Effects of ulinastatin therapy in deep vein thrombosis prevention after brain tumor surgery: A single-center randomized controlled trial.

BACKGROUND: Venous thromboembolism (VTE) is a common neurosurgical complication after brain tumor resection, and its prophylaxis has been widely studied. There are no effective drugs in the clinical management of venous thromboembolism, and there is an absence of evidence-based medicine concerning the treatment of severe multiple traumas. AIM: To explore whether ulinastatin (UTI) can prevent VTE after brain tumor resection. METHODS: The present research included patients who underwent brain tumor resection. Patients received UTIs (400,000 IU) or placebos utilizing computer-based random sequencing (in a 1:1 ratio). The primary outcome measures were the incidence of VTE, coagulation function, pulmonary emboli, liver function, renal function, and drug-related adverse effects. RESULTS: A total of 405 patients were evaluated between January 2019 and December 2021, and 361 of these were initially enrolled in the study to form intention-to-treat, which was given UTI (n = 180) or placebo (n = 181) treatment in a random manner. There were no statistically significant differences in baseline clinical data between the two groups. The incidence of VTE in the UTI group was remarkably improved compared with that in the placebo group. UTI can improve coagulation dysfunction, pulmonary emboli, liver function, and renal function. No significant difference was identified between the two groups in the side effects of UTI-induced diarrhea, vomiting, hospital stays, or hospitalization costs. The incidence of allergies was higher in the UTI group than in the placebo group. CONCLUSION: The findings from the present research indicated that UTI can decrease the incidence of VTE and clinical outcomes of patients after brain tumor resection and has fewer adverse reactions.

A Predictive Model for Chronic Hydrocephalus After Clipping Aneurysmal Subarachnoid Hemorrhage.

Chronic hydrocephalus after clipping aneurysmal subarachnoid hemorrhage (aSAH) often results in poor outcomes. This study was to establish and validate model to predict chronic hydrocephalus after aSAH by least absolute shrinkage and selection operator logistic regression. The model was constructed from a retrospectively analyzed. Two hundred forty-eight patients of aSAH were analyzed retrospectively in our hospital from January 2019 to December 2021, and the patients were divided into chronic hydrocephalus (CH) group (n=55) and non-CH group (n=193) according to whether occurred CH within 3 months. In summary, 16 candidate risk factors related to chronic hydrocephalus after aSAH were analyzed. Univariate analysis was performed to judging the risk factors for CH. The least absolute shrinkage and selection operator regression was used to filter risk factors. Subsequently, the nomogram was designed by the above variables. And area under the curve and calibration chart were used to detect the discrimination and goodness of fit of the nomogram, respectively. Finally, decision curve analysis was constructed to assess the practicability of the risk of chronic hydrocephalus by calculating the net benefits. Univariate analysis showed that age (60 y or older), aneurysm location, modified Fisher grade, Hunt-Hess grade, and the method for cerebrospinal fluid drainage, intracranial infections, and decompressive craniectomy were significantly related to CH ( P <0.05). Whereas 5 variables [age (60 y or older), posterior aneurysm, modified Fisher grade, Hunt-Hess grade, decompression craniectomy] from 16 candidate factors were filtered by LASSO logistic regression for further research. Area under the curve of this model was 0.892 (95% confidence interval: 0.799-0.981), indicating a good discrimination ability. Meanwhile, the result of calibration indicated a good fitting between the prediction probability and the actual probability. Finally, decision curve analysis showed a good clinical efficacy. In summary, this model could conveniently predict the occurrence of chronic hydrocephalus after aSAH. Meanwhile, it could help physicians to develop personalized treatment and close follow-up for these patients.

Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation.

