Delayed onset of fat embolus in the cerebral venous system after breast and hip augmentation: a case report.

BACKGROUND: Cerebral fat embolism (CFE) is a subtype of fat embolism syndrome which tends to cause ischemic cerebral infarction. Fat embolism in the cerebral venous system have not been reported. We hereby present a rare case of fat embolus formed in the cerebral venous system 10 days after cosmetic surgery, and describe our management of this patient. CASE PRESENTATION: A 26-year-old woman with the disturbance of consciousness and recurrent convulsions of the right upper extremity over a 21-h period was admitted to our hospital. The patient was initially diagnosed with haemorrhagic infarction, and cerebral venous thrombosis (CVT) was suspected based on computed tomography (CT). A diagnosis of CFE was confirmed based on surgical findings. Breast and hip augmentation performed 10 days ago was considered the underlying cause. Drug-induced hypothermia, low molecular weight heparin, atorvastatin, dexamethasone, piperacillin/tazobactam, valproic acid, and mannitol were applied. On hospital day 30, she was discharged with a Montreal Cognitive Assessment score of 25. CONCLUSIONS: Fat embolism can occur in the cerebral venous system, and may mimic CVT symptoms rather than CFE symptoms. Early identification of the nature of the embolus is essential. The use of heparin may prevent secondary thrombus formation, and accelerate fat embolus decomposition.

The predictive value of RDW in AKI and mortality in patients with traumatic brain injury.

BACKGROUND: Red blood cell distribution width (RDW) has been validated valuable in predicting outcome and acute kidney injury (AKI) in several clinical settings. The aim of this study was to explore whether RDW is associated with outcome and AKI in patients with traumatic brain injury (TBI). METHODS: Patients admitted to our hospital for TBI from January 2015 to August 2018 were included in this study. Multivariate logistic regression analysis was performed to identify risk factors of AKI and outcome in patients with TBI. The value of RDW in predicting AKI and outcome was evaluated by receiver operating characteristic (ROC) curve. RESULTS: Three hundred and eighteen patients were included in this study. The median of RDW was 14.25%. We divided subjects into two groups based on the median and compared difference of variables between two groups. The incidence of AKI and mortality was higher in high RDW (RDW > 14.25) group (31.45% vs 9.43%, P < .001; 69.81% vs 29.56%, P < .001). Spearman's method showed RDW was moderately associated with 90-day Glasgow Outcome Scale (GOS) (P < .001). In multivariate logistic regression analysis, RDW, lymphocyte, chlorine, and serum creatinine were risk factors of AKI. And Glasgow Coma Scale (GCS), glucose, chlorine, AKI, and RDW were risk factors of mortality. The area under the ROC curve (AUC) of RDW for predicting AKI and mortality was 0.724 (0.662-0.786) and 0.754 (0.701-0.807), respectively. Patients with higher RDW were likely to have shorter median survival time (58 vs 70, P < .001). CONCLUSIONS: Red blood cell distribution width is an independent risk factor of AKI and mortality in patients with TBI.

Encapsulating N­doped graphite carbon in MoO2 as a novel cocatalyst for boosting photocatalytic hydrogen evolution.

Generally, it is important to ameliorate the co-catalyst used in photocatalytic hydrogen evolution reactions (PHERs) to achieve efficient transfer and separation of photogenerated carriers, decrease the surface reaction energy barrier, and hence improve the photocatalytic activity. In this study, N-doped graphite carbon (GC) was introduced in situ to MoO2 to ensure the presence of well-dispersed active sites, lower the overpotential of hydrogen evolution, and further achieve high conductivity. Then, the MoO2/GC composite obtained was used as a co-catalyst of ZnIn2S4 (ZIS) in a PHER, resulting in a great improvement in the photocatalytic activity. Given the metallicity and large work function of MoO2/GC, a Schottky interface can form between MoO2/GC and ZIS, which accelerates the transmission of photogenerated electrons. As a result, the separation efficiency of photogenerated carriers improves, whereas the surface overpotential of PHERs clearly decreases for ZIS. This study proposes a new idea for exploiting efficient co-catalysts and promotes the wide and heavy use of carbon materials in the field of solar energy conversion.

