The Optimal Velocity Criterion in the Diagnosis of Unilateral Middle Cerebral Artery Stenosis by Transcranial Doppler

We evaluated the optimal flow velocity of transcranial doppler (TCD) in detecting unilateral middle cerebral artery (MCA) stenosis and stenosis grading by magnetic resonance angiography (MRA) as the reference standard. 302 nonconsecutive patients with unilateral MCA stenosis detected by TCD underwent MRA of the intracranial arteries. The peak systolic velocity (PSV), mean flow velocity (MFV), and end-diastolic velocity (EDV) of each MCA were recorded. 604 MCA were categorized into four groups depending on the stenosis severity: normal MCA (n = 319, 52.8 %), mild stenosis (n = 94, 15.6 %), moderate stenosis (n = 66, 10.9 %), and severe stenosis (n = 125, 20.7 %). Significant differences in PSV, MFV, and EDV between these four groups were observed (P < 0.001, respectively). The optimal cutoff velocities for detecting MCA stenosis were: PSV = 160 cm/s, MFV = 100 cm/s, EDV = 60 cm/s; the optimal cutoff points to distinguish mild from moderate stenosis were: PSV = 200 cm/s, MFV = 120 cm/s, EDV = 80 cm/s; the cutoffs to distinguish moderate from severe stenosis were: PSV = 280 cm/s, MFV = 180 cm/s, EDV = 110 cm/s. Using PSV as the diagnostic criteria, the correlation for diagnosing MCA stenosis using TCD and MCA was good (Kappa number κ = 0.668); using as MFV criteria, κ = 0.641. The optimal cutoff PSV values in stenosis grading on TCD were 160, 200, and 280 cm/s. The optimal cutoff MFV values were 100, 120, and 180 cm/s. PSV is more accurate than MFV in detecting and grading MCA stenosis.     

Cerebral blood flow during cardiopulmonary bypass in pediatric cardiac surgery: the role of transcranial Doppler – a systematic review of the literature

Background

Transcranial Doppler Ultrasound (TCD) is a sensitive, real time tool for monitoring cerebral blood flow velocity (CBFV). This technique is fast, accurate, reproducible and noninvasive. In the setting of congenital heart surgery, TCD finds application in the evaluation of cerebral blood flow variations during cardiopulmonary bypass (CPB).

Methodology

We performed a search on human studies published on the MEDLINE using the keyword "trans cranial Doppler" crossed with "pediatric cardiac surgery" AND "cardio pulmonary by pass", OR deep hypothermic cardiac arrest", OR "neurological monitoring".

Discussion

Current scientific evidence suggests a good correlation between changes in cbral blood flow and mean cerebral artery (MCA) blood flow velocity. The introduction of Doppler technology has allowed an accurate monitorization of cerebral blood flow (CBF) during circulatory arrest and low-flow CPB. TCD has also been utilized in detecting cerebral emboli, improper cannulation or cross clamping of aortic arch vessels. Limitations of TCD routine utilization are represented by the need of a learning curve and some experience by the operators, as well as the need of implementing CBF informations with, for example, data on brain tissue oxygen delivery and consumption.

Conclusion

In this light, TCD plays an essential role in multimodal neurological monitorization during CPB (Near Infrared Spectroscopy, TCD, processed electro encephalography) that, according to recent studies, can help to significantly improve neurological outcome after cardiac surgery in neonates and pediatric patients.     

In Vivo Validation of Simultaneous Non-Contrast Angiography and intraPlaque Hemorrhage (SNAP) Magnetic Resonance Angiography: An Intracranial Artery Study

Objectives

Simultaneous Non-contrast Angiography and intraPlaque hemorrhage (SNAP) technique was recently proposed for joint MRA and intraplaque hemorrhage (IPH) imaging. The purpose of this study is to validate SNAP’s MRA performance in patients with suspected intracranial artery disease.

Methods

SNAP and time-of-flight (TOF) techniques with matched field of view and resolution were applied on 15 patients with suspected intracranial artery disease. Both techniques were evaluated based on their detection of luminal stenosis of bilateral middle cerebral arteries (MCA) and the delineation of smallest visible branches (SVB) of the MCA. Statistical analysis was conducted on the artery level.

