Leachate recirculation effects on waste degradation: study on columns.

The purpose of this study is to determine the impact of leachate recirculation on the degradation of municipal solid wastes (bioreactor concept). The study was carried out using columns containing approximately 50 kg of waste, in order to follow waste degradation over a limited time. Three types of waste were studied: fresh waste of standard composition, fresh waste of fermentable composition and some 8-yr-old waste extracted from a site in France. Measurement of the global parameters, such as chemical oxygen demand (COD), volatile acidity, alkalinity, leachate conductivity, methane potential of the wastes and biogas production monitoring (volume of CO2 and CH4 produced), were carried out. The quantity of oxydizable matter and biogas production was increased by the leachate recirculation, and the duration of the first degradation phases was reduced in all cases. Chloride, ammonium and organic pollution accumulation was observed according to the duration of recirculation. After 400 days of degradation, waste stabilization seemed to be reached for all of the recirculated columns (COD<300 mg/L O2, and methane potential reached).

Indicating the parameters of the state of degradation of municipal solid waste.

This study related to the analysis of the physical (granulometry and composition) and chemical (organic matter, organic carbon and nitrogen contents) characteristics, as well as those relating to release (leaching tests and determining the methanogene potential) of several domestic wastes, with an aim of evaluating stabilization indicators. Values thresholds for a known stabilized waste were thus deduced by correlation (% paper-cardboard = 0-1; % volatile solid (VS) = 18-19; % OC = 5-6; % fines = 44-45; % degraded components = 75-76, COD of leachate = 141-155 mg O2/L; DOC from leachate = 45-49 mg C/L and 0.9-1 m3 CH4/t of dry waste). However, these values thresholds remain specific to the method employed for the analyses. The results obtained represent a considerable advance in the definition of a waste stabilized state and propose the importance of certain parameters, such as the paper-cardboard content and the measurement of leachates by using the SUVA index for determining a stabilization state.

Expression of Epstein-Barr nuclear antigen 2 in kidney tubule cells induce tumors in transgenic mice.

The effect of EBNA2 in normal cells in vivo has not as yet been explored. The experiments described here were initiated to follow the consequences of the expression of EBNA2 in different tissues in transgenic mice. EBNA2 transgenic strains were generated using a vector containing EBNA2 encoding sequences under the control of the simian virus 40 (SV 40) early enhancer/promoter fused to the endogenous EBNA2 Wp promoter. Control mice carrying a transgene with the same sequence but lacking the EBV DNA part remained healthy during observation periods of up to 15 months. The SV-EBNA2 transgenic animals, however, over time developed abdominal masses that on necropsy showed to be due to kidney tumors. Histological examination revealed the presence of tumors with the morphology of kidney adenocarcinoma with a solid growth pattern. At the age of 20 weeks the kidneys of all animals investigated showed disseminated islands of tubular hyperplasia but no true malignant neoplasms. At about 50 weeks of age multiple foci of microscopic tubular adenocarcinomas were found in both kidneys. Eventually, tumors could be diagnosed in about 90% of the SV-EBNA2 transgenic mice. EBNA2-encoding RNA was expressed in both non-malignant kidney tissue and in tumors as shown by cDNA/PCR analysis. Immunoprecipitation and immunoblot analysis showed that the tumor cells contained a polypeptide of the same size as EBNA2 in B95-8 cells that reacted with a monoclonal anti-EBNA2 antibody. Immunohistochemistry demonstrated nuclear expression of EBNA2 in hyperplastic tubules and in tumor tissue.

17-year trends in incidence and prognosis of cardiogenic shock in patients with acute myocardial infarction in western Sweden.

BACKGROUND: Cardiogenic shock remains the leading cause of in hospital death in acute myocardial infarction (AMI) and is associated with a mortality rate of approximately 50%. Here we investigated the 17-year trends in incidence and prognosis of AMI-induced cardiogenic shock in Västra Götaland in western Sweden, an area with approximately 1.6 million inhabitants. The study period includes the transition from thrombolysis to primary percutaneous coronary intervention (PCI) as the region-wide therapy of choice for patients with ST-elevation myocardial infarction (STEMI). METHODS: Data on patients hospitalized in cardiac care units in Västra Götaland, Sweden between 1995 and 2013 were obtained from the Swedish Websystem for Enhancement of Evidence-based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART). We determined the incidence of cardiogenic shock among patients diagnosed with AMI and the risk of death associated with developing cardiogenic shock. We fitted logistic regression models to study which factors predicted post-AMI cardiogenic shock. Analyses were performed on complete case data as well as after multiple imputation of missing data. RESULTS: Incidence of cardiogenic shock as a complication of AMI declined in western Sweden in the past decade, from 14% in 1995 to 4% in 2012. The risk of dying once cardiogenic shock had developed increased during the study period (p<0.01). Patients presenting with STEMI were more likely to develop cardiogenic shock than patients presenting with non STEMI (p<0.001). CONCLUSIONS: The incidence of cardiogenic shock has declined but cardiogenic shock carries a worse prognosis today than in 1995.

