Impact of hyperglycemia on neuronal apoptosis after subarachnoid hemorrhage in rodent brain: An experimental research.

BACKGROUND: Hyperglycemia, a derangement after subarachnoid hemorrhage (SAH), is known to be associated with unfavorable outcomes. Whether the connection between hyperglycemia and poor prognosis results from severe neuronal apoptosis is unknown, and we aim at investigating their relationship. MATERIAL AND METHODS: Streptozotocin (STZ) was administrated to trigger hyperglycemia before SAH induction in Sprague-Dawley rats that were assigned to one of four groups: control, SAH only, hyperglycemia only, and SAH with hyperglycemia. The severity of neuronal apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated dUTP nickend labelling (TUNEL) staining of cerebral cortex. RESULTS: When subjected to SAH, hyperglycemic animals had worse neurobehavioral functions than normoglycemic ones. Hyperglycemia-exacerbated apoptosis was evident by greater increases in cleaved caspase-3 expression and TUNEL-positive cell density in the SAH with hyperglycemia group than those in the SAH only group, whereas there was no significant difference in cleaved caspase-9 expression and Bax/Bcl-2 ratio between the two groups. Furthermore, there was a remarkable decrease in the ratio of phosphorylated extracellular regulated kinase (ERK)/total ERK in the hyperglycemic rats after SAH. CONCLUSION: Hyperglycemia aggravated neuronal apoptosis after SAH and was associated with impaired neurological outcomes. Activation of the extrinsic caspase cascade through the ERK signal pathway may contribute to hyperglycemia-mediated apoptosis.

Hyperglycemia Aggravates Cerebral Vasospasm after Subarachnoid Hemorrhage in a Rat Model.

BACKGROUND: Hyperglycemia is common and showed to be risky for poor prognosis in patients with subarachnoid hemorrhage (SAH). However, the causality and mechanism underlying this observation are not well established. OBJECTIVE: To investigate the relationship between hyperglycemia and cerebral vasospasm with its pathogenesis in a rat model of SAH. METHODS: One-shot SAH model was employed in male Sprague-Dawley rats. Hyperglycemia was triggered by intraperitoneal streptozotocin administration (50 mg/kg) 7 days before SAH induction. The severity of cerebral vasospasm was determined by the cross-sectional area of basilar artery (BA) in male rats randomly assigned to 1 of 4 groups: control, hyperglycemia only, SAH only, and SAH with hyperglycemia. The expression of endothelial nitric oxide synthase (eNOS) and induced nitric oxide synthase (iNOS) in the BA were analyzed by immunohistochemistry. RESULTS: The mean (standard deviation) blood glucose level was 433.0 (98.3) and 156.5 (31.7) mg/dL in streptozotocin -treated and untreated rats, respectively. Hyperglycemic rats exhibited poorer neurobehavioral performance than normoglycemic rats when subjected to SAH. Hyperglycemia-mediated exacerbation of vasospasm was evident by the greater decrease in the BA cross-sectional area in the hyperglycemic SAH group than in the SAH only group. Furthermore, there was more decreased expression of eNOS and increased expression of iNOS within the vessels of the hyperglycemic SAH rats. CONCLUSION: Hyperglycemia exacerbated cerebral vasospasm and was associated with poorer neurological outcomes following SAH. Our findings also suggested the nitric oxide pathway as a potential underlying mechanism via the dysregulation of eNOS and iNOS.

Motor outcome of deep intracerebral haemorrhage in diffusion tensor imaging: comparison of data from different locations along the corticospinal tract.