Decompressive craniectomy is an effective strategy to reduce intracranial hypertension after traumatic brain injury (TBI), but it is related to many postoperative complications, such as delayed intracranial hematoma and diffuse brain swelling. Our previous studies have demonstrated that controlled decompression (CDC) surgery attenuates brain injury and reduces the rate of complications after TBI. Here, we investigated the potential molecular mechanisms of CDC in experimental models. The in vitro experiments were performed in a traumatic neuronal injury (TNI) model following compression treatment in primary cultured cortical neurons. We found that compression aggravates TNI-induced neuronal injury, which was significantly attenuated by CDC for 2 h or 3 h. The results of immunocytochemistry showed that CDC reduced neuronal necroptosis and activation of RIP3 induced by TNI and compression, with no effect on RIP1 activity. These protective effects were associated with decreased levels of inflammatory cytokines and preserved intracellular Ca2+ homeostasis. In addition, the expression of the two-pore domain K+ channel TREK-1 and its activity was increased by compression and prolonged by CDC. Treatment with the TREK-1 blockers, spadin or SID1900, could partially prevent the effects of CDC on intracellular Ca2+ metabolism, necroptosis, and neuronal injury following TNI and compression. Using a traumatic intracranial hypertension model in rats, we found that CDC for 20 min or 30 min was effective in alleviating brain edema and locomotor impairment in vivo. CDC significantly inhibited neuronal necroptosis and neuroinflammation and increased TREK-1 activation, and the CDC-induced protection in vivo was attenuated by spadin and SID1900. In summary, CDC is effective in alleviating compressive neuronal injury both in vitro and in vivo, which is associated with the TREK-1-mediated attenuation of intracellular Ca2+ overload, neuronal necroptosis, and neuroinflammation.

IP3R-mediated activation of BK channels contributes to mGluR5-induced protection against spinal cord ischemia-reperfusion injury.

Spinal cord ischemia-reperfusion injury (SCIRI) can cause dramatic neuron loss and lead to paraplegia in patients. In this research, the role of mGluR5, a member of the metabotropic glutamate receptors (mGluRs) family, was investigated both in vitro and in vivo to explore a possible method to treat this complication. In vitro experiment, after activating mGluR5 via pretreating cells with (RS)-2-Chloro-5-hydroxyphenylglycine (CHPG) and 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB), excitotoxicity induced by glutamate (Glu) was attenuated in primary spinal cord neurons, evidenced by higher neuron viability, decreased lactate dehydrogenase (LDH) release and less detected TUNEL-positive cells. According to Western Blot (WB) results, Glu treatment resulted in a high level of large-conductance Ca2+- and voltage-activated K+ (BK) channels, with activation relying on the mGluR5-IP3R (inositol triphosphate) pathway. In vivo part, a rat model of SCIRI was built to further investigate the role of mGluR5. After pretreating them with CHPG and CDPPB, the rats showed markedly lower spinal water content, attenuated motor neuron injury in the spinal cord of L4 segments, and better neurological function. This effect could be partially reversed by paxilline, a blocker of BK channels. In addition, activating BK channels alone using specific openers: NS1619 or NS11021 can protect spinal cord neurons from injury induced by either SCIRI or Glu. In conclusion, in this research, we proved that mGluR5 exerts a protective role in SCIRI, and this effect partially works via IP3R-mediated activation of BK channels.

Bioinformatics-based Identification of Key Pathways and Hub Genes of Traumatic Brain Injury in a Rat Model.

Traumatic brain injury (TBI) is a common injury caused by external forces that lead to damaged brain function or pathological changes in the brain tissue. To explore the molecular mechanism and the hub genes of TBI, we downloaded gene expression profiles of the TBI model of rat and the sham control for the subsequent gene set enrichment analysis, pathway analysis and protein-protein interactions analysis. The results of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis indicated that multiple biological pathways, including immune response, inflammatory response and cellular response to interleukin-1, as well as signaling pathways, such as tumor necrosis factor signaling pathway, chemokine signaling pathway, cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway and nuclear factor kappa B signaling pathway were implicated in the TBI. In conclusion, this study provides insights into the molecular mechanism of TBI by screening the differentially expressed genes and hub genes that can be used as biomarkers and therapeutic targets.

