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PubMed1989

The impact and experience of adventitious deafness.

Relatively little well controlled, empirical research has examined the problems, experiences, functional limitations and coping strategies of late-deafened individuals. The present paper summarizes, integrates and evaluates the literature on adventitious deafness. Several issues are explored in detail, including: a) a comparison of congenital and acquired deafness; b) a critical review of the literature investigating the psychiatric problems experienced by late-deafened individuals; c) an examination of the effects of acquired deafness on identity and personal control; and d) a consideration of adventitious deafness among the elderly.

Aged↗
PubMed2006

Fgf9 and Wnt4 act as antagonistic signals to regulate mammalian sex determination.

The genes encoding members of the wingless-related MMTV integration site (WNT) and fibroblast growth factor (FGF) families coordinate growth, morphogenesis, and differentiation in many fields of cells during development. In the mouse, Fgf9 and Wnt4 are expressed in gonads of both sexes prior to sex determination. Loss of Fgf9 leads to XY sex reversal, whereas loss of Wnt4 results in partial testis development in XX gonads. However, the relationship between these signals and the male sex-determining gene, Sry, was unknown. We show through gain- and loss-of-function experiments that fibroblast growth factor 9 (FGF9) and WNT4 act as opposing signals to regulate sex determination. In the mouse XY gonad, Sry normally initiates a feed-forward loop between Sox9 and Fgf9, which up-regulates Fgf9 and represses Wnt4 to establish the testis pathway. Surprisingly, loss of Wnt4 in XX gonads is sufficient to up-regulate Fgf9 and Sox9 in the absence of Sry. These data suggest that the fate of the gonad is controlled by antagonism between Fgf9 and Wnt4. The role of the male sex-determining switch--Sry in the case of mammals--is to tip the balance between these underlying patterning signals. In principle, sex determination in other vertebrates may operate through any switch that introduces an imbalance between these two signaling pathways.

Animals↗
PubMed1986

Respiratory function during pressure support ventilation.

Pressure support ventilation (PSV) is a pressure assist form of mechanical ventilatory support that augments the patient's spontaneous inspiratory efforts with a clinician selected level of positive airway pressure. To understand the effects of PSV on respiratory function, experiments were performed on 15 stable patients requiring synchronized intermittent mandatory ventilation (SIMV), as well as on a mechanical model simulating these patients' ventilatory systems. In the clinical study, gas exchange, airway pressures, blood pressure and heart rate were measured while SIMV was replaced by enough PSV to approximate the baseline SIMV tidal volume (VT). Measurements were repeated while this PSV level was then reduced in three 5 cm H2O steps every 10 to 15 minutes. It was found that PSV was a reasonable form of mechanical ventilatory support in patients with spontaneous ventilatory drives. It improves patient comfort, reduces the patient's ventilatory work, and provides a more balanced pressure and volume change form of muscle work to the patient. The clinical significance of these properties during the weaning process remain to be determined.

Adult↗
PubMed2006

Genomic reconstruction by serial mitotic recombination of yeast artificial chromosomes.

DNA cloned in yeast artificial chromosomes (YACs) is a valuable resource for functional experiments in cell culture as well as whole animal systems. Where the size or chimerism of a YAC clone are limiting factors it may be desirable to generate recombinant YAC clones. One such approach is based on mitotic recombination, and we describe the development of a methodology that allows multiple recombination cycles for serial reconstruction of overlapping YACs. This approach employs retrofitting with standard plasmid vectors, transfer of YACs to a common haploid host by Kar1 mating, and selection for recombination with 5-fluoro-orotic acid.

Chromosomes, Artificial, Yeast↗
PubMed2003

Molecular mechanisms that regulate auditory hair-cell differentiation in the mammalian cochlea.

Mechanosensory hair cells of the vertebrate cochlea offer an excellent developmental system to study cell-fate specification, and to gain insight into the many human neurological deficits which result in a hearing loss, by affecting primarily the hair cells. Therefore, there is great interest in studying the molecular mechanisms that regulate their specification and differentiation. Recent studies, based mostly on loss-of-function experiments that target the role of Notch signaling and basic helix-loop-helix genes in inner-ear development have indicated that they can regulate mechanosensory hair cell-fate specification and their initial differentiation.

