Integration and Extension of Specialty Mental Healthcare Services to Community Practice in Parkinson Disease

Parkinson disease (PD) is a progressive neurodegenerative disease with a higher prevalence of neuropsychiatric symptoms compared with the general population. Symptoms such as anxiety, depression, psychosis, impulse control disorders, and cognitive impairment cause a greater worsening of quality of life than even the motor symptoms that define PD. Despite the ubiquity and impact of neuropsychiatric symptoms, specialty mental healthcare is not routinely available, accessible, or integrated in most neurology practices. Currently, training in PD-specific mental healthcare is not standard in most programs, and the need for subspecialty-trained, mental healthcare providers will only increase over time, as the prevalence of PD will more than double by 2060. Many barriers limit extension of mental healthcare into existing models of integrated or multidisciplinary care and the community at large. Foundations and professional societies have played an important role in raising awareness of mental healthcare needs in PD; however, their initiatives to promote integrated or multidisciplinary care have traditionally focused on disciplines outside of mental health such as physical, occupational, and speech therapy. This article examines these issues and suggests strategies to better address mental healthcare needs for PD patients in the future.     

A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning

Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) are potentially lethal plants after ingestion. Poisoning by these plants is a common toxicological emergency in tropical and subtropical parts of the world and intentional self-harm using T. peruviana is prevalent in South Asian countries, especially India and Sri Lanka. All parts of these plants are toxic, and contain a variety of cardiac glycosides including neriifolin, thevetin A, thevetin B, and oleandrin. Ingestion of either oleander results in nausea, vomiting, abdominal pain, diarrhoea, dysrhythmias, and hyperkalemia. In most cases, clinical management of poisoning by either N. oleander or T. peruviana involves administration of activated charcoal and supportive care. Digoxin specific Fab fragments are an effective treatment of acute intoxication by either species. However, where limited economic resources restrict the use of such Fab fragments, treatment of severely poisoned patients is difficult. Data from case reports and clinical studies were reviewed to identify treatments supported by evidence for the management of poisoning by N. oleander and T. peruviana.     

Chondrocyte activation by interleukin-1: synergism with fibroblast growth factor and phorbol myristate acetate

Exposure to synovial factors or purified interleukin-1 (IL-1) induces the production of prostaglandin E2 (PGE2) and the neutral proteinases (NP) collagenase, gelatinase and stromelysin by lapine articular chondrocytes. Having frequently found our partially purified synovial preparations to elicit this process of chondrocyte activation more strongly than recombinant IL-1, Phadke's report of synergism between IL-1 and fibroblast growth factor (FGF) intrigued us. In our hands, basic FGF (1 ng/ml-1 micrograms/ml) did not activate chondrocytes but, in a dose-dependent manner, enhanced the production of PGE2 and NP by chondrocytes exposed to IL-1 alpha or IL-1 beta (1-10 U/ml). Further examination determined that the basic FGF was a better synergist than acidic FGF. In view of reports that FGF activates protein kinase C, we tested whether phorbol myristate acetate (PMA) could substitute for FGF as a synergist. Not only did it do so, but PMA alone (0.1 ng/ml-100 ng/ml), unlike FGF, provoked the production of PGE2 by chondrocytes. The Ca2+ ionophore A23187 could not substitute for FGF in enhancing induction of the NP. Using a cDNA probe, we confirmed that the synergistic effects of both FGF and PMA upon IL-1 mediated collagenase induction, were associated with an increased abundance of collagenase mRNA.     

Distribution and localization of endotoxin in the reticulo-endothelial system (RES) and in the main vessels of the rat during shock

The fate of endotoxin was followed with immunohistochemistry and radio-labelled lipopolysaccharide (LPS) in organs of the reticulo-endothelial system (RES), in the great vessels and the thoracic duct of rats during a 14 day period after the injection of a shock-inducing amount of endotoxin. The immunohistochemical detectability of LPS in most tissues increased continuously during the first 48 hours, showing the strongest LPS staining in the liver and adrenal gland. Macrophages were found to be the most important cells of primary LPS uptake in all organs except the adrenal glands, where endotoxin was mainly present in phagocytic vacuoles of the cortical epithelium. The comparison of results obtained with the immunoperoxidase method and radioactivity measurements revealed that at a later stage of the experiment the persisting LPS in liver and spleen looses its antigenic activity. The correlation between the appearance of LPS positive macrophages and histological signs of tissue injury during endotoxin shock is striking.     

