Nonocclusive mesenteric ischemia caused by type B aortic dissection: a case report.

BACKGROUND: Nonocclusive mesenteric ischemia (NOMI) is defined as acute intestinal ischemia because of decreased blood flow in mesenteric vessels. Only a few cases of NOMI that occur secondary to aortic dissection (AD) have been reported, resulting in the lack of sufficient knowledge of diagnosis and treatment. CASE PRESENTATION: We aimed to report a case of NOMI caused by type B Aortic Dissection. A 26-year-old male patient was transferred to our hospital with the diagnose of NOMI and aortic dissection in April 2018. The abdominal computed tomography (CT) assists the diagnosis of paralytic intestinal obstruction, intestinal wall pneumatosis, and perforation. Emergency laparotomy revealed that the bowel wall supplied by the superior mesenteric artery (SMA) was pale with the palpable but weak pulsation of the parietal artery. The small intestine was extremely dilated with a paper-thin, fragile wall that was ruptured easily and could not be sutured. In this case, extensive resection and segmental drainage were done. Postoperatively, the digestive tract was reconstructed. However, the patient suffered from iron deficiency anemia and short bowel syndrome eight months later, and unfortunately died from long-term complications. CONCLUSION: Aortic dissection leads to continuous decrease in blood pressure and blood flow to the SMA, considering as a predisposing factor for NOMI. During the treatment, extensive resection and segmental drainage are the optimal surgical strategy, which can make benefit in emergencies especially.

Risk factors of postoperative septic cardiomyopathy in perioperative sepsis patients.

OBJECTIVE: This study aimed to clarify the relevant risk factors of septic cardiomyopathy (SCM) in perioperative sepsis patients. METHODS: This retrospective study evaluated patients who were diagnosed with sepsis during the perioperative period and postoperatively admitted to the intensive care unit (ICU) in the Second Affiliated Hospital of Soochow University, the First Affiliated Hospital of Soochow University, and the Suzhou Municipal Hospital between January 2017 and November 2020. They were divided into two groups as the septic cardiomyopathy group (SCM group) and the non-SCM group (NSCM group). Factors with P < 0.1 were compared between groups and were analyzed by multivariate logistic regression to screen the risk factors of sepsis cardiomyopathy. The area under the receiver operating characteristic (ROC) curve was used to verify the discriminative ability of multivariate logistic regression results. Hosmer-Lemeshow goodness of fit test was used to verify the calibration ability of multiple logistic regression results. RESULT: Among the 269 patients, 49 patients had SCM. Sequential Organ Failure Assessment (SOFA) score (adjusted odds ratio [AOR] = 2.535, 95% confidence interval (CI): 1.186-1.821, P = 0.000]) and endoscopic surgery (AOR = 3.154, 95% CI: 1.173-8.477, P = 0.023]) were identified to be independent risk factors for SCM. Patients with a SOFA score ≥ 7 had a 46.831-fold higher risk of SCM (AOR =46.831, 95% CI: 10.511-208.662, P < 0.05). The multivariate logistic regression results had good discriminative (area under the curve: 0.902 [95% CI: 0.852-0.953]) and calibration (c2 = 4.401, P = 0.819) capabilities. The predictive accuracy was 86.2%. The rates of mechanical ventilation and tracheotomy were significantly higher in the SCM group than in the NSCM group (both P < 0.05). The SCM group also had a significantly longer duration of mechanical ventilation (P < 0.05) and significantly higher rates of continuous renal replacement therapy (CRRT) and CRRT-related mortality (P < 0.05). Further, the total length of stay and hospitalization cost were significantly higher in the SCM group than in the NSCM group (P < 0.05). CONCLUSION: Endoscopic surgery and SOFA score ≥ 7 during postoperative ICU admission were independent risk factors for SCM within 48 hours postoperatively in patients with perioperative sepsis.

Cystatin C improves blood-brain barrier integrity after ischemic brain injury in mice.