Impairment of cardiac function and bioenergetics in adult transgenic mice overexpressing the bovine growth hormone gene.

Cardiovascular abnormalities represent the major cause of death in patients with acromegaly. We evaluated cardiac structure, function, and energy status in adult transgenic mice overexpressing bovine GH (bGH) gene. Female transgenic mice expressing bGH gene (n = 11) 8 months old and aged matched controls (n = 11) were used. They were studied with two-dimensional guided M-mode and Doppler echocardiography. The animals (n = 6) for each group were examined with 31P magnetic resonance spectroscopy to determine the cardiac energy status. Transgenic mice had a significantly higher body weight (BW), 53.2+/-2.4 vs. 34.6+/-3.7 g (P < 0.0001) and hypertrophy of left ventricle (LV) compared with normal controls: LV mass/BW 5.6+/-1.6 vs. 2.7+/-0.2 mg/g, P < 0.01. Several indexes of systolic function were depressed in transgenic animals compared with controls mice such as shortening fraction 25+/-3.0% vs. 39.9+/-3.1%; ejection fraction, 57+/-9 vs. 77+/-5; mean velocity of circumferential shortening, 4.5+/-0.8 vs. 7.0+/-1.1 circ/sec, p < 0.01. Creatine phosphate-to-ATP ratio was significantly lower in bGH overexpressing mice (1.3+/-0.08 vs. 2.1+/-0.23 in controls, P < 0.05). Ultrastructural examination of the hearts from transgenic mice revealed substantial changes of mitochondria. This study provides new insight into possible mechanisms behind the deteriorating effects of long exposure to high level of GH on heart function.

Induction of growth hormone receptor and insulin-like growth factor-I mRNA in aorta and caval vein during hemodynamic challenge.

Induction of two-kidney, one clip hypertension (renal hypertension) is characterized by a slow increase in left ventricular tension and aortic wall stress, as opposed to aortocaval fistula or shunt volume overload, which induces a marked and rapid onset of wall stress in the caval vein and right ventricle. In the present study, we applied hemodynamic challenge to study the growth response involving gene expression of insulin-like growth factor-I (IGF-I) and growth hormone receptor (GH-R) mRNA in aorta and caval vein. Volume overload and pressure overload were induced in Wistar rats by means of shunt and renal hypertension, respectively. Systolic pressure was measured before excision of the great vessels, which was performed between 2 and 12 days postoperatively. Aortic and caval vein IGF-I and GH-R mRNA expressions were measured by means of a solution hybridization assay, and the caval vein was analyzed for IGF-I protein by immunohistochemistry. In the volume-distended but not pressurized caval vein in shunt rats, verified by telemetry recordings, there was an eightfold increase in IGF-I and 3.5-fold increase in GH-R mRNA at day 4 versus control. The IGF-I protein appeared to be localized in smooth muscle cells. In the aorta of the renal hypertension group, changes were of a slower onset. At day 7, there was a fourfold increase in IGF-I and five-fold increase of GH-R mRNA expressions versus sham-operated rats. Both the shunt caval vein and renal hypertension aorta showed evidence of a structural adaptation of the growth response. The present study suggests that acute elevation in vascular wall stress is an important triggering factor for overexpression of IGF-I and GH-R mRNA in great vessels. The growth hormone/insulin-like growth factor axis may be an important link in mediating structurally adaptive growth responses in the blood vessel wall.

Cortisol decreases IGF-I mRNA levels in human osteoblast-like cells.

Excess levels of glucocorticoids are known to cause osteoporosis. It is speculated that the effect of glucocorticoids could be mediated via regulation of IGF-I. The aims of the present study were to detect and quantify the expression of IGF-I and/or IGF-II mRNA transcripts in human osteoblast-like cells and to investigate whether glucocorticoids regulate the expression of IGF-I mRNA transcripts in human osteoblast-like cells. Cultures of human osteoblast-like cells from trabecular bone were established. The IGF-IA and IGF-IB transcripts were detected in human osteoblast-like cells from seven out of nine patients while the IGF-II transcript was detected in human osteoblast-like cells from eight out of nine patients, as determined by RT-PCR assays. Human osteoblast-like cells, as well as human muscle tissue, expressed approximately 1/10 of the IGF-I mRNA levels found in liver, as determined by RNase protection solution hybridization assay. The IGF-I mRNA levels did not decrease with age in the human osteoblast-like cells and no difference was seen between males and females. However, cortisol (10(-6) mol/l) decreased IGF-I mRNA levels. In summary, the present study has shown that human osteoblast-like cells express IGF-I and IGF-II mRNA transcripts and that cortisol down-regulates the IGF-I mRNA levels, indicating that some of the inhibitory effect of glucocorticoids on bone formation in humans is mediated via a reduced autocrine/paracrine expression of IGF-I.

