Martian wave of darkening: a frost phenomenon?

A new hypothesis attributes the Martian "wave of darkening" to soil frost phenomena. Diurnal thawing and freezing of the ground, which uses moisture transported by the atmosphere from the melting polar cap, can produce various minute, frost-heaved, soil surface features. These microrelief features result in a complex porous surface structure, which causes optical darkening. The boundary at which the wave of darkening terminates on the winter hemisphere correlates with the latitude at which the diurnal peak surface temperature drops below 0 degrees C. The hypothesis is examined in terms of known properties of the Martian atmosphere and surface and the availability of water.

Stimulation in vitro by 1,25-dihydroxy-vitamin D3 of intestinal cell calcium uptake and calcium-binding protein.

Treatment of duodenal tissue from rats deficient in vitamin D with 1,25-dihydroxy-vitamin D3 [1,25-(OH)2-D3] led to more than a doubling of calcium uptake by the isolated cells and the appearacne in those cells of previously undetectable calcium-binding protein (CaBP). Treatment with the precursor, 25-hydroxy-vitamin D3, was without effect on calcium uptake or CaBP. Cells from vitamin D-replete animals took up three and a half times more calcium than cells from deficient animals. This rapid (90-minute) effect of in vitro treatment with a physiological dose (4.7 X 10(-8)M) of 1,25-(OH)2-D is the first such report and is in accord with the regulatory role of the hormone-like sterol.

Vitamin D-dependent calcium-binding protein from rat kidney.

A calcium-binding protein has been partially purified from rat kidney. It is found in the cortex, but not in the medulla. It is Vitamin D-dependent, as it occurs in normal, but not in Vitamin D-deficient rats. The molecular weight is 28 000, more than twice that of the Vitamin D-dependent calcium-binding proteins from rat intestinal mucosa. The apparent dissociation constant of the partially purified renal calcium-binding protein is approx. 10-5 M.

[Post-denervation renal artery stenosis - a matter of concern?]. / Les sténoses artérielles rénales post-dénervation - une problématique préoccupante ?

Renal denervation, an invasive technique indicated in resistant hypertension patients insufficiently controlled by antihypertensive drugs, has a good safety profile. However, an increasing number of post-denervation renal artery stenosis cases has recently been reported. We describe the case of a 49-year-old woman with resistant hypertension who was referred to our university hypertension center for renal sympathetic denervation. Her daily treatment included six antihypertensive drugs. CT angiography prior to denervation showed no renal artery stenosis or vessel wall lesions. A standard renal denervation procedure using the St Jude protocol was performed. After an initial improvement in blood pressure profile, she presented with a blood pressure impairment at 3 months after renal denervation leading to the diagnosis of a severe right renal artery stenosis.

Calcium and osteoporosis.

Skeletal size and mass are genetically programmed. Optimum skeletal size can be attained if the nutrient supply, ie, calcium, is ample, but the age-dependent decrease in skeletal mass that begins in the third decade cannot be arrested by adequate calcium intake alone. The decrease in skeletal mass is primarily caused by the age-dependent decrease in gonadal hormones. The dramatic drop in hormones in menopause is associated with a sharp decrease in trabecular bone and a slower decrease in cortical bone. In men this decrease is gradual. Replacement therapy with gonadal hormones can markedly slow this decrease in bone mass, provided calcium intake is adequate. Soluble forms of calcium are preferred to ensure adequate calcium absorption. Vitamin D supplementation beyond the recommended dietary allowance does not appear beneficial in osteoporosis, but may be so in cases of senile hyperparathyroidism. Calculations based on bone calcium turnover indicate that the recommended dietary allowance for calcium is adequate for boys and men, but is insufficient for adolescent girls. Calcium intake by women is probably too low to slow bone calcium turnover to its programmed minimum. Adequate calcium intake in childhood and adolescence is essential to attain the optimal bone mass and size.

Vitamin D deficiency and rickets.

