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1.
Oper Neurosurg (Hagerstown) ; 22(6): 400-408, 2022 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-35867080

RESUMO

BACKGROUND: The current transsylvian or transopercular approaches make access difficult because of the limited exposure of insular tumors. Hence, maximal and safe removal of insular gliomas is challenging. In this article, a new approach to resect insular gliomas is presented. OBJECTIVE: To determine whether the new transfrontal limiting sulcus approach is helpful for maximal and safe removal of insular gliomas. METHODS: The authors reported surgical techniques for insular gliomas resected through the transfrontal limiting sulcus approach. The authors evaluated the surgical resections of 69 insular gliomas performed through the new approach in their department. The extents of resection and postoperative neurological outcomes were analyzed to determine the value of this new approach. RESULTS: Based on the Berger-Sanai classification, most insular gliomas were giant tumors (59.42%), followed by zone I + IV tumors (24.64%). The median (interquartile range) extent of resection of all patients was 100% (91%, 100%). The total resection rate for all gliomas was (55 of 69, 79.7%), and the total resection rate for low-grade gliomas was (28 of 40, 70%), which was significantly lower than that for high-grade gliomas (27 of 29, 93.1%) (P = .019). All patients had muscle strength greater than grade 4 3 months after surgery. Only 1 patient had a speech disorder 3 months after surgery. The median Karnofsky Performance Status score at the time of the 3-month follow-up was 90. CONCLUSION: The transfrontal limiting sulcus approach can help to achieve maximal and safe removal of insular gliomas.


Assuntos
Neoplasias Encefálicas , Glioma , Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/cirurgia , Córtex Cerebral/cirurgia , Glioma/patologia , Glioma/cirurgia , Humanos , Procedimentos Neurocirúrgicos/métodos , Resultado do Tratamento
2.
Biomed Pharmacother ; 141: 111839, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34174505

RESUMO

If mitochondrial energy availability or oxidative metabolism is altered, patients will suffer from insufficient energy supply Phosphocreatine (PCr) not only acts as an energy carrier, but also acts as an antioxidant and defensive agent to maintain the integrity and stability of the membrane, to maintain ATP homeostasis through regulating mitochondrial respiration. Meanwhile, PCr can enhance calcium balance and reduce morphological pathological changes, ultimately, PCr helps to reduce apoptosis. On the other aspect, the activities of ATP synthase and MitCK play a crucial role in the maintenance of cellular energy metabolic function. It is interesting to note, PCr not only rises the activities of ATP synthase as well as MitCK, but also promotes these two enzymatic reactions. Additionally, PCr can also inhibit mitochondrial permeability transition in a concentration-dependent manner, prevent ROS and CytC from spilling into the cytoplasm, thereby inhibit the release of proapoptotic factors caspase-3 and caspase-9, and eventually, effectively prevent LPS-induced apoptosis of cells. Understandably, PCr prevents the apoptosis caused by abnormal mitochondrial energy metabolism and has a protective role in a non-energy manner. Moreover, recent studies have shown that PCr protects cell survival through PI3K/Akt/eNOS, MAPK pathway, and inhibition of Ang II-induced NF-κB activation. Furthermore, PCr antagonizes oxidative stress through the activation of PI3K/Akt/GSK3b intracellular pathway, PI3K/AKT-PGC1α signaling pathway, while through the promotion of SIRT3 expression to maintain normal cell metabolism. Interestingly, PCr results in delaying the time to enter pathological metabolism through the delayed activation of AMPK pathway, which is different from previous studies, now we propose the hypothesis that the "miRNA-JAK2/STAT3 -CypD pathway" may take part in protecting cells from apoptosis, PCr may be further be involved in the dynamic relationship between CypD and STAT3. Furthermore, we believe that PCr and CypD would be the central link to maintain cell survival and maintain cell stability and mitochondrial repair under the mitochondrial dysfunction caused by oxidative stress. This review provides the modern progress knowledge and views on the molecular mechanism and molecular targets of PCr in a non-energy way.


Assuntos
Sobrevivência Celular/fisiologia , Fosfocreatina/fisiologia , Animais , Sobrevivência Celular/genética , Metabolismo Energético/fisiologia , Humanos , Estresse Oxidativo , Fosfocreatina/genética , Transdução de Sinais/fisiologia
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