The Lost Diary of Annie Westburg

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This book has really excellent information on causes of miscarriage and ectopic pregnancy as well as options in subsequent pregnancies. Useful glossary of terms too.

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It has a strong feminist perspective and includes personal stories about elective abortion as well as miscarriage and ectopic pregnancy. Sue Sanders Penguin, Auckland, The first hand experience of a patient undergoing the complicated procedures of infertility treatment. Beer M. This new book contains information on the latest medical tests and treatments to help women conceive and carry to term.

This book is a wonderful resource for all those struggling with recurrent failure and loss. Nicola is a practising midwife and childbirth educator and has lost 4 babies at various stages of pregnancy. Yet, one out of four pregnancies ends in this tragedy. Where are these women, Samantha wondered, after her miscarriage? Samantha realized that she had unwittingly become a member in an underground, secret society of women who suffer alone in silence. Ann Oakley, Ann Macpherson and Helen Roberts Britain, , revised Contains lots of good medical information and common sense advice.

A comprehensive and insightful perspective on possible causes, medical terminology, choices and decisions, emotional aspects, planning for the future, coping suggestions and resources. Supportive and comforting. Professor Lesley Regan Bloomsbury, London, An extremely interesting and informative book, written for both patients and doctors.

In addition to addressing miscarriage causes, Dr. Regan also includes a section on answering common questions and offers practical advice on preparing for your next pregnancy.

Good Grief: A Companion for Every Loss

Henry Lerner M. D Introduction by Robert Barbieri, M. Perseus Publishing. Christine Moulder Britain, This very comprehensive book includes personal stories, medical information and useful tips and suggestions. Louise Conway This is the memoir of Louise who at age 30 experienced 3 recurrent miscarriages and who 2 years later was diagnosed with Thyroid Cancer. Emma Patton Penguin, Auckland, Contains a very sensitive section on miscarriage and baby death.

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Jane Warland Australia, This book was self-published by an Australian midwife and survivor of miscarriage and stillbirth. Worthwhile reading if you are pregnant again or contemplating becoming so. Julie Reid Tandem Press, Auckland, An increasingly common problem discussed frankly and practically. Lists many steps that you can take at home before seeking either alternative or medical help. Stacey McLaughlin Published by iUniverse McLaughlin addresses the variety of emotions a woman experiences after a miscarriage and focuses on how to mend your soul.

Diana Plater Double Day, Auckland, A must read for those who enjoy taking control. Sarah Murphy Sheldon Press, London, An easy to read book by another woman whose experience of miscarriage left her wanting to help others through the process. Lynne Friedman with Irene Daria A very down to earth book with up-to-date information. It also has stories from women in several different circumstances. A guide to gynaecological health for women of all ages, from puberty to menopause and beyond. Easy to read and well illustrated. The illustrations are beautiful with little text.

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Preschoolers and older toddlers would understand what the book is saying. There are suggestions at the end of the book for helping adults help their children deal with their grief which is processed differently. Covers everything from the first period to the last — and everything that can go wrong in between. One allele in the tumor sample showed a reduced intensity when compared with the normal sample Fig. Amplification and gene scan analysis of microdissected normal stromal cells showed two alleles of comparable heights Fig.

LOH analysis using marker D6S LOH analysis was performed on normal microdissected epithelial or stromal cells, nonmicrodissected tumor cells and microdissected tumor cells. Sections were used for microdissection were stained by toluidin blue 2a and 2c, 3a and 3c. The figures show the areas of tumor 2c and 3c or normal cells 2a and 3a that were microdissected.

For LOH analysis of the nonmicrodissected tumor, the whole section was used, of which only a part is shown. Tumor cells are indicated with asterisks.

Amplification and subsequent gene scan analysis of the samples was performed using marker D15S 2a to 2c or marker D6S 3a to 3c. The numbers and are the peak heights of allele 1 and allele 2, respectively, of the nonmicrodissected tumor sample Fig. The numbers and 90 are the peak heights of allele 1 and allele 2, respectively, of the control sample Fig.

DNA was isolated from microdissected tumor cells Fig. The numbers and are the peak heights of allele 1 and allele 2, respectively, of the microdissected tumor sample Fig. A panel of nine paired tumor samples derived from primary HN and metastatic lesions L of the head and neck, were subjected to high density microsatellite analysis. None of the tumors displayed down-regulated or lost TAP2 expression. Results obtained by application of these markers are shown in Table 1 , right panel. In addition, a marker located on the 6q arm, D6S, was used. Each primary tumor with down-regulated HLA expression HN37, 38, 41, 54, 20, and 8 displayed allelic loss at 6p, and specifically at 6p Of these tumors, three primary tumors HN38, 54, and 20 displayed allelic loss at the majority of the informative 6p One of these tumors HN38 displayed allelic loss at all informative 6p markers, whereas heterozygosity was retained at the chromosome 6q marker D6S Three primary tumors with down-regulated HLA class I expression HN37, 41, and 8 displayed allelic loss at 1—3 loci, only.

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Telomeric 6p loss was found in HN8 and HN To study the role of chromosomal deletions at 6p, and in particular at 6p Table 1 includes the results obtained by high density microsatellite analysis of the lymph node metastases L. The primary tumor contained two noncontinuous regions of loss: one region between D6S and C, and the second region between D6S and D6S Marker C was not informative.

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The lymph node metastasis contained one region of allelic loss ranging from D6S to D6S Allelic loss at this marker was not found in the primary tumor. Down-regulation of HLA class I expression has been reported in various tumors and this singularity may provide tumor cells with a mechanism to escape immune recognition by cytotoxic T cells. Loss of HLA class I expression in tumors has mainly been established by immunohistochemical procedures using monoclonal antibodies mAbs directed against monomorphic, locus-, and allele-specific determinants of HLA class I molecules Garrido et al, Due to the cross-reactivity of several locus-specific mAbs and the scarcity of allele-specific mAbs, the exact frequency and nature of altered HLA class I expression are still unclear.

Moreover, immunohistochemical procedures are limited in revealing the underlying mechanisms responsible for down-regulated HLA class I expression. Interpretation of HLA class loss phenotypes in tumors is even more complicated by the heterogeneity of tumors. The development of reliable and robust molecular techniques is required to study HLA class I loss in tumors.

One important innovation in these studies is microdissection, which enables isolation of tumor cells without co-isolation of normal cells that could mask alterations in tumor cells. In addition, this technique offers the possibility to study heterogeneity in tumors. One of these mechanisms, LOH of chromosome 6p, has been reported in various tumors of different origin Foulkes et al, a; Randerson et al, Previously, we studied chromosomal deletions of the HLA region at 6p Normal DNA was used as a control because the efficiency of amplification varies between alleles and between samples.

The ratio between two alleles in a heterozygous sample should remain constant. By comparing tumor and normal DNA, a change in the ratio indicates allelic loss. Most samples showed residual amplification of the lost allele in the tumor from co-isolated DNA derived from stromal and infiltrating cells.

In four tumors, near-threshold values of signal reduction were found. In addition, normal stromal and epithelial cells of these tumors were microdissected and used as a control.

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Microdissection of tumor resulted in clear allelic loss in these tumors. The initial low signal reduction in the nonmicrodissected tumor tissue, may have resulted from the heterogeneity of these tumors. Due to this heterogeneity, only a low percentage of the tumor cells may contain allelic loss. Alternatively, the initial low signal reduction in the nonmicrodissected tumor tissue may result from the high percentage of infiltrating cells.

The presence of a high percentage of infiltrating cells in tissue impedes estimation of the percentage of tumor cells.