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Biomedical subjects

Carsten Sand

Publications and source records attributed to Carsten Sand.

10 recordsLinked to original sources
PubMed2006

[The first HPV vaccine is now available].

More than two thirds of carcinomas of the uterine cervix are caused by human papilloma virus (HPV) types 16 and 18, and 90% of all genital warts are caused by HPV 6 and 11. In June 2006, the US Food and Drug Administration accepted the first prophylactic HPV vaccine against HPV 6, 11, 16 and 18 to be offered to girls and young women. This new vaccine is also now available in Denmark. Questions concerning economics, ethics, organization, and vaccine monitoring need to be discussed in connection with the establishment of a vaccine program. In addition, information to the general population as well as to health care providers and decision-makers should have been given a high priority.

Adolescent↗
PubMed2005

[Dermatologic problems arising during foreign travel].

The skin is a highly exposed organ during vacation times, especially during travel to countries with subtropical and tropical climates. Prolonged stay in these countries significantly increases the risk of contracting rarely seen dermatoses such as leishmaniasis, larva migrans and myiasis. The bites of various flies may provoke itching and excoriations that may be infected with Staphylococcus aureus and/or hemolytic streptococci, resulting in impetigo, furunculosis or erysipelas. Elderly persons spending weeks in the tropical sun may develop drug-induced phototoxic or photoallergic rash due to concomitant medication for cardiovascular or rheumatic diseases. Acute sunburn is considered a short-lasting problem, but in children it increases the risk of malignant melanoma in later years. Also of concern is chronic UV exposure, which increases the risk of premalignant and malignant skin tumors. Finally, mucocutaneous manifestations arising weeks and months after returning from vacation should raise suspicions of sexually transmitted syphilis and HIV.

Adult↗
PubMed2005

Referral pattern of skin diseases in an acute outpatient dermatological clinic in Copenhagen.

The referral pattern of acute dermatologic conditions is not well described in either outpatients or hospitalized patients. The aim of this study is to describe in more detail the skin diseases that were referred for evaluation in an acute outpatient clinic at Bispebjerg Hospital, Copenhagen. In a 3-month period in 2003 a total of 428 consecutive new patients were referred for various skin diseases that needed subacute and acute dermatological evaluation in a university hospital setting. Referral pattern, age ratio and sex ratio were examined retrospectively. Two hundred and twenty-five (53%) of the 428 patients were referred from other hospital clinics in the local area. Sixty-six (15%) were referred from private practising dermatologists and 64 (15%) from general practitioners in the City of Copenhagen. Referral information was not noted in 35 (8%) of the 428 patients. The most prevalent diagnoses were: unspecified eczema (10.7%), drug eruptions (6.3 %), psoriasis (6.3%), atopic dermatitis (5.6%), bacterial skin infections (4.0%), inflammatory skin disorders (3.7%), seborrhoeic dermatitis (3.5%), urticaria (3.0%), seborrhoeic keratosis (3.0%), toxic contact dermatitis (2.8%), ulcus cruris (2.8%), autoimmune diseases (2.8%), malignant skin tumours (2.5%), candidiasis (2.5%), pruritus/prurigo (2.5%) and viral skin infections (2.5%). The fact that drug eruptions are one of the leading causes of acute referral conditions probably reflects the proximity to other hospital settings, where a large number of patients receive several systemic medicaments for various conditions.

Acute Disease↗
PubMed2004

Vasopressin-induced vasoconstriction is dependent on MAPKerk1/2 phosphorylation.

To investigate the involvement of the mitogen-activated protein kinase (MAPK) family of extracellular signal-regulated kinase (ERK) 1 and 2 (MAPKerk1/2) in the vasopressin-mediated vasoconstriction in the rat aorta. Vasopressin-induced vasoconstriction was measured in isolated rat thoracic aortae in the presence or absence of MAPKerk1/2 kinase (MKKmek1/2) inhibitors. Thereafter the MAPKerk1/2 phosphorylation in the rat aorta was quantified using Western blot analysis. Vasopressin (1-300 nm) induced a concentration-dependent vasoconstriction, which could be inhibited concentration dependently by the selective MKKmek1/2 inhibitors, PD 98059 (10 and 100 microm) and U 0126 (10 and 100 microm). Western blot analysis revealed a 2.7 +/- 0.6-fold increase in the MAPKerk1/2 phosphorylation induced by vasopressin (300 nm). This phosphorylation could be dose dependently prevented by both PD 98059 (100 microm) and U 0126 (10 and 100 microm). These results indicate that vasoconstriction induced by vasopressin is partly regulated by the MAPKerk1/2 pathway.

Animals↗
PubMed2003

The influence of endogenously generated reactive oxygen species on the inotropic and chronotropic effects of adrenoceptor and ET-receptor stimulation.

