Predictive value of the Trauma Rating Index in Age, Glasgow Coma Scale, Respiratory rate and Systolic blood pressure score (TRIAGES) for the short-term mortality of older patients with isolated traumatic brain injury: a retrospective cohort study.

OBJECTIVES: This study aimed to evaluate the effectiveness of the Trauma Rating Index in Age, Glasgow Coma Scale, Respiratory rate and Systolic blood pressure score (TRIAGES) in predicting 24-hour in-hospital mortality among patients aged 65 years and older with isolated traumatic brain injury (TBI). DESIGN: A retrospective, single-centre cohort study. SETTING: This study was conducted at a government-run tertiary comprehensive hospital. PARTICIPANTS: This study included 982 patients aged 65 years or older with isolated TBI, who were admitted to the emergency department between 1 January 2020 and 31 December 2021. INTERVENTIONS: None. PRIMARY OUTCOME: 24-hour in-hospital mortality was the primary outcome. RESULTS: Among the 982 patients, 8.75% died within 24 hours of admission. The non-survivors typically had higher TRIAGES and lower GCS scores. Logistic regression showed significant associations of both TRIAGES and GCS with mortality; the adjusted ORs were 1.98 (95% CI 1.74 to 2.25) for TRIAGES and 0.72 (95% CI 0.68 to 0.77) for GCS. Receiver operating characteristic (ROC) analysis indicated an area under the ROC curve of 0.86 for GCS and 0.88 for TRIAGES, with a significant difference (p=0.012). However, precision-recall curve (PRC) analysis revealed an area under the PRC of 0.38 for GCS and 0.47 for TRIAGES, without a significant difference (p=0.107). CONCLUSIONS: The TRIAGES system is a promising tool for predicting 24-hour in-hospital mortality in older patients with TBI, demonstrating comparable or slightly superior efficacy to the GCS. Further multicentre studies are recommended for validation.

Predictive value of the Trauma Rating Index in Age, Glasgow Coma Scale, Respiratory rate and Systolic blood pressure score (TRIAGES) and Revised Trauma Score (RTS) for the short-term mortality of patients with isolated traumatic brain injury.

BACKGROUND: Ensuring rapid and precise mortality prediction in patients with traumatic brain injury (TBI) at the emergency department (ED) is paramount in patient triage and enhancing their outcomes. We aimed to estimate and compare the predictive power of the Trauma Rating Index in Age, Glasgow Coma Scale, Respiratory rate, and Systolic blood pressure score (TRIAGES) and Revised Trauma Score (RTS) for 24-h in-hospital mortality in patients with isolated TBI. METHODS: We conducted a retrospective single-center study analyzing clinical data from 1156 patients with isolated acute TBI treated in the ED of the Affiliated Hospital of Nantong University from January 1, 2020, to December 31, 2020. We calculated each patient's TRIAGES and RTS scores and estimated their predictive value for short-term mortality using receiver operating characteristic (ROC) curves. RESULTS: 87 patients (7.53%) died within 24 h of admission. The non-survival group had higher TRIAGES and lower RTS than the survival group. Compared to non-survivors, survivors exhibited higher Glasgow Coma Scale scores (GCS) with a median score of 15 (12, 15) compared to a median score of 4.0 (3.0, 6.0). The crude and adjusted odds ratios (ORs) for TRIAGES were 1.79, 95% CI (1.62 to 1.98) and 1.79, 95% CI (1.60 to 2.00), respectively. The crude and adjusted ORs for RTS were 0.39, 95% CI (0.33 to 0.45) and 0.40, 95% CI (0.34 to 0.47), respectively. The area under the ROC (AUROC) curve of TRIAGES, RTS, and GCS was 0.865 (0.844 to 0.884), 0.863 (0.842 to 0.882), and 0.869 (0.830 to 0.909), respectively. The optimal cut-off values for predicting 24-h in-hospital mortality were 3 for TRIAGES, 6.08 for RTS, and 8 for GCS. The subgroup analysis showed a higher AUROC in TRIAGES (0.845) compared to GCS (0.836) and RTS (0.829) among patients aged 65 and above, although the difference was not statistically significant. CONCLUSIONS: TRIAGES and RTS have shown promising efficacy in predicting 24-h in-hospital mortality in patients with isolated TBI, with comparable performance to GCS. However, improving the comprehensiveness of assessment does not necessarily translate into an overall increase in predictive ability.