Classical experimental rickets in the rat is a dual deficiency, resulting from both phosphate and vitamin D deficiency, with many of the features of rickets reproducible by simple phosphorus deficiency. Simple vitamin D deficiency differs markedly from experimental rickets, with only the absence of the vitamin D-dependent calcium-binding proteins common to both situations. The expression at the bone level of vitamin D deficiency differs in the two conditions, with rickets leading to profound structural and metabolic changes, whereas simple vitamin deficiency primarily compromises the regulatory function of bone, without obvious structural alterations. It is proposed that human nutritional rickets is the result of a nutritional vitamin D deficiency that aggravates the expression of a pre-existing metabolic defect in phosphate transport. Simple nutritional vitamin D deficiency, unaccompanied by rickets, may occur, but probably has always been rare.

Net calcium absorption in premature infants: results of 103 metabolic balance studies.

Net calcium absorption was evaluated in 103 low-birth-weight preterm infants by a 72-h balance technique. At birth the infants had a mean (+/- SE) gestational age of 30.9 +/- 0.2 wk and weighed 1.43 +/- 0.03 kg. When tested 3 wk later, their net calcium absorption averaged 58 +/- 1% with an intake of 80 +/- 2 mg Ca.kg body wt-1.d-1. Of the 103 infants, 58 had been fed low-birth-weight formulas supplemented with vitamin D. The remainder received banked human milk, of whom 34 were supplemented with vitamin D and calcium; 11 infants received no supplementation. Calcium absorption in the four subgroups did not differ significantly, with neither vitamin D supplementation nor supplementation with vitamin D and calcium affecting percent absorption significantly. Net calcium absorption was a linear function of intake (40-130 mg Ca.kg body wt-1.d-1) with a zero intercept. Because vitamin D supplementation did not increase net calcium absorption, it is concluded that in preterm low-birth-weight infants calcium absorption proceeds by a nonsaturable route, with the transcellular, vitamin D-regulated mechanism not yet expressed.

A human periodontal ligament fibroblast clone releases a bone resorption inhibition factor in vitro.

The conditioned media (CM) obtained from three lines of cloned human periodontal ligament (PDL) cells were analyzed to determine whether they altered the parathyroid hormone (PTH)-stimulated resorption rates (45Ca release) in 48-hour cultures of 45Ca-labeled rat long bones. One PDL cell line, PDL-5, produced a heat-resistant factor in its CM that inhibited the PTH-stimulated resorption by 43.8 +/- 9.7 (SE) percent (p less than or equal to 0.02), whereas the CM from the other cell lines were without statistically significant effect. The CM from the PDL-5 line did not diminish organ culture viability, as determined by 3H-thymidine incorporation, and did not enhance or diminish the resorption-inhibiting activity of calcitonin added to the PTH-stimulated cultures. The addition of CM from PDL-5 did not alter the bone-resorbing effect of interleukin-1 (IL-1). These results indicate that CM from PDL-5 inhibits only the PTH-induced and not the IL-1-mediated resorption processes, whose mechanisms are therefore likely to differ.

Bone and calcium homeostasis.

The principal repository of calcium is bone. Calcium enters bone largely via the trabeculae, with the rate of calcium clearance by bone approximating 50 percent. Calcium enters bone as an ion in solution, but undergoes a phase change to a solid as soon as in contact with the bone surfaces. Calcium removal from and redistribution in bone is mediated by the bone cells, principally osteoblasts and osteoclasts. Calcium enters the body via intestinal absorption, a transport process that is the vectorial result of a saturable and an non-saturable step. Calcium leaves the body in the urine and stool, with a circulating calcium ion having one chance in about four of being lost via excretion. Ions like lead can compete with calcium at the sites of calcium deposition and transport. Their rate in the body should therefore parallel that of calcium, but may be modified by differing binding affinities or interactions with specific sites and molecules.

Microdistribution of lead in bone: a new approach.