Animals↗
PubMed2004

Brain-derived neurotrophic factor plays a critical role in contextual fear conditioning.

In this study, brain-derived neurotrophic factor (BDNF) heterozygous knock-outs were tested on fear conditioning, and their wild-type littermates were used as controls. Results showed that BDNF(+/-) mice are impaired in contextual learning, whereas tone learning remains intact. Because BDNF is involved in synaptic transmission and contextual learning is hippocampal dependent, we hypothesized that this deficit is attributable to abnormal BDNF-modulated synaptic plasticity in the hippocampus. A "gain-of-function" experiment was performed next by infusing recombinant BDNF protein into the hippocampal formation to investigate whether this deficit can be rescued. Infusion of BDNF protein into the hippocampus appeared to partially restore contextual fear learning of BDNF(+/-) mice. In conclusion, the present study suggests that BDNF plays a critical role in fear conditioning. Loss of one copy of the BDNF gene leads to impairment of contextual fear learning in BDNF(+/-). This deficit can be partially rescued by infusing BDNF protein into the hippocampus. Other brain regions interacting with the hippocampus in the context conditioned stimulus pathway, for example, the amygdala, may also require normal BDNF expression levels to fully rescue this impairment.

Amygdala↗
PubMed2007

Hepatocyte growth factor acts as a motogen and guidance signal for gonadotropin hormone-releasing hormone-1 neuronal migration.

Reproduction in mammals is under the control of the hypothalamic neuropeptide gonadotropin hormone-releasing hormone-1 (GnRH-1). GnRH-1-secreting neurons originate during embryonic development in the nasal placode and migrate into the forebrain along olfactory nerves. Gradients of secreted molecules may play a role in this migratory process. In this context, hepatocyte growth factor (HGF) is a potential candidate, because it promotes cell motility in developing brain and has been shown previously to act as a motogen on immortalized GnRH-1 neurons (GN11). In this study, the role of HGF and its receptor Met during development of the GnRH-1 system was examined. GnRH-1 cells express Met during their migration and downregulate its expression once they complete this process. Tissue-type plasminogen activator (tPA), a known HGF activator, is also detected in migratory GnRH-1 neurons. Consistent with in vivo expression, HGF is present in nasal explants, and GnRH-1 neurons express Met. HGF-neutralizing antibody was applied to explants to examine the role of the endogenous growth factor. Migration of GnRH-1 cells and olfactory axon outgrowth were significantly reduced, in line with disruption of a guidance gradient. Exogenous application of HGF to explants increased the distance that GnRH-1 cells migrated, suggesting that HGF also acts as a motogen to GnRH-1 neurons. Functional experiments, performed on organotypic slice cultures, show that creation of an opposing HGF gradient inhibits GnRH-1 neuronal migration. Finally, tPA(-/-):uPA(-/-) (urokinase-type plasminogen activator(-/-)) knock-out mice exhibit strong reduction of the GnRH-1 cell population. Together, these data indicate that HGF signaling via Met receptor influences the development of GnRH-1.

Animals↗
PubMed2026

Protective TGFβ2/SMAD3 axis identified by TWAS in papillary thyroid cancer.

Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy. Although generally indolent, a subset shows aggressive behaviour. Furthermore, the genetic heterogeneity of PTC is not fully explained by known driver mutations, underscoring the need to identify additional susceptibility genes and regulatory mechanisms. To identify additional susceptibility genes and regulatory mechanisms, we integrated transcriptome-wide association studies (TWAS) with summary-data-based Mendelian randomisation (SMR), joint/conditional testing (JCT), and colocalisation analyses across multiple independent cohorts, followed by heterogeneity in dependent instruments (HEIDI) test. Gene prioritisation analyses consistently highlighted TGFB2 and SMAD3 as candidate susceptibility genes for PTC, with SMR supporting putative protective effects. Besides, GEPIA confirmed the positive correlation between TGFB2 and SMAD3 expression in TCGA-THCA. Functional experiments in TPC-1 cells showed that TGFβ2 treatment inhibited cell proliferation and migration, induced apoptosis, and resulted in G0/G1 cell-cycle arrest, accompanied by increased SMAD3 phosphorylation, suggesting activation of canonical TGFβ signalling. Collectively, these findings bridge population-based genetic inference with mechanistic validation and suggest convergent evidence supporting a tumour-suppressive role of the TGFβ2/SMAD3 axis in PTC.

