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<title>AMU, Nº 3, octubre 2015</title>
<link href="https://hdl.handle.net/10481/68140" rel="alternate"/>
<subtitle/>
<id>https://hdl.handle.net/10481/68140</id>
<updated>2026-04-18T08:18:58Z</updated>
<dc:date>2026-04-18T08:18:58Z</dc:date>
<entry>
<title>Sarcoidosis and primary hyperparathyroidism</title>
<link href="https://hdl.handle.net/10481/69322" rel="alternate"/>
<author>
<name>Zarza Arribas, María</name>
</author>
<author>
<name>Alonso Santor, Juan Ernesto</name>
</author>
<id>https://hdl.handle.net/10481/69322</id>
<updated>2021-06-21T11:23:01Z</updated>
<summary type="text">Sarcoidosis and primary hyperparathyroidism
Zarza Arribas, María; Alonso Santor, Juan Ernesto
The etiopathogenical relationship between&#13;
sarcoidosis and primary hyperparathyroidism&#13;
is not yet fully defined. This coexistence&#13;
remains rare in medical literature despite their&#13;
relatively high prevalence. Therefore, this&#13;
potential association should be considered in the&#13;
differential diagnosis of a patient with sarcoidosis&#13;
presenting symptoms of hyperparathyroidism.&#13;
In this paper we describe the case of a patient&#13;
diagnosed with sarcoidosis who presented an initial&#13;
episode of symptomatic hypercalcemia successfully&#13;
treated with corticoids. After remaining asymptomatic&#13;
for years, hypercalcemia reappears in several tests.&#13;
The complete study on calcium metabolism leads the&#13;
diagnosis toward primary hyperparathyroidism.&#13;
This case is relevant as it emphasizes the need to avoid&#13;
attributing to hypercalcemia a reaction proper to&#13;
sarcoidosis. Thus, it is intended to highlight the need&#13;
to approach differential diagnosis of hypercalcemia&#13;
instead of administering a treatment with corticoids.
</summary>
</entry>
<entry>
<title>Prevention and treatment of burns in diabetic patients' feet</title>
<link href="https://hdl.handle.net/10481/69321" rel="alternate"/>
<author>
<name>Castro, L.</name>
</author>
<id>https://hdl.handle.net/10481/69321</id>
<updated>2021-06-21T11:18:27Z</updated>
<summary type="text">Prevention and treatment of burns in diabetic patients' feet
Castro, L.
THE LOSS OF SENSIBILITY CAUSED BY DIABETIC&#13;
NEUROPATHY REQUIRES THE PATIENT'S SELF-CARE&#13;
TO AVOID FAINT WOUNDS. IN THIS CASE, THE PATIENT&#13;
SUFFERS BURNS DESPITE BEING EDUCATED IN THE&#13;
MATTER. THIS CAN BE ATTRIBUTED TO THE THERMAL&#13;
SOURCE'S RARITY (SAND). THE PATIENT DOES NOT&#13;
IDENTIFY THE RISK BECAUSE HE DOES NOT RELATE IT&#13;
TO HIS PATHOLOGY. THIS CLINICAL CASE IS AIMED AT&#13;
STRESSING THE NEED FOR A PROPER EDUCATION IN&#13;
CASES OF DIABETIC NEUROPATHY, INCLUDING THE RISKS&#13;
THAT, ALTHOUGH INFREQUENT, ARE REMARKABLE.