OBJECTIVES: Although diffusion tensor imaging (DTI) is widely studied to assess the motor outcome after ischaemic stroke, there is paucity of data regarding outcomes of intracerebral haemorrhage (ICH). The aim of this study was to determine the DTI data from different locations along the corticospinal tract (CST) and association to motor outcome. METHODS: We prospectively recruited patients with deep ICH admitted to our hospital from November 2010 to July 2012.Diffusion tensor imaging was performed within 14  days after the onset of ICH. Fractional anisotropy (FA) was measured along the CST at corona radiata, perihaematomal oedema, cerebral peduncle and pons. Corticospinal tract integrity was classified into three types by diffusion tensor tractography (DTT): type A with preserved CST, type B with partially interrupted CST and type C with completely interrupted CST. Motor outcome was assessed by Motricity index (MI) at admission, after 1 and 3  months. RESULTS: Forty-eight patients were enrolled with a mean age of 62  years. The median time interval from onset of ICH to DTI study was 7  days. The patients in type C had significantly worse MI at admission (P < 0.001), after 1  month (P < 0.001) and after 3  months (P < 0.001) as compared to those with type A and type B. Lower rFA at the corona radiata was significantly correlated with poorer motor outcome at admission, after 1  month and after 3  months. DISCUSSION: Clinical motor outcome of ICH within 2  weeks can be identified with a statistically significant decrease in rFA at the corona radiata.

Impact of body mass index on adjacent segment disease after lumbar fusion for degenerative spine disease.

BACKGROUND: Adjacent segment disease is an important complication after fusion of degenerative lumbar spines. However, the role of body mass index (BMI) in adjacent segment disease has been addressed less. OBJECTIVE: To examine the relationship between BMI and adjacent segment disease after lumbar fusion for degenerative spine diseases. METHODS: For this retrospective study, we enrolled 190 patients undergoing lumbar fusion surgery for degeneration. BMI at admission was documented. Adjacent segment disease was defined by integration of the clinical presentations and radiographic criteria based on the morphology of the dural sac on magnetic resonance images. RESULTS: Adjacent segment disease was identified in 13 of the 190 patients, accounting for 6.8%. The interval between surgery and diagnosis as adjacent segment disease ranged from 21 to 66 months. Five of the 13 patients required subsequent surgical intervention for clinically relevant adjacent segment disease. In the logistic regression model, BMI was a risk factor for adjacent segment disease after lumbar fusion for degenerative spine diseases (odds ratio, 1.68; 95% confidence interval, 1.27-2.21; P < .001). Any increase of 1 mean value in BMI would increase the adjacent segment disease rate by 67.6%. The patients were subdivided into 2 groups based on BMI, and up to 11.9% of patients with BMI ≥ 25 kg/m were diagnosed as having adjacent segment disease at the last follow-up. CONCLUSION: BMI is a risk factor for adjacent segment disease in patients undergoing lumbar fusion for degenerative spine diseases. Because BMI is clinically objective and modifiable, controlling body weight before or after surgery may provide opportunities to reduce the rate of adjacent segment disease and to improve the outcome of fusion surgery.

Comparison of surface markers between human and rabbit mesenchymal stem cells.

This study investigated whether there are marked differences in surface markers between rabbit and human mesenchymal stem cells (MSCs). Murine and rabbit MSCs have been reported to be CD90-negative. Rat MSCs have been reported to be CD71-negative. Our previous study also shows that rabbit MSCs are CD29-negative. However, human MSCs are generally considered to be CD29-, CD71-, and CD90-positive. Therefore, the surface markers of human MSCs might differ from those of other species. Rabbit bone marrow MSCs were obtained that had a multi-differentiation potential. The phenotype of these cells was studied using flow cytometry antibodies for 25 rabbit surface markers, namely, CD13, CD14, CD29, CD31, CD34, CD44, CD45, CD49d, CD49f, CD51, CD54, CD59, CD71, CD73, CD90, CD105, CD106, CD133, CD166, MHC I, MHC II, α-smooth muscle actin (α-SMA), cytokeratin, desmin, and vimentin. The phenotype of commercially available human MSCs was similarly studied using antibodies for human surface markers. CD14, CD31, CD34, CD45, CD49d, CD49f, CD51, CD54, CD71, CD106, CD133, MHC II, and cytokeratin were absent from both rabbit and human MSCs, while CD44, α-SMA, and vimentin were present on both cell lines. CD13, CD29, CD59, CD73, CD90, CD105, CD166, and MHC I were present on human MSCs, but not on rabbit MSCs. However, desmin was present on rabbit MSCs, but not on human MSCs. In total, the surface expression of nine markers differed between human and rabbit MSCs, whereas the surface expression of 16 markers was the same in the two cell lines.

