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Biomedical subjects

J Roberts

Publications and source records attributed to J Roberts.

At least 235 records · Page 13Linked to original sources
PubMed1996

A second look at the second stage of labor.

This article focuses on the primary clinical issues during the second stage of labor: diagnosis, duration, maternal bearing-down efforts, and fetal descent, and ways to help women with their expulsive efforts during this time. A pattern of progression for the second stage/expulsive phase of labor is presented, with an emphasis on the importance of delaying direction to or encouragement of the woman to push until the obstetric conditions are optimal for descent and the women has entered the active phase of the second stage. Ongoing assessment of fetal status and descent, the quality of uterine contractions, and maternal condition are emphasized, rather than arbitrary time limits for the second stage. The use of various care practices, including maternal position and alternative bearing-down techniques, which optimize maternal and fetal outcomes, is described. Finally, women's concerns about this major life experience are considered in the context of the care that they receive during the second stage of labor.

Cervix Uteri↗
PubMed1996

Perceptions of the significant other of the effects of psychodynamic psychotherapy. Implications for thinking about psychodynamic and systemic approaches.

BACKGROUND: Clinical suggests that partners of psychotherapy patients often have powerful feelings about the therapy and therapist. The repercussions of psychotherapy on those close to the patient are rarely considered. A small exploratory study was therefore conducted. METHOD: All patients who had completed at least two months of weekly psychodynamic psychotherapy in 1990 at an out-patient unit of a psychiatric hospital (n = 35) and had a partner with whom they were living at the time of starting therapy (n = 23) were contacted. Eight gave permission for their partner to be contacted directly. All eight partners agreed to participate in a semi-structured interview exploring their perceptions of the effects of the therapy on a number of family relationships. The impact of the process of the study was also investigated by means of a questionnaire sent to all partners some weeks after the interview. RESULTS: Considerable changes were perceived to have taken place in association with therapy affecting not only the relationship between the couple but also their parenting relationship, the children, and at time members of the extended family. Partner's views about the direction of such changes seemed to influence other perceptions about the therapy. CONCLUSION: The repercussions of individual psychotherapy may well spread extensively within a family. This further blurs the boundary between individual and family therapy, both theoretically and clinically. Research procedures are themselves a major intervention and may have a considerable emotional impact on participants.

Adult↗
PubMed1996

Mutations in the human skeletal muscle chloride channel gene (CLCN1) associated with dominant and recessive myotonia congenita.

Myotonia, defined as delayed relaxation of muscle after contraction, is seen in a group of genetic disorders that includes autosomal dominant myotonia congenita (Thomsen's disease) and autosomal recessive myotonia congenita (Becker's disease). Both disorders are characterized electrophysiologically by increased excitability of muscle fibers, reflected in clinical myotonia. These diseases are similar except that transient weakness is seen in patients with Becker's, but not Thomsen's disease. Becker's and Thomsen's diseases are caused by mutations in the skeletal muscle voltage-gated chloride channel gene (CLCN1). Genetic screening of a panel of 18 consecutive myotonia congenita (MC) probands for mutation in CLCN1 revealed that a novel Gln-68-Stop nonsense mutation predicts premature truncation of the chloride channel protein. Four previously reported mutations, Arg-894-stop, Arg-338-Gln, Gly-230-Glu, and del 1437-1450, were also noted in our sample set. The Arg-338-Gln and Gly-230-Glu mutations were found in patients with different phenotypes from those of previous reports. Further study of the Arg-338-Gln and Gln-230-Glu alleles may shed light on variable modes of transmission (dominant versus recessive) in different families. Physiologic study of these mutations may lead to better understanding of the pathophysiology of myotonia in these patients and of voltage-gated chloride channel structure/function relationships in skeletal muscles.

Chloride Channels↗
PubMed1996

Recurrent miscarriage is associated with increased numbers of CD5/20 positive lymphocytes and an increased incidence of thyroid antibodies.

The aim of this study was to determine whether recurrent miscarriage (three or more miscarriages, no live children) was associated with an increased incidence of autoantibodies. Five groups were enrolled into the study; healthy non-pregnant women, healthy first-trimester pregnant women, women suffering spontaneous abortion, those undergoing termination of pregnancy and those with a previous history of miscarriage. The number of total B cells and the numbers of the antibody producing B cell subset CD5+/CD20+ were determined for each group. Samples were tested for anticardiolipin antibodies, antinuclear antibodies and thyroid microsomal and thyroglobulin antibodies. The results showed that compared to normal pregnancy or spontaneous abortion, recurrent miscarriage was associated with a significant increase in the number of CD5+/20+ positive cells (0.8 +/- 0.3 vs 0.5 +/- 0.1 vs 1.1 +/- 0.3 x 10(8)/l; p < 0.001). These women were also found to have a higher incidence of thyroid antibodies, with four out of the 11 patients being positive for thyroid microsomal antibodies. These results suggest that there may be an association between autoimmunity and recurrent miscarriage.

Abortion, Habitual↗
PubMed1996

Gene therapy in the adult primate brain: intraparenchymal grafts of cells genetically modified to produce nerve growth factor prevent cholinergic neuronal degeneration.

Gene therapy may be a useful means of delivering substances to the brain that are capable of preventing neuronal degeneration. In the present experiment, we determined whether intraparenchymal transplants of primary autologous cells genetically modified to produce nerve growth factor (NGF) would prevent injury-induced degeneration of cholinergic neurons. Cultured primary monkey fibroblasts were genetically modified to produce human NGF, and secreted 13.2 ng NGF/10(6) cells/h in vitro. Adult monkeys then underwent fornix transections to induce degeneration of basal forebrain cholinergic neurons, and received autologous grafts of either NGF-producing or control, beta-galactosidase-producing fibroblasts directly into the basal forebrain region. One month later, 61.7 +/- 8.9% of cholinergic neurons remained indentifiable in NGF-graft recipients compared to 26.2 +/- 5.0% in control graft recipients (P < 0.02). Neuronal protection correlated with the accuracy of graft placement: up to 92% protection from neuronal degeneration occurred when NGF-secreting grafts were accurately placed immediately adjacent to injured neurons. Thus, intraparenchymal NGF delivery to the adult primate brain by gene transfer can prevent the degeneration of basal forebrain cholinergic neurons. Gene therapy can target intraparenchymal brain sites for regionally specific neurotrophin delivery, thereby avoiding limitations imposed by diffusion of substances across the blood-brain barrier and through CNS parenchyma, while avoiding adverse effects of neurotrophic factors delivered in a non-directed manner to the central nervous system. The delivery of NGF by gene transfer to the brain merits further study as a means of preventing cholinergic neuronal degeneration in human disorders such as Alzheimer's disease.

Animals↗