MicroRNAs (miRNAs) are small noncoding regulatory RNAs that reduce stability and/or translation of fully or partially sequence-complementary target mRNAs. Recent evidence indicates that miRNAs can function both as tumor suppressors and as oncogenes. It has been demonstrated that in glioblastoma multiforme miR-21 and 221 are upregulated whereas miR-128 and 181 are downregulated. Expression of miR-21, 221, 128a, 128b, 128c, 181a, 181b, 181c was studied using real-time quantitative reverse transcriptase polymerase chain reaction and northern blotting for human astrocytic tumors with different grade of malignancy. miR-21 and 221 were overexpressed in glioma samples, whereas miRNA 181b was downregulated compared with normal brain tissue. miRNA-21 was hyperexpressed in all tumor samples whereas higher levels of miRNA-221 were found in high-grade gliomas. This study is the first analysis of miRNAs in astrocytic tumor at different stages of malignancy. The different expression pattern observed in tumors at different stages of malignancy is probably dependent on the cell-specific repertoire of target genes of tumors sharing different molecular pathways activity and suggests miRNAs may have also a place in diagnosis and staging of brain tumors.

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BACKGROUND Antiapoptotis resulting from hyperactivation of the transcription factor NF‐κB has been described in several cancer types. It is triggered by the interaction of the tumor necrosis factor (TNF) with its receptors and recruitment of the intermediate factor TNF‐receptor associated factor (TRAF) 2. The NF‐κB transcriptional activity could amplify the expression of antiapoptotic genes. The authors investigated the activity of NF‐κB, and the mRNA expression of TNFα, TNFα receptor, TRAF1, TRAF2, and TRAF‐associated NF‐κB activator (TANK), and the antiapoptotic genes Bcl‐2, c‐IAP 1 and 2, and Survivin in human astrocytic tumors. METHODS Eight low‐grade astrocytomas (LGA), 10 anaplastic astrocytomas (AAs), 10 glioblastoma multiforme (GBM) samples were used; 4 samples of normal brain tissue were used as controls. The NF‐κB activation was analyzed by electrophoretic mobility shift assay; TRAF1, TRAF2, TANK/I‐TRAF, Bcl‐2, c‐IAP 1 and 2, and Survivin mRNA expressions were studied using real‐time quantitative reverse‐transcriptase polymerase chain reaction. RESULTS NF‐κB hyperactivity was detected in tumor samples. mRNA of antiapoptotic genes, particularly BCL‐2 and Survivin, was hyperexpressed in gliomas. Interestingly, BCL‐2 was hyperexpressed in LGAs, whereas a very high level of Survivin featured high‐grade gliomas. The differential expression of antiapoptotic genes yielded a tight clustering of all LGA and nearly all GBM samples in cluster analysis. CONCLUSIONS NF‐κB and factors involved in its intracellular activation were up‐regulated in gliomas. NF‐κB‐activated antiapoptotic genes were hyperexpressed in tumor samples, but showed a differential expression with higher levels of Bcl‐2 in LGAs and higher levels of Survivin in GBMs. Cancer 2008. © 2008 American Cancer Society.

BACKGROUND: Since January 2020, when the pathogen causing the coronavirus disease was identified in humans, the literature on coronavirus disease 2019 (COVID-19) has grown exponentially to more than 4000 publications. There is the need to provide an update for each single medical discipline, including neurosurgery, to be used by single professionals or to be distributed through the neurosurgical community and to be used by governments in designing new scenario of care.-CONCLUSIONS: The neurosurgical scientific community has promptly reacted to the COVID-19 outbreak by producing a growing number of documents that could serve as guidance for neurosurgeons all over the world. Neurosurgical societies will represent the key institutions for guiding the neurosurgical community to overcome the COVID-19 crisis.

A number of experimental studies have reported that moderate hypothermia can produce significant protection against behavioral deficits and/or morphopathological alterations following traumatic brain injury; a Phase 3 clinical trial is currently examining the therapeutic potential for moderate hypothermia (32 degrees C) to improve outcome following severe traumatic brain injury in humans. The current study examined whether hypothermia (32 degrees C) provided behavioral protection following experimental cortical impact injury. The extent of focal cortical contusion was also examined in the same rats. A total of 30 male Sprague-Dawley rats were trained on beam balance and beam walking tasks prior to injury. Under isoflurane anesthesia, cortical impact was produced on the right parietal cortex of 20 rats. Ten rats underwent all surgical procedures but were not impacted (sham-injured rats). Ten of the injured rats were cooled to 32 degrees C (measured in temporalis muscle) beginning 5 min postinjury, maintained for 2 h and rewarmed slowly for 1 h. In the other 10 injured rats, normothermic temperatures (37.5 degrees C) were maintained for the same duration. Beam balance and beam walking performance was assessed daily for 5 days following injury. At 11 days postinjury, rats were assessed for 5 days on acquisition of the Morris water maze task. Following behavioral assessments, rats were perfused and the brain removed. Coronal sections were cut through the site of cortical impact injury and stained with hematoxylin and eosin. Hypothermic treatment resulted in significantly less beam balance and beam walking deficits than observed in normothermic rats. Hypothermia also significantly attenuated spatial memory performance deficits. Quantitative morphometric analyses failed to detect any significant differences in volumes of necrotic tissue cavitation in cortices of hypothermic and normothermic rats. Hypothermic treatment also had no effect on volumes of dorsal hippocampal tissue or numbers of cells in CA1 or CA3 regions of the hippocampus. These data suggest that hypothermia, consistent with the reports of others, can produce significant behavioral protection following cortical impact injury that is not necessarily correlated with changes in focal cortical necrosis within the first 15 days following injury.

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The standard sylvian and basal cistern opening may be insufficient to guarantee preservation of olfactory function. Early identification and arachnoidal dissection of the nerve may reduce the rate of olfaction compromise. The opening of the subarachnoidal space should be performed in a proximal-to-distal manner to allow early visualization of the olfactory bulb and its dissection. The arachnoidal dissection should be performed with sharp instruments, avoiding any traction on the posterior portion of the olfactory tract. Any direct retractor compression should also be avoided to spare the microvasculature lying on the dorsal surface of the nerve.

Pituitary apoplexy is a rare clinical syndrome due to ischemic or haemorrhagic necrosis of the pituitary gland which complicates 2–12% of pituitary tumours, especially nonfunctioning adenomas. In many cases, it results in severe neurological, ophthalmological, and endocrinological consequences and may require prompt surgical decompression. Pituitary apoplexy represents a rare medical emergency that necessitates a multidisciplinary approach. Modalities of treatment and times of intervention are still largely debated. Therefore, the management of patients with pituitary apoplexy is often empirically individualized and clinical outcome is inevitably related to the multidisciplinary team's skills and experience. This review aims to highlight the importance of a multidisciplinary approach in the management of pituitary apoplexy and to discuss modalities of presentation, treatment, and times of intervention.