'Ectopic' suprasellar type IIa PRL-secreting pituitary adenoma.

BACKGROUND: Ectopic pituitary adenomas (EPAs) are rare, and the suprasellar cistern seems to be the most common location. At this time, no detailed original classification, diagnosis, or treatment protocols for suprasellar pituitary adenomas (SPAs) have been described. CASE DESCRIPTION: A 19-year-old man showed visual disturbances and lack of libido for 3 years, he suffered a sharp decline in vision with only light perception in the last week. Magnetic resonance imaging scans revealed a large suprasellar cystic lesion with a normal pituitary in the sella turcica. Endocrinological findings showed an extremely high prolactin level of 1250 ng/mL. Because of the sharp decline in vision, the patient underwent total removal of the suprasellar lesion using a transfrontal interhemispheric approach. The tumor pedicle originated in the lower pituitary stalk without any connection to the anterior pituitary gland in the sella turcica, while the diaphragma sellae was incomplete. Clinical and endocrinological cure criteria were fulfilled and postoperative pathology confirmed a prolactin-secreting pituitary adenoma. CONCLUSION: Ectopic suprasellar pituitary adenomas (ESPAs) are extremely rare intracranial extracerebral tumors. SPAs can be classified into three types according to their origin and their relationship with surrounding tissue. Only type III is theoretically a true ectopic, based on previous reports. Thus, ESPAs are uncommon compared to other EPAs. Our case is the first reported case of a type IIa 'E'SPA and the first description of this subtype classification until now. The pars tuberalis may be different from the pars distalis, and each subtype of adenohypophyseal cells may have different migration characteristics, which leads to different proportions of each hormone-secreting subtype in SPAs and EPAs. Transsphenoidal surgery is minimally invasive, but transcranial surgery may remain a universal option for the treatment of suprasellar lesions.

Plasma 8-iso-Prostaglandin F2α, a possible prognostic marker in aneurysmal subarachnoid hemorrhage.

BACKGROUND: 8-iso-Prostaglandin F2α (8-iso-PGF2α) is a potential biomarker of oxidative stress. This study clarified whether plasma 8-iso-PGF2α concentrations were affected and its underlying relevance to prognosis in aneurysmal subarachnoid hemorrhage (aSAH). METHODS: In this prospective, observational study, a total of 170 controls and 170 aSAH patients were enrolled. Plasma 8-iso-PGF2α concentrations were detected using an ELISA. Severity was assessed by World Federation of Neurological Surgeons (WFNS) scale and modified Fisher grading scale. Clinical outcomes included 6-month mortality and poor outcome referred to as Glasgow outcome scale score of 1-3. RESULTS: As compared to controls, admission plasma 8-iso-PGF2α concentrations were significantly enhanced. Increased concentrations of plasma 8-iso-PGF2α correlated with WFNS scores and modified Fisher scores. 8-iso-PGF2α in plasma was an independent predictor for clinical outcomes. Under ROC curve, the predictive values of 8-iso-PGF2α concentrations resembled those of WFNS scores and modified Fisher scores for clinical outcomes. CONCLUSIONS: An elevation in plasma 8-iso-PGF2α concentrations is associated with the severity and poor outcome after aSAH, substantializing 8-iso-PGF2α as a potential prognostic biomarker of aSAH.

