A therapeutic regimen of ceftazidime-avibactam for a critical patient receiving prolonged intermittent renal replacement therapy.

The present report firstly described a critically ill patient receiving a dosing regimen of ceftazidime-avibactam (CAZ-AVI) (1.875g q24h) to eliminate multidrug-resistant Klebsiella pneumoniae and a scheduled time for prolonged intermittent renal replacement therapy (PIRRT) every 48h (6h-session beginning 12h after the previous dosage on hemodialysis day). This dosing regimen for CAZ-AVI and a scheduled time for PIRRT allowed pharmacodynamic parameters of ceftazidime and avibactam to have little difference on hemodialysis and non-hemodialysis days so that we can maintain a relatively stable drug concentration. Our report highlighted not only the importance of dosing regimens in patients with PIRRT but also the significance of hemodialysis time points during the dosing interval. The innovative therapeutic plan proved to be suitable for patients infected with Klebsiella pneumoniae when on PIRRT according to the trough plasma concentrations of ceftazidime and avibactam which were maintained above the minimum inhibitory concentration during the dosing interval.

Utilizing reclassification to explore characteristics and prognosis of KDIGOSCr AKI subgroups: a retrospective analysis of a multicenter prospective cohort study.

BACKGROUND: Acute kidney injury (AKI) is widespread in the intensive care unit (ICU) and affects patient prognosis. According to Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, the absolute and relative increases of serum creatinine (Scr) are classified into the same stage. Whether the prognosis of the two types of patients is similar in the ICU remains unclear. METHODS: According to the absolute and relative increase of Scr, AKI stage 1 and stage 3 patients were divided into stage 1a and 1b, stage 3a and 3b groups, respectively. Their demographics, laboratory results, clinical characteristics, and outcomes were analyzed retrospectively. RESULTS: Of the 345 eligible cases, we analyzed stage 1 because stage 3a group had only one patient. Using 53 or 61.88 µmol/L as the reference Scr (Scrref), no significant differences were observed in ICU mortality (P53=0.076, P61.88=0.070) or renal replacement therapy (RRT) ratio, (P53=0.356, P61.88=0.471) between stage 1a and 1b, but stage 1b had longer ICU length of stay (LOS) than stage 1a (P53<0.001, P61.88=0.032). In the Kaplan-Meier survival analysis, no differences were observed in ICU mortality between stage 1a and 1b (P53=0.378, P61.88=0.255). In a multivariate analysis, respiratory failure [HR = 4.462 (95% CI 1.144-17.401), p = 0.031] and vasoactive drug therapy [HR = 4.023 (95% CI 1.584-10.216), p = 0.003] were found to be independently associated with increased risk of death. CONCLUSION: ICU LOS benefit was more prominent in KDIGOSCr AKI stage 1a patients than in stage 1 b. Further prospective studies with a larger sample size are necessary to confirm the effectiveness of reclassification.

Treatment of traumatic cerebrospinal fluid rhinorrhea via extended extradural anterior skull base approach.

OBJECTIVE: To describe and assess the repair technique and perioperative management for cerebrospinal fluid (CSF) leak resulting from extensive anterior skull base fracture via extradural anterior skull base approach. METHODS: This was a retrospective review conducted at the Department of Neurosurgery of the Shanghai Tenth People's Hospital from January 2015 to April 2020. Patients with traumatic CSF rhinorrhea resulting from extensive anterior skull base fracture treated surgically via extended extradural anterior skull base approach were included in this study. The data of medical and radiological records, surgical approaches, repair techniques, peritoperative management, surgical outcome and postoperative follow-up were analyzed. Surgical repair techniques were tailored to the condition of associated injuries of the scalp, bony and dura injuries and associated intracranial lesions. Patients were followed up for the outcome of CSF leak and surgical complications. Data were presented as frequency and percent. RESULTS: Thirty-five patients were included in this series. The patients' mean age was 33 years (range 11-71 years). Eight patients were treated surgically within 2 weeks; while the other 27 patients, with prolonged or recurrent CSF rhinorrhea, received the repair surgery at 17 days to 10 years after the initial trauma. The mean overall length of follow-up was 23 months (range 3-65 months). All the patients suffered from frontobasal multiple fractures. The basic repair tenet was to achieve watertight seal of the dura. The frontal pericranial flap alone was used in 20 patients, combined with temporalis muscle and/or its facia in 10 patients. Free fascia lata graft was used instead in the rest 5 patients. No CSF leak was found in all the patients at discharge. There was no surgical mortality in this series. Bilateral anosmia was the most common complication. At follow-up, no recurrent CSF leak or meningitis occurred. No patients developed mucoceles, epidural abscess or osteomyelitis. One patient ultimately required ventriculoperitoneal shunt because of progressive hydrocephalus. CONCLUSION: Traumatic CSF rhinorrhea associated with extensive anterior skull base fractures often requires aggressive treatment via extended intracranial extradural approach. Vascularized tissue flaps are ideal grafts for cranial base reconstruction, either alone or in combination with temporalis muscle and its fascia---fascia lata sometimes can be opted as free autologous graft. The approach is usually reserved for patients with traumatic CSF rhinorrhea in complex frontobasal injuries.

