Prevalence of and risk factors for thirst in the intensive care unit: An observational study.

AIM AND OBJECTIVES: This study investigated the incidence of thirst and contributing factors in intensive care unit (ICU) patients by analysing differences in physiologic, psychological, and disease- and environment-related parameters in ICU patients with vs without thirst. BACKGROUND: Little is known about the factors that influence thirst, and there are no standardised methods for identifying at-risk patients in the ICU. Previous studies generalised the risk of thirst in ICU patients because of a lack of data on relevant variables. Here, we examined the factors contributing to thirst based on symptom management theory. DESIGN: Prospective descriptive design. METHODS: Physiologic, psychological, disease-related and environment-related data were collected for 301 patients from 4 ICUs (medical, surgical, cardiac and emergency ICUs) of a hospital from 15 December 2017-10 July 2019 through a screening interview, questionnaires and from electronic medical records. The data were analysed with descriptive statistics, the t-test and chi-squared test, and by logistic regression. Binary stepwise logistic regression was used to identify thirst-associated factors. The findings are reported according to the STROBE checklist for cross-sectional studies. RESULTS: In total, 210/301 (69.8%) ICU patients experienced thirst. Risk factors were nil per os order (odds ratio [OR] = 4.10, 95% confidence interval [CI]: 1.44-11.69), surgery (OR = 2.96, 95% CI: 1.11-7.93), high glucose (OR = 3.36, 95% CI: 1.01-11.17) and greater disease severity (OR = 1.13, 95% CI: 1.02-1.24). CONCLUSION: Thirst is common in ICU patients. Timely detection of patients' thirst and identification of those at high risk by ICU nurses can ensure the implementation of effective and safe interventions. RELEVANCE TO CLINICAL PRACTICE: The results of this study highlight the need to evaluate thirst symptoms in patients with severe disease and develop relief strategies for fasting, perioperative, and hyperglycaemic patients and others who are at high risk of thirst.

Cadmium exposure reprograms energy metabolism of hematopoietic stem cells to promote myelopoiesis at the expense of lymphopoiesis in mice.

Cadmium (Cd) is a highly toxic heavy metal in our living environment. Hematopoietic stem cells (HSC) are ancestors for all blood cells. Therefore understanding the impact of Cd on HSC is significant for public health. The aim of this study was to investigate the impact of Cd2+ on energy metabolism of HSC and its involvement in hematopoiesis. Wild-type C57BL/6 mice were treated with 10 ppm of Cd2+ via drinking water for 3 months, and thereafter glycolysis and mitochondrial (MT) oxidative phosphorylation (OXPHOS) of HSC in the bone marrow (BM) and their impact on hematopoiesis were evaluated. After Cd2+ treatment, HSC had reduced lactate dehydrogenase (LDH) activity and lactate production while having increased pyruvate dehydrogenase (PDH) activity, MT membrane potential, ATP production, oxygen (O2) consumption and reactive oxygen species (ROS), indicating that Cd2+ switched the pattern of energy metabolism from glycolysis to OXPHOS in HSC. Moreover, Cd2+ switch of HSC energy metabolism was critically dependent on Wnt5a/Cdc42/calcium (Ca2+) signaling triggered by a direct action of Cd2+ on HSC. To test the biological significance of Cd2+ impact on HSC energy metabolism, HSC were intervened for Ca2+, OXPHOS, or ROS in vitro, and thereafter the HSC were transplanted into lethally irradiated recipients to reconstitute the immune system; the transplantation assay indicated that Ca2+-dependent MT OXPHOS dominated the skewed myelopoiesis of HSC by Cd2+ exposure. Collectively, we revealed that Cd2+ exposure activated Wnt5a/Cdc42/Ca2+ signaling to reprogram the energy metabolism of HSC to drive myelopoiesis at the expense of lymphopoiesis.

Lead suppresses interferon γ to induce splenomegaly via modification on splenic endothelial cells and lymphoid tissue organizer cells in mice.

