[Dynamic palatography: Diagnostic tool for dysfunc­tional swallowing? Feasibility study].

Objective: Dysfunctional swallowing may cause transverse occlusal disorders. The speech re-education of dysfunctional swallowing aims to correct or prevent the recurrence of occlu­sal disorders. The main objective was to test the dynamic palato­graphy as a diagnosis and quantification tool of the dysfunctional swallowing. Material and methods: The study was prospective and descriptive. Twelve average 23.5 years old women with a clinical dysfunctional swallowing have been included between January and May 2014. None was aware of presenting an atypical swallowing or dento-facial dysmorphism of class II. The dynamic palatography device measured the pressure force of the language on the palate during the lingual rest, swallowing saliva and water. Parameters measured were the duration and magnitude of support of the tongue on the palate. Results: Dynamic palatography showed a trend to predominant anterior contact during rest position (25%), and lower position of the language with little contact during swallo­wing of saliva and water. Discussion: Palatography results are consistent with the clinical diagnostic criteria of atypical swallo­wing. Our palatography tool has the advantage of being unobtrusive in the mouth compared to other pre existing systems. This device should be tested on larger patient popu­la­tions and could enable monitore atypical swallowing rehabili­ta­tion efficiency. The palatography could complete the swallo­wing assessment and be a monitoring and rehabilitation tool in real time.

A PCR for the detection of mycoplasmas belonging to the Mycoplasma mycoides cluster: application to the diagnosis of contagious agalactia.

Contagious agalactia is a mycoplasmal infection caused by Mycoplasma agalactiae, Mycoplasma mycoides subsp. mycoides LC, M. mycoides subsp. capri, Mycoplasma capricolum subsp. capricolum and Mycoplasma putrefaciens. Identification of the causative organisms is usually performed by isolation and classical biochemical and serological tests, though this is a lengthy and cumbersome process for mycoplasmas. Specific PCR assays have been developed for the identification of Mycoplasma agalactiae and M. putrefaciens. For members of the M. mycoides cluster existing PCR tests are based on the amplification of highly conserved genes coding for ribosomal proteins, hence a possibility of cross-reactions. The gene glk, coding for a glucokinase, that is found in this cluster is very distantly related to any other bacterial glucokinase described so far. It was therefore chosen as target to design a new PCR test. The validation was performed independently in three laboratories in France and India using over 100 mycoplasma strains of various geographical origins. All strains belonging to the M. mycoides cluster were detected by amplification of the expected PCR product (428 bp) while no amplification was obtained from M. agalactiae strains. Our results demonstrate the universality of this PCR in spite of the great heterogeneity found within this cluster. This new tool may be of great help for the implementation of control measures directed towards contagious agalactia.

Improved analogs and novel delivery systems for somatostatin octapeptides.

Appropriate N-terminus modification can result in somatostatin (SRIF) octapeptide analogs that are both more potent and more selective in vitro for the human SRIF receptor type 2 (hsst2). In addition, these modifications can improve the duration of action and bioavailability of SRIF analogs following parenteral administration, as shown by both pharmacological and distribution studies in vivo with BIM-23190 and BIM-23197 in the rat.

Renal tubular absorption of beta 2 microglobulin.

125Iodinated human beta 2 microglobulin (beta 2m, 5 to 30 mg) was administered to anesthetized rats. Clearance studies showed a low threshold of excretion of injected beta 2m and a high Tm of 400 to 600 micrograms X min-1 X kg-1. A glomerular sieving coefficient of 0.97 was calculated as the slope of the curve: beta 2m excretion rate = F (plasma beta 2m X glomerular filtration rate) for values above saturation. Electrophoresis analysis of proteinuria in agarose gel and sodium dodecyl sulfate polyacrylamide gel showed that injection of saturating doses of beta 2m induced the excretion of proteins of similar size but different charge and that of other proteins of different size. Among the latter, some were excreted transiently in association with beta 2m, whereas others had a delayed excretion suggesting existence of a complex mechanism of reabsorption whose steps remain to be elucidated.

Turnover studies of human beta 2-microglobulin in the rat: evidence for a beta 2-microglobulin-binding plasma protein.

1. 125I-labelled beta 2-microglobulin (beta 2m) was injected into rats and protein or non protein-bound radioactivity was determined in plasma urine and several organs. 2. The observed kinetics differed from those expected according to the bicompartmental model for plasma protein turnover. The difference was attributed to the binding of a part of the tracer to a plasma component. Chromatography of plasma taken after injection of beta 2m showed an additional peak of radioactivity at the 55,000-80,000 daltons position. 3. In animals with ligated renal arteries, disappearance of the tracer from the plasma was markedly prolonged, and little non-protein-bound radioactivity was detectable in plasma, indicating that the kidney was the major site of catabolism of beta 2m. 4. Chromatography of plasma from control rats and rats with ligated renal arteries showed that the kidney was the major site of catabolism for free beta 2m only. 5. In normal rats, the urine was found to contain only non-protein-bound radioactivity.