Trans-foramen ovale biopsy of a parasellar lesion guided by intraoperative CT neuronavigation with MRI fusion: a case report.

A 23-year-old male presented with a parasellar lesion which was suspected as disseminated intracranial germ cell tumour. The diagnosis of germinoma was made using immunohistochemistry from percutaneous trans-foramen ovale biopsy. This report describes the role of neuronavigation-guided biopsy through the foramen ovale for lesions in the parasellar region.

Characterization and spinal fusion effect of rabbit mesenchymal stem cells.

BACKGROUND: The surface markers of mesenchymal stem cells (MSCs) of rabbits have been reported only sporadically. However, interest in the spinal fusion effect of MSCs has risen recently. The purpose of this research was to study the surface markers and spinal fusion effect of rabbit MSCs. RESULTS: Of our rabbit MSCs, 2% expressed CD14, CD29, and CD45, 1% expressed CD90 and 97% expressed CD44. These results implied the MSCs were negative for CD14, CD29, CD45, and CD90, but positive for CD44. The surgical results showed that satisfactory fusion occurred in 10 rabbits (83%) in the study group and unsatisfactory fusion in 2 (17%). In the control group, satisfactory fusion was found in 3 rabbits (25%) and unsatisfactory fusion in 9 (75%). Statistical analysis showed the study group had significantly better spinal fusion results than the control group. CONCLUSIONS: The surface markers of human and rabbit MSCs are not exactly the same. Rabbit MSCs do not have positive reactivity for CD29 and CD90, which are invariably present on human MSCs. The allogeneic undifferentiated rabbit MSCs were able to promote spinal fusion and did not induce an adverse immune response.

Clinical Characteristics of Endogenous Cushing's Syndrome at a Medical Center in Southern Taiwan.

From January 1987 to December 2011, over a total of 25 years, 84 patients with Cushing's syndrome (CS) were identified at a medical center in southern Taiwan. We observed a higher incidence of ACTH-independent CS (75%) than ACTH-dependent CS (25%). A higher incidence of adrenocortical adenoma (58.3%) than Cushing's disease (CD, 21.4%) was also found. The sensitivity of the definitive diagnostic tests for CS, including loss of plasma cortisol circadian rhythm, a baseline 24 h urinary free cortisol (UFC) value >80 µ g, and overnight and 2-day low-dose dexamethasone suppression test, was between 94.4% and 100%. For the 2-day high-dose dexamethasone suppression test for the differential diagnosis of CD, the sensitivity of 0800 h plasma cortisol and 24 h UFC was 44.4% and 85.7%, respectively. For the differential diagnosis of adrenal CS, the sensitivities of the 0800 h plasma cortisol and 24 h UFC were 95.5% and 88.9%, respectively. In patients with ACTH-independent CS and ACTH-dependent CS, the baseline plasma ACTH levels were all below 29 pg/mL and above 37 pg/mL, respectively. The postsurgical hospitalization stay following retroperitoneoscopic adrenalectomy was shorter than that observed for transabdominal adrenalectomy (4.3 ± 1.6 versus 8.8 ± 3.7 days, P < 0.001). It was easy to develop retroperitoneal and peritoneal seeding of adrenocortical carcinoma via laparoscopic adrenalectomy.

Is timing of cranioplasty following posttraumatic craniectomy related to neurological outcome?

