This article presents a framework of ethical analysis for anticipatory evaluation of advanced biopreservation technologies and employs the framework illustratively in three domains. The framework features four clusters of general ethical considerations: (1) Producing Benefits, Minimizing Harms, Balancing Benefits, Risk, and Costs; (2) Justice, Fairness, Equity; (3) Respect for Autonomy; and (4) Transparency, Trustworthiness, and Public Trust.

Advanced biopreservation technologies using subzero approaches such as supercooling, partial freezing, and vitrification with reanimating techniques including nanoparticle infusion and laser rewarming are rapidly emerging as technologies with potential to radically disrupt biomedicine, research, aquaculture, and conservation. These technologies could pause biological time and facilitate large-scale banking of biomedical products including organs, tissues, and cell therapies.

Research on advanced biopreservation — technologies that include, for example, partial freezing, supercooling, and vitrification with nanoparticle infusion and laser rewarming — is proceeding at a rapid pace, potentially affecting many areas of medicine and the life sciences, food, agriculture, and environmental conservation. Given the breadth and depth of its medical, scientific, and corresponding social impacts, advanced biopreservation is poised to emerge as a disruptive technology with real benefits, but also ethical challenges and risks. Early engagement with potentially affected groups can help navigate possible societal barriers to adoption of this new technology and help ensure that emerging capabilities align with the needs, desires, and expectations of a broad range of interested parties.

The application of advanced biopreservation to organs donated for transplantation may make possible their indefinite storage and thereby improve the utility and equity they provide to patients. The technology is still at a preclinical stage, with many difficult, scientific issues that remain to be answered. At the moment, however, the actual capabilities of the technology are too indefinite to begin formulating the statutes, regulations, and ethical guidance that will be needed to obtain the benefits expected from its use.

To understand the future of informed consent, we should pay attention to two ethical-legal sources in addition to the revised Common Rule. Physicians acting as investigators and patients serving as research subjects bring to that relationship a long history regarding consent to treatment, and everyone dealing with research ethics needs to be aware of the Nuremberg Code and other human-rights documents. These three streams make separate and distinctly different contributions to informed consent doctrine.

Public health law courses typically focus a good deal of attention on two related topics: the duty of government agencies to control the spread of communicable diseases and their use of the police power to do so. While governments sometimes take forceful actions in responding to disease outbreaks, they can also act to prevent their occurrence. Indeed, one of the great triumphs of public health in the 20th century was the development of vaccines and their widespread use, which seemed on course to relegate many formerly crippling or deadly diseases to the history books. Particular success occurred with vaccinations against childhood diseases such as polio, smallpox, and measles, outbreaks of which once routinely closed schoolrooms, playgrounds, and community swimming pools. By the last quarter of the century, completion of an elaborate schedule of immunizations was not merely the standard in pediatric practice but an official requirement for school enrollment. As a result, the range of communicable diseases that had once terrified parents had become threats to be feared only in memory.

Emulsions are usually metastable systems of two non-miscible phases stabilized by surface active species like surfactant molecules. Emulsions stabilized by solid colloidal particles adsorbed at the interface (Pickering emulsions) offer some competitive advantages with respect to classical emulsions. Most studies published up to now concern emulsions stabilized by inorganic (metallic oxides, exfoliated clays, carbonates and phosphates) or polymeric particles while biomass derived alternatives have only been explored to a limited extent. For the first time, we report the stabilization of emulsions by unmodified cellulose nanocrystals [1, 2] . Cellulose nanocrystals were produced from bacterial cellulose and used to form Pickering emulsions. We demonstrate by SEM that the nanocrystals are adsorbed at the oil/water interface. We also study the size distribution of the droplets that was found to range around 4μm in diameter with very narrow dispersity. The stability of the emulsions was also investigated. The fabrication of new armored microparticles exposing cellulose acicular nanocrystals from cellulose nanocrystals opens opportunities to build materials from low cost and environmental friendly resource.

In 1990, I voiced strong doubts about a bill entitled the Patient Self-Determination Act (PSDA), which had been introduced in the U.S. Senate by John Danforth (R-MO) and Daniel Patrick Moynihan (D-NY). I hoped to see it defeated. In 1991, after the bill had become a small part of a massive status (the Omnibys Budget Reconciliation Act of 1990) adopted in the waning hours of the 101st Congress, I devoted countless hours to its implementation. I wanted to see it succeed. Why the change?