Piretanide and urinary excretion of ions in rat. Effect of indomethacin.

1. Piretanide is a new loop diuretic resembling furosemide. The effects of this diuretic on various parameters of renal function and on the excretion of the major ions were studied on anaesthetized, hydrated rats. 2. Piretanide induced a marked diuresis and increased sodium, potassium, chloride and calcium excretion. Calcium excretion increased more than that of sodium. Urinary osmolality and water reabsorption decreased. 3. Inulin clearance and phosphate excretion were significantly altered by piretanide. 4. Pretreatment of rats with indomethacin did not suppress the effects of piretanide on diuresis nor its effects on urinary excretion of sodium, chloride and potassium, since these parameters increased in the same proportion in the presence or in the absence of indomethacin. 5. Pretreatment with indomethacin abolished piretanide-induced dissociation of sodium and calcium excretions.

Acute effect of high dose (48 mg) of piretanide in advanced renal insufficiency.

1 The acute effects of a high dose of piretanide, a new potent diuretic were studied in eight patients with severely impaired renal function (GFR between 0.09 and 0.17 ml s-1 1.73 m-2). 2 After hydration and following two control periods, a single dose of 48 mg piretanide was ingested. Thereafter, urine was collected every 30 min for 2 h and every hour for the next 4 h. Urinary fluid losses were replaced orally (100 ml of water ever hour) and intravenously (isotonic saline + glucose infusion). 3 The following measurements were made: urine flow rate, clearances of inulin, PAH, urea, creatinine, uric acid, osmolar and free water clearances, excretion rates of sodium, chloride, potassium, calcium, phosphate, bicarbonate, ammonium, titratable acidity and urine pH. 4 Piretanide (48 mg) appeared to be effective in advanced renal insufficiency, producing a significant increase in urine flow rate, in sodium, chloride, potassium and calcium excretion and in Cosm. 5 There was no significant change in GFR, as measured by inulin clearance, or in the other measured parameters.

Fate of glutamate carbon and nitrogen in isolated guinea-pig kidney-cortex tubules. Evidence for involvement of glutamate dehydrogenase in glutamine sythesis from glutamate.

1. The pathways and the fate of glutamate carbon and nitrogen were investigated in isolated guinea-pig kidney-cortex tubules. 2. At low glutamate concentration (1 mM), the glutamate carbon skeleton was either completely oxidized or converted into glutamine. At high glutamate concentration (5 mM), glucose, lactate and alanine were additional products of glutamate metabolism. 3. At neither concentration of glutamate was there accumulation of ammonia. 4. Nitrogen-balance calculations and the release of 14CO2 from L-[1-14C]glutamate (which gives an estimation of the flux of glutamate carbon skeleton through alpha-oxoglutarate dehydrogenase) clearly indicated that, despite the absence of ammonia accumulation, glutamate metabolism was initiated by the action of glutamate dehydrogenase and not by transamination reactions as suggested by Klahr, Schoolwerth & Bourgoignie [(1972) Am. J. Physiol. 222, 813-820] and Preuss [(1972) Am. J. Physiol. 222, 1395-1397]. Additional evidence for this was obtained by the use of (i) amino-oxyacetate, an inhibitor of transaminases, which did not decrease glutamate removal, or (ii) L-methionine DL-sulphoximine, an inhibitor of glutamine synthetase, which caused an accumulation of ammonia from glutamate. 5. Addition of NH4Cl plus glutamate caused an increase in both glutamate removal and glutamine synthesis, demonstrating that the supply of ammonia via glutamate dehydrogenase is the rate-limiting step in glutamine formation from glutamate. NH4Cl also inhibited the flux of glutamate through glutamate dehydrogenase and the formation of glucose, alanine and lactate. 6. The activities of enzymes possibly involved in the glutamate conversion into pyruvate were measured in guinea-pig renal cortex. 7. Renal arteriovenous-difference measurements revealed that in vivo the guinea-pig kidney adds glutamine and alanine to the circulating blood.

Activity of a new high efficiency diuretic in man: piretanide (HOE 118).

