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PubMed1980

Interaction of cardiopulmonary and somatic reflexes in humans.

Activation of cardiopulmonary receptors with vagal afferents results predominantly in reflex inhibition of efferent sympathetic activity, whereas activation of somatic receptors reflexly increases sympathetic activity to the heart and circulation. Previous studies in experimental animals indicate that there is an important interaction between these excitatory and inhibitory reflexes in the control of the renal circulation. The purpose of this study was to determine whether there is a similar interaction between somatic and cardiopulmonary reflexes in humans. The activity of the cardiopulmonary receptors was altered (reduced) with lower body negative pressure (-5 mm Hg), which causes a decrease in cardiac filling pressure and a small reflex increase in forearm vascular resistance without accompanying changes in arterial pressure. Activation of somatic receptors by isometric handgrip for 2 min at 10 and 20% of maximum voluntary contraction resulted in reflex vasoconstriction in the nonexercising arm. Lower body negative pressure at -5 mm Hg produced a threefold augmentation in the forearm vasoconstrictor response to isometric handgrip in the nonexercising arm. This increase in resistance was significantly greater (P < 0.05) than the algebraic sum of the increases in resistance resulting from lower body suction alone plus isometric handgrip alone. Furthermore, it occurred despite a greater rise in arterial pressure, which would be expected to decrease forearm vascular resistance through activation of arterial baroreceptors and through passive dilatation of forearm vessels. Thus, removal of the inhibitory influence of cardiopulmonary receptors by pooling blood in the lower extremities enhances the somatic reflex. These data suggest an interaction between cardiopulmonary and somatic reflexes in the control of forearm vascular resistance in man.

Adult↗
PubMed1997

Molecular single-cell analysis reveals that CD5-positive peripheral blood B cells in healthy humans are characterized by rearranged Vkappa genes lacking somatic mutation.

B cells expressing the CD5 cell surface antigen are involved in certain B cell malignancies and autoimmune diseases. From studies in the mouse, it emerged that CD5+ B cells represent a separate lineage of B lymphocytes that, in contrast to conventional (CD5-) B cells, are not driven into T cell-dependent immune responses in which rearranged variable (V) region genes are diversified by somatic hypermutation. Against this background it came as a surprise that human disease-involved CD5-positive autoreactive B cells as well as B cell chronic lymphocytic leukemias can harbor somatically mutated V region genes. Recent V gene analyses on CD5+ B cells in healthy adults did not give rise to a clear picture about the fraction of somatically mutated among all CD5+ B cells. In this work we used a molecular single-cell analysis to determine reliably the frequency of mutated CD5+ B cells in healthy humans: single, kappa light chain-expressing CD5+ peripheral blood B cells were isolated by flow cytometry, and rearranged Vkappa genes were amplified by PCR. From one donor, CD5+CD19+ B cells were analyzed. Since CD5+ B cells were found among IgM+IgD+ and IgM+IgD- cells (but almost not among class-switched cells) from two other donors, individual cells corresponding to these IgM-expressing subsets were investigated separately. The sequence analysis of rearranged Vkappa genes revealed that most if not all CD5+ B cells in healthy humans carry unmutated V region genes. From one of the donors, a novel polymorphic Jkappa2 gene segment was identified. To explain the discrepancy between the frequent occurrence of disease-associated somatically mutated CD5+ B cells and the low incidence or absence of somatic mutation in normal CD5+ B cells, we speculate that CD5+ B cells usually do not participate in germinal center reactions, but if they occasionally do so, they may be at an increased risk to become involved in autoimmune diseases or B cell malignancies.

Adult↗
PubMed1985

Linguistic dimensions of affect and thought in somatization disorder.

DSM-III has established diagnostic criteria that separate somatization disorder from other overlapping symptom configurations. Nevertheless, information regarding the experience of somatization disorder is far from complete. Terms such as "masked depression" or "alexithymia" imply that a disturbance of affect is a central but guarded issue for at least some somatizing patients. Through content analysis of speech, the authors investigated the self-experience of somatization disorder in relation to affective disorder. Rather than defended depression, a distinctive characteristic found in the language of patients with somatization disorder reflects a confused, negative self-identity.

Adult↗
PubMed1986

A prospective follow-up and family study of somatization in men and women.

