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PubMed1989

Somatization among refugees: an epidemiologic study.

Somatization has been widely reported among refugee psychiatric patients since World War II, and some psychological theorists have viewed somatization as an alternative to depression. These and other theories were tested in a population survey of 97 Hmong refugees who had lived in the U.S. for several years. Four different measures of somatization were employed, including a 12-item self-rating scale, a single-item global rating based on the total interview, and somatic subscales of the two Hamilton interview-rating scales. These data demonstrate that somatization accompanies certain demographic characteristics that are associated with failure to acculturate. Somatization in this non-patient, refugee population was associated with treatment seeking and self-identified "medical problems" and with psychiatric symptoms and disorders, but not with objective evidence of medical disorder.

Acculturation↗
PubMedDate not supplied

Late-onset psychosis with somatic delusions.

The authors studied 10 patients who had late-onset psychosis with somatic delusions and 2 comparison groups similar in age and education: 9 late-onset psychosis patients without somatic delusions and 10 normal control subjects. Demographic, clinical, and neuropsychological data were obtained. Brain magnetic resonance imaging was also done and compared. The patients with somatic delusions were somewhat more likely to be women, have been ill longer, and meet DSM-III-R criteria for delusional disorder, compared with late-onset psychotic patients without somatic delusions. Patients with somatic delusions also had lower scores on a full-scale IQ test, compared with the normal comparison subjects. The patients with somatic delusions rarely benefitted from and poorly complied with treatment with psychotropics. The study's limitations, such as small sample size and heterogeneity of diagnosis, as well as the possible clinical implications of these findings are also discussed.

Age of Onset↗
PubMed1998

Increased stem cell somatic mutation in the non-neoplastic colorectal mucosa of patients with familial adenomatous polyposis.

Colorectal tumorigenesis in familial adenomatous polyposis (FAP) results from somatic mutation of either the normal APC allele or another growth control gene in epithelial cells bearing a germline APC defect. The rate at which tumors develop is therefore dependent on the somatic mutation frequency; it is not known whether this is normal or elevated in FAP. We aimed to quantify stem cell somatic mutation in FAP, comparing it with hereditary nonpolyposis colorectal cancer (HNPCC) and Crohn's disease (CD). Stem cell somatic mutation frequency was studied in 47 FAP patients, 5 HNPCC patients, and 13 CD patients, all younger than 49 years, by quantifying crypt-restricted loss of O-acetyltransferase activity in sections of morphologically normal colonic mucosa from individuals heterozygous for this monogenically inherited polymorphism. Median stem cell somatic mutation frequency was significantly higher in FAP than HNPCC (4.2 x 10(-4) v 1.4 x 10(-4), Mann-Whitney U, P < .02). The level in CD (4.0 x 10(-4)) was similar to FAP. Mutated crypts occurred in groups more frequently in FAP (22%) than HNPCC (12%) or CD (10%), suggesting an increase in stem cell division associated with crypt fission in FAP. We conclude that stem cell somatic mutation frequency is raised in non-neoplastic colorectal mucosa in FAP. This is probably related to increased stem cell proliferation and contributes to the high rate of tumor formation in this condition.

Adenomatous Polyposis Coli↗
PubMed1997

The natural somatic mutation frequency and human carcinogenesis.

