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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.
Maternal prenatal stress during pregnancy is associated with fetal growth restriction and adverse neurodevelopmental outcomes, which may be mediated by impaired placental function. Imprinted genes control fetal growth, placental development, adult behaviour (including maternal behaviour) and placental lactogen production. This study examined whether maternal prenatal depression was associated with aberrant placental expression of the imprinted genes paternally expressed gene 3 (PEG3), paternally expressed gene 10 (PEG10), pleckstrin homology-like domain family a member 2 (PHLDA2) and cyclin-dependent kinase inhibitor 1C (CDKN1C), and resulting impaired placental human placental lactogen (hPL) expression.
A diagnosis of depression during pregnancy was recorded from Manchester cohort participants’ medical notes (n = 75). Queen Charlotte's (n = 40) and My Baby and Me study (MBAM) (n = 81) cohort participants completed the Edinburgh Postnatal Depression Scale self-rating psychometric questionnaire. Villous trophoblast tissue samples were analysed for gene expression.
In a pilot study, diagnosed depression during pregnancy was associated with a significant reduction in placental PEG3 expression (41%, p = 0.02). In two further independent cohorts, the Queen Charlotte's and MBAM cohorts, placental PEG3 expression was also inversely associated with maternal depression scores, an association that was significant in male but not female placentas. Finally, hPL expression was significantly decreased in women with clinically diagnosed depression (44%, p < 0.05) and in those with high depression scores (31% and 21%, respectively).
This study provides the first evidence that maternal prenatal depression is associated with changes in the placental expression of PEG3, co-incident with decreased expression of hPL. This aberrant placental gene expression could provide a possible mechanistic explanation for the co-occurrence of maternal depression, fetal growth restriction, impaired maternal behaviour and poorer offspring outcomes.
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.
Irrigation for intensive sugar cultivation started in the early 1980s at Richard Toll, some 100 km from the mouth of the Senegal River. Infections with Schistosoma mansoni were first seen in late 1988. This study records quantitative snail surveys for over 3 years from 1992 at sites representing different habitats in and around the irrigation scheme. Populations of both Biomphalaria pfeifferi (the intermediate host of S. mansoni) and Bulinus spp. (mainly B. truncatus, the local host of S. bovis) peaked in late ‘spring' or early ‘summer', depending on the habitat, and then remained low until the following ‘spring'. B. pfeifferi favoured smaller, man-made habitats with most transmission between May and August each year. The less abundant Bulinus spp. favoured larger natural and man-made habitats with most S. bovis transmission between April and July. S. mansoni infections were more, but S. bovis infections were less abundant than other trematodes in their respective snail hosts. Ecological changes in the early 1980s due to sugar irrigation pre-dated similar, more widespread changes in the late 1980s when the completion of dams across the Senegal River prevented seasonal rain fed floods and sea water intrusion. S. mansoni has since spread rapidly around Richard Toll. The incompatibility of the local S. haematobium strains with the dominant bulinid snails has so far prevented an epidemic of urinary schistosomiasis at Richard Toll, but the invasion of similar downstream habitats by susceptible B. globosus is worrying. The principal control measure, chemotherapy, given in the ‘winter' would minimise the rate of reinfection. It could be reinforced by judicious mollusciciding within the sugar irrigation scheme but not elsewhere.
A few years ago a battered infant was admitted to
a California hospital. After a period of observation
and testing, the physicians concluded that the infant had
been beaten so badly that his brain was almost completely
destroyed, leaving him permanently unconscious. The hospital
had just adopted a policy specifying that life-sustaining
treatment for permanent unconsciousness was futile and,
therefore, not indicated. According to this policy, after
suitable subspecialty consultations and deliberations,
including efforts to gain parental agreement and documentation
of unanimous ethics committee support, the patient's
physician had the authority to discontinue life-sustaining
treatment. The infant's physician wished to do this.
The mother, however, who was the prime battery suspect,
insisted that the baby be kept alive.
