Remote Continuous Glucose Monitoring With a Computerized Insulin Infusion Protocol for Critically Ill Patients in a COVID-19 Medical ICU: Proof of Concept

OBJECTIVEThe use of remote real-time continuous glucose monitoring (CGM) in the hospital has rapidly emerged to preserve personal protective equipment and reduce potential exposures during coronavirus disease 2019 (COVID-19).RESEARCH DESIGN AND METHODSWe linked a hybrid CGM and point-of-care (POC) glucose testing protocol to a computerized decision support system for continuous insulin infusion and integrated a validation system for sensor glucose values into the electronic health record. We report our proof-of-concept experience in a COVID-19 intensive care unit.RESULTSAll nine patients required mechanical ventilation and corticosteroids. During the protocol, 75.7% of sensor values were within 20% of the reference POC glucose with an associated average reduction in POC of 63%. Mean time in range (70–180 mg/dL) was 71.4 ± 13.9%. Sensor accuracy was impacted by mechanical interferences in four patients.CONCLUSIONSA hybrid protocol integrating real-time CGM and POC is helpful for managing critically ill patients with COVID-19 requiring insulin infusion.     

Prevalencia del síndrome complejo de malnutrición e inflamación y su correlación con las hormonas tiroideas en pacientes en hemodiálisis crónica

Introduction

Low levels of thyroid hormones, total triiodothyronine (T3) and free triiodothyronine (FT3) in haemodialysis patients is a marker of malnutrition and inflammation and are predictors of mortality. The aim of this study was to determine the prevalence of malnutrition-inflammation complex syndrome in haemodialysis and its relationship with the thyroid hormones thyrotropin, T3, FT3 and free thyroxine (FT4), as well as to evaluate the prevalence of low FT3 syndrome and its correlation with nutritional and inflammatory markers.

Progressive age-related changes in pulmonary tuberculosis images and the effect of diabetes

Atypical radiologic images of pulmonary tuberculosis are common in elderly and in diabetic patients. To investigate the relationship of chest radiographic findings of tuberculosis to age in diabetic and nondiabetic patients, we compared the chest radiographic findings of 192 inpatients with pulmonary tuberculosis and diabetes with those of 130 patients with pulmonary tuberculosis alone. The proportion of patients with lower lung field lesions progressively increased with age (r(S) = 0.89, p < 0.01), whereas the frequency of cavitation steadily decreased with age (r(S) = -0.79, p < 0.05). In diabetic patients, a high frequency of lower lung lesions and cavitation was observed in all age groups. We speculated that, in older patients and in diabetics, the increased alveolar oxygen pressure in the lower lobes favors development of lower lobe disease in these groups.     

Decreased dendritic spine density of neurons of the prefrontal cortex and nucleus accumbens and enhanced amphetamine sensitivity in postpubertal rats after a neonatal amygdala lesion

A neonatal basolateral‐amygdala (nBLA) lesion in rats could be a potential animal model to study the early neurodevelopmental abnormalities associated with the behavioral and morphological brain changes observed in schizophrenia. Morphological alterations in pyramidal neurons from the prefrontal cortex (PFC) have been observed in postmortem schizophrenic brains, mainly because of decreased dendritic arbor and spine density. We assessed the effects of nBLA‐lesion on the dendritic morphology of neurons from the PFC and the nucleus accumbens (NAcc) in rats. nBLA lesions were made on postnatal day 7 (PD7), and later, the dendritic morphology was studied by the Golgi‐Cox stain procedure followed by Sholl analysis at PD35 (prepubertal) and PD60 (adult) ages. We also evaluated the effects of the nBLA‐lesion on locomotor activity caused by a novel environment, apomorphine, and amphetamine. Adult animals with nBLA lesions showed a decreased spine density in pyramidal neurons from the PFC and in medium spiny cells from the NAcc. An increased locomotion in a novel environment and in amphetamine‐treated adult animals with an nBLA‐lesion was observed. Our results indicate that nBLA‐lesion alters the neuronal dendrite morphology of the NAcc and PFC, suggesting a disconnection between these limbic structures. The locomotion paradigms support the idea that dopaminergic transmission is altered in the nBLA lesion model. This could help to understand the consequences of an earlier amygdala dysfunction in schizophrenia. Synapse 63:1143–1153, 2009. © 2009 Wiley‐Liss, Inc.     

