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Les sarcomes des tissus mous sont des tumeurs rares avec une grande variété histologique et des modalités de traitement différentes. Le pazopanib a été récemment mis sur le marché pour le traitement des métastases non adipocytaires des sarcomes des tissus mous résistants au traitement par chimiothérapie conventionnelle. Les pneumothorax spontanés font partie des éventuelles complications de cette molécule et leur prise en charge reste complexe. Le cas rapporté concerne la prise en charge chirurgicale d’un pneumothorax bilatéral spontané chez un patient avec des métastases pulmonaires d’un sarcome traité par pazopanib. L’objectif principal est de pouvoir maintenir ce traitement chez les patients qui en bénéficient. Une collaboration étroite entre les équipes oncologiques et chirurgicales est cruciale pour la prise en charge des effets secondaires liés à l’action anti-angiogénique du pazopanib.

1α,25(OH)2‐vitamin D strongly regulates the expression of the epithelial calcium channel CaT1. CaT1 expression is reduced in ERKOα mice and induced by estrogen treatment, pregnancy, or lactation in VDR WT and KO mice. Estrogens and vitamin D are thus independent potent regulators of the expression of this calcium influx mechanism, which is involved in active intestinal calcium absorption.

1α,25(OH)2‐vitamin D strongly regulates the expression of the epithelial calcium channel CaT1. CaT1 expression is reduced in ERKOα mice and induced by estrogen treatment, pregnancy, or lactation in VDR WT and KO mice. Estrogens and vitamin D are thus independent potent regulators of the expression of this calcium influx mechanism, which is involved in active intestinal calcium absorption.Introduction:Active duodenal calcium absorption consists of three major steps: calcium influx into, transfer through, and extrusion out of the enterocyte. These steps are carried out by the calcium transport protein 1 (CaT1), calbindin‐D9K, and the plasma membrane calcium ATPase (PMCA1b), respectively. We investigated whether estrogens or hormonal changes during the female reproductive cycle influence the expression of these genes, and if so, whether these effects are vitamin D‐vitamin D receptor (VDR) dependent.Materials and Methods:We evaluated duodenal expression patterns in estrogen receptor (ER)α and ‐β knockout (KO) mice, as well as in ovariectomized, estrogen‐treated, pregnant, and lactating VDR wild‐type (WT) and VDR KO mice.Results:Expression of calcium transporter genes was not altered in ERKOβ mice. CaT1 mRNA expression was reduced by 55% in ERKOα mice, while the two other calcium transporter genes were not affected. Ovariectomy caused no change in duodenal expression pattern of VDR WT and KO mice, whereas treatment with a pharmacologic dose of estrogens induced CaT1 mRNA expression in VDR WT (4‐fold) and KO (8‐fold) mice. Pregnancy enhanced CaT1 expression equally in VDR WT and KO mice (12‐fold). Calbindin‐D9Kand PMCA1bexpression increased to a lesser extent and solely in pregnant VDR WT animals. In lactating VDR WT and KO mice, CaT1 mRNA expression increased 13 times, which was associated with a smaller increase in calbindin‐D9Kprotein content and PMCA1bmRNA expression.Conclusions:Estrogens or hormonal changes during pregnancy or lactation have distinct, vitamin D‐independent effects at the genomic level on active duodenal calcium absorption mechanisms, mainly through a major upregulation of the calcium influx channel CaT1. The estrogen effects seem to be mediated solely by ERα.