</summary>
</entry>
<entry>
<title>Choosing the right cell line for rectal cancer research</title>
<link href="https://hdl.handle.net/10481/69319" rel="alternate"/>
<author>
<name>Moya Ramírez, Miguel Ángel</name>
</author>
<author>
<name>Sánchez Martín, Victoria</name>
</author>
<author>
<name>Herrera Merchán, Antonio</name>
</author>
<author>
<name>Medina Vico, Pedro Pablo</name>
</author>
<author>
<name>Cuadros Celorrio, Marta Eugenia</name>
</author>
<id>https://hdl.handle.net/10481/69319</id>
<updated>2021-06-21T11:13:20Z</updated>
<summary type="text">Choosing the right cell line for rectal cancer research
Moya Ramírez, Miguel Ángel; Sánchez Martín, Victoria; Herrera Merchán, Antonio; Medina Vico, Pedro Pablo; Cuadros Celorrio, Marta Eugenia
Up to date no effective method exists that predicts&#13;
response to preoperative chemoradiation (CRT) in&#13;
locally advanced rectal cancer (LARC). Nevertheless,&#13;
identification of patients who have a higher likelihood&#13;
of responding to preoperative CRT could be crucial in&#13;
decreasing treatment morbidity and avoiding expensive&#13;
and time-consuming treatments. Using the Gng4, c-Myc,&#13;
Pola1, and Rrm1 signature, we were able to establish&#13;
a model to predict response to CRT in rectal cancer&#13;
with a sensitivity of 60% and 100% specificity. The aim&#13;
of this study was to characterize c-Myc status in DNA,&#13;
RNA and protein levels in 3 tumoral cell lines (SW480,&#13;
SW620 and SW837) to establish the best cell line model&#13;
and, subsequently, carry out genome silencing of&#13;
c-Myc by means of RNA interference (iRNA). To study&#13;
the expression levels of c-Myc, we used Polymerase&#13;
Chain Reaction (PCR) amplifications and sequencing;&#13;
quantitative real time PCR (qRT-PCR); and western blot&#13;
analysis in each cell line. SW480 and SW620 showed a&#13;
variation A &gt; G in exon 2, which caused a substitution&#13;
of aspargine to serine, and SW837 revealed a G &gt; A&#13;
transition in the same, which caused a mutation at&#13;
codon 92. The three cell lines expressed c-Myc mRNA.&#13;
SW837 showed a decrease of c-Myc expression levels&#13;
compared with SW480, and SW620. At protein level,&#13;
SW620 showed the highest expression of c-Myc.&#13;
According to the results obtained, we can perform&#13;
c-Myc gene silencing experiments to analyze the&#13;
role of this biomarker in response to treatment.
</summary>
</entry>
<entry>
<title>Oncostatic effect of melatonin in head and neck cancer cells: clonogenic assay</title>
<link href="https://hdl.handle.net/10481/69318" rel="alternate"/>
<author>
<name>González Díez, Manuel</name>
</author>
<author>
<name>Guerra Librero Rite, Ana</name>
</author>
<author>
<name>González Gil, Beatriz</name>
</author>
<author>
<name>Escames Rosa, Germaine</name>
</author>
<id>https://hdl.handle.net/10481/69318</id>
<updated>2022-02-16T12:12:19Z</updated>
<summary type="text">Oncostatic effect of melatonin in head and neck cancer cells: clonogenic assay
González Díez, Manuel; Guerra Librero Rite, Ana; González Gil, Beatriz; Escames Rosa, Germaine
Background: The oncostatic effect of melatonin&#13;
has been previously described among different&#13;
neoplastic types. One of these is head and neck&#13;
squamous cell cancer (HNSCC) with a high rate of&#13;
mortality and morbidity. Melatonin (aMT) could cause&#13;
cell death in this neoplastic cell type. To determine&#13;
this, we performed a clonogenic assay with CAL-27&#13;
cells treated with melatonin and/or radiation.&#13;
Methods: Cells were plated in a 6-well plate, with 800&#13;
cells per well. Assays were performed at least twice&#13;
and each time in triplicates. Cells were allowed to&#13;
grow 15 days to form colonies of at least 50 cells&#13;
each one. Cells were treated with melatonin (100,&#13;
500, 1000, 1500 and 2000 µM) alone or in combination&#13;
with irradiation (8 Gy). To visualize colonies, cells&#13;
were fixed in 100 % ethanol on days 12, 13, 14 and 15&#13;
after they were plated and stained with crystal violet&#13;
solution. Colonies were scored with Image J Software.&#13;
Results: The results clearly show that melatonin&#13;
inhibits colony growth of CAL-27 cells in a dosedependent manner in the groups treated with melatonin&#13;
alone 1500 µM or in combination with irradiation.&#13;
Conclusion: The results show the capability of aMT&#13;
to prevent colony growth and causing cell death on&#13;
CAL-27 cancer cells, especially when combined with&#13;
radiation. This is consistent with previous studies on&#13;
aMT oncostatic effects and suggests that usage of&#13;
aMT in vivo should have future clinical application.
</summary>
</entry>
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