The Predictive Value of Serum Uric Acid on Acute Kidney Injury following Traumatic Brain Injury.

BACKGROUNDS: Acute kidney injury (AKI) is a prevalent nonneurological complication in patients with traumatic brain injury (TBI). We designed this study to explore the association between serum uric acid (SUA) level and the occurrence of AKI following TBI. METHODS: This is a retrospective single-center study. A total of 479 patients admitted with TBI were included in this study. We utilized SUA and other risk factors for AKI to construct a predictive model by performing multivariate logistic regression. 374 patients and 105 patients were, respectively, divided into a training set and validation set. The predictive value of the single SUA and constructed model was evaluated by drawing a receiver operating characteristic (ROC) curve. AKI was diagnosed according to the KIDGO criteria. RESULTS: 79 (21.12%) patients were diagnosed with AKI in the training cohort. The patients in the AKI group are older than those in the non-AKI group (p = 0.01). And the Glasgow Coma Scale (GCS) of the AKI group was lower than that of the non-AKI group (p < 0.001). In a multivariate logistic regression analysis, we found that heart rate (p = 0.041), shock (p = 0.018), serum creatinine (p < 0.001), and serum uric acid (SUA) (p < 0.001) were significant risk factors for AKI. Bivariate correlation analyses showed that serum creatinine was moderately positively correlated with SUA (r = 0.523, p < 0.001). Finally, the area under the receiver operating characteristic curve (AUC) of SUA for predicting AKI in the training set and validation set was 0.850 (0.805-0.895) and 0.869 (0.801-0.938), respectively. CONCLUSIONS: SUA is an effective risk factor for AKI following TBI. Combining SUA with serum creatinine could more accurately identify TBI patients with high risk of developing AKI.

Serum Procalcitonin Level Predicts Acute Kidney Injury After Traumatic Brain Injury.

BACKGROUND: A common non-neurologic complication after traumatic brain injury (TBI), acute kidney injury (AKI) is a risk factor of mortality. Some studies confirmed the predictive value of procalcitonin (PCT) on AKI in several clinical settings. We designed this study to explore the predictive value of PCT on AKI after TBI. METHODS: We retrospectively enrolled patients with TBI admitted to our hospital from February 2015 to June 2019. Multivariate logistic regression analysis was performed to find the risk factors of AKI and construct a predictive model for AKI. Receiver operating characteristics curves were drawn to compare the predictive value of PCT and the constructed model. RESULTS: A total of 214 patients were included in this study. The incidence of AKI after TBI was 25.70% in this study. Compared with the non-AKI group, the AKI group had higher age (P = 0.031), lower Glasgow Coma Scale (P < 0.001), and higher incidence of coagulopathy (P < 0.001) and shock (P < 0.001). Moreover, patients complicated with AKI had higher in-hospital mortality (P < 0.001) and worse 90-day outcome (P < 0.001). Multivariate logistic regression analysis indicated that age (P = 0.033), PCT (P = 0.002), serum chlorine (P = 0.011), and creatinine (P < 0.001) were independent risk factors of AKI. We constructed a predictive model using these 4 risk factors. The area under receiver operating characteristics curves of the predictive model was 0.928, which was significantly higher than that of a single PCT value (area under receiver operating characteristics curves = 0.833) (Z = 2.395, P < 0.05). CONCLUSIONS: PCT is valuable in predicting AKI after TBI. To avoid AKI after TBI, physicians can adjust treatment strategies according to the level of PCT.

[Characteristics and treatment of multiple organ dysfunction syndrome in patients with trauma in the Wenchuan earthquake on 12th May, 2008].