Association between admission systemic immune-inflammation index and mortality in critically ill patients with sepsis: a retrospective cohort study based on MIMIC-IV database.

Systemic immune-inflammation index (SII) has been identified as a prognostic biomarker for various diseases. Our study aimed to investigate the association between SII and mortality risk in critically ill patients with sepsis, thus exploring possible tools for rapid screening. This retrospective cohort study was conducted using clinical data extracted from the Medical Information Mart for Intensive Care Database. The study included only patients diagnosed with sepsis admitted to the intensive care unit for the first time. We used the restricted cubic splines to explore the relationship between SII and 28-day mortality. Kaplan-Meier curve and Cox regression models were performed to evaluate the association between SII and mortality. Subgroup analysis was performed to explore the stability of the primary results. A total of 16,007 patients with sepsis were eligible in the final analysis. We found a J-shaped relationship between SII and mortality risk. The SII level associated with the lowest mortality risk was 774.46*109/L. Compared with the reference group (second SII quartile), the 28-day mortality was increased in the highest quartile and third quartile groups of SII levels; fully adjusted HRs were 1.16 (1.02 to 1.32) and 1.40 (1.23 to 1.58), respectively. However, although the lower SII (Q1 group) also showed a trend toward a higher hazard of 28-day mortality, there was no statistical difference, with a fully adjusted HR of 1.05 (0.92 to 1.21). In the population of critically ill patients with sepsis, low and high SII levels were associated with an increased risk of short-term mortality. The 28-day mortality risk was lowest at SII levels of 774.46*109/L.

Blocking vicious cycle of cardiac dysfunction by external cardiopulmonary resuscitation is the key to rescue acute aluminium phosphide poisoning.

Aluminium phosphide (ALP) and aluminium zinc phosphide (ZnP), the two main ingredients of fumigation drugs, are commonly used to kill insects or rodents in grain. When exposed to water, highly toxic phosphine gas is released and absorbed through the respiratory or digestive tract. Phosphine gas could non-selectively block cytochrome oxidase, inhibit electron transfer and suppress oxidative phosphorylation, leading to cellular hypoxia and organ dysfunction. The characteristic clinical manifestations are refractory shock and metabolic acidosis with high mortality. However, patients with ALP poisoning have a chance to be cured. Here, we report a case of oral ALP poisoning that was successfully treated by extracorporeal membrane oxygenation (ECMO) combined with continuous renal replacement therapy (CRRT) during frequent ventricular fibrillation and cardiac dysfunction.

Optimal Strategy on Radiation Estimation for Calculating Universal Thermal Climate Index in Tourism Cities of China.

The Universal Thermal Climate Index (UTCI) is believed to be a very powerful tool for providing information on human thermal perception in the domain of public health, but the solar radiation as an input variable is difficult to access. Thus, this study aimed to explore the optimal strategy on estimation of solar radiation to increase the accuracy in UTCI calculation, and to identify the spatial and temporal variation in UTCI over China. With daily meteorological data collected in 35 tourism cities in China from 1961 to 2020, two sunshine-based Angstrom and Ogelman models, and two temperature-based Bristow and Hargreaves models, together with neural network and support vector machine-learning methods, were tested against radiation measurements. The results indicated that temperature-based models performed the worst with the lowest NSE and highest RMSE. The machine-learning methods performed better in calibration, but the predictive ability decreased significantly in validation due to big data requirements. In contrast, the sunshine-based Angstrom model performed best with high NSE (Nash-Sutcliffe Efficiency) of 0.84 and low RMSE (Root Mean Square Error) of 35.4 J/m2 s in validation, which resulted in a small RMSE of about 1.2 °C in UTCI calculation. Thus, Angstrom model was selected as the optimal strategy on radiation estimation for UTCI calculation over China. The spatial distribution of UTCI showed that days under no thermal stress were high in tourism cities in central China within a range from 135 to 225 days, while the largest values occurred in Kunming and Lijiang in southwest China. In addition, days under no thermal stress during a year have decreased in most tourism cities of China, which could be attributed to the asymmetric changes in significant decrease in frost days and slightly increase in hot days. However, days under no thermal stress in summer time have indeed decreased, accompanying with increasing days under strong stress, especially in the developed regions such as Yangze River Delta and Zhujiang River Delta. Based on the study, we conclude that UTCI can successfully depict the overall spatial distribution and temporal change of the thermal environments in the tourism cities over China, and can be recommend as an efficient index in the operational services for assessing and predicting thermal perception for public health. However, extreme cold and heat stress in the tourism cities of China were not revealed by UTCI due to mismatch of the daily UTCI with category at hourly scale, which makes it an urgent task to redefine category at daily scale in the next research work.