The authors evaluated alternative criteria for somatization disorder in 277 female and 129 male psychiatric outpatients. In women, the diagnosis of somatization disorder based on DSM-III criteria was highly concordant with the diagnosis of Briquet's syndrome based on Guze's original criteria. There was familial aggregation for Briquet's syndrome in women but none among individuals of either sex who had somatization disorder without the full Briquet's syndrome. In men, the diagnosis of somatization disorder was rarer and less stable than in women. The findings show that somatization usually has a different clinical picture and different familial antecedents in men than in women.

Ambulatory Care↗
PubMedDate not supplied

Trauma spectrum adaptation: somatic symptoms in long-term pediatric cancer survivors.

The authors assessed somatic symptoms and the degree of association among somatic symptoms, global adjustment, trauma symptoms, and personality characteristics in long-term pediatric cancer survivors. Forty cancer survivors completed self-report questionnaires and clinical interviews. Participants' level of somatic symptoms fell between nonclinic and psychiatric populations. Somatic symptom scores correlated with general adjustment in the negative direction and with posttraumatic stress disorder (PTSD) scores in the positive direction. The majority of participants met at least partial current PTSD criteria. Because these survivors demonstrate a repressive adaptive style but endorse somatic symptoms, the latter may represent a method for detecting trauma-related distress in this population.

Adaptation, Psychological↗
PubMedDate not supplied

Somatic symptoms for diagnosing major depression in cancer patients.

Diagnosing depression in cancer patients has been challenging because the diagnostic criteria include somatic symptoms frequently attributed to the cancer itself or its treatment. However, few studies have explored how to appropriately deal with individual somatic symptoms. The authors used data from 220 cancer patients with major depression to examine the intercorrelations among the DSM-IV somatic and nonsomatic symptom criteria as well as whether the presence of an individual somatic symptom could discriminate the severity of major depression. Appetite changes and a diminished ability to think were positively associated with anhedonia. Sleep disturbance and fatigue were not significantly associated with nonsomatic symptoms. These associations were consistent after adjusting for physical functioning and pain. Only patients with appetite changes showed a higher severity of depression. These results suggest that individual somatic symptoms differ in nature and that appetite-related symptoms and a diminished ability to think may be useful for diagnosing depression in cancer patients, whereas sleep disturbances and fatigue may not be as useful.

Adolescent↗
PubMedDate not supplied

PTSD and somatization in women treated at a VA primary care clinic.

The authors examined the association between trauma, posttraumatic stress disorder (PTSD), and somatization in 264 women attending a Department of Veterans Affairs primary care clinic. Using a structured computerized interview (Composite International Diagnostic Interview), they found that traumatic events were reported by 81% of the women. The lifetime prevalence of PTSD was 27%; for somatization it was 19%. PTSD was the best predictor of somatization after control for demographic variables, veteran status, and other mood and anxiety disorders. Psychological numbing symptoms of PTSD emerged as a particularly strong predictor of somatization. The link between PTSD and somatization deserves further study.

Adult↗
PubMed2002

Attention-Deficit/Hyperactivity Disorder and methylphenidate: a dose-response analysis and parent-child comparison of somatic complaints.

The authors examined parent and child ratings of somatic complaints in 65 children with Attention-Deficit/Hyperactivity Disorder (ADHD) who received four doses (5 mg, 10 mg, 15 mg, 20 mg) of methylphenidate (MPH) in the context of a double-blind, placebo controlled, within-subject (crossover) experimental design. Results indicated that parent and child ratings of somatic complaints decreased in a linear fashion from baseline levels as a function of increasing MPH dose and showed minimal variation across MPH conditions. Statistical comparisons of specific somatic complaints indicated minimal agreement between parents and children in contrast to the nearly identical parent-child dose-response curves. The paradoxical findings of fewer somatic complaints associated with MPH, importance of obtaining children's perceptions of MPH treatment, and implications for measuring somatic complaints are discussed.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

Somatic and depressive symptoms in female Japanese and American students: a preliminary investigation.

The present study examined the relationship between common somatic symptoms and depression in samples of Japanese and American college students. Fifty Japanese and 44 American women completed the Beck Depression Inventory (BDI) and rated 56 somatic-distress items for 7 days. Japanese had higher levels of somatic distress than Americans. ANOVA of somatic distress by BDI-level revealed that the High BDI Japanese group reported 26 somatic symptoms (including stomach ache, dizziness, and shoulder pain) with significantly higher means when compared with the low BDI group. High BDI Americans had a significantly higher mean for joint pain compared to the Low BDI group. The importance of the body in transcultural psychiatry is explored, and implications for primary and mental health care are discussed.