Splenomegaly is a symptom characterized by the presence of an enlarged spleen. The impact of environmental factors on splenomegaly is largely unknown. In this study, C57BL/6 mice were treated with 125 ppm or 1250 ppm lead (Pb) via drinking water for 8 wk, and the process of splenomegaly was evaluated. Treatment with 1250 ppm Pb, but not 125 ppm Pb, caused splenomegaly, which was associated with increased capacity for erythrocyte clearance. Intriguingly, Pb-caused splenomegaly was independent of lymphoid tissue inducer (LTi) cells, which produce lymphotoxins α and ß (LTα/ß) to activate endothelial cells and LT organizer (LTo) cells and drive the development of spleen physiologically. A direct action of Pb on endothelial cells and LTo cells did not impact their proliferation. On the other hand, during steady state, a tonic level of interferon (IFN)γ acted on endothelial cells and LTo cells to suppress splenomegaly, as IFNγ receptor (IFNγR)-deficient mice had enlarged spleens relative to wild-type mice; during Pb exposure, splenic IFNγ production was suppressed, thus leading to a loss of the inhibitory effect of IFNγ on splenomegaly. Mechanically, Pb acted on splenic CD4+ T cells to suppress IFNγ production, which impaired the Janus kinase (Jak)1/ signal transducer and activator of transcription (STAT)1 signaling in endothelial cells and LTo cells; the weakened Jak1/STAT1 signaling resulted in the enhanced nuclear factor-κB (NF-κB) signaling in endothelial cells and LTo cells, which drove their proliferation and caused splenomegaly. The present study reveals a previously unrecognized mechanism for the immunotoxicity of Pb, which may extend our current understanding for Pb toxicology.

[Development of residual voltage testing equipment].

For the existing measurement methods of residual voltage which can't turn the power off at peak voltage exactly and simultaneously display waveforms, a new residual voltage detection method is put forward in this paper. First, the zero point of the power supply is detected with zero cross detection circuit and is inputted to a single-chip microcomputer in the form of pulse signal. Secend, when the zero point delays to the peak voltage, the single-chip microcomputer sends control signal to power off the relay. At last, the waveform of the residual voltage is displayed on a principal computer or oscilloscope. The experimental results show that the device designed in this paper can turn the power off at peak voltage and is able to accurately display the voltage waveform immediately after power off and the standard deviation of the residual voltage is less than 0.2 V at exactly one second and later.

[Advances in salivary exosomal miRNAs in head and neck squamous carcinoma].

Salivary exosomes are extracellular vesicles of 30-150 nm in diameter that exist in saliva and play an important role in substance exchange and signal transduction between cells, delivering the lipids, proteins and nucleic acids they carry to the recipient cells and regulating the physiological and pathological processes of the recipient cells. miRNA, as an important "cargo" in exosomes, is transported to the recipient cells and regulates the signaling pathways of the recipient cells, thus playing a regulatory role in disease progression. The miRNAs are transported to the recipient cells and regulate the signaling pathways of the recipient cells, thus playing a regulatory role in the progression of diseases. With the development of technological tools this year, numerous studies have revealed the important role of salivary exosomal miRNAs in the development of head and neck squamous carcinoma and the role of salivary exosomal miRNAs in the diagnosis and treatment of head and neck squamous carcinoma. This paper reviews the occurrence, treatment and prognosis of salivary exosomal miRNA in head and neck squamous carcinoma, and discusses the potential prospects and importance of salivary exosomal miRNA as a biomarker in the diagnosis of head and neck squamous carcinoma.

ICU nurses' knowledge and attitude towards electrocardiogram interpretation in Fujian province, China: a cross-sectional study.

