Impacts of pollution, fishing pressure, and reef rugosity on resource fish biomass in West Hawaii.

Human activities and land-use drivers combine in complex ways to affect coral reef health and, in turn, the diversity and abundance of reef fauna. Here we examine the impacts of different marine protected area (MPA) types, and various human and habitat drivers, on resource fish functional groups (i.e., total fish, herbivore, grazer, scraper, and browser biomass) along the 180 km west coast of Hawaii Island. Across survey years from 2008 to 2018, we observed an overall decrease in total fish biomass of 45%, with similar decreases in biomass seen across most fish functional groups. MPAs that prohibited a combination of lay nets, aquarium collection, and spear fishing were most effective in maintaining and/or increasing fish biomass across all functional groups. We also found that pollution, fishing, and habitat drivers all contributed to changes in total fish biomass, where the most negative impact was nitrogen input from land-based sewage disposal. Fish biomass relationships with our study drivers depended on fish functional grouping. For surgeonfish (grazers), changes in biomass linked most strongly to changes in reef rugosity. For parrotfish (scrapers), biomass was better explained by changes in commercial catch where current commercial fishing levels are negatively affecting scraper populations. Our observations suggest that regional management of multiple factors, including habitat, pollution, and fisheries, will benefit resource fish biomass off Hawaii Island.

Retraction Note: Aluminum in Neurological and Neurodegenerative Disease.

The Editor-in Chief of Molecular Neurobiology has retracted this article [1] at the request of the corresponding author. This is because it significantly overlaps with their previous publication [2]. Both articles report the same results and as such this article is redundant.Walter J. Lukiw, Maire E. Percy, and Zhide Fang agree to this retraction.William J.Walsh and Yuhai Zhao do not agree to this retraction. Aileen I. Pogue, Nathan M. Sharfman, Vivian Jaber, and Wenhong Li have not responded to any correspondence from the editor/publisher about this retraction. Donald R. C. McLachlan, Catherine Bergeron, Peter N. Alexandrov, and Theodore P. A. Kruck are deceased.[1] McLachlan, D.R.C., Bergeron, C., Alexandrov, P.N. et al. Mol Neurobiol (2019) 56: 1531. https://doi.org/10.1007/s12035-018-1441-x[2] McLachlan, D.R.C., Alexandrov, P.N., Walsh, W.J. et al. J Alzheimers Dis Parkinsonism (2018) 8(6): 457. https://doi.org/10.4172/2161-0460.1000457.

Aluminum in neurological disease - a 36 year multicenter study.

Aluminum is a ubiquitous neurotoxin highly enriched in our biosphere, and has been implicated in the etiology and pathology of multiple neurological diseases that involve inflammatory neural degeneration, behavioral impairment and cognitive decline. Over the last 36 years our group has analyzed the aluminum content of the temporal lobe neocortex of 511 high quality coded human brain samples from 18 diverse neurological and neurodegenerative disorders, including 2 groups of age-matched controls. Brodmann anatomical areas including the inferior, medial and superior temporal gyrus (A20-A22) were selected for analysis: (i) because of their essential functions in massive neural information processing operations including cognition and memory formation; and (ii) because subareas of these anatomical regions are unique to humans and are amongst the earliest areas affected by progressive neurodegenerative disorders such as Alzheimer's disease (AD). Coded brain tissue samples were analyzed using the analytical technique of: (i) Zeeman-type electrothermal atomic absorption spectrophotometry (ETAAS) combined with (ii) an experimental multi-elemental analysis using the advanced photon source (APS) ultra-bright storage ring-generated hard X-ray beam (7 GeV) and fluorescence raster scanning (XRFR) spectroscopy device at the Argonne National Laboratory, US Department of Energy, University of Chicago IL, USA. These data represent the largest study of aluminum concentration in the brains of human neurological and neurodegenerative disease ever undertaken. Neurological diseases examined were AD (N=186), ataxia Friedreich's type (AFT; N=6), amyotrophic lateral sclerosis (ALS; N=16), autism spectrum disorder (ASD; N=26), dialysis dementia syndrome (DDS; N=27), Down's syndrome (DS; trisomy21; N=24), Huntington's chorea (HC; N=15), multiple infarct dementia (MID; N=19), multiple sclerosis (MS; N=23), Parkinson's disease (PD; N=27), prion disease (PrD; N=11) including bovine spongiform encephalopathy (BSE; 'mad cow disease'), Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Sheinker syndrome (GSS), progressive multifocal leukoencephalopathy (PML; N=11), progressive supranuclear palsy (PSP; N=24), schizophrenia (SCZ; N=21), a young control group (YCG; N=22) and an aged control group (ACG; N=53). Amongst these 18 common neurological conditions and controls we report a statistically significant trend for aluminum to be increased only in AD, DS and DDS compared to age- and gender-matched brains from the same anatomical region. The results continue to suggest that aluminum's association with AD, DDS and DS brain tissues may contribute to the neuropathology of these neurological diseases but appear not to be a significant factor in other common disorders of the human central nervous system (CNS).