Adult↗
PubMed2005

Somatic mutations in the mitochondria of rheumatoid arthritis synoviocytes.

Somatic mutations have a role in the pathogenesis of a number of diseases, particularly cancers. Here we present data supporting a role of mitochondrial somatic mutations in an autoimmune disease, rheumatoid arthritis (RA). RA is a complex, multifactorial disease with a number of predisposition traits, including major histocompatibility complex (MHC) type and early bacterial infection in the joint. Somatic mutations in mitochondrial peptides displayed by MHCs may be recognized as non-self, furthering the destructive immune infiltration of the RA joint. Because many bacterial proteins have mitochondrial homologues, the immune system may be primed against these altered peptides if they mimic bacterial homologues. In addition, somatic mutations may be influencing cellular function, aiding in the acquirement of transformed properties of RA synoviocytes. To test the hypothesis that mutations in mitochondrial DNA (mtDNA) are associated with RA, we focused on the MT-ND1 gene for mitochondrially encoded NADH dehydrogenase 1 (subunit one of complex I - NADH dehydrogenase) of synoviocyte mitochondria from RA patients, using tissue from osteoarthritis (OA) patients for controls. We identified the mutational burden and amino acid changes in potential epitope regions in the two patient groups. RA synoviocyte mtDNA had about twice the number of mutations as the OA group. Furthermore, some of these changes had resulted in potential non-self MHC peptide epitopes. These results provide evidence for a new role for somatic mutations in mtDNA in RA and predict a role in other diseases.

Arthritis, Rheumatoid↗
PubMed2007

Somatic sequence alterations in twenty-one genes selected by expression profile analysis of breast carcinomas.

INTRODUCTION: Genomic alterations have been observed in breast carcinomas that affect the capacity of cells to regulate proliferation, signaling, and metastasis. Re-sequence studies have investigated candidate genes based on prior genetic observations (changes in copy number or regions of genetic instability) or other laboratory observations and have defined critical somatic mutations in genes such as TP53 and PIK3CA. METHODS: We have extended the paradigm and analyzed 21 genes primarily identified by expression profiling studies, which are useful for breast cancer subtyping and prognosis. This study conducted a bidirectional re-sequence analysis of all exons and 5', 3', and evolutionarily conserved regions (spanning more than 16 megabases) in 91 breast tumor samples. RESULTS: Eighty-seven unique somatic alterations were identified in 16 genes. Seventy-eight were single base pair alterations, of which 23 were missense mutations; 55 were distributed across conserved intronic regions or the 5' and 3' regions. There were nine insertion/deletions. Because there is no a priori way to predict whether any one of the identified synonymous and noncoding somatic alterations disrupt function, analysis unique to each gene will be required to establish whether it is a tumor suppressor gene or whether there is no effect. In five genes, no somatic alterations were observed. CONCLUSION: The study confirms the value of re-sequence analysis in cancer gene discovery and underscores the importance of characterizing somatic alterations across genes that are related not only by function, or functional pathways, but also based upon expression patterns.

Breast Neoplasms↗
PubMed2004

Somatic symptoms in depression: evaluation of their diagnostic weight in an African setting.

BACKGROUND: Somatic symptoms are extremely common features of depression and other mental disorders in African countries such as Nigeria, but their weight in the diagnosis of depression is not certain. AIM: To determine what weight should be assigned to these symptoms in comparison with other well-known symptoms in the diagnosis of depression. METHOD: A sample of 829 persons completed the Patient Health Questionnaire which was earlier modified by the inclusion of the somatic symptoms being studied. Using principal component analysis and a logistic regression model, the contributions of these symptoms in comparison with others were determined. RESULTS: Core depressive symptoms accounted for most of the total variance for depression. The somatic symptoms studied loaded separately from the core depressive symptoms and were not as good predictors of depression. A cognitive factor emerged as well as some somatic factors. CONCLUSIONS: Although somatic symptoms may be florid among patients with depression, they have considerably less weight than core depressive symptoms in the diagnosis of depression. The emerging cognitive factor could be similar to that described by previous authors.

Adolescent↗
PubMed2006

The Knudson's two-hit model and timing of somatic mutation may account for the phenotypic diversity of focal congenital hyperinsulinism.