The Epidemiology of Sepsis in Chinese ICUs: A National Cross-Sectional Survey.

OBJECTIVES: We performed a national cross-sectional survey to determine the epidemiologic characteristics of patients with sepsis in ICU in China. DESIGN: A cross-section survey study. SETTING: Forty-four hospitals in mainland China from December 1, 2015, to January 31, 2016. PATIENTS: All septic patients diagnosed according sepsis-1 criteria admitted to participating ICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We recorded demographic, physiologic, and microbiological data with follow-up for 90 days or death, if sooner. The frequency of sepsis and 90-day mortality rate were computed, and the relationship with gross domestic product determined. Multivariate logistic regression analysis was used to determine risk factors for 90-day mortality in patients with sepsis. Two-thousand three-hundred twenty-two patients with sepsis were included in the analysis, of whom 786 patients (33.9%) had hospital-acquired sepsis. The most common infection site was the lung (68.2%), followed by abdomen (26.6%) and bloodstream (7.8%). The frequency of sepsis in the ICU was 20.6 cases per 100 ICU admissions (95% CI, 15.8-25.4) with a 90-day mortality of 35.5%. The proportion of sepsis, severe sepsis, and septic shock were 3.10%, 43.6%, and 53.3% with a 90-day mortality of 2.78%, 17.69%, and 51.94%, respectively. Older age, low body weight, higher Sequential Organ Failure Assessment score, the number of systemic inflammatory response syndrome criteria, comorbid with heart failure, hematologic cancer, immunosuppression, higher level of lactate, infection site (pneumonia and bloodstream) were associated with 90-day mortality. CONCLUSIONS: Sepsis affects a fifth of patients admitted to ICUs in mainland China with a 90-day mortality rate of 35.5%. Our findings indicate that a large burden of sepsis, and we need to focus on sepsis as a quality improvement target in China given the high mortality. In addition, further studies are needed to delineate the epidemiology of sepsis outside the ICU.

Gene expression profile of the hippocampus of rats subjected to traumatic brain injury.

Traumatic brain injury (TBI) is a serious public health problem as well as a leading cause of severe posttraumatic disability. Numerous studies indicate that the differentially expressed genes (DEGs) of neural signaling pathways are strongly correlated with brain injury. To further analyze the roles of the DGEs in the central nervous system, here we systematically investigated TBI on the hippocampus and its injury mechanism at the whole genome level. On the basis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes Analyses, we revealed that the DEGs were involved in many signaling pathways related to the nervous system, especially neuronal survival-related pathways. Finally, we verified the microarray results and detected the gene expression of neuronal survival-related genes in the hippocampus by using real-time quantitative polymerase chain reaction. With Western blot and axon growth assay, the expression of P2rx3 was upregulated in rats subjected to TBI, and overexpression of P2rx3 promoted neurite growth of NG108 cells. Our results suggested that the DEGs (especially P2rx3) and several signaling pathways might play a pivotal role in TBI. We also provided several targeted genes related to TBI for future investigation.

Does training improve diagnostic accuracy and inter-rater agreement in applying the Berlin radiographic definition of acute respiratory distress syndrome? A multicenter prospective study.

BACKGROUND: Poor inter-rater reliability in chest radiograph interpretation has been reported in the context of acute respiratory distress syndrome (ARDS), although not for the Berlin definition of ARDS. We sought to examine the effect of training material on the accuracy and consistency of intensivists' chest radiograph interpretations for ARDS diagnosis. METHODS: We conducted a rater agreement study in which 286 intensivists (residents 41.3%, junior attending physicians 35.3%, and senior attending physician 23.4%) independently reviewed the same 12 chest radiographs developed by the ARDS Definition Task Force ("the panel") before and after training. Radiographic diagnoses by the panel were classified into the consistent (n = 4), equivocal (n = 4), and inconsistent (n = 4) categories and were used as a reference. The 1.5-hour training course attended by all 286 intensivists included introduction of the diagnostic rationale, and a subsequent in-depth discussion to reach consensus for all 12 radiographs. RESULTS: Overall diagnostic accuracy, which was defined as the percentage of chest radiographs that were interpreted correctly, improved but remained poor after training (42.0 ± 14.8% before training vs. 55.3 ± 23.4% after training, p < 0.001). Diagnostic sensitivity and specificity improved after training for all diagnostic categories (p < 0.001), with the exception of specificity for the equivocal category (p = 0.883). Diagnostic accuracy was higher for the consistent category than for the inconsistent and equivocal categories (p < 0.001). Comparisons of pre-training and post-training results revealed that inter-rater agreement was poor and did not improve after training, as assessed by overall agreement (0.450 ± 0.406 vs. 0.461 ± 0.575, p = 0.792), Fleiss's kappa (0.133 ± 0.575 vs. 0.178 ± 0.710, p = 0.405), and intraclass correlation coefficient (ICC; 0.219 vs. 0.276, p = 0.470). CONCLUSIONS: The radiographic diagnostic accuracy and inter-rater agreement were poor when the Berlin radiographic definition was used, and were not significantly improved by the training set of chest radiographs developed by the ARDS Definition Task Force. TRIAL REGISTRATION: The study was registered at ClinicalTrials.gov (registration number NCT01704066 ) on 6 October 2012.

