Prediction Value of Epilepsy Secondary to Inferior Cavity Hemorrhage Based on Scalp EEG Wave Pattern in Deep Learning.

Objective: To search the predictive value of epilepsy secondary to acute subarachnoid hemorrhage (aSAH) based on EEG wave pattern in deep learning. Methods: A total of 156 cases of secondary epilepsy with lower cavity hemorrhage in our hospital were selected and divided into the late epilepsy group and the early epilepsy group according to seizure time, and the nonseizure group and the seizure group according to seizure condition. General data of patients were collected, the EEG types of each group were analyzed, and the disease recurrence rate, treatment effect, and symptom onset time were compared. Results: Rapid and slow and rapid blood flow velocity were the main abnormal manifestations of epilepsy secondary to inferior cavity hemorrhage, accounting for 33.3% and 18.6%, respectively. Compared with the seizure group, the proportion of type ii and type iii in the nonseizure group was higher, and the proportion of type ii and type iii in the early epilepsy group was higher than in the late epilepsy group (P < 0.05). The diagnostic accuracy, missed diagnosis rate, misdiagnosis rate, specificity, and sensitivity of the EEG wave pattern were 94.9%, 3.2%, 1.9%, 91.7%, and 96.2%, respectively. Compared with the early epilepsy group, the recurrence rate of type iii and type iv in the late epilepsy group was higher (P < 0.05). The effective rates of the attack group and the nonattack group were 72.7% and 97.0%, respectively. Compared with the attack group, the effective rate of the nonattack group was higher (P < 0.05). The effective rates of the early epilepsy group and the late epilepsy group were 91.7% and 85.0%, respectively. Compared with the late epilepsy group, the effective rate of the early epilepsy group was higher (P < 0.05). Compared with the early epilepsy group, the late epilepsy group had longer tonic-clonic seizures, atonic seizures, and absent seizures, and the difference between the groups was statistically significant (P < 0.05). Conclusion: In aSAH secondary epilepsy disease prediction, based on indepth study of the scalp EEG wave type prediction, they play an important role, including aSAH high-risk secondary epilepsy wave types for V, III, and IV types, as well as early and late epilepsy associated with disease stage. Through the diagnosis method to predict the severity of disease, this builds a good foundation for clinical treatment. It is beneficial to improve the effective rate of treatment.

[Effects of glucocorticoid receptor agonists on hyperalgesia of rats with neuropathic pain and its mechanisms].

OBJECTIVE: To investigate the effects of glucocorticoid receptor agonists on hyperalgesia in rats with neuropathic pain (NPP) by regulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin-1ß (IL-1ß) pathway and its mechanisms. METHODS: Forty SD rats were divided into control group, NPP model group, NPP treated with NLRP3 inhibitor group and dexamethasone treatment group with 10 rats in each group. The NPP rat model was induced by vincristine. The model group was established according to the above method, the NLRP3 inhibitor group was treated with NLRP3 inhibitor (MCC950) after the NPP model was established, and the treatment group was treated with glucocorticoid receptor agonist (dexamethasone) after the model was established according to the design. The rats of the control group were given the same amount of normal saline. After 7 days of intervention, the mechanical pain threshold, thermal pain threshold, morphological changes of spinal dorsal horn, pain factors (prostaglandin E2 (PGE2), substance P (SP), 5-hydroxytryptamine (5-HT)), inflammatory factors (interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6)), and NLRP3/IL-1ß protein expressions were determined and compared among the four groups. RESULTS: Compared with the model group, the pathological changes of spinal dorsal horn neurons in NLRP3 inhibitor group and treatment group were alleviated significantly, the arrangement of neurons was tended to be close, the number of neurons was gradually returned to normal, and the pyknosis of neurons was decreased. Compared with the control group, the mechanical pain threshold and thermal pain threshold of the model group were decreased significantly (P＜0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1ß protein were increased significantly (P＜0.05); compared with the model group, the mechanical pain threshold and thermal pain threshold of the NLRP3 inhibitor group and the dexamethasone treatment group were increased significantly (P＜0.05), and the expressions of inflammatory factors, pain factors and NLRP3, IL-1ß protein were decreased significantly (P＜ 0.05). The difference between NLRP3 inhibitor group and treatment group was not statistically significant (P＞0.05). CONCLUSION: Glucocorticoid receptor agonists may reduce the hyperalgesia of neuropathic pain rat model by down regulating NLRP3/IL-1ß pathway, which may be the mechanism of dexamethasone on antiinflammatory of analgesia in early stage of NPP.

Zwitterionic Hydrogel Activates Autophagy to Promote Extracellular Matrix Remodeling for Improved Pressure Ulcer Healing.