Elevation of serum CXC chemokine ligand-12 levels predicts poor outcome after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: CXC chemokine ligand-12 (CXCL12) is involved in the innate immune system. Elevation of its level in the peripheral blood is associated with severity and outcome of ischemic stroke. This study aimed to investigate its relation to severity and prognosis following aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Serum CXCL12 levels were determined in a total of 182 controls and 182 aSAH patients. Hemorrhagic severity was assessed using the World Federation of Neurological Surgeons (WFNS) scale and modified Fisher grading scale. Unfavorable outcome was defined as Glasgow outcome scale score of 1-3. Prognostic predictors of 6-month mortality and unfavorable outcome were identified using multivariate analysis. RESULTS: The serum CXCL12 levels were significantly higher in patients as compared to controls (14.5±6.7ng/mL vs. 1.7±0.6ng/mL, P<0.001) and were independently associated with WFNS scores (t=5.927, P<0.001) and modified Fisher scores (t=5.506, P<0.001). Serum CXCL12 levels predicted 6-month mortality and 6-month unfavorable outcome with the area under curves of 0.815 [95% confidence (CI), 0.751-0.868] and 0.809 (95% CI, 0.745-0.864) respectively and were related independently to 6-month mortality (odds ratio, 4.428; 95% CI, 1.977-12.031; P=0.004) and 6-month unfavorable outcome (odds ratio, 3.821; 95% CI, 1.097-9.251; P=0.001). Moreover, the predictive values of CXCL12 levels were in the range of WFNS scores and modified Fisher scores. CONCLUSIONS: Elevation of serum CXCL12 levels is associated highly with hemorrhagic severity and poor outcome after aSAH, suggesting CXCL12 might have the potential to be a prognostic predictive biomarker of aSAH.

Change of serum levels of thioredoxin in patients with severe traumatic brain injury.

BACKGROUND: Thioredoxin (TRX), a potent anti-oxidant, is released during inflammation and oxidative stress. The purpose of this study was to establish the relationship between serum TRX concentrations and trauma severity and outcome in severe traumatic brain injury (STBI). METHODS: We determined serum TRX concentrations in 112 patients and 112 controls. Multivariate analyses were performed to analyze the predictive factors of 1-week mortality, 6-month mortality and 6-month unfavorable outcome. The predictive values were investigated under receiver operating characteristic curves. RESULTS: Serum TRX concentrations were markedly higher in patients than in controls (19.1±7.8ng/ml vs. 8.0±2.3ng/ml, P<0.001). There was a significant negative association between serum TRX concentrations and Glasgow coma scale (GCS) scores (r=-0.543, P<0.001). Increased TRX was identified as an independent prognostic marker of 1-week mortality [Odds ratio (OR), 1.220; 95% confidence interval (CI), 1.101-1.367; P<0.001], 6-month mortality (OR, 1.201; 95% CI, 1.097-1.324; P<0.001) and 6-month unfavorable outcome (OR, 1.189; 95% CI, 1.090-1.311; P<0.001). TRX concentrations improved area under curve of GCS scores for 6-month unfavorable outcome, but not for 1-week mortality and 6-month mortality. CONCLUSIONS: Increased serum TRX concentration, associated highly with trauma severity and poor outcome, might be a novel prognostic marker in patients with STBI.

A novel method for culturing neural stem cells.

The standard culture method for neural stem cells cannot prevent the attachment of neurospheres, which eventually result in differentiation. This study developed a new method for long-term neural stem cell cultivation. In the antiattachment group, neural stem cells were cultured in flasks coated with 1.5% agarose gel. As a control, cells were cultured in plastic flasks. The 5-bromine-deoxyuridine incorporation assay was used to determine the S-phase labeling index of both groups. The methyl thiazolyl tetrazolium (MTT) colorimetric assay was used to determine the total cell vitality. After a 3-mo culture, the spontaneous differentiation of stem cells was studied using immunocytochemistry for neuroepithelial stem cell protein. We found that neural stem cells grew rapidly in the antiattachment flasks. There was no statistically significant difference between the two groups in terms of the S-phase labeling index or MTT assay. When cultured for 3 mo in vitro, many more cells differentiated in the control than in the antiattachment group (32.05 vs. 0.64%, P < 0.01). Moreover, the neural stem cells in the antiattachment group remained multipotent. Therefore, flasks coated with agarose gel are suitable for long-term neural stem cell culture.

Transplantation of neural stem cells into the traumatized brain induces lymphocyte infiltration.

