No abstract

Traumatic acute subdural hematoma (ASDH) is a major clinical entity in traumatic brain injury (TBI). It acts as a space occupying lesion to increase intracranial pressure, and is often complicated by co-existing lesions, and is modified by cerebral blood flow (CBF) changes, coagulopathy, and delayed hematomas. Because of its complicated pathophysiology, the mortality of ASDH is still remaining high. In this review article, its epidemiology, pathophyiology, surgical treatment, and salvage ability are described. With regard to epidemiology, as the population ages, growing number of elderly patients with ASDH, especially patients with prehospital anticoagulant and antiplatelets, increase. Concerning pathophysiology, in addition to well-known initial intracranial hypertension and subsequent ischemia, delayed hyperemia/hyperperfusion, or delayed hematoma is being recognized frequently in recent years. However, optimal treatments for these delayed phenomenons have not been established yet. With regard to surgical procedures, all of craniotomy, decompressive craniectomy, and initial trephination strategies seem to be effective, but superiority of each procedure have not been established yet. Since Glasgow Coma Scale (GCS) scores, age, papillary reaction, and computed tomographic findings are strongly correlated to outcome, each factor has been investigated as an indicator of salvage ability. None of them, however, has been defined as such one. In future studies, epidemiological changes as population ages, management of delayed pathophysiology, superiority of each surgical procedures, and salvage ability should be addressed.

It is believed that the plastids in green plants lost peptidoglycan (i.e., a bacterial cell wall-containing D-amino acids) during their evolution from an endosymbiotic cyanobacterium. Although wall-like structures could not be detected in the plastids of green plants, the moss Physcomitrella patens has the genes required to generate peptidoglycan (Mur genes), and knocking out these genes causes defects in chloroplast division. Here, we generated P. patens knockout lines (ΔPp-ddl) for a homolog of the bacterial peptidoglycan-synthetic gene encoding D-Ala:D-Ala ligase. ΔPp-ddl had a macrochloroplast phenotype, similar to other Mur knockout lines. The addition of D-Ala-D-Ala (DA-DA) to the medium suppressed the appearance of giant chloroplasts in ΔPp-ddl, but the addition of L-Ala-L-Ala (LA-LA), DA-LA, LA-DA, or D-Ala did not. Recently, a metabolic method for labeling bacterial peptidoglycan was established using ethynyl-DA-DA (EDA-DA) and click chemistry to attach an azidemodified fluorophore to the ethynyl group. The ΔPp-ddl line complemented with EDA-DA showed that moss chloroplasts are completely surrounded by peptidoglycan. Our findings strongly suggest that the moss plastids have a peptidoglycan wall containing D-amino acids. By contrast, no plastid phenotypes were observed in the T-DNA tagged ddl mutant lines of Arabidopsis thaliana.

No abstract

The effects of three risk factors for valproate (VPA) hepatotoxicity (i.e., young age, polypharmacy, and high VPA serum level) on the metabolism of VPA to its monounsaturated metabolites [2-en-VPA (2-en), 3-en-VPA (3-en) and 4-en-VPA (4-en)] were investigated in 106 patients treated with VPA (56 cases of monotherapy and 50 cases of polytherapy). In the monotherapy group, there was a significant negative correlation between age and 4-en/VPA ratio. In the same group, the 4-en/VPA ratio showed a significant positive correlation with serum VPA level, while 3-en/VPA and 2-en/VPA ratios showed significant negative correlations. In patients greater than 10 years, the 4-en/VPA ratio was significantly higher, while the 2-en/VPA ratio was significantly lower in the polytherapy group than in the monotherapy group. Our results indicate that all three risk factors clearly increase the metabolic conversion of VPA to 4-en, the most toxic VPA metabolite, and that polytherapy and high VPA serum level result in the inhibited beta-oxidative metabolism of VPA to 2-en. These altered VPA metabolic profiles are strikingly similar to the abnormal VPA metabolism previously reported in cases with fatal hepatic failure. Although VPA-induced fatal hepatotoxicity has been regarded as an idiosyncratic reaction, it is possible that these three factors enhance susceptibility to VPA hepatotoxicity by altering the metabolism of VPA.