinated by two O,O'-bidentate Hspar neutral mol-ecules (which exist as zwitterions) and an O,O'-bidentate bdc dianion to generate a distorted MnO6 trigonal prism. A very long bond [2.580 (12) Å] from the Mn(2+) ion to a 0.25-occupied water mol-ecule projects through a square face of the prism. In (II), the Cu(2+) ion lies on a crystallographic inversion centre and a CuO4 square-planar geometry arises from its coordination by two O,O'-bidentate Hspar mol-ecules. The bdc dianion acts as a counter-ion to the cationic complex and does not bond to the metal ion. The Hspar ligands in both (I) and (II) feature intra-molecular N-H⋯O hydrogen bonds, which close S(6) rings. In the crystals of both (I) and (II), the components are linked by N-H⋯O, O-H⋯O and C-H⋯O hydrogen bonds, generating three-dimensional networks.

Radiotherapy with temozolomide provides better survival in the newly diagnosed glioblastoma multiforme: A meta-analysis.

BACKGROUND: The optimal treatment for patients with newly diagnosed glioblastoma multiforme (GBM) remains controversial. The purpose of this meta-analysis was to systematically evaluate radiotherapy/temozolomide (TMZ) versus radiotherapy for treating newly diagnosed GBM. MATERIALS AND METHODS: Six electronic databases (PubMed, EMBASE, MEDLINE, Web of Science, Cochrane Library, and CNKI) were searched for relevant publications up to November 05, 2014. RevMan version 5.2 software was used for statistical analysis. RESULTS: A total of 9 studies were identified in this analyses, which included 986 patients. The summary risk ratio (RR) for overall survival and the progression-free survival (PFS) was the measure of interest. Results revealed that the addition of TMZ to radiotherapy resulted in a statistically significant survival benefit in poor prognosis patients with newly diagnosed glioblastoma (RR = 2.93 [95% confidence interval (CI) 2.29, 3.75], P < 0.00001). Moreover, radiotherapy plus TMZ was more beneficial than radiotherapy alone in improving PFS (RR = 3.52, [95% CI 2.53, 4.89], P < 0.00001). However, certain grade 3-4 hematological toxicities were significantly more common with TMZ. CONCLUSIONS: This meta-analysis suggests that radiotherapy/TMZ provides better survival than radiotherapy alone in treating GBM.

MicroRNA let-7: Regulation, single nucleotide polymorphism, and therapy in lung cancer.

Lung cancer (LC) is the leading cause of cancer-related deaths worldwide. MicroRNAs (miRNAs) are highly evolutionarily conserved noncoding small RNAs, which were first identified in Caenorhabditis elegans. There are 1100 or more miRNAs have been identified in Homo sapiens. Let-7 miRNA is involved in the regulation of gene expression in cells. Several novel factors and feedback loops involved in the regulation of the synthesis of let-7 have been identified and additional let-7 target genes have been found. Let-7 has also been shown to be significantly correlated with the occurrence and development of cancer and the results of preliminary studies suggest that it is involved in the regulation of oncogenic pathways in numerous types of tumors, such as, LC. As let-7 is a potential molecular target for tumor therapy, a mass of studies have been conducted focus on the relationship between let-7 and LC. With the mechanism becoming revealed, more and more groups are looking for the anti-tumor role of let-7 family in anti-tumor therapy development. In this review, we summarize the newest investigations on let-7 and LC, the regulation of let-7 and its targets gene have been discussed, and the attempts for new therapy for LC have also been summarized.

Apolipoprotein A5 and apolipoprotein C3 single nucleotide polymorphisms are correlated with an increased risk of coronary heart disease: a case-control and meta-analysis study.

BACKGROUND: Triglycerides (TGs) are proatherogenic lipoproteins involving the risk of coronary heart disease (CHD), while apolipoprotein A5 (APOA5) and apolipoprotein C3 (APOC3) are main lipoproteins composing TG-rich lipoproteins. In this study, we aim to explore the correlation of CHD with APOA5 -1131 T > C and APOC3 -455 T > C single nucleotide polymorphisms (SNPs). METHODS: A sum of 210 CHD patients, hospitalized between Jan. 2013 and Mar. 2015 at China-Japan Union Hospital, Jilin University, were selected as our case group and 223 healthy individuals who had physical examination at same hospital at the same period were selected as control group. The frequency distribution of genotypes of APOA5 -1131 T > C and APOC3 -455 T > C SNPs were measured by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The Stata 12.0 software was utilized for statistical analyses. RESULTS: There was no significant difference on age and sex between case and control group (P > 0.05). History of smoking, drinking, hypertension and diabetes mellitus, body mass index and levels of TG and fasting blood sugar in case group were shown to be higher than control group (P < 0.05), while levels of total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol in case group were lower than control group (P < 0.05). Both CC and TC' + CC frequencies of APOA5 -1131 T > C and APOC3 -455 T > C in case group were higher compared to control group (both P < 0.05). Additionally, T allele frequencies of the two SNPs in case group were lower than control group, while C allele in case group has higher frequencies compared to control group (both P < 0.05). The results of meta-analysis under allele and dominant models showed that APOA5 -1131 T > C and APOC3 -455 T > C SNPs are likely to increase the risk of CHD (both P < 0.05). CONCLUSION: APOA5 -1131 T > C and APOC3 -455 T > C SNPs may play potent roles in the development and progression of CHD.

