An atretic parietal cephalocele associated with multiple intracranial and eye anomalies

We present the cranial MRI findings in a 4-month-old girl with an atretic parietal cephalocele associated with multiple cerebral and ocular anomalies including lobar holoprosencephaly, a Dandy-Walker malformation, agenesis of the corpus callosum, grey-matter heterotopia, extra-axial cysts in various locations, bilateral microphthalmia and a retroocular cyst

The effect of pentoxifylline on cerebral vasospasm following experimental subarachnoid hemorrhage

Objects: Cerebral vasospasm is an important event that occurs following subarachnoid hemorage which has significant mortality and morbidity. The goal in this study was to investigate the effect of pentoxifylline on vasospasm in an experimental subarachnoid hemorrhage model.Methods: In this study, 20 male New Zeland White rabbits weighing 3000-3500 g were assigned randomly to four groups. Animals in group 1 served as controls. Animals in group two received only intravenous pentoxifylline injection 3 times in 12 h intervals. In group 3, SAH was induced and no injection was given. Animals in group 4 received intravenous pentoxifylline (6 mg/kg) injections 3 times at 12th, 24th and 36th hours after subarachnoid hemorrhage induction. All animals were sacrificed and basilar arteries were removed at 48th hour. Basilar artery vessel diameters, wall thicknesses and luminal section areas were measured with Spot for Windows version 4.1. Statistical analysis was performed using ANOVA and Kruskall-Wallis tests.Results: Mean basilar artery luminal section areas and luminal diameters in group 4 were significantly higher compared to group 3 (p < 0.05). Basilar artery wall thicknesses and were found to be higher in group 3 than in other groups and this was also statistically significant (p < 0.05).Conclusion: Our study demonstrated that intravenous administration of pentoxifylline significantly decreases vasospasm after subarachnoid hemorrhage.Wo

Effects of an acetylcholinesterase inhibitor and an N-methyl-D-aspartate receptor antagonist on inflammation and degeneration of the nucleus pulposus

OBJECTIVE: The study aimed to examine the effects of two drugs, an acetylcholinesterase inhibitor (AChEI) and an N-methyl-D-aspartate receptor (NMDAR) antagonist, on degenerated annulus fibrosus (AF) and nucleus pulposus (NP) cells and the extracellular matrix (ECM) structure in vitro. PATIENTS AND METHODS: Tissue samples were obtained from patients with intervertebral disc herniation (four males and four females; classified as Pfirmann stage IV) and used to prepare cell cultures. Untreated cell culture samples served as the control group. Study group samples were treated with donepezil, memantine or a combination of the two drugs. Cell viability, toxicity and proliferation were evaluated in all groups. Western blotting was used to examine changes in protein expression of signal transducer and activator of transcription 3 (STAT3), phospho-STAT3 (ser727), hypoxia-inducible factor (HIF)-1 alpha (HIF-1 alpha) and nucleotide-binding oligomerisation domain (NOD) leucine-rich repeat (LRR)-containing proteins (NLR) family pyrin domain containing 3 (NLRP3) inflammasome. The alpha significance value was < 0.05. RESULTS: Analysis of the microscopy and commercial kit results revealed that cell proliferation was suppressed. and no cell death was observed. The protein expression levels of NLRP3, STAT3, ser727 and HIF-1 alpha were lower in the samples treated with donepezil and memantine at 72 h (p < 0.05). The protein expression levels of NLRP3, STAT3, ser727 and HIF-1 alpha were higher in the samples treated with the combination of donepezil and memantine (p < 0.05). CONCLUSIONS: The combined administration of memantine a NMDAR antagonist which can prevent neurodegeneration and donepezil an AChEI used for pain relief increased the protein expression levels in the anabolic pathway. However, it did not reduce the protein expression levels in the catabolic pathway. Therefore, further studies are needed to provide extensive insight into whether it may be among the potential targets for the therapy of intervertebral disc (IVD) diseases

Does oseltamivir protect human chondrocyte and nucleus pulposus cells from degeneration by inhibiting senescence and proinflammation mediated by the NLRP3 inflammasome and NF-?B?