Reactive oxygen species (ROS) play a role in cardiovascular diseases such as heart failure and hypertension. Furthermore, increasing evidence has accumulated suggesting that ROS can also be formed subsequent to the stimulation of various receptors, thus functioning as second messengers. The objective of the present study was to elucidate the role of intracellular-generated ROS in the inotropic and chronotropic effects of the alpha1- and beta-adrenoceptor and the ET-receptor stimulation in isolated rat atria. In addition, we investigated whether the MAPKerk pathway is involved in the ROS-provoked rise of contractile force. For this purpose hydrogen peroxide was applied, which is known to serve several endogenous functions as a second messenger. Moreover, hydrogen peroxide readily crosses cell membranes, which thus allows to mimic the intracellular formation. Preincubation of atria with EUK 8 (400 microM), a cell permeable superoxide dismutase- and catalase-mimetic, reduced the positive inotropic effect upon alpha1-adrenoceptor and ET-receptor stimulation. The responsiveness to beta-adrenoceptor stimulation remained unaffected by this pretreatment. The chronotropic effects were not altered by preincubation with EUK 8. In contrast to the MAPK(p38) inhibitor SB203580 (2 and 10 microM), the two MKKmek inhibitors PD98059 (30 and 100 microM) and U0126 (10 microM) significantly attenuated the positive inotropic response to hydrogen peroxide in isolated rat left atria. In addition, inhibition of the Na+/H+ exchange (NHE) by cariporide (1 microM) counteracted ROS-provoked increase of contractile force. From the present study we conclude that the inotropic responses to alpha1-adrenoceptor and ET-receptor stimulation are, at least partially, caused by intracellular-formed ROS, that subsequently may activate the MAPKerk pathway and the NHE.

Animals↗
PubMed2003

Effects of hypochlorite and hydrogen peroxide on cardiac autonomic receptors and vascular endothelial function.

1. Reactive oxygen species (ROS) are known to be involved in the progression of various cardiovascular diseases. One source of ROS is activated neutrophils, which can release superoxide anion radicals and hydrogen peroxide by membrane-bound NAD(P)H oxidases. These ROS not only destroy bacteria, but may also affect mammalian tissue. In addition, hydrogen peroxide serves as a substrate for myeloperoxidase, an enzyme that is released by activated neutrophils during inflammatory processes, as seen, for instance, in reperfusion injury and atherosclerosis. Myeloperoxidase catalyses the oxidation of chloride by hydrogen peroxide, yielding hypochlorite, an extremely potent oxidant. 2. The purpose of the present study was to evaluate the effects of hypochlorite on a variety of receptor-dependent processes in rat isolated left atria and rat thoracic aorta and to compare these results with the phenomena observed after incubation with hydrogen peroxide. 3. In the presence of hypochlorite (300 micro mol/L), the positive inotropic response of alpha1-adrenoceptor stimulation by methoxamine (300 micro mol/L) was converted into a negative inotropic response. In contrast, the positive inotropic effects of the beta1/beta2-adrenoceptor agonist isoprenaline (3 micro mol/L) and endothelin (ET)-1 (100 nmol/L) remained largely unaffected. 4. The inversion of alpha1-adrenoceptor-mediated inotropy was not obtained in the presence of hydrogen peroxide (500 micro mol/L). Hydrogen peroxide did not affect the positive inotropic response of isoprenaline, but it completely abolished the inotropic effect of ET-1. 5. The effect of cardiac M2-receptor stimulation was studied in the presence of hypochlorite and hydrogen peroxide. The negative inotropic response to acetylcholine (ACh) was significantly enhanced after hypochlorite incubation compared with control. 6. In the rat thoracic aorta, endothelial function, evaluated by means of ACh-induced vasodilation, was completely abolished in the presence of hypochlorite (100 micro mol/L), but remained unaffected by treatment with the same concentration of hydrogen peroxide. 7. From these data, we conclude that hypochlorite exerts more toxic properties than its precursor hydrogen peroxide, leading to substantial physiological alterations in cardiac and vascular tissue.

Acetylcholine↗
PubMed2002

A mitogen-activated protein kinase is involved in the inotropic but not chronotropic actions of adrenoceptor agonists and endothelin-1.

The activation of mitogen-activated protein kinase (MAPK) pathways in the heart, for instance by alpha(1)-adrenoceptor agonists and endothelin-1, has primarily been associated with cellular growth regulation. Here we have investigated a possible role of MAPK pathways in the inotropic and chronotropic effects of adrenoceptor agonists and endothelin-1 in isolated rat left and right atria. Inotropic and chronotropic responses of the isolated atria to methoxamine, isoprenaline and endothelin-1 were measured in the absence and presence of inhibitors of MAPK pathways. The MAPK kinase (MKK(mek)) inhibitors PD98059 (100 microM) and U0126 (10 microM) significantly inhibited the inotropic responses to the alpha(1)-adrenoceptor agonist methoxamine (300 microM) and endothelin-1 (50 nM), but not the chronotropic responses to these agonists. U0126 but not PD98059 inhibited the inotropic response to 3 microM isoprenaline. None of the aforementioned inotropic and chronotropic effects were inhibited by the MAPKP(p38) inhibitor SB203580 (2 microM). We conclude that activation of the PD98059/U0126-sensitive MAPK pathway is essential for the inotropic but not chronotropic actions of adrenoceptor agonists and endothelin-1.

Adrenergic Agonists↗