Expression of GH receptor, IGF-I receptor and IGF-I mRNA in the kidney and liver of rats recovering from unilateral renal ischemia.

The role of the growth-hormone (GH), insulin-like growth factor-I (IGF-I) axis in the kidney has been extensively studied in recent years. To further elucidate the role for GH and IGF-I in renal regeneration, the expression of the GH-rec, IGF-I-rec and IGF-I mRNA was studied in the post-ischemic regenerating kidney and in the liver of the same rats, using a solution hybridization assay. Rats were subjected to 90 min of unilateral renal ischemia followed by reperfusion. The kidneys and livers were collected 1, 3 and 7 days after injury. Five animals were operated on in each group. An additional five animals were sham-operated and killed on day 4. In the kidney, significant alterations were found in the expression of mRNAs for the GH-rec and the IGF-rec. The GH-rec mRNA decreased significantly at day 1 (P < 0.01) to less than one-fifth of the initial value, and normalized at days 3 and 7. The IGF-rec mRNA levels increased more than three-fold at day 3 (P < 0.01) and more than five-fold at day 7 (P < 0.01). In the kidneys there was no significant alteration in the IGF-I mRNA level. In the liver, significant alteration in the level of the GH-rec mRNA was found, while the levels of IGF-rec and the IGF-I mRNA did not change significantly. The levels of GH-rec mRNA increased two-fold at day 3 (P < 0.05), while the levels were unchanged at days 1 and 7. In the early phase of renal regeneration, there is a sharp decrease in the expression of GH-rec mRNA in the kidney. This suggests that there are no direct effects on renal tissue mediated by GH in this situation. There is a significant increase in the intrarenal IGF-I-rec mRNA levels from day 3, suggesting an increased need for IGF-I during regeneration. In the liver, the concentration of GH-mRNA is increased significantly at day 3. These data show on alterations that suggest a role for these factors in renal regeneration.

High dosage growth hormone treatment and post-ischemic acute renal failure in the rat.

The positive effect of insulin-like growth factor I (IGF-I) on the outcome of experimental acute renal failure has gained much attention in recent years. However, the potential positive effects of GH have been less intensively studied. Therefore, a study was designed in which rats suffering from post-ischemic renal failure were treated with high dosage growth hormone (GH). Forty-six rats were subjected to bilateral renal ischemia for 45 min. Following reperfusion the animals were treated with either human recombinant GH in a dosage of 2 mg/day given as subcutaneous injection or placebo. The animals were monitored daily for body weight, s-creatinine, s-urea and B-glucose. S-IGF levels were determined at the start of the experiment and at days 3 and 7. IGF-I and GH receptor mRNA were measured in the kidney and the liver of the surviving animals at the end of the experiment. Survival in the GH-treated rats was 42.9% as compared to 32.0% in the control group (not significant). Both groups of animals lost body weight in the initial phase. The loss in body weight was less pronounced for the GH-treated animals and the difference was significant at day 2 (P<0.05). The s-creatinine levels tended to be lower in the GH-group at all times studied, but the difference was not significant. The s-urea levels were significantly reduced by GH-treatment at day 2 (P<0.05). GH treatment caused no adverse effects on carbohydrate metabolism as studied by daily B-glucose determinations. The serum IGF-I levels were identical in both the groups at day zero. At day 3 the serum IGF-I levels had increased by approximately 30% in both groups. At day 7 the serum IGF-I level was 1600 ng/ml in the GH-treated group as compared to 1400 ng/ml in the placebo group (not significant). When placebo-treated uremic rats were compared to normal sham-operated animals GH-rec mRNA was down-regulated in the kidney and liver, while IGF-I mRNA was down-regulated only in the liver (P<0.05). GH treatment partly restored the GH-rec and IGF-I mRNA levels in both organs. The data are compatible with a severe GH resistance syndrome in acute renal failure.

Distribution and development of G alpha i-2 mRNA in the rat cerebral cortex investigated with in situ hybridization and RNAse protection assay.

