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M Allard

Publications and source records attributed to M Allard.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Treatment of chronic ankle instability with the Chrisman-Snook's technique].

PURPOSE OF THE STUDY: We report our experience on lateral ankle instability treated by the Chrisman Snook procedure. We studied the objective and subjective results as well as the effect on peroneus brevis tendon function. MATERIAL AND METHODS: Among 110 patients treated for chronic lateral ankle instability between 1991 and 1997, 32 cases were treated with this technique. The average age was 25 years (16-37) and the average time to surgery from the initial trauma was 30 months. This was a retrospective study using the Karlson Peterson form while the laxity was measured with Telos device (120 N). Cybex testing was performed on 10 patients. Twenty-seven patients participated in sport. RESULTS: The follow-up ranged from 6 to 65 months (average 25 months). The average Karlson's score was 82.6 with 78 per cent excellent and good results. Lateral ligament laxity was reduced from 17 mm to 4 mm on Telos measurements and no osteoarthritis was noticed radiographically. The joint mobility consistently returned to the preoperative level. Twenty four patients returned to sport although half of the patients had some pain during sport activities or with fast walking. DISCUSSION: Males and patients participating in sporting activities had the best results and none of the patients had recurrent instability despite new sport injuries. The persistence of some pain may be associated with the long period of instability prior to reconstruction in this group of patients. CONCLUSION: The Chrisman Snook lateral ligament reconstruction is a technically easy and solid technique and we recommend it in patients with significant chronic lateral ligament instability.

Adolescent↗
PubMed1998

Evidence for a hypothalamic oxytocin-sensitive pattern-generating network governing oxytocin neurons in vitro.

During lactation and parturition, magnocellular oxytocin (OT) neurons display a characteristic bursting electrical activity responsible for pulsatile OT release. We investigated this activity using hypothalamic organotypic slice cultures enriched in magnocellular OT neurons. As shown here, the neurons are functional and actively secrete amidated OT into the cultures. Intracellular recordings were made from 23 spontaneously bursting and 28 slow irregular neurons, all identified as oxytocinergic with biocytin and immunocytochemistry. The bursting electrical activity was similar to that described in vivo and was characterized by bursts of action potentials (20.1 +/- 4.3 Hz) lasting approximately 6 sec, over an irregular background activity. OT (0.1-1 microM), added to the medium, increased burst frequency, reducing interburst intervals by 70%. The peptide also triggered bursting in 27% of nonbursting neurons. These effects were mimicked by the oxytocin receptor (OTR) agonist [Thr4, Gly7]-OT and inhibited by the OTR antagonist desGly-NH2d(CH2)5[D-Tyr2,Thr4]OVT. Burst rhythmicity was independent of membrane potential. Hyperpolarization of the cells unmasked volleys of afferent EPSPs underlying the bursts, which were blocked by CNQX, an AMPA/kainate receptor antagonist. Our results reveal that OT neurons are part of a hypothalamic rhythmic network in which a glutamatergic input governs burst generation. OT neurons, in turn, exert a positive feedback on their afferent drive through the release of OT.

Animals↗
PubMed1998

Regulated expression of the cell adhesion glycoprotein F3 in adult hypothalamic magnocellular neurons.

F3, a glycoprotein of the immunoglobulin superfamily implicated in axonal growth, occurs in oxytocin (OT)-secreting and vasopressin (AVP)-secreting neurons of the adult hypothalamo-neurohypophysial system (HNS) whose axons undergo morphological changes in response to stimulation. Immunocytochemistry and immunoblot analysis showed that during basal conditions of HNS secretion, there are higher levels of this glycosylphosphatidyl inositol-anchored protein in the neurohypophysis, where their axons terminate, than in the hypothalamic nuclei containing their somata. Physiological stimulation (lactation, osmotic challenge) reversed this pattern and resulted in upregulation of F3 expression, paralleling that of OT and AVP under these conditions. In situ hybridization revealed that F3 expression in the hypothalamus is restricted to its magnocellular neurons and demonstrated a more than threefold increase in F3 mRNA levels in response to stimulation. Confocal and electron microscopy localized F3 in secretory granules in all neuronal compartments, a localization confirmed by detection of F3 immunoreactivity in granule-enriched fractions obtained by sucrose density gradient fractionation of rat neurohypophyses. F3 was not visible on any cell surface in the magnocellular nuclei. In contrast, in the neurohypophysis, it was present not only in secretory granules but also on the surface of axon terminals and glia and in extracellular spaces. Taken together, our observations reveal that the cell adhesion glycoprotein F3 is colocalized with neurohypophysial peptides in secretory granules. It follows, therefore, the regulated pathway of secretion in HNS neurons to be released by exocytosis at their axon terminals in the neurohypophysis, where it may intervene in activity-dependent structural axonal plasticity.

