Children With Down Syndrome Can Learn

Teaching Down Syndrome

Although Home is Where the Smart Is is packed with information in its 104 pages, it is not an exhaustive work. It's a consideration of the basics of teaching your child with Down syndrome, starting from birth through the foundational elementary years. What's inside: Why Down syndrome is Not mental retardation .page 14 How you really can reat Down syndrome. . page 17 How you can save frustration and diapers with an old method of potty training . pg 49 How you can keep that tongue from sticking out . page 38, 69 The fastest way to teach your child to read . page 60 Developmental milestones, word lists, websites and resources . page 90 And, if you must be involved with the public school system, basic guidelines for Individual Educational Plans (Ieps) and 15 snippy questions to ask educators.

Teaching Down Syndrome Summary

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Author: Helen Middlebrooke

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CASE 1 Child With Sclerosing Papillary Cancer Case Description

A 9-yr-old girl was referred to an endocrinologist in November 1995 after her pediatrician found a goiter. Her paternal grandmother and paternal uncle (who also had Down syndrome) both had thyroidectomies by age 20 yr for unknown reasons. The endocrinologist found the patient had high titers of antithyroid peroxidase antibodies, diagnosed Hashimoto's thyroiditis, and initiated thyroxine suppression therapy.

Consequences Of Congenital Or Acquired Human Herpesvirus 6 And 7 Infections

Several case reports have described fetuses or infants with HHV-6 infection, yet most have no abnormalities. Aubin et al. (25) first described in utero infection with HHV-6. These investigators examined 52 electively aborted fetuses from HIV-infected women from France and noted one fetus (26 weeks) with HHV-6 DNA distributed throughout fetal tissues. No abnormalities were identified. One study from Japan identified HHV-6 antigens in tissues from 2 of 30 (7 ) fetuses spontaneously aborted at 6-12 weeks fetal abnormalities were not described (26). HHV-6 DNA has also been found in fetal tissues of two of eight cases (25 ) of fetal hydrops (17 and 19 weeks of gestation) (27). However, both fetuses also had a chromosomal abnormality (Down syndrome and Turner's syndrome) possibly contributing to the hydrops. Fulminant hepatitis in two neonates (aged 3 and 5 days) has purported to be linked to congenital HHV-6 infection based on HHV-6 viremia in mother and baby (28) further...

Identifying the Dementia Syndrome History

An accurate history of the current illness is particularly important in the diagnostic evaluation of dementia, in order to 1) establish the temporal relationship between possible etiological factors and the onset of cognitive decline, which can help to identify the underlying pathophysiological process causing dementia and 2) permit the potentially important distinction between early- and late-onset Alzheimer's disease. Accordingly, multiple sources of information, including the patient's medical records, should be used to supplement information provided by the patient and the patient's primary caregiver, and an attempt should be made to establish detailed timelines. It is particularly important to focus on trauma signs or symptoms of neurological or psychiatric illness substance use, including alcohol and medications past and present exposure to potential toxins past surgeries and past and present psychosocial stressors. The family history should include inquiry about Down syndrome,...

PAPPA as a Marker for Plaque Stability

The progression and destabilization of atheromatous plaques involve major changes in the structure ofthe arterial wall. Matrix metalloproteinases (MMPs) are potential indicators of arterial inflammation, and by degrading extracellular matrix, they contribute to the fragility of the lipid-rich, atherosclerotic plaque and finally to its rupture. PAPP-A is a high-molecular-weight, zinc-binding MMPs enzyme that is measured during pregnancy in maternal blood for the fetal diagnosis of Down syndrome. However, low levels of circulating PAPP-A are also physiologically present in both men and women. As previously described for several other MMPs (MMP-1, MMP-3, MMP-12, or MMP-13) (26, 27), data from patients with ACS also indicate the presence of PAPP-A in atherosclerotic plaques (28). Among patients who died suddenly from cardiac causes, PAPP-A was abundantly expressed in ruptured and eroded unstable plaques, but PAPP-A was absent or minimally expressed in stable plaques (28). In plaques with...

Conclusion Context Placebos and Nocebos

It should now be clear that the major issue, the major concern, the major variable in all of these discussions about the ethics and social consequences of genetic disclosure is not whether information is disclosed, but the character of the social milieu into which that disclosure is disseminated. And the width and band of that social milieu is critical, from nation to culture to region to family unit. One family environment (or nation-state) may be safe and supportive for a child with Down syndrome, another quite hostile. It is not so much the disclosure that should occupy the focus of our analysis, but the context of that disclosure. As we have seen, under the highly commendable and politically safe banner of prospectively bringing greater health, molecular biologists assume that what they are doing will ultimately come down on the side of increasing public health (Hood 1992 Gilbert 1992).