A knowledge of the microdistribution of lead in bone is important in order to understand the mechanisms for accumulation and release of lead. The availability of the synchrotron x-ray microscope for sensitive measurements of bone content and distribution of lead provides a valuable tool which, when combined with kinetic, balance, and tissue measurements, can lead to better evaluation of lead toxicity. It may also provide the basis for the development of a suitable model of how lead behaves in the human body. An outline of an experimental protocol for exploitation of the x-ray microscope is given, along with synchrotron x-ray microscope measurements of the distribution of gallium in rat bone that demonstrate the feasibility of the experimental approach.

The molecular nature of 1,25-(OH)2-D3-induced calcium-binding protein biosynthesis in the rat.

Exogenous 1,25-(OH)2-D3, administered to vitamin D-replete animals on a high calcium diet, induces biosynthesis of the duodenal, cytosolic calcium-binding protein (CaBP) in less than 2 h. This process can be blocked by simultaneously administered cycloheximide, but not by actinomycin D. In vitamin D-replete animals on a low Ca diet, on the other hand, 1,25-(OH)2-D3 administration leads to new CaBP synthesis only after about 7 h; this process can be blocked by actinomycin D. In vitamin D-deficient animals on a high calcium diet who have no CaBP, treatment with 1,25-(OH)2-D3 induces CaBP formation in congruent to 8 h; this process is known to be blocked by actinomycin D. Thus in D-replete animals on a low calcium diet and in D-deficient animals, CaBP biosynthesis proceeds by a transcriptional route, whereas in D-replete animals on a high calcium diet the rapid response appears to be posttranscriptional. This finding points to the possibility of a more rapid regulatory action of vitamin D than previously reported and how vitamin D might function in the D-replete state.

Extracellular and intracellular regulation of calcium homeostasis.

An organism with an internal skeleton must accumulate calcium while maintaining body fluids at a well-regulated, constant calcium concentration. Neither calcium absorption nor excretion plays a significant regulatory role. Instead, isoionic calcium uptake and release by bone surfaces causes plasma calcium to be well regulated. Very rapid shape changes of osteoblasts and osteoclasts, in response to hormonal signals, modulate the available bone surfaces so that plasma calcium can increase when more low-affinity bone calcium binding sites are made available and can decrease when more high-affinity binding sites are exposed. The intracellular free calcium concentration of body cells is also regulated, but because cells are bathed by fluids with vastly higher calcium concentration, their major regulatory mechanism is severe entry restriction. All cells have a calcium-sensing receptor that modulates cell function via its response to extracellular calcium. In duodenal cells, the apical calcium entry structure functions as both transporter and a vitamin D--responsive channel. The channel upregulates calcium entry, with intracellular transport mediated by the mobile, vitamin D-dependent buffer, calbindin D9K, which binds and transports more than 90% of the transcellular calcium flux. Fixed intracellular calcium binding sites can, like the body's skeleton, take up and release calcium that has entered the cell, but the principal regulatory tool of the cell is restricted entry.

[Value of the analysis of pulmonary venous flow in the evaluation of hemodynamics in dialysed patients]. / De l'intérêt de l'analyse du flux veineux pulmonaire dans l'estimation d'un état hémodynamique. Exemple de la dialyse.

The aim of this study was to assess the value of analysis of pulmonary venous flow in the evaluation of the haemodynamic status of patients with chronic renal failure with normal left ventricular function, treated by haemodialysis. Pulmonary venous flow was recorded immediately before and after haemodialysis in 27 patients with chronic renal failure and a mean age of 44 years. Three groups of patients were defined according to the change in mitral E/A ratio: Group I (E/A < 1 before and after dialysis), Group II (E/A > 1 before and < 1 after dialysis) and Group III (E/A > 1 before and after dialysis). There was a significant difference between these subgroups before dialysis with respect to age, S, D, VTI S, Total VTI, VTI S/Total (p < 0.05). However, because the values overlapped, only a VTI S/Total ratio greater than 59% differentiated patients in Group II from those in group III (p < 0.05). After dialysis, the change in S/D and VTI S/Total ratios increased in Groups I and II and decreased in Group III. The authors concluded that 63% of patients without LV dysfunction on haemodialysis have abnormalities of relaxation which are latent in 47% of cases due to increased filling pressures diagnosed by a VTI S/Total ratio > 59% or simply because the patients are over 50 year old.