Animals↗
PubMed1998

Periganglionic foraminal steroid injections performed under CT control.

PURPOSE: The purpose of our study was to evaluate the efficacy of direct intraforaminal steroid injections into the periganglionic space in the treatment of radicular pain. METHODS: Periganglionic infiltrations were performed in 41 patients with acute or chronic radicular pain. Neuroradiologic imaging in all patients showed foraminal stenosis due to degenerative disorders or herniated disk. All injections were performed under CT control. RESULTS: Seventy percent of patients had significant pain reduction, with the greatest success (90% of patients) in those whose foraminal stenosis was due to degenerative disorders; 45% of patients with foraminal herniated disks had pain relief. CONCLUSION: Intraforaminal steroid injection is useful in the treatment of radicular pain, particularly in cases of foraminal degenerative stenosis.

Adult↗
PubMed1997

Expression of high levels of the extracellular matrix glycoprotein, tenascin-C, in the normal adult hypothalamoneurohypophysial system.

Glia and neurons of the hypothalamoneurohypophysial system (HNS) undergo reversible morphological changes, which are concomitant with the remodelling of afferents onto the neurons, under different conditions of neurohormone secretion. Here, we show that the adult rat HNS contains high levels of tenascin-C (TN-C), which is an extracellular matrix glycoprotein whose expression is usually associated with neuronal-glial interactions in the developing and lesioned central nervous system (CNS). By using light and electron microscopic immunocytochemical procedures, we visualized TN-C immunoreactivity in the hypothalamic supraoptic (SON) and paraventricular nuclei, where somata of the neurons are localized; in the median eminence, where their axons transit; and in the neurohypophysis, where they terminate. Hypothalamic areas adjacent to the magnocellular nuclei were devoid of immunoreactivity. Electron microscopy of the neurohypophysis showed immunolabelling of perivascular spaces, glial (pituicyte) and axonal surfaces, a type of labelling that also characterized the median eminence. In the hypothalamic nuclei, there was labelling of extracellular spaces and astrocytic surfaces. In normal animals, we detected no cytoplasmic reaction in glia somata, neurons, or endothelial cells. However, in animals treated with the intracellular transport blocker colchicine, there was intracytoplasmic labelling of all HNS glial cells, indicating a glial source for TN-C. Immunoblot analysis revealed TN-C isoforms of apparent high molecular weight (225, 240, and 260 kD) in the SON and median eminence, whereas lower MW forms (190/200 kD) predominated in the neurohypophysis. By using immunocytochemistry and immunoblot analysis, we found no visible differences in TN-C expression in relation to age, sex, or differing neurohypophysial secretion, which suggests that the expression of TN-C is a permanent feature of the HNS.

Animals↗
PubMed1997

Nutrition and successful aging: a study of 520 elderly persons from the Toulouse and New-Mexico Aging Process Study.

Epidemiological studies of aging are usually confronted with the presence of numerous pathologies or environmental factors which make it difficult to identify the effects of aging individually. One way of reducing the variability among individuals is to use well defined criteria to select the study population. This is the choice that was made for the New Mexico and Toulouse Aging Process Studies, which were particularly turned towards successful aging. In this study we have sought to explain the diversity of states of health of the subjects of these two studies by means of an aging classification exploring the medical history, balance and walking, and the cognitive functions. This reveals that the poorer health of certain subjects (about 10% and 30% of the populations of Toulouse and Albuquerque respectively) is slightly associated with changes in eating behaviour relative to subjects who age successfully. We have, however observed a decrease in vitamin E intake in Toulouse associated with a reduction of lipids in the food. But the poorer state of health is predominantly explained by advancing age and the occurrence of pathological states. This study confirms that aging was generally successful in the two populations studied.