The distribution of the G alpha i-2 mRNA was investigated with in situ hybridization on tissue sections of the rat cerebral cortex. A non-radioactive method based on digoxygenin labelled cRNA was used for in situ hybridization. The G alpha i-2 mRNA was shown to be present predominantly in large neuronal shaped cells in laminae II-III. The ontogenic development of the expression of G alpha i-2 mRNA in the rat cerebral cortex was quantified using a solution hybridization RNAse protection assay. The abundancy of G alpha i-2 mRNA was shown to increase significantly from embryonic day 16 to adult age. The amount of G alpha i-2 mRNA in adult cerebral cortex of the rat brain was 23 amol/micrograms RNA. The distribution and ontogenic development of G alpha i-2 mRNA are discussed.

Hypertriglyceridaemia and Lewis (A-B-) phenotype in non-insulin-dependent diabetic patients.

A relationship between Lewis (a-b-) phenotype and the metabolic syndrome X has been suggested. We studied the frequency of Lewis (a-b-) phenotype in subjects with non-insulin-dependent diabetes mellitus (NIDDM) as well as the relationship between Lewis phenotype and lipid concentration in NIDDM patients. Lewis red blood cell phenotyping was done in 207 NIDDM subjects and 345 non-diabetic control subjects by immuno-agglutination with anti-Lewis a and b monoclonal antibodies. Among NIDDM patients, the proportion with the Lewis (a-b-) phenotype was significantly increased (23.6% vs 14.3%, p = 0.01), and this phenotype was associated with higher levels of triglycerides (2.40 +/- 2.58 vs 1.97 +/- 1.25, p = 0.03). This study shows a relationship between NIDDM and Lewis (a-b-) phenotype. Hypertriglyceridaemia in Lewis-negative NIDDM could suggest an increased risk of ischaemic heart disease for these subjects.

Fractionation and characterisation of dissolved organic matter from composting green wastes.

A new fractionation procedure using membrane ultrafiltration (UF), followed by chemical characterisation--measurement of total organic carbon (TOC), chemical oxygen demand (COD) and organic nitrogen and spectroscopic study--was applied to aqueous extracts of composting green wastes. Three membranes of molecular weight (MW) cut-offs of 1, 10 and 100 kDa were used. The study demonstrated the first step of the transfer of organic matter from the solids to the aqueous biofilm surrounding the solids. The microbiological consumption of the dissolved organic matter mainly used molecules smaller than 1 kDa, while the aromatisation of the organic matter, observed after 100 days composting, involved molecules larger than 10 kDa.

[Food-dependent Cushing syndrome: a new entity of organic hypercorticism]. / Le syndrome de Cushing alimentaire: une nouvelle entité d'hypercorticisme organique.

Diagnosis of Cushing's syndrome is quite difficult in endocrinology. Spontaneous Cushing's syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing's syndrome have usually diffusely enlarged adrenal glands. In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing's syndrome with food dependent periodic hormonogenesis. This food dependent Cushing's syndrome is an ACTH-independent Cushing's syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion. Food dependent Cushing's syndrome is a new cause of Cushing's syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing's syndrome.

[Primary hyperparathyroidism and pregnancy]. / Hyperparathyroïdie primaire et grossesse.

We report a case of primary Hyperparathyroidism (HPT) occuring in a 36 year old woman, during pregnancy. This woman received medical therapy to the delivery, then underwent parathyroidectomy in post-partum. Primary HPT during pregnancy is associated with increased risk of fetal loss, neonatal and maternal morbidity. Neonatal hypocalcemia is due to transient hypoparathyroidism consequent to abnormal suppression of fetal parathyroid hormone secretion by maternal hypercalcemia. Maternal hypercalcemia may be masked by hypoalbuminemia during pregnancy and often leads to aspecific symptoms which will differ the diagnosis. The recommanded treatment is parathyroidectomy which should preferably be performed during the second trimester of pregnancy; the efficacity of medical treatment is poor and transient.

[Thymic carcinoid tumor causing paraneoplastic Cushing syndrome. Diagnostic value of double-labelled tomoscintigraphy]. / Tumeur carcinoïde thymique responsable d'un syndrome de Cushing paranéoplasique. Intérêt diagnostique de la tomoscintigraphie en double marquage.

Cushing's syndromes caused by ectopic corticotropin secretion represent 10 to 15% in the causes of Cushing's syndrome. Somatostatin receptor scientigraphy can be successful in the localization of ACTH-secreting neuroendocrine tumors. We report a case of Cushing's syndrome caused by ectopic corticotropin secretion from a thymic carcinoid tumor. Conventional localization techniques failed but the tumor was detected by a double binding thoracic scintigraphy using 111Indium-octreotide and 99mTechnetium-albumine macroagregates.