Humans↗
PubMed2000

Effect of acute immunoneutralization of endogenous leptin on prolactin and LH secretion during the afternoon of pro-oestrus or in steroid-treated ovariectomized female rats.

Recent data indicate that leptin is involved in the control of reproductive function. Experiments were carried out to analyse the role of endogenous leptin in the regulation of LH and prolactin secretion during the afternoon of pro-oestrus and that induced by ovarian steroids in ovariectomized rats. In the first experiment, cyclic female rats were implanted with intra-auricular and intracerebroventricular (i.c.v.) cannulae and, at pro-oestrus, were injected (i.c.v.) with 10 microliters normal rabbit serum or leptin antiserum (at 13:00 and 14:00 h). Blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the second experiment, female rats in pro-oestrus were injected with normal rabbit serum or leptin antiserum at 16:00 and 18:00 h and blood samples were taken every 10 min between 18:00 and 20:00 h. In the third experiment, adult female rats that had been ovariectomized 2 weeks before were implanted with intra-auricular and i.c.v. cannulae and treated with oestradiol benzoate (30 micrograms s.c.) at 10:00 h and progesterone (2 mg s.c.) 48 h later. Normal rabbit serum (10 microliters) or leptin antiserum (10 microliters) were injected (i.c.v.) at 13:00 and 14:00 h, and blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the fourth experiment, hemipituitaries from ovariectomized steroid-treated female rats were incubated in the presence of leptin116-130 (an active fragment of the native molecule), GnRH or leptin + GnRH. Prolactin and LH secretion during the afternoon of pro-oestrus in females treated with leptin antiserum was similar to that observed in animals injected with normal rabbit serum. In ovariectomized female rats, the steroid-induced LH surge increased slightly after administration of leptin antiserum, whereas the prolactin surge remained unchanged. In vitro, leptin116-130 (10(-5) to 10(-8) mol l-1) inhibited LH secretion and modulated the effect of GnRH on LH release, depending on the concentration of GnRH: leptin116-130 (10(-6) mol l-1) reduced the effectiveness of 10(-7) mol GnRH l-1 and increased that of 10(-9) mol GnRH l-1. In conclusion, these experiments indicate that acute immunoneutralization of endogenous leptin does not interfere with spontaneous or steroid-induced LH and prolactin surges. In addition, the finding that leptin116-130 inhibited LH release and modulated the effectiveness of GnRH in vitro provides evidence of the direct modulatory role of leptin on LH secretion acting at the pituitary.

Analysis of Variance↗
PubMed2005

Acetylcholine-induced aortic relaxation studied in salbutamol treated rats.

It has been proposed that the acetylcholine (ACh)-induced relaxation of the rat aorta is entirely mediated by endothelium derived-nitric oxide (NO). However, some authors have reported that indomethacin pretreatment attenuates ACh-induced relaxation of rat aortic ring preparations. Moreover, it has also been suggested that cAMP accumulation may regulate either nitric oxide synthase (NOS) or cyclooxygenase (COX) expression in different tissues. Thus, in this in vitro study we have investigated the endothelial mechanisms involved in the ACh-induced relaxation of ring preparations of the rat thoracic aorta, as well as the influence chronic treatment with the selective beta(2)-agonist salbutamol had upon such mechanisms. Results of functional experiments show that N(G)-monomethyl-L-arginine (L-NMMA, 3 x 10(-4) M) considerably inhibited the ACh-induced relaxation of rat aortic ring preparations. However, indomethacin (10(-5) M) was also found to partially attenuate this ACh response, suggesting that although NO is the most important mediator of the ACh-induced relaxation of the rat aortic ring preparations, vasorelaxation may also involve prostanoids. Moreover, the results suggest that treatment with salbutamol failed to produce any change in the ACh-induced relaxation of rat aortic ring preparations.

Acetylcholine↗
PubMed2005

[Valve replacement with the Omnicarbon valve prosthesis. A 10-year follow-up].

