Translation and validation of traditional Chinese version of the pediatric eating assessment Tool-10.

BACKGROUND: /Purpose: The Pediatric Eating Assessment Tool-10 (Pedi-EAT-10) is a caregiver-administrated subjective questionnaire for evaluating swallowing and feeding disorders among children. This study translated the Pedi-EAT-10 into Traditional Chinese and tested the translated version's reliability and validity. METHODS: Pedi-EAT-10 was translated into Traditional Chinese by experts and finalized after discussion and testing. A total of 168 participants, consisting of 32 children with dysphagia from a tertiary medical center and 136 healthy controls from its Children Care Center for Employees, were recruited. All participants were assessed by an otolaryngologist and speech-language pathologist. The reliability, validity, and efficacy of the translated Pedi-EAT-10 were analyzed to ensure it could be used to identify pediatric dysphagia and feeding problems. RESULTS: The Traditional Chinese version of the Pedi-EAT-10 had significant clinical discriminative validity between the dysphagia group and the control group (total score = 9.6 vs. 2.6, P < 0.001), acceptable test-retest reliability (intraclass correlation = 0.63), and excellent internal consistency (Cronbach's α = 0.91 for the entire cohort). The overall performance of the test for distinguishing children with dysphagia from normal controls was acceptable, and the area under the curve was 74.8% (sensitivity = 71.9%; specificity = 69.9%). The optimal cutoff score was ≥3 on the Youdex index. CONCLUSIONS: The Traditional Chinese version of the Pedi-EAT-10 has fair reliability and validity and can be quickly and easily completed by caregivers. The translated Ped-EAT-10 can be used as a first-line tool for assessing the need for further referral and instrumental examination.

A newly proposed heatstroke-induced coagulopathy score in patients with heat illness: A multicenter retrospective study in China.

PURPOSE: In patients with heatstroke, disseminated intravascular coagulation (DIC) is associated with greater risk of in-hospital mortality. However, time-consuming assays or a complex diagnostic system may delay immediate treatment. Therefore, the present study proposes a new heatstroke-induced coagulopathy (HIC) score in patients with heat illness as an early warning indicator for DIC. METHODS: This retrospective study enrolled patients with heat illness in 24 Chinese hospitals from March 2021 to May 2022. Patients under 18 years old, with a congenital clotting disorder or liver disease, or using anticoagulants were excluded. Data were collected on demographic characteristics, routine blood tests, conventional coagulation assays and biochemical indexes. The risk factors related to coagulation function in heatstroke were identified by regression analysis, and used to construct a scoring system for HIC. The data of patients who met the diagnostic criteria for HIC and International Society on Thrombosis and Haemostasis defined-DIC were analyzed. All statistical analyses were performed using SPSS 26.0. RESULTS: The final analysis included 302 patients with heat illness, of whom 131 (43.4%) suffered from heatstroke, including 7 death (5.3%). Core temperature (OR = 1.681, 95% CI 1.291 - 2.189, p < 0.001), prothrombin time (OR = 1.427, 95% CI 1.175 - 1.733, p < 0.001) and D-dimer (OR = 1.242, 95% CI 1.049 - 1.471, p = 0.012) were independent risk factors for heatstroke, and therefore used to construct an HIC scoring system because of their close relation with abnormal coagulation. A total score ≥ 3 indicated HIC, and HIC scores correlated with the score for International Society of Thrombosis and Hemostasis -DIC (r = 0.8848, p < 0.001). The incidence of HIC (27.5%) was higher than that of DIC (11.2%) in all of 131 heatstroke patients. Meanwhile, the mortality rate of HIC (19.4%) was lower than that of DIC (46.7%). When HIC developed into DIC, parameters of coagulation dysfunction changed significantly: platelet count decreased, D-dimer level rose, and prothrombin time and activated partial thromboplastin time prolonged (p < 0.05). CONCLUSIONS: The newly proposed HIC score may provide a valuable tool for early detection of HIC and prompt initiation of treatment.

