Cheng-Guang Huang

Cholesterol Levels and Risk of Hemorrhagic Stroke A Systematic Review and Meta-Analysis

Background and Purpose— Cholesterol levels are inconsistently associated with the risk of hemorrhagic stroke. The purpose of this study is to assess their relationships using a meta-analytic approach. Methods— We searched PubMed and Embase for pertinent articles published in English. Only prospective studies that reported effect estimates with 95% confidential intervals (CIs) of hemorrhagic stroke for ≥3 categories of cholesterol levels, for high and low comparison, or for per 1 mmol/L increment of cholesterol concentrations were included. We used the random-effects model to pool the study-specific results. Results— Twenty-three prospective studies were included, totaling 1 430 141 participants with 7960 (5.6%) hemorrhagic strokes. In high versus low analysis, the summary relative risk of hemorrhagic stroke was 0.69 (95% CI, 0.59–0.81) for total cholesterol, 0.98 (95% CI, 0.80–1.19) for high-density lipoprotein cholesterol, and 0.62 (95% CI, 0.41–0.92) for low-density lipoprotein cholesterol. In dose–response analysis, the summary relative risk of hemorrhagic stroke for 1 mmol/L increment of total cholesterol was 0.85 (95% CI, 0.80–0.91), for high-density lipoprotein cholesterol was 1.11 (95% CI, 0.99–1.25), and for low-density lipoprotein cholesterol was 0.90 (95% CI, 0.77–1.05). The pooled relative risk for intracerebral hemorrhage was 1.17 (95% CI, 1.02–1.35) for high-density lipoprotein cholesterol. Conclusions— Total cholesterol level is inversely associated with risk of hemorrhagic stroke. Higher level of low-density lipoprotein cholesterol seems to be associated with lower risk of hemorrhagic stroke. High-density lipoprotein cholesterol level seems to be positively associated with risk of intracerebral hemorrhage.

Nutritional Support for Patients Sustaining Traumatic Brain Injury: A Systematic Review and Meta-Analysis of Prospective Studies

Background In traumatic brain injury (TBI), the appropriate timing and route of feeding, and the efficacy of immune-enhancing formulae have not been well established. We performed this meta-analysis aiming to compare the effects of different nutritional support modalities on clinical outcomes of TBI patients. Methods We systematically searched Pubmed, Embase, and the Cochrane Library until October, 2012. All randomized controlled trials (RCTs) and non-randomized prospective studies (NPSs) that compared the effects of different routes, timings, or formulae of feeding on outcomes in TBI patients were selected. The primary outcomes included mortality and poor outcome. The secondary outcomes included the length of hospital stay, the length of ventilation days, and the rate of infectious or feeding-related complications. Findings 13 RCTs and 3 NPSs were included. The pooled data demonstrated that, compared with delayed feeding, early feeding was associated with a significant reduction in the rate of mortality (relative risk [RR] = 0.35; 95% CI, 0.24–0.50), poor outcome (RR = 0.70; 95% CI, 0.54–0.91), and infectious complications (RR = 0.77; 95% CI, 0.59–0.99). Compared with enteral nutrition, parenteral nutrition showed a slight trend of reduction in the rate of mortality (RR = 0.61; 95% CI, 0.34–1.09), poor outcome (RR = 0.73; 95% CI, 0.51–1.04), and infectious complications (RR = 0.89; 95% CI, 0.66–1.22), whereas without statistical significances. The immune-enhancing formula was associated with a significant reduction in infection rate compared with the standard formula (RR = 0.54; 95% CI, 0.35–0.82). Small-bowel feeding was found to be with a decreasing rate of pneumonia compared with nasogastric feeding (RR = 0.41; 95% CI, 0.22–0.76). Conclusion After TBI, early initiation of nutrition is recommended. It appears that parenteral nutrition is superior to enteral nutrition in improving outcomes. Our results lend support to the use of small-bowel feeding and immune-enhancing formulae in reducing infectious complications.

Expression of ubiquitin-conjugating enzyme E2C/UbcH10 in astrocytic tumors.