Aluminum in Neurological and Neurodegenerative Disease.

With continuing cooperation from 18 domestic and international brain banks over the last 36 years, we have analyzed the aluminum content of the temporal lobe neocortex of 511 high-quality human female brain samples from 16 diverse neurological and neurodegenerative disorders, including 2 groups of age-matched controls. Temporal lobes (Brodmann areas A20-A22) were selected for analysis because of their availability and their central role in massive information-processing operations including efferent-signal integration, cognition, and memory formation. We used the analytical technique of (i) Zeeman-type electrothermal atomic absorption spectrophotometry (ETAAS) combined with (ii) preliminary analysis from the advanced photon source (APS) hard X-ray beam (7 GeV) fluorescence raster-scanning (XRFR) spectroscopy device (undulator beam line 2-ID-E) at the Argonne National Laboratory, US Department of Energy, University of Chicago IL, USA. Neurological diseases examined were Alzheimer's disease (AD; N = 186), ataxia Friedreich's type (AFT; N = 6), amyotrophic lateral sclerosis (ALS; N = 16), autism spectrum disorder (ASD; N = 26), dialysis dementia syndrome (DDS; N = 27), Down's syndrome (DS; trisomy, 21; N = 24), Huntington's chorea (HC; N = 15), multiple infarct dementia (MID; N = 19), multiple sclerosis (MS; N = 23), Parkinson's disease (PD; N = 27), and prion disease (PrD; N = 11) that included bovine spongiform encephalopathy (BSE; "mad cow disease"), Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Sheinker syndrome (GSS), progressive multifocal leukoencephalopathy (PML; N = 11), progressive supranuclear palsy (PSP; N = 24), schizophrenia (SCZ; N = 21), a young control group (YCG; N = 22; mean age, 10.2 ± 6.1 year), and an aged control group (ACG; N = 53; mean age, 71.4 ± 9.3 year). Using ETAAS, all measurements were performed in triplicate on each tissue sample. Among these 17 common neurological conditions, we found a statistically significant trend for aluminum to be increased only in AD, DS, and DDS compared to age- and gender-matched brains from the same anatomical region. This is the largest study of aluminum concentration in the brains of human neurological and neurodegenerative disease ever undertaken. The results continue to suggest that aluminum's association with AD, DDS, and DS brain tissues may contribute to the neuropathology of those neurological diseases but appear not to be a significant factor in other common disorders of the human brain and/or CNS.

Micronutrient Therapy for Violent and Aggressive Male Youth: An Open-Label Trial.