BACKGROUND: With the use of decompressive craniectomy for traumatic brain injury (TBI) come a corresponding number of cranioplasties. TBI causes dynamic processes to commence or change during the period from injury to recovery; hence, the role of the timing of surgical intervention should be emphasized. AIMS: We attempt to identify the relationship between the timing of cranioplasty and neurological outcomes following posttraumatic craniectomy. METHODS: In this 3-year retrospective study, 105 patients undergoing decompressive craniectomies and subsequent cranioplasties for TBI were enrolled. We documented the patients' demographic information, including Glasgow Coma Scale (GCS) at admission for trauma. The follow-up period was terminated by death or a minimum of 6 months after TBI. Glasgow Outcome Scale (GOS) at the end of follow-up was used as an outcome measure. Unfavorable outcome was defined as a GOS score of 1-3. RESULTS: The 105 patients included 71 male and 34 female subjects. The mean age was 41.94 ± 19.73 years. Neurological assessment showed that admission GCS was 8.50 ± 3.15, on average. The mean time interval between cranioplasty and craniectomy was 78.84 ± 49.04 days (range, 13-245 days). Univariate logistic regression analysis showed that the association between the timing of cranioplasty and unfavorable outcomes was not statistically significant (odds ratio = 1.005, confidence interval 0.997-1.013; p = 0.195). CONCLUSION: The timing of cranioplasty following posttraumatic craniectomy was not related to the neurological outcomes of TBI. Despite the limitations of the retrospective design, the analyses provide preliminary information to elucidate the question.

Surgical and endovascular treatment for ruptured anterior circulation cerebral aneurysms: a comparison of outcomes--a single centre study from Taiwan.

The purpose of this 2-year retrospective study is to compare the outcomes of patients with either surgical clipping or endovascular coiling treatment for ruptured anterior circulation cerebral aneurysms. We enrolled 100 patients with spontaneous subarachnoid hemorrhage resulting from ruptured anterior circulation cerebral aneurysms. We reviewed the demographic information, operative details, and image examinations including computed tomography (CT), digital subtraction angiography, and magnetic resonance imaging of brains. The patients were subdivided into two groups on the basis of treatment modalities: surgical clipping (N = 44) or endovascular coiling (N = 56). The modified Rankin's scale (mRS) was used as an outcome measures. Unfavorable outcome was defined by a mRS score of 1-3. The mean age of 100 patients, comprising 35 men and 65 women, was 57.48 ± 12.68 years. The follow-up period was 18.91 ± 13.05 months in average. The differences between the clipping and coiling groups in terms of admission Glasgow Coma Scale, Hunt and Hess grade, World Federation of Neurosurgical Societies grade, and Fisher's grade by CT scans were not statistically significant. There was no intergroup difference in the following results: symptomatic or radiographic vasospasm, post-treat rebleeding, and recurrence of aneurysms. Although the incidences of unfavorable outcome at the end of follow-up were 32.0% and 27.0% in the clipping and coiling group respectively, it revealed no significant difference (p = 0.202). In dealing with the patients with ruptured anterior circulation cerebral aneurysms, our results provide helpful information when discussing projected outcome before surgical or endovascular treatment.

Bilateral chronic subdural hematoma: what is the clinical significance?

BACKGROUND: Bilateral chronic subdural hematoma (CSDH) is not uncommon, although information on this condition is limited. AIMS: We aim to identify the differences in clinical characteristics between patients with bilateral or unilateral CSDH. METHODS: Ninety-eight patients with CSDH were enrolled in the two-year retrospective study. We investigated neurological outcome, morbidity, mortality, and recurrences after burr hole craniostomy for CSDH. RESULTS: Bilateral convexity hematomas were identified in 25 of 98 CSDH (25.51%). The patients with bilateral lesions had a lower incidence of hemiparesis than those having unilateral lesions (p = 0.004). Analysis of the neuro-images revealed significant differences in the presence of a midline shift (p = 0.001) and thickness of the hematoma (p < 0.001). The mean Markwalder subdural hematoma grade at admission was 1.89 ± 0.66 and 1.64 ± 0.49 in the unilateral and bilateral hematoma groups, respectively (p = 0.010). After a minimum follow-up period of 6 months, the mean Glasgow Outcome Scale was not significantly different (p = 0.060). The recurrence rate of up to 28.00% observed for the bilateral disease was found to be higher than 9.59% observed for the unilateral disease (p = 0.042). CONCLUSION: The frequency of focal neurological deficits was found to be lesser in patients with bilateral CSDH, and it may confound the diagnosis and delay treatment. To prevent neurological deterioration resulting from the thicker hematomas, early surgical decompression for bilateral CSDH should be implemented. Additionally, clinicians must be aware of the higher recurrent rate of bilateral CSDH after burr hole craniostomy.