Introduction: The series of electrocardiograms (ECGs) can help track cardiac abnormalities in patients' conditions and make an earlier clinical decision. It is crucial for nurses working in critical care environments to acquire ECG knowledge for effective ECG monitoring and act accordingly in case of a change in patient condition. This study aimed at investigating intensive care unit (ICU) nurses' knowledge and attitude towards ECG interpretation in Fujian province, China. The study also analyzed the relationship between participants' demographic characteristics and level of ECG knowledge. Methods: This study was done online at twenty-one hospitals in Fujian province using a quantitative cross-sectional design involving 357 registered nurses working in the ICU between October and December 2021. The selection of hospitals and potential participants involved purposive and convenient sampling methods, respectively. Binary logistic regression was carried out to determine factors that predict ICU nurses' knowledge of ECG interpretation, and a p-value <0.05 was deemed statistically significant. Results: The majority of nurses (70.9%) demonstrated a low level of ECG knowledge. The mean score for ECG knowledge was 5.95 (SD = 2.14), with only 0.8% of ICU nurses answering all questions correctly. The majority portrayed positive attitude towards ECG interpretation; however, more than half (61.6%) believed that nurses should rely on a doctor's opinion about ECG interpretation. Previous ECG training (AOR = 3.98, 95% CI: 2.12-7.45); frequency of ECG interpretation in comparison with no frequency of ECG interpretation (1-3 times per day: AOR = 15.55, 95% CI: 6.33-38.18; 1-3 times per week: AOR = 18.10, 95% CI: 6.38-51.34); and current working unit in comparison to those working in cardiac ICU (general ICU: AOR = 0.45, 95% CI: 0.21-0.94; medical ICU; AOR = 0.28, 95% CI: 0.12-0.67; and surgical ICU; AOR = 0.05, 95% CI: 0.01-0.43) remained statistically significant after adjusting for confounders. Conclusion: The present study revealed a low level of knowledge about ECG interpretation among ICU nurses. Although the participants demonstrated positive attitudes toward ECG interpretation, the negative attitude still existed. Nurses should acknowledge ECG interpretation as part of their duties and responsibilities in nursing care instead of merely relying on doctors' opinions.

Bioinformatics and system biology approach to identify the influences of SARS-CoV-2 on metabolic unhealthy obese patients.

Introduction: The severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) has posed a significant challenge to individuals' health. Increasing evidence shows that patients with metabolic unhealthy obesity (MUO) and COVID-19 have severer complications and higher mortality rate. However, the molecular mechanisms underlying the association between MUO and COVID-19 are poorly understood. Methods: We sought to reveal the relationship between MUO and COVID-19 using bioinformatics and systems biology analysis approaches. Here, two datasets (GSE196822 and GSE152991) were employed to extract differentially expressed genes (DEGs) to identify common hub genes, shared pathways, transcriptional regulatory networks, gene-disease relationship and candidate drugs. Results: Based on the identified 65 common DEGs, the complement-related pathways and neutrophil degranulation-related functions are found to be mainly affected. The hub genes, which included SPI1, CD163, C1QB, SIGLEC1, C1QA, ITGAM, CD14, FCGR1A, VSIG4 and C1QC, were identified. From the interaction network analysis, 65 transcription factors (TFs) were found to be the regulatory signals. Some infections, inflammation and liver diseases were found to be most coordinated with the hub genes. Importantly, Paricalcitol, 3,3',4,4',5-Pentachlorobiphenyl, PD 98059, Medroxyprogesterone acetate, Dexamethasone and Tretinoin HL60 UP have shown possibility as therapeutic agents against COVID-19 and MUO. Conclusion: This study provides new clues and references to treat both COVID-19 and MUO.

Discovering common pathogenetic processes between COVID-19 and tuberculosis by bioinformatics and system biology approach.