Much recent attention has been paid to the important role of the DNA mismatch repair system in controlling the accumulation of somatic mutations in human tissues and the association of mismatch repair deficiency with carcinogenesis. In the absence of an intact mismatch repair system, cells accumulate mutations at a rate some 1000 times faster than normal cells, and this mutator phenotype is easily measured by the detection of the formation of new variant alleles at microsatellite loci. However, the mismatch repair system is not 100% efficient, even when intact, and the pattern of microsatellite alterations in a wide variety of tumors is consistent with these being due to clonal amplification from tissues that are genetically heterogeneous at microsatellite loci rather than mismatch repair deficiency in the tumor itself. On this basis, it can be estimated that the mutation frequency of microsatellites in normal human tissues is approximately 10(-2) per locus per cell. Similarly, a frequency of mutation at minisatellite loci in normal tissues of around 10(-1) per locus per cell can be estimated. Such elevated levels of mutation are consistent with a recent study of the frequency of HPRT mutation in human kidneys that demonstrated these to be frequent (average 2.5 x 10(-4) in individuals of 70 years or more) and exponentially related to age. Taken as a whole, the data suggest that somatic mutation in human epithelial cells may be some 10-fold higher than in peripheral blood lymphocytes and that the underlying rate of spontaneous mutation is sufficient to account for a large proportion of human carcinogenesis without the need to evoke either stepwise alteration to a mutator phenotype of clonal expansion at all the mutation steps in carcinogenesis. The exponential increase in mutation frequency with age is predictable on the basis that the mutation rate is controlled at the level of repair and that mutation in genes that affect the efficiency of these processes will gradually increase the underlying rate. In addition, the age relatedness of mutation frequency strongly supports the concept that mutation is cell division dependent and that cellular proliferation per se is an important risk factor for cancer. Comparison of somatic mutations with those in the human germline mutation suggests common mechanistic origins and that the high levels of somatic mutation that occur are a direct reflection of the germline mutation rate selected over evolutionary time. Thus, the somatic accumulation of mutations can be seen as a natural process within the human body and cancer a normal part of the human life cycle. This point of view may explain why it has been so difficult to significantly reduce cancer incidence and suggests that, for this to be achieved, the means of altering the natural somatic mutation rate needs to be identified.

Cell Division↗
PubMed1998

Quantification of somatic and spermatogenic cell proliferation in the testes of ruminants, using a proliferation marker and flow cytometry analysis.

We compared 2 methods for the quantification of proliferation in somatic and spermatogenic compartments of post mortem-collected testes in cattle and roe deer. Proliferation was evaluated by estimation of the tissue polypeptid specific antigen (TPS) using an ELISA. This proliferation-specific marker was detected in homogenized cells after selective enrichment of different cell types by density gradient centrifugation. The haploid, diploid and tetraploid cells were monitored by one-parameter flow cytometry and analyzed for mitotic cell cycle. Somatic and spermatogenic cells were discriminated by dual-parameter flow cytometry after DNA staining with propidium iodide and selective labelling of stromatic cells with a vimentin antibody. The TPS was related to the ploidy of cells and their somatic or spermatogenic type. High concentrations of TPS were found in both species. The TPS values varied with different contents of spermatogenic and somatic cells in the fractions of the density gradient. The TPS was positively correlated with spermatogenic cells in the G2/M phase of mitotic cycle (r = 0.474; P < 0.01) and negatively correlated with somatic cells (r = -0.676; P < 0.0001) in roe deer (n = 40). Discrimination of germinative and stromatic cells in the G2-M phase showed their varying proliferation during the annual cycle in roe deer. The quantification of tetraploid spermatogenic cells allowed the calculation of an exact meiotic transformation (ratio haploid:tetraploid cells). In conclusion, TPS indicates proliferation in the germinative compartment of the testes. However, this marker provides only relative values, without information on the number and type of proliferating cells. Dual-parameter flow cytometry using specific staining for vimentin proves to be a better method for studying changing mitotic and meiotic steps during the involution and recrudescence of testes in seasonally breeding ruminants, as it relates proliferative processes directly to both spermatogenic and somatic cells.

Animals↗
PubMedDate not supplied

Somatic DNA alterations in endometriosis: high frequency of chromosome 17 and p53 loss in late-stage endometriosis.