OBJECTIVE: To analyze the characteristics and treatment of the multiple organ dysfunction syndrome (MODS) in patients in the Wenchuan earthquake on 12th May, 2008, in order to provide theoretical reference for future care for such patients. METHODS: Characteristics of MODS in these patients were analyzed, differences between survivors and non-survivors were compared, and therapeutic measures, and the time of the treatment for MODS in patients with earthquake related injury or illness who were admitted to West China Hospital from 12th May to 20th June, 2008, were retrospectively analyzed. RESULTS: A total of 42 MODS patients were admitted to intensive care unit (ICU). Both the acute physiology and chronic health evaluation II (APACHE II) score and predicted death risk were lowering during the course of therapy. Fractures of bones of extremities were predominant in the earthquake related diseases, with an incidence of 45.2%. The actual mortality of MODS (33.3%) was lower than the predicted death risk (41.5%). The age, the time of receiving the first treatment in ICU after the earthquake, the Glasgow score, the oxygen index, blood creatinine level, platelet count, and vasoactive agent pumping velocity were significantly different between survivors and non-survivors (all P<0.05). The overall mortality was 9.8%, the morbidity of cardiac dysfunction, the incidence of acute renal failure (ARF) and sepsis were significantly different between non-survivors and survivors (all P<0.05). The use of mechanical ventilation, continuous renal replacement therapy (CRRT), and vasoactive agent reached peak level on the 14-29 days after the earthquake. CONCLUSION: Fracture of bones of extremities are predominant injury in the earthquake related diseases, and the cause of death is closely associated with multiple trauma and ARF, systemic infection of large wound surfaces. The central nervous system, respiratory system, circulatory system, renal function, circulatory system should be monitored during the treatment. Adequate preparedness is essential in order to cope with the peak period of occurrence of serious complications after a disaster.

The prognostic value of COX-2 expression on circulating tumor cells in nasopharyngeal carcinoma: A prospective analysis.

BACKGROUND AND PURPOSE: The prognostic significance of circulating tumor cells (CTCs) in head and neck cancer is still under debate, as only a few studies have been reported and limited conclusions are reached. Besides, CTCs' count alone was utilized as an indicator in the previous researches. As a form of 'liquid biopsy', the further identification of genetic or phenotypic biomarkers on CTCs could possibly provide further clinical significance. MATERIALS AND METHODS: The prospective study enrolled 131 patients with nasopharyngeal carcinoma (NPC). CTCs were isolated at baseline and at the end of concurrent chemoradiotherapy, and cyclooxygenase-2 (COX-2) expression status of CTCs was detected by RNA-in situ hybridization (ISH) method. Results were correlated with patient's clinicopathological parameters and treatment outcomes. Univariate and multivariate survival analyses were performed to determine the prognostic significance. RESULTS: COX-2 expression was found in 87/131 (66.4%) patients at baseline and 53/115 (46.1%) patients at the end of concurrent chemoradiotherapy. Patients with post-therapeutic COX-2 expression had significantly poorer treatment response (P = 0.011) and higher risk of tumor relapse (P = 0.026) and metastasis (P = 0.007). Besides, multivariate analysis revealed that post-therapeutic COX-2 expression on CTCs remained an independent prognostic indicator for poorer progression-free survival (HR 2.17, P = 0.019) and overall survival (HR 2.41, P = 0.024). CONCLUSION: The study demonstrated that post-therapeutic COX-2 expression on CTCs was a novel and promising prognostic indicator for NPC patients. Future studies are needed to validate our findings and further clarify the value of integrating the indicator with current clinical strategies in improving survival of NPC patients.

The efficacy of intensity modulated radiation therapy in treating thyroid-associated ophthalmopathy and predictive factors for treatment response.

The study evaluated clinical efficacy of intensity modulated radiation therapy (IMRT) in treating patients with thyroid-associated ophthalmopathy (TAO) and defined predictive factors that associated with treatment response. A total of 178 TAO patients were treated with retro-orbital IMRT with radiation dose of 20 Gy in 10 fractions. The immediate and long-term treatment response and complications were evaluated. Besides, logistic-regression analysis was conducted to identify possible predictive factors. TAO symptom score significantly fell from the initiation to 6-month post-treatment (P < 0.001). 134 patients (73.2%) had mild to significant response to IMRT, and 172 patients (96.6%) achieved stabilization of TAO without future progression. Current smoker (OR 2.88, 95% CI 1.32-6.29; P = 0.008) and symptom duration longer than 18 months (OR 3.33, 95% CI 1.24-8.93; P = 0.017) were identified as independent predictive factors for non-response of TAO to retro-orbital IMRT. Immediate complications were slight and self-limited, and long-term complications mainly included chronic xerophthalmias in12 patients (6.74%) and cataract formation in 4 patients (2.25%). The study suggested that IMRT was a viable option for treating TAO patients, with a satisfactory symptom control ability and acceptable post-treatment complications.

