Plant development: the making of a leaf.
A transcription factor of the Myb family has been found to couple dorsoventral patterning and proximodistal outgrowth during leaf development.
Meristem↗
Biomedical subjects
S Christensen
Publications and source records attributed to S Christensen.
[Patients and attitudes to a palliative unit in H:S--a questionnaire study].
A questionnaire was mailed to 42 representative in-patient departments of hospitals in the City of Copenhagen asking the medical staff to state what number of their patients could possibly be referred to a future hospital--associated palliative care unit. All-together 215 answers were returned from two questionnaire dates two weeks apart, comprising more than 1750 patients each day. Furthermore, 42 of 60 general practitioners answered another questionnaire on the same topic. From the hospital questionnaire it was concluded that approximately 8% of all patients were admitted for palliative care reasons, 75% suffering from incurable cancer. More than 50% of patients admitted for palliative care reasons were assessed to be suitable candidates for a palliative care unit. The general practitioners recognised at least 50 patients treated only for palliative reasons. In the same month the general practitioners referred more than 20 patients to hospital wards, but two-thirds of the practitioners would have preferred that these patients could have had the option of staying at home for terminal care. In general, more than 50% of the medical staff opted for establishing a palliative care unit.
Adult↗
[Teratogenic effects of ACE-inhibitors and angiotensin II receptor antagonists].
Since the introduction of angiotensin converting enzyme-inhibitors (ACE-inhibitors) in the 1980's, more than 50 cases of foetotoxic effects ascribed to intrauterine exposure to inhibitors have been published. Among the most commonly reported effects are: Hypotension, renal dysplasia, anuria/oliguria, oligohydramios, intrauterine growth retardation, pulmonary hypoplasia, unclosed ductus arteriosus, incomplete ossification of the skull, intrauterine og neonatal death. Recent animal studies have confirmed that intrauterine or neonatal exposure to ACE-inhibitors or the AT1-receptor antagonist losartan can cause death and serious, irreversible organ damage. These effects are similar to the complications previously reported in humans. Animal studies suggest that the foetotoxic actions are most common after exposure during the last trimester. However, due to the severity of these complications, the use of ACE-inhibitors and AT1-receptor antagonists should be avoided throughout pregnancy and in women who are breast feeding.
Abnormalities, Drug-Induced↗
[Orbital injury following accidental fall. Intra-orbital wooden foreign body].
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Accidental Falls↗
RNA expression from a site-specific non-LTR retrotransposon microinjected into Xenopus oocytes.
Tx1L is a site-specific non-LTR retrotransposon (NLR) that has been identified in the genome of Xenopus laevis. Using microinjection into Xenopus oocytes, several aspects of RNA expression by these elements were investigated. With constructs carrying various parts of the element we saw no evidence of promoter activity, unlike what has been shown for several other elements of this class. Tx1L transcription was induced by linking a whole element to a promoter that is active in oocytes. Among the RNAs produced, about half had 3' ends located near the end of the element, suggesting that instruction for 3' end formation are encoded in the element or its target. Deletion of the 3' UTR of Tx1L and of surrounding target sequences indicated that these regions are not required for termination or processing of the RNA. PolyA or very A-rich sequences were added at these 3' ends, despite the absence of canonical polyA addition signals. A significant proportion of non-A residues was found in the 3' untemplated tails, and this is reminiscent of non-templated insertions often found at the 3' junction of new genomic copies of some NLRs.
3' Untranslated Regions↗
Mechanism of antidiuresis caused by bendroflumethiazide in conscious rats with diabetes insipidus.