Cystatin C, a well-established biomarker of renal function, has been associated with a protective effect against stroke. However, the potential neuroprotective mechanism of cystatin C in ischemic brain injury remains unclear. Our study hypothesized that cystatin C can ameliorate blood-brain barrier (BBB) disruption by up-regulating caveolin-1 expression, thereby improving neurological outcomes in cerebral ischemic injury. Western blotting, immunohistochemistry, immunofluorescence staining, and immunoprecipitation were performed to investigate target proteins. Evans Blue and gelatin zymography were used to examine the effect of cystatin C on BBB disruption. Plasmid and small interfering RNA transfection was used to observe alterations in caveolin-1 and occludin expression induced by changes in cystatin C expression. Intriguingly, our study showed that the expression of both cystatin C and caveolin-1 was increased in middle cerebral artery occlusion-injured mice, and pretreatment with exogenous cystatin C significantly increased caveolin-1 expression, reduced Evans Blue leakage in the injured brain region, and decreased the enzymatic activity of matrix metallopeptidase-9. Meanwhile, our study also showed that the over-expression of cystatin C greatly enhanced caveolin-1 expression, which later increased occludin expression in oxygen-glucose deprivation-exposed brain microvascular endothelial cells. The knockdown of cystatin C induced the opposite outcomes. These experimental results indicate a positive role for cystatin C in the regulation of caveolin-1 and occludin expression in cerebral ischemic injury. Taken together, these data unveil a new mechanism of the regulation of caveolin-1 expression by cystatin C in the maintenance of BBB integrity after ischemic brain injury and provide new clues for the identification of potential therapeutic strategies for stroke.

Rescue fecal microbiota transplantation for antibiotic-associated diarrhea in critically ill patients.

BACKGROUND: Antibiotic-associated diarrhea (AAD) is a risk factor for exacerbating the outcome of critically ill patients. Dysbiosis induced by the exposure to antibiotics reveals the potential therapeutic role of fecal microbiota transplantation (FMT) in these patients. Herein, we aimed to evaluate the safety and potential benefit of rescue FMT for AAD in critically ill patients. METHODS: A series of critically ill patients with AAD received rescue FMT from Chinese fmtBank, from September 2015 to February 2019. Adverse events (AEs) and rescue FMT success which focused on the improvement of abdominal symptoms and post-ICU survival rate during a minimum of 12 weeks follow-up were assessed. RESULTS: Twenty critically ill patients with AAD underwent rescue FMT, and 18 of them were included for analysis. The mean of Acute Physiology and Chronic Health Evaluation (APACHE) II scores at intensive care unit (ICU) admission was 21.7 ± 8.3 (range 11-37). Thirteen patients received FMT through nasojejunal tube, four through gastroscopy, and one through enema. Patients were treated with four (4.2 ± 2.1, range 2-9) types of antibiotics before and during the onset of AAD. 38.9% (7/18) of patients had FMT-related AEs during follow-up, including increased diarrhea frequency, abdominal pain, increased serum amylase, and fever. Eight deaths unrelated to FMT occurred during follow-up. One hundred percent (2/2) of abdominal pain, 86.7% (13/15) of diarrhea, 69.2% (9/13) of abdominal distention, and 50% (1/2) of hematochezia were improved after FMT. 44.4% (8/18) of patients recovered from abdominal symptoms without recurrence and survived for a minimum of 12 weeks after being discharged from ICU. CONCLUSION: In this case series studying the use of FMT in critically ill patients with AAD, good clinical outcomes without infectious complications were observed. These findings could potentially encourage researchers to set up new clinical trials that will provide more insight into the potential benefit and safety of the procedure in the ICU. TRIAL REGISTRATION: ClinicalTrials.gov, Number NCT03895593 . Registered 29 March 2019 (retrospectively registered).

miR-181b-5p suppresses starvation-induced cardiomyocyte autophagy by targeting Hspa5.