The relationship between initial mobilization of 11-S globulin storage protein (leading to solubilization of its B-subunit) and germination performance after priming was studied in sugarbeet (Beta vulgaris L.) seeds. Priming was conducted for 2 d either in water (hydropriming) or in –2.0 MPa polyethylene glycol-8000 (osmopriming), at various temperatures ranging from 5 to 40°C and oxygen concentrations in the atmosphere ranging from 0 to 21%. For both types of pre-treatments, the range of temperatures and the concentrations of oxygen which were effective in priming were very similar to those which allowed solubilization of the B-subunit of 11-S globulin, supporting the robustness of this protein marker for optimization of sugarbeet seed priming. Furthermore, the temperature and oxygen dependence of priming efficiency closely paralleled that for germination of the untreated seeds, reinforcing the finding that the beneficial effect of priming corresponded to the advancement of germination sensu stricto (i.e. phase II of the germination process). For priming times longer than 2 d, particularly for osmopriming, there was a very dramatic decrease in germination of the treated seeds. For instance, following a 14 d osmopriming at 25°C as much as 60% of the pre-treated seed population failed to germinate when transferred to water. This loss in germination performance quite closely paralleled degradation of LEA (late embryogenesis abundant) proteins, notably a heat-stable seed-specific protein of about 60 kDa and a seed-specific biotinylated LEA protein.
Is information about a person's genome, whether derived from the analysis of DNA or otherwise, protected by the right to privacy? If it is, why and in what manner? It often appears that some people believe that the answer to this question is to be found in molecular genetics itself. They point to the rapid progress being made in basic and applied aspects of this field of biology; this progress has remarkably increased what is known about human genetics. Since knowledge of a particular person's genetic makeup entails a potential intrusion into that person's most private realms and exposes him or her to dire results if revealed to others, they argue, the law needs to protect “genetic privacy.” There is nothing inherently wrong with this account, but it certainly presupposes that we know—and agree about—what it means to protect privacy and, indeed, what interests are implicated in the concept and why they matter. Rather than make this assumption, in this essay I first elaborate a concept of privacy before turning to the potential privacy implications that arise at the intersection of human genetics and the field of insurance. I argue that the core value here is self-determination broadly conceived—that control over one's genetic information may be important for achieving self-determination—but that at least in the context of contracts for life insurance, we should be reluctant to recognize “rights” that would permanently preclude the use of genetic data by insurers.
The isolation of 2 genomic clones has allowed us to further characterize
a Schistosoma mansoni serine protease designated
SmSP1. The deduced amino acid sequence (248aa) considered as a ‘light
chain’ encoding the active site, presents
significant homologies with mouse plasma kallikrein and human factor I
light chain. The secondary structure of SmSP1
‘light chain’ is correctly predicted and may be sufficient
by itself to constitute an active enzyme. The biological function
of SmSP1 is unknown, however, the homology with 2 serine proteases suggests
that SmSP1 may play a role in the evasion
of the host immune response. This is supported by the presence of the native
protein corresponding to SmSP1 particularly
in schistosomula released products (SRP) and in male dorsal spines. The
expression of this enzyme is differentially
regulated throughout the parasite life-cycle. However, infected animals
with S. mansoni did not produce specific antibodies
to recombinant SmSP1. The lack of such response could be advantageous to
the parasite by protecting itself from host
The genetic differences between praziquantel-resistant (R) and
strains of Schistosoma mansoni (Fallon &
Doenhoff, 1994) were explored using RAPD and by cloning differentially
expressed mRNAs by subtractive PCR. No
differences between the 2 strains were detectable by RAPD using 41 different
primers indicating that no major genomic
rearrangements were present. Subtractive PCR generated a number of fragments,
1 of which was shown to correspond
to an over-expressed mRNA in the R strain and to encode a fragment of the
subunit 1 of cytochrome-c oxidase (SCOX1).
In the absence of a complete sequence for this gene, we used EST sequences
to compile a consensus sequence for the
904 bp at the 3′ end that enabled us to choose primers for semi-quantitative
RT–PCR. This technique showed that SCOX1
was indeed over-expressed about 5 to 10-fold in the R strain whereas the
encoding the 28 kDa glutathione S-transferase, glutathione peroxidase,
NADH dehydrogenase subunit 5 and the ATP-binding cassette family protein
SMDR2 were not. In contrast, cytochrome-c oxidase enzyme
activity was 4-fold lower in the R strain than in the S strain.
