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Marine natural products are promising sources of green antifoulants. Here, a new compound (1) was isolated from the soft coral Sinularia flexibilis. This compound, another nine cembranoids (2–10) from S. flexibilis, and three eunicellin-type diterpenoids (11–13) from the gorgonian Muricella sp. were tested for antifouling activity against larval settlement of the bryozoan Bugula neritina. Compounds 2, 3, 4, 9, 12, and 13 exhibited significant antifouling activity, with EC50 values of 18.2, 99.7, 67.9, 35.6, 33.9, and 49.3 μM, respectively. Analysis of the structure-activity relationships suggested that the hydroxy group at C-13 in compound 4 reduced its antifouling activity. [ABSTRACT FROM AUTHOR]

Objective: Subdural hygroma (SDG) is a common complication that can occur after head trauma or secondary to decompressive craniectomy (DC). SDGs can be located not only ipsilateral or contralateral to the side of the DC, but also bilateral or unilateral in patients without DC. This study investigated the incidence and risk factors for different types of SDG in a large cohort of patients with traumatic brain injury (TBI). Methods: A retrospective study was conducted involving 379 adult patients with TBI who were admitted to Huashan Hospital, Fudan University between January 2009 and December 2013. As the outcome was dichotomous (SDG vs no SDG or hydrocephalus vs no hydrocephalus), multivariate logistic regression analyses were used to identify independent risk factors for the development of SDGs in patients without DC, ipsilateral SDG after unilateral DC, contralateral SDG after unilateral DC or SDG after bilateral DC. Risk factors for the development of hydrocephalus were also evaluated in patients with and without DC. Results: Among the 207 (54.6%) patients without DC, 30 (14.5%) had unilateral SDGs and 34 (16.4%) had bilateral SDGs. Of the 172 patients (45.4%) with DC, 134 (77.9%) underwent unilateral DC and 38 (22.1%) underwent bilateral DC. Of the 134 patients who underwent unilateral DC, 49 developed SDG, including 22 (16.4%) ipsilateral SDG, 19 (14.2%) contralateral SDG and eight (6.0%) both ipsilateral and contralateral SDGs. For patients undergoing bilateral DC, 13 (34.2%) developed a SDG. No significant difference in the incidence of SDG was observed between the patients with and without DC (36.0% vs 30.9%, p = 0.291), but the characteristics of SDGs were different between the two groups. Logistic regression analysis showed that factors independently associated with the development of SDG were male sex (odds ratio [OR] = 3.861; 95% CI = 1.642-9.091; p = 0.002), older age (OR = 1.046; 95% CI = 1.021-1.070; p < 0.001), basal cistern haemorrhage (OR = 4.608; 95% CI = 1.510-14.064; p = 0.007), diffuse injury and swelling (OR = 3.158; 95% CI = 1.341-7.435; p = 0.008) or diffuse injury and shift (OR = 3.826; 95% CI = 1.141-12.830; p = 0.030) in patients without DC. Temporal haematoma or contusion in the non-DC side (OR = 2.623; 95% CI = 1.070-6.428; p = 0.035) and traumatic SAH (OR = 3.751; 95% CI = 1.047-13.438; p = 0.042) were independently associated with the development of ipsilateral SDG in patients who underwent unilateral DC. However, factors independently associated with the development of contralateral SDG were frontal haematoma or contusion on the non-DC side (OR = 3.145; 95% CI = 1.272-7.774; p = 0.013) and SDH on the non-DC side (OR = 7.024; 95% CI = 1.477-33.390; p = 0.014). Only craniectomy area (OR = 1.030; 95% CI = 1.008-1.052; p = 0.008) was independently associated with the development of SDG in patients with bilateral DC. In the multivariate analysis, SDG in patients without DC was not associated with the development of hydrocephalus. However, SDG was significantly associated with the development of hydrocephalus for patients who underwent DC (OR = 2.173; 95% CI = 1.362-3.467; p = 0.001). Conclusions: This study suggested that the incidence of SDG in patients who have and have not undergone DC was identical; however, the patients' characteristics and risk factors differed. Therefore, the management and prediction of SDG should be performed according to SDG type. [ABSTRACT FROM AUTHOR]

Objective: To prospectively investigate the predictive value of initial intracranial pressure (ICP) for refractory intracranial hypertension and outcomes in persons with diffuse traumatic brain injury (TBI). Methods: A prospective observational study was conducted in 107 adult persons with diffuse TBI (Marshall CT Class II-IV). Initial ICP was defined as the first ICP recorded in the operating room. Refractory intracranial hypertension was defined as ICP increases to more than 30 mmHg and/or reduces in cerebral perfusion pressure to less than 60 mmHg for a period longer than 15 minutes and failure to respond to the maximum medical treatment. Baseline demographics and injury-specific data were recorded. Multiple logistic regression models were used to determine independent risk factors for refractory intracranial hypertension and unfavourable outcomes. A receiver-operating characteristic (ROC) curve was then drawn. Results: The initial ICP allowed for a better refractory intracranial hypertension prediction (ROC area = 0.868; 95% CI = 0.799-0.937) than the Marshall Classification (ROC area = 0.670; 95% CI = 0.569-0.772) or Rotterdam Classification scores (ROC area = 0.679; 95% CI = 0.577-0.780). An initial ICP value higher than 20 mmHg had 83% sensitivity and 83% specificity, whereas an initial ICP value higher than 25 mmHg had 64% sensitivity and 92% specificity for refractory intracranial hypertension. A multivariable logistic regression model showed that any 5 mmHg pressure increase in a patient with initial ICP led to 2.884-times higher odds of refractory intracranial hypertension (95% CI = 1.893-4.395; p < 0.001). Head Abbreviated Injury Scale score, initial Glasgow Coma Scale (GCS) and initial GCS motor scores were not predictive of refractory intracranial hypertension ( p > 0.05). Conclusion: For persons with diffuse TBI, the initial ICP provides great prognostic discrimination and is an independent predictor of refractory intracranial hypertension. [ABSTRACT FROM AUTHOR]