How the origin of fresh household waste affects its ability to be biodegraded: an assessment using basic tools and its application to the city of Kara in Togo.

Waste biodegradation has been largely investigated in the literature by using conventional tests like the BMP test and the respirometric test, whereas only few studies deal with the use of leaching tests in combination with biological activity measurements. Consequently, this study used an improved leaching test to evaluate the biodegradability of two deposits of fresh household waste from the city of Kara in Togo. The first deposit came from households in neighborhoods located in the outskirts of the city and the second consisted of fresh waste, mainly composed of business waste and household waste, collected in the urban center and aimed at being deposited in the landfill. A physicochemical characterization of the two deposits completed the leaching test. The biological activity was monitored by measuring O(2) consumption and CO(2) production. pH, DOC/OM, VFA/DOC ratios and the SUVA index was measured in the leaching juice to assess both the state of degradation of the waste in the deposits and the ability of the organic matter to be mobilized quickly and to be easily assimilated by microorganisms. The biodegradability of waste from the city of Kara correlated with their origin even though the physical characteristics of the two deposits studied differed greatly.

Local infusion of IGF-I into the kidney of pituitary intact rats induces renal growth.

To determine whether insulin-like growth factor I (IGF-I) exerts growth-promoting actions on the kidneys of pituitary-intact animals IGF-I was infused into the kidney via two different routes using osmotic pumps. In a first set of experiments IGF-I was infused directly into the tissue by the use of an implanted catheter traversing the kidney. It was found that a dosage of 50 micrograms IGF-I wk-1 but not 20 micrograms wk-1 caused a gain in weight of the kidney. The growth was accompanied with morphological alterations among the cortical distal tubules. As a marker for hyperplasia, a monoclonal antibody directed against the M1 subunit of ribonucleotide reductase (RR) was used. The altered cells stained with RR, as also did the tubule cells of the medullary thick ascending limb (mTAL). No RR staining was found in the bulk of renal mass, i.e. the proximal tubules, indicating that possible growth in these cells did not involve cell division. In a second set of experiments IGF-I at 50, 100 and 300 micrograms wk-1 was infused into the renal circulation via a side branch of the renal artery, the suprarenal artery. In these experiments, no growth response or morphological alterations of the tissue were found. These findings demonstrate that IGF-I, when administered directly into the parenchyma, causes growth of the kidney in normal animals. The data are compatible with a causative role for IGF-I in the course of renal growth.

IGF-I binding and IGF-I mRNA expression in the post-ischemic regenerating rat kidney.

The localization of IGF-I peptide and IGF-I mRNA was investigated in the post-ischemic regenerating rat kidney using immunohistochemistry and non-radioactive in situ hybridization techniques. In addition, the distribution and relative quantity of IGF-I binding sites were studied by autoradiographic ligand-binding techniques. Two and three days after the injury, morphological signs of an intense regenerative activity was evident. By this time a substantial number of the regenerating cells were stained with a monoclonal antibody against the M1 subunit of ribonucleotide reductase, a proliferative marker used. Low proliferative tubular cells, replacing those that had been injured, were seen lining the tubular basement membrane. By seven days, the morphology in the cortex was quite normalized, while cells of the S3 segments in the outer medulla remained dedifferentiated. The regenerative cells expressed IGF-I peptide and IGF-I mRNA in a transient manner and this was found to correlate better to cell differentiation than cell division. In addition, non-tubular cells, predominantly macrophages, expressed both the IGF-I peptide and the mRNA. The IGF-I binding was significantly increased in the regenerative zone at all times studied and began to decline at day seven. The binding characteristics were found to be compatible with binding to the IGF-I receptor. Altogether, these findings provide circumstantial evidence that IGF-I is of trophic importance in the regeneration of renal tubular cells. The data are compatible with a local production and action of IGF-I, suggesting an autocrine and/or paracrine mode of action during the regenerative process.

IGF-I binding and IGF-I expression in regenerating muscle of normal and hypophysectomized rats.

Binding of iodinated IGF-I to tissue sections from regenerating muscle was studied by autoradiography in normal and in hypophysectomized rats. Binding of IGF-I was low in control muscle in both groups of animals, but increased transiently about 10-fold during regeneration after injury. Maximal binding occurred later in hypophysectomized rats than in control rats, and there was also a slower regeneration process in these animals. IGF-I, as demonstrated by immunohistochemistry, and IGF-I mRNA, as demonstrated by in situ hybridization, were expressed by the regenerating muscle cells in both groups of animals. It is concluded that locally produced IGF-I is the most likely ligand for IGF-I receptors during muscle regeneration.