Improvement of nutritional support strategies after surgery for benign liver tumor through nutritional risk screening: a prospective,randomized, controlled,single-blind clinical study

Objective

The rising of individualized therapy requires nutritional risk screening has become a major topic for each particular disease, yet most of the screenings were for malignancies, less for benign diseases. There is no report on the screening of patients with benign liver tumors postoperatively. We aim to evaluate the nutritional support strategies post operation for benign liver tumors through nutritional risk screening.

Methods

In this prospective, randomized, controlled study, 95 patients who underwent hepatectomy for benign tumors were divided into two groups. Fifty patients in the control group were given routine permissive underfeeding nutritional supply (75 kJ/kg/d), and 45 patients in the experimental group were given lower energy (42 kJ/kg/d) in accordance of their surgical trauma. Routine blood tests, liver/kidney function were monitored before surgery and at the day 1, 3, 5, 9 after surgery, patients were observed for the time of flatus, complications, length of hospitalization (LOH), nutrition-related costs, and other clinical parameters. This completed study is registered with Clinicaltrials.gov, number NCT01292330.

Results

The nutrition-related expenses (494.0±181.0 vs. 1,514.4±348.4 RMB, P<0.05) and the total hospital costs (18,495.2±4735.0 vs. 21,432.7±8,291.2 RMB, P<0.05) for patients in the experimental group were significantly lower than those in the control group. Meanwhile, the lowered energy supply after the surgeries did not have adverse effects on clinical parameters, complications, and LOH.

Conclusions

Patient with benign liver tumors can adopt an even lower postoperative nutritional supply that close to that for mild non-surgical conditions, and lower than the postoperative permissive underfeeding standard.Key Words: Nutritional risk screening, benign liver tumor, individualized therapy, nutrition therapy, permissive underfeeding     

Surgical treatment of high grade dural arteriovenous fistulae

Dural arteriovenous fistulae (dAVF) with direct cortical venous drainage (CVD, Borden Type III) have a high risk of hemorrhage, particularly when symptomatic. Stereotactic radiosurgery is therefore not recommended, and endovascular treatment can be limited by access, incomplete obliteration, and recanalization. Of 70 cerebral dAVF seen at our institution over the past 8 years, 35 were Borden Type III (50%). Twenty-four were treated via microsurgery (69%). Presentation included hemorrhage in nine patients (38%), nonhemorrhagic neurologic deficits in five (21%), asymptomatic in five (21%), headache in three (13%), and seizure in two patients (8%). Only eight of 19 patients with symptomatic dAVF were independent (modified Rankin Scale [mRS] 0–2) preoperatively (42%). The dAVF location was tentorial in six patients (25%), petrosal in six (25%), superior sagittal sinus in four (17%), torcular in two (7%), floor of the anterior fossa in two (7%), and sphenoid ridge, transverse-sigmoid, inferior sagittal sinus and jugular in one patient each (4%). Four patients had failed endovascular therapy (17%). The angiographic obliteration rate was 96%. The combined permanent morbidity and mortality rate was 17%. After a mean follow-up of 2.1 years, 13 patients improved (54%), seven were the same, (29%) and four were worse (17%). Thirteen patients were asymptomatic (mRS 0, 54%), and 18 were independent (mRS 0–2, 75%). Our results reinforce that surgical treatment of dAVF with direct CVD is associated with a high angiographic cure rate with acceptable morbidity and mortality, particularly in light of the lesions’ natural history.     

Cerebrovascular neurosurgery in 2012

Considerable advances in our understanding of the natural history and treatment of cerebrovascular disease were made in 2012. The landmark Unruptured Cerebral Aneurysm Study in Japan was published, illustrating a significantly greater rupture risk than previously reported for small anterior and posterior communicating artery aneurysms, those with daughter domes, and giant aneurysms. Results from the Cerecyte (DePuy Synthes, West Chester, PN, USA) coil trial did not demonstrate a statistically significant positive impact of these bioactive coils on angiographic occlusion rates or outcome. The Clazosentan to Overcome Neurological Ischemia and Infarct Occurring after Subarachnoid Hemorrhage study was also published and unfortunately did not demonstrate an overall favorable long-term functional outcome rate for patients with aneurysmal subarachnoid hemorrhage receiving clazosentan. Studies furthering our understanding of the natural history and treatment of vascular malformations were also published, including large prospective natural history studies of cavernous malformations from the Mayo Clinic and the Scottish Audit of Intracranial Vascular Malformations database. Although pregnancy was found to be a significant risk factor for arteriovenous malformation hemorrhage, several studies did not demonstrate pregnancy as a significant risk factor for cavernous malformation hemorrhage. Finally, prospective randomized control trials illustrated significantly improved angiographic and clinical outcome results for both the Solitaire (ev3 Endovascular, Plymouth, MN, USA; SWIFT trial) and Trevo (Concentric Medical, Mountainview, CA, USA; TREVO 2 trial) stent retrievers as compared to the Merci (Concentric Medical) clot retriever.     