OBJECTIVES: Pharmacotherapy for problematic aggressive and violent behavior disorders in male children and adolescents is associated with significant adverse events. Treatments with more acceptable risk-benefit ratios are critically needed. Micronutrient intervention will be investigated as an alternative to bridge the therapeutic gap in the management of these behaviors. METHODS: Males aged 4-14 who displayed ongoing violent and aggressive behaviors received micronutrient intervention containing alpha-tocopherol (vitamin E), ascorbic acid (vitamin C), biotin, chromium, pyridoxal-5-phosphate (P5P), pyridoxine (vitamins B6), selenium, and zinc, in a 16-week open-label trial. Plasma zinc, plasma copper, copper/zinc ratio, and urinary hydroxyhemopyrroline-2-one (HPL) tests were conducted at baseline and endpoint. Participants were examined for changes in aggressive and violent behaviors measured using the Children's Aggression Scale (CAS) and the Modified Overt Aggression Scale (MOAS), improvements in family functioning measured using the Family Functioning Style Scale, improvements in health-related quality of life (HRQoL) measured using the Pediatric Quality of Life Inventory (PedsQL) at baseline, 8 weeks, endpoint, and at 4-6-month follow-up. RESULTS: Thirty-two male children and adolescents met inclusion criteria. Thirty-one (mean 8.35 ± standard deviation 2.93 years) completed the study, with one participant lost to follow-up. Micronutrient therapy significantly improved parent-reported aggressive and violent behaviors measured using the CAS for all domains except the use of weapons (p < 0.001 to p = 0.02) with medium to large effect size (Cohen's d = 0.72-1.43) and the MOAS (p < 0.001) with large effect size (Cohen's d = 1.26). Parent-reported HRQoL (p < 0.001; Cohen's d = -1.69) and family functioning (p = 0.03; Cohen's d = -0.41) also significantly improved. CONCLUSION: Micronutrient therapy appeared well tolerated, with a favorable side effect profile. It appeared effective in the reduction of parent-reported aggressive and violent behaviors, and showed improvement in family functioning and HRQoL in male youth after 16 weeks. Further research in the form of a double-blinded, randomized controlled trial is required to verify these initial positive observations.

Pufferfish mortality associated with novel polar marine toxins in Hawaii.

Fish die-offs are important signals in tropical marine ecosystems. In 2010, a mass mortality of pufferfish in Hawaii (USA) was dominated by Arothron hispidus showing aberrant neurological behaviors. Using pathology, toxinology, and field surveys, we implicated a series of novel, polar, marine toxins as a likely cause of this mass mortality. Our findings are striking in that (1) a marine toxin was associated with a kill of a fish species that is itself toxic; (2) we provide a plausible mechanism to explain clinical signs of affected fish; and (3) this epizootic likely depleted puffer populations. Whilst our data are compelling, we did not synthesize the toxin de novo, and we were unable to categorically prove that the polar toxins caused mortality or that they were metabolites of an undefined parent compound. However, our approach does provide a template for marine fish kill investigations associated with marine toxins and inherent limitations of existing methods. Our study also highlights the need for more rapid and cost-effective tools to identify new marine toxins, particularly small, highly polar molecules.

Marine protected area networks: assessing whether the whole is greater than the sum of its parts.

Anthropogenic impacts are increasingly affecting the world's oceans. Networks of marine protected areas (MPAs) provide an option for increasing the ecological and economic benefits often provided by single MPAs. It is vital to empirically assess the effects of MPA networks and to prioritize the monitoring data necessary to explain those effects. We summarize the types of MPA networks based on their intended management outcomes and illustrate a framework for evaluating whether a connectivity network is providing an outcome greater than the sum of individual MPA effects. We use an analysis of an MPA network in Hawai'i to compare networked MPAs to non-networked MPAs to demonstrate results consistent with a network effect. We assert that planning processes for MPA networks should identify their intended outcomes while also employing coupled field monitoring-simulation modeling approaches, a powerful way to prioritize the most relevant monitoring data for empirically assessing MPA network performance.

Discerning the Mauve factor, Part 2.

