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Dupuytren's contracture of the fingers: a simplified approach to the surgical treatment.

Hematoma formation, delay in healing, pain, stiffened finger joints are complications that sometimes follow classical surgical approaches to Dupuytren's contracture. A new surgical approach to the disease that can correct the contractures without the attendant morbidity is urgently needed. By treating Dupuytren's as any other scar contracture (division of the contracting soft tissue at its point of maximal tension and interposing normal free full-thickness skin) postoperative morbidity can be greatly decreased. Full return of function was achieved within 21 days following operation in 85 percent of the cases in which finger contractures were present before operation. Contracture release of 100 joints was done by this means, with loss of only one graft and without recurrence of the disease. This technique offers simple surgical control of progressive and recurrent Dupuytren's contracture of the fingers with minimal postoperative morbidity.

Aged↗

Evaluation of inferior check ligament desmotomy for treatment of acquired flexor tendon contracture in the horse.

The usefulness of inferior check ligament desmotomy as a treatment for acquired tendon contracture in horses was evaluated in 13 cases of deep digital flexor (DDF) contracture and in 3 cases of combined superficial digital flexor (SDF) and DDF contracture. In 8 of 9 cases of DDF contracture in which the dorsal surface of the hoof had not passed beyond being vertical to the ground, the surgical procedure was successful in returning the limb to a normal position and function. Compared with DDF tenotomy, inferior check ligament desmotomy was a superior treatment technique because of decreased postoperative pain, better postoperative appearance, and improved return to function. In 4 cases of DDF contracture in which the dorsal SDF contracture was also involved, inferior check ligament desmotomy was generally insufficient to allow return of the limb to normal alignment and function.

Animals↗

[Pathogenesis of quadriceps contracture in children and adolescence (author's transl)].

Forty-one limbs in 35 patients were examined about the findings concerning with quadriceps contracture at operation and moreover pathohistological examination was carried out for the whole length of the resected rectus femoris muscle in every patient in order to study pathogenesis of contracture of the quadriceps muscles. The age of patients at operation was two years and 3 months for the youngest and 17 years and 3 months for the oldest. Among these patients, the previous history of injection was positive in 29 cases, negative in 5 cases and unknown in one case. In cases with nor previous history of injection, the cross sections of the rectus femoris muscle macroscopically revealed that scar exists over the whole length of this muscle, showing clear boundary between scar and adjacent muscles. Pathohistological examination showed that fibrosis of the muscle fibers in addition to infiltration of fibrous tissues between muscle fibers. On the other hand, in cases with previous history of injection, pathohistological findings revealed that atrophy and degeneration were marked in the whole area of the muscle fibers in comparison with non-injection cases although scar in muscle was not so clear macroscopically. As the operative findings in the cases with or without injection in the previous history, considerable adhesion and scar were seen in the muscles and fascias surrounding the rectus femoris muscle. Therefore, in order to release contracture it was necessary to detach these adhesions, to remove scar tissues and to cut the contracted fascia. From these results, it is considered that the chief cause for the contracture of the quadriceps muscles treated by us can be attributable to the muscles showing contracture over the whole length and lacking normal elasticty, which produce adhesions caused in scar formation with surrounding muscles and fascias. The various clinical symptoms associated with quadriceps contracture depend upon the severity of such pathologic changes. The follow-up results obtained in these cases were to be satisfied. Therefore, the findings at operation, pathohistological findings, operative technique and follow-up results in our cases are fully justified in recommending our method. However, it was impossible to classify clearly our cases into rectus type, vastus type or mixed type according to the general criteria. In other words, all of our cases could be classified into mixed type. It may be explained by small number of cases as well as 41 limbs included in our study.

Adolescent↗

Factors affecting appearance patterns of hip-flexion contractures and their effects on postural and gait abnormalities.