Insulin-like growth factor-binding protein-1 (IGFBP-1) is believed to be an inhibitory factor for fetal growth. The regulation of IGFBP-1 secretion in the fetus is uncertain, although insulin and oxygen tension (PO2) and saturation are thought to play a role. We studied IGFBP-1 levels in umbilical cord artery (UA) and vein (UV) of 98 singleton fetuses at term with clinical signs of distress during labor, i.e. meconium-stained liquor or/and an abnormal fetal heart rate tracing. Blood gas values and serum C-peptide and IGFBP-1 concentrations were measured in both UA and UV. Twenty-five fetuses had an UA pH<7.20. The concentrations of IGFBP-1 were similar in UA and UV and were highly correlated (r=0.98). IGFBP-1 levels were inversely correlated with birth weight, with increased concentrations in small-for-gestational age fetuses (< or =10th weight percentile). IGFBP-1 levels were negatively correlated with C-peptide concentrations, and remained so after correction for birth weight (r=-0.37 for both UA and UV; P<0.001); more specifically, IGFBP-1 levels were increased in the lowest C-peptide quartile (<0.23 nmol/l) compared with the other quartiles. In addition, IGFBP-1 levels were inversely correlated with PO(2) values (r=-0.39 in UA and r=-0.34 in UV; P<0.001); quartiles of UA and UV PO2 showed a gradual increase in IGFBP-1 concentrations with lower PO2 values. A regression model with C-peptide and PO2 values as independent variables predicted IGFBP-1 concentrations (R2 of model was 0.25 and 0.22 for UA and UV respectively; P<0.001). Other blood gas values (pH, PCO2, HCO3- and base deficit) did not correlate with IGFBP-1 levels. The data of this study indicate that serum IGFBP-1 levels in term fetuses are determined by both insulin and PO2 levels, and suggest that acute hypoxemia stimulates IGFBP-1 secretion in the fetus.

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) concentrations have been found to be decreased in diabetic humans and rats. To investigate further the regulation of plasma Ca in diabetes, first we measured Ca(2+), P, Mg, parathyroid hormone(1-34) (PTH), and total and free 1,25(OH)(2)D(3) in male spontaneously diabetic rats 7 and 28 days after the onset of glycosuria. Secondly, we studied changes in the levels of PTH and 1,25(OH)(2)D(3) in response to hypocalcaemia induced by an i.v. infusion of EGTA (2.5%, wt/vol.) for 24 h, and changes in the levels of 1,25(OH)(2)D(3) in response to an i.v. infusion of rat PTH (10 microgram over 24 h) without or with concomitant EGTA infusion (producing hypercalcaemia or normo/hypocalcaemia respectively), in diabetic and control rats. Ca(2+), P, Mg and PTH concentrations remained within the control ranges after 7 and 28 days of glycosuria; 1,25(OH)(2)D(3) concentrations were decreased after 7, but not after 28, days of glycosuria. PTH concentrations showed a similar rise during EGTA-induced hypocalcaemia in control and diabetic rats compared with saline-infused rats, whereas 1,25(OH)(2)D(3) concentrations were unchanged in both groups. Total and free 1,25(OH)(2)D(3) levels were comparably (about 3-fold) increased during PTH, but not during combined PTH and EGTA infusion in control and diabetic rats. Total 1, 25(OH)(2)D(3) concentrations were lower in the diabetic groups infused with saline or PTH than in their respective controls, and there was a similar trend in the PTH+EGTA-infused group; free 1, 25(OH)(2)D(3) levels, however, were normal or increased in the diabetic groups, confirming our previous data. The novel finding of this study is that, despite severe insulin deficiency and altered 1, 25(OH)(2)D(3) levels, the in vivo response of PTH levels to hypocalcaemia and the in vivo response of 1,25(OH)(2)D(3) levels to PTH in diabetic rats are comparable with those found in nondiabetic rats.

Summary The foraging activities of four genera (six species) of grassland ants (Formica rufibarbis, Tapinoma erraticum, Myrmica schenki, M. sabuleti, Tetramorium caespitum andT. impurum) were observed in June–July 1985 at Treignes (Belgium).

Spontaneously diabetic BB rats were sham operated (SO) or ovariectomized (OVX) within days after onset and studied after 4, 8, and 12 weeks. Analyses included histomorphometry of proximal tibial metaphyses, biochemical analyses of humeri, DXA analyses, and biomechanical testing of femora. In SO diabetic rats, no osteoblasts, osteoid tissue, or osteoclasts were present on the trabecular bone surface, but trabecular bone volume (TBV) remained normal compared with control BB rats. The concentration of IGF‐I per dry weight of humerus was decreased after 12 weeks of diabetes, whereas the concentrations of calcium and osteocalcin did not change. DXA analysis showed normal bone mineral density (BMD) at both diaphyseal and metaphyseal femoral areas. On biomechanical testing, angular deformation, energy absorption, and torsional strength of the femora were decreased after 8–12 weeks of diabetes, but stiffness was normal. Ovariectomy in diabetic rats caused a decrease in femoral BMD especially at the metaphysis, and there was a trend toward decreased TBV in the tibial metaphysis; TBV loss was less marked than in control OVX rats, however. The increase in BMD at the femoral diaphysis, measured after 12 weeks of OVX in control rats, was absent in diabetic rats. Multiple‐regression analysis indicated that the presence of diabetes but not ovariectomy, weight, and mineral content correlated with decreased energy absorption, angular deformation, and strength of the femora. The data infer that the (near) absence of unmineralized bone matrix in severely diabetic rats alters bone microarchitecture and ultimately results in brittle bones, which is not predicted by BMC or BMD measurements.