FGF-2 suppresses neuronal autophagy by regulating the PI3K/Akt pathway in subarachnoid hemorrhage.

The degree of early brain injury (EBI) is a significant factor that affects the prognosis of patients with subarachnoid hemorrhage (SAH). Evidence has shown that fibroblast growth factor-2 (FGF-2) may alleviate the serious consequences of EBI after SAH. The objective of the current study was to investigate the underlying mechanism that mediates the neuroprotective effects of FGF-2 in the SAH rat model. Sprague-Dawley (SD) rats that underwent different treatments were divided into various groups. FGF-2 was administered intranasally to rats in the treatment group within 30 min after modeling. Rapamycin (an autophagy activator) or LY294002 (a PI3K/Akt pathway inhibitor) was administered intracerebroventricularly (i.c.v.) 30 min before modeling. Neurological scale and brain water content were measured in the brain tissue of the rats. TUNEL staining, Western blot, and immunofluorescence staining were performed to examine and compare the diverse effects of FGF-2 treatment, activated autophagy, and inhibited the PI3K/Akt pathway. We found that FGF-2 treatment effectively reduced the number of TUNEL-positive cells, decreased the brain water content, and improved the neurological function of rats after SAH. Additionally, the expression levels of autophagy-related proteins (LC3 and Beclin-1) were obviously decreased in the FGF-2 treatment group compared with the SAH + vehicle group. The therapeutic effects of FGF-2 in the SAH + FGF-2+rapamycin group were weakened compared with that in the SAH + FGF-2+DMSO group. In the event of the PI3K/Akt pathway inhibition, the expression levels of LC3 and Beclin-1 were enhanced, and the therapeutic effects of FGF-2 were compromised. In summary, our data collectively demonstrated that FGF-2 may suppress autophagy levels to play a neuroprotective role, at least partially by activating the PI3K/Akt pathway. These results highlight FGF-2 as a promising solution to the clinical intervention of SAH.

Posttraumatic Giant Intradiploic Epidermoid Cyst of Orbital Roof.

ABSTRACT: Epidermoid cysts are rare benign tumors that account for 0.3% to 1.8% of all intracranial space-occupying lesions. They are usually congenital in origin and are thought to derived from ectodermal cell inclusions occurring during closure of the neural tube around third to fifth week of gestation. They are most commonly located in the cerebellopontine angle and the parasellar area, and their location in the diploic space is very rare. In this article, a case of giant epidermoid cyst located in the orbital roof intradiploic space is presented with clinical, radiologic features and surgical treatment.

The AMPAR Antagonist Perampanel Regulates Neuronal Necroptosis via Akt/GSK3ß Signaling After Acute Traumatic Injury in Cortical Neuron.

BACKGROUND: Perampanel is a highly selective and non-competitive α-amino-3-hydroxy- 5 -methyl-4-isoxazole propionate (AMPA) receptor (AMPAR) antagonist, which has been licensed as an orally administered antiepileptic drug in more than 55 countries. Recently, perampanel was found to exert neuroprotective effects in hemorrhagic and ischemic stroke models. OBJECTIVE: In this study, the protective effect of perampanel was investigated. METHODS: The protective effect of perampanel was investigated in an in vitro Traumatic Neuronal Injury (TNI) model in primary cultured cortical neurons. RESULTS: We found that perampanel significantly preserved morphological changes, attenuated lactate dehydrogenase (LDH) release and inhibited caspase-3 activation after TNI. The TNI-induced necroptosis, as evidenced by flow cytometry, was markedly reduced by perampanel treatment. The results of western blot showed that perampanel decreased the expression and phosphorylation of the necroptotic factors, receptor protein interacting kinase 1 (RIPK1) and RIPK3. In addition, treatment with perampanel increased the phosphorylation of Akt and GSK3ß in a time-dependent manner up to 24 h after TNI. Treatment with the Akt inhibitor LY294002 partially reversed the protective effects of perampanel. CONCLUSION: Our present data suggest that necroptosis plays a key role in the pathogenesis of neuronal death after TNI, and that perampanel might have therapeutic potential for patients with Traumatic Brain Injury (TBI).