OBJECTIVE: We retrospectively examined the outcomes of 264 patients who underwent consecutive Omnicarbon valve implantation surgery between April 1985 and May 1995. METHODS: At the time of surgery, patients who received this mechanical prosthesis averaged 57+/-11 years of age. Omnicarbon valves were placed in the aortic position in 36% of the cases, in the mitral position in 44%, and in both positions in 20%. Follow-up was carefully performed, with most patients undergoing physical examination at our clinic. While taking the case history, cardiac physicians specifically questioned the patient about valve-related complications. RESULTS: Accumulated total patient-years is 1291, with a mean follow-up time of 5.4 years. Survival at 10 years is 79.4+/-3.9%, including all causes of death and early mortality. Complications recorded during the 11-year study include: thromboembolism (0.1%), hemorrhage (0.4%), endocarditis (0.2%), and nonstructural failure (1.2%). No hemolytic anemia, valve thrombosis, or structural failure was detected during this long-term experience. Functional capability of these patients was subjectively assessed by the NYHA classification system. With follow-up time averaging over 5 years, 97% of our Omnicarbon valve patients are in NYHA I or II. CONCLUSION: The Omnicarbon mechanical prosthesis provides a good clinical performance for up to 10 years in both the aortic and mitral positions. Results indicated a low incidence of thromboembolism and of hemorrhagic complications.

Adult↗
PubMed1999

The conveyor belt hypothesis for thymocyte migration: participation of adhesion and de-adhesion molecules.

Thymocyte differentiation is the process by which bone marrow-derived precursors enter the thymus, proliferate, rearrange the genes and express the corresponding T cell receptors, and undergo positive and/or negative selection, ultimately yielding mature T cells that will represent the so-called T cell repertoire. This process occurs in the context of cell migration, whose cellular and molecular basis is still poorly understood. Kinetic studies favor the idea that these cells leave the organ in an ordered pattern, as if they were moving on a conveyor belt. We have recently proposed that extracellular matrix glycoproteins, such as fibronectin, laminin and type IV collagen, among others, produced by non-lymphoid cells both in the cortex and in the medulla, would constitute a macromolecular arrangement allowing differentiating thymocytes to migrate. Here we discuss the participation of both molecules with adhesive and de-adhesive properties in the intrathymic T cell migration. Functional experiments demonstrated that galectin-3, a soluble beta-galactoside-binding lectin secreted by thymic microenvironmental cells, is a likely candidate for de-adhesion proteins by decreasing thymocyte interaction with the thymic microenvironment.

Antigens, Differentiation↗
PubMed2026

CST2 promotes melanoma malignant phenotypes through the IL-6-STAT3-NF-κB signaling axis.

BACKGROUND: Melanoma is a highly aggressive malignancy with increasing incidence and mortality over recent decades. Cystatin SA (CST2) encodes a secreted cysteine protease inhibitor that is overexpressed in various cancers and promotes tumor progression; however, its role in melanoma remains unclear. This study aimed to investigate the expression and clinical significance of CST2 in melanoma as well as its biological functions and underlying molecular mechanisms in melanoma progression. METHODS: CST2 expression was analyzed in melanoma tissues using The Cancer Genome Atlas (TCGA) dataset. The prognostic value of CST2 was assessed using Kaplan-Meier analysis. In vitro gain- and loss-of-function experiments were performed to evaluate the effect of CST2 on melanoma cell proliferation, colony formation, and migration. Mechanistic studies included protein-protein docking and co-immunoprecipitation to detect the interaction between CST2 and interleukin-6 (IL-6). Western blotting was used to examine the activation status of IL-6 downstream signaling pathways. RESULTS: CST2 was significantly upregulated in melanoma tissues and was correlated with poor patient prognosis. Overexpression of CST2 promoted melanoma cell proliferation, clonogenicity, and migration, whereas CST2 knockdown suppressed these malignant behaviors. CST2 interacted with IL-6, and its knockdown reduced the expression of IL-6, phospho-STAT3, and phospho-NF-κB. These suppressive effects were reversed by IL-6 overexpression, indicating that CST2 exerted its oncogenic effects through the IL-6-STAT3-NF-κB axis. CONCLUSIONS: CST2 promotes melanoma progression by activating the IL-6-STAT3-NF-κB signaling pathway, and may serve as a potential prognostic biomarker and therapeutic target in melanoma.

CST2↗
PubMed2026

Hypoxia-inducible factor-1α promotes the malignant progression of cervical cancer cells by regulating lactate dehydrogenase A-mediated glycolysis.