B-CAN: a resource sharing platform to improve the operation, visualization and integrated analysis of TCGA breast cancer data.

Breast cancer is a high-risk heterogeneous disease with myriad subtypes and complicated biological features. The Cancer Genome Atlas (TCGA) breast cancer database provides researchers with the large-scale genome and clinical data via web portals and FTP services. Researchers are able to gain new insights into their related fields, and evaluate experimental discoveries with TCGA. However, it is difficult for researchers who have little experience with database and bioinformatics to access and operate on because of TCGA's complex data format and diverse files. For ease of use, we build the breast cancer (B-CAN) platform, which enables data customization, data visualization, and private data center. The B-CAN platform runs on Apache server and interacts with the backstage of MySQL database by PHP. Users can customize data based on their needs by combining tables from original TCGA database and selecting variables from each table. The private data center is applicable for private data and two types of customized data. A key feature of the B-CAN is that it provides single table display and multiple table display. Customized data with one barcode corresponding to many records and processed customized data are allowed in Multiple Tables Display. The B-CAN is an intuitive and high-efficient data-sharing platform.

Tazarotene-induced gene 2 is associated with poor survival in non-small cell lung cancer.

The aim of the present study was to investigate the expression of tazarotene-induced gene 2 (TIG2) and evaluate the clinicopathological variables and prognostic value for non-small cell lung cancer (NSCLC) patients. Reverse transcription-polymerase chain reaction and western blotting were utilized to detect TIG2 expression in NSCLC specimens and adjacent noncancerous tissue. Furthermore, the present study investigated the protein expression and the clinicopathological significance of TIG2 in 98 paraffin-embedded NSCLC samples by using immunohistochemistry. The results of the present study demonstrated that the expression of TIG2 mRNA (P=0.003) and protein (P=0.0024) was significantly reduced in NSCLC compared with corresponding noncancerous tissue. TIG2 protein expression in NSCLC was significantly associated with lymph node metastasis (P=0.006), Tumor-Node-Metastasis stage (P=0.021) and degree of differentiation (P=0.025). The Kaplan-Meier method and log-rank test revealed that high TIG2 expression was significantly associated with increased survival of NSCLC patients (P=0.003). Multivariate analysis revealed that TIG2 expression was an independent prognostic factor of the overall survival of NSCLC patients. Decreased expression of TIG2 may be useful as a biomarker for poor prognosis in NSCLC carcinogenesis and may act as a target for gene therapy for the treatment of NSCLC patients.

Comparison of minocycline and azithromycin for the treatment of mild scrub typhus in northern China.

Scrub typhus, caused by Orientia tsutsugamushi, has recently emerged in northern China where the disease had not been known to exist. Although doxycycline and azithromycin are the recommended agents for the treatment of scrub typhus, clinical responses depend both on the susceptibilities of various O. tsutsugamushi strains and the severity of the disease. A retrospective analysis was conducted on patients diagnosed with mild scrub typhus from August 2013 to January 2016 in the Affiliated Hospital of Nantong University, northern China. A total of 40 patients who received minocycline treatment and 34 patients who received azithromycin treatment were included in the analysis. All patients except one defervesced within 120 h after initiating antimicrobial therapy. Kaplan-Meier curves in association with log-rank test showed that the median time to defervescence was significantly shorter for the minocycline-treated group than the azithromycin-treated group (P = 0.003). There were no serious adverse events during treatment. No relapse occurred in either group during the 1-month follow-up period. In conclusion, both minocycline and azithromycin are effective and safe for the treatment of mild scrub typhus, but minocycline is more active than azithromycin against O. tsutsugamushi infection acquired in northern China.

TRAM1 protects AR42J cells from caerulein-induced acute pancreatitis through ER stress-apoptosis pathway.