UbcH10 is one of the key regulators of cell cycle progression through the mitotic spindle assembly checkpoint pathway. Recently, aberrantly high UbcH10 expression has been demonstrated in a variety of malignancies. However, its role in astrocytic carcinogenesis is not well defined. This study investigated the splice pattern of the UbcH10 gene and its expression status in astrocytomas of different grades. Consequently, UbcH10 splice variant 1 (GenBank accession nos. NM_007019) was detected in astrocytomas and normal brain tissues by RT-PCR and sequence analysis. Expression levels of UbcH10 mRNA were elevated in high- versus low-grade astrocytomas (64.33+/-60.98 vs 8.36+/-8.15, respectively; p=0.000) or normal controls (64.33+/-60.98 vs 1.00+/-1.57, respectively; p=0.000), as determined by quantitative real time PCR analysis. Similarly, immunohistochemistry study showed increased UbcH10 labelling index in high-grade astrocytomas versus low-grade tumors (10.53+/-5.79% vs 4.23+/-2.85%, respectively; p=0.000) or normal controls (10.53+/-5.79% vs 0.0+/-0.0%, respectively; p=0.000) and, a positive correlation between UbcH10 immunoreactivity and Ki-67 immunostaining was also noted (Spearman r=0.63, p<0.001). These data suggest that overexpression of UbcH10 may serve as one important molecular mechanism that underlies the astrocytic carcinogenesis.

Knockdown of ubiquitin-conjugating enzyme E2C/UbcH10 expression by RNA interference inhibits glioma cell proliferation and enhances cell apoptosis in vitro

PurposeTo address the role of ubiquitin-conjugating enzyme, E2C/UbcH10, in astrocytic carcinogenesis.MethodsExpression pattern of UbcH10 in U251 glioma cells was evaluated by immunohistochemistry and western blot. RNA interference was employed to downregulate UbcH10 expression in U251 cell line. The effect of UbcH10 silencing on cell proliferation was assessed by MTT assay and cell cycle analysis. Cell apoptosis was determined by flow cytometry, TUNEL staining and western blot.ResultsLevels of UbcH10 protein were significantly upregulated in U251 cells compared with normal brain tissues. Marked immunoreactivity for UbcH10 was demonstrated in the cytoplasm of U251 glioma cells, especially in the mitotic cells. The growth rate of U251 cells was significantly inhibited by depletion of UbcH10 by short interference RNA. Further, UbcH10 RNAi induced apoptosis through induction of Bax and p53, downregulation of Bcl-2 and G2/M arrest of the cell cycle.ConclusionThese data imply that knocking-down UbcH10 protein expression may represent a potential therapeutic option for glioma.

Expression of targeting protein for Xenopus kinesin-like protein 2 is associated with progression of human malignant astrocytoma.

In humans, the targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a cell cycle-associated protein, and altered TPX2 expression has been found in various malignancies. However, the contribution of TPX2 expression to astrocytoma progression is unclear. The aim of this study was to investigate TPX2 expression in human astrocytoma samples and cell lines. TPX2 protein expression was detected in the nucleus of astrocytoma tissues by immunohistochemistry and immunofluorescence staining. Real-time PCR and Western blot analysis showed that the expression levels of TPX2 were higher in high-grade astrocytoma tissues and cell lines than that in low-grade astrocytoma tissues and normal cell lines. Immunohistochemical analysis of tumor tissues from 52 patients with astrocytoma showed that TPX2 over-expression was significantly associated with decreased patient survival. In addition, down-regulation of the TPX2 gene by RNA interference inhibited proliferation of U87 cells. TPX2 gene silencing also increased early-stage apoptosis in U87 cells. Western blotting and real-time PCR showed changes in the protein and mRNA expression of Aurora A, Ran, p53, c-Myc and cyclin B1 in U87 cells that had been transfected with pSUPER/TPX2/siRNA. These data suggest that TPX2 expression is associated with the progression of malignant astrocytoma.

3-Dimensional rotational angiography for the treatment of spinal cord vascular malformations.