Results

The SNAP MRA was found to provide similar stenosis detection performance when compared with TOF (Cohen’s κ 0.79; 95% Confidence Interval: 0.56–0.99). For the SVB comparison, SNAP was found to provide significantly better small artery delineation than TOF (p = 0.017). Inter-reader reproducibility for both measurements on SNAP was over 0.7. SNAP also detected IPH lesions on 13% of the patients.

Conclusions

The SNAP technique’s MRA performance was optimized and compared against TOF for intracranial artery atherosclerosis imaging and was found to provide comparable stenosis detection accuracy. Along with its IPH detection capability, SNAP holds the potential to become a first-line screening tool for high risk intracranial atherosclerosis disease evaluation.     

Assessment of Dynamic Cerebral Autoregulation in Patients with Basilar Artery Stenosis

Background and Aims

Previous studies have shown impaired cerebral autoregulation (CA) in carotid and middle cerebral artery (MCA) stenosis/occlusion. Little is known about CA in patients with basilar artery (BA) stenosis. We therefore investigated dynamic CA patterns in BA stenosis using transfer function analysis (TFA).

Methods

We measured spontaneous oscillations of blood flow velocity (CBFV) in the right posterior cerebral artery (PCA), and left MCA and mean arterial pressure (ABP) continuously in 25 patients with BA stenosis (moderate n=16 with 50-69% occlusion and severe n=9 with ≥70% occlusion) and 22 healthy volunteers in supine position during 6 circles per minute deep breath. Analysis was based on the ‘black-box’ model of transfer function deriving phase and gain in both PCA and MCA.

Results

Though changes of phase shift and gain between the patients and healthy controls were observed in MCA, the differences are however not significant. Phase shift in PCA was significantly decreased in severe stenosis when comparing with healthy controls and moderate stenosis (4.2±34.2° VS 41.1±40.4°, 4.2±34.2° VS 34.2±27.2°, both p<0.05), whilst the gain in PCA is increased for moderate BA stenosis and decreased for severe BA stenosis. Furthermore, we found that phase shift were almost abolished in patients with ischemic stroke who developed unfavorable clinical outcome (mRs>2) on the 90 days after stroke onset.

Conclusion

Dynamic CA in PCA reduces in patients with severe BA stenosis and those with ischemic stroke who present poor outcome in 90 days after stroke onset. Phase shift might be a sensitive index prompting impaired CA in posterior circulation.     

Peak systolic velocity Doppler of middle cerebral artery in small for gestational age (SGA) fetus

Background

Small for gestational age (SGA) has high frequency which increases the risk of long-term adverse outcomes. Thus the aim of this study was to evaluate peak systolic velocity Doppler of middle cerebral artery (MCA) in SGA fetus in order to find appropriate method to diagnosis SGA sooner.

Materials and Methods

This prospective longitudinal study was conducted on 90 pregnant women with a diagnosis of SGA fetus and 90 pregnant women with normal fetus. Then MCA and umbilical artery assessment were performed for all subjects and compared between two groups.

Results

Doppler assessment showed that umbilical artery PI was significantly higher in SGA group as compared to normal group (1.11±0.37 vs 0.98±0.18, P = 0.003), while MCA PI was significantly lower in SGA group (1.77±0.44 vs 1.92±0.47, P = 0.028). On the other hand, PSV did not differ between the groups (P = 0.592). Moreover, we found that PSV was more in SGA group by grouping maternal age (<27 years) (P = 0.006), and gestational age (>34 weeks) (P<0.001).

Conclusion

The results of this study suggest that MCA PI decreased significantly in SGA fetuses, while UA PI increased in this group. Moreover, PSV increased in this group when evaluated in different subgroups (based on maternal age and gestational age).

     

Differentiation between attention-deficit/hyperactivity disorder and autism spectrum disorder by the Social Communication Questionnaire

The differentiation of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) poses a clinical challenge. In children, overlap of psychopathological and cognitive findings has been found for both disorders. In addition, some children suffer from both disorders. The Social Communication Questionnaire (SCQ) is a screening instrument for ASD symptoms which indicates the presence of ASD in a rapid and economic way. However, validity to differentiate ASD and ADHD as differential or comorbid diagnoses has not been studied. Here, the differential validity was compared in groups of children with ASD, ADHD, ASD + ADHD, and typically developing (TD) children and IQ > 70. ROC analyses indicated an excellent differentiation between ASD and TD with ROC–AUC = .941 and between ASD + ADHD with ROC–AUC = .993. The optimal cutoff was below the originally recommended one of 15. The differentiation between children with ASD with (ROC–AUC = .982) or without ADHD (ROC–AUC = .864) and ADHD alone also showed acceptable differential validity, and here, the optimal cutoff corresponded to the recommended. Taken together, the SCQ can be recommended as a screening instrument for a first differentiation between children with ASD and typically developing children as well as children with ADHD.     

