[Management of communication between inpatients isolated due to COVID-19 and their families]. / Gestión de la comunicación de los pacientes hospitalizados, aislados con sus familias por la COVID-19.

BACKGROUND AND GOAL: Quality of healthcare has been affected by the current dimensions of the COVID-19 pandemic and the strict hospital isolation to which some inpatients have been subjected. Therefore, we propose to describe the process designed to facilitate the communication of inpatients with their families to detect their needs and perform individualized treatments in each case. METHOD: Qualitative study with action research methodology, responding to the following algorithm: plan the action, diagnosis of the need and hypothesis-action; apply the action, creation of the group of case managers and training of the members; observe the action, collect and analyse the information. During the month of April 2020. RESULTS: 1,754 interactions were undertaken, that affected 490 inpatients. Case Managers made 767 calls, to provide information about admissions (71.45%), changes in inpatient location or operation of units (18.84%), among others. One thousand and ninety-eight calls from family members were received requesting medical information (43.8%), to talk to inpatients (18.48%), to deliver personal articles or manage lost objects (12.84%), and seeking information about patient location or medical discharge (10.20%). Sixty-six percent of the requests were solved by Case Managers, 30% were referred on and 4% could not be solved. CONCLUSIONS: Implementation of the Case Manager Group contributed to encourage communication of inpatients isolated due to COVID-19 with their families, responding to needs raised, improving quality of care and promoting humanization of care.

The expression of thyroid hormone transporters in the human fetal cerebral cortex during early development and in N-Tera-2 neurodifferentiation.

Associations of neurological impairment with mutations in the thyroid hormone (TH) transporter, MCT8, and with maternal hypothyroxinaemia, suggest that THs are crucial for human fetal brain development. It has been postulated that TH transporters regulate the cellular supply of THs within the fetal brain during development. This study describes the expression of TH transporters in the human fetal cerebral cortex (7­20 weeks gestation) and during retinoic acid induced neurodifferentiation of the human N-Tera-2 (NT2) cell line, in triiodothyronine (T3) replete and T3-depleted media. Compared with adult cortex, mRNAs encoding OATP1A2, OATP1C1, OATP3A1 variant 2, OATP4A1, LAT2 and CD98 were reduced in fetal cortex at different gestational ages, whilst mRNAs encoding MCT8, MCT10, OATP3A1 variant 1 and LAT1 were similar. From the early first trimester, immunohistochemistry localised MCT8 and MCT10 to the microvasculature and to undifferentiated CNS cells. With neurodifferentiation, NT2 cells demonstrated declining T3 uptake, accompanied by reduced expressions of MCT8, LAT1, CD98 and OATP4A1. T3 depletion significantly reduced MCT10 and LAT2 mRNA expression at specific time points during neurodifferentiation but there were no effects upon T3 uptake, neurodifferentiation marker expression or neurite lengths and branching. MCT8 repression also did not affect NT2 neurodifferentiation. In conclusion, many TH transporters are expressed in the human fetal cerebral cortex from the first trimester, which could regulate cellular TH supply during early development. However, human NT2 neurodifferentiation is not dependent upon T3 or MCT8 and there were no compensatory changes to promote T3 uptake in a T3-depleted environment.

Differential triiodothyronine responsiveness and transport by human cytotrophoblasts from normal and growth-restricted pregnancies.

CONTEXT: Abnormal placentation in human pregnancy is associated with intrauterine fetal growth restriction (IUGR). Our group has previously reported the association between severe IUGR, lower fetal circulating concentrations of thyroid hormones (THs), and altered expression of TH receptors and TH transporters within human placental villi. We postulate that altered TH bioavailability to trophoblasts may contribute to the pathogenesis of IUGR. DESIGN AND OBJECTIVE: Cytotrophoblasts were isolated from normal and IUGR human placentae to compare their responsiveness to T(3) and their capability for T(3) transport. RESULTS: Compared with normal cytotrophoblasts, the viability of IUGR cytotrophoblasts (assessed by methyltetrazoleum assay) was significantly reduced (P < 0.001), whereas apoptosis (assessed using caspase 3/7 activity and M30 immunoreactivity) was significantly increased after T(3) treatment for 48 h (P < 0.001 and P < 0.01, respectively). The secretion of human chorionic gonadotropin was significantly increased by IUGR cytotrophoblasts compared with normal cytotrophoblasts (P < 0.001), independently of T(3) treatment. Net transport of [(125)I]T(3) was 20% higher by IUGR cytotrophoblasts compared with normal cytotrophoblasts (P < 0.001), and this was accompanied by a 2-fold increase in the protein expression of the TH transporter, monocarboxylate transporter 8, as assessed by Western immunoblotting (P < 0.01). CONCLUSIONS: IUGR cytotrophoblasts demonstrate altered responsiveness to T(3) with significant effects on cell survival and apoptosis compared with normal cytotrophoblasts. Increased monocarboxylate transporter 8 expression and intracellular T(3) accumulation may contribute to the altered T(3) responsiveness of IUGR cytotrophoblasts.