Hip flexion contractures accompanying various orthopedic and neurologic conditions not only limits the physical activities of the patients but also distorts their postures and gait patterns. The purposes of this study were to characterize the appearance patterns of flexion contracture at the hip joints and to elucidate how this disability affects their postural and gait abnormalities. Seventy-eight patients (mean age of 68.1 +/- 10.5 years) with hemiplegia, femoral neck fractures, osteoarthritis of the hip and other conditions causing hip flexion contractures were studied. The presence and degree of hip flexion contracture were estimated in the supine position using the Thomas maneuver with a goniometer. Relationship between appearance patterns and 12-survey variables was also analyzed statistically. As a result, it was revealed that whether lack of mobility caused by hip flexion contracture was compensated for by pelvic tilt an an increase of lumbar lordosis or not was affected by four factors. It was also revealed that whether it appeared unilaterally or bilaterally was affected by five factors. In addition, some postural and gait abnormalities caused by hip flexion contracture were observed in many patients. These results suggest that clinical pictures of the patient's posture and gait abnormality depend on his ability to regulate the position of the trunk and knees as well as the mobility of his spine.

Adolescent↗

C1840-T mutation in the human skeletal muscle ryanodine receptor gene: frequency in northern German families susceptible to malignant hyperthermia and the relationship to in vitro contracture response.

In swine, a point mutation in the ryanodine receptor gene can account for all cases of malignant hyperthermia (MH). The frequency of a corresponding mutation in humans (C1840-T) and its relationship to the in vitro contracture profile is unknown. We screened 192 patients from 28 unrelated northern German families for the C1840-T mutation in the human ryanodine receptor gene and tested for MH susceptibility using the in vitro contracture test (IVCT) according to the European MH Protocol. In our patients 106 revealed MH susceptible (MHS), 56 MH nonsusceptible and 30 MH equivocal status following IVCT. In each family one or two individuals had developed clinical signs of MH or a MH crisis. All of these patients were classified MHS. The C1840-T mutation was found in 2 of 28 families (7.1%). All eight individuals of the two families characterized by this mutation revealed MHS status following IVCT. The thresholds for halothane- and caffeine-induced contractures as well as the contracture profiles following cumulative (0.4-10.0 mumol/l every 3 min) and bolus (10 mumol/l) administration of ryanodine were found to be similar in MHS patients with and without the C1840-T mutation. In conclusion, the C1840-T mutation in the human ryanodine receptor gene is a rare abnormality in MHS families. Similar contracture profiles in the presence and absence of this mutation might imply no major functional role with respect to the contracture response. At present, molecular genetic analysis cannot replace IVCT to discover MH susceptibility in humans.

Adolescent↗

Potassium contractures and mechanical activation in mammalian skeletal muscles.

Potassium (K-) contractures were recorded from slow-twitch (mouse soleus and fast-twitch (mouse extensor digitorum longus (EDL) and rat sternomastoid) muscles. The mouse limb muscles responded to a maintained increase in external potassium concentration with a rapid increase in tension (fast contracture) which inactivated and was followed by a slow contracture. Rat sternomastoid muscles responded with fast contractures only. The threshold potassium concentration for contraction was higher in fast-twitch muscles than in soleus muscles, at 22 and at 37 degrees C. After corrections had been made for the more rapid depolarization of soleus fibers, the threshold potential for soleus fiber contraction was 15mV closer to the resting membrane potential than the threshold for fast-twitch fiber contraction. The K-contracture results were confirmed by two microelectrode voltage-clamp experiments. Activation of fast twitch fibers required depolarizing pulses that were 15 to 20mV greater than the pulses required to activate soleus fibers. When the time courses of K-contractures were compared it was evident that inactivation with prolonged depolarization was much faster in the fast-twitch muscles than in the soleus muscles. The results suggest that the voltage dependence and kinetics of the process coupling T-tubule depolarization with calcium release from the sarcoplasmic reticulum may depend on fiber atype in mammalian skeletal muscle.

Animals↗

Hyperthyroidism is associated with preserved preconditioning capacity but intensified and accelerated ischaemic contracture in rat heart.