[Investigation on the predictive value of the dynamic changes of EVLWI and PVPI on the prognosis of ARDS patients].

OBJECTIVE: To investigate the dynamic changes of extra vascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) on the prognosis of acute respiratory distress syndrome (ARDS), and predict the risk factors affecting prognosis of ARDS. METHODS: 70 patients meeting ARDS Berlin definition, who were admitted to the ICU from July 2012 to July 2014, were analyzed with a prospective method. The patients were divided into a survival group and a death group according to their survival situation in 28 days. EVLWI (EVLWI1-EVLWI4), PVPI (PVPI1-PVPI4), DeltaEVLWI (subtracting EVLWI day 4 from day 1), and DeltaPVPI (subtracting PVPI day 4 from day 1) of the two groups of patients from the 1st day to the 4th day were monitored by the pulse indicator continuous cardiac output (PiCCO). Parameters including the acute physiology and chronic health evaluation (APACHE II) score, sequential organ failure assessment (SOFA) score, EVLWI, PVPI, DeltaEVLWI, DeltaPVPI, oxygenation index (OI), CVP, the number of organ dysfunction were compared between the two groups. Univariate analysis and multivariate logistic regression were used to analyze the independent risk factors associated with prognosis. Receiver operating characteristic curve (ROC curve) was drawn to evaluate the prediction performance of those risk factors in the prognosis of ARDS. RESULTS: Comparison of EVLWI and PVPI between the survival group and the death group of ARDS patients at different time points: EVLWI and PVPI showed no statistical difference from the 1st day to the 2nd day after admission, but those two parameters in the death group were higher than those in the survival group form the 3rd day to the 4th day after admission (P<0.01). The comparison of the dynamic changes of EVLWI and PVPI within the two groups: the EVLWI and PVPI in the survival group declined gradually from 1st day to 4th day after treatment, but that changing trend in the death group showed no statistical difference. DeltaEVLWI and DeltaPVPI changes in the survival group were higher than in the death group (P<0.01). They were independent risk factors of patients 28-day prognosis (P<0.05). ROC curve and 28-day survival curve showed that the area under ROC curve of DeltaPVPI predicting prognosis of patients with ARDS was 0.812, when the optimal cut off value was 1.2, and the median survival period in DeltaPVPI>1.2 group was longer than that in the Delta PVPI≤1.2 group. CONCLUSIONS: The continuous dynamic observation of EVLWI and PVPI changes is better than that of a single detection. DeltaEVLWI and DeltaPVPI are independent risk factors and can be used as an auxiliary indicator for the prognosis of patients with ARDS.

Characteristics of critically ill patients in ICUs in mainland China.

OBJECTIVES: We sought to describe the demographics, case mix, interventions, and clinical outcome of critically ill patients admitted to ICUs in Mainland China. DESIGN: A 2-month (July 1, 2009, to August 31, 2009) prospective, observational cohort study. SETTING: Twenty-two ICUs in Mainland China. PATIENTS: Adult patients admitted to participating ICUs during the study period with an ICU length of stay >24 hrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patient characteristics, including demographics, underlying diseases, severity of illness, admission status, complications, intervention and treatment during ICU stay, and clinical outcome were recorded in case report form. The primary outcome measure was all-cause hospital mortality. Independent predictors for hospital mortality were determined with multivariate logistic regression analysis. One thousand two hundred ninety-seven patients met the inclusion criteria for the study, 821 (63.3%) were male, and mean age was 58.5 ± 19.2 yrs. Mean Acute Physiology and Chronic Health Evaluation II score was 18.0 ± 8.1, and mean Sequential Organ Failure Assessment score was 6.5 ± 3.8. One third of the patients were postoperative ICU admissions. Seven hundred sixty-five patients (59.0%) developed infections, followed by severe sepsis or septic shock (484, 37.3%), acute kidney injury (398, 30.7%), and acute lung injury/acute respiratory distress syndrome (351, 27.1%). Mechanical ventilation was used in almost three fourths of the patients, whereas any type of renal replacement therapy was used in 173 patients (13.3%). Hospital mortality was 20.3%. Multivariate logistic regression analysis found that Acute Physiology and Chronic Health Evaluation II score, solid tumor, severe sepsis/septic shock, acute lung injury/acute respiratory distress syndrome, and acute kidney injury were independent risk factors for hospital mortality. CONCLUSIONS: Critically ill patients in ICUs in Mainland China exhibited a case mix similar to those of Western countries, although there are significant differences in intensive care unit admission rates and disease severity between Western and Chinese ICUs.