Giant aneurysm of the bilateral vertebrobasilar junction treated by pipeline and coils: A case report and literature review.

Giant aneurysm of the posterior circulation is associated with a higher risk of rupture compared with that of the anterior circulation. Furthermore, surgical clipping and interventional embolization for giant aneurysm of the posterior circulation are more difficult and complex to perform. The present study reported on the case of a 26-year-old female who exhibited a giant spherical aneurysm of the vertebrobasilar junction (VBJ) with a maximum diameter of ~35 mm that caused cervical discomfort. In addition, the patient experienced symptoms including left-sided walking and hoarseness caused by the compression of the brainstem and the posterior cranial nerves. The risks associated with performing surgery in this area are high and the prognosis is mainly poor. The patient of the present study was treated using the Pipeline Flex device with coil embolization. As a giant aneurysm of the VBJ simultaneously affects the bilateral vertebral arteries (VAs) and basilar artery, it is a unique condition and the treatment strategy must be personalized. Based on an analysis of the hemodynamic influence on the aneurysm in the present case, the Pipeline was placed through the left VA, the coils were packed through the right VA, and finally, the right VA was proximally occluded. At 7 months after embolization, the patient's modified Rankin scale score was 1 point. Upon analysis of the hemodynamic influence on the aneurysm of the VBJ, the VA with the larger shear force on the wall of the aneurysm was selected for occlusion to simplify the treatment of the aneurysm and to maximize the probability to achieve recovery.

Forniceal deep brain stimulation in severe Alzheimer's disease: A case report.

BACKGROUND: Forniceal deep brain stimulation (DBS) has been proposed as an alternative treatment for Alzheimer's disease (AD). Previous studies on mild to moderate AD patients demonstrated improvements in cognitive functions brought about by forniceal DBS. Here, we report our longitudinal findings in one severe AD patient for whom the activities of daily living (ADL) rather than cognitive function significantly improved after 3 mo of continuous stimulation. CASE SUMMARY: In 2011, a 62-year-old Chinese male with no previous history of brain injury or other neuropsychological diseases and no family history of dementia developed early symptoms of memory decline and cognitive impairment. Five years later, the symptoms had increased to the extent that they affected his daily living. He lost the ability to work as a businessman and to take care of himself. The patient was given a clinical diagnosis of probable AD and was prescribed donepezil and subsequently memantine, but no improvement in symptoms was observed. The patient then received DBS surgery. After 3 mo of continuous stimulation, the patient's ADL score decreased from 65 points to 47 points, indicating the quality of the patient's daily living improved distinctly. Other scores remained unchanged, suggesting no significant improvement in cognitive function. A follow-up positron emission tomography scan demonstrated perceivable increased glucose metabolism in the classical AD-related brain regions. CONCLUSION: Based on this case we hypothesize that forniceal DBS may improve ADL through elevating regional glucose metabolism in the brain.

Up-regulation of circular RNA hsa_circ_01844 induces apoptosis and suppresses proliferation and migration of glioblastoma cells.