Pathologic Features

Down syndrome with Alzheimer's disease. A well-adjusted, neat woman with Down syndrome was easy to get along with and able to perform simple housework until about age 38, when her behavior gradually changed. She neglected her appearance became irritable with screaming and cursing and was unable to help with housework. She developed seizures, and her physical and mental condition progressively deteriorated. During the final stage of her illness, she was mute and totally helpless, dying at age 56 years. The cerebral cortex shows numerous neuritic plaques and neurofibrillary tangles (Bodian stain). Down syndrome with Alzheimer's disease. A well-adjusted, neat woman with Down syndrome was easy to get along with and able to perform simple housework until about age 38, when her behavior gradually changed. She neglected her appearance became irritable with screaming and cursing and was unable to help with housework. She developed seizures, and her physical and mental condition progressively...

Genetic Mutation

Genetic mutation plays a pivotal role in the etiology of ALL in children born with Down syndrome with the associated trisomy 21 chromosome abnormality. Alteration and activation of the GATA-1 hematopoietic transcription factor increases the risk for development of ALL and increases the incidence of acute megakaryocytic leukemia as well.31-35 That hematologic malignancies representing different cell lines may become malignant suggests that multiple signaling pathways may be affected by this and other chromosome abnormalities.36 Of interest, the more detrimental chromosome abnormalities, t(9 22) and t(4 11), occur infrequently in Down syndrome.33-35 Favorable abnormalities of the TEL AML1 fusion, denoted by the t(12 21) translocation, are also less frequent in Down syndrome.

Figure

Genetic syndromes have been reported in an estimated 2.6 of British children diagnosed with leukemia 90 of these attributable to Down syndrome (DS, constitutional trisomy 21) 9 . Whereas the pathogenic basis for the 10- to 20-fold increased risk of ALL in individuals with DS has not been elucidated, somatic mutations of the GATA1 gene are seen in virtually all cases of DS-associated AML and may be implicated in the development of megakaryoblastic AML seen in these patients 10, 11 . Such mutations may also confer enhanced leukemic sensitivity to cytarabine via dysreg-ulation of cytidine deaminase gene expression 12 .

Etiology

There are only a few proven etiologic factors for childhood AML, for example in utero exposure to alcohol, exposure to benzene, ionizing radiation, or different drugs that may contribute to AML in young children. The risk of AML is increased in children with congenital syndromes such as Fanconi anemia, Shwachman syndrome, and Down syndrome. Somatic mutations of the GATA 1 gene are seen in virtually all cases of AML associated with Down syndrome and may be implicated in

Trypanosomiasis

A 7-year-old girl with Down syndrome died 2 weeks following an acute Entameba histolytica enterocolitis. The brain shows a poorly demarcated abscess in the temporal lobe with purulent necrotic walls. Entameba histolytica abscess. A 7-year-old girl with Down syndrome died 2 weeks following an acute Entameba histolytica enterocolitis. The brain shows a poorly demarcated abscess in the temporal lobe with purulent necrotic walls.

S100b

S100B protein is not essential for survival since S100B- -mice present only mild phenotypes (Table 3). They show an enhanced spatial and fear memory associated with strengthened neuronal plasticity (Nishiyama et al., 2002). In addition, enhanced epileptogenesis has been reported (Dyck et al., 2002), probably because of abnormalities in calcium-handling in astrocytes, as evidenced by increased Ca2+ transients upon KCl and caffeine treatment in S100B-deficient neonatal cerebellar glia cells (Xiong et al., 2000). Transgenic mice overexpressing S100B exhibit enhanced explorative activity, reduced anxiety and impaired learning and memory capabilities (Bell et al., 2003 Gerlai et al., 1995 Gerlai and Roder, 1996 Winocur et al., 2001). Interestingly, in humans, higher S100B concentration has been detected after brain trauma and ischemia, making S100B a potential diagnostic protein in traumatic brain damage (Rothermundt et al., 2003). An increased concentration of S100B has also been found in...

Stages Of Mitosis

The DNA molecules of an interphase cell can only be observed using an electron microscope (page 8). However, at mitosis, when they condense, individual chromosomes can be made out easily using a standard light microscope (page 76). Mitotic cells can then be screened for chromosome abnormalities such as the presence of three copies of chromosome 21, a condition that causes Down syndrome, and the Philadelphia chromosome, a rearrangement between chromosomes 9 and 21 (which results in a form of leukemia).