Optic nerve decompression through pterional and supraorbital approaches in the treatment of severe traumatic optic neuropathy.

To investigate the effectiveness of optic nerve decompression (OND) in the treatment of severe traumatic optic neuropathy (TON) through pterional and supraorbital approaches, and to identify the prognostic factor for postoperative visual acuity (VA) following OND. Patients with severe TON treated with OND through either pterional or supraorbital approach in our institute from September 2019 to June 2022 were retrospectively reviewed in this study. Demographic information, trauma factors, the interval between trauma and complete blindness, the interval between trauma and surgery, and the associated craniofacial traumas were recorded. Hospitalization days and the postoperative VA of patients in two groups were compared. There were 54 severe TON patients with NLP included in this study; 21 patients underwent OND through the pterional approach, and the other 33 underwent the supraorbital approach. Respectively, in groups of pterional and supraorbital approaches, the average hospitalization days were 9.8 ± 3.2 and 10.7 ± 2.9 days (p = 0.58), the mean durations of follow-up were 18.9 ± 4.3 and 20.8 ± 3.7 months (p = 0.09), and the average circumference of OND were 53.14 ± 15.89 ◦ (range 220 ◦ -278◦) and 181.70 ± 6.56◦ (range 173 ◦ -193◦) (p<0.001). The overall improvement rates of pterional and supraorbital approaches are 57.1% and 45.5% (p = 0.40), respectively. Optic canal fracture (OCF) was revealed to be significantly associated with postoperative VA in the supraorbital approach (Binary: p = 0.014, CI: 1.573-57.087; Ordinal: p = 0.003, CI: 1.517-5.503), but not in the pterional approach. In the group of supraorbital approach, patients with OFC had a higher rate of a better outcome (78.6%) than those without (21.4%). Patients with severe traumatic TON may benefit from OND through either the pterional or supraorbital approach. OCF is a potential prognostic factor for postoperative VA following OND through the supraorbital approach.

Combined surgical and endovascular treatment for spinal arteriovenous fistula associated with Parkes Weber syndrome.

BACKGROUND: Parkes Weber syndrome (PWS) is a rare and congenital vascular malformation manifesting as hemihypertrophy of the extremities, cutaneous hemangiomas, varicose veins, and arteriovenous fistula of the affected limbs. The incidence rate of spinal arteriovenous fistula (AVF) associated with PWS is extremely rare. CASE PRESENTATION: We reported a case of an adolescent girl with PWS who presented with a rupture spinal perimedullary AVF at the level of T12-L1. She was successfully treated with emergent surgical decompression and subsequent endovascular embolization. The clinical features and treatment of spinal AVF associated with PWS were discussed and a brief literature review was presented. CONCLUSION: Based on this case report, we suggested that the management of spinal AVF in PWS should also be individualized and be tailored according to the condition and expectation of the patients as well as the angioarchitecture of the vascular malformation.

Activation of 4-1BB signaling in bone marrow stromal cells triggers bone loss via the p-38 MAPK-DKK1 axis in aged mice.

Senile osteoporosis can cause bone fragility and increased fracture risks and has been one of the most prevalent and severe diseases affecting the elderly population. Bone formation depends on the proper osteogenic differentiation of bone marrow stromal cells (BMSCs) in the bone marrow microenvironment, which is generated by the functional relationship among different cell types in the bone marrow. With aging, bone marrow provides signals that repress osteogenesis. Finding the signals that oppose BMSC osteogenic differentiation from the bone marrow microenvironment and identifying the abnormal changes in BMSCs with aging are key to elucidating the mechanisms of senile osteoporosis. In a pilot experiment, we found that 4-1BBL and 4-1BB were more abundant in bone marrow from aged (18-month-old) mice than young (6-month-old) mice. Meanwhile, significant bone loss was observed in aged mice compared with young mice. However, very little data have been generated regarding whether high-level 4-1BB/4-1BBL in bone marrow was associated with bone loss in aged mice. In the current study, we found upregulation of 4-1BB in the BMSCs of aged mice, which resulted in the attenuation of the osteogenic differentiation potential of BMSCs from aged mice via the p38 MAPK-Dkk1 pathway. More importantly, bone loss of aged mice could be rescued through the blockade of 4-1BB signaling in vivo. Our study will benefit not only our understanding of the pathogenesis of age-related trabecular bone loss but also the search for new targets to treat senile osteoporosis.

