Evidence-based cognitive rehabilitation: recommendations for clinical practice.

OBJECTIVE: To establish evidence-based recommendations for the clinical practice of cognitive rehabilitation, derived from a methodical review of the scientific literature concerning the effectiveness of cognitive rehabilitation for persons with traumatic brain injury (TBI) or stroke. DATA SOURCES: A MEDLINE literature search using combinations of these key words as search terms: attention, awareness, cognition, communication, executive, language, memory, perception, problem solving, reasoning, rehabilitation, remediation, and training. Reference lists from identified articles also were reviewed; a total bibliography of 655 published articles was compiled. STUDY SELECTION: Studies were initially reviewed according to the following exclusion criteria: nonintervention studies; theoretical, descriptive, or review papers; papers without adequate specification of interventions; subjects other than persons with TBI or stroke; pediatric subjects; pharmacologic interventions; and non-English language papers. After screening, 232 articles were eligible for inclusion. After detailed review, 61 of these were excluded as single case reports without data, subjects other than TBI and stroke, and nontreatment studies. This screening yielded 171 articles to be evaluated. DATA EXTRACTION: Articles were assigned to 1 of 7 categories according to their primary area of intervention: attention, visual perception and constructional abilities, language and communication, memory, problem solving and executive functioning, multi-modal interventions, and comprehensive-holistic cognitive rehabilitation. All articles were independently reviewed by at least 2 committee members and abstracted according to specified criteria. The 171 studies that passed initial review were classified according to the strength of their methods. Class I studies were defined as prospective, randomized controlled trials. Class II studies were defined as prospective cohort studies, retrospective case-control studies, or clinical series with well-designed controls. Class III studies were defined as clinical series without concurrent controls, or studies with appropriate single-subject methodology. DATA SYNTHESIS: Of the 171 studies evaluated, 29 were rated as Class I, 35 as Class II, and 107 as Class III. The overall evidence within each predefined area of intervention was then synthesized and recommendations were derived based on consideration of the relative strengths of the evidence. The resulting practice parameters were organized into 3 types of recommendations: Practice Standards, Practice Guidelines, and Practice Options. CONCLUSIONS: Overall, support exists for the effectiveness of several forms of cognitive rehabilitation for persons with stroke and TBI. Specific recommendations can be made for remediation of language and perception after left and right hemisphere stroke, respectively, and for the remediation of attention, memory, functional communication, and executive functioning after TBI. These recommendations may help to establish parameters of effective treatment, which should be of assistance to practicing clinicians.

Effect of Fas+ and Fas- target cells on the ability of NK cells to repeatedly fragment DNA and trigger lysis via the Fas lytic pathway.

We and others have recently shown that human NK cells express the Fas ligand (FasL) constitutively and that they can trigger the lysis of Fas positive (Fas+) target cells (TC) by apoptosis. We have also previously demonstrated that NK cells exposed to sensitive TC temporarily lose their ability to lyse sensitive TC via the granule-mediated pathway and that this loss is recovered when inactivated NK cells (NKi) are incubated in medium supplemented with IL-2, IL-12 or IL-15. In this study, we investigated the fate of the Fas-lytic pathway in NK cells exposed to either Fas+ or Fas- TC. To this end, we exposed NK cells to Jurkat (Fas-) or Jurkat (Fas+) TC for up to 6 h, separated NK cells from the TC and assessed the residual lytic activity against K562, a traditional human NK cell target, Jurkat Fas+ and Jurkat Fas- TC. Fas lytic activity was determined in calcium free medium, in the presence or absence of two distinct Fas-blocking monoclonal antibodies and a Fas.Fc fusion protein. In parallel experiments, the extent of DNA fragmentation in the three TCs was also assayed by the JAM test. Our results indicate that: (i) NK cells exposed to susceptible Fas+ TC temporarily lose most of their lytic potential due to the granule-mediated pathway, while only partially losing the Fas-lytic pathway. They also partially lose their ability to fragment DNA. (ii) NK cells exposed to Fas+ TC completely recover the Fas lytic pathway and the ability to fragment DNA via the Fas/Fas ligand when incubated in medium supplemented with IL-2 for 18 h.

Alcohol cue reactivity, negative-mood reactivity, and relapse in treated alcoholic men.