Summary A study of global recruitment inTetramorium impurum has shown its main characteristics.

Summary During food recruitment, three phases were recognized in the behaviour of the recruiter.

The HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) is a pathological entity in obstetrics that is related to preeclampsia. Recognition and early treatment are mandatory, because of the high fetal and maternal morbidity and fetal mortality rates. This report features the CT and MRI findings in two patients with HELLP syndrome, upper abdominal pain, and severe liver cell dysfunction. Despite the extensive hepatic abnormalities seen on CT and MRI studies, both patients recovered fully after delivery. The role of imaging studies for diagnosis and treatment planning in the clinical setting of HELLP syndrome is discussed.

This paper identifies the symptom profile associated with the four main diagnoses of functional digestive disorders (dyspepsia, gastrooesophageal reflux disease (GORD), gastritis, and constipation) made by general practitioners in Belgium. Results are also presented from a multicentre study in which the effects of cisapride, administered as an oral tablet or suspension, were evaluated in patients with these functional digestive disorders. Analysis of symptom patterns revealed that early satiety and postprandial abdominal bloating were the most prominent symptoms, followed by eructation (belching), heartburn, regurgitation, postprandial epigastric burning or discomfort, and nausea. These symptoms occurred in all diagnostic groups. However, different symptom patterns were associated with each of the disorders; for example, heartburn and regurgitation were the core symptoms in patients diagnosed as having GORD, early satiety and abdominal bloating were characteristic of patients diagnosed with dyspepsia, and fasting or postprandial pain were characteristic of patients given the diagnosis of gastritis. Therefore, it appears that these diagnoses used by general practitioners in Belgium closely correspond to reflux-like, dysmotility-like and ulcer-like dyspepsia, as defined by an international working party. Cisapride improved the core symptoms in about 80% of patients with GORD or dyspepsia, relieved all epigastric symptoms in about 80% of patients with gastritis, and significantly decreased the use of laxatives and increased stool frequency in constipated patients. Cisapride was well tolerated and thus appears to be a useful option in the treatment of functional digestive disorders in a general practice setting.

The maternal and fetal endocrine pancreas were investigated in the diabetic BB rat on day 21 of pregnancy. The maternal pancreas of the diabetic rat contained practically no insulin-positive B cells. The A and D cell mass were also decreased, while plasma glucagon and somatostatin levels were normal or increased, confirming previous data. Six of 11 diabetic rats had B-cell-specific surface antibodies (ICSA), whereas only 1 of 10 nondiabetic rats was ICSA-positive. The volume density of insulin-positive cells was decreased in the fetal pancreas of diabetic BB rats compared to fetuses of nondiabetic rats, but the volume density of glucagon- and somatostatin-positive cells remained normal. The B cells of these fetuses were ultrastructurally less granulated and showed signs of increased cellular activity. Plasma insulin levels were decreased while plasma glucagon and somatostatin concentrations were normal. ICSA were not detected in fetuses of nondiabetic and diabetic rats. There were no differences in the histology of the spleen and thymus between both groups of fetuses. Metabolic characterization of the growth-retarded fetuses of diabetic rats revealed, besides lower plasma insulin concentrations, increased branched chain amino acid levels, and normal plasma Sm/IGF-I levels. The main conclusions from this study are: (1) Severe maternal diabetes decreases the pancreatic insulin-positive cell mass and plasma insulin levels in the fetus, but not the A and D cell mass and function; (2) ICSA are not detectable in fetal plasma; (3) the influence of maternal BB rat diabetes on fetal endocrine pancreas and metabolic environment resembles that of severe streptozotocin-induced diabetes.

The heads of maleT. caespitum contain 4-methyl-3-hexanol (1.7 µg, only the erythro isomer(s) detected) and 4-methyl-3-hexanone (0.8 µg). The heads of alate females contain 0.1 µg of each compound, whereas only the alcohol (0.1 ?g) was found in the heads of workers. Both compounds act as attractants for the workers and their possible functions are discussed.