Chronic endoplasmic reticulum (ER) stress in pancreatic acinar cells has emerged as a major contributor to the recovery of acute pancreatitis (AP). However, the molecular mechanisms linking AP and ER stress remain not fully understood. In this study, we employed caerulein to induce AP-like inflammation in the AR42J rat pancreatic acinar cells to mimic the AP-like acinar cell injury. Caerulein can activate ER stress in AR42J cells, but the molecular link between AP and ER stress remains to be identified. We here reported that translocating chain-associated membrane protein 1 (TRAM1), an ER-resident multispanning membrane protein, was involved in the onset of AP-like injury on AR42J cells. TRAM1 was significantly elevated in caerulein-treated AR42J cells. Furthermore, we showed that knockdown of TRAM1 led to hyperactivation of 78 kDa glucose-regulated protein precursor (GRP78) and C/EBP homologous protein (CHOP) and the activation of downstream apoptosis pathway. Given the fact that the activation of ER stress played a protection role in AP, the pro-inflammatory mediators TNF-α and IL-6 and the marker of cell injury LDH were also analyzed. We found that depletion of TRAM1 markedly increased the secretion of TNF-α, IL-6, and LDH in the cells. Moreover, flow cytometry indicated that treatment with caerulein induced a significant decrease of apoptotic index and increase of necrosis index in TRAM1-siRNA cells, compared with control groups, as indicated by downregulated expression of cleaved caspase-3, caspase-8, and caspase-9 mRNA expression activity in TRAM1-siRNA cells. These data implicated that TRAM1 might protect AR42J cells against caerulein-induced AP in AR42J cells through alleviating ER stress.

Karyopherin Alpha 2 Promotes the Inflammatory Response in Rat Pancreatic Acinar Cells Via Facilitating NF-κB Activation.

BACKGROUND: Activation of the transcription factor NF-κB and expression of pro-inflammatory mediators have been considered as major events of acute pancreatitis (AP). Karyopherin alpha 2 (KPNA2), a member of the importin α family, reportedly modulates p65 subcellular localization. AIM: This study aimed to investigate the expression and possible functions of KPNA2 in the AP cell and animal model, focusing on its association with NF-κB activation. METHODS: An AP cell model was established with the cerulein-stimulated AR42J and isolated rat pancreatic acinar cells. The AP rat model was induced by the intraperitoneal injection of cerulein. The secretion of TNF-α, IL-6, and LDH was detected by ELISA kits and the production of NO using nitric oxide kit. Expression of KPNA2 was measured by RT-PCR and Western blot. Expression levels of IKKα, phosphorylation of p65, and total p65 were detected by Western blot. Co-localization of KPNA2 with p65 was observed by immunofluorescence assay. To determine the biological functions of KPNA2 in cerulein-induced inflammatory response, RNA interference was employed to knockdown KPNA2 expression in AR42J and isolated pancreatic acini cells. RESULTS: Cerulein stimulated KPNA2 expression and IL-6, TNF-α, NO, and LDH production in rat pancreatic acinar cells. Cerulein triggered the phosphorylation and nuclear translocation of NF-κB p65 subunit, indicating the NF-κB activation. The co-localization and nuclear accumulation of KPNA2 and p65 were detected in cerulein-treated cells. Knocking down KPNA2 hindered cerulein-induced nuclear transportation of p65 and alleviated the subsequent inflammatory response in rat pancreatic acinar cells. Additionally, KPNA2 expression was significantly up-regulated in cerulein-induced AP rat model. CONCLUSIONS: KPNA2-facilitated p65 nuclear translocation promotes NF-κB activation and inflammation in acute pancreatitis.

OGT-mediated O-GlcNAcylation promotes NF-κB activation and inflammation in acute pancreatitis.

