Spaces:
Build error
Build error
Commit
·
06c0c59
1
Parent(s):
72fa22c
Update app.py
Browse files
app.py
CHANGED
@@ -147,18 +147,13 @@ with st.form(key="my_form"):
|
|
147 |
|
148 |
|
149 |
with c2:
|
150 |
-
|
151 |
|
152 |
doc = st.text_area(
|
153 |
"Paste your text below",
|
|
|
154 |
height=400,
|
155 |
-
|
156 |
-
if ex_but:
|
157 |
-
doc = st.text_area(
|
158 |
-
"Paste your text below",
|
159 |
-
value='He denies synophrys. Individual II-1 is a 10 year old boy. He was born at term with normal birth parameters and good APGAR scores (9/10/10). The neonatal period was uneventful, and he had normal motor development during early childhood: he began to look up at 3 months, sit by himself at 5 months, stand up at 11 months, walk at 13 months, and speak at 17 months. He attended a regular kindergarten, without any signs of difference in intelligence, compared to his peers. Starting at age 6, the parents observed ever increasing behavioral disturbance for the boy, manifesting in multiple aspects of life. For example, he can no longer wear clothes by himself, cannot obey instruction from parents/teachers, can no longer hold subjects tightly in hand, which were all things that he could do before 6 years of age. In addition, he no longer liked to play with others; instead, he just preferred to stay by himself, and he sometimes fell down when he walked on the stairs, which had rarely happened at age 5. The proband continued to deteriorate: at age 9, he could not say a single word and had no action or response to any instruction given in clinical exams. Additionally, rough facial features were noted with a flat nasal bridge, a synophrys (unibrow), a long and smooth philtrum, thick lips and an enlarged mouth. He also had rib edge eversion, and it was also discovered that he was profoundly deaf and had completely lost the ability to speak. He also had loss of bladder control. The diagnosis of severe intellectual disability was made, based on Wechsler Intelligence Scale examination. Brain MRI demonstrated cortical atrophy with enlargement of the subarachnoid spaces and ventricular dilatation (Figure 2). Brainstem evoked potentials showed moderate abnormalities. Electroencephalography (EEG) showed abnormal sleep EEG.',
|
160 |
-
height=400,
|
161 |
-
)
|
162 |
|
163 |
|
164 |
|
|
|
147 |
|
148 |
|
149 |
with c2:
|
150 |
+
|
151 |
|
152 |
doc = st.text_area(
|
153 |
"Paste your text below",
|
154 |
+
value='The clinical features of Angelman syndrome (AS) comprise severe mental retardation, postnatal microcephaly, macrostomia and prognathia, absence of speech, ataxia, and a happy disposition. We report on seven patients who lack most of these features, but presented with obesity, muscular hypotonia and mild mental retardation. Based on the latter findings, the patients were initially suspected of having Prader-Willi syndrome. DNA methylation analysis of SNRPN and D15S63, however, revealed an AS pattern, ie the maternal band was faint or absent. Cytogenetic studies and microsatellite analysis demonstrated apparently normal chromosomes 15 of biparental inheritance. We conclude that these patients have an imprinting defect and a previously unrecognised form of AS. The mild phenotype may be explained by an incomplete imprinting defect or by cellular mosaicism.'
|
155 |
height=400,
|
156 |
+
)
|
|
|
|
|
|
|
|
|
|
|
|
|
157 |
|
158 |
|
159 |
|