[Effects and mechanisms of heme oxygenase-1 on rats with postresuscitation myocardial dysfunction].

OBJECTIVE: To explore the effects and mechanisms of heme oxygenase-1 on rats with postresuscitation myocardial dysfunction. METHODS: Male Sprague-Dawley rats were asphyxiated for 9 minutes and resuscitated. They were randomly divided into 4 groups: sham-operated, cardiopulmonary resuscitation (CPR), hemin and hemin + ZnPP (zinc protoporphyrin IX). Resuscitated groups had 2 observation points: 6 and 24 hours post-CPR (n = 8 for each time point). And the sham-operated group of 12 rats were divided in two observation points, according to 6 or 24 hours post-operation (n = 6 each). Hemodynamic was observed. The expression of heme oxygenase-1 (HO-1) in cardiac tissue was detected by Western blot. And the activity of cardiac homogenate superoxide dismutase (SOD) was determined by xanthine oxidase method and the level of malondialdehyde (MDA) measured by the thiobarbituric acid method. Nitrotyrosine protein expression in cardiac tissue was analyzed by immunohistochemistry. RESULTS: (1) The mean blood pressure (MAP) significantly decreased in resuscitated groups after resuscitation (all P < 0.05). No difference existed between the subgroups. The scores of dP/dt40 and -dP/dt significantly decreased in CPR and hemin + ZnPP groups after resuscitation (all P < 0.05). But dP/dt40 in hemin group did not differ significantly after resuscitation and -dP/dt decreased only 0.5 hour and 1 hour post-resuscitation (3341.60 ± 524.85 and 3711.40 ± 502.39 vs 4284.20 ± 800.87, all P < 0.05). The scores of dP/dt40 and -dP/dt in hemin group at all time points post-resuscitation were significantly higher than those in CPR and hemin + ZnPP groups (all P < 0.05). (2) Compared with the sham-operated group, the HO-1 expression, MDA level and nitrotyrosine protein expression significantly increased while the activities of SOD decreased after resuscitation in the CPR, hemin and hemin + ZnPP groups (all P < 0.05). Compared with the CPR and hemin + ZnPP groups, the expression of HO-1 and the activity of SOD increased, while MDA level and nitrotyrosine protein expression were decreased in group hemin (all P < 0.05). No difference existed in the above indices between the CPR and hemin + ZnPP groups. CONCLUSION: HO-1 can reduce myocardial oxidative stress injury after cardiopulmonary resuscitation and effectively improve post-resuscitation myocardial function in rats.

[Evaluation of accuracy and influence factors of bedside blood glucose monitoring in critically ill patients].

OBJECTIVE: To evaluate the accuracy and influence factors of point-of-care testing (POCT) for glucose in critically ill patients. METHODS: Two hundred and forty critically ill patients aged ≥18 years in department of critical care medicine were enrolled. According to blood glucose level (BGL) during glucose control, patients were divided into three groups: (1) hypoglycemia group, BGL<4.5 mmol/L, n=32; (2) euglycemia group, BGL 4.5-8.3 mmol/L, n=138; (3) hyperglycemia group, BGL>8.3 mmol/L, n=70. The blood samples from vein, artery and capillary of patients were collected synchronically and the blood glucose of POCT were determined with glucose oxidase (GOD) and glucose dehydrogenase (GDH) methods, respectively, compared with blood glucose reference values of laboratory [hexokinase method (HK method)]. The accuracy of POCT for glucose and influence factors were analyzed statistically by the logistic regression method. RESULTS: (1) The inaccurate rates of glucose values in blood samples from vein, artery and capillary in hypoglycemia group (GDH method: 25.00%, 40.62%, 40.62%; GOD method: 59.38%, 71.88%, 71.88%) were significantly higher than those in euglycemia group (GDH method: 2.90%, 9.42%, 7.97%; GOD method: 18.12%, 27.54%, 27.54%) and hyperglycemia group (GDH method: 1.43%, 8.57%, 4.28%; GOD method: 11.43%, 8.57%, 11.43%, all P<0.01). (2) The average levels of difference for the glucose reference value of laboratory and the glucose value measured by glucometer in hypoglycemia group were 0.41-0.69 mmol/L (GDH method) and 0.92-1.18 mmol/L (GOD method), in euglycemia 0.16-0.33 mmol/L and 0.77-0.90 mmol/L, in hyperglycemia group -0.06-0.18 mmol/L and 0.56-0.76 mmol/L, respectively. (3) The correlation coefficients between the laboratory and glucometer in hypoglycemia group were respectively 0.812-0.853 (GDH method) and 0.723-0.816 (GOD method). The correlation coefficients in euglycemia group were 0.862-0.890 and 0.768-0.857. They were elevated to 0.922-0.957 and 0.896-0.922 in hyperglycemia group (all P<0.01). (4)On the influence factors of accuracy in POCT for glucose, BGL, acute physiology and chronic health evaluation II (APACHEII) score and hematocrit level were into the logistic regression equation. CONCLUSIONS: The accuracy of POCT for glucose was markedly affected by the BGL, severity of patients and hematocrit level during glucose control. Under hypoglycemia, the agreement between laboratory and glucometer measurements was obviously fallen and it tended to overestimate the patient's real glucose value.

