The GLAS editing procedures for the FGGE level II-B data collected during SOP-1 and 2

The modifications made to the FGGE Level II-b data are discussed and the FORTRAN program developed to perform the modifications is described. It is suggested that the edited database is the most accurate one available for FGGE SOP-1 and 2

Objective analysis of observational data from the FGGE observing systems

An objective analysis procedure for updating the GLAS second and fourth order general atmospheric circulation models using observational data from the first GARP global experiment is described. The objective analysis procedure is based on a successive corrections method and the model is updated in a data assimilation cycle. Preparation of the observational data for analysis and the objective analysis scheme are described. The organization of the program and description of the required data sets are presented. The program logic and detailed descriptions of each subroutine are given

Documentation of the GLAS fourth order general calculation model. Volume 3: Vectorized code for the Cyber 205

Volume 3 of a 3-volume technical memoranda which contains documentation of the GLAS fourth order genera circulation model is presented. The volume contains the CYBER 205 scalar and vector codes of the model, list of variables, and cross references. A dictionary of FORTRAN variables used in the Scalar Version, and listings of the FORTRAN Code compiled with the C-option, are included. Cross reference maps of local variables are included for each subroutine

Documentation of the GLAS fourth order general circulation model. Volume 2: Scalar code

Volume 2, of a 3 volume technical memoranda contains a detailed documentation of the GLAS fourth order general circulation model. Volume 2 contains the CYBER 205 scalar and vector codes of the model, list of variables, and cross references. A variable name dictionary for the scalar code, and code listings are outlined

Short stature, hyperkalemia and acidosis: A defect in renal transport of potassium

Short stature, hyperkalemia, and acidosis: A defect in renal transport of potassium. An eleven-year-old boy presented with short stature, hyperkalemia, and metabolic acidosis. No endocrine cause for a short stature could be demonstrated. Renal function, as assessed by inulin and PAH clearances, concentrating and diluting capacity, and ability to acidify the urine and to excrete net acid, was normal. No defect was detected in adrenal secretion of, or renal responsiveness to, aldosterone. A low renal threshold for bicarbonate was documented which apparently explained the acidosis. However, correction of the acidosis by administration of sodium bicarbonate did not influence the hyperkalemia, making it unlikely that an abnormality in bicarbonate reabsorption was the primary defect. Chlorothiazide induced a fall in serum potassium and a rise in serum bicarbonate to normal levels. During bicarbonate loading the rates of excretion of potassium in urine were consistently below those observed in control subjects. It appeared, therefore, that the patient had a primary abnormality in potassium excretion. The resulting hyperkalemia caused urinary loss of bicarbonate and systemic acidosis. Correction of both the acidosis and hyperkalemia by chronic administration of chlorothiazide and sodium bicarbonate has resulted in resumption of normal growth.Retard de croissance, hyperkaliéme et acidose: Un déficit du transport rénal du potassium. Un enfant de 11 ans avait un retard de croissance, une hyperkaliémie et une acidose métabolique. Aucune cause endocrine du retard de croissance n'a été trouvée. La fonction rénale, estimée par les clearances de l'inuline et du PAH, la capacité de concentration et de dilution et la capacité d'acidifier l'urine, était normales. Aucun déficit de la secrétion d'aldostérone ou de la réponse rénale à l'aldostérone n'a été mis en évidence. Un seuil rénal bas des bicarbonates a été découvert, qui explique apparemment l'acidose. Cependant la correction de l'acidose par l'administration de bicarbonate de sodium n'a pas influencé l'hyperkaliémie, ce qui rend peu probable que le déficit de la réabsorption de bicarbonate soit la cause de l'ensemble. Le Chlorothiazide a déterminé une baisse de la kaliéme et une augmentation du bicarbonate plasmatique jusqu'à des valeurs normales. Pendant une charge en bicarbonate les débits d'excretion du potassium dans les urines ont été nettement inférieurs à ceux obtenus chez des sujets témoins. Il apparaît donc que le malade a une anomalie primitive de l'excrétion de potassium. L'hyperkaliémie qui en est la conséquence a déterminé une perte de bicarbonate dans les urines et une acidose systémique. La correction de l'acidose et de l'hyperkaliémie par l'administration permanente de Chlorothiazide et de bicarbonate de sodium a eu pour résultat une reprise de la croissance normale