Relapsed alcoholic individuals frequently report that negative emotional states trigger their return to drinking. A parametric laboratory study was conducted to assess the separate and combined effects of exposure to alcohol-related stimuli and induced negative moods in abstinent alcoholic persons. The authors also sought to determine if reactivity to alcohol cues or reactivity to negative mood induction predicted relapse soon after treatment. Men with alcoholism (N = 50) undergoing inpatient treatment participated in a guided imagery procedure designed to induce negative moods and were then exposed to either their favorite alcoholic beverage or to spring water. Results indicated that both alcoholic beverage presentation and negative affect imagery led to increased subjective reporting of desire to drink. These effects were additive but not multiplicative (i.e., the interaction of mood state with beverage type was not significant). Reported urge to drink during the trial that combined negative mood imagery with alcoholic beverage exposure predicted time to relapse after inpatient discharge.

Hypochondriasis influences quality-of-life outcomes in patients with chronic fatigue.

BACKGROUND: To determine how hypochondriacal symptoms influence the quality-of-life outcomes of patients with a chief complaint of chronic fatigue. METHODS: Cross-sectional cohort study of a consecutive sample of 71 patients (mean duration of fatigue of 4.1 years). Forty-eight (68%) patients met criteria for current major depression and 32 (45%) met criteria for chronic fatigue syndrome (CFS). All patients received a comprehensive medical and psychiatric evaluation. Quality-of-life and physical, depressive and hypochondriacal symptom scores were assessed through reliable self-report questionnaires and a structured interview. A path model expressing the relation between predictor variables (hypochondriasis and depression), intervening variables (physical symptoms) and quality of life was postulated and evaluated using structural equation methods. RESULTS: The paths linking hypochondriasis with physical symptoms and mental health and the path connecting physical symptoms and quality of life were each statistically significant. The model applied especially well to patients who fulfilled CFS criteria. CONCLUSIONS: The quality of life of chronic fatigue patients correlates with the severity of their physical symptoms and their hypochondriacal disposition toward illness.

Alpha 1-adrenoceptor-induced contractility in rat aorta is mediated by the alpha 1D subtype.

Adrenoceptor agonists were used to characterize the alpha 1-adrenoceptor subtype responsible for mediating tension (phasic and tonic combined) in the denuded rat aorta and compared with radioligand binding at alpha 1-adrenoceptor subtypes. The rank order of potency at the rat aorta was the same as that obtained for binding affinity at the rat clonal alpha 1d-adrenoceptor: norepinephrine > epinephrine > cirazoline > phenylephrine > oxymetazoline > A-61603 > methoxamine. Correlation coefficients comparing rat aortic contraction (pD2) to binding (pKi) were 0.09-0.21 for alpha 1A/a receptors, 0.66 for clonal alpha 1b and 0.94 for clonal alpha 1d-adrenoceptors. Correlation coefficients comparing the clonal alpha 1d-adrenoceptor binding affinity to in vitro contractile responses were 0.03 and 0.10 for the rat vas deferens and canine prostate alpha 1A-adrenoceptor responses, respectively, 0.09 for the rat spleen alpha 1B and as noted, 0.94 for the rat aorta. The agreement observed between agonist potency at the rat aorta and affinity for the alpha 1d binding site provide new evidence that the alpha 1D-adrenoceptor subtype is responsible for mediating contractions in the rat aorta.

Synergistic inhibition of human cell-mediated cytotoxicity by complement component antisera indicates that target cell lysis may result from an enzymatic cascade involving granzymes and perforin.

A widely accepted theory of lymphocyte-mediated cytotoxicity (CMC) proposes that upon effector cell (EC) and target cell (TC) interaction, release of perforin, serine proteases and other lytic moieties contained within cytoplasmic granules results in TC lysis. Complement activation and the activation of the various enzymatic activities associated with cytotoxic granules have strikingly similar modes of action and both lead to pore formation in their respective targets. We report here that by using antisera to early and late complement components we were able to inhibit CTL, NK and ADCC cytotoxicity up to 100%, even though binding of EC to TC was unaffected. Furthermore, we showed that addition of C1q or C1s (two serine proteases) antisera to C9 antisera, at titers too low to inhibit separately, resulted in synergistic inhibition of CMC. Anti-C1s together with anti-C1q (or anti-C8 with anti-C9) did not result in synergy. This finding supports a cascade model of activation for lytic molecules released from EC. In addition, we demonstrated that anti-C1q and anti-C1s bind to proteins in the 30-kD region and anti-C9 binds to proteins in the 70-kD region, coinciding with published molecular weights of granzymes and perforin, respectively. Finally, lytic ability of purified granules was also inhibited by complement antisera, further suggesting that activation occurs outside of TC. Taken as a whole, these data indicate that TC lysis may be the result of a cascade of events involving granzymes and perforin, analogous to that seen with the complement system.

