[Predictive value of stroke-related early tracheotomy score for tracheotomy in neurocritical patients].

OBJECTIVE: To explore the predictive value of stroke-related early tracheotomy score (SET) for tracheotomy in neurocritical patients. METHODS: A retrospective analysis of the clinical data of neurocritical patients admitted to the department of intensive care unit (ICU) of the Xindu District People's Hospital of Chengdu from January 1st to December 31st, 2019. Patients were divided into tracheostomy group and non-tracheostomy group according to whether they underwent tracheotomy during hospitalization; according to SET score, patients were divided into groups with SET score < 10 points and SET score ≥ 10 points. The differences in gender, age, acute physiology and chronic health evaluation II (APACHE II), Glasgow coma score (GCS), SET score, the length of ICU stay and mechanical ventilation time were compared between the two groups. The receiver operator characteristic curve (ROC curve) was used to analyze the predictive value of SET score for the length of ICU stay > 10 days, mechanical ventilation time > 5 days, and tracheotomy treatment, and the predictive value of APACHE II score for tracheotomy treatment. RESULTS: Among 66 patients, 35 cases underwent a tracheotomy, 31 cases did not; SET score < 10 points in 19 cases, while SET score ≥ 10 points in 47 cases. Compared with the non-tracheostomy group, there were more male patients in the tracheostomy group (cases: 27 vs. 13), the GCS score was lower (7.00±2.41 vs. 11.52±2.00), the APACHE II score and the SET score were higher (22.43±4.45 vs. 19.58±5.86, 16.11±3.67 vs. 8.61±4.27), and the length of ICU stay and mechanical ventilation time was longer [days: 27.54±18.82 vs. 7.45±5.30, 13 (9, 19) vs. 0 (0, 2)], and all differences were statistically significant (all P < 0.05). Compared with SET score < 10 points group, the proportion of traumatic brain injury and tracheotomy in the SET score ≥ 10 points group was higher (44.68% vs. 15.79%, 70.21% vs. 5.26%), the GCS score was lower (8.00±2.87 vs. 11.89±1.97), APACHE II score was higher (22.30±4.80 vs. 18.11±5.49), and the length of ICU stay and mechanical ventilation time was longer [days: 22.38±18.74 vs. 7.53±4.60, 9 (4, 16) vs. 0 (0, 2)], and the differences were statistically significant (all P < 0.05). ROC curve analysis showed that the area under the curve (AUC) of SET score predicting the length of ICU stay > 10 days of neurocritical patients was 0.877, and the 95% confidence interval (95%CI) was 0.790-0.964 (P = 0.000), and its cut-off value was 13.50, the sensitivity was 80.0%, and the specificity was 87.1%. The SET score predicts the AUC for mechanical ventilation time > 5 days was 0.915, the 95%CI was 0.851-0.979 (P = 0.000), the cut-off value was 13.50, the sensitivity was 78.4%, and the specificity was 89.7%. SET score predicts the AUC of tracheotomy treatment was 0.919, 95%CI was 0.853-0.985 (P = 0.000), its cut-off value was 13.50, the sensitivity was 82.9%, and the specificity was 90.3%, which was significantly better than that of APACHE II score in predicting the value of tracheotomy (AUC was 0.647, 95%CI was 0.512-0.783, P = 0.040, its cut-off value was 17.50, the sensitivity was 91.4%, and the specificity was 41.9%). CONCLUSIONS: SET score has a good predictive value for the length of ICU stay, mechanical ventilation time and tracheotomy in neurocritical patients.

Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5.

Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.

Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5

Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.