BACKGROUND: Previous studies have demonstrated that various circular RNAs are involved in the malignant proliferation of cancers, such as liver cancer, lung cancer, breast cancer, and others. The potential role of circular RNAs in glioblastoma, however, is still uncertain. In this study, we aimed to study the potential role of hsa_circ_01844 in glioblastoma. METHODS: Using reverse transcription-polymerase chain reaction (RT-PCR) method, hsa_circ_01844 expression was measured in five glioblastoma samples and five normal brain samples. To evaluate the potential function of hsa_circ_01844 in glioblastoma, hsa_circ_01844 was overexpressed in glioblastoma cell lines (U251 and U87 cells). Using these two cell lines, in vitro experiments including the flow cytometry assay, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, Transwell assay, and cell apoptosis assay were performed to investigate the role of hsa_circ_01844 in glioblastoma. Student t test and one-way analysis of variance were used for statistical analysis. RESULTS: The expression of circular RNA hsa_circ_01844 was lower in glioblastoma tissues when compared with the normal brain tissues by RT-PCR method (0.034 ±â€Š0.036 vs. 1.630 ±â€Š0.891, P < 0.001). Using two glioblastoma cell lines, we found that overexpression of hsa_circ_01844 in glioblastoma cells suppressed their proliferation, colony formation, migration, and increased the apoptotic rate compared with empty vector group and blank control group (all P < 0.05). CONCLUSION: Hsa_circ_01844 shows decreased expression in glioblastoma and its overexpression induces apoptosis and inhibits proliferation, migration, and invasion of glioblastoma cells.

Infections under Skin Flap After Cranioplasty and a Simple Effective Treatment.

AIM: To report treatment experiences with titanium mesh cranioplasty infection at a single institution over the last 5 years. MATERIAL AND METHODS: We retrospectively reviewed 11 consecutive patients who were diagnosed with infection under the skin flap after titanium mesh cranioplasty and received our new treatment between Feb 2008 and Feb 2013. We performed a 2- to 6-year follow-up to evaluate prognosis and security. RESULTS: All 11 patients were cured and discharged, and all saved their infected bone flap (titanium mesh) completely. There was no recurrence of infection after follow-up for 2-6 years. CONCLUSION: Sensitive antibiotics combined with enclosed continuous irrigation and drainage is a safe, easy, economical and effective treatment for infection after titanium mesh cranioplasty that can save the infected bone flap.

The Value of Managing Severe Traumatic Brain Injury During the Perioperative Period Using Intracranial Pressure Monitoring.

This study aimed to investigate the clinical efficacy of intracranial pressure (ICP) monitoring regarding the perioperative management of patients with severe traumatic brain injury (sTBI). This was a cohort study performed between Jan 2013 and Jan 2016 and included all patients with sTBI. All patients were split into ICP monitoring and non-ICP monitoring groups. The primary outcomes were in-hospital mortality and Glasgow Outcome Scale (GOS) scores 6 months after injury, whereas the secondary outcomes include rate of successful nonsurgical treatment, rate of decompression craniotomy (DC), the length of stay in the ICU, and the hospital and medical expenses. This retrospective analysis included 246 ICP monitoring sTBI patients and 695 without ICP monitoring sTBI patients. No significant difference between groups regarding patient demographics. All patients underwent a GOS assessment 6 months after surgery. Compared to the non-ICP monitoring group, a lower in-hospital mortality (20.3% vs 30.2%, P < 0.01) and better GOS scores after 6 months (3.3 ±â€Š1.6 vs 2.9 ±â€Š1.6, P < 0.05) with ICP monitoring. In addition, patients in the ICP monitoring group had a lower craniotomy rate (41.1% vs 50.9%, P < 0.01) and a lower DC rate (41.6% vs 55.9%, P < 0.05) than those in the non-ICP monitoring group. ICU length of stay (12.4 ±â€Š4.0 days vs 10.2 ±â€Š4.8 days, P < 0.01) was shorter in the non-ICP monitoring group, but it had no difference between 2 groups on total length of hospital stay (22.9 ±â€Š13.6 days vs 24.6 ±â€Š13.6 days, P = 0.108); Furthermore, the medical expenses were significantly higher in the non-ICP monitoring group than the ICP monitoring group (11.5 ±â€Š7.2 vs 13.3 ±â€Š9.1, P < 0.01). Intracranial pressure monitoring has beneficial effects for sTBI during the perioperative period. It can reduce the in-hospital mortality and DC rate and also can improve the 6-month outcomes. However, this was a single institution and observational study, well-designed, multicenter, randomized control trials are needed to evaluate the effects of ICP monitoring for perioperative sTBI patients.