"Mauve Factor" was once mistaken for kryptopyrrole but is the hydroxylactam of hemopyrrole, hydroxyhemopyrrolin-2-one (HPL). Treatment with nutrients--particularly vitamin B6 and zinc--reduces urinary excretion of HPL and improves diverse neurobehavioral symptoms in subjects with elevated urinary HPL. Heightened HPL excretion classically associates with emotional stress, which in turn is known to associate with oxidative stress. For this review, markers for nutritional status and for oxidative stress were examined in relationship to urinary HPL. In cohorts with mixed diagnoses, 24-hour urinary HPL correlated negatively with vitamin B6 activity and zinc concentration in red cells (P < .0001). Above-normal HPL excretion corresponded to subnormal vitamin B6 activity and subnormal zinc with remarkable consistency. HPL correlated inversely with plasma GSH and red-cell catalase, and correlated directly with plasma nitric oxide (P < .0001). Thus, besides implying proportionate needs for vitamin B6 and zinc, HPL is a promising biomarker for oxidative stress. HPL is known to cause non-erythroid heme depression, which lowers zinc, increases nitric oxide, and increases oxidative stress. Administration of prednisone reportedly provoked HPL excretion in animals. Since adrenocorticoid (and catecholamine) stress hormones mediate intestinal permeability, urinary HPL was examined in relationship to urinary indicans, presumptive marker for intestinal permeability. Urinary HPL associated with higher levels ofindicans (P < .0001). Antibiotics reportedly reduce HPL in urine, suggesting an enterobic role in production. Potentially, gut is reservoir for HPL or its precursor, and stress-related changes in intestinal permeability mediate systemic and urinary concentrations.

A multivariate assessment of the coral ecosystem health of two embayments on the lee of the island of Hawai'i.

Four coral-dominated coastal sites within two embayments (Kealakekua Bay and Honokohau Bay) on the lee of the island of Hawai'i were studied to assess evidence of anthropogenic impacts in these relatively pristine locales. Nutrient-loading parameters were analyzed in relation to benthic composition data. Statistically, there were significant positive relationships between nitrate+nitrite, silicate, and ammonium with the abundance of macroalgae, coralline algae, and dead coral, and between delta(15)N and dead coral abundance. The north outside site of Kealakekua Bay and the south outside site of Honokohau Bay appear to be most impacted by nutrient-loading factors in each bay, respectively. Comparisons with past nutrient data indicate that nutrient inputs have increased to the two bays, and that early impacts of these increased loadings are evident. It is predicted that at current nutrient-loading rates, the north sites of Kealakekua Bay and the south sites of Honokohau Bay will exhibit evidence of further degradation in future years.

Discerning the Mauve Factor, Part 1.

"Mauve Factor" was once mistaken for kryptopyrrole but is the hydroxylactam of hemopyrrole, hydroxyhemopyrrolin-2-one (HPL). Treatment with nutrients--particularly vitamin B6 and zinc--reduces urinary excretion of HPL and improves diverse neurobehavioral symptoms in subjects with elevated urinary HPL. Heightened HPL excretion classically associates with emotional stress, which in turn is known to associate with oxidative stress. For this review, markers for nutritional status and for oxidative stress were examined in relationship to urinary HPL. In cohorts with mixed diagnoses, 24-hour urinary HPL correlated negatively with vitamin B6 activity and zinc concentration in red cells (P < .0001). Above-normal HPL excretion corresponded to subnormal vitamin B6 activity and subnormal zinc with remarkable consistency. HPL correlated inversely with plasma glutathione and red-cell catalase, and correlated directly with plasma nitric oxide (P < .0001). Thus, besides implying proportionate needs for vitamin B6 and zinc, HPL is a promising biomarker for oxidative stress. HPL is known to cause non-erythroid heme depression, which lowers zinc, increases nitric oxide, and increases oxidative stress. Administration of prednisone reportedly provoked HPL excretion in animals. Since adrenocorticoid (and catecholamine) stress hormones mediate intestinal permeability, urinary HPL examined in relationship to urinary indicans, presumptive marker for intestinal permeability. Urinary HPL associated with higher levels of indicans (P < .0001). Antibiotics reportedly reduce HPL in urine, suggesting an enterobic role in production. Potentially, gut is a reservoir for HPL or its precursor, and stress-related changes in intestinal permeability mediate systemic and urinary concentrations.