Aged↗
PubMed1996

Cardiovascular effects induced by the stimulation of neuropeptide FF receptors in the dorsal vagal complex: an autoradiographic and pharmacological study in the rat.

Previous studies have suggested that central administration of neuropeptide FF-related peptides may modulate cardiovascular parameters in the rat. In the present study, we investigated the role of dorsal vagal complex neuropeptide FF receptors in the central regulation of cardiovascular parameters. The fate of neuropeptide FF receptors in normal and nodose ganglionectomized rats was investigated using an autoradiographic approach with 125I-[DTyr1, (NMe)Phe3]NPFF as ligand for these receptors. We showed that neuropeptide FF binding sites are preferentially located postsynaptically with respect to the vagal afferent fibers in the nucleus tractus solitarius. Thus, ganglionectomy reduced by only 30% and 17% the density of peptide binding sites in the rostral and caudal regions of this nucleus, respectively. Bilateral microinjection of neuropeptide FF (1 nmol) into the commissural nucleus tractus solitarius produced an increase in blood pressure (+13.8 +/- 0.8 mmHg, n = 6), bradycardia (-29.0 +/- 3.2 bpm) and a significant inhibition (-47.6 +/- 3.1%) of the cardiac component of the baroreceptor reflex. Further studies with doses below 1 nmol indicate that NTS microinjections of the neuropeptide produced a dose-dependent decrease in heart rate. Similar cardiovascular effects were observed after bilateral NTS microinjections of one analog neuropeptide FF receptor agonist, [DTyr1, (NMe)Phe3]NPFF (1 nmol). Pretreatment with prazosin (100 micrograms/kg), an alpha 1-adrenoreceptor antagonist, inhibited the neuropeptide FF-evoked blood pressure effect. In addition, the neuropeptide FF-induced heart rate decrease was abolished by pretreatment with atropine (30 micrograms/kg), a muscarinic receptor antagonist. Taken together, these anatomical and pharmacological data suggest that neuropeptide FF receptors within the nucleus tractus solitarius, preferentially located on the postsynaptic component, are involved in the central reflex regulation of cardiovascular parameters.

Animals↗
PubMed1996

Spontaneous coronary artery dissection in young women.

Spontaneous dissection of the coronary arteries is quite rare. It is usually a catastrophic event with fatal outcome. We report two interesting cases of spontaneous dissection whose presentations exemplify the variable course the disorder may take. The first is the only report to our knowledge associated with aerobic exercise; the second is the only reported attempt at treatment with intracoronary thrombolysis.

Adolescent↗
PubMed1996

Evidence for multiple opioid receptors in the human posterior pituitary.

The distribution and quantification of opioid receptor types in post-mortem human pituitary cryostat sections was determined by quantitative in vitro receptor autoradiography. Highly specific radioligands were used for each opioid receptor type i.e. [125l]-FK-33-824 for mu-opioid sites, [125l][D.Ala2]-Deltorphin-l for delta-opioid sites and 3H-U69,593 for kappa-opioid sites. None of the five specimens tested exhibited any labeling in the anterior lobe of the pituitary for the three radioligands. As for the posterior pituitary, all 5 specimens contained both mu and kappa-opioid binding sites whereas none of them showed delta-binding sites. The presence of both mu- and kappa-opioid binding sites in the human posterior pituitary contrasts with previous findings in the rat where only kappa-sites have been found. The present study could contribute to understanding of the functional action of opioids in the human pituitary.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Reduction by (-)-cicletanine of the vascular reactivity to angiotensin II in rats.