ROS-Mediated Mitochondrial Dysfunction and ER Stress Contribute to Compression-Induced Neuronal Injury.

Intracranial hypertension (IH) is a medical or surgical emergency that can be the common ending of various neurological disorders, such as traumatic brain injury, cerebral vascular diseases and brain tumors. However, the molecular mechanisms underlying IH-induced neuronal apoptosis have not been fully determined, and the treatments are symptomatic, insufficient and complicated by side-effects. In this study, a cellular model induced by compressed gas treatment in primary cultured rat cortical neurons was performed to mimic IH-induced neuronal injury in vitro. We found that compression induced cytotoxicity and apoptosis in cortical neurons in a dose- and time-dependent manner. Compression resulted in oxidative stress, which could be prevented by the ROS scavenger N-acetylcysteine (NAC). Compression produced mitochondrial oxidative stress, ATP loss and mitochondrial fragmentation. The results of western blot showed that compression differently regulated the expression of mitochondrial dynamic proteins, and the Drp1 inhibitor mdivi-1 partially reversed the compression-induced cytotoxicity. Compression significantly increased the expression of ER stress-associated factors in a time-dependent manner. The results of calcium imaging showed that compression induced intracellular calcium overload via promoting ER calcium release. Furthermore, the results using inhibitors of each signaling pathway demonstrated that ROS mediated the compression-induced ER stress and mitochondrial dysfunction in cortical neurons. In conclusion, our results demonstrated that compression induced apoptosis in primary cultured cortical neurons, which was associated with ROS mediated ER stress and mitochondrial dysfunction. Pharmacological compounds or agents targeting mitochondrial dysfunction and ER stress associated oxidative stress might be ideal candidates for the treatment of IH-related neurological diseases.

Expression signatures of long non-coding RNA and mRNA in human traumatic brain injury.

Long non-coding RNAs (lncRNAs) play a key role in craniocerebral disease, although their expression profiles in human traumatic brain injury are still unclear. In this regard, in this study, we examined brain injury tissue from three patients of the 101st Hospital of the People's Liberation Army, China (specifically, a 36-year-old male, a 52-year-old female, and a 49-year-old female), who were diagnosed with traumatic brain injury and underwent brain contusion removal surgery. Tissue surrounding the brain contusion in the three patients was used as control tissue to observe expression characteristics of lncRNAs and mRNAs in human traumatic brain injury tissue. Volcano plot filtering identified 99 lncRNAs and 63 mRNAs differentially expressed in frontotemporal tissue of the two groups (P < 0.05, fold change > 1.2). Microarray analysis showed that 43 lncRNAs were up-regulated and 56 lncRNAs were down-regulated. Meanwhile, 59 mRNAs were up-regulated and 4 mRNAs were down-regulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed 27 signaling pathways associated with target genes and, in particular, legionellosis and influenza A signaling pathways. Subsequently, a lncRNA-gene network was generated, which showed an absolute correlation coefficient value > 0.99 for 12 lncRNA-mRNA pairs. Finally, quantitative real-time polymerase chain reaction confirmed different expression of the five most up-regulated mRNAs within the two groups, which was consistent with the microarray results. In summary, our results show that expression profiles of mRNAs and lncRNAs are significantly different between human traumatic brain injury tissue and surrounding tissue, providing novel insight regarding lncRNAs' involvement in human traumatic brain injury. All participants provided informed consent. This research was registered in the Chinese Clinical Trial Registry (registration number: ChiCTR-TCC-13004002) and the protocol version number is 1.0.

Reduced inflammatory cell recruitment and tissue damage in spinal cord injury by acellular spinal cord scaffold seeded with mesenchymal stem cells.