1. The mechanism underlying the antidiuretic effect of thiazide diuretics in diabetes insipidus (DI) is unknown. This study addressed two specific questions: is the reduction in urine flow rate (V) related to a decrease in the delivery of fluid from the pars recta of the proximal tubules ('distal delivery'), and are there any changes in the expression and/or intracellular distribution of vasopressin stimulated water channels (AQP2) in the collecting ducts, during chronic thiazide-induced antidiuresis? 2. Nine Brattleboro rats with vasopressin-deficient DI were treated for 5 days with bendroflumethiazide (BFTZ), 9 mg kg(-1) day(-1) orally, and 9 Brattleboro rats were left untreated. BFTZ-treated DI rats showed a fall in V from approximately 200 to approximately 75 ml day(-1) and an increase in urine osmolality from approximately 130 to approximately 400 mosmol kg(-1). 3. BFTZ-induced antidiuresis was associated with a persistent loss of sodium, but not of potassium. After 5 days of treatment, clearance studies in conscious rats showed a tendency towards decreases in effective renal plasma flow (-7%), GFR (-12%) and lithium clearance (C(Li); used as marker for distal delivery) (-25%), compared with untreated controls, but none of these changes were statistically significant. There was no apparent relationship between C(Li) and V in BFTZ-treated or untreated DI rats. 4. BFTZ treatment did not change the expression of AQP2 in homogenates of cortex, outer or inner medulla from DI rats, or from normal Long Evans rats. Light and electron microscopic immunocytochemistry revealed no changes in intracellular distribution of AQP2 in principal cells from inner medullary collecting ducts of BFTZ-treated DI rats. 5. We concluded, (i) that although the antidiuretic effect of BFTZ in rats with DI is associated with a net loss of Na, the decrease in V shows no association with changes in distal delivery, as estimated by C(Li). (ii) Antidiuretic treatment with BFTZ does not alter the expression of subcellular distribution of AQP2 water channels in the collecting ducts. The mechanism underlying the chronic antidiuresis caused by thiazide diuretics in DI remains elusive.
Animals↗
Model explaining the relation between distal nephron Li+ reabsorption and urinary Na+ excretion in rats.
Li+ may be reabsorbed via an amiloride-sensitive mechanism in the collecting ducts of rats administered a low-Na+ diet. This was investigated by measuring the increase in fractional urinary excretion of Li+ (FELi) in response to amiloride in conscious rats at two different levels of plasma Li+ concentration and after administration of bendroflumethiazide (BFTZ), angiotensin III (ANG III), and aldosterone (Aldo). The results confirmed that amiloride increased (FELi) in rats on a low-Na+ diet (20 +/- 1 to 35 +/- 1%, means +/- SE), whereas no increase was observed in rats on a normal Na+ diet (37 +/- 1 to 38 +/- 1%). The lithiuretic effect of amiloride was 1) abolished by preadministration of BFTZ (32 +/- 1 to 33 +/- 2%) to Na(+)-deprived rats and 2) increased by ANG III (27 +/- 3 to 33 +/- 2%) and Aldo (25 +/- 2 to 37 +/- 2%) in Na(+)-replete rats. Amiloride-induced changes in FELi were independent of plasma Li+ concentration but inversely related to the fractional excretion of Na+ and the amiloride-sensitive excretion of K+. These results are compatible with the hypothesis that a low tubular Na+ concentration reduces end-tubular Na+ reabsorption and results in hyperpolarization of the apical membrane, thus favoring Li+ uptake into the cells.
Aldosterone↗
Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis.
Experiments were performed to investigate vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in cirrhotic rats with sodium retention but without ascites. In addition, the expression of the furosemide-sensitive type 1 Na-K-2Cl cotransporter (BSC-1) and the natriuretic response to an intravenous test dose furosemide (7.5 mg/kg) during acute V2-receptor blockade was measured. Acute V2-receptor blockade with the selective nonpeptide antagonist OPC-31260 (800 microg . kg-1 . h-1) was performed during conditions in which volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 150 mM glucose. OPC-31260 produced a significantly smaller increase in urine flow rate (-26%) and free water clearance (-18%) in cirrhotic rats than in control rats. The natriuretic response to an intravenous test dose furosemide (7.5 mg/kg) was significantly increased in cirrhotic rats (+52%), but pretreatment with OPC-31260 did not affect the natriuretic response to furosemide in neither cirrhotic nor in control rats. Semiquantitative immunoblotting showed a significant downregulation of AQP-2 in the renal cortex (-72%) and in the outer medulla (-44%). The relative expression of BSC-1 in the outer medulla was unchanged in cirrhotic rats. The corticopapillary gradient of Na was significantly increased in cirrhotic rats. Since daily urine flow rate was similar in cirrhotic and sham-operated rats, we suggest that non-vasopressin-mediated water reabsorption is increased in cirrhotic rats probably as a result of an increased corticomedullary gradient due to exaggerated NaCl reabsorption in the thick ascending limb of Henle's loop.
Alanine Transaminase↗
SB 207499 (Ariflo), a second generation phosphodiesterase 4 inhibitor, reduces tumor necrosis factor alpha and interleukin-4 production in vivo.