This study aimed to investigate the role of microRNA­181b­5p (miR­181b­5p) in starvation­induced cardiomyocyte autophagy by targeting heat shock protein family A member 5 (Hspa5). For this purpose, H9c2 cardiomyocytes and neonatal rat ventricular myocytes (NRVMs) were glucose­starved in Earle's Balanced Salt Solution (EBSS) for different periods of time (0, 2, 4, 6 and 8 h). RT­qPCR analysis was performed to examine the expression of miR­181b­5p in the different groups. Immunofluorescence was performed to detect the expression of LC3. In addition, the H9c2 cardiomyocytes and NRVMs were transfected with miR­181b­5p mimic, miR­181b­5p inhibitor, siHspa5 or their respective controls. An MTT assay was performed to measure cell proliferation in the different groups. Western blot analysis was performed to determine the expression of Beclin­1, Hspa5, phosphorylated phosphoinositide 3­kinase PI3K (p­PI3K), phosphorylated Akt (p­Akt), phosphorylated mammalian target of rapamycin (p­mTOR), Bcl­2, Bax and cleaved caspase­3. Flow cytometry was performed to assess cell apoptosis. A luciferase reporter assay was performed to determine whether Hspa5 is a direct target of miR­181b­5p. The results revealed that the downregulation of miR­181b­5p promoted cell autophagy in the cardiomyocytes. Moreover, miR­181b­5p negatively regulated Beclin­1 and Hspa5. Beclin­1 is a well­known autophagy­ and apoptosis­related protein. In addition, cell apoptosis was attenuated by the decreased expression of miR­181b­5p in the cardiomyocytes. Bcl­2 prevented apoptosis and autophagy by binding to Bax and Bcl­2, respectively. The upregulation of miR­181b­5p inhibited autophagy and promoted apoptosis via Hspa5. miR­181b­5p inhibition promoted p­mTOR, p­Akt and p­PI3K expression via Hspa5. The results of luciferase reporter assay also confirmed that Hspa5 is a direct target of miR­181b­5p. On the whole, the findings of this study suggest that miR­181b­5p contributes to starvation­induced autophagy and apoptosis in cardiomyocytes by directly targeting Hspa5 via the PI3K/Akt/mTOR signaling pathway.

Efficiency and safety of ketamine for pain relief after laparoscopic cholecystectomy: A meta-analysis from randomized controlled trials.

OBJECTIVE: This meta-analysis aims to evaluate the effectiveness of intravenous infusion of ketamine for pain control after laparoscopic cholecystectomy (LC). METHODS: A systematic search was performed in PubMed (1966-2017.08), Medline (1966-2017.08), Embase (1980-2017.08), ScienceDirect (1985-2017.08) and the Cochrane Library. Only randomized controlled trials (RCTs) were included. Meta-analysis was performed using Stata 11.0 software. RESULTS: A total of six RCTs were retrieved involving 294 patients. The present meta-analysis showed that there were significant differences between groups in terms of visual analogue scale scores at 12 h (WMD = -0.478, 95% CI: -0.934 to -0.021, P = 0.040), 24 h (WMD = -0.550, 95% CI: -1.099 to -0.002, P = 0.049), and 48 h (WMD = -0.350, 95% CI: -0.678 to -0.021, P = 0.037) after LC. Significant differences were found regarding opioid consumption at 12 h (WMD = -2.820, 95% CI: -5.170 to -0.470, P = 0.019), 24 h (WMD = -3.816, 95% CI: -7.155 to -0.478, P = 0.025), and 48 h (WMD = -2.210, 95% CI: -4.046 to -0.375, P = 0.018) after LC. CONCLUSION: Intravenous ketamine infusion significantly reduced postoperative pain scores and opioid consumption after LC. In addition, there were fewer adverse effects in the ketamine groups. Higher quality RCTs are still required for further research.

Molecular hydrogen inhalation attenuates postoperative cognitive impairment in rats.

Postoperative cognitive decline is a major clinical problem with high morbidity and mortality after surgery. Many studies have found that molecular hydrogen (H2) has significant neuroprotection against acute and chronic neurological injury by regulating inflammation and apoptosis. In this study, we hypothesized that H2 treatment could ameliorate the development of cognitive impairment following surgery. Adult male rats were subjected to stabilized tibial fracture operation under anesthesia. Two percent of H2 was inhaled for 3 h beginning at 1 h after surgery. Separate cohorts of rats were tested for cognitive function with fear conditioning and the Y-maze test, or euthanized to assess blood-brain barrier integrity, and systemic and hippocampal proinflammatory cytokine and caspase-3 activity. Surgery-challenged animals showed significant cognitive impairment evidenced by a decreased percentage of freezing time and an increased number of learning trials on days 1, 3, and 7 after operation, which were significantly improved by H2 treatment. Furthermore, H2 treatment significantly ameliorated the increase in serum and hippocampal proinflammatory cytokines tumor necrosis factor-α, interleukin-1ß, interleukin-6, and high-mobility group protein 1 in surgery-challenged animals. Moreover, H2 treatment markedly improved blood-brain barrier integrity and reduced caspase-3 activity in the hippocampus of surgery-challenged animals. These findings suggest that H2 treatment could significantly mitigate surgery-induced cognitive impairment by regulating inflammation and apoptosis.