Encephalitis with antibodies against the GABAB receptor: seizures as the most common presentation at admission.

OBJECTIVE: Autoimmune encephalitis associated with antibodies against gamma-aminobutyric-acid B receptor (GABABR) has not been described in detail in Chinese patients. METHODS: Patients with anti-GABABR encephalitis treated between January 2013 and December 2015 were analyzed in terms of clinical characteristics, laboratory findings, tumor presence, autoantibody patterns, treatment response and outcomes. RESULTS: Eleven patients were identified (male, N = 8; female, N = 3), with the median age of 51 years. All patients presented with seizures (N = 11; 100%), and they were given anti-epileptic drugs and first-line immunotherapy to address the disease. Seizures always accompanied by limbic manifestations (N = 10; 90.9%). Extralimbic manifestations were present in 4 patients (N = 4; 36.4%). MRI Brain abnormality with increased medio-temporal lobe T2/FLAIR signal were present in 2 patients (N = 2; 18.2%), and epileptiform epileptiform activity on electroencephalography were observed in 2 patients (N = 2; 18.2%). Small-cell lung cancer was histologically confirmed in 3 patients (N = 3; 27.3%). Seven patients showed good outcomes (mRS 1-2; N = 7; 63.6%), one patient showed poor neurological status with minimal changes (mRS 4; N = 1; 9.1%), and three patients died during follow-up (mRS = 6; N = 3; 27.3%). Outcomes were correlated with age-of-onset, and were worse among older patients (P = 0.0112). CONCLUSION: Anti-GABABR encephalitis is a potentially treatable disorder involving seizures as the most predominant presentation at admission. It should be considered as a possible diagnosis in middle-aged and older patients with refractory new-onset epilepsy.

[Correlation between intravascular coagulation/fibrinolysis system and cytokines].

Bacterial factors stimulate the release of tissue factor as well as proinflammatory and antiinflammatory cytokines. TNF augments inflammation, TNF and IFN-gamma induce coagulation, and IL-1beta induces coagulation and fibrinolysis. IL-8 augments synergistic inflammation and coagulation. IL-6 augments coagulation and inhibits fibrinolysis. IL-10 inhibits inflammatory process and inhibits fibrinolysis. IL-4, IL-13, and TGF-beta act for anticoagulation. Administration of IL-2, G-CSF or IFN-gamma has been reported to have side effect of induction of coagulation. IL-12 induces coagulation first and fibrinolysis later. On the other, tissue factor induces proinflammatory (except TNF) and antiinflammatory cytokines, and thrombin enhances inflammation. Patients who died of SIRS/sepsis have been complicated with hypercoagulopathy and impaired fibrinolysis correlated with increased IL-10 production. Inhibition of IL-10 production or administration of fiblynolitic agents may be useful. Recently, activated protein C (APC) which has antiinflammatory effect has been paid attention in the treatment of SIRS/sepsis.

The effects of arginine and selective inducible nitric oxide synthase inhibitor on pathophysiology of sepsis in a CLP model.

BACKGROUND: Sepsis is an arginine-deficient state and is associated with overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS). It has been indicated that low plasma levels of arginine are related to high mortality rates in sepsis. Arginine, however, is also known to be a precursor of NO. Therefore, administration of arginine in septic patients remains controversial. We examined the effects of co-administration of arginine and aminoguanidine, a selective iNOS inhibitor, on sepsis, using rat models. METHOD: Sepsis was induced in rats by cecal ligation and puncture (CLP). Effects of separate and combined administration of arginine and aminoguanidine were investigated by comparing plasma levels of arginine, expressions of heme oxygenase (HO)-1 and HO-2 in liver and lung, and nitrite + nitrate (NOx) excretion in urine, as well as neuroendocrine responses in urine in the early phase of sepsis. Seven-day survival rates were also examined. RESULTS: A combination of arginine and aminoguanidine recovered the plasma level of arginine at 6 h post-CLP, decreased expression of HO-1 in liver and lung at 24 h post-CLP, decreased urinary excretion of epinephrine, norepinephrine, dopamine, and 17-hydroxycorticosteroid in the first 24 h post-CLP, and increased 7-d survival. CONCLUSION: It is demonstrated that administration of arginine together with the selective iNOS inhibitor in the early phase of sepsis restores plasma arginine, reduces oxidative stress by probably maintaining NO derived from constitutive NOS, and attenuates neuroendocrine stress responses. This co-administration may be a beneficial treatment approach against sepsis.

