Paradoxical herniation associated with hyperbaric oxygen therapy after decompressive craniectomy: A case report.

BACKGROUND: Whether hyperbaric oxygen therapy (HBOT) can cause paradoxical herniation is still unclear. CASE SUMMARY: A 65-year-old patient who was comatose due to brain trauma underwent decompressive craniotomy and gradually regained consciousness after surgery. HBOT was administered 22 d after surgery due to speech impairment. Paradoxical herniation appeared on the second day after treatment, and the patient's condition worsened after receiving mannitol treatment at the rehabilitation hospital. After timely skull repair, the paradoxical herniation was resolved, and the patient regained consciousness and had a good recovery as observed at the follow-up visit. CONCLUSION: Paradoxical herniation is rare and may be caused by HBOT. However, the underlying mechanism is unknown, and the understanding of this phenomenon is insufficient. The use of mannitol may worsen this condition. Timely skull repair can treat paradoxical herniation and prevent serious complications.

Neuroprotective effect of exosomes derived from bone marrow mesenchymal stem cells via activating TGR5 and suppressing apoptosis.

Cerebral infarction has become one of the most common neurovascular diseases, and it leads to a high disability and death rate. The exosomes derived from bone marrow mesenchymal stem cells (BM-MSCs-exo) have been viewed as a potential therapeutic method for some diseases. However, the role of BM-MSCs-exo in cerebral infarction remains unclear. Middle cerebral artery occlusion (MCAO) rat and oxygen and glucose deprived cell models were established. Neurological score, animal behaviors, TTC-staining, HE staining, and immunohistochemical staining were performed to evaluate neuro function recovery. Floy cytometry was applied to detect apoptosis and cell cycle. BM-MSCs-exo significantly improved infarction ratio and neurological function after MCAO, and the influence of BM-MSCs-exo on neuro function recovery could be reversed by knocking down TGR5. Meanwhile, BM-MSCs-exo could remarkably activate TGR5 in vivo. The suppression of apoptosis by BM-MSCs-exo in vivo and in vitro was remarkably reversed by siRNA TGR5. BM-MSCs-exo promoted the animal recovery after MCAO. The neuroprotective effect by BM-MSCs-exo might be achieved by activating TGR5 and inhibiting apoptosis. Our findings provide a potential therapeutic thought for the treatment of cerebral infarction through BM-MSCs-exo targeting TGR5 and inhibiting apoptosis.

[Activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of type II focal cortical dysplasia].

OBJECTIVE: To investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy. METHODS: A total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry. RESULTS: The expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group. CONCLUSION: Abnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.

[Expression and clinical significance of tumor necrosis factor-alpha and its receptors in non-specific chronic encephalitis and non-encephalitis relative intractable epilepsy].

OBJECTIVE: To explore the expression and clinical significance of tumor necrosis factor-alpha (TNF-α) and its receptors p55 and p75 in non-specific chronic encephalitis relative intractable epilepsy (NCERE) and non-NCERE. METHODS: Immunohistochemical SABC staining was employed to detect the foci of 24 cases of intractable epilepsy (NCERE, n = 10; non-NCERE, n = 14) and 10 cases of the expression of TNF-α and its receptors p55 and p75 in normal brain tissues (control group) to analyze their clinical significance. RESULTS: All expressions of the control group were negative. TNF-α and its receptors p55 and p75 were differentially expressed in neuron cytoplasm between NCERE and non-NCERE. No statistical significance existed between NCERE and non-NCERE (P > 0.05). There was a positive correlation between the expressions of receptors p55 and p75 (r = 0.897, P < 0.05). CONCLUSION: By binding its receptors and the synergistic effect between receptors p55 and p75, TNF-αis involved in the generation and development of NCERE and non-NCERE. However it appears to have nothing to do with the etiology of epilepsy.

Huber fractal image coding based on a fitting plane.

Recently, there has been significant interest in robust fractal image coding for the purpose of robustness against outliers. However, the known robust fractal coding methods (HFIC and LAD-FIC, etc.) are not optimal, since, besides the high computational cost, they use the corrupted domain block as the independent variable in the robust regression model, which may adversely affect the robust estimator to calculate the fractal parameters (depending on the noise level). This paper presents a Huber fitting plane-based fractal image coding (HFPFIC) method. This method builds Huber fitting planes (HFPs) for the domain and range blocks, respectively, ensuring the use of an uncorrupted independent variable in the robust model. On this basis, a new matching error function is introduced to robustly evaluate the best scaling factor. Meanwhile, a median absolute deviation (MAD) about the median decomposition criterion is proposed to achieve fast adaptive quadtree partitioning for the image corrupted by salt & pepper noise. In order to reduce computational cost, the no-search method is applied to speedup the encoding process. Experimental results show that the proposed HFPFIC can yield superior performance over conventional robust fractal image coding methods in encoding speed and the quality of the restored image. Furthermore, the no-search method can significantly reduce encoding time and achieve less than 2.0 s for the HFPFIC with acceptable image quality degradation. In addition, we show that, combined with the MAD decomposition scheme, the HFP technique used as a robust method can further reduce the encoding time while maintaining image quality.