A PCR strategy using degenerate oligonucleotide primers based upon
consensus sequences of the active site of serine
proteases yielded a 467 bp fragment from genomic DNA from
Schistosoma mansoni cercariae. The sequence presented a
continuous open reading frame and the deduced amino acid sequence (156
presented homologies with various serine
proteases, in particular the highest percentage identity was observed with
a mammalian plasma kallikrein. The expression
of this serine protease was studied first at the mRNA level and it was
detected by RT-PCR in cercariae and in adult
worms. At the protein level we were able to detect it by Western blotting
and by using antigen extracts from metabolically
radio-isotope labelled worms. The absence of any positive signal in
Northern blot and the detection of the protein suggest
that the mRNA has a very short half-life, however the protein may be
accumulated in the parasite. The significance of
identity with mammalian kallikrein was confirmed by cross-immunoreactivity
with a native porcine pancreatic kallikrein.
However, no cross-reactivity was observed with S. mansoni
elastase, another serine protease. Thus, we suggest that the
serine protease described in this paper is a kallikrein-like protease.
The potential of a recombinant Schistosoma bovis-derived
glutathione S-transferase (rSb28GST) to protect cattle against
S. mattheei infection was tested in Zambia. All animals were
challenged 2 weeks after the second inoculation with either
0·250 mg rSb28GST in adjuvants (vaccinated calves, n=14)
or adjuvants alone (controls, n=14). In a first experiment,
7 vaccinated and 7 control animals were exposed to 10000 S. mattheei
cercariae percutaneously. All animals developed
clinical schistosomiasis 7–8 weeks after challenge.
At perfusion, 12 weeks after challenge, vaccinated and control groups
had averages of 887 and 541 eggs per gramme (epg) faeces, 6515 and 5990
and 4·2 and 3·4 million tissue eggs,
respectively. These results indicate that the immunization protocol used
did not protect these calves against the massive
single experimental challenge. In a second experiment, another 2 groups
(n=7) of vaccinated and control animals were
challenged naturally over a period of 9 months on a farm known to be
endemic for S. mattheei. The natural infections were
much lighter in intensity, as indicated by the mean faecal egg count
(13 epg), worm count (139) and tissue egg count
(294000) in non-vaccinated controls. In vaccinated calves, significant
reductions in female worm burdens (50%), faecal
egg counts (89%) and miracidial counts (93%) were recorded. Total tissue
egg counts were also reduced by 42% in
vaccinated animals. It therefore appears that the rSb28GST can provide
significant protection in cattle against S. mattheei
under conditions of low to moderate natural infection.
Many aspects of modern medicine provoke spirited ethical argument, but few engender as much disagreement about what exactly is at issue as does the futility debate. The relationships of physicians and nurses, on the one side, and patients (especially dying patients dependent on extensive medical support) and their families, on the other, are viewed very differently by various commentators. As characterized by some, physicians have become pathetic characters in a modern day Molière play, technically sophisticated servants doing the bidding of their patients. Professionals with this perception feel misused and justify their rebelliousness by invoking medical futility. The simple recognition of the limits of medicine's power to cure and to extend life denotes that health care professionals should not be obliged to provide further treatment or, more powerfully, that they would exceed their role-based authority as healers to continue to do so. Yet other commentators claim that medical futility is an empty concept that does not provide any ground for decision that would not be present had the concept never been coined. They characterize medical futility as nothing more than a cover for physician's rearguard action to regain the dominance in decision making that they possessed before autonomy and informed consent shifted authority to patients and their families beginning in the 1960s.
This book surveys the clinical, ethical, religious, legal, economic and personal dimensions of decision making in situations when the choice is between extending costly medical treatment of uncertain effectiveness, or terminating treatment thereby ending the patient's life. Contributors from a wide range of disciplines offer perspectives on issues ranging from the definition of medical futility to the implications for care in various clinical settings, including intensive care, neonatal and paediatric practice and nursing homes. An important contribution towards the more humane and consistent handling of these situations, Medical Futility will be obligatory reading for health care professionals, students and scholars concerned with ethical standards in medical care.