Therapy using acellular spinal cord (ASC) scaffolds seeded with bone marrow stromal cells (BMSCs) has previously been shown to restore function of the damaged spinal cord and improve functional recovery in a rat model of acute hemisected spinal cord injury (SCI). The aim of the present study was to determine whether BMSCs and ASC scaffolds promote the functional recovery of the damaged spinal cord in a rat SCI model through regulation of apoptosis and immune responses. Whether this strategy regulates secondary inflammation, which is characterized by the infiltration of immune cells and inflammatory mediators to the lesion site, in SCI repair was investigated. Basso, Beattie, and Bresnahan scores revealed that treatment with BMSCs seeded into an ASC scaffold led to a significant improvement in motor function recovery compared with treatment with an ASC scaffold alone or untreated controls at 2 and 8 weeks after surgery (P<0.05). Two weeks after transplantation, the BMSCs seeded into an ASC scaffold significantly decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, as compared with the ASC scaffold only and control groups. These results suggested that the use of BMSCs decreased the apoptosis of neural cells and thereby limited tissue damage at the lesion site. Notably, the use of BMSCs with an ASC scaffold also decreased the recruitment of macrophages (microglia; P<0.05) and T lymphocytes (P<0.05) around the SCI site, as indicated by immunofluorescent markers. By contrast, there was no inhibition of the inflammatory response in the control and ASC scaffold only groups. BMSCs regulated inflammatory cell recruitment to promote functional recovery. However, there was no significant difference in IgM-positive expression among the three groups (P>0.05). The results of this study demonstrated that BMSCs seeded into ASC scaffolds for repair of spinal cord hemisection defects promoted functional recovery through the early regulation of inflammatory cell recruitment with inhibition of apoptosis and secondary inflammation.

[Mass Transfer Kinetics Model of Ultrasonic Extraction of Pomegranate Peel Polyphenols].

OBJECTIVE: The dynamic mathematical model of ultrasonic extraction of polyphenols from pomegranate peel was constructed with the Fick's second law as the theoretical basis. METHODS: The spherical model was selected, with mass concentrations of pomegranate peel polyphenols as the index, 50% ethanol as the extraction solvent and ultrasonic extraction as the extraction method. In different test conditions including the liquid ratio, extraction temperature and extraction time, a series of kinetic parameters were solved, such as the extraction process (k), relative raffinate rate, surface diffusion coefficient(D(S)), half life (t½) and the apparent activation energy (E(a)). RESULTS: With the extraction temperature increasing, k and D(S) were gradually increased with t½ decreasing,which indicated that the elevated temperature was favorable to the extraction of pomegranate peel polyphenols. The exponential equation of relative raffinate rate showed that the established numerical dynamics model fitted the extraction of pomegranate peel polyphenols, and the relationship between the reaction conditions and pomegranate peel polyphenols concentration was well reflected by the model. CONCLUSION: Based on the experimental results, a feasible and reliable kinetic model for ultrasonic extraction of polyphenols from pomegranate peel is established, which can be used for the optimization control of engineering magnifying production.

Sirt3 attenuates hydrogen peroxide-induced oxidative stress through the preservation of mitochondrial function in HT22 cells.

Sirtuins (Sirt) are a family of phylogenetically conserved nicotinamide adenine nucleotide (NAD(+))-dependent protein deacetylases, among which Sirt3 resides primarily in the mitochondria and serves as a stress responsive deacetylase, playing a role in protecting cells from damage under stress conditions. The present study aimed to investigate the role of Sirt3 in hydrogen peroxide (H(2)O(2))-induced oxidative neuronal injury in HT22 mouse hippocampal cells. Treatment with H(2)O(2) increased the expression of Sirt3 in a dose- and time-dependent manner, and the knockdown of Sirt3 using specific small interfering RNA (siRNA) exacerbated the H(2)O(2)-induced neuronal injury. The overexpression of Sirt3 induced by lentiviral transfection significantly reduced the generation of reactive oxygen species (ROS) and lipid peroxidation following injury, whereas the activities of endogenous antioxidant enzymes were not affected. Further experiments revealed that the H(2)O(2)-induced inhibition of mitochondrial complex activity and adenosine triphosphate (ATP) synthesis, the decrease in mitochondrial Ca(2+) buffering capacity and mitochondrial swelling were all partly reversed by Sirt3. Furthermore, the overexpression of Sirt3 attenuated the release of cytochrome c, the increase in the Bax/Bcl-2 ratio, as well as caspase-9/caspase-3 activity induced by H(2)O(2), and eventually inhibited apoptotic neuronal cell death. These results suggest that Sirt3 acts as a prosurvival factor, playing an essential role in protecting HT22 cells under H(2)O(2)-induced oxidative stress, possibly by inhibiting ROS accumulation and the activation of the mitochondrial apoptotic pathway.