OBJECTIVE: Activation of the transcription factor κB (NF-κB) and secretion of pro-inflammatory mediators are major events in acute pancreatitis (AP). Recently, O-linked-N-acetylglucosamine (O-GlcNAc) modification, one type of posttranslational modifications, reportedly attunes NF-κB function. However, the expression of O-GlcNAc transferase (OGT), the enzyme responsible for O-GlcNAcylation of proteins, in AP, and the possible contribution of OGT-mediated O-GlcNAcylation to the NF-κB inflammatory activation in pancreatic acinar cells and to the AP progression have not been understood. This study focused on the effects and mechanisms of OGT-mediated O-GlcNAcylation during AP. METHODS: An AP cell model was established with the caerulein-stimulated AR42 J rat pancreatic acinar cells. The secretion of pro-inflammatory cytokines TNF-α was detected by ELISA kits, and the production of NO was determined using the colorimetric Griess reaction. Expression of OGT was measured by RT-PCR and Western blot. Expression levels of RL2, phosphorylation of p65, total p65, IKKα were detected by Western blot. The NF-κB activity was evaluated by luciferase reporter gene assay. To determine the biological functions of OGT in caerulein-induced inflammatory response, RNA interference and PUGNAc, the inhibitor of O-GlcNAcase (OGA) was employed to regulate OGT expression in AR42 J cells. RESULTS: Caerulein significantly up-regulated the expression of OGT, and increased the global protein O-GlcNAcylation level in AR42 J cells. Reduction of OGT by small interfering RNA (siRNA) inhibited caerulein-triggered inflammation, assessed by the production of pro-inflammatory mediators (TNF-α and NO). We also demonstrated that O-GlcNAcylation directly modified the NF-κB p65 subunit and its upstream activating kinases IKKα in AR42 J cells. Lowering O-GlcNAcylation by OGT knockdown attenuated p65 activating phosphorylation, nuclear translocation, NF-κB transcriptional activity and levels of NF-κB transcriptional targets TNF-α and NO; on the contrary, elevating O-GlcNAc through PUGNAc increased IKKα and p65 O-GlcNAcylation accompanied by increased p65 phosphorylation, activity and levels of TNF-α and NO in caerulein-treated cells. CONCLUSIONS: Our results demonstrate for the first time that OGT-mediated O-GlcNAcylation promotes NF-κB signaling activation and inflammation in pancreatic acinar cells, which might promote the progression of AP.

Transformer 2ß (Tra2ß/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation.

Transformer 2ß (Tra2ß), a member of the serine/arginine-rich-like protein family, is an important RNA-binding protein involved in alternative splice. Deregulation of Tra2ß has been observed in several cancers. However, the detailed role of Tra2ß in non-small cell lung cancer (NSCLC) has not been elucidated. In this study, the contribution of Tra2ß to NSCLC development was investigated. On histological level, the expression of Tra2ß was determined by Western and immunohistochemistry assays. It demonstrated that Tra2ß was expressed higher in NSCLC tumor tissues compared with adjacent non-tumor tissues. In addition to confirm the association of Tra2ß expression with histological differentiation and clinical stage (p < 0.05), we also confirmed significant positive correlation between the expression level of Tra2ß and that of Ki67 (p < 0.05, r = 0.446) by Spearman rank correlation test. Moreover, high expression of Tra2ß predicted poor prognosis by Kaplan-Meier survival analysis. And Tra2ß among with other clinicopathologic variables was an independent prognostic indicator for patients' overall survival by multivariate analysis. On cellular level, Tra2ß expression was demonstrated to promote proliferation of NSCLC cells through a series of assays, including serum starvation and release assay, Western blot assay and flow cytometry analysis. Moreover, knockdown of Tra2ß was confirmed to inhibit proliferation and to induce apoptosis of NSCLC cells through flow cytometry analysis, western analysis, cell counting kit-8 assay and Tunnel assay. Our results indicated that Tra2ß was involved in the tumorigenesis of NSCLC and might be a potential therapeutic target of NSCLC.

Angiotensin-converting enzyme gene 2350 G/A polymorphism and susceptibility to atrial fibrillation in Han Chinese patients with essential hypertension.

OBJECTIVE: The angiotensin-converting enzyme gene is one of the most studied candidate genes related to atrial fibrillation. Among the polymorphisms of the angiotensin-converting enzyme gene, the 2350 G/A polymorphism (rs4343) is known to have the most significant effects on the plasma angiotensin-converting enzyme concentration. The aim of the present study was to investigate the association of the angiotensin-converting enzyme 2350 G/A polymorphism with atrial fibrillation in Han Chinese patients with essential hypertension. METHODS: A total of 169 hypertensive patients were eligible for this study. Patients with atrial fibrillation (n = 75) were allocated to the atrial fibrillation group, and 94 subjects without atrial fibrillation were allocated to the control group. The PCR-based restriction fragment length polymorphism technique was used to assess the genotype frequencies. RESULTS: The distributions of the angiotensin-converting enzyme 2350 G/A genotypes (GG, GA, and AA, respectively) were 40.43%, 41.49%, and 18.08% in the controls and 18.67%, 46.67%, and 34.66% in the atrial fibrillation subjects (p = 0.037). The frequency of the A allele in the atrial fibrillation group was significantly greater than in the control group (58.00% vs. 38.83%, p = 0.0007). Compared with the wild-type GG genotype, the GA and AA genotypes had an increased risk for atrial fibrillation. Additionally, atrial fibrillation patients with the AA genotype had greater left atrial dimensions than the patients with the GG or GA genotypes (p<0.01 and p<0.05, respectively). CONCLUSIONS: The results obtained in this study indicate that the angiotensin-converting enzyme 2350 G/A polymorphism is associated with atrial fibrillation and that the A allele shows an increased risk for atrial fibrillation in Han Chinese patients with essential hypertension.