Mechanism of lncRNA SNHG16 in oxidative stress and inflammation in oxygen-glucose deprivation and reoxygenation-induced SK-N-SH cells.

Cerebral ischemia-reperfusion injury imposes a clinical challenge for physicians in the wake of ischemic stroke. Meanwhile, recent evidence has come to light eliciting the neuroprotective function of SNHG16 in cerebrovascular diseases. Accordingly, the current study sought to analyze the regulatory mechanism of long non-coding RNA small nucleolar RNA host gene16 (SNHG16) in oxidative stress (OS) injury and cell inflammation. Firstly, models of oxygen-glucose deprivation and reoxygenation (OGD/R) were established in SK-N-SH cells. Cell proliferation and apoptosis were appraised using cell counting kit-8 and flow cytometry. Additionally, SNHG16, X-linked inhibitor of apoptosis protein (XIAP), microRNA (miR-421), reactive oxygen species (ROS), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor -α, interleukin (IL)-1ß, and IL-10 expression patterns were determined. In addition, we determined and validated the subcellular localization of SNHG16 and the binding relationships between SNHG16 and miR-421, and miR-421 and XIAP. It was found that SNHG16 was poorly-expressed in OGD/R-treated cells. On the other hand, SNHG16 over-expression enhanced cell proliferation, inhibited apoptosis, and alleviated OS and cell inflammation. Furthermore, SNHG16 bound to miR-421 to facilitate the expression of XIAP. Up-regulation of miR-421 or down-regulation of XIAP could reverse the suppressive effects of SNHG16 on OS and cell inflammation. Collectively, our findings indicated that SNHG16 bound to miR-421 to facilitate XIAP expression, thus alleviating OS injury and inflammation in OGD/R-induced SK-N-SH cells.

[Value of serum amyloid protein dynamic changes on evaluating condition and prognosis of patients with viral and mycoplasma community-acquired pneumonia].

OBJECTIVE: To investigate the predictive role of dynamic changes of plasma biomarkers in patients with viral and mycoplasma community-acquired pneumonia (CAP). METHODS: From January 2020 to June 2020, 141 patients with viral and mycoplasma CAP in People's Hospital of Ningxia Hui Autonomous Region were enrolled. Pneumonia severity index (PSI) scores [grade I-II (PSI score ≤ 70), grade III (PSI score 71-90) and grade IV-V (PSI score ≥ 91)], serum amyloid A (SAA), hypersensitive C-reactive protein (hs-CRP), procalcitonin (PCT), erythrocyte sedimentation rate (ESR) and white blood cell (WBC) on the 1 day after admission were compared between the different pathogens (viral and mycoplasma) or different disease severity. The change in level of SAA, hs-CRP on the third day (Δ3 d = 1 d-3 d) were compared among different disease outcome groups (patients were divided into improved group, stable group and exacerbation group based on PSI scores or lung CT images on the third day). The change in the level of SAA, hs-CRP on the seventh day (Δ7 d = 1 d-7 d) were compared among different disease prognosis groups (patients were divided into survival group and death group based on 28-day survival data). The receiver operating characteristic curve (ROC) were drawn to evaluate the value of SAA in the evaluation of disease and prediction prognosis. RESULTS: The level of SAA in mycoplasma group (43 cases) was significantly higher than that in virus group (98 cases) on the 1 day after admission. There were no significant differences in other plasma biomarkers between the two groups. The more severe the illness, the higher the SAA level on the 1 day after admission. The trends of other plasma biomarkers in the two groups were consistent with SAA. The levels of SAA in the patients with exacerbation of the virus group and mycoplasma group (12 cases, 9 cases) were significantly higher than those of the improved group (57 cases, 26 cases) and the stable group (29 cases, 8 cases). SAA increased gradually in the exacerbation group, decreased gradually in the improved group, and slightly increased in the stable group. ΔSAA3 d were differences among three groups. The change trend of hs-CPR was consistent with SAA. The level of SAA in the death group was higher than that in the survival group on the seventh day. SAA increased in the death group and decreased in survival group with time from hospital admission. There were differences according to ΔSAA7 d between death group and survival group. The change trend of hs-CPR was consistent with SAA. ROC curve showed that the value of SAA was better than hs-CRP in assessing the severity of patients on admission day, and the area under ROC curve (AUC) was respectively 0.777 [95% confidence interval (95%CI) was 0.669-0.886], 0.729 (95%CI was 0.628-0.830). The value of ΔSAA3 d was better than SAA on the third day predicting disease trends, and AUC was respectively 0.979 (95%CI was 0.921-1.000), 0.850 (95%CI was 0.660-1.000). hs-CRP on the third day and Δhs-CRP3 d had no predictive value. Both SAA on the seventh day and ΔSAA7 d have predictive value for prognosis. AUC was respectively 0.954 (95%CI was 0.898-0.993) and 0.890 (95%CI was 0.689-1.000). SAA on the seventh day and ΔSAA7 d were better than hs-CRP on the seventh day. Δhs-CRP7 d have no predictive value. CONCLUSIONS: SAA is a sensitive and valuable indicator for CAP patients with viruses and mycoplasma. Dynamic monitoring of SAA can evaluate the patient's progression, prognosis, and assist diagnosis and treatment.