Malignant ventricular tachycardia in acromegaly: a case report / Taquicardia ventricular maligna na acromegalia: relato de caso

CONTEXT: In patients with acromegaly, cardiovascular complications are the main cause of death; sudden death has been associated with ventricular tachyarrhythmias. In other patients with life-threatening malignant ventricular tachyarrhythmias, surgical placement of an implantable cardioverter-defibrillator (ICD) has proved highly effective in reducing sudden death rates. CASE REPORT: The present article reports the case of a 50-year-old male acromegalic patient who presented symptoms of syncope induced by ventricular tachycardia. An ICD was surgically implanted and a pituitary adenoma, which was responsible for the acromegaly, was completely removed in the same procedure. The surgery was successful and the ventricular arrhythmias were effectively terminated. During six months of follow-up, no documented arrhythmic episodes occurred. CONCLUSION: In patients with acromegaly, malignant ventricular tachyarrhythmia might be effectively controlled by implantation of an ICD and surgical removal of the pituitary adenoma. .

CONTEXTO: As complicações cardiovasculares são a principal causa de morte em pacientes com acromegalia, e a morte súbita tem sido associada a taquiarritmias ventriculares. Em outros pacientes com risco de vida por taquiarritmias ventriculares malignas, a aplicação cirúrgica de um cardioversor-desfibrilador implantável (CDI) provou ser altamente eficaz na redução das taxas de morte súbita. RELATO DE CASO: O presente artigo relata o caso de um paciente acromegálico de 50 anos de idade e do sexo masculino, que apresentava sintomas de síncope induzida por taquicardia ventricular. Foi implantado cirurgicamente nesse paciente um CDI e na mesma intervenção cirúrgica foi completamente removido um adenoma hipofisário responsável pela acromegalia. A cirurgia foi bem-sucedida e o paciente deixou de sofrer de arritmias ventriculares. Durante seis meses de acompanhamento, não se documentaram, nesse paciente, episódios arrítmicos. CONCLUSÃO: A taquiarritmia ventricular maligna pode ser efetivamente controlada em pacientes com acromegalia pela implantação de um CDI combinado com a remoção cirúrgica do adenoma hipofisário. .

Malignant ventricular tachycardia in acromegaly: a case report.

CONTEXT: In patients with acromegaly, cardiovascular complications are the main cause of death; sudden death has been associated with ventricular tachyarrhythmias. In other patients with life-threatening malignant ventricular tachyarrhythmias, surgical placement of an implantable cardioverter-defibrillator (ICD) has proved highly effective in reducing sudden death rates. CASE REPORT: The present article reports the case of a 50-year-old male acromegalic patient who presented symptoms of syncope induced by ventricular tachycardia. An ICD was surgically implanted and a pituitary adenoma, which was responsible for the acromegaly, was completely removed in the same procedure. The surgery was successful and the ventricular arrhythmias were effectively terminated. During six months of follow-up, no documented arrhythmic episodes occurred. CONCLUSION: In patients with acromegaly, malignant ventricular tachyarrhythmia might be effectively controlled by implantation of an ICD and surgical removal of the pituitary adenoma.

Bis(µ-biphenyl-2,2'-dicarboxyl-ato)bis-[aqua-(2,2'-bipyridine)cadmium(II)].

In the centrosymmetric dinuclear mol-ecule of the title compound, [Cd(2)(C(14)H(8)O(4))(2)(C(10)H(8)N(2))(2)(H(2)O)(2)], the Cd(2+) ion is coordinated by three O atoms from two different diphenyl-dicarboxyl-ate (dpa) ligands (one O,O'-bidentate and one monodentate), a chelating bipyridine ligand and a water mol-ecule, generating an extremely distorted trigonal-prismatic (or irregular) CdN(2)O(4) coordination geometry for the metal ion. The bridging ligands generate an 18-membered ring, which is stabilized by two pairs of intra-molecular O-H⋯O hydrogen bonds.

Poly[bis-[µ(2)-8-ethyl-5-oxo-2-(piperazin-1-yl)-5,8-dihydro-pyrido[2,3-d]pyrimidine-6-carboxyl-ato]nickel(II)].

The title compound, [Ni(C(14)H(16)N(5)O(3))(2)](n) or [Ni(ppa)(2)](n), where ppa is 8-ethyl-5-oxo-2-(piperazin-1-yl)-5,8-dihydro-pyrido[2,3-d]pyrimidine-6-carboxyl-ate, was synthesized under hydro-thermal conditions. The Ni(II) atom (site symmetry ) exhibits a distorted trans-NiN(2)O(4) octa-hedral geometry defined by two monodentate N-bonded and two bidentate O,O'-bonded ppa monoanions. The extended two-dimensional structure is a square grid. An inter-molecular N-H⋯O hydrogen bond occurs.