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PubMed1998

[Clarification of Amae as a concept--response to the criticism by K. Nagayama].

Nagayama wrote a lengthy paper in order to demonstrate that the amae theory which I propounded is all confused. I should say on the contrary that the confusion is his own because he dose not realize that he and I may mean different things by the same word amae. Apparently he means those phenomena that indicate the fulfilment of amae, while I take amae as a verbnoun of amaeru meaning the operation of amaeru in one way or another irrespective of the outcome, its prototype being that of an infant seeking its mother. In short, for Nagayama amae is a characteristic of certain Japanese phenomena and for me a concept. It may refer, in psychoanalytic thinking, to that primordial urge for object relations. It makes no sense therefore to censure my wording of amae like 'narcissistic amae' as not measuring up to the true state of amae as Nagayama defines it, because my usage of the word amae is entirely different from his. In this connection I may point out a curious resemblance between the dismissive manner of his criticism and the behavior of a small group embodying amae which he characterizes as distinctly exclusive of outsiders. There is a good reason to believe that the resemblance is not accidental. I must say that Nagayama is most confused in his critical appraisal of the amae theory against Balint's theory. He completely ignores the fact that these two theories developed independently though there is a definite parallel between them. He then takes me to task that I did not properly incorporate Balint's late ideas into my thinking, even though those ideas became known only in the books published after that book of mine which is the butt of his criticism. Nagayama attempts to trace the amae phenomena back to some racial unconscious underlying Japanese culture. He may believe so, but it sharply contrasts with my view that the very availability of such a concept like amae is indicative of the tenor of Japanese culture. It is interesting to note here that all critics of the amae theory including Nagayama stumble on amae as a concept. They just cannot imagine that one can fetch a Japanese word and make it a universal concept. It must be their unspoken belief that all the valid concepts in whatever field of study come from abroad, notably the West.

Cultural Characteristics↗
PubMed2005

Changing demographics of advanced maternal age (AMA) and the impact on the predicted incidence of Down syndrome in the United States: Implications for prenatal screening and genetic counseling.

This study documents the changes in the percentages of advanced maternal age (AMA) pregnancies in the United States and in Washington State, underlying demographic factors, the impact on the predicted incidence of Down syndrome, and its impact on Down syndrome screening. Data on births in the United States from 1933 to 2002 were obtained from publications and the website of the National Center for Health Statistics. Data for Washington State were obtained from the website of the Washington State Department of Health. Information on births at Swedish Medical Center was obtained from hospital records. The percentage of AMA pregnancies in the US was about 14% before World War II, dropped steadily to about 5% in the 1970s and rose since the 1980s to about 14% in 2002. AMA Fractions are greatest among non-Hispanic Caucasians and Asian/Pacific Islanders, women who have college education and beyond, and are married. However, since 1980, the AMA Fractions have increased across all racial/ethnic groups, educational levels, and married and unmarried women. In Washington State in 2001, the overall AMA Fraction was about 14%, but there was considerable variation in the AMA Fraction across counties. In 1980, AMA pregnancies accounted for about 25% of pregnancies with Down syndrome in the United States. In 2002, AMA pregnancies accounted for more than 50% of Down syndrome pregnancies. Given the current AMA Fraction, offering amniocentesis to women of age 35 and above would result in one in seven pregnant women undergoing amniocentesis. Based on likelihood ratios, AMA as a screening strategy for Down syndrome is significantly inferior to combined serum and sonographic screening.

Adult↗
PubMed2001

[Induced expression of the variable region of AMA-1 from Plasmodium falciparum].

OBJECTIVE: To express the variable region of AMA-1 gene from Plasmodium falciparum in Escherichia coli. METHODS: Genomic DNA of FCC1/HN was used as template and the variable region of AMA-1 gene was amplified by polymerase chain reaction(PCR). The PCR products were digested by endonuclease BamH I and Hind III, cloned into pBlu2KSP. The nucleotide sequences of the variable region of AMA-1 gene were determined by sequencing. The AMA-1 gene fragment was subcloned into plasmid pQE, expressed in E. coli and induced by IPTG. The fusion product as identified by SDS-PAGE gel electrophoresis and Western blotting were proceeded with anti-AMA-1 sera from rabbit. RESULTS: The size of the variable region of AMA-1 gene from FCC1/HN was 506 bp and encoded 168 amino acids. On SDS-PAGE gel dyed with Coomassie brilliant blue R250, no specific protein band can be discerned, but Western blotting proceeded with anti-AMA-1 sera from rabbit demonstrated that the specific protein band was about 23.0 kDa. CONCLUSION: The variable region of AMA-1 gene from FCC1/HN was able to be expressed in E. coli and analysis of Western blotting demonstrated that the AMA-1 fussion protein contained specific antigenic epitopes.

Amino Acid Sequence↗
PubMed1996

Report 59 of the AMA Board of Trustees (A-96). Physician-assisted suicide. Reference Committee on Amendments to Constitution and Bylaws.