Knowledge and attitudes of healthcare workers in Chinese intensive care units regarding 2009 H1N1 influenza pandemic.

BACKGROUND: To describe the knowledge and attitudes of critical care clinicians during the 2009 H1N1 influenza pandemic. METHODS: A survey conducted in 21 intensive care units in 17 provinces in China. RESULTS: Out of 733 questionnaires distributed, 695 were completed. Three hundred and fifty-six respondents (51.2%) reported their experience of caring for H1N1 patients. Despite the fact that 88.5% of all respondents ultimately finished an H1N1 training program, only 41.9% admitted that they had the knowledge of 2009 H1N1 influenza. A total of 572 respondents (82.3%) expressed willingness to care for H1N1 patients. Independent variables associated with increasing likelihood to care for patients in the logistic regression analysis were physicians or nurses rather than other professionals (odds ratio 4.056 and 3.235, p = 0.002 and 0.007, respectively), knowledge training prior to patient care (odds ratio 1.531, p = 0.044), and the confidence to know how to protect themselves and their patients (odds ratio 2.109, p = 0.001). CONCLUSION: Critical care clinicians reported poor knowledge of H1N1 influenza, even though most finished a relevant knowledge training program. Implementation of appropriate education program might improve compliance to infection control measures, and willingness to work in a pandemic.

[An investigation of the relationship of inflammatory response and insulin and its components during stress hyperglycemia in critically ill patients].

OBJECTIVE: To observe the relationship between inflammatory response and the constituents of islet ß cell secretion during stress hyperglycemia (SHG) in critically ill patients, in order to study the impact of inflammatory response on insulin resistance and the secretion function of islet ß cells. METHODS: According to the state of inflammatory response, 45 critical patients with SHG were divided into two groups: stress and the convalescence period. Twenty five healthy individuals were enrolled as control group. The blood levels of tumour necrosis factor ß (TNF-ß), blood glucose (BG), and insulin components including proinsulin (PI), immunoreactive insulin (IRI), true insulin (TI), C-peptide (C-P) were measured respectively. The levels of BG, TNF-ß, insulin components, insulin resistance index (HOMA-IR) and the secretion index (HOMA-ß) were compared among groups. The relationship between TNF-ß and BG, insulin components, HOMA-IR, HOMA-ß were analyzed. RESULTS: (1)There was no difference in concentrations of TI among stress period, convalescence stage and control group [3.68 (1.57, 7.70), 3.42 (2.41, 7.40), 1.46 (0.35, 4.90) mU/L, all P >0.05], whereas the concentration of BG [(10.04 ± 2.43) mmol/L], TNF-ß [13.70 (11.77, 20.00) ng/L], PI [6.20 (3.22, 9.27) pmol/L], IRI [13.45 (9.88, 19.88) mU/L] and C-P [3.01 (2.37, 4.00) µg/L]in stress period were significantly higher than those in the convalescence stage[BG: (6.09 ± 0.84) mmol/L, TNF-ß: 11.58 (8.80, 13.22) ng/L,PI: 1.54 (0.36, 11.82) pmol/L, IRI: 10.80 (5.35, 12.60) mU/L, C-P: 2.42 (1.17, 3.56) µg/L] and control group [BG: (4.87 ± 0.56) mmol/L,TNF-ß: 9.27 (7.48, 12.16) ng/L, PI: 2.20 (1.88, 4.54) pmol/L, IRI: 5.50 (4.00, 8.00) mU/L, C-P: 1.15 (0.87, 1.76) µg/L, P <0.05 or P <0.01]. (2)The HOMA-IR [5.17 (3.41, 11.51)] in stress period was significantly higher than that in the convalescence[3.24 (1.51, 6.95)] and control group [1.14 (0.81, 1.79), P <0.05 and P<0.01]. The HOMA-ß [10.80 (3.72, 31.40)] of isletß cell in stress period was significantly lower than that in the convalescence [28.42 (6.46, 125.01)] and control group [21.94 (7.77, 62.01), P <0.01 and P <0.05]. (3)There were positive correlations between the concentration of TNF-ß and PI, IRI, C-P and HOMA-IR ( r 1=0.292, r 2=0.344, r 3=0.397, r 4=0.324, P <0.05 or P <0.01). There were negative correlation between concentration of TNF-ß and HOMA-ß ( r =-0.235 , P <0.05) . CONCLUSION: The severer the inflammatory response, the higher PI, IRI and C-P, while the secretion of TI is relatively deficient.Inflammatory response could affect insulin resistance and the secretion function of islet ßcell during SHG in critically ill patients.