Cicletanine [particularly the levorotatory (-)enantiomer] inhibits calcium/calmodulin cyclic GMP phosphodiesterase (PDE) in vascular smooth muscle (VSM) and potentiates the vasorelaxant actions of the guanylate cyclase activators sodium nitroprusside (SNP) and atriopeptin II, but the possible interference with vasopressor mechanisms remains to be determined. We tested racemic (+/-) cicletanine for its ability to modify the vascular responses to vasocontractant agents in pithed rats. The most significant results were obtained with angiotensin II (AII). Therefore, the dose of AII that increased the carotid artery blood pressure (BP) 50 mm Hg was twice as high in cicletanine-pretreated (50 mg/kg orally, p.o.) as that in vehicle-pretreated animals (ED50 = 0.48 +/- 0.012 vs. 0.25 +/- 0.007 microgram/kg, p < 0.05). The displacement by cicletanine represented 47.2% of that obtained with losartan (40 micrograms/kg, intravenously, i.v.). Similar results were obtained with (-)-cicletanine (p.o. or i.v.), but not with (+)-cicletanine. In isolated rat aorta, the contraction induced by AII was reduced by (-)-cicletanine in a noncompetitive manner (the percent reduction was independent of the AII concentration). (-)-Cicletanine reduces the vascular reactivity to AII, which plays a key role in several forms of hypertension. These findings are compatible with an action of (-)-cicletanine at any of the numerous steps that couple the occupation of AII receptors to the final contractile response, such as calcium/calmodulin cyclic GMP PDE.

Administration, Oral↗
PubMed1996

[Gleno-humeral arthroscopic arthrolysis for shoulder stiffness. Apropos of 26 cases. Société Française d'Arthroscopie].

UNLABELLED: Shoulder stiffness is a problem which covers many different conditions. In fact there is still a semantic and pathogenetic confusion. The words: capsulite retractile, frozen shoulder, adhesive capsulitis, stiff shoulder contracture have been successively used and this ambiguity renders the literature difficult to interpret. Moreover the cause of the stiffness which depends on the aetiology, is not always clearly known: capsular contraction, capsular adhesion, capsular scarring following trauma or surgery, extra capsular phenomenons in the subacromial bursa, muscles or tendons. MATERIALS AND METHODS: 26 shoulders (25 patients) were reviewed with a follow up of 21 months using the Constant's scoring system. Patients had an average duration of symptoms for 13 months (1 to 27). Pre op passive motion was: abduction: 74 degrees, external rotation: 6 degrees, forward flexion: 84 degrees. The average motion core was 12.9/40. We distinguished three groups: primary frozen shoulder (13 cases) ; bipolar stiffness (3 cases) due to rotator cuff disease ; acquired "surgical" stiffness, (10 cases). The capsular release was performed, at the anterior rim of the glenoid fossa, purely anterior or anterior and inferior, followed by gentle manipulation. If external rotation was not improved the coraco-humeral ligament was detached from its coracoid attachment. Additional procedures were performed:acromioplasty (5 cases), bursectomy (3 cases), SLAP lesion debridement (1 case). Only 2 out 13 primary shoulders required an additional procedure. RESULTS: 1-There were no intra-operative complications (vascular or neural). 2-Range of Motion: the average gain under anesthesia was: abduction: 72 degrees, external rotation: 34 degrees, forward flexion: 86 degrees. Final result was obtained with a mean duration of seven months. There was no difference according to the aetiology. Gain was more important in the primary group (9.69 to 34.9 vs 15.8 to 30.6). 3-Subjective results were better in the primary group. 4-Objective results demonstrated an absolute Constant's score of 70.3, that is to say 83.4 per cent of the contralateral supposed healthy shoulder. There were 3 excellent, 5 very good, 7 good, but 11 fair or poor results. The relative Constant's score was 91 per cent in the primary group and only 76 per cent in the acquired group. The difference was due to the pain and strength which were greatly improved in the primary group. DISCUSSION: Arthroscopic release of shoulder contracture is feasible, safe and effective. For primary frozen shoulder, there is usually spontaneous recovery. Indications for surgery are very few. There is no evidence that arthroscopic release shortens spontaneous evolution. Therefore, we propose it in very selected cases of dramatically limited motion. One year of evolution is an acceptable time. For bipolar stiffnesses, arthroscopy allows one to recognize the exact cause of the stiffness and to treat it, especially the subacromial pathology. In this occurrence, buroscopy must be performed and cuff pathology treated. For acquired surgical stiffnesses, gain of motion is significant. Subjective and objective results are less satisfactory than those of primary frozen shoulder, due to persistance of pain and lack of strength. The alternative is open release, but arthroscopic release has less morbidity. It can be proposed early as soon as capsular tissue has healed (for instance 6 months).

Adult↗
PubMed1995

Evidence for (+)-cicletanine sulfate as an active natriuretic metabolite of cicletanine in the rat.