Attempts were made to manipulate specific responses of baboons to protect them from infection with Schistosoma mansoni. In Experiment 1, cosinophilia was induced in naive baboons with Trichinella spiralis larvae given intravenously before intraperitoneal injection of globulin fractions from S. mansoni-infected baboon sera and subsequent percutancous exposure to S. mansoni cercariac. In Experiment 2, baboons with 8- or 32-week-old primary S. mansoni infections received T spiralis i.v. before an S. mansoni challenge. In experiments 3 to 5 respectively, naive baboons received intramuscularly before challenge: formalin-fixed S. mansoni schistosomula, with Bordetella pertussis as an adjuvant; a preparation of S. mansoni adult worm teguments; and a preparation of NE-immune complexes obtained from S. mansoni-infected rat sera, with Freunds Complete Adjuvant. Minor, but statistically insignificant, protection was obtained in Experiments 2 (32-week infections) and 3, but was far less than that given by intact, irradiated living vaccines. There are signs on the horizon of non-living vaccines protecting rodents against S. mansoni infection and it would be prudent, as with drugs, to test these in primates before proceeding to man. The results of our experiments, though essentially negative, should help the design of any future vaccine trials in primates.

Physician aid in dying is a broader topic than euthanasia in that the latter usually refers to active euthanasia, while physician assistance also encompasses the issue of assisted suicide. Volumes could be and have been written on physician-assisted death. But my purpose here is to address a specific aspect of the topic: the policy implications with regard to proposed legislation on physician-aided death.

Although the title's reference to physician assistance suggests a focus on the role of the professional, what people often take to be most important and at the heart of the topic is the issue of the patient's rights, usually seen as being manifested in four different ways. First is the right to a dignified death, as free from pain and suffering as possible. In crossing national boundaries and preceding the organization of the professions and the creation of societies, this right is viewed as one that ought to be recognized.

Shared antigens between Brugia malayi and Aedes aegypti were studied. The experiments carried out with sera from infected Mastomys natalensis indicated that an immunological response against A. aegypti antigens (Mr 185, 35, 32 kDa) appeared often when animals became microfilaraemic and increased progressively in intensity during the time-course of infection. Sera of animals immunized with B. malayi reacted with the crude extract of mosquitoes and conversely, antibodies from animals immunized with A. aegypti reacted with the surface of B. malayi microfilariae. The implications of these findings for the natural history of B. malayi infection are discussed.

The roles of different antibody isotypes in the transfer of protection with serum from rats vaccinated with irradiated cercariae were investigated by immunoadsorption of IgG, IgG2a and IgG2c, and by heating at 56°C to remove IgE. Only depletion of IgG2a reduced the levels of vaccine-induced immunity transferred, whereas immunity transferred by infection serum was reduced by both IgG2a and IgE depletion. It was also shown that exposure to irradiated parasites did not lead to either specific or non-specific induction of an IgE response. The successful passive-transfer experiments using serum from non-resistant 25 week-infected rats into recipient animals demonstrated that the waning of resistance observed in 25 week-infected rats was not due to a failure of the humoral response to protective antigens.

The A subunit of NF-Y nuclear factor from Schistosoma mansoni was expressed in E. coli fused to a histidine tag and purified by affinity chromatography using a Ni2+-Agarose matrix. Antibodies against the recombinant protein were prepared and used for Western blot and immunolocalization. The presence of SMNF-YA in all stages of the parasite life-cycle was determined by RT-PCR and Western blot analysis. The immunolocalization of SMNF-YA showed the presence of this factor in a parenchymal cell population of cercariae and adult worms and in embryos within eggs. The expression of SMNF-YA was demonstrated to decrease in maturating spermatozoites whereas an accumulation of this factor was observed in the nucleus from oocytes during their maturation processes.