1 The pharmacological actions of piretanide, a new high efficiency diuretic, were studied in sixteen patients with GFR (inulin clearance) varying from 0.1--2.5 ml/s. 2 After hydration and following two control periods, a single dose of 6 mg piretanide was ingested. Thereafter, urine was collected every 30 min for 2 h and every hour for the next 4 h. Fluid losses were replaced. 3 The following measurements were made: urine flow rate, clearances of inulin, PAH, urea, creatinine, uric acid, osmolar and free water clearances, excretion rates of sodium, chloride, potassium, calcium, phosphate, bicarbonate, ammonium, titratable acidity and urine pH. 4 Main results showed piretanide was efficient in the group with normal GFR (inulin clearance greater than 1.5 ml/s) and in the group with slightly decreased GFR (1.0 less than inulin clearance less than 1.4 ml/s), in terms of diuresis, natriuresis, kaliuresis and calciuresis. It was inefficient in the group with severe renal insufficiency (inulin clearance less than 0.3 ml/s). 5 Free water clearance showed preservation of diluting ability to a large extent. 6 In the three groups, no significant change in inulin clearance and PAH clearance occurred.

Effect of acidosis, alkalosis and monofluoroacetate administration on citrate and ATP content of rat renal medulla and papilla.

1. --Renal distribution of citrate showed that there is an increase in citrate content from cortex to medulla and a decrease from medulla to papilla. Alkalosis produced an increase in citrate content and acidosis a decrease in renal citrate content, in each of the studied renal area. Monofluoroacetate produced no significant change in citrate content of medulla or papilla; it did not interfere with the acido-basic related changes in cortex citrate content, but its effect was additive. 2. --Renal distribution of ATP significantly decreased from cortex to medulla and from medulla to papilla. Acid or basic diet had no influence on intratissular ATP content. Fluoroacetate decreased renal ATP content.

A new device for differentiated tissue sampling in rat kidney.

Since freeze-clamping does not allow to sample the diffrent renal areas a new method of kidney tissue sampling in anesthetized rats is described. It consists in sectioning a slice in the middle of the rat kidney and immediately freezing. This device allows quick and accurate separation of the different renal areas, and especially of the papilla which is almost entirely sampled. Complete freezing is obtained within 7s after clamping of the renal artery. As proof of adequate "in vivo" fixing, adenine nucleotide levels were assessed in each tissue sample. ATP concentration in cortex samples was 1.62 +/- 0.33 mumole/g wet tissue, this value is comparable with those obtained in the cortex by freeze-clamping.

Glutamine metabolism in isolated dog kidney tubules: inhibition by dialysed albumin preparation.

The metabolic fate of L-glutamine (1 and 5 mM) was studied in isolated dog kidney tubules. At 1 and 5 mM substrate concentration, and after 60 min of incubation, glucose represented 40% and 25% of the glutamine removed; the glutamine unaccounted for (which was probably completely oxidized) represented about one-half and one-third of glutamine removal at 1 and 5 mM glutamine concentrations, respectively. Due to contaminating fatty acids, addition of dialysed bovine serum albumin (fraction V) greatly altered the metabolic fate of glutamine. This observation emphasizes the need for using albumin with great caution for experiments with kidney tubules.

Effect of monofluoroacetate on renal H+ excretion in the rat.

In order to investigate the effect of monofluoroacetate (MFA) on renal H+ excretion, anesthetized rats under mannitol diuresis were given intraperitoneally MFA and some of the acido-basic status parameters were determined. Urinary pH and pCO2 did not change after MFA administration, while urinary flow rate increased. MFA induced a decrease in H+ net excretion and in ammonia excretion. Titratable acidity did not change significantly within the experiment.

In vitro citrate synthesis by the dog kidney. Investigations with cortex, red and white medulla slices.

In vitro utilization or production of citrate by the cortex, outer medulla or inner medulla of dog kidney was measured. Our data show: 1. An in vitro citrate synthesis or utilization capacity of the cortex greater than that of the red medulla. 2. An effect of pH on citrate synthesis or utilization capacity of the cortex, an effect not seen with medullary slices. 3. An absence of citrate synthesis or utilization by white medulla slices. It would seem that the citrate found in the white medulla and the papilla of the dog kidney in vivo was not produced in situ.

Lactate and pyruvate metabolism in isolated renal tubules of normal dogs.

The kinetics of lactate and pyruvate (1 and 5 mM in each case) metabolism was studied in isolated dog renal tubules. Utilization of these two substrates and the production of glucose, pyruvate, or lactate, and alanine were determined. The rates of lactate and pyruvate utilization and of glucose production were constant during 60 min of incubation. Glucose production from pyruvate was less than that from lactate. Addition of albumin to the incubation medium greatly inhibited lactate and pyruvate utilization at both substrate concentrations. It stimulated, however, glucose production from 1 mM, but not 5 mM, lactate or pyruvate. These effects were found to be due to the presence of fatty acids in the albumin solution used. In the absence of fatty acids, glucose production represented 35 to 40% of lactate uptake, but represented less than 20% of pyruvate uptake. Fatty acids markedly enhanced the percentage of transformation of lactate and pyruvate into glucose, and that of pyruvate into lactate. Alanine represented 20% or less of lactate and pyruvate uptake. These results suggest that fatty acids have a regulatory influence on lactate and pyruvate dog kidney metabolism.