OBJECTIVE: Recent drug design studies suggest that inflammation is among the most important factors in the development of both intervertebral disc (IVD) degeneration (IVDD) and osteoarthritis (OA) due to cartilage damage. This study aimed to investigate whether the anti-inflammatory drug oseltamivir has a toxic effect on IVD and cartilage tissue cells. It assessed what effect oseltamivir has on hypoxia-inducible factor (HIF)-1 alpha (HIF1?), which plays an important role in anabolic pathways in IVD and cartilage tissue. In addition, the study analyzed whether oseltamivir could inhibit the release of inflammatory interleukin-1 beta (IL-1?) via the nuclear factor kappa-B (NF-?B) signaling pathway by activating the nucleotide-binding oligomerization domain and leucine-rich repeat protein-3 (NLRP3) inflammasome. MATERIALS AND METHODS: Human lumbar IVD (n = 8) tissues were isolated for annulus fibrosus (AF) and nucleus pulposus (NP) primary cell cultures, and human tibial and femoral cartilage tissues (n = 8) were isolated for primary chondrocyte cultures. Untreated groups served as the control and oseltamivir-treated groups as the study sample. Cell viability and cytotoxicity were evaluated at 0, 24, 48, and 72 h in all groups for changes in HIF-1?, IL-1?, NF-?B, and the NLRP3-inflammasome protein expressions using Western blotting. The ? significance value was < 0.05. RESULTS: In the oseltamivir-treated groups, cell proliferation decreased in both AF/NP cell and chondrocyte cultures obtained from IVD cartilage tissues. After Western blotting analysis, changes were observed in the protein expressions of HIF-1?, IL-1?, NF-?B, and the NLRP3 inflammasome in both AF/NP cells and chondrocytes. The results were statistically significant (p < 0.05). CONCLUSIONS: Oseltamivir treatment may be a promising regenerative strategy to manage IVDD and osteoarthritic cartilage tissues. © 2022 Verduci Editore s.r.l. All rights reserved

Does oseltamivir protect human chondrocyte and nucleus pulposus cells from degeneration by inhibiting senescence and proinflammation mediated by the NLRP3 inflammasome and NF-kappa B?

OBJECTIVE: Recent drug design studies suggest that inflammation is among the most important factors in the development of both intervertebral disc (IVD) degeneration (IVDD) and osteoarthritis (OA) due to cartilage damage. This study aimed to investigate whether the anti-inflammatory drug oseltamivir has a toxic effect on IVD and cartilage tissue cells. It assessed what effect oseltamivir has on hypoxia-inducible factor (HIF)-1 alpha (HIF1 alpha), which plays an important role in anabolic pathways in IVD and cartilage tissue. In addition, the study analyzed whether oseltamivir could inhibit the release of inflammatory interleukin-1 beta (IL-1 beta) via the nuclear factor kappa-B (NF-kappa B) signaling pathway by activating the nucleotide-binding oligomerization domain and leucine-rich repeat protein-3 (NLRP3) inflammasome. MATERIALS AND METHODS: Human lumbar IVD (n = 8) tissues were isolated for annulus fibrosus (AF) and nucleus pulposus (NP) primary cell cultures. and human tibial and femoral cartilage tissues (n = 8) were isolated for primary chondrocyte cultures. Untreated groups served as the control and oseltamivir-treated groups as the study sample. Cell viability and cytotoxicity were evaluated at 0, 24, 48. and 72 h in all groups for changes in HIF-1 alpha, IL-18, NF-kappa B. and the NLRP3-inflammasome protein expressions using Western blotting. The a significance value was < 0.05. RESULTS: In the oseltamivir-treated groups, cell proliferation decreased in both AF/NP cell and chondrocyte cultures obtained from IVD cartilage tissues. After Western blotting analysis, changes were observed in the protein expressions of HIF-1 alpha, IL-1 beta, NF-kappa B, and the NLRP3 inflammasome in both AF/NP cells and chondrocytes. The results were statistically significant (p < 0.05). CONCLUSIONS: Oseltamivir treatment may be a promising regenerative strategy to manage IVDD and osteoarthritic cartilage tissues

Can transcription factors in the intervertebral disc of lopinavir/ritonavir prevent degeneration in the nucleus pulposus by mediating the regulation of inflammation through signaling pathways?