Introduction: The coronavirus disease 2019 (COVID-19) pandemic, stemming from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has persistently threatened the global health system. Meanwhile, tuberculosis (TB) caused by Mycobacterium tuberculosis (M. tuberculosis) still continues to be endemic in various regions of the world. There is a certain degree of similarity between the clinical features of COVID-19 and TB, but the underlying common pathogenetic processes between COVID-19 and TB are not well understood. Methods: To elucidate the common pathogenetic processes between COVID-19 and TB, we implemented bioinformatics and systematic research to obtain shared pathways and molecular biomarkers. Here, the RNA-seq datasets (GSE196822 and GSE126614) are used to extract shared differentially expressed genes (DEGs) of COVID-19 and TB. The common DEGs were used to identify common pathways, hub genes, transcriptional regulatory networks, and potential drugs. Results: A total of 96 common DEGs were selected for subsequent analyses. Functional enrichment analyses showed that viral genome replication and immune-related pathways collectively contributed to the development and progression of TB and COVID-19. Based on the protein-protein interaction (PPI) network analysis, we identified 10 hub genes, including IFI44L, ISG15, MX1, IFI44, OASL, RSAD2, GBP1, OAS1, IFI6, and HERC5. Subsequently, the transcription factor (TF)-gene interaction and microRNA (miRNA)-gene coregulatory network identified 61 TFs and 29 miRNAs. Notably, we identified 10 potential drugs to treat TB and COVID-19, namely suloctidil, prenylamine, acetohexamide, terfenadine, prochlorperazine, 3'-azido-3'-deoxythymidine, chlorophyllin, etoposide, clioquinol, and propofol. Conclusion: This research provides novel strategies and valuable references for the treatment of tuberculosis and COVID-19.

Cadmium impairs the development of natural killer cells and bidirectionally modifies their capacity for cytotoxicity.

Cadmium (Cd) is a highly toxic heavy metal in the environment. The aim of this study was to investigate the impact of Cd on natural killer (NK) cells. C57BL/6 mice were treated with 10 ppm Cd via drinking water for 3 months, and the development of NK cells in the bone marrow (BM) and the cytotoxicity of mature NK (mNK) cells in the peripheral immune organs were evaluated thereafter; the impact of Cd on the cytotoxicity of mNK cells from human peripheral blood mononuclear cells (PBMC) was also investigated. Whereas Cd treatment impaired the differentiation of NK progenitors in the BM, Cd treatment activated the JAK3/STAT5 signaling to drive the proliferation of mNK cells and thereby lead to a compensation increase of mNK cells in the peripheral immune organs of mice. Additionally, Cd treatment bidirectionally regulated the cytotoxicity of mouse mNK cells to differential tumor cells, dependent on the levels of Fas expression in the tumor cells; mechanically, Cd treatment activated the JAK3/STAT5 signaling to promote the expression of FasL in mNK cells to increase their cytotoxicity, while Cd treatment reduced the expression of granzyme B in mNK cells to impair their cytotoxicity in the peripheral immune organs of mice. Likewise, in vitro assays indicated that Cd treatment also activated the JAK3/STAT5 signaling to increase the expression of FasL, whereas Cd treatment reduced the expression of granzyme B in human mNK cells. Thus Cd treatment impaired the development of NK cells in the BM and bidirectionally regulated the cytotoxicity of mNK cells in the peripheral immune organs, which may extend our current understanding for the immunotoxicity of Cd.

Effects of a spray-based oropharyngeal moisturising programme for patients following endotracheal extubation after cardiac surgery: A randomised, controlled three-arm trial.