Trail pheromone production and trail following behaviour of workers ofMyrmica rubra of different age groups, categorized by their cuticular pigmentation, were analysed.

Spontaneously diabetic BB rats have a markedly depressed longitudinal bone growth and bone formation/turnover. In this study, male diabetic BB rats were infused intraperitoneally or subcutaneously for 2 weeks with hormones that are believed to stimulate skeletal growth and/or trabecular bone formation: insulin (3 or 4 U/day), human GH (hGH; 400 mU/day), recombinant human insulin-like growth factor-I (rhIGF-I; 300 or 600 μg/day) and testosterone (80 μg/100 g body weight per day).Saline-treated diabetic BB rats had decreased plasma concentrations of IGF-I and osteocalcin (OC) (OC, 3·7 ±0·3 vs 13·1 ± 0·8 (s.e.m.) nmol/l in controls); bone histomorphometry showed decreased epiphyseal width, osteoblast surface (0·04±0·04 vs 1·5±0·3%) and osteoid surface, and mineral apposition rate (MAR) (1·8±0·5 vs 7·9±0·6 μm/day).Testosterone and hGH infusions had no effect on weight loss or on decreased skeletal growth and bone formation of diabetic rats, nor did they increase plasma IGF-I concentrations. Insulin infusions into diabetic rats resulted in hyperinsulinaemia and accelerated weight gain. The epiphyseal width, osteoblast/osteoid surfaces and OC levels of insulin-treated rats were normalized or stimulated well above control values (osteoblast surface, 4·3 ±0·8%; plasma OC, 16·1 ± 1·4 nmol/l); the MAR (4·0 ± 0·9 μm/day) was only partly corrected after the 2-week infusion. Infusions of rhIGF-I into diabetic rats doubled but did not restore plasma IGF-I levels to normal; weight gain, however, was similar to that in control rats. IGF-I treatment had no effect on epiphyseal width, osteoblast/osteoid surfaces and OC concentrations, but improved the decreased MAR (4·6±1·2 μm/day).These results indicate (1) that the decreased epiphyseal width and osteoblast recruitment of diabetic BB rats are directly related to their insulin deficiency, and (2) that IGF-I, administered systemically, corrects, in part, the decreased MAR in diabetes, suggesting a role in osteoblast function and/or mineralization.Journal of Endocrinology(1992) 134,485–492

Concentrations of osteocalcin were measured in plasma and bone of normal and diabetic rats during the reproductive cycle and compared with plasma 1,25-dihydroxyvitamin D3(1,25-(OH)2D3) concentrations. The age-dependence of osteocalcin was also examined. Plasma concentrations of osteocalcin levels were low but detectable in 21-day-old fetuses (3·7 ± 0·3 nmol/l); osteocalcin concentrations were highest in weaning rats (104 ± 9 nmol/l) and decreased thereafter. In adult rats, plasma concentrations of both osteocalcin and 1,25-(OH)2D3increased during the last days of normal pregnancy, and even more so in rats fed a diet low in calcium and phosphate. After an early post-partum decline, osteocalcin concentrations in plasma remained at non-pregnant levels in lactating rats fed a high calcium/phosphate diet while their 1,25-(OH)2D3concentrations were higher than in non-pregnant rats; however, lactating rats fed a low calcium/phosphate diet showed increasing osteocalcin concentrations.In spontaneously diabetic BB rats, plasma osteocalcin concentrations were severely decreased compared with those in non-diabetic rats, more than would have been expected from their decreased 1,25-(OH)2D3concentrations. Moreover, plasma osteocalcin did not increase during pregnancy or lactation in diabetic rats, even when fed a low calcium/phosphate diet. Fetuses of diabetic rats also had lower plasma osteocalcin levels than fetuses from non-diabetic rats or than weight-matched fetuses from semistarved rats. In contrast to plasma osteocalcin concentrations, bone osteocalcin concentrations and content were not altered by pregnancy, lactation, low calcium/phosphate diet or diabetes.These data show that plasma osteocalcin concentrations change during the reproductive period in normal rats but not in diabetic rats, and that osteocalcin levels do not seem to be regulated solely by 1,25-(OH)2D3.Journal of Endocrinology(1989) 120,143–151

