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Honokiol is a polyphenolic compound that exerts neuroprotective properties through a variety of mechanisms. It has therapeutic potential in anxiety, pain, cerebrovascular injury, epilepsy, and cognitive disorders including Alzheimer’s disease. It has been traditionally used in medical practices throughout much of Southeast Asia, but has now become more widely studied due to its pleiotropic effects. Most current research regarding this compound has focused on its chemotherapeutic properties. However, it has the potential to be an effective neuroprotective agent as well. This review summarizes what is currently known regarding the mechanisms involved in the neuroprotective and anesthetic effects of this compound and identifies potential areas for further research.

Galloylated flavonol rhamnosides identified as kaempferol-3-O-(2″,3″,4″-tri-O-galloyl)-α-l-rhamnopyranoside, quercetin-3-O-(3″,4″-di-O-galloyl)-α-l-rhamnopyranoside, and quercetin-3-O-(2″,3″,4″-tri-O-galloyl)-α-l-rhamnopyranoside, together with five known galloylated and non-galloylated flavonol rhamnosides, were isolated from leaves of Calliandra tergemina (L.) Benth. Their structures were established using spectroscopic methods and their antibacterial activities against methicillin-resistant Staphylococcus aureus (MRSA) were evaluated by a microdilution method., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Many medicinal plants from Leguminosae family can be found easily in Malaysia. These plants have been used as traditional medicines by local ethnic groups, where they are prepared as decoction, pastes for wound infections, and some have been eaten as salad. This paper focused on the assessment of antioxidant potential, antibacterial activity and classes of phytochemicals of nine plants from the Leguminosae family., Methods: Acacia auriculiformis, Bauhinia kockiana, Bauhinia purpurea, Caesalpinia pulcherrima, Calliandra tergemina, Cassia surattensis, Leucaena leucocephala, Peltophorum pterocarpum, and Samanea saman were extracted with aqueous methanol and dichloromethane:methanol mixture to test for antioxidant and antibacterial activities. The Folin-Ciocalteu assay was conducted to quantify the total phenolic content and 2, 2-diphenyl-1-picrylhydrazyl (DPPH) assay was used to determine the free radical quenching capacity. Antibacterial activity was assessed using disc diffusion (Kirby-Bauer) assay. Screening for major classes of phytochemical was done using standard chemical tests., Results: B. kockiana flowers and C. pulcherrima leaves contained high total phenolic content (TPC) and strong DPPH radical scavenging ability with TPC of 8280 ± 498 mg GAE/100 g, IC(50) of 27.0 ± 5.0 μg/mL and TPC of 5030 ± 602 mg GAE/100 g, IC(50) of 50.0 ± 5.0 μg/mL respectively. Positive correlation was observed between TPC and free radical scavenging ability. Most extracts showed antibacterial activity against Gram positive bacteria at 1 mg, while none showed activity against Gram negative bacteria at the same dose. All extracts (except Samanea saman flower) showed antibacterial activity against two strains of methicillin resistant Staphylococcus aureus (MRSA) with MID values ranging between 100 μg/disc and 500 μg/disc., Conclusion: The potential source of antioxidant and antibacterial agents, especially for MRSA infection treatments were found in B. kockiana, C. pulcherrima, C. tergemina and P. pterocarpum. These preliminary results would be a guide in the selection of potential candidates for further pharmacological study and in search of new drug candidate in treating MRSA infections.

Objectives: To determine morphine pharmacokinetics in premature neonates varying in postconceptional age (PCA) and evaluate behavioral pain response in relationship to serum morphine concentrations., Methods: Premature neonates (n = 48), stratified by weeks of PCA (group 1 = 24-27 weeks, group 2 = 28-31 weeks, group 3 = 32-35 weeks, and group 4 = 36-39 weeks) received morphine infusions. Blood samples were drawn at 48, 60, and 72 hours and at discontinuation of morphine, followed by 3 samples obtained during the next 24 hours. Newborns were videotaped during heel lances and restful states, with morphine at steady-state concentrations and without morphine. Pain was assessed by using the Neonatal Facial Coding System (NFCS). Statistical analysis included regression between NFCS score changes from baseline to painful procedure with and without morphine., Results: Morphine clearance for groups 1, 2, 3, and 4 was calculated as 2.27 +/- 1.07, 3.21 +/- 1.57, 4.51 +/- 1.97, and 7.80 +/- 2.67 mL/kg/min, respectively, and correlated with PCA (r = 0.63, P <.001). Pain measured by facial expression was diminished; however, it did not correlate with morphine concentrations., Conclusion: Morphine clearance in premature neonates is less than reported, increasing with PCA. Facial activity discloses morphine analgesia; however, it is unrelated to morphine concentrations.