It was previously shown that the urinary sulfo-conjugate metabolite of cicletanine (cicletanine sulfate), and not free cicletanine, is salidiuretic in rats. Here we investigated potential differences between the resolved (+/-) enantiomers of cicletanine sulfate. Two groups of rats (n = 10) received either (+)- or (-)-cicletanine p.o. High performance capillary electrophoresis revealed that the 24-h urinary excretion of (+)-cicletanine sulfate was 5 times higher than that of (-)-cicletanine sulfate (18.9% vs. 3.8% of the oral dose). The same relative trend was observed after 5 and 10 days of oral administration. Following direct administration into the renal artery of anesthetized rats, (+)-cicletanine sulfate was 3-4 times more potent, in terms of active doses, than (-)-cicletanine sulfate to increase sodium excretion (ED50 = 1.86 +/- 0.28 mg/kg vs. 6.1 +/- 1.0 mg/kg, mean +/- S.E.M., n = 4). The maximal natriuretic potency of (+)-cicletanine sulfate was intermediate between that of furosemide and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonate). In rat erythrocytes, (+)-cicletanine sulfate was between 2 and 3 times more potent to inhibit the Na(+)-dependent Cl-/HCO3- anion exchanger than (-)-cicletanine sulfate (IC50 = 61 +/- 3 microM vs. 142 +/- 31 microM, n = 4). In conclusion, (+)-cicletanine was more sulfo-conjugated and more potent natriuretic agent in rats than (-)-cicletanine. These results strongly suggest that (+)-cicletanine sulfate is the active natriuretic metabolite of racemic cicletanine in rats. This compound may probably act by inhibiting the Na(+)-dependent Cl-/HCO3- anion exchanger at the cortical diluting segment.

Acetates↗
PubMed1995

Changes in CNS neuropeptide FF-like material, pain sensitivity, and opiate dependence following chronic morphine treatment.

Tolerance and dependence to opiates may be an adaptive process that limits excessive effects of morphine on the CNS. Because no consistent opiate receptor reduction in chronically treated rats seems to underlie the hyposensitivity to morphine, an alternative hypothesis has postulated a role of "antiopioid" peptides. It is possible to speculate that the administration of morphine stimulates antiopioid systems such as neuropeptide FF (NPFF), as part of an homeostatic mechanism contributing to the development of tolerance. To test this hypothesis, pain sensitivity, opiate dependence, and CNS NPFF-IR levels were estimated at different times after implantation of morphine pellets (2 x 75 mg; NIDA). Three hours after morphine pellet treatment the analgesic effect was maximum and it decreased rapidly during the following 12 h. Naloxone-precipitated withdrawal syndrome was detected as soon as 3 h after morphine pellet implantation and was maximal after 24 h. NPFF-IR levels were measured in the spinal cord, brain stem, and hypothalamus. A significant decrease of NPFF-IR was observed 1 h after morphine pellet implantation (-25% to -45% depending on the structures) followed by a drastic increase of NPFF-IR levels (+60 to +140%) between 3 and 6 h. NPFF-IR levels rapidly returned to baseline after 24-36 h. It is suggested that the activity of these NPFF-IR neurones may increase gradually as a consequence of the continuous stimulation of opiate receptors and be part of an adaptive process that is able to counteract morphine effects and to induce dependence and tolerance to the analgesic effects of opiates.

Adaptation, Biological↗
PubMed1995

Neuropeptide FLFQRFamide receptors within the ventral mesenchephalon and dopaminergic terminal areas: localization and functional antiopioid involvement.