Angiotensin-converting enzyme gene 2350 G/A polymorphism and susceptibility to atrial fibrillation in Han Chinese patients with essential hypertension

OBJECTIVE: The angiotensin-converting enzyme gene is one of the most studied candidate genes related to atrial fibrillation. Among the polymorphisms of the angiotensin-converting enzyme gene, the 2350 G/A polymorphism (rs4343) is known to have the most significant effects on the plasma angiotensin-converting enzyme concentration. The aim of the present study was to investigate the association of the angiotensin-converting enzyme 2350 G/A polymorphism with atrial fibrillation in Han Chinese patients with essential hypertension. METHODS: A total of 169 hypertensive patients were eligible for this study. Patients with atrial fibrillation (n = 75) were allocated to the atrial fibrillation group, and 94 subjects without atrial fibrillation were allocated to the control group. The PCR-based restriction fragment length polymorphism technique was used to assess the genotype frequencies. RESULTS: The distributions of the angiotensin-converting enzyme 2350 G/A genotypes (GG, GA, and AA, respectively) were 40.43%, 41.49%, and 18.08% in the controls and 18.67%, 46.67%, and 34.66% in the atrial fibrillation subjects (p = 0.037). The frequency of the A allele in the atrial fibrillation group was significantly greater than in the control group (58.00% vs. 38.83%, p = 0.0007). Compared with the wild-type GG genotype, the GA and AA genotypes had an increased risk for atrial fibrillation. Additionally, atrial fibrillation patients with the AA genotype had greater left atrial dimensions than the patients with the GG or GA genotypes (p<0.01 and p<0.05, respectively). CONCLUSIONS: The results obtained in this study indicate that the angiotensin-converting enzyme 2350 G/A polymorphism is associated with atrial fibrillation and that the A allele shows an increased risk for atrial fibrillation in Han Chinese patients with essential hypertension. .

[Protective effect of reduced glutathione on multiple organ function in patient with acute pancreatitis].

OBJECTIVE: To study the protective effect of reduced glutathione (GSH) on multiple organ function in patient with acute pancreatitis. METHODS: A total of 45 patients with acute pancreatitis was randomly divided into two groups, 22 patients were given GSH in a dose of 1.2 g/d through intravenous drip for 7 days as GSH group, and 23 patients were not given GSH to serve as control group. The same treatment was given to both groups other than GSH. Plasma contents of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) and biochemistry indexes were determined. RESULTS: After the treatment, the levels of TNF-alpha and IL-6 were significantly decreased in both groups (all P<0.05). The levels of TNF-alpha and IL-6 were decreased much more obviously in GSH group compared with those in control group (P<0.05). Plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine (Cr), blood urea nitrogen (BUN), lactate dehydrogenase (LDH), creatine kinase (CK), and MB isoenzyme of creatine kinase (CK-MB) were significantly decreased in both treatment groups, but the decrease of all these indexes was more marked in GSH group (P<0.05). CONCLUSION: The results suggest that GSH has beneficial effects in protecting visceral organ function in patients with acute pancreatitis.

A phytochemical in the edible Tamogi-take mushroom (Pleurotus cornucopiae), D-mannitol, inhibits ACE activity and lowers the blood pressure of spontaneously hypertensive rats.

D-Mannitol, one of the main phytochemicals of the edible Tamogi-take mushroom (Pleurotus cornucopiae), was found to inhibit an angiotensin I converting enzyme (ACE). The antihypertensive effect of D-mannitol and a hot water extract of Tamogi-take mushroom was demonstrated in spontaneously hypertensive rats (SHR) by oral administration.