The ability of the second generation phosphodiesterase 4 inhibitor SB 207499 (Ariflo), [c-4-cyano-4-(3-cyclopentyloxy-4-methoxyphenyl)-r-l-cyclohexane carboxylic acid], to inhibit inflammatory cytokine production in vivo was evaluated and compared to that of rolipram, a first generation phosphodiesterase 4 inhibitor. To examine human tumor necrosis factor alpha (TNFalpha) production, human monocytes were adoptively transferred into Balb/c mice and challenged with lipopolysaccharide (LPS). In this model, SB 207499 inhibited human TNFalpha production with oral ED50 of 4.9 mg/kg. Similarly, R-rolipram inhibited human TNFalpha production with an ED50 of 5.1 mg/kg, p.o. In contrast to their equipotent activity against TNFalpha production, SB 207499 (ED50 = 2.3 mg/kg, p.o.) was 10-fold less potent than R-rolipram (ED50 = 0.23 mg/kg, p.o.) in reversing reserpine-induced hypothermia, a model of antidepressant activity. In time course studies, SB 207499 (30 mg/kg, p.o.) inhibited TNFalpha production for at least 10 hr; substantial plasma concentrations of SB 207499 were detected over the same interval. The ability of SB 207499 to modulate interleukin-4 production in vivo was assessed in a chronic oxazolone-induced contact sensitivity model in Balb/c mice. In this model, topical administration of SB 207499 (1000 microgram) inhibited intralesional concentrations of interleukin-4 (55%; P <.01). The results demonstrate that SB 207499 is a potent inhibitor of inflammatory cytokine production in a variety of settings in vivo. Moreover, although it is as potent as R-rolipram in inhibiting TNFalpha production, it has substantially less central nervous system activity. Thus SB 207499 represents an excellent candidate with which to evaluate the antiinflammatory potential of PDE4 inhibitors.
3',5'-Cyclic-AMP Phosphodiesterases↗
Aldosterone receptor blockade inhibits increased furosemide-sensitive sodium reabsorption in rats with liver cirrhosis.
We examined the role of chronic aldosterone receptor blockade on the altered furosemide-sensitive sodium reabsorption in rats with liver cirrhosis induced by common bile duct ligation. CBL and sham-operated control animals were treated with the aldosterone receptor antagonist canrenoate (20 mg/day i.v.) for 4 weeks. Untreated CBL and sham-CBL served as control groups. The plasma concentration of aldosterone was within the normal range in all groups. Sodium balance studies showed that aldosterone receptor blockade prevented sodium retention in cirrhotic rats. Clearance studies showed that the glomerular filtration rate was unchanged, whereas the renal plasma flow was increased in CBL rats. A test dose of furosemide (7.5 mg/kg b.wt. i.v.) produced significantly greater diuretic (+59%) and natriuretic (+56%) responses in CBL rats than in sham-operated controls. The urinary furosemide excretion rate (UFURV) reflects delivery of furosemide to the thick ascending limb. When the natriuresis was expressed relative to UFURV (i.e., the natriuretic efficiency), we found that natriuretic efficiency of furosemide was significantly increased in untreated CBL rats (+59%). However, the natriuretic efficiency of furosemide was normalized in CBL rats treated with canrenoate. The urinary excretion of furosemide was unchanged in untreated CBL rats, but it was significantly increased in cirrhotic rats treated with canrenoate (+43%). This suggests that in CBL rats, chronic canrenoate treatment increases the renal elimination of furosemide as a consequence of reduced metabolism. These data suggest that chronic aldosterone receptor blockade with canrenoate prevents sodium retention in cirrhotic rats partly by inhibition of increased sodium reabsorption in the thick ascending limb.
Animals↗
Ribonucleoprotein formation by the ORF1 protein of the non-LTR retrotransposon Tx1L in Xenopus oocytes.