Baicalin induces apoptosis in human osteosarcoma cell through ROS-mediated mitochondrial pathway.

Baicalin is extracted from a traditional Chinese herb, Scutellaria baicalensis. In this study, the anticancer activity and underlying mechanisms of baicalin towards human osteosarcoma cell (HOS) were investigated. Baicalin could inhibit HOS cell proliferation in a concentration-dependent manner. Mitochondrial membrane potential decreased obviously after treated with different concentration of baicalin by flow cytometry assay and revealed that baicalin triggered a significant generation of reactive oxygen species (ROS). Western blotting assay further revealed that baicalin-induced cell apoptosis by suppressing Bcl-2 level, then activating caspase-9 and caspase-3. In vivo experiment, baicalin significantly suppressed tumour growth in female BALB/C nude mice bearing HOS tumours. In addition, baicalin did show toxicity to treated animal by comparing the body weight increase and mortality. In general, the present results demonstrated that baicalin-induced apoptosis in human osteosarcoma cell via a ROS-mediated mitochondrial pathway. The paper indicated that baicalin is a promising candidate for the treatment of HOS.

siRNA-mediated knockdown of JUB expression suppresses the proliferation of glioblastoma cells.

BACKGROUND: Glioma is one of the most common primary malignant brain tumors. However, the potential molecular mechanism of glioma tumorigenesis is limited. In this study, we aimed to investigate the functional relationship between glioma and a potential tumor related gene JUB. METHODS: Lentivirus-based RNA interference was carried out to knock down JUB expression in human glioma cells U251. The effects of JUB on cell proliferation and cell cycle were detected by MTT, colony formation and flow cytometry assays. RESULTS: Lentivirus-mediated shRNA could effectively suppress JUB expression in U251 cells, resulting in significant decreases in cell proliferation and colony formation. Flow cytometry analysis showed that JUB silencing blocked cell cycle at S and G2/M phases, and induced apoptosis, which could contribute to cell growth suppression. Furthermore, knockdown of JUB caused downregulation of CDK6 and activations of Caspase 3 and PARP. CONCLUSIONS: The results in this study uncovered that JUB was a regulator involved in proliferation of glioma cells, and it could be used as a potential therapeutic target for glioma.

Operative treatment of huge adult frontal nasoethmoid meningoencephalocele.

A retrospective study was undertaken in order to choose the operative methods of adult huge frontal nasoethmoid meningoencephalocele. Ten patients were admitted to hospital for their craniofacial mass. Of these, 9 cases suffered meningocele and 1 case meningoencephalocele. Four cases undertook the mass resection and repairing operation with postoperative lumbar drainage; at final, they had to receive shunt operation. Six cases underwent mass resection and repairing operation with shunt surgery at one stage; they recovered smoothly. Our results suggest that the adult patients with huge meningoencephalocele have larger subarachnoid cavity. When they receive repairing operation, their subarachnoid cavity would be decreased in volume and cerebrospinal fluid (CSF) circulation could be disturbed. In order to maintain the balance of CSF production and absorption, the shunt operation should be given at the same stage.

Surgical treatment of parapontine epidermoid cysts presenting with trigeminal neuralgia.

We retrospectively reviewed the management of 49 patients with parapontine epidermoid cyst presenting with trigeminal neuralgia, emphasizing the importance of fully removing the tumor to relieve the trigeminal neuralgia. Clinical symptoms, MRI, the operative approach, and post-operative results were examined. Trigeminal neuralgia was noted in all patients. The mean duration from onset of symptoms to surgery was 18 months. Total removal was achieved in 23 patients, near-total removal in 21, and subtotal removal in five patients. However, all tumor capsule that adhered to the trigeminal nerve was completely removed. After the operation, 33 patients developed facial hypoesthesia, three complained of double vision, and two developed acute hydrocephalus. At six months of follow-up, all patients had recovered and returned to their normal lives. At 2 years of follow-up, one patient experienced pain recurrence and underwent another operation. Parapontine epidermoid cysts either encase cranial nerve (CN) V but with intact arachnoid between the capsule and the nerve, or compress and distort the nerve with tumor capsule adherent or attached to the nerve surface. Resecting the tumor capsule's attachment to CN V is critical in relieving pain, even though this method may damage the nerve.