Chinese expert consensus on diagnosis and treatment of trauma-induced hypercoagulopathy.

Trauma-induced coagulopathy (TIC) is caused by post-traumatic tissue injury and manifests as hypercoagulability that leads to thromboembolism or hypocoagulability that leads to uncontrollable massive hemorrhage. Previous studies on TIC have mainly focused on hemorrhagic coagulopathy caused by the hypocoagulable phenotype of TIC, while recent studies have found that trauma-induced hypercoagulopathy can occur in as many as 22.2-85.1% of trauma patients, in whom it can increase the risk of thrombotic events and mortality by 2- to 4-fold. Therefore, the Chinese People's Liberation Army Professional Committee of Critical Care Medicine and the Chinese Society of Thrombosis, Hemostasis and Critical Care, Chinese Medicine Education Association jointly formulated this Chinese Expert Consensus comprising 15 recommendations for the definition, pathophysiological mechanism, assessment, prevention, and treatment of trauma-induced hypercoagulopathy.

Chinese expert consensus on diagnosis and treatment of coagulation dysfunction in COVID-19.

Since December 2019, a novel type of coronavirus disease (COVID-19) in Wuhan led to an outbreak throughout China and the rest of the world. To date, there have been more than 1,260,000 COVID-19 patients, with a mortality rate of approximately 5.44%. Studies have shown that coagulation dysfunction is a major cause of death in patients with severe COVID-19. Therefore, the People's Liberation Army Professional Committee of Critical Care Medicine and Chinese Society on Thrombosis and Hemostasis grouped experts from the frontline of the Wuhan epidemic to come together and develop an expert consensus on diagnosis and treatment of coagulation dysfunction associated with a severe COVID-19 infection. This consensus includes an overview of COVID-19-related coagulation dysfunction, tests for coagulation, anticoagulation therapy, replacement therapy, supportive therapy and prevention. The consensus produced 18 recommendations which are being used to guide clinical work.

Expert consensus on the diagnosis and treatment of heat stroke in China.

Heat stroke (HS) is a fatal disease caused by thermal damage in the body, and it has a very high mortality rate. In 2015, the People's Liberation Army Professional Committee of Critical Care Medicine published the first expert consensus on HS in China, Expert consensus on standardized diagnosis and treatment for heat stroke. With an increased understanding of HS and new issues that emerged during the HS treatment in China in recent years, the 2015 consensus no longer meet the requirements for HS prevention and treatment. It is necessary to update the consensus to include the latest research evidence and establish a new consensus that has broader coverage, is more practical and is more in line with China's national conditions. This new expert consensus includes new concept of HS, recommendations for laboratory tests and auxiliary examinations, new understanding of diagnosis and differential diagnosis, On-site emergency treatment and In-hospital treatment, translocation of HS patients and prevention of HS.

Expert consensus on the diagnosis and treatment of thrombocytopenia in adult critical care patients in China.

Thrombocytopenia is a common complication of critical care patients. The rates of bleeding events and mortality are also significantly increased in critical care patients with thrombocytopenia. Therefore, the Critical Care Medicine Committee of Chinese People's Liberation Army (PLA) worked with Chinese Society of Laboratory Medicine, Chinese Medical Association to develop this consensus to provide guidance for clinical practice. The consensus includes five sections and 27 items: the definition of thrombocytopenia, etiology and pathophysiology, diagnosis and differential diagnosis, treatment and prevention.

[The effect of telomerase reverse transcriptase on 5-HT induced pulmonary artery smooth muscle cells proliferation].