The Tx1L elements constitute a family of site-specific non-LTR retrotransposons found in the genome of the frog Xenopus laevis . The elements have two open reading frames (ORFs) with homology to proteins of retroviruses and other retroelements. This study demonstrates an expected activity of one of the element-encoded proteins. The RNA binding properties of ORF1p, the product of the first ORF of Tx1L, were examined after expression from RNA injected into Xenopus oocytes. Using sucrose gradient sedimentation and non-denaturing gel electrophoresis, we show that ORF1p associates with RNA in cytoplasmic ribonucleoprotein (RNP) particles. Discrete RNPs are formed with well-defined mobilities. The ORF1p RNPs are distinct from endogenous RNPs that contain stored oocyte mRNAs and two specific endogenous mRNAs do not become associated with ORF1p. ORF1p appears to be capable of associating with its own mRNA and with other injected RNAs, independent of specific recognition sequences. Although nuclear localization of ORF1p was anticipated, based both on the supposed mechanism of transposition and on the presence of a potential nuclear localization signal, no significant fraction of the protein was found in the oocyte nucleus. Nonetheless, the RNA binding capability of ORF1p is consistent with the proposed model for transposition of non-LTR retrotransposons.
Animals↗
On the role of calcium in the regulatory volume decrease (RVD) response in Ehrlich mouse ascites tumor cells.
The putative role for Ca2+ entry and Ca2+ mobilization in the activation of the regulatory volume decrease (RVD) response has been assessed in Ehrlich cells. Following hypotonic exposure (50% osmolarity) there is: (i) no increase in cellular Ins(1,4,5)P3 content, as measured in extracts from [2-3H]myoinositol-labeled cells, a finding at variance with earlier reports from our group; (ii) no evidence of Ca2+-signaling recorded in a suspension of fura-2-loaded cells; (iii) Ca2+-signaling in only about 6% of the single, fura-2-loaded cells at 1-mm Ca2+ (1% only at 0.1-mM Ca2+ and in Ca2+-free medium), as monitored by fluorescence-ratio imaging; (iv) no effect of removing external Ca2+ upon the volume-induced K+ loss; (v) no significant inhibition of the RVD response in cells loaded with the Ca2+ chelator BAPTA when the BAPTA-loading is performed in K+ equilibrium medium; (vi) an inhibition of the swelling-induced K+ loss (about 50%) at 1-mM Ba2+, but almost no effect of charybdotoxin (100 nm) or of clotrimazole (10 microM), reported inhibitors of the K+ loss induced by Ca2+-mobilizing agonists. Thus, Ca2+signaling by Ca2+ release or Ca2+ entry appears to play no role in the activation mechanism for the RVD response in Ehrlich cells.
Animals↗
Assignment of a single disulphide bridge in human alpha2-antiplasmin: implications for the structural and functional properties.
Human alpha2-antiplasmin (alpha2AP) is a serpin involved in the regulation of blood coagulation. Most serpins, unlike smaller serine proteinase inhibitors, do not contain disulphide bridges. alpha2AP is an exception from this generalization and has previously been shown to contain four Cys residues organized into two disulphide bridges [Lijnen, Holmes, van Hoef, Wiman, Rodriguez and Collen (1987) Eur. J. Biochem. 166, 565-574]. However, we found that alpha2AP incorporates iodo[14C]acetic acid, suggesting that the protein contains reactive thiol groups. This observation prompted a re-examination of the state of the thiol groups, which revealed (i) a disulphide bridge between Cys43 and Cys116, (ii) that Cys76 is bound to a cysteinyl-glycine dipeptide, and (iii) and Cys125 exists as either a free thiol or in a mixed disulphide with another Cys residue. The disulphide identified between Cys43 and Cys116 appears to be conserved in orthologous proteins since the homologous Cys residues form disulphide bonds in bovine and possibly mouse alpha2AP. The conservation of this disulphide bridge suggests that it is important for functional aspects of alpha2AP. However, the structural and functional analysis described in this study does not support this conclusion.
Animals↗
The DIA illness probably was the flu!
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Bias↗
[Ultrasound examination of the liver in HELLP syndrome].
A 33-year-old multiparous woman in the 34th gestational week presented with severe upper abdominal pain, nausea and vomiting. Clinical examination revealed severe epigastric tenderness. Abdominal ultrasound examination showed geographical areas with increased echogenicity in the right lobe of the liver. Through haematological examination, we found severe thrombocytopenia and fibrinolysis. The diagnosis of HELLP syndrome was suspected and a caesarean section was performed. We suggest that obstetrical patients with upper abdominal pain and abnormal liver sonography should immediately be haematologically investigated to exclude the life-threatening condition of the HELLP syndrome.
Adult↗
Renal function after myocardial infarction and cardiac arrest in rats: role of ANP-induced albuminuria?