Elevated serum copper levels in women with a history of post-partum depression.

Previous observations suggested that there may be an association between elevated serum copper (Cu) levels and post-partum depression (PPD). In this study, we examined Zn and Cu levels in women with completed pregnancies who had a history of PPD and compared them to women who did not have depression, and to women who reported having been depressed, but without a history of PPD. Cu levels were significantly higher in women having a history of PPD compared both to non-depressed women and to depressed women without a history of PPD. The mean serum Cu level of 78 women with a history of PPD was 131+/-39microg/dL compared with 111+/-25microg/dL in 148 women without such a history, and 106+/-20microg/dL in non-depressed controls (p<0.001). Zn levels did not differ across the three groups. Cu/Zn ratios were significantly higher in the PPD-history-positive group, due to the significant differences in Cu levels. Cu and Zn levels were not significantly different in depressed and non-depressed men, nor between non-depressed women and non-depressed men. Depressed women had higher Cu, but not Zn, levels compared with men. The nature of the association between elevated Cu values and PPD is, as yet, unknown; however Cu has roles in a variety of physiological systems that may be implicated in the development of PPD.

Altered vascular phenotype in autism: correlation with oxidative stress.

BACKGROUND: Autism is a neurologic disorder characterized by impaired communication and social interaction. Results of previous studies showed biochemical evidence for abnormal platelet reactivity and altered blood flow in children with autism. OBJECTIVE: To evaluate the vascular phenotype in children with autism. DESIGN AND MAIN OUTCOME MEASURES: Urinary levels of isoprostane F(2alpha)-VI, a marker of lipid peroxidation; 2,3-dinor-thromboxane B(2), which reflects platelet activation; and 6-keto-prostaglandin F(1alpha), a marker of endothelium activation, were measured by means of gas chromatography-mass spectrometry in subjects with autism and healthy control subjects. SETTING AND SUBJECTS: Children with a clinical diagnosis of autism attending the Pfeiffer Treatment Center. RESULTS: Compared with controls, children with autism had significantly higher urinary levels of isoprostane F(2alpha)-VI, 2,3-dinor-thromboxane B(2), and 6-keto-prostaglandin F(1alpha). Lipid peroxidation levels directly correlated with both vascular biomarker ratios. CONCLUSION: Besides enhanced oxidative stress, platelet and vascular endothelium activation also could contribute to the development and clinical manifestations of autism.

Reduced violent behavior following biochemical therapy.

UNLABELLED: Reduced violent behavior following biochemical therapy. We conducted an outcome study to measure the effectiveness of biochemical therapy for 207 consecutive patients presenting with a diagnosed behavior disorder. The treatment protocols were based on clinical evaluation and our past experience in the treatment of 8000 patients with behavior disorders at the Pfeiffer Treatment Center (PTC) over a 10-year period. Each test subject was screened for chemical imbalances previously found in high incidence in this population, including metal-metabolism disorders, methylation abnormalities, disordered pyrrole chemistry, heavy-metal overload, glucose dyscontrol, and malabsorption. The clinical procedure included a medical history, assay of 90 biochemical factors, and a physical examination. Standardized treatment protocols were applied for each imbalance that was identified. The frequencies of physical assaults and destructive episodes were determined using a standardized behavior scale before and after treatment, with follow-up ranging from 4 to 8 months. RESULTS: Seventy-six percent of the test subjects achieved compliance during the treatment period. The remaining 24% were reported to have discontinued the therapy. A reduced frequency of assaults was reported by 92% of the compliant assaultive patients, with 58% achieving elimination of the behavior. A total of 88% of compliant destructive patients exhibited a reduced frequency of destructive incidents and 53% achieved elimination of the behavior. Statistical significance was found for reduced frequency of assaults (t=7.74, p<0.001) and destructive incidents (t= 8.77, p<0.001). The results of this outcome study strongly suggest that individualized biochemical therapy may be efficacious in achieving behavioral improvements in this patient population.