Nanosecond pulsed electric fields modulate the expression of Fas/CD95 death receptor pathway regulators in U937 and Jurkat Cells

In this publication, we demonstrate that exposure of Jurkat and U937 cells to nanosecond pulsed electrical fields (nsPEF) can modulate the extrinsic-mediated apoptotic pathway via the Fas/CD95 death receptor. An inherent difference in survival between these two cell lines in response to 10 ns exposures has been previously reported (Jurkat being more sensitive to nsPEF than U937), but the reason for this sensitivity difference remains unknown. We found that exposure of each cell line to 100, 10 ns pulses at 50 kV/cm caused a marked increase in expression of cFLIP (extrinsic apoptosis inhibitor) in U937 and FasL (extrinsic apoptosis activator) in Jurkat, respectively. Measurement of basal expression levels revealed an inherent difference between U937 cells, having a higher expression of cFLIP, and Jurkat cells, having a higher expression of FasL. From these data, we hypothesize that the sensitivity difference between the cells to nsPEF exposure may be directly related to expression of extrinsic apoptotic regulators. To validate this hypothesis, we used siRNA to knockdown cFLAR (coding for cFLIP protein) expression in U937, and FasL expression in Jurkat and challenged them to 100, 10 ns pulses at 150 kV/cm, a typical lethal dose. We observed that U937 survival was reduced nearly 60 % in the knockdown population while Jurkat survival improved ~40 %. These findings support the hypothesis that cell survival following 10 ns pulse exposures depends on extrinsic apoptotic regulators. Interestingly, pretreatment of U937 with a 100-pulse, 50 kV/cm exposure (to amplify cFLAR expression) significantly reduced the lethality of a 150 kV/cm, 100-pulse exposure applied 24 h later. From these data, we conclude that the observed survival differences between cells, exposed to 10 ns pulsed electric fields, is due to inherent cell biochemistry rather than the biophysics of the exposure itself. Understanding cell sensitivity to nsPEF may provide researchers/clinicians with a predicable way to control or avoid unintended cell death during nsPEF exposure.     

Marker features for malignancy in ectocervical cells

Marker features for malignancy have recently been observed in ectocervical cells, even in cells that are visually normal in appearance. This study assessed the statistical significance of these marker features using a mixed-model nested-design analysis of variance (ANOVA). Features in blue intermediate cells from patients with normal cytology, moderate dysplasia, and severe dysplasia/carcinomain situ, nonkeratinizing cells from patients with moderate dysplasia, severe dysplasia/carcinomain situ, and invasive cancer, and dysplastic cells from areas of metaplasia from patients with moderate dysplasia, severe dysplasia/carcinomain situ, and invasive cancer were tested. ANOVA clearly demonstrated that the marker features differentiate between cells of the same cell type originating from patients in different diagnostic categories. In every instance, the differences owing to the diagnostic category were statistically significantly greater than those caused by patient-to-patient variability. Although the discriminating marker features in the intermediate cells were almost exclusively spectral features reflecting staining differences, morphometric features were also marker features in the dysplastic cells.     

Effects of Mild and Moderate Hypothemia Therapy on Expression of Cerebral Neuron Apoptosis Related Proteins and Glial Fiber Acidic Protein After Rat Cardio-pulmonary Resuscitation