BACKGROUND: Enhanced glycolysis is a hallmark of metabolic reprogramming in cervical cancer and plays a key role in tumor progression. Hypoxia-inducible factor-1α (HIF-1α), a core regulator of glycolytic metabolism, remains incompletely characterized in cervical cancer. This study aimed to investigate the expression pattern and clinical significance of HIF-1α in cervical cancer, and to explore its association with malignant biological behavior and lactate dehydrogenase A (LDHA)-related glycolytic metabolism in cervical cancer cells. METHODS: The expression level, clinicopathological features, immune infiltration correlation, and prognostic value of HIF-1α in cervical cancer were analyzed based on the The Cancer Genome Atlas (TCGA) database. HIF-1α overexpression and knockdown models were established in HeLa and Caski cells. Cell viability and invasive ability were assessed by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect changes in LDHA expression. Lactate production was measured using a lactate assay kit, and intracellular reactive oxygen species (ROS) levels were determined by flow cytometry. RESULTS: Bioinformatics analysis showed that HIF-1α was highly expressed in cervical cancer and was closely associated with patient age, menopausal status, immune cell infiltration, and poor prognosis. Kaplan-Meier survival analysis demonstrated that patients with high HIF-1α expression had significantly worse overall survival (OS) than those with low expression. In vitro functional experiments further confirmed that HIF-1α overexpression significantly enhanced the viability and invasive ability of HeLa and Caski cells, whereas HIF-1α knockdown produced the opposite effects. HIF-1α overexpression was associated with increased messenger RNA (mRNA) and protein expression levels of LDHA, a key glycolytic molecule, along with increased lactate production and elevated intracellular ROS levels. CONCLUSIONS: HIF-1α is aberrantly highly expressed in cervical cancer and may enhance glycolytic activity by upregulating LDHA expression, thereby promoting the proliferation and invasion of cervical cancer cells. These findings suggest that HIF-1α could serve as a potential diagnostic, prognostic, and therapeutic target biomarker for cervical cancer.

Hypoxia-inducible factor-1α (HIF-1α)↗
PubMed2026

KLK6 is Associated with a Neutrophil-Dominant Immunosuppressive Microenvironment and Epigenetic Deregulation in Lung Adenocarcinoma.

INTRODUCTION: Lung adenocarcinoma (LUAD) is the most prevalent histological subtype of lung cancer and is associated with poor survival despite advances in targeted therapies. Kallikrein-related peptidase 6 (KLK6) has been implicated in several malignancies, but its expression pattern, clinical relevance, and biological function in LUAD remain incompletely characterized. This study aimed to evaluate KLK6 expression and its associations with prognosis, epigenetic regulation, immune infiltration, and migratory phenotypes in LUAD. METHODS: RNA-seq expression and clinical data were obtained from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Gene Expression Omnibus (GEO) databases. KLK6 expression was analyzed in relation to clinicopathological parameters, survival outcomes, promoter methylation status (via UALCAN), and tumor-infiltrating immune cell abundance (via TIMER2.0). In vitro, KLK6 was knocked down using shRNA in A549 and H1299 LUAD cell lines. Cell migration was assessed by transwell assays, and the expression of Epithelial-Mesenchymal Transition (EMT)- and Wnt signaling-related markers was examined by qRT-PCR and Western blotting. RESULTS: KLK6 expression was significantly upregulated in LUAD tissues compared with normal lung tissues. High KLK6 expression was associated with poorer overall survival (HR = 1.52, P = 0.009) and disease-specific survival (HR = 1.55, P = 0.03). ROC analysis showed that KLK6 discriminated stage I LUAD from normal tissues with an AUC of 0.73. Promoter hypomethylation was observed in LUAD tumors and correlated with increased KLK6 expression. Immune infiltration analysis revealed that KLK6-high tumors exhibited reduced B-cell infiltration and increased neutrophil infiltration. Functional experiments demonstrated that KLK6 knockdown significantly suppressed cell migration, accompanied by increased E-cadherin and decreased N-cadherin, Vimentin, Wnt5a, and β-catenin expression. DISCUSSION: These findings suggest that KLK6 overexpression in LUAD is driven in part by promoter hypomethylation and is closely linked to a neutrophil-dominant immunosuppressive microenvironment. Furthermore, KLK6 appears to promote LUAD cell migration through EMT- and Wnt-related signaling pathways. Collectively, these multi-layered data position KLK6 as a potential driver of aggressive tumor behavior and a candidate biomarker for risk stratification. CONCLUSION: KLK6 is aberrantly overexpressed in LUAD and is associated with poor prognosis and enhanced migratory capacity. It may serve as a promising prognostic biomarker and a potential therapeutic target for LUAD.