Thirty-day mortality in traumatically brain-injured patients undergoing decompressive craniectomy.

OBJECT: Decompressive craniectomy is a life-saving measure for patients who have sustained traumatic brain injury (TBI), but patients undergoing this procedure may still die during an early phase of head injury. The aim of this study was to investigate the incidence, causes, and risk factors of 30-day mortality in traumatically brain-injured patients undergoing decompressive craniectomy. METHODS: The authors included 201 head-injured patients undergoing decompressive craniectomy in this 3-year retrospective study. The main outcome evaluated was 30-day mortality in patients who had undergone craniectomy after TBI. Demographic and clinical data, including information on death, were obtained for subsequent analysis. The authors identified differences between survivors and nonsurvivors in terms of clinical parameters; multivariate logistic regression was used to adjust for independent risk factors of short-term death. RESULTS: The 30-day mortality rate was 26.4% in traumatically brain-injured patients undergoing decompressive craniectomy. The majority of deaths following decompression resulted from uncontrollable brain swelling and extensive brain infarction, which accounted for 79.2% of mortality. In the multivariate logistic regression mode, the 2 independent risk factors for 30-day mortality were age (OR 1.035 [95% CI 1.006-1.064]; p = 0.018) and Glasgow Coma Scale (GCS) score before decompressive craniectomy (OR 0.769 [95% CI 0.597-0.990]; p = 0.041). CONCLUSIONS: There is a high 30-day mortality rate in traumatically brain-injured patients undergoing decompressive craniectomy. Most of the deaths are attributed to ongoing brain damage, even after decompression. Risk factors of short-term death, including age and preoperative GCS score, are important in patient selection for decompressive craniectomy, and these factors should be considered together to ensure the highest chance of surviving TBI.

Tracheostomy in craniectomised survivors after traumatic brain injury: a cross-sectional analytical study.

BACKGROUND: Decompressive craniectomy (DC) is a life-saving measure for traumatic brain injury (TBI). However, survivors may remain in a vegetative or minimally conscious state and require tracheostomy to facilitate airway management. In this cross-sectional analytical study, we investigated the predictors for tracheostomy requirement and influence of tracheostomy timing on outcomes in craniectomised survivors after TBI. METHODS: We enrolled 160 patients undergoing DC and surviving >7 days after TBI in this 3-year retrospective study. The patients were subdivided into 2 groups based on whether tracheostomy was (N=38) or was not (N=122) performed. We identified intergroup differences in early clinical parameters. Multivariable logistic regression was used to adjust for independent predictors of the need for tracheostomy. Early tracheostomy was defined as the performance of the procedure within the first 10 days after DC. Intensive care unit (ICU) stay, hospital stay, mortality, and Glasgow outcome scale (GOS) were analysed according to the timing of the tracheostomy procedure. RESULTS: After TBI, 24% of craniectomised survivors required tracheostomy. In the multivariate logistic regression mode, the significant factors related to the need for tracheostomy were age (odds ratio=1.041; p=0.002), the Glasgow coma score (GCS) at admission (odds ratio=0.733; p=0.005), and normal status of basal cisterns (odds ratio=0.000; p=0.008). The ICU stay was shorter for patients with early tracheostomy than for those undergoing late tracheostomy (p=0.004). The timing of tracheostomy had no influence on the hospital stay, mortality, or GOS. CONCLUSION: Age and admission GCS were independent predictors of the need for tracheostomy in craniectomised survivors after TBI. If tracheostomy is necessary, an earlier procedure may assist in patient care.