BACKGROUND: The present study was undertaken to define the effects of thyroxine administration on ischaemic preconditioning (PC) and the ischaemic contracture. METHODS: Hyperthyroidism was induced by administration of L-thyroxine in rats (THYR) while normal animals served as controls (NORMa). Isolated rat hearts were perfused in a Langendorff preparation. NORMa control (n = 16) and THYR control (n = 9) hearts underwent 20 min of ischaemia and 45 min reperfusion while NORMa PC (n = 16) and THYR PC (n = 14) were subjected to PC before ischaemia. Additional normal hearts were subjected to 30 min of ischaemia with and without PC, NORMb control, n = 8 and NORMb PC, n = 6. Postischaemic recoveries of left ventricular (LV) developed pressure were expressed as % of the initial value (LVDP%). Severity of contracture was measured by the time (Tmax) and magnitude (Cmax) of peak contracture. RESULTS: LVDP% was significantly higher after PC, both in NORMa and THYR rats. In NORMa control hearts, ischaemic contracture had not yet reached a plateau at 20 min of ischaemia. Contracture appeared earlier in THYR control and PC than in NORMa control and PC groups. Tmax was 22.1 (0.9) vs 16.8 (1.4) min for NORMb control and PC, p < 0.05 and 12.5 (1.0) vs 9.3 (1.1) min for THYR control and PC hearts, p < 0.05. Tmax was earlier in both THYR groups compared to NORMb groups, p < 0.05. Cmax was significantly higher in both THYR groups compared to both NORMb groups. CONCLUSION: Ischaemic contracture is both accelerated and accentuated in thyroxine treated hearts while preconditioning capacity is preserved. Preconditioning and thyroxine administration shorten Tmax in an additive way, whereas Cmax in hyperthyroid hearts did not further increase by preconditioning.

Adenosine Triphosphate↗

Caffeine-evoked contractures in single slow (tonic) muscle fibres of the frog (Rana temporaria and R. esculenta).

Single slow (tonic) muscle fibres were dissected from cruralis muscles of Rana temporaria and R. esculenta. Increasing concentrations of caffeine were applied in Ringer solution, and contractures were measured isometrically. Sigmoid caffeine concentration-response curves were obtained, the threshold value being near 1.2 mmol/l, and maximum contractures being obtained with 10 to 20 mmol/l concentrations of caffeine. Contracture solutions were modified by varying the Ca2+ concentration or by replacing Ca2+ with 1.8 mmol/l Mg2+, Ni2+, Co2+ or with 0.1-5.0 mmol/l La3+. The effects of low pH (5.3), K+ (6,10 and 95 mmol/l), adenosine (10 mmol/l) and gallopamil (D600; 30 micromol/l) were examined too. The caffeine threshold was lowered by Mg2+, K+, 0 .1 mmol/l La3+ and D600, while all other substances including 0.5-5.0 mmol/l La3+ increased it. The amplitude of contractures evoked by high caffeine concentrations was unaffected. Caffeine (1-40 mmol/l) was also pressure injected into slow fibres. The composition of the solution was modified in a number of ways, but a contractile response was not observed or measured. Extracellular application of caffeine from the same pipettes evoked local contractures. Similar injection experiments in twitch fibres revealed the same results. These observations suggest that an extracellular binding site seems to be involved in the initiation of caffeine-evoked contractures in intact frog muscle fibres. Possible reasons for the ineffectiveness of intracellular caffeine are discussed.

Adenosine↗

Similar inhibitory effects of dantrolene sodium on twitch tension and on silver ion-induced contracture in skeletal muscle.

To determine the mechanism by which Ag+ induces a transient contracture in skeletal muscle, the effect of dantrolene sodium on the Ag+ contracture was examined and the findings compared with those for the twitch, tetanus and caffeine contracture. The inhibition of twitch by dantrolene was equivalent to that of the Ag+ contracture at concentrations of 1, 2 or 5 microM of dantrolene. The tetanus tension was slightly inhibited by dantrolene, but not the caffeine contracture. These observations suggest that the Ag+ contracture may be governed by the same mechanism as that involved in the development of twitch tension.

Animals↗

Inhibition of hypoxic myocardial contracture by Cobalt in the rat.

We studied the relationship between the slow inward current, tissue ATP content, and the development of hypoxic myocardial contracture in the rat. Resting tension and active isometric tension were measured using isolated left ventricular papillary muscle preparations. Action potentials and membrane currents were studied using a single sucrose gap voltage clamp technique. The slow inward current (isi) was partially inhibited by verapamil and completely inhibited by cobalt but was not reduced by ryanodine. Active tension was reduced by all three drugs. Non-stimulation, verapamil, and ryanodine did not prevent contracture development with hypoxia, but contracture was markedly reduced by pre-treatment with cobalt. Despite contrasting effects on contracture, both non-stimulation and cobalt partially prevented ATP depletion with hypoxia, suggesting that contracture is not directly related to total muscle ATP content. Cobalt appears to block hypoxic contracture via a mechanism other than simple blockade of isi, inhibition of contraction, or preservation of tissue ATP content.