To explore the effects of different degrees of hypothermia on brain tissue apoptosis after cardio-pulmonary resuscitation (CPR). Cardiac arrest for 5 min induced by asphyxia method was used to create CPR model. 30 SD rats were randomly divided into control group (normothermia), 33 °C hypothermia group and 30 °C hypothermia group with ten rats in each. Rats in control group received routine treatment at 25 °C room temperature after CPR; Rats in mild hypothermia and moderate hypothermia groups were given hypothermia treatment 0.5 h after CPR. Brain tissue in all groups was taken 24 h after CPR, and immunohistochemistry was used to detect the caspase-3 in cerebral cortex and glial fiber acidic protein (GFAP) expression in astrocyte. Western blotting was used to detect Bcl-2 and Bax protein expression, and histopathological change was observed in brain tissue. Compare to the control group, caspase-3 expression in cerebral neurons in hypothermia group was significantly decreased (p<0.01), which was significantly lower in 30 °C group than that in 33 °C group (p > 0.05); GFAP level in hypothermia groups was significantly increased (p < 0.01), which was higher in 30 °C hypothermia group than that in 33 °C hypothermia group (p < 0.05); Bcl-2 expression level in hypothermia group was significantly increased (p < 0.01), which was higher in 30 °C hypothermia group than that in 33 °C hypothermia group (p < 0.05); The level of Bax had no significant difference among the three groups. Hypothermia-regulated GFAP expression by decreasing caspase-3 expression and increasing Bcl-2 expression to promote brain cell signaling transduction, and further inhibited cell apoptosis and reduced brain injury. Moderate hypothermia therapy is more effective than mild hypothermia in preventing brain injure.     

Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis

We investigated the presence of inflammatory signs in the progression of fatty liver disease induced by fasting. Sixty standard black American mink (Neovison vison) were fasted for 0, 1, 3, 5, or 7 days and one group for 7 days followed by re-feeding for 28 days. Liver sections were evaluated histologically and liver mRNA levels indicating endoplasmic reticulum (ER) stress, adipogenic transformation, and inflammation were assessed by quantitative real-time PCR. After 3 days of fasting, the mink had developed moderate liver steatosis. Increased hyaluronan reactivity in lymphocytic foci but no Mallory–Denk bodies were seen in livers of the mink fasted for 5–7 days. Up-regulation of glucose-regulated protein, 78 kDa was observed on day 7 indicating ER stress, especially in the females. Liver lipoprotein lipase and monocyte chemoattractant protein 1 mRNA levels increased in response to 5–7 days of food deprivation, while tumor necrosis factor α (TNF-α) was the highest in the mink fasted for 5 days. The expression of the genes of interest, except for TNF-α, correlated with each other and with the liver fat content. The mRNA levels were found to change more rapidly below n-3/n-6 polyunsaturated fatty acid ratio threshold of 0.15. Following re-feeding, hepatocyte morphology and mRNA abundance returned to pre-fasting levels. Within the studied timeframe, evidence for ER stress, adipogenic transformation, and liver inflammation suggested incipient transition from steatosis to steatohepatitis with potential for development of more severe liver disease. This may present a possibility to influence disease progression before histologically observable steatohepatitis.     

Respiratory Nursing Interventions Following Tracheostomy in Acute Traumatic Cervical Spinal Cord Injury

Tracheostomy is frequently performed in severe cervical spinal cord injury (SCI) patients with the pulmonary dysfunction. A series of respiratory nursing interventions are required to plan tracheostomy removal. Tracheostomy was performed in 29 patients after acute traumatic cervical SCI. A series of respiratory nursing interventions were introduced in these patients after closed tracheostomy and decannulation, including closed tracheostomy tube training, manually assisted cough. Chacheostomy was successfully removed in 21 patients after the respiratory nursing interventions. In contrast, eight patients died from associated injuries. The average time from tracheostomy to decannulation was 40 days (14–104 days), the average time from closed tracheostomy to decannulation was 18.80 ± 13.50 days. Second tracheostomy was performed in one patient after 29 days’ removal due to pulmonary infection. One patient presented with delayed incision healing for 29 days. Closed tracheostomy tube training and manually assisted cough are key factors for tracheostomy removal, although intensive nursing are also needed. The time from tracheostomy to decannulation and from closed tracheostomy to decannulation is increased in case of "late" (>24 h) tracheostomy and longer mechanical ventilation.     