BACKGROUND: When a patient emerges from cardiac surgery, they may experience intense thirst and discomfort or even impaired swallowing after endotracheal extubation. This may lead to feelings of suffocation, desperation, fear, and anxiety. Although thirst relief and dysphagia prevention share similar mechanisms, there is limited evidence for a combined intervention to alleviate thirst and prevent dysphagia. Furthermore, no studies to date have targeted postoperative cardiac patients. OBJECTIVE: To evaluate the safety, feasibility, and effects of a spray-based oropharyngeal moisturising programme for cardiac surgery patients following endotracheal extubation. DESIGN: A randomised, controlled three-arm trial was conducted from October 2017 to December 2019. SETTING: Tertiary medical centre cardiac care unit. PARTICIPANTS: Participants (N = 145) were patients who underwent cardiac surgery and received mechanical ventilation. METHODS: Participants were randomly assigned to one of three groups: a four-part programme offering spray-based therapy with either a constant low-temperature cold spray (programme A; n = 47) or low-to-normal temperature spray (programme B; n = 49), or those that received usual care (control group; n = 49). Control group patients who complained of thirst were given wet cotton swabs to moisten their mouths. The primary outcomes included discomfort and various levels of thirst intensity; secondary outcomes included dysphagia and adverse events. Outcomes were evaluated at Time 0 (baseline), Time 1 (3 h), Time 2 (6 h) and Time 3 (96 h) post intervention. Repeated-measures analyses was performed using generalised estimating equations. RESULTS: The baseline evaluation indicated no significant differences between the groups. Participants (average age: 55 years; 53.8% men) underwent cardiac surgery for; valvular heart disease (64.8%), coronary atherosclerotic heart disease (25.5%), or aortic dissection (9.7%). Baseline scores indicated moderately severe thirst (6.24±1.57) and discomfort (9.88±2.23). Post intervention, the thirst intensity in the intervention groups was significantly lower than that of the control group (p<0.001). The generalised estimating equation analysis showed no significant difference in reduced thirst intensity between programmes A and B (adjusted ß=0.08, 95% CI: -0.59-0.76, p = 0.810) when controlling for intervention condition and time. Comparable results were found for reduced thirst discomfort (adjusted ß=0.36, 95% CI: -0.66-1.38, p = 0.493). The three groups showed no significant differences for dysphagia frequency. No observable adverse events were reported during the intervention period. CONCLUSIONS: A spray-based oropharyngeal moisturising programme is a practical and effective intervention to alleviate patient thirst after cardiac surgery and tracheal intubation that could be integrated into comfort care for post-surgical patients' critical care management. TWEETABLE ABSTRACT: A spray-based oropharyngeal moisturising programme for cardiac surgery recipients following endotracheal extubation may alleviate thirst.

Cadmium Suppresses Bone Marrow Thrombopoietin Production and Impairs Megakaryocytopoiesis in Mice.

Cadmium (Cd) is a highly toxic heavy metal in our environment. The influence of Cd on the development of platelets, or megakaryocytopoiesis, remains to be defined. The aim of this study was to investigate the impact of Cd on megakaryocytopoiesis. C57BL/6 (B6) mice aged 6-8 weeks were treated with 10 ppm Cd via drinking water or control for 3 months, and megakaryocytopoiesis was evaluated thereafter. Mice treated with Cd had a decreased number of platelets in the blood, which was associated with the reduced number of megakaryocyte progenitors (MkP) and megakaryocytes (MK) in the bone marrow (BM). Functional analyses indicate that Cd treatment impaired the proliferation and differentiation of MkP as well as the maturation of MK in the BM, suggesting that Cd treatment impeded megakaryocytopoiesis. Intriguingly, the impaired megakaryocytopoiesis in the BM of mice treated with Cd was not caused by increased apoptosis of MkP. Moreover, in vitro treatment of MkP with Cd did not impact their proliferation or differentiation, indicating that the impeded megakaryocytopoiesis in the BM of mice was likely not caused by direct action of Cd on MkP. On the other hand, Cd treatment selectively suppressed thrombopoietin (TPO) production in the BM and decreased the cellular myelocytomatosis oncogene signaling in MkP, thus likely leading to the impeded megakaryocytopoiesis in the BM and thrombocytopenia in the blood of mice. This study revealed a previously unrecognized hematopoietic toxicity of Cd, which may extend our current understanding of Cd toxicity.

Mercury Chloride Impacts on the Development of Erythrocytes and Megakaryocytes in Mice.

