Differences in efficacy and safety of midazolam vs. dexmedetomidine in critically ill patients: A meta-analysis of randomized controlled trial.

The present study aimed to compare the efficacy and safety of dexmedetomidine and midazolam in patients that are critically ill. Full text articles reporting the clinical effects and complications of dexmedetomidine and midazolam were retrieved from multiple databases. Review Manager 5.0 was adopted for meta-analysis, sensitivity and bias analysis. Finally, a total of 1,379 patients from 8 studies, which met the eligibility criteria, were included. The meta-analysis suggested that the length of stay at the intensive care unit [mean absolute difference (MD)=-1.80; 95% confidence interval (CI), -2.13, -1.48; P<0.00001; P-value for heterogeneity=0.41; I²=3%], time to extubation (MD=-2.18; 95% CI, -2.66, -1.69; P<0.00001; P-value for heterogeneity=0.84; I²=0%) and delirium (MD=0.46; 95% CI, 0.37, 0.57; P<0.00001; P-value for heterogeneity=0.65; I²=0%) was higher following midazolam treatment compared with dexmedetomidine, while bradycardia [odds ratio (OR)=5.03; 95% CI, 3.86, 6.57; P<0.00001; P-value for heterogeneity=0.13; I²=38%] was higher in dexmedetomidine treated patients compared with midazolam. However, no difference was observed in the incidence of hypotension (OR=0.88; 95% CI, 0.70, 1.10; P=0.26; P-value for heterogeneity=0.99; I²=0%) and mortality (OR=0.96; 95% CI, 0.74, 1.25; P=0.77; P-value for heterogeneity=0.99; I²=0%). Taking clinical effects and safety into account, the present study suggested dexmedetomidine to be the preferred option of anesthesia for patients that are critically ill.

COVID-19 patients managed in psychiatric inpatient settings due to first-episode mental disorders in Wuhan, China: clinical characteristics, treatments, outcomes, and our experiences.

Data are scarce regarding the comorbid mental disorders and their management among COVID-19 patients. This study described the clinical characteristics and management of COVID-19 patients treated in psychiatric inpatient settings due to comorbid first-onset mental disorders in Wuhan, China. This electronic medical records-based study included 25 COVID-19 patients with first-onset mental disorders and 55 patients with first-onset mental disorders without COVID-19 (control group). Data collected included ICD-10 diagnoses of mental disorders, psychiatric and respiratory symptoms, treatments, and outcomes. Adjustment disorder (n = 11, 44.0%) and acute and transient psychotic disorders, with associated acute stress (n = 6, 24.0%) were main clinical diagnoses in the COVID-19 group while serious mental illnesses (i.e., schizophrenia, 24.5%) and alcohol use disorders (10.9%) were overrepresented in the control group. On admission, the most common psychiatric symptom in COVID-19 patients was insomnia symptoms (n = 18, 72.0%), followed by aggressive behaviors (n = 16, 64.0%), delusion (n = 10, 40.0%), and severe anxiety (n = 9, 36.0%). In addition to respiratory treatments, 76.0% COVID-19 patients received antipsychotics, 40.0% sedative-hypnotics, and 24.0% mood stabilizers. At the end of inpatient treatment, 4 (16.0%) COVID-19 patients were transferred to other hospitals to continue respiratory treatment after their psychiatric symptoms were controlled while the remaining 21 (84.0%) all recovered. Compared to the control group, COVID-19 group had significantly shorter length of hospital stay (21.2 vs. 37.4 days, P < 0.001). Adjustment disorder and acute and transient psychotic disorders are the main clinical diagnoses of COVID-19 patients managed in psychiatric inpatient settings. The short-term prognosis of these patients is good after conventional psychotropic treatment.

TROP2 promotes cell proliferation and migration in osteosarcoma through PI3K/AKT signaling.

Human trophoblast cell surface antigen 2 (TROP2) has been noted to serve an important role in the proliferation and migration of various types of human cancers. However, the potential role and the molecular mechanisms of TROP2 in osteosarcoma (OS) remain largely unclear. In the present study, high expression of TROP2 in human OS tissues and cell lines was observed. Overexpression of TROP2 promoted the proliferation and migration of OS cell lines, while TROP2 knockdown markedly decreased cell growth and migration. Furthermore, it was revealed that TROP2 overexpression significantly activated the phosphoinositide 3­kinase/protein kinase B (PI3K/AKT) signaling pathway. Collectively, these results suggested that TROP2 may promote OS cell proliferation and migration via PI3K/AKT signaling and may serve as a novel treatment target for OS.

Enriched housing promotes post-stroke functional recovery through astrocytic HMGB1-IL-6-mediated angiogenesis.