[Paradoxal lowering of parasympathetic indices in myasthenic patients]. / Diminution paradoxale des paramètres parasympathiques chez les patients myasthéniques.

Myasthenia gravis is an autoimmune disease presenting antibodies developed against the nicotinic receptors of acetylcholine. The aim of this study was to evaluate heart rate variability in these patients. Heart rate variability was studied with 24 hour Holter recordings. Eighteen myasthenic patients, 7 men and 11 women, under pyridostigmine treatment, with an average age of 40 years (25 to 63 years) were aged and gender matched to a control group of 18 healthy subjects. All patients exhibited normal cardiac status and Doppler echocardiography. The following parameters were collected over 24 hours and the data further differentiated between night and day: for the temporal domain: heart rate, SDNN, pNN50, rMSSD; and for the spectral domain: total power, high frequency (HF) and low frequency (LF) power. The mean heart rate was slightly higher in the myasthenic group (non significant), due to a less marked nocturnal bradycardia. There was a decrease in the observed absolute values of SDNN as well as temporal and spectral parasympathetic indices (pNN50, rMSSD, HF) (p < 0.01) over the 24 hour period. The results were more significant during the night. Cardiac parasympathetic modulation is significantly modified in myasthenic patients. Considering that lack of bradycardia argues against an over active vagal tone, three hypothesis are discussed that favor of a low vagal tone: antibodies effects on the nicotinic receptors of the autonomic nervous system, respiratory impairment and a desensitization of the acetylcholine receptors.

[Variability of heart rate after heart surgery under extracorporeal circulation: aortocoronary bypass or aortic valve replacement]. / Evolution de la variabilité de la fréquence cardiaque après chirurgie cardiaque sous circulation extra-corporelle: pontages aorto-coronariens ou remplacements valvulaires aortiques.

The study of heart rate variability allows analysis of modulations of heart rate by the sympathetic vagal system. The authors studied the course of sinus variability by 24-hour Holter monitoring preoperatively, and on the 6th and 42nd postoperative day, in 25 patients undergoing coronary bypass graft (group I) and 10 patients undergoing aortic valve replacement (group II). Surgery was performed under cardiopulmonary bypass with selective antegrade cold crystalloid cardioplegia. The preoperative ejection fraction of these patients was 62% with a mean age of 59.5 years in group I and 61.5 years in group II. All temporal or spectral parameters were significantly decreased in the two groups on the sixth day (p < 0.05). Parameters which remain altered on D42 compared to baseline values were temporal parameters: pNN50 and rMSSD for group I and ASDNN for group II, with a tendency to return to baseline values, but with a higher mean heart rate in group II on D6 and D42 (p < 0.05). In the spectral domain, TP (total power of the spectrum) and LF (Low frequencies) remained decreased in both groups. A reversible alteration of sinus variability parameters was therefore observed in the two groups of patients. Other studies are necessary to define the mechanisms of these alterations, which are most probably related to catecholaminergic flooding related to CPB or partial vagal denervation by ischaemic or surgical damage to nerve structures.

[About an implantable cardioverter-fibrillator]. / Fibrillateur automatique implantable.

A 61-year-old man has been implanted with a Ventritex Profile MD V-186 HV3 ICD for ischemic cardiomyopathy with sustained inducible VT. Three years later, this patient received several inappropriate shocks during the device's interrogation. These shocks provoked ventricular fibrillation. They were caused by a failing soldering between the system random accessory memory (SRAM) module and the hybrid circuit of the device. The device was explanted in emergency.