BACKGROUND This study was conducted to evaluate the effect of 3D-RA on the treatment of SCVMs. METHODS Twelve patients with SCVM were retrospectively reviewed for details of 2D and 3D-RA findings. Pretherapeutic 2D and 3D-RA angiograms were compared with respect to 4 critical categories of parameters: (1) the exact anatomic location, size, and extent; (2) the definitive diagnosis; (3) the precise angioarchitectural configuration; and (4) the contribution to further intervention. RESULTS Overall, 2D and 3D-RA were equally effective in demonstrating the exact anatomic location, size, and extent, and establishing the definitive diagnosis of SCVM in all 12 cases. 3-Dimensional rotational angiography demonstrated precise angioarchitectural configuration in 8 (8/12) cases, facilitated treatment in 6 (6/12) cases, and modified therapeutic strategies in 2 (2/12) cases via information not available from 2D-DSA images. Both 2D and 3D-RA contributed equally to the therapeutic intervention in 4 (4/12) patients. No complications occurred as a result of 3D-RA. CONCLUSIONS 3-Dimensional rotational angiography may enhance our ability to treat SCVMs with complex angioarchitecture and is an ideal addition to conventional 2D angiography in the management of these vascular lesions.

Endoscopic transmaxillary transMüller's muscle approach for decompression of superior orbital fissure: A cadaveric study with illustrative case

BACKGROUND In an effort to avoid the damage and inconvenience associated with transcranial approaches, we developed an endoscopic transmaxillary transMüllers muscle approach for decompression of the superior orbital fissure (SOF). METHODS The endoscopic transmaxillary transMüllers muscle route was performed in ten cadaveric heads. We measured important anatomic landmarks, and angles radiographically. This approach was initially attempted in one patient with traumatic superior orbital fissure syndrome (tSOFS). RESULTS A maxillary antrostomy was carried out with a buccal sulcus incision. The sinus ostium and the course of infraorbital nerve were used as endoscopic anatomic landmarks. Then the inferior orbital fissure was drilled out, followed by separating the Müllers muscle. The periorbita were peeled off from the lateral wall, followed by the endoscope going along the periorbital space, until the lateral aspect of the SOF could be visualized. Decompression was successfully performed in all specimens. The initial clinical application justified this approach. The patient had an uneventful postoperative course and satisfactory recovery. CONCLUSION This approach offers sufficient endoscopic visualization and reliable decompression of SOF. It avoids the need for brain retraction, temporalis muscle manipulation, or any external incision, and appears to be able to deliver satisfying aesthetic results as well as favourable functional recovery.

Intracranial haemophilic pseudotumor associated with factor VIII deficiency.

Haemophilic pseudotumor is a rare complication of haemophilia occurring in 1–2% of patients and is more frequently located is in the long bones of the lower extremities and in the pelvis. We present the first case of an intracranial haemophilic pseudotumor in a patient with factor VIII deficiency.

miR-448-3p controls intracranial aneurysm by regulating KLF5 expression

microRNAs (miRNAs) control several processes known to be involved in progression of aneurysm. Here, intracranial aneurysms (IAs) were surgically induced in Sprague-Dawley rats, and we found that miR-448-3p was downregulated and KLF5 was upregulated in IA rats. We identified Klf5 as a direct target of miR-448-3p in smooth muscle cells (SMCs). In addition, aneurysms size and the lumen area of the aneurysms were smaller 4 weeks after IA induction in the miR-448-3p-treated group. miR-448-3p treatment protected the wall thickness ratio and suppressed macrophage infiltration after IA induction. IAs caused a significant increase in KLF5 expression and were alleviated by miR-448-3p. Moreover, the anti-inflammatory effect of miR-448-3p was verified in lipopolysaccharide -stimulated RAW 264.7 macrophage cells. The expression levels of KLF5, MMP2, and MMP9 levels were elevated by LPS, and were attenuated by miR-448-3p. These data suggest that miR-448-3p plays the inhibitory role in IA progression, indicating that miR-448-3p overexpression is crucial for preventing the development of IA through downregulation of macrophage-mediated inflammation.

Measures to Improve the Existing Problems in the Medical Records of the Neurosurgery Department

AbstractSome problems such as one-sidedness in parsing problems, lack of connotation, time limit error, missing items in content, and copy error commonly occur during the writing of medical records by neurosurgeons. We need to strengthen “three bases” during the training of resident physicians, standardize medical record writing, highlight the regulatory functions of attending physicians, strengthen the “three-level” supervision of medical record quality, and implement a system to continuously improve the quality of medical records, along with a series of measures to standardize the diagnosis and treatment behaviors, in order to improve the medical record writing quality, and to enhance the connotation of medical records.