OBJECTIVE: This study was con-ducted to examine whether lopinavir/ritonavir (Lop/r), an HIV protease inhibitor, can improve disc physiology and slow down intervertebral disc (IVD) degeneration through in vitro experimental methods, as well as whether it can suppress inflammation with interleukin-1 beta (IL-113) and sex-determining region Y (SRY) protein-related high-mobility group box genes-9 (SOX9) through hypoxia-inducible factor 1-alpha (HIF-1 alpha) and the nuclear factor kappa B (NF-KB) signaling pathway. The aim was to investigate whether Lop/r application is toxic to IVD cells and the microenvironment simultaneously. PATIENTS AND METHODS: Human primary cell cultures were prepared using herniated IVD tissues obtained from patients with lumbar disc hernia who were unresponsive to conservative and medical treatment, and thereby, were operated on. The untreated culture samples served as control group, and the samples treated with Lop/r served as study group. Microscopic evaluations were performed simultaneously using fluorescent and supravital dyes in all groups. In addition to cell viability, toxicity, and proliferation analysis through a commercial kit, IL-113, SOX9, HIF-1 alpha, and NF-KB protein expressions were evaluated using Western blotting. In the statistical comparison of the obtained data, an alpha value less than 0.05 was considered significant. RESULTS: Cell proliferation decreased in the Lop/r group, but no cell death was observed (p < 0.05). Moreover, at the end of 72 hours after Lop/r application, IL-113 and NF-kB protein expressions decreased by 40% and 52%, respectively, while HIF-1 alpha and SOX9 protein expressions increased by 4% and 59%, respectively (p < 0.05). CONCLUSIONS: Although these data were obtained from an in vitro experimental study, it is believed that these findings could make significant contributions to the pharmaco-regenerative treatment modalities of IVD degeneration. Lop/r suppresses the IL-113 and NF-KB and induces SOX9 and HIF-1 alpha, since these signaling path-ways may be related to human IVD degeneration

Intracranial Ependymomas in Childhood - A Retrospective Review of Sixty-Two Children

Of the 818 tumours of the central nervous system diagnosed between 1972 and 1991, 62 patients (35 males and 27 females) with histopathologically confirmed ependymomas were treated and followed-up at the Children's Hospital of Hacettepe University during that period. The median age was 6 years (range 1-17 years). Headache, nausea and vomiting were the most frequent symptoms; papilledema was the most common sign in our patients. Tumour sites were in the posterior fossa in 47 patients and supratentorial in 15 patients. All patients underwent surgery. Gross- total resection was performed in 27 patients, subtotal resection in 32 patients and biopsy in the remaining 3 patients. Initially, 53 patients were given postoperative radiotherapy. Four patients did not receive radiotherapy because of their young age, whereas five patients died prior to starting radiotherapy. Two slightly different types of chemotherapy protocols were applied for an average of one year in 47 patients. Event-free and overall survival rates at 10 years were 36% and 50%, respectively. Twenty children suffered relapse 4 to 55 months after diagnosis (median 16 months). Relapses were distant in 3 cases and local in 17. Age was the only statistically significant prognostic factor, patients younger than 5 years of age having a poorer outcome. Sex, histopathologic type, localization of the tumour, extent of surgery, and chemotherapy did not influence the prognosis in our study. Because the majority of recurrences were local, better local tumour control is required. New treatment strategies should be developed in order to improve local control.WoSScopu

How much do plastic surgeons add to the closure of myelomeningoceles?

Purpose This study reviews the outcomes of children undergoing myelomeningocele (MMC) repair in the paediatric neurosurgical department in Cardiff. These procedures are historically performed by paediatric neurosurgeons with occasional support from plastic surgeons for the larger lesions. We reviewed the postoperative outcomes over a 9-year period to assess the efficacy of having a plastic surgeon present at all MMC closures. Methods Analysis of a prospectively collected database of all MMC closures performed at University Hospital Wales from April 2009 to August 2017 was used. Comparison was made with the published literature especially with regard to complications. Results Thirty-one children, 13 males and 18 females, underwent MMC closure over the 9-year period. Twenty-four (77.4%) defects were closed by direct approximation. Seven patients (22.5%) required a more complex plastic procedure to obtain closure. Two patients (6.5%) had a wound complication, one wound infection and one flap edge necrosis both healing with dressings alone. Two patients had cerebrospinal fluid (CSF) leaks that responded to ventriculo-peritoneal shunting. Two patients died from unrelated conditions during the study period. Conclusion In our series, 7/31 (22.5%) cases involved a more complex closure in keeping with the literature. The authors feel that having the plastic surgeon at all closures has led to a low wound complication rate