Antiangiogenic therapy effects on age-associated matrix metalloproteinase-9 (MMP-9) and insulin-like growth factor receptor-1 (IGFR-1) responses: a comparative study of prostate disorders in aged and TRAMP mice

Senescence is associated with hormonal imbalance and prostatic disorders. Angiogenesis is fundamental for the progression of malignant lesions and is a promising target for prostate cancer treatment. The aim was to characterize matrix metalloproteinase-9 (MMP-9) and insulin-like growth factor receptor-1 (IGFR-1) responses in the prostate during senescence and following antiangiogenic and/or androgen ablation therapies, comparing them to cancer progression features in TRAMP mice. Aged male mice (52-week-old FVB) were submitted to antiangiogenic treatments with SU5416 (6 mg/kg; i.p.) and/or TNP-470 (15 mg/kg; s.c). Finasteride (20 mg/kg; s.c.) was administered alone or associated to both inhibitors. Dorsolateral prostate was collected for light microscopy, and immunohistochemistry and Western blotting collected for MMP-9 and IGFR-1. Senescence led to inflammation and different proliferative lesions in the prostate, as well as to increased MMP-9 and IGFR-1, resembling TRAMP mice prostatic microenvironment. Antiangiogenic therapies promoted recovery and/or interruption of age-associated alterations, presenting differential effects on the molecules studied. SU5416 acted mainly on MMP-9, whereas TNP-470 showed its best influence on IGFR-1 levels. Finasteride administration, alone or in combination with antiangiogenic agents, also resulted in regression of inflammation and neoplastic lesions, besides having a negative modulatory effect on both MMP-9 and IGFR-1. We concluded that stimulated tissue remodeling and proliferative processes during senescence predisposed the prostate to malignant disorders. The combination of different agents was more effective to minimize prostatic imbalance during this period, probably due to the differential action of each drug on factors involved in cell proliferation and extracellular matrix remodeling, resulting in a broader spectrum of effects following the combined treatment.     

Pain ratings, psychological functioning and quantitative EEG in a controlled study of chronic back pain patients

Objectives

Several recent studies report the presence of a specific EEG pattern named Thalamocortical Dysrhythmia (TCD) in patients with severe chronic neurogenic pain. This is of major interest since so far no neuroscientific indicator of chronic pain could be identified. We investigated whether a TCD-like pattern could be found in patients with moderate chronic back pain, and we compared patients with neuropathic and non-neuropathic pain components. We furthermore assessed the presence of psychopathology and the degree of psychological functioning and examined whether the strength of the TCD-related EEG markers is correlated with psychological symptoms and pain ratings.

Design

Controlled clinical trial with age and sex matched healthy controls.

Methods

Spontaneous EEG was recorded in 37 back pain patients and 37 healthy controls.

Results

We were not able to observe a statistically significant TCD effect in the EEG data of the whole patient group, but a subsample of patients with evidence for root damage showed a trend in this direction. Pain patients showed markedly increased psychopathology. In addition, patients'' ratings of pain intensity within the last 1 to 12 months showed strong correlations with EEG power, while psychopathology was correlated to the peak frequency.

Conclusion

Out of several possible interpretations the most likely conclusion is that only patients with severe pain as well as root lesions with consecutive thalamic deafferentation develop the typical TCD pattern. Our primary method of defining ‘neuropathic pain’ could not reliably determine if such a deafferentation was present. Nevertheless the analysis of a specific subsample as well as correlations between pain ratings, psychopathology and EEG power and peak frequency give some support to the TCD concept.

Trial Registration

ClinicalTrials.gov {"type":"clinical-trial","attrs":{"text":"NCT00744575","term_id":"NCT00744575"}}NCT00744575     

The prognostic value of osteopontin expression in non-small cell lung cancer: a meta-analysis

To investigate the association of Osteopontin (OPN) expression in tumor tissue with clinicopathological features of non-small cell lung carcinoma (NSCLC) patients. Publications assessing the clinicopathological characteristics and prognostic significance of OPN in expression NSCLC were identified up to March 2014. A meta-analysis of eligible studies was performed using standard statistical methods to clarify the association between OPN expression and these clinical parameters. A total of eleven studies met the inclusion criteria, and included 1536 cases of NSCLC tumor tissue and 340 cases of normal lung tissue. The OPN expression rate in NSCLC tissue was higher than normal tissue [Odds ratio (OR) 6.427; 95 % confidence interval (CI) 4.689–8.808; P = 0.000]. Simultaneously, we also found that OPN expression was positively associated with stage (OR 0.332; 95 % CI 0.250–0.440; P = 0.000), lymph node metastasis (OR 3.094; 95 % CI 2.295–4.172; P = 0.000), tumor size (tumor size <3 cm vs. ≥3 cm; OR 0.484; 95 % CI 0.303–0.773; P = 0.002) and pathology (OR 0.611; 95 % CI 0.466–0.800; P = 0.000). It was unrelated that OPN expression in NSCLC tissue with and degree of differentiation and other clinical features (P > 0.05). Experimental findings indicate that, OPN plays a crucial role in the development of NSCLC.     