The in vitro interaction between rat peritoneal macrophages and Dipetalonema viteae microfilariae in the presence of amicrofilaraemic rat immune serum was studied by transmission electron microscopy. The probable sequence of events leading to the killing of D. viteae microfilaria by macrophages is as follows. (a) Rat peritoneal macrophages in the presence of amicrofilaraemic rat immune serum adhere to the parasite surface, (b) the macrophages extend their pseudopodia around the parasite, (c) the ‘lysosome-like’ granules discharge their contents on to the parasite surface, (d) the lytic activity of these products begins at the parasite surface and (e) subsequent breaking of the microfilarial cuticle occurs, exposing the parasite intracellular material.

After hamsters have been infected with Dipetalonema viteae for about 4 months, microfilariae disappear from the circulation but the adult worms remain alive and active. Such hamsters are said to harbour a ‘latent’ infection. Additional adult worms implanted into such hamsters produce no microfilariae, but adult worms recovered from hamsters with latent infections resume microfilariae production when surgically transplanted into new hosts. In vitro, worms from hamsters with latent infections renewed microfilariae production in the presence of serum from uninfected but not infected hamsters. Serum from infected animals had a marked suppressive effect on the microfilariae production of adult worms implanted into passively immunized hamsters. This suggests that microfilarial release is regulated by a serum factor. Microfilarial production in in vitro and in vivo experiments was more strongly inhibited by serum taken from hamsters with latent infections and hamsters infected for only 30 days (pre-patent) than by serum taken 90 days after infection (whilst microfilariae were in the circulation of the serum donors). A cytotoxic effect of sera from infected hamsters on the microfilariae could not be demonstrated.

In animals immunized by extracts of adult worms or microfilariae, microfilaraemia was considerably reduced. In contrast, animals immunized repeatedly with the extract from small numbers of microfilariae during the pre-patent phase of an infection had an enhanced microfilaraemia. Adult worm numbers were not affected by immunization except in animals given extract from a single female worm which harboured fewer worms than controls.

The expression of the Schistosoma mansoni 28 kDa glutathione S-transferase (Sm28) was studied using molecular (PCR, in situ hybridization), and immunocytochemical techniques. The presence of Sm28 was demonstrated in all developmental stages of the parasite except the intra-uterine immature egg. In the parenchyma of male and female adult worms the distribution of Sm28 was limited to a subpopulation of parenchymal cells and to the dorsal tubercles of the male. The tegument, the muscles, the digestive tract, the neural mass, the vitelline glands, and mature gametes were not immunoreactive. Immature germinal cells in both sexes, and the ootype in the female genital system, were found to express Sm28. Deposits of immunoreactive material on host skin following cercarial penetration, exfoliation from the male tubercles, and especially emission of Sm28 from eggs in hepatic granulomas are suspected to be a source of antigen during the parasite infection. The reduction in worm fecundity previously observed in immunization experiments may result from an antibody response directed against Sm28 present in the ootype. There was no cross-reactivity observed, under the experimental conditions used, between the anti-Sm28 sera and either vertebrate or invertebrate host tissue.

A total of 129 children were treated for Schistosoma mansoni infections, and followed for intensity of reinfection at 3-monthly intervals over a 21-month period. Blood samples were taken before treatment and at 5 weeks and 6, 12 and 18 months after treatment. This paper presents a statistical analysis of the relationship between various immune responses and subsequent reinfection. Responses analysed were: blood eosinophil levels; IgE antibodies against schistosomulum antigens; IgG antibodies mediating eosinophil-dependent killing of schistosomula; antibodies inhibiting the binding to schistosomulum antigens of two rat monoclonal antibodies that also recognize egg antigens; the levels of anti-adult worm and of anti-egg (total, IgM and IgG) antibodies; and IgM anti-schistosomulum antibodies. Results for each assay were well correlated for each of the five separate blood samples. None of the assays were predictive of resistance to reinfection, but susceptibility to reinfection was strongly correlated with results in the preceding blood samples for total anti-egg antibodies and the inhibition of binding of one of the two monoclonal antibodies. Further analysis also revealed a correlation between reinfection intensities and both IgM anti-schistosomulum antibodies and IgM and IgG anti-egg antibodies. These results are consistent with the hypothesis that early infections elicit the development, in response to egg antigens, of antibodies that block immune mechanisms directed against schistosomula. Blocking antibodies may be IgM, but might also be of an ineffective IgG isotype. The existence of such antibodies in young children would explain the slow development of immunity in the face of a range of detectable, potentially protective immune responses.