Endoscopy-assisted cerebral falx incision via unilateral approach for treatment of dissymmetric bilateral frontal contusion.

OBJECTIVE: To investigate the clinical features and treatment strategy of dissymmetric bilateral frontal contusion, and to summarize our experience in treating these patients by minimally invasive surgery. METHODS: Over the past 3 years, we have treated a total of 31 patients with dissymmetric bilateral frontal contusion using endoscopy-assisted unilateral cerebral falx incision. Other 30 patients treated by routine bilateral approaches within the same period were taken as control. RESULTS: Seventeen cases (54.8%) in the unilateral operation group survived and were in good condition, 8 (25.8%) had moderate disability, 4 (12.9%) had severe disability, 1 (3.2%) was in vegetative state, and 1 (3.2%) died. Compared with the control group, the Glasgow Outcome Scale score was not significantly different in the unilateral operation group, but the operation time, blood transfusion volume, the length of hospital stay, the incidences of mental disorder and olfactory nerve injury were greatly reduced in the unilateral operation group. CONCLUSIONS: Endoscopy-assisted unilateral cerebral falx incision can shorten the operation time, reduce surgical trauma and complications in treatment of patients with dissymmetric bilateral frontal contusion. It can obviously diminish the chance of delayed intracerebral hematoma and subsequently minimize the incidences of subfalcial and centrencephalic herniation.

[Identification of Tritielytrigia alien disomic addition line shannong 87074-519 with yellow rust resistance].

In this paper, Shannong 87074-519, a derivative of wheat-decaploid Elytrigia elongata, was identified by inoculation assessment, cytological analysis, simple sequence repeat (SSR), molecular marker technique,and genomic in situ hybridization (GISH). The results are as follows: the chromosome number of Shannong87074-519 in root tip cells was 2n=44, 22 bivalents were observed in most PMC at MI, and the average chromosome configuration was 2n=44=21.82 II+0.36 I , and the chromosome configuration (2n=43=21 II +1 I) was observed in most PMC of F1 between Shannong87074-519 and C.S. at MI. Therefore, it was an alien disomic addition line with one pair chromosome of Elytrigia elongata. Then the St total genomic DNA was labeled as probe in GISH, the green-yellow hybridization signal was observed in two intact chromosomes, indicating that Shannong87074-519 was added by one pair chromosome of St genome. The SSR-PCR technique was employed in the primer filtration, and the molecular marker BARC165 was singled out from 170 primers, which could amplify the specific molecular marker BARC165(268) of Elytrigia elongata in Shannong87074-519. Subsequently, the specific segment in Elytrigia elongata was cloned and labeled as probe in GISH of root tip cells of Shannong87074-519, the light yellow hybridization signal was observed in both chromatin at interphase and chromosome at mitotic metaphase, thus the BARC165(268) could be applied as a specific molecular marker to detect alien chromatin of Elytrigia elongata in Shannong87074-519. Because of the good agronomic characteristics, high immunity to yellow rust, and dominant new yellow rust resistant gene located at the added chromosome St, assigned as YrSt temporarily, Shannong87074-519 has very important value in wheat breeding and genetics improvement.