This study aimed to evaluate whether recombinant human growth hormone (rhGH) or insulin‐like growth factor‐I (rhIGF‐I) can reverse or prevent further bone loss in aged osteopenic ovariectomized (OVX) rats and to compare their effects with those of 17β‐estradiol (E2). Twelve‐month‐old rats were OVX, remained untreated for 8 weeks, and subsequently received daily subcutaneous (SC) injections of rhGH (75 μ/day), rhIGF‐I (250 μg/day), E2(1.5 μg/day), and their respective combinations during 8 weeks, and were then compared with sham‐operated, pretreatment OVX, and saline‐treated OVX rats. A single sc injection of rhGH resulted in peak hGH concentrations after 90 minutes, with a half‐life of 124 minutes; the highest plasma IGF‐I concentrations were reached 45 minutes after rhIGF‐I injection (+57% vs. baseline) with a gradual decline thereafter. Measurements included: biochemical parameters of bone remodeling (plasma osteocalcin and urinary pyridinolines); histomorphometry of proximal tibial metaphysis; DXA of femur; biomechanical analysis of femur and fifth lumbar vertebra (L5); plasma 1,25‐dihydroxyvitamin D3(1,25(OH)2D3), and calbindin‐D9Kin duodenal mucosa. Whereas all E2‐treated OVX rats had much suppressed bone remodeling, rhGH or rhIGF‐I had no effect on any biochemical or histomorphometrical parameter of remodeling. The bone mineral density (BMD) at the distal femoral metaphysis as well as parameters of strength at L5 were maintained at pretreatment values in OVX rats treated with E2, GH, or IGF‐I, but not in saline‐treated OVX rats; their effects were not additive, however. Trabecular bone volume in the tibial metaphysis was also higher in rats treated with these agents than in saline‐treated rats, but this was more apparent at the primary than at the secondary spongiosa, suggesting that their mechanism of action is on primary spongiosa formation or breakdown. E2alone was ineffective to augment the BMD at the femoral diaphysis; however, the diaphyseal BMD was 12–14% higher (p< 0.01) after 8 weeks of GH treatment than in pretreatment or saline‐treated OVX rats and sham‐operated rats, while IGF‐I was less effective than GH. GH or IGF‐I treatment had no effect on plasma 1,25(OH)2D3or duodenal calbindin‐D9Kconcentrations, but the combination of GH or IGF‐I with E2potentiated the effect of E2to stimulate calbindin‐D9Kconcentrations and urinary calcium excretion, indicating “hyperabsorption hypercalciuria”. In conclusion, the administration of rhGH and rhIGF‐I, like that of E2, into aged OVX rats prevents further loss of bone mass and strength at sites containing trabecular bone. In addition, rhGH increases cortical bone mass above pretreatment values. (J Bone Miner Res 1996;11:1723‐1735)

Scintillators for the detection of slow neutrons were obtained by pressing mixtures of H3BO3and ZnS(Ag) phosphor into thin, slightly transparent disks. In order to obtain optimal conditions, we studied the influence of mixing-ratio, thickness and pressure on detection efficiency. The scintillator obtained in this way was compared with a commercial NE 400 slow neutron boronpolyester detector.

The specific heat of two ferrites with respective chemical composition Mn1-aZna, Fe2O4(a≈ 0.38) and Ni1-aZnaFe2O4(a≈ 0.50) has been measured with a Nernst adiabatic calorimeter in the temperature range 20°C–350°C. Associated with the ferrimagnetic transition an enhanced specific heat, due to the magnetic contribution, is observed, having a maximum at the Curie-point (172°C and 308.5°C respectively). The results of the measurements are tabulated and discussed.

IT is well known that ferrimagnetic materials become anisotropic upon application of a magnetic field and that consequently the permeability of a magnetically saturated ferrite medium is described by a tensor1: For a positive and negative circularly polarized wave, the tensor is diagonalized, and the effective permeability is a scalar, μ ± k. The real and the imaginary parts of the elements of the tensor have been measured by several workers2,3, using resonance cavities excited with circularly polarized modes. In order to study ferrite itself, it was pointed out by Spencer et al.3that it is necessary to determine the intrinsic magnetic quantities μ and k. Because of the radiofrequency demagnetizing fields the values &μtilde; and \k̃ derived from the measurements depend on the sample shape. Those intrinsic values are computed from the experimental values using a magnetostatic approximation for the internal field.