Pressure ulcer (PU) is a worldwide problem that is hard to heal because of its prolonged inflammatory response and impaired ECM deposition caused by local hypoxia and repeated ischemia/reperfusion. Our previous study discovered that the non-fouling zwitterionic sulfated poly (sulfobetaine methacrylate) (SBMA) hydrogel can improve PU healing with rapid ECM rebuilding. However, the mechanism of the SBMA hydrogel in promoting ECM rebuilding is unclear. Therefore, in this work, the impact of the SBMA hydrogel on ECM reconstruction is comprehensively studied, and the underlying mechanism is intensively investigated in a rat PU model. The in vivo data demonstrate that compared to the PEG hydrogel, the SBMA hydrogel enhances the ECM remolding by the upregulation of fibronectin and laminin expression as well as the inhibition of MMP-2. Further investigation reveals that the decreased MMP-2 expression of zwitterionic SBMA hydrogel treatment is due to the activation of autophagy through the inhibited PI3K/Akt/mTOR signaling pathway and reduced inflammation. The association of autophagy with ECM remodeling may provide a way in guiding the design of biomaterial-based wound dressing for chronic wound repair.

Dl-3-n-butylphthalide attenuates hypoxic-ischemic brain injury through inhibiting endoplasmic reticulum stress-induced cell apoptosis and alleviating blood-brain barrier disruption in newborn rats.

Dl-3-n-butylphthalide (NBP) has been demonstrated to exert neuroprotective effects in experimental models and human patients. This study was performed to assess the therapeutic effects and the underlying molecular mechanisms of NBP in a neonatal hypoxic-ischemic rat model. The results showed that NBP treatment significantly reduced the infarct volume, improved histological recovery, decreased neuronal cell loss, enhanced neuronal cell rehabilitation, promoted neurite growth and decreased white matter injury. In addition, NBP treatment effectively improved long-term neurobehavioral development and prognosis after HI injury. We further demonstrated an inhibitory effect of NBP on endoplasmic reticulum (ER) stress-induced apoptosis, evidenced by reduction in ER stress-related protein expressions (GRP78, XBP-1, PDI and CHOP), decrease in TUNEL-positive cells, down-regulation in pro-apoptosis protein (Bax and cleaved caspase-3), up-regulation in anti-apoptosis protein (Bcl-2). Moreover, NBP exerted a protective effect in blood-brain barrier disruption, which ameliorated brain edema and reduced the degeneration of the tight junction proteins (Occludin and Claudin-5) and adherens junction proteins (P120-Catenin, VE-Cadherin and ß-Catenin). Overall, our findings demonstrated that NBP treatment attenuated HI brain injury through inhibiting ER stress-induced apoptosis and alleviating blood-brain barrier disruption in newborn rats. This work provides an effective therapeutic strategy to reduce brain damage and enhance recovery after neonatal HI brain injury.

Protective effects of FGF10 on neurovascular unit in a rat model of neonatal hypoxic-ischemic brain injury.

Neonatal hypoxic-ischemic (HI) brain injury remains a devastating clinical disease associated with high mortality and lifetime disability. Neonatal HI injury damages the architecture of neurovascular unit (NVU), thus, therapy targeting the NVU may provide effective neuroprotection against HI. This study was designed to investigate whether fibroblast growth factor 10 (FGF10) protected the NVU against HI and afforded observable neuroprotection in a rat model of neonatal HI brain injury. The results showed that FGF10 treatment significantly reduced brain damage post HI, characterized by reduction in brain infarct volume and tissue loss. Further interesting findings showed that FGF10 treatment exerted neuroprotective effects on HI brain injury in neonate rats through protecting the NVU against HI, evidenced by inhibition of neuronal cell apoptosis, suppression of gliosis, and amelioration of blood-brain barrier disruption. Collectively, our study indicates that FGF10 treatment exhibits great potential for protecting NVU against HI and attenuates neonatal brain injury, suggesting a potential novel therapeutic agent to this disease.

Biodegradable copolypeptide hydrogel prodrug accelerates dermal wound regeneration by enhanced angiogenesis and epithelialization.

Hydrogels are one of the most promising wound dressings. However, their effectiveness on wound healing is still largely limited due to either the non-degradability or the release of non-therapeutic degradable products. Herein, a biodegradable copolypeptide hydrogel based on the glutamic acid and lysine was synthesized and applied as both wound dressing and therapeutic prodrug. The hydrogel can degrade in the existence of elevated degradative enzymes in a wound environment, which will release therapeutic amino acids to enhance the wound healing. In vivo results found that the hydrogel could effectively promote wound regeneration in both macroscopic and microscopic scales. Further investigation revealed that the wound healing effect of the hydrogel was highly attributed to its enhanced impact on angiogenesis, cell proliferation and re-epithelialization of the wound. All in all, the present study proves that the degradable copolypeptide hydrogel can efficiently improve wound healing and indicates its potent clinical application for wound regeneration.