The objectives of this paper are to examine (a) the survival of extremely low-gestational-age (ELGA) infants born at 23-28 weeks' gestational age (GA) and (b) the neurodevelopmental outcome at 18 months corrected age for those born at 23-25 weeks' GA during 1991-1993, when antenatal steroids, surfactant, and dexamethasone for bronchopulmonary dysplasia had become accepted treatments; and to compare with an earlier (1983-1989), previously published large cohort (in a presurfactant era) from our institution. Perinatal and neonatal data on all births delivered at 23-28 weeks' GA at British Columbia's tertiary perinatal center were analyzed for survival rates by GA. Survivors of those born at 23-25 weeks' GA underwent neurodevelopmental assessment at a corrected chronological age of 18 months. The recent cohort (n = 333) of live birth infants, compared to the earlier cohort (n = 911 ) showed a trend toward an overall improved survival to discharge (72 vs. 65%, p = 0.06). Further analysis showed that improved survival was seen only in 26- to 28-week GA infants (86 vs. 76%, p = 0.01), but not in 23- to 25-week GA infants (44 vs. 44%, p = 0.9), even when adjusted for gender or twin births. In addition, the incidence of major impairment at 18 months (36% in both periods) remained high. Reanalysis of 24- to 25-week GA infants again showed no evidence of improved survival (53 vs. 50%) or improved outcome at 18 months (major handicap rate 32%; vs. 34%). Survival rates improved for 26- to 28-week GA infants, but the survival rate and incidence of major impairment had not improved for of 23- to 25-week GA infants.

The meningeal inflammatory response to a heat-killed mutant unencapsulated strain of type III group B Streptococcus (GBS) was studied in a newborn piglet model. GBS (10(9) colony-forming unit equivalents) or saline (control) was inoculated intraventricularly. Serial cerebrospinal fluid measurements were done at baseline and over the course of the next 24 h for cytochemical changes and production of tumor necrosis factor (TNF) and prostaglandins. In separate experiments, we defined the time course of early changes during the first 6 h and dose response relationship over a range of inocula 10(6) to 10(9) colony-forming unit equivalents. The intraventricular inoculation of the heat-killed unencapsulated GBS induced marked leukocytosis and increased protein by 6 h. These changes were preceded by a several hundredfold increase in TNF (maximum at 2 h) and prostaglandins (maximum at 2-4 h). The early and sharp rise in TNF suggests its pivotal role in initiating the inflammatory cascade. The magnitude of the inflammatory response increased with increasing bacterial dose over the range studied. To study the effect of encapsulation of GBS in the induction of meningeal inflammation, we compared the response to the unencapsulated mutant strain with that to the encapsulated parent strain. The encapsulated strain produced much smaller inflammatory changes, and only with high doses of bacteria. The GBS cell wall appeared to be the primary bacterial product triggering inflammation. Intraventricular injection of the heat-killed unencapsulated GBS with exposed cell wall can serve as a valid model for studying neonatal meningitis.

We prospectively studied the pharmacokinetic parameters of vancomycin in premature neonates given vancomycin according to a dosage protocol developed in our neonatal unit. Study infants were administered vancomycin according to four postconceptional age (PCA) groups: (0) 18 mg/kg every 36 h for PCA < 27 weeks; (I) 16 mg/kg every 24 h for PCA 27-30 weeks; (II) 18 mg/kg every 18 h for PCA 31-36 weeks; and (III) 15 mg/kg every 12 h for PCA > or = 37 weeks. Pharmacokinetic parameters were calculated from peak and trough serum vancomycin concentrations at steady state. Results in 44 infants (PCA, 27-44 weeks) showed that our dosage regimen achieved target peak serum vancomycin concentrations in 64% of neonates in Groups I-III, although it tended to undershoot the target trough concentrations. Volume of distribution (Vd), normalized for body weight, remained constant throughout the PCA range, with a mean value of 0.56 L/kg, whereas absolute clearance (r = 0.81) and normalized clearance (r = 0.48) increased with PCA (p < 0.005). The increase in clearance with PCA is associated with a greater elimination rate constant and shorter half-life. Vancomycin therapy can be initiated in a standard fashion according to our protocol or by individualizing the dosage regimen based on a Vd of 0.56 L/kg and clearance estimated from the infant's body weight and PCA groups.