Preclinical pharmacological actions of (+/-)-(1'R*,3R*)-3-phenyl-1- [1',2',3',4'-tetrahydro-5',6'-methylene-dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200), a potential antidepressant agent that antagonizes alpha-2 adrenergic receptors and inhibits the neuronal uptake of norepinephrine.

(+/-)-(1'R*,3R*)-3-phenyl-1-[(1',2',3',4'-tetrahydro-5',6'-methylene- dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200) was evaluated in a number of biological tests to establish its pharmacological profile of activity. ABT-200 antagonized the uptake of [3H]-norepinephrine into synaptosomes of rat hypothalamus (IC50 = 841 nM) and blocked 4,alpha-dimethyl-m-tyramine- induced hypermotility in rats. In addition, ABT-200 potently inhibited binding of [3H]-rauwolscine to alpha-2 adrenergic receptors with a Ki value in radioligand binding assays of approximately 1 nM in the rat cortex and was much less potent at other receptor binding sites. ABT-200 antagonized alpha-2 receptors in vitro in the rat vas deferens and dog saphenous vein, where pA2 values of 7.7 and 8.2, respectively, were obtained. ABT-200 also antagonized clonidine-induced mydriasis and increased the overflow of [3H]-norepinephrine in guinea pig hippocampal slices, manifestations of blockade of alpha-2 adrenoceptors in the central nervous system. ABT-200 was active in antagonizing nocturnal hyperactivity in olfactory bulbectomized rats, a test for putative antidepressant activity. In cardiovascular studies, ABT-200 exhibited negligible activity in affecting hemodynamic parameters and was free of postural hypotensive activity. In both in vitro and in vivo, ABT-200 was devoid of antihistaminic or anticholinergic activity. This profile of activity of moderate inhibition of norepinephrine uptake with blockade of alpha-2 adrenoceptors suggests potential dual-action effects for ABT-200, which may represent a putative antidepressant with minimal cardiovascular side-effect liability.

Upregulation of B7 molecules by the Epstein-Barr virus enhances susceptibility to lysis by a human NK-like cell line.

The original human NK-like line YT was reported to lyse K562 and several B- and T-cell lines. The YT subline we are investigating, YT-INDY, does not lyse K562 or the T-cell line Molt-4. It does, however, lyse the EBV+ Burkitt lymphoma (BL) B-cell line Raji and EBV-immortalized B-cell lines. Several EBV- BL lines and an EBV- pre-B-cell leukemia line that we tested were not appreciably lysed by YT-INDY. To determine if EBV plays a role in TC susceptibility to lysis by YT-INDY, we compared YT-INDY's ability to lyse the EBV- BL line BL41 to its ability to lyse an EBV-infected derivative of BL41. The EBV-infected cell line was lysed, on average, at twice the level of the uninfected line. CD28/B7 interactions appeared to be involved in TC recognition by YT-INDY. Therefore, we examined the level of expression of B7 molecules on the infected and uninfected BL41 lines. An average of 15% of the uninfected BL41 cells expressed B7-1/B7-3, compared to 79% of the infected. B7-2 expression was similar in the two cell lines. Lysis of EBV-infected BL41 was reduced by anti-B7-1/B7-3 (BB1) or anti-CD28 antibodies (Abs) to the level of lysis of the uninfected line, indicating that upregulation of B7-1/B7-3 by the virus may be responsible for the enhanced susceptibility. We attempted to determine the particular EBV latent protein responsible for B7-1/B7-3 upregulation by analyzing BL41 clones expressing LMP1, EBNA-2/EBNA-LP, or EBNA-1. All of the high-expressing clones showed a higher level of B7-1/B7-3 expression than the vector-transfected control cell line, with LMP1-expressing clones expressing the highest amount. EBNA-1 clones and a high-expressing EBNA-2/EBNA-LP clone had a slightly higher density of B7-2 on their surface than the remaining clones. The increased expression of molecules of the B7 family correlated with increased susceptibility of the clones to lysis by YT-INDY. Anti-CD28 or a combination of anti-B7-1/B7-3 and anti-By-2 did not inhibit lysis of the clones to the level of lysis of the vector-transfected control cell line in all cases. We conclude that intact EBV enhances susceptibility to YT-INDY lysis by upregulating B7-1/B7-3. EBV proteins expressed individually also enhance susceptibility to lysis and upregulate members of the B7 family.(ABSTRACT TRUNCATED AT 400 WORDS)