BACKGROUND: Congenital hyperinsulinism (CHI) is associated with focal hyperplasia of endocrine tissue in 40-65% of patients. Focal CHI is sporadic and is caused by a germline, paternally inherited, mutation of the SUR1 (ABCC8) or KIR6.2 (KCNJ11) genes (encoding subunits of the pancreatic ATP-dependent potassium channel) together with somatic maternal haploinsufficiency for 11p15.5. Plurifocal or large forms of focal CHI are a cause of apparent failure of surgery, and their underlying mechanism has not been thoroughly investigated. PATIENTS: We here report two patients with bifocal CHI as evidenced by relapsing hypoglycemia after removal of the first focal lesion and the detection of a second, distinct, focal adenomatous hyperplasia during later surgery (patients 1 and 2) and a patient with a giant focal lesion involving the major part of the pancreas (patient 3). RESULTS: In the three patients, a germline, paternally inherited, mutation of SUR1 was found. In patients 1 and 2, haploinsufficiency for the maternal 11p15.5 region resulted from a somatic deletion specific for each of the focal lesions, as shown by the diversity of deletion break points. In patient 3, an identical somatic maternal 11p15 deletion demonstrated by similar break points was shown in two independent lesion samples, suggesting a very early event during pancreas embryogenesis. CONCLUSION: Individual patients with focal hyperinsulinism may have more than one focal pancreatic lesion due to separate somatic maternal deletion of the 11p15 region. These patients and those with solitary focal lesions may follow the two-hit model described by Knudson. The stage of embryogenesis at which the somatic event occurs may account for the observed histological diversity (early event giant lesion, later event small lesion).

ATP-Binding Cassette Transporters↗
PubMed2003

Somatic motoneurone specification in the hindbrain: the influence of somite-derived signals, retinoic acid and Hoxa3.

We have investigated the mechanisms involved in generating hindbrain motoneurone subtypes, focusing on somatic motoneurones, which are confined to the caudal hindbrain within rhombomeres 5-8. Following heterotopic transplantation of rhombomeres along the rostrocaudal axis at various developmental stages, we have found that the capacity of rhombomeres to generate somatic motoneurones is labile at the neural plate stage but becomes fixed just after neural tube closure, at stage 10-11. Grafting of somites or retinoic acid-loaded beads beneath the rostral hindbrain induced the formation of somatic motoneurones in rhombomere 4 only, and Hox genes normally expressed more caudally (Hoxa3, Hoxd4) were induced in this region. Targeted overexpression of Hoxa3 in the rostral hindbrain led to the generation of ectopic somatic motoneurones in ventral rhombomeres 1-4, and was accompanied by the repression of the dorsoventral patterning gene Irx3. Taken together, these observations suggest that the somites, retinoic acid and Hox genes play a role in patterning somatic motoneurones in vivo.

Animals↗
PubMed2004

Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as on milliways(mili(Alk)) as receptor for Jeb signalling.

The visceral muscles of the Drosophila midgut consist of syncytia and arise by fusion of founder and fusion-competent myoblasts, as described for the somatic muscles. A single-step fusion results in the formation of binucleate circular midgut muscles, whereas a multiple-step fusion process produces the longitudinal muscles. A prerequisite for muscle fusion is the establishment of myoblast diversity in the mesoderm prior to the fusion process itself. We provide evidence for a role of Notch signalling during establishment of the different cell types in the visceral mesoderm, demonstrating that the basic mechanism underlying the segregation of somatic muscle founder cells is also conserved during visceral founder cell determination. Searching for genes involved in the determination and differentiation of the different visceral cell types, we identified two independent mutations causing loss of visceral midgut muscles. In both of these mutants visceral muscle founder cells are missing and the visceral mesoderm consists of fusion-competent myoblasts only. Thus, no fusion occurs resulting in a complete disruption of visceral myogenesis. Subsequent characterisation of the mutations revealed that they are novel alleles of jelly belly (jeb) and the Drosophila Alk homologue named milliways (mili(Alk)). We show that the process of founder cell determination in the visceral mesoderm depends on Jeb signalling via the Milliways/Alk receptor. Moreover, we demonstrate that in the somatic mesoderm determination of the opposite cell type, the fusion-competent myoblasts, also depends on Jeb and Alk, revealing different roles for Jeb signalling in specifying myoblast diversity. This novel mechanism uncovers a crosstalk between somatic and visceral mesoderm leading not only to the determination of different cell types but also maintains the separation of mesodermal tissues, the somatic and splanchnic mesoderm.

Anaplastic Lymphoma Kinase↗
PubMed1994

Sex determination of the Drosophila germ line: tra and dsx control somatic inductive signals.