Objectives: To determine gestational age (GA)-specific mortality rates; the effects of GA, birth weight, sex, and multiple gestation on mortality rates; short-term morbidity for infants born at 23 to 28 weeks GA; and impairment rates at a corrected chronologic age of 18 months for those born at 23 to 25 weeks GA., Methods: A data base analysis was performed with a linked obstetric and a neonatal database. GA was determined by obstetric data and confirmed by early ultrasonography (available in 88%) on all births < 30 weeks GA at British Columbia's tertiary perinatal center from 1983 to 1989., Results: Of 1024 births occurring between 23 and 28 weeks GA, 911 were live born. The mortality rate decreased with increasing GA: 84% at 23 weeks; 57% at 24 weeks; 45% at 25 weeks; 37% at 26 weeks; 23% at 27 weeks; and 13% at 28 weeks GA. For each GA, mortality rate versus birth weight plots showed a decreasing mortality rate with increasing birth weight, except for infants who were large for GA. Male infants had a higher mortality rate than female infants (odds ratio, 1.8; confidence interval, 1.4 to 2.5). Twins fared worse than singletons with a decreasing effect from 24 weeks GA (odds ratio, 10.3) to no effect at 28 weeks GA. The median number of days supported by mechanical ventilation and the length of stay in the neonatal intensive care unit decreased markedly with increasing GA. Eighteen-month outcome of survivors between 23 and 25 weeks GA with 93% follow-up rate revealed an overall impairment rate of 36%, but 6 of the 9 surviving 23-week infants had major impairments., Conclusions: The GA-specific perinatal outcome results of this large cohort provide information to assist in perinatal management decision making and for counseling parents prenatally.

Two major factors can interfere with normal development of the fetal lungs: mechanical constriction resulting in decreased intrathoracic space and reduced or absent fetal breathing movements. We report a unique case in which both factors contribute to the development of lethal pulmonary hypoplasia. This full-term neonate had an isolated unilateral lesion in the cervical spinal cord resulting in ipsilateral neurogenic atrophy of the diaphragm, bilateral pulmonary hypoplasia, and lung immaturity. Evenetration of the atrophied diaphragm decreased intrathoracic space, compromising fetal lung growth. This was compounded by impaired fetal respiration due to the diaphragmatic atrophy, further aggravating pulmonary hypoplasia on the affected side. The other lung was also hypoplastic, although to a lesser degree, suggesting that its growth was also affected by either or both of these factors.

With improvement in perinatal management and advances in neonatal intensive care, congenital anomalies have emerged as a major cause of neonatal mortality and morbidity. A 1 year review (1985) of all the admissions to our neonatal intensive care unit (NICU) showed that 78 of 790 (10%) had one or more congenital anomalies. Of these, 26% died in the NICU; another 10% died during the first year; therefore the total mortality of infants with congenital anomalies in the first year of life was 36%. Even though they accounted for only 10% of the total admissions, the infants with congenital anomalies were responsible for 13% of the total NICU patient-days, 26% of the total NICU mortality, 32% of all deaths within the first year, and 35% of all NICU infants with intrauterine growth retardation (IUGR). Of interest, 67% of the infants with anomalies were suspected or diagnosed prenatally. Of these, 54% were delivered by cesarean section, done for fetal reasons in the majority of cases. The highest mortality was associated with (1) multiple abnormal prenatal ultrasound findings; (2) extreme prematurity (less than 30 weeks gestation); and (3) the presence of IUGR. These findings raise concerns about the use of resources in the management of the pregnancy and the delivery of infants with congenital anomalies, particularly when diagnosed prenatally.

Pulmonary hypoplasia was diagnosed in 14 of 88 infants (16%) delivered in 1983 to 1986 after rupture of the membranes of greater than or equal to 7 days with onset before 29 weeks' gestation. Logistic regression analysis applied to examine the relative importance of perinatal risk factors in the prediction of pulmonary hypoplasia showed that gestational age at onset of rupture of the membranes had a significant effect (p = 0.002) on the odds that pulmonary hypoplasia developed in the neonate, whereas the duration of rupture of the membranes (p = 0.11) and the degree of oligohydramnios (p = 0.65) did not. Postnatally, the presence of pulmonary hypoplasia was associated with the severity of skeletal compression deformities (p less than 0.0001). The development of skeletal compression deformities was associated with severe oligohydramnios (p = 0.05) and duration of rupture of the membranes (p = 0.02) but not gestational age at rupture of the membranes (p = 0.77). Gestational age at onset of rupture of the membranes being the best single predictor of pulmonary hypoplasia suggests that the stage of lung development at rupture of the membranes may be important.