Acute autologous bone flap infection after cranioplasty for postinjury decompressive craniectomy.

BACKGROUND: Acute bone flap infection is a devastating complication after cranioplasty for postinjury decompressive craniectomy. We aim to identify the risk factors of autologous bone flap infection. METHODS: We enrolled 151 patients undergoing 153 cranioplasties in the 4-year retrospective study. Autologous bones stored at -75°C were used in the cranioplasties. Acute bone flap infection was defined as the onset of infection ≤14 days after cranioplasty. The epidemiological data of patients and details of the cranioplasty procedure were recorded. RESULTS: Acute bone flap infection was identified in five of the 153 cranioplasties, accounting for 3.3% of all episodes. Three of the 5 infected patients and five of 143 uninfected patients presented with dysfunction of subgaleal drainage comparatively, which was significantly different (p=0.001). Statistical analysis of the cranioplasty procedures and subsequent results of the two patient groups revealed the following significant findings: the duration of operation (p=0.03) and the length of hospital stay after cranioplasty (p<0.001). CONCLUSIONS: Dysfunction of subgaleal drainage and long operative duration of cranioplasty are risk factors of acute autologous bone flap infection. Regarding the prolonged hospital stay in complicated patients, better surgical techniques should be implemented in order to eliminate the risks of infection.

Remote epidural hemorrhage after unilateral decompressive hemicraniectomy in brain-injured patients.

Epidural hemorrhage (EDH) that develops remote from the decompressed hemisphere can be associated with devastating morbidity after hemicraniectomy for traumatic brain injury (TBI). In this study, we investigated the incidence, risk factors, and outcome influence of post-craniectomy remote EDH. For this retrospective study, we enrolled 139 patients undergoing unilateral hemicraniectomy for TBI. The patients were subdivided into two groups based on whether EDH remote from the site of bone decompression was present (n=11) or not (n=128). We identified the intergroup differences in clinical parameters and outcomes. Multivariate odds regression was used to adjust for independent risk factors of the development of EDH. The incidence of remote EDH following decompressive hemicraniectomy for TBI was 7.9%. There were two independent risk factors for remote EDH, including absence of contusional hemorrhage (odds ratio, 95% confidence interval=6.158, 1.090-34.802; p=0.040) and presence of remote skull fracture (odds ratio, 95% confidence interval=19.770, 2.194-178.152; p=0.008) in preoperative computed tomography scans. The mean Glasgow Outcome Scale did not differ between the patients with and without EDH. In conclusion, remote EDH in patients undergoing unilateral decompressive hemicraniectomy for TBI is not uncommon. The absence of contusional hemorrhage and presence of remote skull fracture are independent risk factors. Although postcraniectomy remote EDH is devastating, timely computed tomography scanning and immediate hematoma evacuation are efficient and crucial for patient outcomes.

Dioscorea alata attenuates renal interstitial cellular fibrosis by regulating Smad- and epithelial-mesenchymal transition signaling pathways.

Renal interstitial fibrosis is characterized by increased extracellular matrix (ECM) synthesis. Epithelial-mesenchymal transition (EMT) in kidneys is driven by regulated expression of fibrogenic cytokines such as transforming growth factor-beta (TGF-ß). Yam, or Dioscorea alata (DA) is an important herb in Chinese medicine widely used for the treatment of clinical diabetes mellitus. However, the fibrosis regulatory effect of DA is unclear. Thus, we examined TGF-ß signaling mechanisms against EMT in rat fibroblast cells (NRK-49F). The characterization of DA water-extracts used various methods; after inducing cellular fibrosis in NRK-49F cells by treatment with ß-hydroxybutyrate (ß-HB) (10 mM), we used Western blotting to examine the protein expression in the TGF-ß-related signal protein type I and type II TGF-ß receptors, Smads2 and Smad3 (Smad2/3), pSmad2 and Smad3 (pSmad2/3), Smads4, Smads7, and EMT markers. These markers included E-cadherin, alpha-smooth muscle actin (α-SMA), and matrix metalloproteinase-2 (MMP-2). Bioactive TGF-ß and fibronectin levels in the culture media were determined using ELISA. Expressions of fibronectin and Snail transcription factor, an EMT-regulatory transcription factor, were assessed by immunofluorescence staining. DA extract dose-dependently (50-200 µg/mL) suppressed ß-HB-induced expression of fibronectin in NRK-49F cells concomitantly with the inhibition of Smad2/3, pSmad2/3, and Smad4. By contrast, Smad7 expression was significantly increased. DA extract caused a decrease in α-SMA (α-smooth muscle actin) and MMP-2 levels, and an increase in E-cadherin expression. We propose that DA extract might act as a novel fibrosis antagonist, which acts partly by down regulating the TGF-ß/smad signaling pathway and modulating EMT expression.