CHRFAM7A Overexpression Attenuates Cerebral Ischemia-Reperfusion Injury via Inhibiting Microglia Pyroptosis Mediated by the NLRP3/Caspase-1 pathway.

Cerebral ischemia-reperfusion (I/R) injury is an inflammation-related disease. CHRFAM7A can regulate inflammatory responses. Therefore, the present study investigated the mechanism of CHRFAM7A in cerebral I/R injury. CHRFAM7A expression and inflammatory cytokine levels in patients with cerebral I/R injury and oxygen-glucose deprivation/reperfusion (OGD/R)-treated microglia were detected. The proliferation, inflammatory cytokine expressions, nod-like receptor protein 3 (NLRP3) level, cell pyroptosis, and viability and lactate dehydrogenase (LDH) activity in OGD/R-treated microglia were detected after CHRFAM7A overexpression. The NLRP3/Caspase-1 pathway was activated to assess the effect of CHRFAM7A on microglia. Expressions of microglial M1 phenotype marker iNOS and M2 marker Arg1 were detected. Downregulated CHRFAM7A and elevated inflammatory cytokine levels were observed in patients with cerebral I/R injury and OGD/R-treated microglia. In OGD/R-treated microglia, CHRFAM7A overexpression promoted cell proliferation and viability, reduced inflammation and LDH activity, and inhibited NLRP3 inflammasome activation and cell pyroptosis. Mechanically, CHRFAM7A inhibited microglia pyroptosis via inhibiting the NLRP3/Caspase-1 pathway and reduced cell inflammatory injury via promoting microglia polarization from M1 to M2. Overall, CHRFAM7A overexpression attenuated cerebral I/R injury by inhibiting microglia pyroptosis in a NLRP3/Caspase-1 pathway-dependent manner and promoting microglia polarization to M2 phenotype.

[Comparison of computer-driven weaning and physician-directed weaning from mechanical ventilation: a randomized prospective study].

OBJECTIVE: To evaluate if the computer-driven weaning (CDW) with a closed-loop knowledge-based system introduced in a ventilator is superior to physician-directed weaning (PDW) in difficult-to-wean patients in the intensive care unit (ICU). METHODS: Sixty-two difficult-to-wean patients were randomized into 2 groups: weaning with Smart Care/PS (SC group, n = 32) or with synchronize intermittent mandatory ventilation add positive support ventilation (SP group, n = 30). In the SC group, the automated system titrated pressure support, conducted a spontaneous breathing trial and provided notification of success (separation potential). In the SP group, weaning from ventilators was carried out by gradually decreasing respiratory support. The length of mechanical ventilation and stay in ICU, the rate of ventilator-associated pneumonia (VAP), the retubing rate in 48 h, manual ventilator setting changes before extubation were compared between the 2 groups. RESULTS: In the SC group, the weaning time was (49 +/- 13) h, (67 +/- 37) h, and (254 +/- 96) h, respectively in patients with neuromuscular diseases, for post-operative respiratory support and patients with respiratory diseases; while in the SP group, the weaning time was (223 +/- 38) h, (106 +/- 34) h and (502 +/- 91) h, respectively; the difference between the 2 groups being statistically significant (chi(2) = 8.33, 4.77, 4.43, all P < 0.05). The time of stay in ICU was (9.0 +/- 1.7) d and (7.3 +/- 1.9) d in the SC group for patients with neuromuscular diseases and patients with post-operative respiratory support, respectively, while that was (20.8 +/- 5.1) d and (14.6 +/- 1.7) d in the SP group, respectively. Time of stay in ICU was significantly shorter in the SC group (chi2 = 6.74, 7.68, both P < 0.05). The number of manual ventilator setting changes was (5 +/- 1) times in the SC group, significantly less than that of the SP group (13 +/- 3, t = 2.73, P < 0.05). There were no significant differences between the SC and the SP groups in the rate of re-intubation, the rate of tracheotomy, the incidence of pneumothorax, the incidence of VAP and the incidence of subcutaneous emphysema. CONCLUSION: The CDW method used in patients with difficult weaning from ventilators was shown to shorten the weaning time, reduce stay in ICU, and decrease the need for manual adjustment of ventilators.

Subarachnoid Osteoma of the Right Frontal Lobe.

BACKGROUND: Intracranial osteoma arising from nonosseous tissue and surrounded by brain parenchyma is extremely rare. We report an intracranial osteoma surgical case with no heterotopic ossification. CASE DESCRIPTION: A 32-year-old woman presented with headache, vertigo, and weakness. Preoperative neuroimaging revealed a spherelike, calcified intracranial lesion in the right frontal region. The bone-hard mass was completely removed by right frontal craniotomy; adhesion and invasion of the skull inner plate and dura were not found. The subarachnoid lesion was surrounded by right middle frontal gyrus, and the blood supply was from branches of pia mater. Postoperative histologic examination suggested an extensive intracranial ossification. At 6-month follow-up, the patient demonstrated a good recovery without any neurological deficits and no recurrence. CONCLUSIONS: In this rare surgical case of subarachnoid osteoma, comprehensive preoperative neuroradiologic examinations, accurate surgical management of adjacent brain tissue, and vessel protection were the cornerstones of successful resection.