In Drosophila, the sex of germ cells is determined by cell-autonomous and inductive signals. XY germ cells autonomously enter spermatogenesis when developing in a female host. In contrast, XX germ cells non-autonomously become spermatogenic when developing in a male host. In first instar larvae with two X chromosomes, XX germ cells enter the female or the male pathway depending on the presence or absence of transformer (tra) activity in the surrounding soma. In somatic cells, the product of tra regulates the expression of the gene double sex (dsx) which can form a male-specific or a female-specific product. In dsx mutant larvae, XX and XY germ cells develop abnormally, with a seemingly intersexual phenotype. This indicates that female-specific somatic dsx products feminize XX germ cells, and male-specific somatic dsx products masculinize XX and XY germ cells. The results show that tra and dsx control early inductive signals that determine the sex of XX germ cells and that somatic signals also affect the development of XY germ cells. XX germ cells that develop in pseudomales lacking the sex-determining function of Sxl are spermatogenic. If, however, female-specific tra functions are expressed in these animals, XX germ cells become oogenic. Furthermore, transplanted XX germ cells can become oogenic and form eggs in XY animals that express the female-specific function of tra. Therefore, TRA product present in somatic cells of XY animals or in animals lacking the sex-determining function of Sxl, is sufficient to support developing XX germ cells through oogenesis.

Animals↗
PubMed2000

Two waves of programmed cell death occur during formation and development of somatic embryos in the gymnosperm, Norway spruce.

In the animal life cycle, the earliest manifestations of programmed cell death (PCD) can already be seen during embryogenesis. The aim of this work was to determine if PCD is also involved in the elimination of certain cells during plant embryogenesis. We used a model system of Norway spruce somatic embryogenesis, which represents a multistep developmental pathway with two broad phases. The first phase is represented by proliferating proembryogenic masses (PEMs). The second phase encompasses development of somatic embryos, which arise from PEMs and proceed through the same sequence of stages as described for their zygotic counterparts. Here we demonstrate two successive waves of PCD, which are implicated in the transition from PEMs to somatic embryos and in correct embryonic pattern formation, respectively. The first wave of PCD is responsible for the degradation of PEMs when they give rise to somatic embryos. We show that PCD in PEM cells and embryo formation are closely interlinked processes, both stimulated upon withdrawal or partial depletion of auxins and cytokinins. The second wave of PCD eliminates terminally differentiated embryo-suspensor cells during early embryogeny. During the dismantling phase of PCD, PEM and embryo-suspensor cells exhibit progressive autolysis, resulting in the formation of a large central vacuole. Autolytic degradation of the cytoplasm is accompanied by lobing and budding-like segmentation of the nucleus. Nuclear DNA undergoes fragmentation into both large fragments of about 50 kb and multiples of approximately 180 bp. The tonoplast rupture is delayed until lysis of the cytoplasm and organelles, including the nucleus, is almost complete. The protoplasm then disappears, leaving a cellular corpse represented by only the cell wall. This pathway of cell dismantling suggests overlapping of apoptotic and autophagic types of PCD during somatic embryogenesis in Norway spruce.

Apoptosis↗
PubMed2003

Gibberellin is essentially required for carrot (Daucus carota L.) somatic embryogenesis: dynamic regulation of gibberellin 3-oxidase gene expressions.

A GA biosynthesis inhibitor, uniconazole, caused many shrunken embryos when it was supplied to cultured carrot (Daucus carota L.) cells at the induction of somatic embryos. The abnormality was prevented by exogenous GA(1) or GA(4). To analyze the status of GA biosynthesis during somatic embryogenesis, expression patterns of newly isolated genes encoding GA biosynthetic enzymes, two GA 20-oxidases, three GA 3-oxidases, and two GA 2-oxidases were observed by using a semi-quantitative reverse-transcription-polymerase chain reaction with gene-specific primers. Transcript levels of GA 20-oxidases and GA 2-oxidases did not change greatly during development of the somatic embryo. On the other hand, drastic changes were found in three GA 3-oxidase genes. Strikingly, expression of a GA 3-oxidase gene, DcGA3ox2, was elevated once in somatic embryogenesis, but not in the non-induced suspension cells. The enzymatic functions of these gene products were also confirmed using recombinant proteins expressed in Escherichia coli. Our results indicate that GA biosynthesis is required for carrot somatic embryogenesis.

Base Sequence↗