A prepared anti-MSTN polyclonal antibody reverses insulin resistance of diet-induced obese rats via regulation of PI3K/Akt/mTOR&FoxO1 signal pathways

Suppression of myostatin (MSTN) is associated with skeletal muscle atrophy and insulin resistance. However, the mechanisms by which MSTN regulates insulin resistance are not well known. We have explored the signaling pathways through which MSTN regulates insulin resistance in diet-induced obese rats using a polyclonal antibody for MSTN. The anti-MSTN polyclonal antibody significantly improved insulin resistance and whole-body insulin sensitivity, decreased MSTN protein expression in muscle samples by 39 % in diet-induced obese rats. Furthermore, the anti-MSTN polyclonal antibody significantly enhanced PI3K activity (140 %), Akt phosphorylation (86 %), GLUT4 protein expression (23 %), the phosphorylation of mTOR (21 %), and inhibited the phosphorylation of FoxO1 (57 %), but did not affect the phosphorylation of GSK-3β. Thus, suppression of MSTN by the anti-MSTN polyclonal antibody reverses insulin resistance of diet-induced obesity via MSTN/PI3K/Akt/mTOR and MSTN/PI3K/Akt/FoxO1 signaling pathways.     

Basic amino acids and dimethylarginines targeted metabolomics discriminates primary hepatocarcinoma from hepatic colorectal metastases

Hepatocellular carcinoma (HCC) is a very aggressive neoplasia requiring early and accurate diagnosis to improve patient outcomes with timely treatment. The liver is also very frequently colonized by metastases, and the most frequent differential diagnosis is HCC against intrahepatic cholangiocarcinoma or metastatic adenocarcinoma. Metabolomics is a powerful tool for identification of altered biomarkers in cancer, and to evaluate the efficacy of drug treatments. Here we analyzed by HILIC-MS/MS methylated arginines, basic amino acids (Arg, Cit, Orn), and their ratios in the extracts of primary HCC tissues, liver metastases from colorectal carcinoma (MET), cirrhotic related hepatitis-C-virus (CIR), and non-cirrhotic normal liver (NT) adjacent tissues. We found high levels of Arg (p < 0.0001) and Arg/Orn (p < 0.01) in MET compared to other tissues. In MET, compared to NT and CIR, Arg concentration was fivefold higher, while in HCC it was twofold higher. ADMA increased twofold compared to NT and CIR, while in HCC it was 50 % higher. Arg/Cit and ADMA/SDMA ratios were significantly higher in MET compared to NT and CIR (p < 0.005). Arg/Orn, Arg/Cit, and ADMA/SDMA ratios increased progressively from NT, CIR, HCC, to MET tissues. Arg/Cit correlated significantly with Arg/Orn ratios (r = 0.77; p < 0.0001), and discriminates tumor from non-tumor samples. In addition, the discriminant lactate/glucose ratio we previously found by NMR, also correlated significantly with the Arg levels (r = 0.64; p < 0.0001), and discriminated MET from all other tissues. The results indicated that Arg in MET is higher than other tissue classes, suggesting that, together with the lactate/glucose ratio, it can be considered a further biomarker for HCC-metastases differentiation.     

Kinetics of nitrification in a fixed biofilm reactor using dewatered sludge-fly ash composite ceramic particle as a supporting medium