Receptor interactions of Abbott-81988, a highly potent, non-peptide angiotensin-II antagonist selective for type-1 receptors.

Abbott-81988 (A-81988) was selected from a series of related compounds as a highly potent and selective antagonist of angiotensin receptors. In the rabbit aorta, A-81988 exhibited a pA2 of 10.12 (+/- 0.08) vs. angiotensin-II, for type 1 receptors (AT1), and the antagonism appeared competitive. These results agreed with radioligand assays in which A-81988 inhibited the binding of [125I]-Sar1-Ile8-Angiotensin-II to rat liver membranes with a pKI of 9.12 (+/- 0.63). A-81988 was selective for AT1 receptors based on its lack of activity at other sites, such as aortic alpha 1 receptors. Moreover, A-81988 lacked affinity for AT2 receptors of bovine cerebellar membranes or for alpha or beta adrenergic receptors in binding assays. A-81988 lowered blood pressure significantly in vivo in renal artery-ligated rats at doses of 0.3 mg/kg administered either i.v. or p.o. The compound was rapidly and almost completely absorbed from the duodenum of anesthetized rats and demonstrated very low first-pass metabolism in the rat liver. These properties of selectivity toward and potency for antagonizing AT1 receptors, activity in lowering blood pressure in experimental animals, and favorable pharmacokinetic properties indicate that A-81988 should be a useful antihypertensive agent in man.

Pharmacological characterization of Abbott-81282, a novel, non-peptide angiotensin-II antagonist selective for type-1 receptors.

Abbott-81282 (A-81282) has been identified among a series of related compounds as being a highly potent and selective antagonist of angiotensin receptors. At AT1 receptors of the rabbit aorta, A-81282 exhibited a pA2 of 9.64 (+/- 0.33) vs. angiotensin-II, and demonstrated characteristics consistent with competitive antagonism of this receptor. These results were supported in radioligand binding assays in which A-81282 inhibited the binding of [125I]-Sar-Il8-Angiotensin-II to rat liver membranes with a pKI of 8.505 (+/- 0.102). Selectivity of this agent for AT1 receptors was validated by its lack of activity at other receptor sites, such as alpha 1 receptors of isolated rabbit aorta. Moreover, A-81282 lacked affinity for AT2 receptors of bovine cerebellar membranes or for alpha or beta adrenergic receptor sites in radioligand binding assays. A-81282 lowered blood pressure significantly in vivo in renal artery-ligated rats at doses of 1 mg/kg i.v. or 5 mg/kg p.o. The compound was slowly and moderately absorbed from the duodenum of anesthetized rats and demonstrated low first-pass metabolism in the rat liver. Because of its selectivity and potency for antagonizing AT1 receptors, and its activity in lowering blood pressure in experimental animals, A-81282 has the potential to be a useful antihypertensive agent in man.

Blocking the Ca(2+)-activated cytotoxic mechanisms of cholinergic neuronal death: a novel treatment strategy for Alzheimer's disease.

The major neuropathological finding in Alzheimer's disease (AD) is the death of cholinergic cell bodies originating in the nucleus basalis of Mynert. This paper will review the data suggesting that a pharmacologic strategy designed to slow the rate of cholinergic neuronal death (CND) should be of palliative value in the treatment of AD. Recent data on the biology of cell death (CD) show that there are two patterns of CD: necrosis and apoptosis or genetically controlled, programmed cell death. Regardless of whether cells die by necrosis or apoptosis, four Ca(2+)-activated cytotoxic mechanisms are triggered. Cytosolic free [Ca2+]i increases with aging. After 75 years, this rise may lead to the activation of a putative apoptotic gene in AD that results in CND. Since the increase in cytosolic [Ca2+]i may be mediated by the voltage operated L-type Ca2+ channel on the neuronal cell body, chronic treatment with an L-channel blocker, like nimodipine, might palliate the progression of and possibly prevent the majority of cases of AD.