20-Hydroxyecdysone attenuates TGF-ß1-induced renal cellular fibrosis in proximal tubule cells.

UNLABELLED: Renal fibrosis progresses to end stage of diabetes kidney disease, which causes irreversible progressive proximal tubular injury. In a previous study, 20-hydroxyecdysterone (20-HE), a phytoecdysteroid, attenuated renal injury in diabetes models. However, the fibrosis regulatory role remains to be investigated. METHODS: The proximal tubular epithelial cells (designated as HK-2) were treated for 48 h with TGF-ß1 (5 ng/ml) in different concentrations of 20-HE (0 to 500 nM/ml) in the last 24 h of culture. The extracellular fibronectin was measured by ELISA assay. Western blot and immunofluorescence were used to evaluate the expression of TGF-ß1/Smads transducer (including Smad2/3, 4, and 7), epithelial and mesenchymal markers (e.g. E-cadherin and α-smooth muscle actin) and Snail (transcriptional regulators for EMT). RESULTS: 20-HE reverses TGF-ß1-induced increase in fibronectin (both intracellular and extracellular fibronectin). Simultaneously, 20-HE reverses TGF-ß1-induced down-regulation of Smad7. In addition, 20-HE significantly attenuates TGF-ß1-induced upregulation of Smad2/3 and pSmad2/3, and downregulation of E-Cadherin. Moreover, 20-HE dramatically suppresses TGF-ß1-induced increases in the expression of Snail. CONCLUSION: We propose that 20-HE is a potential fibrosis antagonist for renal proximal tubule cells. 20-HE might act through suppressing post-receptor signaling of TGF-ß1 and restoring tubule epithelial character by blocking the expression of Snail.

Acute clinical deterioration of posterior fossa epidural hematoma: clinical features, risk factors and outcome.

BACKGROUND: This study aimed to present experience in treating patients with posterior fossa epidural hematoma (PFEDH) and to discuss the risk factors, clinical features, and outcome in PFEDH patients with acute clinical deterioration (ACD). METHODS: Twenty-seven patients with PFEDH initially treated conservatively were evaluated. A comparison was made between patients with and without ACD during hospitalization. RESULTS: Eight of the 27 patients subsequently experienced ACD. Local traumatic findings, loss of consciousness due to injury, headache, and vomiting were the four most common clinical features of the 27 cases. Seven of the 8 patients with ACD had good recoveries and 1 died. Eighteen of the 19 patients without ACD had good recoveries, while 1 remained moderately disabled. Stepwise logistic regression demonstrated that the adjusted risk of ACD during hospitalization for patients with vomiting and an occipital fracture across the transverse sinus on computed tomography (CT) had odds ratios of 12.6 (95% confidence interval = 1.03-152.37, p = 0.047) and 8.8 (95% CI = 1.02-75.95, p = 0.048), respectively, compared with those without ACD. CONCLUSION: This study demonstrated that an occipital fracture across the transverse sinus on CT and vomiting on presentation are risk factors for ACD during hospitalization. In this study, PFEDH patients including those with ACD had good outcomes. Further studies are necessary to clarify the clinical course and risk factors for the clinical deterioration of PFEDH patients and to establish a treatment strategy.