Renal function was measured by clearance technique before and after acute myocardial infarction (MI) induced by left coronary artery ligation in male Sprague-Dawley rats. The animals were anaesthetized with halothane-nitrous oxide, paralysed with pancuronium and artificially ventilated. All parameters were stable throughout the experiment in sham-operated time control animals (n = 8). After MI, rats developed left ventricular dysfunction with increased left ventricular end-diastolic pressure and decreased mean arterial pressure. MI produced antidiuresis and antinatriuresis without changes in glomerular filtration rate (GFR), lithium clearance or renal albumin excretion (n = 8). The antidiuretic and antinatriuretic responses to MI were similar in rats with chronic bilateral renal denervation (n = 5). Three additional rats with chronic bilateral renal denervation had cardiac arrest and were resuscitated with cardiac massage, i.v. lidocaine and intracardiac adrenaline administration. These animals showed a transient increase in urine flow rate, sodium and albumin excretion with maximum 30-60 min after resuscitation, while GFR and lithium clearance were normal. Since cardiac ischaemia and sympathetic stimulation are strong stimuli for the release of atrial natriuretic peptide (ANP), we examined if ANP (0.25, 0.50, and 1.00 microg kg(-1) min(-1), n = 8 per dose) affects urinary albumin excretion. ANP increased dose-dependently the urine/plasma concentration ratio of albumin relative to inulin, which suggests that ANP increases the glomerular permeability for albumin. We conclude that MI causes stimulation of renal tubular sodium and water reabsorption by a mechanism which is independent of intact renal innervation. MI does not produce any change in renal albumin excretion in rats, but transient albuminuria may be observed in rats following cardiac arrest and/or manoeuvres used in cardiac resuscitation. Since ANP produces albuminuria, we speculate that ANP may be an important mediator of albuminuria in states with elevated plasma concentrations of ANP.
Albuminuria↗
Functional domains of LAG-2, a putative signaling ligand for LIN-12 and GLP-1 receptors in Caenorhabditis elegans.
The LAG-2 membrane protein is a putative signaling ligand for the LIN-12 and GLP-1 receptors of Caenorhabditis elegans. LAG-2, like its Drosophila homologues Delta and Serrate, acts in a conserved signal transduction pathway to regulate cell fates during development. In this article, we investigate the functional domains of LAG-2. For the most part, mutants were constructed in vitro and assayed for activity in transgenic animals. We find a functional role for all major regions except one. Within the extracellular domain, the N-terminal region, which bears no known motif, and the DSL domain are both required. By contrast, the region bearing epidermal growth factor-like repeats can be deleted with no apparent reduction in rescuing activity. The intracellular region is not required for activity but instead plays a role in down-regulating LAG-2 function. Finally, membrane association is critical for mutant rescue.
Animals↗
Antihypertensive action of non-natriuretic doses of furosemide in Dahl salt-sensitive rats.
BACKGROUND: That non-natriuretic doses of loop diuretics exert an antihypertensive action has been suggested, but not confirmed, by simultaneous measurements of the arterial pressure and sodium balance during therapy. OBJECTIVE: To examine the relationship between changes in arterial pressure and changes in sodium balance during furosemide treatment. DESIGN: Twenty hypertensive Dahl salt-sensitive rats fed a 4% NaCl diet were allocated to four groups and administered the following treatments: placebo once a day intraperitoneally, continuous infusion of 4 mg/day furosemide intraperitoneally, 4 mg furosemide once a day intraperitoneally and 12 mg furosemide once every third day intraperitoneally. METHODS: The mean arterial pressure (MAP) was measured continuously with radiotelemetry and the sodium balance was measured with the rats in metabolic cages. RESULTS: Administration of furosemide as a bolus injection once a day (P < 0.01) or once every third day (P < 0.05) lowered the MAP significantly compared with placebo, whereas continuous infusion of furosemide had no significant effect on the MAP (P < 0.07). Fast Fourier transformation analysis detected an acute antihypertensive action related to the temporary diuretic and natriuretic responses during the period 0-6 h after intraperitoneal bolus injections of 4 and 12 mg furosemide. None of the treatment regimens produced 24 h sodium or potassium losses. At the end of the study, the total body water, extracellular fluid volume, total body sodium and potassium were similar for rats in all groups. CONCLUSIONS: Furosemide has an acute antihypertensive action in Dahl salt-sensitive rats fed a 4% NaCl diet that is related to renal sodium and volume losses whereas the long-term antihypertensive effect is independent of changes in extracellular fluid volume, total body water, sodium and potassium.
Animals↗