Postoperative antibiotic management strategy for febrile patient with posterior cranial fossa tumor resection: Retrospective clinical study.

OBJECTIVE: Postoperative fever (POF), associated with posterior cranial fossa (PCF) surgery, occurs commonly and is a potential intracranial infection indicator of perioperative antibiotics prolongation and advancement. The existing prophylactic approaches to balancing the risk between intracranial infection and antibiotics abuse are debatable. METHODS: We retrospectively assessed 100 patients subjected to PCF tumor resection between December 2015 and December 2018 at a single institution. Forty febrile patients were selected for further analysis. Of them, 16 received basic and 24 advanced antibiotics and were subjected to prophylactic antibiotic assessment. RESULTS: The total POF rate of PCF tumor resection was 49.4%. POF occurred from day 1 to day 5, along with the abnormalities of cerebrospinal fluid (CSF) profiles and the mild meningeal irritation symptom. CSF cultures of all selected patients were negative. In the comparison between the basic and advanced antibiotic therapy, we found no statistically significant differences in the results of the average and dynamic analysis of the body temperature and CSF profiles. Negative results of outcome studies were also obtained in the duration of fever, duration of hospitalization, and total hospitalization expenses. However, the expenses were substantially increased in the advanced antibiotic treatment. CONCLUSIONS: Although POF is a common symptom after PCF tumor resection, definite intracranial infection is rare. A high body temperature and significant abnormal CSF profiles at an early stage may not be a specific and sufficient indicator of intracranial infection to upgrade antibiotics therapy when standard prophylactic protocols have been accurately achieved.

Dexmedetomidine alleviates doxorubicin cardiotoxicity by inhibiting mitochondrial reactive oxygen species generation.

Cardiotoxicity largely limits the application of doxorubicin (Dox) for cancer treatment. Dexmedetomidine (Dex), a selective agonist of α2-adrenergic receptor, has been suggested to exert cardioprotection against myocardial injury. However, the effect and underlying mechanisms of Dex on Dox cardiotoxicity remain unknown. In this study, C57BL/6 mice were treated with Dox followed by Dex administration. Cardiomyocytes were co-incubated with Dox and Dex in vitro. The results showed that Dex markedly attenuated cardiac dysfunction induced by Dox. TUNEL staining exhibited that Dex inhibited Dox-induced cardiomyocyte apoptosis in myocardium. Moreover, the expression of anti-apoptotic protein Bcl-2 was increased, whereas the expression of pro-apoptotic protein Bax was decreased by Dex. Dox-induced the increase of reactive oxygen species (ROS), superoxide anion, and mitochondrial ROS (mROS) generation in myocardial tissues were significantly inhibited after Dex administration. In in vitro study, it was further confirmed that Dex prevented Dox-induced cardiomyocyte apoptosis and injury. However, the stimulation of mROS generation reversed the effect of Dex in cardiomyocytes. Mechanically, Dex blocked Dox-induced the ubiquitination of peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α), leading to the restoration of PGC-1α and downstream oxidative stress-protective molecules uncoupling protein 2 and manganese-dependent superoxide dismutase expression. Taken together, this study demonstrates that Dex exerts cardioprotection against Dox cardiotoxicity by attenuating mitochondrial dysfunction, oxidative stress, and cardiomyocyte apoptosis via inhibiting PGC-1α-signaling pathway inactivation. This suggests that Dex may be a potential therapeutic strategy for Dox cardiotoxicity treatment.

Neuropathic pain releasing calcitonin gene related peptide protects against stroke in rats.

Neuropathic pain (NPP) is deemed as a potential risk of stroke; however, recent pieces of evidence showed that calcitonin gene-related peptide is involving in pain progression as well as organ protection. The mechanisms underlying the neuroprotection of calcitonin gene-related peptide are yet poorly described with respect to stroke. The present study showed that the elevated level of calcitonin gene-related peptide-induced by NPP exerts a protective effect against stroke in rats, which was further confirmed in vivo and vitro via mitigation of inflammatory response, inhibition of neuronal cell apoptosis, and increase in regional cerebral blood flow. Repetitive transcranial magnetic stimulation at trigeminal ganglion was performed to simulate to facilitate the release of calcitonin gene-related peptide for a similar neuroprotective effect. Together, these findings posit that the release of calcitonin gene-related peptide-induced by NPP or repetitive transcranial magnetic stimulation protects against stroke in rats. Thus, repetitive transcranial magnetic stimulation could have high application prospects for the prevention and treatment of stroke.