Neuroendocrine system response modulates oxidative cellular damage in burn patients.

Oxygen-derived free radicals play important roles in pathophysiological processes in critically ill patients, but the data characterizing relationships between radicals and neuroendocrine system response are sparse. To search the cue to reduce the oxidative cellular damage from the point of view of neuroendocrine system response, we studied the indicators of neuroendocrine and inflammatory responses excreted in urine in 14 burn patients (42.3 +/- 31.4 years old, and 32.3 +/- 27.6% burn of total body surface area [%TBSA]) during the first seven days post burn. The daily mean amounts of urinary excretion of 8-hydroxy-2'-deoxy-guanosine (8-OHdG), a marker of oxidative cellular damage, were above the upper limit of the standard value during the studied period. The total amount of urinary excretion of 8-OHdG in the first day post burn correlated with burn severity indices: %TBSA (r = 0.63, p = 0.021) and burn index (r = 0.70, p = 0.008). The daily urinary excretion of 8-OHdG correlated with the daily urinary excretion of norepinephrine and nitrite plus nitrate (NOx) during the studied period except day 2 post burn, and correlated with the daily urinary excretion of 17-hydroxycorticosteriod (17-OHCS) in days 2, 3, and 7 post burn. These data suggest that oxidative cellular damage correlates with burn severity and neuroendocrine system response modulates inflammation and oxidative cellular damage. Modulation of neuroendocrine system response and inflammation in the treatment in the early phase of burn may be useful to reduce the oxidative cellular damage and to prevent multiple organ failures in patients with extensive burn.

AML1/Runx1 recruits calcineurin to regulate granulocyte macrophage colony-stimulating factor by Ets1 activation.

Acute myeloid leukemia 1 (AML1), also denoted Runx1, is a transcription factor essential for hematopoiesis, and the AML1 gene is the most common target of chromosomal translocations in human leukemias. AML1 binds to sequences present in the regulatory regions of a number of hematopoiesis-specific genes, including certain cytokines such as granulocyte macrophage colony-stimulating factor (GM-CSF) up-regulated after T cell receptor stimulation. Here we show that both subunits of the Ca(2+)/calmodulin-dependent protein phosphatase calcineurin (CN), which is activated upon T cell receptor stimulation, interact directly with the N-terminal runt homology domain-containing part of AML1. The regulatory CN subunit binds AML1 with a higher affinity and in addition also interacts with the isolated runt homology domain. The related Runx2 transcription factor, which is essential for bone formation, also interacts with CN. A constitutively active derivative of CN is shown to activate synergistically the GM-CSF promoter/enhancer together with AML1 or Runx2. We also provide evidence that relief of the negative effect of the AML1 sites is important for Ca(2+) activation of the GM-CSF promoter/enhancer and that AML1 overexpression increases this Ca(2+) activation. Both subunits of CN interact with AML1 in coimmunoprecipitation analyses, and confocal microscopy analysis of cells expressing fluorescence-tagged protein derivatives shows that CN can be recruited to the nucleus by AML1 in vivo. Mutant analysis of the GM-CSF promoter shows that the Ets1 binding site of the promoter is essential for the synergy between AML1 and CN in Jurkat T cells. Analysis of the effects of inhibitors of the protein kinase glycogen synthase kinase-3beta and in vitro phosphorylation/dephosphorylation analysis of Ets1 suggest that glycogen synthase kinase-3beta-phosphorylated Ets1 is a target of AML1-recruited CN phosphatase at the GM-CSF promoter.