KLK6↗
PubMed2026

ZUP1 as a Novel Potential Oncogenic Driver and Prognostic Biomarker in Breast Cancer.

INTRODUCTION: Breast cancer is one of the main causes of cancer death in women globally. Identifying new predictive markers and therapeutic targets is important for improving patient outcomes. Zinc finger-containing U-rich RNA-binding protein 1 (ZUP1) is an RNA-binding protein containing a zinc finger structure that has not been systematically analyzed in breast cancer research. MATERIALS AND METHODS: The study used data from 1,231 samples from the Cancer Genome Atlas (TCGA) database. The ZUP1 expression in tumor tissues and normal tissues was compared. Its predictive value was assessed using survival analysis and regression models. Its biological role was explored through gene functional analysis. The immune cell analysis method was used to study the tumor immune environment, and the drug susceptibility database was used to predict drug responses. Predictive models were also built and validated. RESULTS: ZUP1 expression was significantly higher in breast cancer tissues than in normal tissues. High expression of ZUP1 is related to advanced tumor stage and is an independent indicator of poor survival prognosis in univariate and multivariate analyses. Functional enrichment revealed that ZUP1 is closely linked to cell cycle progression, DNA replication, and the Fanconi anemia (FA) pathway. Immune infiltration analysis demonstrated a significant negative link between ZUP1 levels and the abundance of resting mast cells and activated NK cells. Furthermore, high ZUP1 expression was associated with increased sensitivity to several targeted therapies, including Nutlin-3a and PD-0325901. A clinically applicable nomogram combining ZUP1 expression with key clinical factors (age, stage, T, N, M) was developed to predict 3- and 5-year OS with good calibration and discrimination. DISCUSSION: Our study identifies ZUP1 as a potential oncogenic factor and a robust independent prognostic biomarker in breast cancer. Its involvement in critical cellular processes and modulation of the tumor immune microenvironment highlights its potential as a novel therapeutic target. Functional experiments, including immunohistochemical staining and CCK8 proliferation assays, further supported the oncogenic role of ZUP1. The established nomogram provides a valuable tool for personalized risk assessment and clinical decision-making. CONCLUSION: Our findings suggest that ZUP1 is a novel multifaceted biomarker with significant implications for personalized treatment strategies in breast cancer.

ZUP1↗
PubMed2001

Non peptidic ligands at the opioid receptor like-1 (ORL-1).

Opioid receptor like-1 (ORL-1) has recently been indicated as a potentially useful target for the treatment of a number of central disorders and several other diseases. This review deals with non peptidic ligands at the ORL-1 receptor, focusing on their structural and binding properties. Agonism or antagonism evidenced from functional experiments is also commented. For some compounds, possible therapeutic applications are considered.

Amino Acid Sequence↗
PubMed2004

Neurobehavioral assessment of children and adolescents attending a developmental disabilities clinic.

Although the risk of the eventual development of tardive dyskinesia and other persistent adverse effects of neuroleptics is high, among adults with mental retardation and other developmental disabilities, neuroleptics may ameliorate dyskinesias, aggression, and inattention. The effects of traditional neuroleptics on a comparable population of children and adolescents with mental retardation and other developmental disabilities are unknown. The objective of this study was to develop an assessment battery to describe the effects of traditional neuroleptics on the behavior and movements of a small sample of children and adolescents with mental retardation and other developmental disabilities. 13 children and adolescents aged 6 to 16 years attending a developmental disabilities clinic were evaluated utilizing a Movement Assessment Battery to measure behavior and motions. Five subjects took traditional neuroleptic medications. Trained raters can reliably assess the movements and behaviors of children and adolescents with multiple handicaps. Children and adolescents with developmental disabilities may be vulnerable to experience functional impairment and akathisia, tics, and other dyskinesias when administered traditional neuroleptic medications.

Adolescent↗