, a Natural Antisense Transcript of , Promotes Tumour Progression and Metastasis in Melanoma.

The TGFβ family member NODAL, repeatedly required during embryonic development, has also been associated with tumour progression. Our aim was to clarify the controversy surrounding its involvement in melanoma tumour progression. We found that the deletion of the exon 2 in a metastatic melanoma cell line impairs its ability to form tumours and colonize distant tissues.

RETRACTED: Prevalence of unprofessional social media content among young vascular surgeons.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).

Femoral vein transposition is a durable hemodialysis access for patients who have exhausted upper extremity options.

Objective: Access surgeons often encounter patients with end-stage renal disease who have exhausted all upper extremity hemodialysis access options. Although the lower extremity is often the next alternative, prosthetic lower extremity access can be prone to infectious complications and historically has poor patency. We describe our contemporary experience with an autogenous femoral vein transposition (FVT) arteriovenous fistula.

Axillary-bifemoral and axillary-unifemoral artery grafts have similar perioperative outcomes and patency.

Objective: It has been suggested that more bypass outflow targets for bypass grafts improve patency and outcomes. Our objective was to examine this in a multicenter contemporary series of axillary to femoral artery grafts.

Methods: The Vascular Quality Initiative database was queried for all axillary-unifemoral (AxUF) and axillary-bifemoral (AxBF) bypass grafts performed between 2010 and 2017 for claudication, rest pain, and tissue loss.

Paternal Insulin-like Growth Factor 2 (Igf2) Regulates Stem Cell Activity During Adulthood.

Insulin-like Growth Factor 2 (IGF2) belongs to the IGF/Insulin pathway, a highly conserved evolutionarily network that regulates growth, aging and lifespan. Igf2 is highly expressed in the embryo and in cancer cells. During mouse development, Igf2 is expressed in all sites where hematopoietic stem cells (HSC) successively expand, then its expression drops at weaning and becomes undetectable when adult HSC have reached their niches in bones and start to self-renew.

Eagle Syndrome Presenting after Blunt Trauma.

As classically described, Eagle syndrome is an entity where patients develop pain or neurologic manifestations arising from an elongated styloid process and/or an ossified stylohyoid ligament irritating or compressing adjacent cranial nerves or the carotid arteries. Over the past few years, there have been reports of actual injury to the internal carotid artery with dissection, occlusion, and strokes. We present 3 cases identified after blunt trauma: 1 due to carotid compression and 2 due to actual injury to the internal carotid artery.

Insulin-like growth factor-II is produced by, signals to and is an important survival factor for the mature podocyte in man and mouse.

Podocytes are crucial for preventing the passage of albumin into the urine and, when lost, are associated with the development of albuminuria, renal failure and cardiovascular disease. Podocytes have limited capacity to regenerate, therefore pro-survival mechanisms are critically important. Insulin-like growth factor-II (IGF-II) is a potent survival and growth factor; however, its major function is thought to be in prenatal development, when circulating levels are high.

Impaired mesenchymal stem cell differentiation and osteoclastogenesis in mice deficient for Igf2-P2 transcripts.

During embryonic development, Igf2 gene transcription is highly regulated through the use of several promoters whose specific roles are not defined. Here, we show that loss-of-function of one of these promoters, Igf2-P2, results in growth defects that are temporally and quantitatively different from those seen in Igf2-null mutants. In particular, Igf2-P2 mutants exhibit skeletal abnormalities characterized by thin and short bones with reduced mineralization and medullar cavity and with altered bone remodeling.

A model for studying human articular cartilage integration in vitro.

One of the major obstacles hindering cartilage repair is the integration of the reparative cartilage with the recipient cartilage. The purpose of this study was to develop an in vitro model that can be conveniently applied to simulate and improve the integration of tissue engineered cartilage with native articular cartilage. This model, a cartilage integration construct, consists of a cartilage explant and isolated chondrocytes.

Fibroblast growth factor-2 regulates myocardial infarct repair: effects on cell proliferation, scar contraction, and ventricular function.

Fibroblast growth factor-2 (FGF2, bFGF) has been proposed to regulate wound healing and angiogenesis, but skin wound healing in FGF2-knockout (FGF2-KO) animals is only slightly delayed. To determine the role of FGF2 in myocardial infarct repair, we studied the evolution of left ventricular geometry, cell proliferation, matrix content, and cardiac function in mice lacking or overexpressing (FGF2-Tg) FGF2. Despite having no effect on initial infarct size, deletion of FGF2 resulted in reduced fibroblast proliferation and interstitial collagen deposition, decreased endothelial proliferation and vascular density, and decreased cardiomyocyte hypertrophy.

Altered cardiovascular responses in mice lacking the M(1) muscarinic acetylcholine receptor.

Although the M(2) muscarinic acetylcholine receptor (mAChR) is the predominant functional mAChR subtype in the heart, some responses of the cardiovascular system to acetylcholine (ACh) may be mediated by other mAChR subtypes. The potential effect of M(1) mAChR on heart function was investigated using M(1) knockout (M(1)-KO) mice. In vivo cardiodynamic analysis showed that basal values of heart rate (HR), developed left ventricular pressure (DLVP), left ventricular dP/dt(max) (LV dP/dt(max)), and mean blood pressure (MBP) were similar between wild-type (WT) and M(1)-KO mice.

Midkine is involved in kidney development and in its regulation by retinoids.