The neuropeptide FLFQPQRF amide is a FMRFamide-like peptide with some anti-opiate properties. Neuropeptide FLFQPQRFamide receptors are present in the mammalian central nervous system and have been clearly identified as different from opiate receptors. Autoradiography has revealed neuropeptide FLFQPQRFamide receptor localization within the ventral mesencephalon, where opiate receptors are also located. In order to delineate anatomical localization of neuropeptide FLFQPQRFamide receptors, we used selective chemical lesions of dopaminergic cells and intrinsic perikarya of the ventral mesencephalon, coupled with in vitro autoradiographic techniques. We show that: (i) unilateral lesions of dopaminergic perikarya produced by 6-hydroxydopamine did not affect either ipsi or contralateral neuropeptide FLFQPQRFamide receptor density within the mesencephalon; (ii) unilateral lesions of intrinsic perikarya by ibotenic acid injected into the ventral tegmental area produced a significant reduction of neuropeptide FLFQPQRFamide receptors (40%) in this region; (iii) in the substantia nigra pars compacta, ibotenic acid unilateral lesions did not affect the density of neuropeptide FLFQPQRF-amide receptors; (iv) unilateral 6-hydroxydopamine or ibotenic acid lesions failed to affect neuropeptide FLFQPQRFamide binding in the dopaminergic projection areas. These results suggest that, like opiate receptors, the neuropeptide FLFQPQRFamide binding sites are not localized on dopaminergic neurons but are distributed on both soma of non dopaminergic cells in the ventral tegmental area and on fibers afferent to the ventral tegmental area and substantia nigra pars compacta. To evaluate the possibility that the stimulation of neuropeptide FLFQPQRFamide receptors may affect the opioid modulation of mesocorticolimbic dopaminergic neuron activity, we tested the effects of neuropeptide FLFQPQRFamide ventral tegmental area infusion (0.25-10 micrograms) on the behavioral activation induced by intra-ventral tegmental area morphine infusion. We observed that in the ventral tegmental area, the stimulation of neuropeptide FLFQPQRFamide receptors inhibits morphine-induced locomotor hyperactivity. These results suggest that in the ventral tegmental area, neuropeptide FLFQPQRFamide may participate, via an indirect mechanism, to the control of the mesocorticolimbic dopaminergic system activity by counteracting the effect of opioids.

Animals↗
PubMed1995

Distribution of neuropeptide FF (FLFQPQRFamide) receptors in the adult rat spinal cord: effects of dorsal rhizotomy and neonatal capsaicin.

By using quantitative autoradiography and highly selective iodinated ligands, we quantified modifications in neuropeptide FF binding sites in the superficial layers (laminae I and II) of the cervical (C6-C8 segments) and lumbar (L3-L5 segments) enlargements in two models: (i) rats neonatally treated with capsaicin; (ii) rat submitted 15 days before to unilateral dorsal rhizotomies. We comparatively analysed the distribution of mu-opioid binding sites in the same animals. We have shown that the [125I]YLFQPQRFamide (neuropeptide FF sites) labelling is not significantly modified following selective damage of fine afferent fibres by neonatal capsaicin treatment. In the cervical and lumbar enlargements, capsaicin-treated/control binding ratios for [125I]YLFQPQRFamide were 0.90 and 0.86, respectively. While unilateral dorsal rhizotomy induced a drastic decrease in [125I]FK-33-824 labelling in the side ipsilateral to the lesion as compared to the intact side of (yielding ratios of 0.29 and 0.31 for cervical and lumbar levels, respectively), [125I]YLFQPQRFamide labelling was not significantly modified, yielding ratios of 0.98 and 0.91 for cervical and lumbar levels, respectively. These data suggest that, in contrast with a majority of mu-opioid receptors, neuropeptide FF receptors are not located on fine primary afferent fibers carrying nociceptive information from the fore- or hindlimb in the rat. This preferential postsynaptic localization, together with the reported "morphine modulating" action of this peptide, support the proposal of a role for neuropeptide FF in intraspinal modulation of nociceptive input.

Amino Acid Sequence↗
PubMed1995

Lateralization of prefrontal activation during internal mental calculation: a functional magnetic resonance imaging study.

1. Functional magnetic resonance imaging (fMRI) at 1.5 T was used to investigate the lateralization of prefrontal cortex activity during internal mental calculation in 16 human volunteers (8 right-handed and 8 left-handed). Subjects were asked to perform two different tasks: 1) a serial subtraction of prime numbers and 2) a control task in which they mentally recited numbers. 2. Signal modifications were regularly observed in the prefrontal cortex (Brodmann's area 46) during the serial subtraction of prime numbers, whereas the number listing task poorly activated the same areas. 3. In right-handed subjects, activation was clearly lateralized in the left dorsolateral prefrontal cortex, whereas a frequent bilateral activation was found in left-handed subjects. 4. We conclude that prefrontal activation during mental calculation is lateralized in a manner similar to that reported during linguistic tasks, i.e., a clear lateralization in right- but not in left-handed subjects.

Adult↗