OBJECTIVE: To investigate the effect of telomerase reverse transcriptase (TERT) to the proliferation of 5-HT induced pulmonary artery smooth muscle cells (PASMCs). METHODS: The PASMCs proliferation experiment was performed to detect the effort on PASMCs of 5-HT or ASODN TERT (antisense oligoribonucleotides TERT designed according to the rat TERT mRNA sequence of gene bank). The immunohistochemistry staining experiment and the in situ hybridization experiment were to detect the TERT protein and mRNA expression with 5-HT or ASODN TERT. FITC marked ASODN TERT experiment was done to research the distribution of ASODN TERT in PASMCs. RESULTS: 5-HT promoted PASMCs proliferation in a dose-dependent manner (10(-9) - 10(-5) mol/L). 5-HT also significantly increased TERT expression at protein and mRNA levels as shown by immunohistochemistry staining and the in situ hybridization studies. This effect could be blocked by ASODN TERT in a time and dose-dependent manner. CONCLUSIONS: Our experiments show TERT is one of the key factors in the procession of 5-HT induced PASMCs proliferation. ASODN TERT might be a potential therapy agent for pulmonary hypertension.

Inhibition of acid sensing ion channel by ligustrazine on angina model in rat.

Ligustrazine, a compound extracted from roots of Ligusticum chuanxiong, is widely used in Chinese traditional medicine to treat cardiac and cerebrovascular diseases and pain, including angina. The mechanism(s) of ligustrazine's effect to reduce angina is not clear. Angina is mediated by cardiac afferent sensory neurons. These neurons display a large acid-evoked depolarizing sodium current that can initiate action potentials in response to acidification that accompanies myocardial ischemia. Acid-sensing ion channels (ASICs) mediate this current. Here we tested the hypothesis that ligustrazine reduces ischemia-induced cardiac dysfunction and acid-evoked pain by an action to inhibit ASIC-mediated current. The effects of ligustrazine to attenuate ischemia-induced ST-segment depression, T wave changes, and myocardial infarct size in hearts of anesthetized rats were determined. Effects of ligustrazine on currents mediated by ASICs expressed in cultured Chinese hamster ovary cells, and effects of the drug on acid-induced nociceptive behavior and acid-induced currents in isolated dorsal root ganglions cells were measured. Ligustrazine significantly attenuated acid-induced ASIC currents, reduced cardiac ischemia-induced electrical dysfunction and infarct size, and decreased the nociceptive response to injection of acid into the paw of the rat hindlimb. The ASIC channel inhibitor A-317567 similarly reduced electrical dysfunction, infarct size, and nociceptive behavior in the rat. Inhibition of ASICs by ligustrazine may explain at least in part the beneficial effects of the drug that are observed in patients with ischemic heart disease and angina.

Therapeutic effects of DCDDP, a calcium channel blocker, on chronic pulmonary hypertension in rat.

To explore the effect of dimethyl 4-(2-chlorophenyl)-1,4-dihydro-2,6-dimethyl-3,5-pyridinedicarboxylate (DCDDP) on pulmonary hypertension (PH) induced by monocrotaline (MCT), the parameters of pulmonary hemodynamics, the contents of endothelin-like immunoreactivity, nitric oxide (NO), malondialdehyde, and superoxide dismutase in plasma and pulmonary homogenate were measured. DCDDP was administered in 5, 50, and 500 microg x kg(-1) x day(-1) ip doses, once a day for 28 days. The antiserotonin effect of DCDDP was investigated by using immunohistochemistry, image analysis, and cell culture technique. The results showed that pulmonary arterial pressure was significantly dropped and pulmonary resistance was decreased in DCDDP groups, compared with the MCT group. DCDDP had no influence on endothelin-like immunoreactivity levels in plasma and pulmonary homogenate but reduced the contents of NO, superoxide dismutase, and malondialdehyde in pulmonary homogenate enhanced by MCT. DCDDP also significantly inhibited the increase in numbers of 5-hydroxytryptamine (5-HT) and 5-HT receptor-positive cells in pulmonary tissue of PH rats induced by MCT. The proliferation and contraction of pulmonary arterial smooth muscle cells and the increase in concentration of free Ca(2+) in them evoked by 5-HT were inhibited significantly by DCDDP. The results suggest that DCDDP reduces the production of free radicals and content of 5-HT and 5-HT receptor and the increase in NO in pulmonary tissue, which underlies the mechanisms of DCDDP against MCT-induced PH.