Action Potentials↗

Force-velocity and unloaded shortening velocity during graded potassium contractures in frog skeletal muscle fibres.

Steady-state conditions of contraction, at maximal and submaximal forces, were produced in intact single muscle fibres, from Rana esculenta, using full tetani and graded K+-contractures. The uniformity in radial direction. of spreading of activation produced in K+-contractures, was checked in relation to the fibre diameters. The absolute isometric force was similar in tetani and maximal contractures, for fibres with diameters between 40 and 60 microm, but not for fibres with diameters greater than about 70 microm in which contracture force never reached tetanic force. The force [K+]o relation was similar for fibres with diameters between 40 and 60 microm. but it was right shifted and it had a minor slope for fibres with diameters greater than 65-70 microm. This suggests that only in the small diameter fibres (40-60 microm) the activation does not fail to penetrate uniformly from the surface towards the fibre core. For fibres selected in the diameter range between 40 and 60 microm, force-velocity relations and unloaded shortening velocities were determined in tetani and maximal and submaximal contractures. Data were obtained across a force range of 0.3 to 1 P0 (tetanic plateau force). Controlled velocity method was used to obtain force-velocity relations, and slack test to determine the unloaded shortening velocity (VU). The values of the parameters characterising the force velocity relation (V0 and a/P0) and VU as determined by the slack test did not differ significantly in tetani and contractures, independent of the activation level or absolute force developed by the fibre. These results show that. at least within the range of forces tested. crossbridge kinetics is independent of the number of cycling crossbridges, in agreement with the prediction of the 'recruitment' model of myofilament activation.

Animals↗

Contractures in skeletal muscle of malignant hyperthermia susceptible patients after in vitro exposure to sevoflurane.

BACKGROUND: Sevoflurane, a potent inhalational anaesthetic agent that is structurally similar to halothane, has some favourable characteristics, but may also be able to trigger malignant hyperthermia (MH) in susceptible patients. The diagnosis of malignant hyperthermia susceptibility relies on the in vitro contracture test on skeletal muscle. The present study was undertaken to investigate whether exposure to sevoflurane of muscles of malignant hyperthermia susceptible (MHS) patients would also cause an abnormal contracture. METHODS: Muscle fascicles obtained from three MHS patients, one malignant hyperthermia non-susceptible (MHN) patient, two control patients and one malignant hyperthermia equivocal (MHE) patient were exposed to sevoflurane instead of halothane in the in vitro contracture test, carried out according to the protocol of the European Malignant Hyperthermia Group. The muscle fascicles were surplus to diagnostic requirements. Sevoflurane concentrations in the testbath were measured using a headspace gas chromatographic technique. RESULTS: The kinetics of sevoflurane concentration in the testbath were similar to those of halothane. An in vitro contracture response of 2 mN or more was seen in all four MHS/MHE patients with sevoflurane but not in the three control/MHN patients. The magnitude of muscle contracture in the sevoflurane test was less than in the conventional halothane test at comparable testbath concentrations. CONCLUSIONS: Sevoflurane can trigger an abnormal contracture in human muscle in vitro. This is indicative of malignant hyperthermia susceptibility. Exposure to sevoflurane should be avoided in patients thought to be susceptible to malignant hyperthermia.

Anesthetics, Inhalation↗

The differential effect of halothane and 1,2-dichlorohexafluorocyclobutane on in vitro muscle contractures of patients susceptible to malignant hyperthermia.

