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At least 415 records · Page 23Linked to original sources
PubMed2001

Parental [correction of Perinatal] consanguinity: a risk factor for developmental delay in Pakistani children.

OBJECTIVE: To investigate the association of parental consanguinity and delayed development in terms of gross motor, fine motor, speech and social aspects in their children. METHODS: One hundred and seventy seven children (age 15 days--72 months) were evaluated for their developmental status utilizing the Denver Developmental Screening Test (DDST). An unmatched case-control study design was used. Case group consisted of 94 children and control group 83 children. Odds ratios were calculated for parental consanguinity and delay in gross and fine motor, speech and social development in their children, for cases and controls, utilizing Binary Multiple Logistic Regression Analysis. Acquired delay was excluded through detailed birth history in both cases and control group respectively. RESULTS: Univariate analysis showed high significant Odds ratios for all areas of developmental delay (viz. gross and fine motor, speech and social development), between cases and controls (p < .001). At the multivariate analysis level however, our results showed no increased risk of parental consanguinity on delayed gross and fine motor, speech and social development in their children. CONCLUSION: Our results show no increased risk of parental consanguinity on delayed gross and fine motor, speech or social development (as measured by the DDST), in their children.

Analysis of Variance↗
PubMed1994

[Symptoms, self concept and developmental delay in healthy and chronically ill adolescents with type I diabetes].

In a prospective four-year longitudinal study 108 adolescents with diabetes and 107 healthy adolescents are being compared. In this paper data are presented from the initial assessment, in which psychopathology in the two groups was compared. In addition, the effect of diabetes on psychosocial development was examined. Several questionnaires were administered to assess symptomatology, self-concept and progress on certain developmental tasks. Regarding symptomatology, diabetic youths described themselves as more normal, i.e. having fewer clinical symptoms, than did the healthy controls. In addition, they had remarkably high scores on a scale of social desirability. This latter result points to a defence mechanism. Only the group of males with poorly controlled diabetes openly acknowledged that they had problems. All of the diabetics showed clear delays in psychosocial development compared with their healthy agemates. There were significant delays in developmental areas involving achievement of autonomy from parents and orientation towards member of one's own age group (regardless of sex), and the subjects with diabetes put less emphasis than the healthy controls on the importance of being successful in these areas in the future.

Adolescent↗
PubMed2004

A de novo mutation affecting human TrkB associated with severe obesity and developmental delay.

An 8-year-old male with a complex developmental syndrome and severe obesity was heterozygous for a de novo missense mutation resulting in a Y722C substitution in the neurotrophin receptor TrkB. This mutation markedly impaired receptor autophosphorylation and signaling to MAP kinase. Mutation of NTRK2, which encodes TrkB, seems to result in a unique human syndrome of hyperphagic obesity. The associated impairment in memory, learning and nociception seen in the proband reflects the crucial role of TrkB in the human nervous system.

Age Factors↗
PubMed2001

DNA ligase IV mutations identified in patients exhibiting developmental delay and immunodeficiency.

DNA ligase IV functions in DNA nonhomologous end-joining and V(D)J recombination. Four patients with features including immunodeficiency and developmental and growth delay were found to have mutations in the gene encoding DNA ligase IV (LIG4). Their clinical phenotype closely resembles the DNA damage response disorder, Nijmegen breakage syndrome (NBS). Some of the mutations identified in the patients directly disrupt the ligase domain while others impair the interaction between DNA ligase IV and Xrcc-4. Cell lines from the patients show pronounced radiosensitivity. Unlike NBS cell lines, they show normal cell cycle checkpoint responses but impaired DNA double-strand break rejoining. An unexpected V(D)J recombination phenotype is observed involving a small decrease in rejoining frequency coupled with elevated imprecision at signal junctions.

Cell Cycle↗
PubMed1990

Developmental delays associated with prenatal alcohol exposure are reversed by thyroid hormone treatment.

Exposure to alcohol in utero has been associated with hypothyroidism and a variety of developmental defects characteristic of thyroid dysfunction. The present work examined whether these abnormalities could be reversed in infant rats treated with thyroid hormones. Subjects were offspring of dams which were on the following diet regimen during gestation: (1) free access to liquid diet containing ethanol (alcohol pups); (2) an equal volume of isocaloric liquid diet (pair-fed pups); or (3) ad libitum control diet (control pups). Neonates from each group were foster-nursed by control dams, and received triiodothyronine (T3; 0.1 mg/kg/day; s.c.) or saline treatments on postnatal days 1 to 10. The alcohol neonates displayed reduced serum thyroxine which was restored to normal by postnatal day 14. In addition, these pups showed a delayed appearance of developmental landmarks, including righting reflex, dental eruption, auditory startle response and eye opening. The retarded incisor eruption and eye opening were reversed in alcohol pups by T3 treatments. The present data suggest that at least some of the developmental abnormalities associated with prenatal alcohol exposure are attributable to perinatal hypothyroidism and can be restored by early hormone replacement therapy.

Abnormalities, Drug-Induced↗
PubMed1997

Prevalence of maternal depression and its relationship to ADL skills in children with developmental delay.

OBJECTIVE: To determine the prevalence of maternal affective symptoms in children with developmental problems compared to a control group, and to examine their relationship to the child's Activities of Daily Living (ADL), socialization skills and behaviour. METHODOLOGY: This study examined prospectively the prevalence of symptoms of maternal depression, maternal anxiety, stress and adverse life events in 65 mothers whose children were attending a Child Development Clinic. ADL and socialization skills were measured using the Vinelands Adaptive Behaviour Scales, and behaviour using a checklist. RESULTS: Symptoms of maternal depression (P = 0.04), maternal anxiety (P = 0.01) and number of adverse life events (P = 0.03) were increased in the study compared to control mothers. Presence of maternal symptoms was unrelated to ADL or socialization skills though was associated with increased behavioural symptoms in the child. CONCLUSION: Affective disturbance in mothers of children with developmental problems are common and should be addressed as part of a comprehensive assessment of such children.

Activities of Daily Living↗
PubMed2001

Delayed developmental effects following prenatal exposure to drugs.

Increasing evidence points to the possible risks of delayed effects upon prenatal exposure to chemicals; the evaluation of such effects may pose serious problems to clinicians, epidemiologists and toxicologists. In fact, several systems (e.g., nervous, excretory) show important developmental processes well after the organogenetic period, up to the postnatal phase; accordingly, these are also expected to be sensitive targets of developmental toxicants, resulting in impairment of the function and/or functional reserve. This review describes the effects of several groups of drugs on the functional maturation and histogenesis of the kidney (e.g., aminoglycosides, angiotensin-converting enzyme inhibitors, indomethacin) and brain (e.g., anticonvulsivants, antiretroviral compounds, benzodiazepines) upon exposure in utero of humans and laboratory animals. The available data stress the importance for risk assessment of an adequate knowledge of both developmental biology and mechanisms of toxicity. The design of developmental toxicity studies should allow an evaluation of targets most relevant for a given drug (or group of drugs); moreover, the analysis of functional development should receive the due attention within the safety assessment of chemicals.

Animals↗