Enriched environment (EE) is shown to promote angiogenesis, neurogenesis and functional recovery after ischemic stroke. However, the underlying mechanisms remain unclear. C57BL/6 mice underwent middle cerebral artery occlusion (60 min) followed by reperfusion, after which mice were housed in either standard environment (SE) or EE. Here we found that post-ischemic EE exhibited decreased depression and anxiety-like behavior, and promoted angiogenesis and functional recovery compared to SE mice. EE mice treated with high-mobility group box-1 (HMGB1) inhibitor glycyrrhizin had an increased post-stroke depression and anxiety-like behavior, and the angiogenesis and functional recovery were decreased. HMGB1 and interleukin-6 (IL-6) expression in astrocyte were increased in EE mice. EE mice treated with glycyrrhizin decreased, whereas EE mice treated with recombinant HMGB1 (rHMGB1) increased the levels of IL-6 and p-AKT. Blockade of IL-6 with anti-IL-6-neutralizing antibody in EE mice attenuated EE-mediated angiogenesis and functional recovery. Furthermore, our in vitro data revealed that in primary astrocyte cultures rHMGB1 promoted the expression of IL-6 in activated astrocytes. PI3K/AKT signaling pathway was involved in HMGB1-mediated expression of astrocytic IL-6. Thus, our results reveal a previously uncharacterized property of HMGB1/IL-6 signaling pathway in EE-mediated angiogenesis and functional recovery after ischemic stroke.

[The effect of enteral nutritional support and growth hormone on critical patients].

OBJECTIVE: To explore the effect of early enteral nutritional support and growth hormone (GH) on critical patients. METHODS: Sixty-eight critical patients were divided into enteral nutrition (EN) group and EN+GH group, with 34 patients in each group, by random number table. All the patients in both group received early enteral nutritional support, at the same time, the patients in EN+GH group received GH 5 U, once a day for 10 days. The intake was isonitrogenous and isocaloric in both groups. Body weight, blood biochemistry examination, nutrition state and lactulose/mannitol test were performed before and 5 days and 10 days after nutritional support. Immune function was performed after 10 days. Nitrogen balance was measured daily. RESULTS: The changes in body weight, albumin and transferring levels were more obvious in the EN+GH group than those in the EN group before and 5 days and 10 days after nutritional support, but the difference was not significant between the two groups. On the 5th and 10th day after treatment, the level of prealbumin [the 5th day:(25.34+/-4.26) g/L vs. (20.62+/-3.58) g/L; the 10th day: (27.34+/-4.25) g/L vs. (23.87+/-2.96) g/L] and that of fibronectin [the 5th day: (2.68+/-0.37) mg/L vs. (2.01+/-0.27) mg/L; the 10th day: (2.74+/-0.31) mg/L vs. (2.44+/-0.19) mg/L] in the EN+GH group were significantly higher than those in the EN group (all P<0.05). However, the level of lactulose/mannitol was significantly lower in EN+GH group than that in the EN group (the 5th day: 0.065+/-0.004 vs. 0.087+/-0.005, the 10th day: 0.027+/-0.002 vs. 0.053+/-0.004, both P<0.01). On the 10th day after treatment, the level of IgA in the EN+GH group was significantly lower than that in the EN group [(2.10+/-0.09) g/L vs.(3.45+/-0.25) g/L], but the levels of CD3 (0.682+/-0.049 vs. 0.606+/-0.046), CD4 (0.456+/-0.039 vs. 0.372+/-0.032), CD4/CD8 ratio (1.66+/-0.11 vs. 1.41+/-0.12), and the natural killer cell (NK cell, 0.139+/-0.011 vs.0.107+/-0.004) in the EN+GH group were significantly higher than those in the EN group (all P<0.05). The gut barrier function in the EN+GH group was superior to that in the EN group during nutritional support period. Nitrogen balance was positive in the EN+GH group [(27.54+/-23.15) mg/kg] and negative in the EN group [-(5.13+/-4.26) mg/kg]. CONCLUSION: Early enteral nutritional support can improve state of nutrition, and it is combined with GH composition of protein may be improved and the immune function may be enhanced.

[The effects of somatostatin on serum interleukin-6 and tumor necrosis factor-alpha in lipopolysaccharide-induced septic shock: experiment with rats].

OBJECTIVE: To explore the effect of somatostatin on serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in lipopolysaccharide (LPS)-induced septic shock. METHODS: 24 male Wistar rats were randomly divided into 2 groups: intervention group (injected with LPS of Escherichia coli via femoral vein to induce septic shock) and control group (injected with LPS of Escherichia coli and then injected with somatostatin). The mean arterial pressure (MAP), heart rate, respiration rater, and mortality rate were observed before the injection of LPS, and 30, 90, and 360 min after the injection, and the serum IL-6 and TNF-alpha level were detected before the injection of LPS, 30, 90, and 360 min after the injection, or after the death. RESULTS: The IL-6 levels 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 233 +/- 47, 212 +/- 33, and 217 +/- 26 mg/L respectively, all significantly lower then those of the control group (308 +/- 56, 260 +/- 32, and 230 +/- 92 mg/L, all P < 0.05). The TNF-alpha level 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 450 +/- 82, 417 +/- 92, and 440 +/- 49 mg/L, all significantly lower than those of the control group (607 +/- 149, 517 +/- 74, and 474 +/- 219 mg/L, all P < 0.05). In addition, compared with the control group, the MAP of the somatostatin intervention group increased after 90 min. Two rats in the control group died 30 to 90 min later and 4 rats died 90 to 360 min later, however, 360 min later all rats in the somatostatin intervention group were alive (P = 0.0054). CONCLUSION: Somatostatin can inhibit the level of serum IL-6 and TNF-alpha in septic shock induced by LPS and improve the survival rate.