UNLABELLED: Malignant hyperthermia (MH) is an autosomal dominant, potentially fatal pharmacogenetic disorder of skeletal muscle. Approximately half of all known MH families show a linkage to the ryanodine receptor type 1 (RY1) gene. Although our knowledge of the diagnosis, genetics, and therapy of MH has improved, the exact pathogenesis and the role of volatile anesthetics as trigger substances for an MH crisis remain unknown. Compounds that do not obey the Meyer-Overton hypothesis (i.e., nonimmobilizers) are today an important part of research on anesthetic mechanisms. We designed this study to test the hypothesis that the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N) compared with halothane has different effects on in vitro muscle contractures of muscle bundles from MH-susceptible (MHS) individuals. In vitro muscle contracture tests were performed with either halothane (approximately 660 microM, equivalent to approximately 4 minimum alveolar anesthetic concentration [MAC]) or 2N ( approximately 100 microM, equivalent to approximately 5 times predicted MAC). MAC is defined as the anesthetic concentration that prevents nocifensive movements after a surgical stimulus in 50% of subjects. In contrast to halothane, 2N caused only minimal muscle contractures in muscle bundles from six MHS patients (0.13 g [0.04-0.31 g] vs 1.95 g [1.60-4.70 g], median values and ranges; P = 0.004). Halothane and 2N differ in their effects on muscle contractures of MHS individuals, possibly because of a differing action on MH RY1. IMPLICATIONS: Using in vitro contracture tests, we showed that halothane and the nonimmobilizer 1,2-dichlorohexafluorocyclobutane differ in their effects on contractures of muscle bundles from individuals susceptible to malignant hyperthermia (MH) as a result of their differing action on MH ryanodine receptors. These findings render this receptor a possible molecular target for volatile anesthetic action.

Adult↗

Capsular contracture in silicone gel and saline-filled breast implants after reconstruction.

Comparisons between results with randomly allotted silicone-gel and saline-filled prostheses in breast reconstruction after mastectomy led to the following conclusions. Neither prosthesis type is ideal. Leakage from saline-filled implants occurred in 2 of the 37 implants, with resultant deflation. Silicone prostheses had a significantly higher rate of capsular contracture [surgeon's evaluation: 54 percent capsular contracture for silicone-gel compared with 20 percent for saline-filled prostheses (p = 0.006); patients' evaluation for the same figures: 54 percent compared with 29 percent (p = 0.03)]. Other authors have shown the presence of silicone in the tissue around silicone-gel-filled silicone implants, but less or none around saline-filled silicone implants. Since the only difference between the two groups was the randomly allotted implants, we assume that the free silicone around silicone-gel-filled prostheses is the major cause of capsular contracture. Since the saline-filled implants showed a 20 percent capsular contracture rate, there could be other causes of capsular contracture in this study. For prevention of contracture, improved implant encapsulation and use of a less reactive filling substance seem to offer possibilities. Surgical technique should aim to preserve the integrity of the prosthesis.

Adult↗

Malignant hyperthermia (MH) diagnostics: a comparison between the halothane-caffeine- and the ryanodine-contracture-test results in MH susceptible, normal and control muscle.

Recent studies demonstrated different contracture responses in muscle from malignant hyperthermia susceptible (MHS) compared to normal (MHN) individuals following exposure to the plant alkaloid ryanodine in-vitro. To confirm if ryanodine has a specific action in MHS muscle, the effect of a single concentration was investigated in skeletal muscle from MHS, MHN and control subjects using a new evaluation technique. In-vitro contracture test (IVCT) and MH diagnosis were performed according to the European Protocol in 86 patients sent to us for MH diagnostic testing and in 24 controls. Viable fresh muscle bundles were exposed to a single bolus of ryanodine 1.0 microM. Contracture onset time (OTp: defined as the time (min) from administration of ryanodine to the start of a contracture as measured by a contracture exceeding predrug baseline height), and the time to an increase of the baseline height to 10 mN above the predrug level (10Tp) were recorded. 29 patients were identified by IVCT to be MHS, 50 MHN, 7 MHE (equivocal) and 24 controls MHN. The indices from the ryanodine test separated all MHS (OTp: < 16 min; 10Tp < 27.4 min) from MHN (> 18 and > 27.7 min) and control subjects (> 17.4 and > 29 min). Values for MHE (equivocal) individuals ranged from 17.1 to 27.8 min for the OTp and from 32 to 49.2 min for the 10Tp. 5 patients with fulminant MH crises were included in the MHS group and showed the 95% confidence intervals (CI) of the median value < or = 8.05 min (OTp) and < or = 13.35 min (10TP) for MHS. In contrast, CI of the median value for the control group were found to be > or = 25.2 min (OTp) and 43.15 min (10Tp) for normal muscle. Thus the ryanodine test protocol showed markedly different contractures in MHS and MHN or control muscle. These results suggest that MHS muscle has a higher sensitivity to ryanodine. However, the protocol should be investigated for reproducibility and validation of thresholds by other laboratories. Ryanodine can help to improve MH diagnostic tests.