Dendritic morphology on neurons from prefrontal cortex, hippocampus, and nucleus accumbens is altered in adult male mice exposed to repeated low dose of malathion

Malathion is a highly neurotoxic pesticide widely used in daily life. Acute and chronic toxicity from this organophosphorus compound may cause damage to health, especially to the central nervous system. In the present work, we show the effects of chronic exposure of malathion on dendritic morphology of neurons from prefrontal cortex (PFC), hippocampus, and nucleus accumbens (NAcc) in adult male mice. Animals were injected i.p. with low dose of malathion (40 mg/kg body weight) for 14 days. Control animals were injected with corn oil, used as vehicle. Fourteen days after the last injection, brains were removed and processed by the Golgi-Cox stain method, and coronal sections were obtained to perform Sholl analysis on pyramidal neurons from the PFC, CA1 area from the hippocampus, and medium spiny cells from the NAcc. Dendritic morphology analysis included the total dendritic length, the maximum branching order, and the dendritic spine density. Results indicated a significant decrement on dendritic morphology in neurons from the hippocampus and the PFC in animals injected with malathion, whereas medium spiny neurons from NAcc showed a significant decrement only on the dendritic spine density in malathion injected mice, as compared to control mice. These results suggest that chronic toxicity of malathion alters the dendritic morphology in adult age, which may affect behavior.     

Corrosion Resistance Measurement of 316L Stainless Steel Manufactured by Selective Laser Melting

Selective laser melting (SLM) technology is ushering in a new era of advanced industrial production of metal components. It is of great importance to understand the relationship between the surface features and electrochemical properties of manufactured parts. This work studied the influence of surface orientation on the corrosion resistance of 316L stainless-steel (SS) components manufactured with SLM. The corrosion resistance of the samples was measured using linear polarization resistance (LPR) and electromechanical noise (EN) techniques under three different environments, H₂O, 3.5 wt.% NaCl, and 20% H₂SO₄, analyzing the horizontal (XY) and vertical (XZ) planes. The microstructure and morphology of the samples were obtained by optical (OM) and scanning electron microscopy (SEM). The obtained microstructure showed the grains growing up from the fusion line to the melt pool center and, via SEM-EDS, the presence of irregular and spherical pores was observed. The highest corrosion rate was identified in the H₂SO₄ solution in the XZ plane with 2.4 × 10⁻² mm/year and the XY plane with 1.31 × 10⁻³ mm/year. The EN technique along with the skewness factor were used to determine the type of corrosion that the material developed. Localized corrosion was observed in the NaCl electrolyte, for the XY and XZ planes (−1.65 and −0.012 skewness factors, respectively), attacking mainly the subgrains of the microstructure and, in some cases, the pores, caused by Cl ions. H₂O and H₂SO₄ solutions presented a uniform corrosion mechanism for the two observed orientations. The morphology identified by SEM was correlated with the results obtained from the electrochemical techniques.     

Neonatal administration of N-omega-nitro-L-arginine induces permanent decrease in NO levels and hyperresponsiveness to locomotor activity by D-amphetamine in postpubertal rats