A mathematical model system was derived to describe the kinetics of ammonium nitrification in a fixed biofilm reactor using dewatered sludge-fly ash composite ceramic particle as a supporting medium. The model incorporates diffusive mass transport and Monod kinetics. The model was solved using a combination of the orthogonal collocation method and Gear’s method. A batch test was conducted to observe the nitrification of ammonium-nitrogen ( \({\text{NH}}_{4}^{ + }\) -N) and the growth of nitrifying biomass. The compositions of nitrifying bacterial community in the batch kinetic test were analyzed using PCR–DGGE method. The experimental results show that the most staining intensity abundance of bands occurred on day 2.75 with the highest biomass concentration of 46.5 mg/L. Chemostat kinetic tests were performed independently to evaluate the biokinetic parameters used in the model prediction. In the column test, the removal efficiency of \({\text{NH}}_{4}^{ + }\) -N was approximately 96 % while the concentration of suspended nitrifying biomass was approximately 16 mg VSS/L and model-predicted biofilm thickness reached up to 0.21 cm in the steady state. The profiles of denaturing gradient gel electrophoresis (DGGE) of different microbial communities demonstrated that indigenous nitrifying bacteria (Nitrospira and Nitrobacter) existed and were the dominant species in the fixed biofilm process.     

Normothermia after decompressive surgery for space-occupying middle cerebral artery infarction: a protocol-based approach

Background

Moderate hypothermia after decompressive surgery might not be beneficial for stroke patients. However, normothermia may prove to be an effective method of enhancing neurological outcomes. The study aims were to evaluate the application of a pre-specified normothermia protocol in stroke patients after decompressive surgery and its impact on temperature load, and to describe the functional outcome of patients at 12 months after treatment.

Methods

We analysed patients with space-occupying middle cerebral artery (MCA) infarction treated with decompressive surgery and a pre-specified temperature management protocol. Patients treated primarily with device-controlled normothermia or hypothermia were excluded. The individual temperature load above 36.5 °C was calculated for the first 96 h after hemicraniectomy as the Area Under the Curve, using °C x hours. The effect of temperature load on functional outcome at 12 months was analysed by logistic regression.

Results

We included 40 stroke patients treated with decompressive surgery (mean [SD] age: 58.9 [10.1] years; mean [SD] time to surgery: 30.5 [16.7] hours). Fever (temperature?>?37.5 °C) developed in 26 patients during the first 96 h after surgery and mean (SD) temperature load above 36.5 °C in this time period was 62,3 (+/? 47,6) °C*hours. At one year after stroke onset, a moderate to moderately severe disability (modified Rankin Scale score of 3 or 4) was observed in 32% of patients, and a severe disability (score of 5) in 37% of patients, respectively. The lethality in the cohort at 12 months was 32%. The temperature load during the first 96 h was not an independent predictor for 12 month lethality (OR 0.986 [95%-CI:0.967–1.002]; p?<?0.12).

Conclusions

Temperature control in surgically treated patients with space-occupying MCA infarction using a pre-specified protocol excluding temperature management systems resulted in mild hyperthermia between 36.8 °C and 37.2 °C and a low overall temperature load. Future prospective studies on larger cohorts comparing different strategies for normothermia treatment including temperature management devices are needed.

     

Alzheimer’s disease: analysis of a mathematical model incorporating the role of prions

We introduce a mathematical model of the in vivo progression of Alzheimer’s disease with focus on the role of prions in memory impairment. Our model consists of differential equations that describe the dynamic formation of \(\upbeta \) -amyloid plaques based on the concentrations of A \(\upbeta \)  oligomers, PrP^C proteins, and the A \(\upbeta \) - \(\times \) -PrP^Ccomplex, which are hypothesized to be responsible for synaptic toxicity. We prove the well-posedness of the model and provided stability results for its unique equilibrium, when the polymerization rate of \(\upbeta \) -amyloid is constant and also when it is described by a power law.     

Tryptase as a marker of severity of aortic valve stenosis

Background

Severe aortic valve stenosis is one of the most common cause of mortality in adult patients affected with metabolic syndrome, a condition associated with an active inflammatory process involving also mast cells and their mediators, in particular tryptase. The aim of this study was to characterize the possible long-term prognostic role of tryptase in severe aortic valve stenosis.

Case presentation

The baseline serum tryptase was measured in 5 consecutive patients admitted to our Hospital to undergo aortic valve replacement for severe acquired stenosis. Within 2 years after, the patients were evaluated for the occurrence of major cardiovascular events (MACE). The tryptase measurements were higher in patients experiencing MACE (10.9, 11.7 and 9.32 ng/ml) than in non-MACE ones (5.69 and 5.58 ng/ml).

Conclusions

In patients affected with severe aortic stenosis, baseline serum tryptase may predict occurence of MACE. Further studies are needed to demonstrate the long-term prognostic role of this biomarker.