Adolescent↗

Effect of temperature variation (22 degrees C-44 degrees C) on halothane and caffeine contracture testing in normal humans.

BACKGROUND: Malignant hyperthermia (MH) susceptibility is diagnosed using halothane-caffeine contracture testing of a muscle sample maintained at 37 degrees C. However, there has not been a systematic study that examines the effect of different temperatures on the response of normal muscle to halothane and caffeine. We hypothesized that altering bath temperature would modify the contracture responses. METHODS: We obtained muscle samples from 20 patients undergoing surgical procedures of the lower extremities. The samples were dissected into 245 bundles and the bundles were exposed to halothane 3% or incremental caffeine, according to the North American MH group protocol. Several bundles from each patient were simultaneously studied at four different temperatures (22 degrees C, 30 degrees C, 37 degrees C and 44 degrees C). Each bundle was studied at only one temperature, the muscle samples of 3 patients were simultaneously studied at all four temperatures for halothane and caffeine. RESULTS: Maximum contracture to caffeine (32 mM) was highest at 37 degrees C; however, at lower caffeine concentrations (2-4 mM), there was no consistent effect of temperature on contracture response. Likewise, temperature did not alter contracture responses to halothane. The extremes of temperature (22 degrees C and 44 degrees C) were associated with lack of twitch in response to electrical stimulation. For the bundles exposed to halothane at 22 degrees C, the absence of a twitch was associated with the presence of a contracture, although these were never above the diagnostic threshold. CONCLUSIONS: We conclude that temperature has little effect on responses of normal muscle to halothane and caffeine.

Aged↗

Potassium contractures and mechanical activation in rat skeletal muscle: effects of multivalent cations, temperature and tetracaine.

The effects of cations, temperature and tetracaine on potassium-induced contractures of rat soleus and extensor digitorus longus (e.d.l.) muscles were investigated. In the soleus, the threshold for the potassium contracture was lower (10-20 vs 20-40 mM), the peak amplitude was up to fourteen times larger, and the time course was about one half that in the e.d.l. muscle. The extent of inactivation of a test potassium contracture was directly related to the concentration of potassium in the conditioning solution and the period of exposure. Removal of calcium reduced the amplitude and time course of potassium contractures in both preparations. Addition of cobalt (10 mM) reduced the amplitude but prolonged the time course of contractures. Exposure of muscles to tetracaine (10(-5)-10(-6) M for 30 min) increased, but higher concentrations reduced, the amplitude of potassium contractures. When present for one minute, tetracaine (1 mM) moved the potassium activation curve to higher, and the potassium inactivation curve to lower, potassium concentrations.

Animals↗

External calcium sensitivity of low sodium contractures in the control and hypertrophied right ventricle of the ferret.

The existence of possible differences of calcium (Ca2+) fluxes through the sarcolemmal sodium-calcium (Na+/Ca2+) exchanger during hypertrophy has been tested by comparing the characteristics of the contracture--as an indicator of the intracellular Ca2+ concentration--induced by partial or total withdrawal of external sodium (Na+), in the absence of external potassium, in the right ventricular trabeculae of adult ferret hearts. Pressure-overload was induced by pulmonary artery clipping and led to an increase of the right ventricular weight of 60%. At an external Ca2+ concentration ([Ca2+]o) of 3 mM, the dependence of the contractures on extracellular sodium concentration ([Na+]o), the rate of tension development, the time course of spontaneous relaxation and the time course for the repriming of the contracture were unchanged by hypertrophy. However, the relationship between [Ca2+]o and contracture amplitude at various [Na+]o showed that the apparent affinity of the contracture for [Ca2+]o was decreased in hypertrophied preparations. Thus, in 0 mM [Na+]o, half-maximal contracture was induced at a [Ca2+]o of 0.012 +/- 0.016 mM and 0.171 +/- 0.021 mM in control (n = 11) and hypertrophy (n = 12) respectively (P less than 0.001). Although these data may be indicative of a decreased Ca2+ influx through the Na+/Ca2+ exchanger, it cannot be excluded that intracellular buffering mechanism may also be involved in this differential response to [Na+]o withdrawal.

Animals↗