In the kidney, in which development depends on epithelial-mesenchymal interactions, it has been shown that retinoids modulate nephrogenesis in a dose-dependent manner in vivo and in vitro. Midkine (MK) is a retinoic acid responsive gene for a heparin-binding growth factor. The aim of the present study was therefore to quantify the expression of MK mRNA during renal development in the rat, to analyze the regulation of MK expression by retinoids in vivo and in vitro, and, finally, to study the role of MK in rat metanephric organ cultures.

Alteration of cardiovascular and neuronal function in M1 knockout mice.

We used gene targeting to generate mice lacking the M1 muscarinic acetylcholine receptor. These mice exhibit a decreased susceptibility to pilocarpine-induced seizures, loss of regulation of M-current potassium channel activity and of a specific calcium channel pathway in sympathetic neurons, a loss of the positive chronotropic and inotropic responses to the novel muscarinic agonist McN-A-343, and impaired learning in a hippocampal-dependent test of spatial memory.

Beta-adrenergic and muscarinic receptor mRNA accumulation in the sinoatrial node area of adult and senescent rat hearts.

The sinoatrial (SA) node is the cardiac pacemaker and changes in its adrenergic-muscarinic phenotype have been postulated as a determinant of age-associated modifications in heart rate variability. To address this question, right atria were microdissected, the SA node area was identified by acetylcholinesterase staining, and, using a RT-PCR method, the accumulation of mRNA molecules encoding beta1- and beta2-adrenergic (beta1- and beta2-AR) and muscarinic (M2-R) receptor was quantified to define the proportion between beta-AR and M2-R mRNAs within the sinoatrial area of adult (3 months) and senescent (24 months) individual rat hearts. In adult hearts, the highest M2-R/beta-AR mRNA ratio was observed within the sinoatrial area compared with adjacent atrial myocardium, while in the senescent hearts, no difference was observed between sinoatrial and adjacent areas.

Heart rate and heart rate variability, a pharmacological target.

Heart rate varies with respiration, blood pressure, emotion, etc., and heart rate variability (HRV) is presently one of the best indices to predict fatal issues in cardiac failure and after myocardial infarction. HRV depends on various reflexes.

beta-Adrenergic and muscarinic receptor expression are regulated in opposite ways during senescence in rat left ventricle.

The well-known attenuated sensitivity of senescent heart to isoproterenol is accompanied by a decreased beta1-adrenergic receptors (beta1-AR) density, a down regulation process which may involve several molecular modifications and whose understanding is incomplete. Data concerning the M2-R muscarinic receptors (M2-R) are more contradictory. Both the absolute and relative concentrations of beta1-AR and M2-R as well as the coupling protein G alpha s and G alpha(i2) mRNAs were determined by slot-blot analysis in the left ventricles (LVs) of 6-7 week and 22-month-old male Wistar rats.

Molecular and cellular biology of the senescent hypertrophied and failing heart.

During aging, experimental studies have revealed various cellular changes, principal among which is myocyte hypertrophy, which compensates for the loss of myocytes and is associated with fibrosis. The expression of alpha-myosin heavy chain is replaced by that of the isogene beta-myosin, which leads to decreased myosin adenosine triphosphatase (ATPase) activity. In consequence, contraction is slower and more energetically economical.

Phosphorylated forms of adrenocorticotropin and corticotropin-like intermediary lobe peptide in human tumors.

Many peptides contribute to the heterogeneity of immunoreactive adrenocorticotropin (ACTH) in man. The use of a radioimmunoassay (RIA) specifically directed against the C-terminal end of ACTH allowed us to study precisely the following four peptides: ACTH itself, corticotropin-like intermediary lobe peptide (CLIP) or ACTH (18-39) and their phosphorylated forms on Ser31. We have set up a high-performance liquid chromatography system that separates these four molecules in a single run, to establish their relative distributions in tumors responsible for Cushing's disease or for the ectopic ACTH syndrome, and to evaluate the possible interference of phospho-Ser31 on various RIA or immunoradiometric assay (IRMA) recognition systems for ACTH.

Is the senescent heart overloaded and already failing?

Heart failure mainly occurs during the last decades of life, and it is important to know if the senescent heart is not an already failing heart. During aging, both contraction and relaxation of papillary muscle are impaired. Such an impairment is compensated in vivo and the cardiac output remains normal.

Decreased accumulation of beta 1-adrenergic receptor, G alpha s and total myosin heavy chain messenger RNAs in the left ventricle of senescent rat heart.

The expression of genes coding for the beta 1-adrenergic receptor (beta 1-AR), the alpha subunit of Gs and total myosin heavy chain (MHC) was compared between left ventricles (LV's) from young (6-7 weeks old) and old (22 months old) rats. The mRNA levels were quantitated by Northern or Slot blots analyses using specific DNA probes. Ageing was found to be associated with a reduction in beta 1-AR (77%), G alpha s (33%) and, total MHC (51%) mRNA levels with no concomitant change in 18S RNA and poly(A+) mRNA levels.

Expression of insulin-like growth factor binding protein-1 and -2 genes through the perinatal period in the rat.

Insulin-like growth factor binding proteins (IGFBPs) are essential mediators of the bioavailability and biological effects of the IGFs. Liver expression of the rat (r) IGFBP-1 and rIGFBP-2 genes has been characterized between day 16 in utero (16 diu) and 16 days postnatally (+16 dpn). Run-on experiments showed transcriptional activity of the rIGFBP-1 and rIGFBP-2 genes at birth (B) to be 25 and 5 times that at 16 diu, respectively.