This Board of Trustees report calls for reaffirmation of the position of the American Medical Association (AMA) in opposition to physicians assisting their patients in committing suicide. The AMA maintains that the appropriate step for physicians is not to assist a patient in death but to provide compassion and palliative care. In providing end-of-life care, the option of allowing physicians to intentionally cause the death of patients is a line that should not be crossed. This position is based on the historical role of physicians as advocates for healing. The report discusses AMA activity to design and implement a comprehensive physician education plan on end-of-life care in response to the House of Delegates' action in adopting Board of Trustees Report 48-I-95, "Quality Care at the End of Life." This plan will further the AMA's commitment that patients should receive high quality care during every stage of life, including the end of life. The goal of this educational campaign is to advance the medical culture by making palliative treatment and care directions based on values-based advance care planning the standard of care for meeting the needs of patients at the end of life. The basis for this activity will be the acknowledgment that physicians, while unable to always provide a cure, should always be able to relieve suffering, address the psychological needs of patients at the end of life, add value to remaining life, and help patients die with dignity. The report presents information on state legislative activities and judicial actions relating to physician-assisted suicide. The report also presents a discussion on the ethical under-pinnings against physician participation in patients' suicides. This report recommends that: the AMA reaffirm current policies 140.952 and 140.966 (AMA Policy Compendium), in accordance with Council on Ethical and Judicial Affairs Opinion 2.211 (opposition to physician-assisted suicide); the AMA initiate an educational campaign to make palliative treatment and care directions based on values-based advance care planning the standard of care for meeting the needs of patients at the end of life; the AMA continue to seek out opportunities to present the views of medicine on physician-assisted suicide and improving the quality of care for patients at the end of life; the AMA disseminate this report throughout the Federation with a request that it be distributed to local physicians; and the Board of Trustees present the House of Delegates with an update on these and related activities at the 1996 Interim Meeting and the 1997 Annual Meeting.

American Medical Association↗
PubMed2006

Synthetic peptides from Plasmodium falciparum apical membrane antigen 1 (AMA-1) specifically interacting with human hepatocytes.

Plasmodium falciparum apical membrane antigen 1 (AMA-1) is expressed during both the sporozoite and merozoite stage of the parasite's life cycle. The role placed by AMA-1 during sporozoite invasion of hepatocytes has not been made sufficiently clear to date. Identifying the sequences involved in binding to hepatocytes is an important step towards understanding the structural basis for sporozoite-hepatocyte interaction. Binding assays between P. falciparum AMA-1 peptides and HepG2 cell were performed in this study to identify possible AMA-1 functional regions. Four AMA-1 high activity binding peptides (HABPs) bound specifically to hepatocytes: 4310 ((74)QHAYPIDHEGAEPAPQEQNL(93)), 4316 ((194)TLDEMRHFYKDNKYVKNLDE(213)), 4321 ((294)VVDNWEKVCPRKNLQNAKFGY(313)) and 4332 ((514)AEVTSNNEVVVKEEYKDEYA(533)). Their binding to these cells became saturable and resistant to treatment with neuraminidase. Most of these peptides were located in AMA-1 domains I and III, these being target regions for protective antibody responses. These peptides interacted with 36 and 58 kDa proteins on the erythrocyte surface. Some of the peptides were found in exposed regions of the AMA-1 protein, thereby facilitating their interaction with host cells. It is thus probable that AMA-1 regions defined by the four peptides mentioned above are involved in sporozoite-hepatocyte interaction.

Amino Acid Sequence↗
PubMed2006

Characterization of AMA, a new AAA protein from Archaeoglobus and methanogenic archaea.

We have previously reported a new group of AAA proteins, which is only found in Archaeoglobus and methanogenic archaea (AMA). The proteins are phylogenetically basal to the metalloprotease clade and their N-terminal domain is homologous to the beta-clam part of the N-domain of CDC48-like proteins. Here we report the biochemical and biophysical characterization of Archaeoglobus fulgidus AMA, and of its isolated N-terminal (AMA-N) and ATPase (AMA-DeltaN) domains. AfAMA forms hexameric complexes, as does AMA-N, while AMA-DeltaN only forms dimers. The ability to hexamerize is dependent on the integrity of a GYPL motif in AMA-N, which resembles the pore motif of FtsH and HslU. While the physiological function of AMA is unknown, we show that it has ATP-dependent chaperone activity and can prevent the thermal aggregation of proteins in vitro. The ability to interact with non-native proteins resides in the N-domain and is energy-independent.

Adenosine Triphosphatases↗
PubMedDate not supplied

Immunisation with recombinant AMA-1 protects mice against infection with Plasmodium chabaudi.

The Plasmodium merozoite surface antigen apical membrane antigen-1 (AMA-1) has previously been shown to provide partial protection to Saimiri and rhesus monkeys immunised with recombinant Plasmodium fragile or parasite-derived Plasmodium knowlesi AMA-1, respectively. In the study reported here we have used the Plasmodium chabaudi/mouse model system to extend our pre-clinical assessment of an AMA-1 vaccine. We describe here the expression of the full-length Plasmodium chabaudi adami AMA-1 and the P. chabaudi adami AMA-1 ectodomain using both baculovirus and Escherichia coli. The ectodomain expressed in E. coli, which contained an N-terminal hexa-his tag, was purified by Ni-chelate chromatography and refolded in vitro in the presence of oxidised and reduced glutathione to generate intramolecular disulphide bonds. In a series of vaccine trials, in both inbred and outbred mice, highly significant protection was obtained by immunising with the refolded AMA-1 ectodomain. Protection was shown to correlate with antibody response and was dependent on intact disulphide bonds. Passive transfer of antibodies raised in rabbits against the refolded AMA-1 ectodomain was also protective. In view of this demonstration that E. coli expression of a soluble P. chabaudi AMA-1 domain can generate a vaccine that is effective in mice, we are pursuing a similar approach to generating a vaccine against P. falciparum for testing in human volunteers.

Animals↗