Akt/Nrf2 Activated Upregulation of Heme Oxygenase-1 Involves in the Role of Rg1 Against Ferrous Iron-Induced Neurotoxicity in SK-N-SH Cells

Iron accumulation is considered to be involved in the pathogenesis of Parkinson’s disease (PD). Our previous studies have observed that Rg1, a major pharmacologically active ingredient from Ginseng, could protect dopaminergic neurons by reducing nigral iron levels through regulating the expression of iron transporters in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced PD mice. The aim of this study is to investigate other mechanism involved in the cytoprotection of Rg1 against iron-induced neurotoxicity in human neuroblastoma SK-N-SH cells. Significant rescue of Rg1 on cell viability against 100 μM ferrous iron-induced neurotoxicity was observed. Upregulation of heme oxygenase-1 (HO-1) and Cu–Zn superoxide dismutase (Cu/Zn SOD) were observed in Rg1 pretreated group. Moreover, Rg1 pretreatment induces Nrf2 nuclear translocation, which is upstream of HO-1 expression, and activated PI3K/Akt pathway was also observed in Rg1 pretreated group. This could antagonize iron-induced increase in intracellular reactive oxygen species and decrease in mitochondrial transmembrane potential. These results suggest that the neuroprotective effects of Rg1 against iron toxicity are attributed to the anti-oxidative properties by activating Akt/Nrf2 pathway and increasing Nrf2-induced expression of HO-1 and Cu/Zn SOD.     

Surgical treatment of hypermotor seizures originating from the temporal lobe

PurposeTo describe the characteristics of electroclinical manifestations in patients with hypermotor seizures (HMSs) originating from the temporal lobe.MethodsWe retrospectively reviewed the data of patients who underwent surgical treatments for seizure to identify patients with HMSs of temporal origin. We systematically reviewed patient seizure histories, imaging reports, video-EEG monitoring data, operative records and pathological findings.ResultsEight of the 9 patients reported auras. The ictal behavior included marked agitation in 5 patients and mild agitation in 4 patients. All of the 9 patients exhibited stiffness or dystonia of the upper limb or contralateral limbs during ictus. Seven of the 9 patients completed intracranial recording and at least 3 seizures were recorded for each patient. The intracranial recordings showed ictal activity originating from mesial temporal lobe in 6 patients and the lateral temporal lobe in 1 patient. The time interval of ictal propagation from the temporal to frontal lobe was 15.0 ± 8.3 s. While the time interval from EEG origination to the beginning of hypermotor behavior was 21.0 ± 8.1 s. Brain MRIs revealed hippocampal sclerosis in 3, neoplastic lesion in 1, and normal images in the remaining 5 patients. Patients were followed for 1–5 years after the anterior temporal lobectomy; 7 patients remained seizure-free throughout follow-up.ConclusionSome HMSs can originate from the temporal lobe. In carefully selected patients, surgical resection may lead to good outcomes.     

Upexpression of Beclin-1-Dependent Autophagy Protects Against Beta-amyloid-Induced Cell Injury in PC12 Cells

Alzheimer’s disease (AD) is an age-related and progressive neurodegenerative disease. Beta-amyloid (Aβ) plays an important role in the pathogenesis of AD. Autophagy is a self-degradative process and its related protein Beclin-1 is involved in the initiation of autophagy. However, the role of Beclin-1 in the pathogenesis of AD is rarely reported. In this study, we examined cell viability and medium levels of neuron-specific enolase (NSE) in PC12 cells incubated with gradient concentrations of Aβ_1-42 (0.625, 1.25, 2.5, 5, 10 μM) for 6, 12, 24, 48, and 72 h, drew the index changes curves, and investigated the correlation between them. The result showed that cell viability was negatively correlated with NSE levels. Based on this study, Beclin-1 expression was quantitatively detected in Aβ_1-42-treated PC12 cells and the dynamic changes curve of Beclin-1 was drawn from 3 to 72 h. Beclin-1 expression was positively correlated with cell viability. Furthermore, both autophagy inhibitor 3-methyladenine (3-MA) and autophagy activator rapamycin were used to investigate the effect of autophagy on Aβ_1-42-induced cell injury. Aβ_1-42-induced Beclin-1 expression was further upregulated by rapamycin but was downregulated by 3-MA. Moreover, cell viability was increased by rapamycin but was decreased by 3-MA, and NSE was decreased by rapamycin but was increased by 3-MA, suggesting that activation of Beclin-1-dependent autophagy before the damage occurred can prevent neuronal cell death, while inhibition of Beclin-1-dependent autophagy can hastened cell death. These findings indicate that increasing Beclin-1-dependent autophagy may have a preventive effect before the AD occurred.     

Saturable Leptin Transport Across the BBB Persists in EAE Mice

We have shown that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, have upregulated leptin receptor expression in reactive astrocytes of the hippocampus, a region involved in sickness behavior. Leptin can exacerbate EAE when its serum concentration is high. Although leptin receptors in astrocytes modulate leptin transport across cultured endothelial cell monolayers, it is not known how leptin transport in EAE mice is regulated. Here, we determined brain and cervical spinal cord uptake of leptin in early and recovery stages of EAE, after either intravenous delivery or in situ brain perfusion of ¹²⁵I-leptin and the vascular marker ¹³¹I-albumin. While increased vascular space and general blood–brain barrier (BBB) permeability after EAE were expected, the specific saturable transport system for leptin crossing the BBB also persisted. Moreover, there was upregulation of leptin transport in hippocampus and cervical spinal cord in the early stage of EAE, shown by higher leptin uptake in these regions and by competitive inhibition with coadministered excess unlabeled leptin. We conclude that EAE induced a time- and region-specific increase of leptin transport. The results provide a link between circulating leptin and enhanced leptin signaling that may play a crucial role in disease progression.