OBJECTIVE: This study examined the lymphocyte infiltration induced by neural stem cell grafts in the traumatized brain. METHODS: Sixty Sprague-Dawley rats were assigned randomly to transplantation (n = 30) or control (n = 30) groups, and each rat was subjected to brain contusion. The neural stem cells derived from Wistar rats were transplanted into the lesion of the transplantation group, and saline was injected instead into the controls. Local lymphocyte infiltration was studied using haematoxylin and eosin staining, immunohistochemistry and flow cytometry. The immunogenicity of neural stem cells was evaluated using MHC-I expression. RESULTS: About 6.57 +/- 0.44% of the neural stem cells expressed MHC-I. In the transplantation group, histological examination and immunohistochemistry revealed significant lymphocyte infiltration in the contusion. The ratio of CD4(+) lymphocytes to total cells in the lesions was 13.28 +/- 1.60% in the transplantation group and 0.41 +/- 0.12% in the controls (p < 0.01). Likewise, the ratio of CD8(+) lymphocytes to total cells was 5.11 +/- 1.03% in the transplantation group and 0.57 +/- 0.26% in the controls (p < 0.01). CONCLUSIONS: Neural stem cells possess immunogenicity and can induce lymphocyte infiltration when transplanted into a traumatised brain. Our findings imply that immunosuppressive treatment is necessary following neural stem cell transplantation.

Inhibitory effect of progesterone on inflammatory factors after experimental traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality in young people. Inflammatory cytokines play an important part in the pathophysiology of TBI. Recent studies demonstrate that progesterone significantly reduces cerebral edema and enhances functional recovery from TBI and stroke in several animal models. This study was designed to investigate the inhibitory effect of progesterone on inflammatory response after traumatic brain injury. METHODS: Progesterone was injected intraperitoneally using rats as a model of traumatic brain injury, and Western blot technique was applied to detect the expression of three inflammation-related factors: nuclear factor kappa B p65 (NFkappaB p65), glial fibrillary acidic protein (GFAP), and tumor necrosis factor-alpha (TNF-alpha). The water content of injured brain was also examined. A neurological severity score was recorded to evaluate the effect of progesterone on neurodeficit recovery. RESULTS: NFkappaB p65, GFAP, and TNF-alpha were increased in all injured animals. In rats treated with progesterone, the expression level of NFkappaB p65 and TNF-alpha were reduced significantly in comparison with vehicle-treated rats. However, progesterone did not alter the expression of GFAP in the injured rats. Progesterone also reduced the water content of injured brain and the lesion volume. In addition, progesterone-treated injured rats showed significant improvements in the Neurological Severity Score test, compared with vehicle-treated ones. CONCLUSIONS: Progesterone inhibits the inflammatory response after experimental traumatic brain injury and mitigates the severity of brain damage.

Establishment of a mechanical injury model of rat hippocampal neurons in vitro.

OBJECTIVE: To establish a simple, reproducible, and practical mechanical injury model of hippocampal neurons of Sprague-Dawley rats in vitro. METHODS: Hippocampal neurons isolated from 1-2-day old rats were cultured in vitro. Mild, moderate and severe mechanical injuries were delivered to the neurons by syringe needle tearing, respectively. The control neurons were treated identically with the exception of trauma. Cell damage was assessed by measuring the Propidium Iodide (PI) uptaking at different time points (0.5, 1, 6, 12 and 24 hours) after injury. The concentration of neuron specific enolase was also measured at some time points. RESULTS: Pathological examination showed that degeneration, degradation and necrosis occurred in the injured cultured neurons. Compared with the control group, the ratio of PI-positive cells in the injured groups increased significantly after 30 minutes of injury (P<0.05). More severe the damage was, more PI-positive neurons were detected. Compared with the control group, the concentration of neuron specific enolase in the injured culture increased significantly after 1 hour of injury (P<0.05). CONCLUSIONS: The established model of hippocampal neuron injury in vitro can be repeated easily and can simulate the damage mechanism of traumatic brain injury, which can be used in the future research of traumatic brain injury.