Categorical perception for voicing contrasts in normal and lead-treated rhesus monkeys: electrophysiological indices.

Categorical perception of voicing contrasts was evaluated in rhesus monkeys. The monkeys had been chronically exposed to subclinical levels of lead either from conception to birth, or for approximately 6 months postnatally beginning at birth, or were never exposed to lead. Auditory evoked responses were recorded at 1 year of age from scalp electrodes placed over the left and right hemispheres during stimulus presentation. A late component of the brain responses recorded from the right temporal region of all monkeys discriminated between stimuli in a categorical manner. This pattern of responses was noted to be similar to that previously reported for humans. Categorical discriminations were also noted earlier in the waveforms for control monkeys and for monkeys exposed to lead prenatally, although this discrimination pattern shifted to the left hemisphere of the latter group. No such effects were noted for monkeys exposed to lead postnatally. These results suggest that the neurocortical mechanisms associated with categorical perception for voicing information may be similar across human and nonhuman primates. However, early exposure to lead appears to alter these processes.

Caroli's disease: new diagnostic and therapeutic approaches.

Cystic dilatations of the intrahepatic and extrahepatic biliary trees are common congenital anomalies that frequently require surgical intervention. We have presented a case of Caroli's disease in which an accurate diagnosis was made noninvasively preoperatively, using computerized tomography, ultrasonography, and cholescintigraphy.

Neuroelectrical correlates of categorical perception for place of articulation in normal and lead-treated rhesus monkeys.

Categorical perception of place of articulation contrasts was evaluated in rhesus monkeys. The monkeys had been chronically exposed to subclinical levels of lead, either from conception to birth, or for approximately 6 months beginning at birth, or were never exposed to lead. Auditory evoked responses were recorded from scalp electrodes placed over left and right hemispheres during stimulus presentation. The brain responses recorded from the right hemisphere of the normal control group of monkeys discriminated between the categories of [dae] and [gae]. Categorical discriminations were also noted for monkeys exposed to lead either prenatally or postnatally. These discriminations, in contrast, were found over only the left hemisphere. In additions, postnatal exposure resulted in categorical discrimination associated with slower latency components, suggesting a less mature pattern than that obtained for prenatally exposed monkeys. Finally, the brain responses of the animals in the normal control and postnatal exposure conditions evidenced reliable within-category, as well as between-category, discriminations. These results suggest that the neurocortical mechanisms associated with categorical perception of place information may differ between human and nonhuman primates and that early exposure to lead alters these processes.

The use of auditory and phonetic memory in vowel discrimination.

A commonly held assumption about memory for speech is that auditory memory is referred to only if phonetic memory does not contain the information needed for a particular trial. However, this assumption is in conflict with recent evidence [Crowder, J. Exp. Psychol.: Learning, Memory, Cognition 8, 153-162 (1982); Repp et al., J. Exp. Psychol.: Human Perception Performance 5, 129-145 (1979)]. The present study provides additional data to help determine how auditory and phonetic memory are used in a vowel discrimination task, and what happens during memory decay. Experiment 1 was conducted to determine whether performance levels decline at similar rates on between- and within-category AX vowel comparison trials when certain methodological problems are removed. This was confirmed. Experiment 2 demonstrated that in the AX task there is a vowel order effect, as Repp et al. found, but that this effect increased across interstimulus delay intervals, in contrast to their findings. The results can be accommodated with a model in which the memory for a vowel is represented as a small, bounded area within the vowel space, and in which memory decay is represented by the expansion of that bounded area over time.

Infant speech recognition in multisyllabic contexts.

In 2 infant speech recognition experiments using trisyllabic sequences, the amount of redundancy within nontarget, context syllables was manipulated. Infants 6 1/2 months old were trained to discriminate the syllables [ba] versus [du] in contexts that were either redundant (e.g., [ko ba ko] or [ti ba ti]) or mixed (e.g., [ko ba ti] or [ti ba ko]) A visually reinforced head-turning procedure was employed. In Experiment 1, context was manipulated between subjects, but in Experiment 2 each subject received all 4 contexts (2 redundant, 2 mixed). Infants consistently recognized the familiar target in all contexts, but did so more successfully in redundant than in mixed trisyllablic contexts. These results suggest that amount of speech redundancy may be an important factor in infants' perceptual capabilities.