Inorganic mercury (Hg2+) is a highly toxic heavy metal. The aim of this study was to investigate the impact of Hg2+ on the development of erythrocytes and megakaryocytes. B10.S mice (H-2s) and DBA/2 mice (H-2d) were administrated with 10 µM HgCl2 or 50 µM HgCl2 via drinking water for four weeks, and erythro-megakaryopoiesis was evaluated thereafter. The administration of 50 µM HgCl2 increased the number of erythrocytes and platelets in B10.S mice, which was not due to a reduced clearance for mature erythrocytes. The administration of 50 µM HgCl2, but not 10 µM HgCl2, increased the number of progenitors for erythrocytes and megakaryocytes in the bone marrow (BM) of B10.S mice, including erythroid-megakaryocyte progenitors (EMPs), burst-forming unit-erythroid progenitors (BFU-Es), colony-forming unit-erythroid progenitors (CFU-Es), and megakaryocyte progenitors (MkPs). Moreover, 50 µM HgCl2 caused EMPs to be more proliferative and possess an increased potential for differentiation into committed progenies in B10.S mice. Mechanistically, 50 µM HgCl2 increased the expression of the erythropoietin receptor (EPOR) in EMPs, thus enhancing the Jak2/STAT5 signaling pathway to promote erythro-megakaryopoiesis in B10.S mice. Conversely, 50 µM HgCl2 did not impact erythro-megakaryopoiesis in DBA/2 mice. This study may extend our current understanding for hematopoietic toxicology of Hg.

Lead in Synergism With IFNγ Acts on Bone Marrow-Resident Macrophages to Increase the Quiescence of Hematopoietic Stem Cells.

Lead (Pb) is a highly toxic heavy metal that broadly exists in our living environment. Although Pb has been shown to influence the development of immune cells, to date, the impact of Pb on hematopoietic stem cells (HSCs) in the bone marrow (BM) remains unknown. As people are ubiquitously exposed to Pb and HSC are essential for human health, understanding the impact of Pb on HSC is significant for public health. In this study, we found that wild-type B6 mice treated with 1250 ppm Pb, but not 125 ppm Pb via drinking water for 8 weeks had increased quiescence of HSC in the BM. Functional analyses demonstrated that wild-type mice treated with 1250 ppm Pb had increased potential for HSC to repopulate the immune system and engraft to the niche in the BM under a competitive chimeric microenvironment of lethally irradiated recipients. Moreover, we found that Pb-increased quiescence of HSC critically relied on a synergetic action of Pb and interferon γ (IFNγ) on BM-resident macrophages (BM-MΦ), but not a direct action of Pb on HSC. Specifically, in steady state, BM-MΦ promoted HSC proliferation; and upon Pb treatment, IFNγ was induced in the BM, and thereafter Pb in synergism with IFNγ acted on BM-MΦ to cause BM-MΦ to become suppressive for HSC proliferation, thus leading to increased quiescence of HSC. Our study suggests that Pb increased the quiescence of HSC via a synergetic action of Pb and IFNγ on BM-MΦ, which was previously unrecognized toxicity of Pb.

Lead Impairs the Development of Innate Lymphoid Cells by Impeding the Differentiation of Their Progenitors.

Lead (Pb) is a heavy metal toxic to the immune system, yet the influence of Pb on innate lymphoid cells (ILC) remains to be defined. In this study, we found that occupationally relevant level of Pb exposure impaired ILC development at the progenitor level by activating Janus Kinase1. C57BL/6 mice treated with 1250 ppm, but not 125 ppm Pb acetic via drinking water for 8 weeks had reduced number of mature ILC, which was not caused by increased apoptosis or suppressed proliferation. Conversely, Pb increased the number of innate lymphoid cell progenitors (ILCP) in the bone marrow. The discordant observation indicated that an obstruction of ILCP differentiation into mature ILC during Pb exposure existed. Pb directly acted on ILCP to suppress their proliferation, indicating that ILCP were less activated during Pb exposure. Reciprocal ILCP transplantation assay confirmed that Pb impeded the differentiation of ILCP into mature ILC, as ILCP gave rise to fewer mature ILC in Pb-treated recipients compared with control recipients. In vitro assays suggested that the obstruction of ILCP differentiation by Pb exposure was due to increased activation of Janus Kinase1. Thus, Pb impeded ILCP differentiation into mature ILC to result in an accumulation of ILCP in the bone marrow and the resultant decreased number of mature ILC in lymphoid and nonlymphoid tissues in mice. Moreover, by analyses of ILC and ILCP in peripheral blood mononuclear cells of human subjects occupationally exposed to Pb, we revealed that Pb might also impede the development of ILC in human.