Nitric oxide (NO) is associated with dopamine (DA) release. Previously, we demonstrated that rats treated with a non-selective nitric oxide synthase inhibitor, N-omega-nitro-l-arginine (l-NNA) at postnatal days 4-6 (PD4-6) show increased locomotion and disrupt neuronal cytoarchitecture after puberty (PD60). Here, we investigate whether the modulation of NO production in rats at PD4-6 causes long term changes of NO system, its impact on DA innervation, and schizophrenia-like behaviors. NO levels were measured in seven brain areas at PD35, PD60, PD90, and PD120. Autoradiographic studies explored the effect of l-NNA on the expression of D₁ and D₂ receptors in the caudate-putamen (CPu) and nucleus accumbens (NAcc) at PD60. Locomotor activity was assessed at PD60 using the non-selective DA agonists, amphetamine and apomorphine, and the selective DA receptor agonist [D₂, quinpirole; D₃, 7-hydroxy-N,N-di-n-propylaminotetralin ((±)-7-OH-DPAT)]. l-NNA treatment produced decreases in NO levels in the frontal cortex, striatum, brainstem and cerebellum, while in the occipital cortex changes were observed at PD120. Hippocampus and temporoparietal cortex showed differential levels of NO. Receptor autoradiography revealed increases in D₁ receptor levels in the NAcc (shell), while decreases in D₂ receptor binding were observed in the CPu and NAcc (core). Amphetamine and quinpirole treatments resulted in increases in locomotion. In contrast, treatment with 7-OH-DPAT produced hypolocomotion at low doses, while increased locomotion was seen at the highest dose. These results show that modulation of NO levels early postnatally (PD4-6) produces long term alteration in NO levels, with possible consequences on DA transmission, and related behaviors relevant to schizophrenia.     

Benzo(a)pyrene induces hepatic AKR1A1 mRNA expression in tilapia fish (Oreochromis niloticus)

AKR1A1 or aldehyde reductase is a member of the aldo-keto reductases superfamily that is evolutionarily conserved among species. AKR1A1 is one of the five AKRs (AKR1A1 and 1C1-1C4) implicated in the metabolic benzo(a)pyrene (BaP) activation to reactive BaP 7,8-dione. BaP is a polycyclic aromatic hydrocarbon (PAH) widely distributed in aquatic ecosystems and its metabolic activation is necessary to produce its toxic effects. Although the presence of AKR1A1 in fish has been reported, its tissue distribution in tilapia (Oreochromis niloticus) and AKR1A1 inducibility by BaP are not known yet. Moreover, cytochrome P4501A (CYP1A) mRNA expression in fish has been used as a PAH biomarker of effect. Therefore, BaP effects on AKR1A1 and CYP1A gene expressions in tilapia, a species of commercial interest, were investigated by real-time RT-PCR. A partial AKR1A1 cDNA was identified, sequenced and compared with AKR1A1 reported sequences in the GenBank DNA database. Constitutive AKR1A1 mRNA expression was detected mainly in liver, similarly to that of CYP1A. BaP exposure resulted in statistically significant AKR1A1 and CYP1A mRNA induction in liver (20- and 120-fold, respectively) at 24 h. On the other hand, ethoxyquin (EQ) was used as control inducer for AKR1A1 mRNA. Interestingly, EQ also induced CYP1A mRNA levels in tilapia liver. Our results suggest that teleost AKR1A1, in addition to CYP1A, are inducible by BaP. The mechanism of AKR1A1 induction by BaP and its role in fish susceptibility to BaP toxic effects remains to be elucidated.     

Apamin induces plastic changes in hippocampal neurons in senile Sprague-Dawley rats

Apamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small‐conductance Ca²⁺‐activated K⁺ channels (SK). Several behavioral and electrophysiological studies indicate that SK‐blockade by apamin may enhance neuron excitability, synaptic plasticity, and long‐term potentiation in the CA1 hippocampal region, and, for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi–Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex as well as on the medium spiny neurons from the nucleus accumbens and granule cells from the dentate gyrus (DG) of the hippocampus. We found that only granule cells from the DG and pyramidal neurons from dorsal and ventral hippocampus were altered in senile rats injected with apamin. Our research suggests that apamin may increase the dendritic morphology in the hippocampus, which could be related to the neuronal excitability and synaptic plasticity enhancement induced by apamin. Synapse 2011. © 2011 Wiley‐Liss, Inc.