Mothers' perceptions of infant distress vocalizations.

In the present study the psychological and acoustic properties of the distress vocalizations of five 3-4-month-old infants were examined. Each vocalization was rated on a 5-point scale from "definitely fuss" to "definitely cry" by mothers on two home visits. On the first home visit, each mother rated a set of her own infant's vocalizations recorded 1/2 hour previously and presented in the order of occurrence. Three weeks later, on the second home visit, mothers were presented with the master tape that contained the vocalizations of all five infants in random order. Analyses of the judgment data and acoustic parameters of the vocalizations revealed that (a) mothers were able to rate infant vocalizations reliably along a fuss-cry continuum, both shortly after these vocalizations were produced and 3 weeks later with fewer available nonacoustic, contextual cues; (b) mothers relied upon mean and peak intensity, mean F2 frequency, the ratio of F1 to F2, and mean duration in their judgments of infant cries versus fusses; and (c) although there was a high level of rating consistency across mothers, there were some discrepancies between visit 1 and 2 ratings due to the contribution of context cues present on visit 1 only.

Echoic storage in infant perception.

Preperceptual auditory of "echoic" storage was investigated in 8-9 week-old infants using a modification of an adult masking paradigm and a nonnutritive sucking discrimination procedure. Experiment 1 provided validation of a new version of the nonnutritive sucking procedure using the standard stimulus contrast [ba] versus [pa]. In experiment 2, infants were presented with repeating pairs of brief vowels with a stimulus onset asynchrony (SOA) of 50 msec for each pair. Within each series, the first vowel in a pair changed (backward masking), the second vowel changed (forward masking), or neither vowel changed (control). Discrimination of the changed occurred in the forward- but not in the backward-masking condition. In experiment 3, discrimination occurred in a backward-masking condition with an SOA of 400 msec, but not with an SOA of 250 msec or in a control condition. In conjunction with the adult literature, these results suggest that echoic storage contributes to auditory perception in infancy, as in adulthood, but that the useful lifetime of an echoic trace may be longer in infancy.

The perception of the sound of silence in early infancy.

When brief periods of silence are inserted between the /s/ and /lit/ portions of the English word "slit" (/slit/), adult listeners typically hear the word as "split" (/split/). 2 experiments were conducted to investigate the ability of 6-8-month-old infants to discriminate brief periods of interconsonantal silence in "slit" versus "split" contrasts. Infants were tested in multiple sessions, using a conditioned head-turning paradigm. 3 sets of stimuli were employed: /slIt/, /slIt/ +Silence, and /splIt/, containing 0, 173, and 90 msec, respectively, of silence duration following the /s/ portion of the stimulus. In both experiments, infants reliably discriminated /slIt/ +Silence from the /slIt/ stimuli but not from the /splIt/ stimuli. Therefore, it appears that infants, like adults, do not treat stimuli containing 90 or 173 msec of silence in this interconsonantal context as different.

Discrimination of voice onset time in infancy.

In an effort to determine whether infants can discriminate speech sounds on the basis of a single acoustic cue, timing onset of periodic voicing, two experiments were conducted employing synthetic speech sounds. Naturally produced syllable pairs were also used for comparison. In the first experiment infants evidenced discrimination of a naturally produced /ba/ versus /pa/ pair and a naturally /du/ versus /tu/ pair. In addition, infants discriminated a synthetic /ba/ versus /pa/ contrast that was cued by several acoustic differences in addition to timing onset of periodic voicing but failed to evidence an ability to discriminate a synthetic /du/ versus /tu/ contrast that contained flat first formants and differed only in timing onset of periodic voicing. A second experiment was conducted in which infants once again evidenced discrimination of naturally produced /du/ versus /tu/ stimuli but not of synthetic /du/ versus /tu/ stimuli containing slight first-formant transitions. These results suggest that timing onset of periodic voicing alone may not be a sufficient cue for infant discrimination of English voicing contrasts.