Association of Actinobacillus pleuropneumoniae capsular polysaccharide with virulence in pigs

The capsular polysaccharide (CP) of Actinobacillus pleuropneumoniae is required for virulence of the bacteria in swine. However, a molecular investigation of whether the type or quantity of CP affects A. pleuropneumoniae virulence has not been reported. To initiate this investigation, a DNA region downstream of conserved genes required for CP export in A. pleuropneumoniae serotype 1 was cloned and sequenced. Three open reading frames, designated cps1A, cps1B, and cps1C, were identified that had amino acid homology to bacterial carbohydrate biosynthesis genes. A kanamycin resistance cassette (Kan(r)) was inserted into a 750-bp deletion spanning cps1AB or into a 512-bp deletion in cps1B only, and the constructs were cloned in a suicide vector. The Kan(r) gene was then transferred into the chromosome of strain 4074 by homologous recombination to produce strain 4074Deltacps1N and strain 4074Deltacps1B, respectively. Strain 4074Deltacps1N produced no detectable CP, but strain 4074Deltacps1B made 15% of the serotype 1 CP made by the parent strain, 4074, as determined by enzyme-linked immunosorbent assay and precipitation of free CP. The cps1ABC genes of strain 4074 and the cps5ABC and cps5ABCDE genes of serotype 5a strain J45 were cloned into the shuttle vector pLS88 and electroporated into 4074Deltacps1N to produce 4074Deltacps1N(pABcps101), 4074Deltacps1N(pJMLcps53), and 4074Deltacps1N(pABcps55), respectively. Strain 4074Deltacps1N(pABcps101) produced about 33% of the serotype 1 CP produced by strain 4074. Strains 4074Deltacps1N(pJMLcps53) and 4074Deltacps1N(pABcps55) produced serotype 5a CP in similar quantity or in fourfold excess, respectively, to that produced by strain 4074. With intratracheal challenge in pigs at similar dosages, the order of virulence of strains producing serotype 1 CP (assessed by mortality, lung consolidation, hemorrhage, and fibrinous pleuritis) was the following: strain 4074 > strain 4074Deltacps1N(pABcps101) > or = strain 4074Deltacps1N > strain 4074Deltacps1B. Strain 4074Deltacps1N(pJMLcps53) was less virulent than strain 4074Deltacps1N(pABcps55). However, both strains produced serotype 5a CP in similar or greater quantities than was observed for production of serotype 1 CP by the parent strain, 4074, but were less virulent than the parent strain. Therefore, the amount of serotype 1 or 5a CP produced by isogenic strains of A. pleuropneumoniae correlated with the virulence of the bacteria in pigs. However, virulence was also influenced by the type of CP produced or by its mechanism of expression.     

Monitoring Attacks on Health Care as a Basis to Facilitate Accountability for Human Rights Violations

Violence against health care systems is an assault on health and human rights. Despite the evolution of global standards to protect health workers and ensure the delivery of health care in times of conflict, attacks against health systems have continued throughout the world—violating humanitarian law, undermining human rights, and threatening public health. The persistence of such violence against health care, especially in humanitarian crises related to armed conflict, has prompted global institutions to develop systematic monitoring mechanisms in an effort to alleviate these harms, seeking to protect health workers from being harmed for their healing efforts. This article examines the development and implementation of the World Health Organization (WHO) Surveillance System of Attacks on Healthcare (SSA) as a systematic mechanism to collect and disseminate data concerning attacks on health care systems. Although the SSA provides a foundation for monitoring attacks in conflict zones, this research considers whether the SSA has collected the necessary data, categorized these data appropriately, and disseminated sufficient information to facilitate human rights accountability, analyzing the political, methodological, and institutional challenges faced by WHO. The article concludes that refinements to this monitoring mechanism are needed to strengthen the political prioritization, research methodology, and institutional implementation necessary to ensure accountability for violations of health and human rights.