PROBLEM: Genetic predisposition to endometriosis is well established, but the gene(s) involved largely remain unknown. Although endometriosis is considered a benign disease, it displays several features similar to malignancy: altered morphology, disregulated growth, invasion. We hypothesize endometriosis arises as result of somatic DNA alterations occurring in a multi-step process, analogous to origin of neoplasia. Since chromosome 17 and TP53 tumor suppressor gene (TSG) alterations occur frequently in premalignant and malignant tissues, including endometrial and ovarian epithelial carcinomas, we sought to determine if similar somatic changes occur in late stage endometriosis. METHOD OF STUDY: To determine the frequencies of monosomy for chromosome 17, as well as for perturbations of p53 and other loci on 17, two different approaches were used. Fluorescent in situ hybridization (FISH) analysis was used to detect monosomy for the 17 centromere and for the p53 locus. For FISH, archival tissue (n=6) and fresh endometriotic touch preparations were prepared from women (n=8) undergoing extirpation of advanced stage endometriosis. Direct-labeled probes specific for p53 (17p13.1) and for the chromosome 17 alpha-satellite centromere region (1711.1-q11.1) were used to compare single glandular and stromal cells from endometriosis and normal tissue. DNA analysis of polymorphic DNA loci were used to detect loss of heterozygosity (LoH) for other loci on 17. We assessed matched endometriotic and normal DNA (peripheral blood) from women with severe/late stage disease (n=15), studying these dinucleotide markers: HGH (located on 17q22-24), D17S250 (17q11.2-q12) and CHRNB1 (17p13.1). RESULTS: Loss of the chromosome 17 centromere (monosomy) was shown by FISH in some cells from all 14 endometriosis specimens, although in no case did every cell show monosomy 17. In 12 of 14 specimens, significant proportions of cells not only were monosomic for the chromosome 17-centromere (8 to 42% of cells) but also showed loss of p53 locus. In the two remaining cases, p53 loss alone was observed in 8 and 14%. LoH for other alleles on chromosome 17 was observed less often, namely only 3 of 15 specimens for HGH, 1 of 15 for D17S250, and 0 of 15 for CHRNB1. CONCLUSIONS: Our study indicates that perturbations of chromosome 17 in general and the p53 locus in particular occur frequently in severe/late stage endometriosis. That not all cells show loss of whole chromosome 17 or the p53 locus suggests somatic mutation, perhaps occurring late in the pathogenesis of endometriosis. Clonal evolution of endometriosis must depend not only on somatic mutations for p53 but also on other oncogenes or TSG. Alternatively, the clone could begin with a germline or somatic mutation involving a nonneoplastic process, followed by one or more somatic mutations involving an oncogene or TSG like p53. Additional candidate genes clearly must be evaluated in order to determine the precise role chromosome 17 and p53 alterations play in endometriosis; however, additional genes seem unlikely to involve region connoted by HGH, D17S250 or CHRNB1.

Chromosomes, Human, Pair 17↗
PubMed2000

Cytokinin-induced somatic embryogenesis and plant regeneration in Corydalis yanhusuo (Fumariaceae) - a medicinal plant.

An efficient method has been developed for regeneration of complete plants via somatic embryogenesis in Corydalis yanhusuo (Fumariaceae), an important medicinal plant, using tuber-derived callus. Primary callus was induced by culturing mature tuber pieces on Murashige and Skoog's (MS) medium supplemented with 2.0 mg l(-1) N(6)-benzyladenine (BA) and 0.5 mg l(-1) alpha-naphthaleneacetic acid (NAA) in darkness. Somatic embryos were induced by subculturing the primary callus on MS medium supplemented with 0.5-4.0 mg l(-1) BA, kinetin, or zeatin, within 2 weeks of culture in light. Embryos with well-developed cotyledonary leaves were transferred in half-strength liquid MS medium supplemented with 1.0 mg l(-1) zeatin riboside for the development of roots. Converted somatic embryos were cultured on half-strength MS medium supplemented with 6% sucrose, and with 0.5-10.0 mg l(-1) abscisic acid (ABA), paclobutrazol, or ancymidol, 0.5-5.0 mg l(-1) GA(3) and 15-100 mg l(-1) polyethylene glycol (PEG) 4000 for further development of plantlets and in vitro tuber formation. The development of somatic embryos over the surface of tuber and/or cotyledonary leaf base region of the converted primary somatic embryo was observed. Before ex vitro establishment of somatic embryo-derived plants, plants with well-developed tubers were cultured on half-strength MS medium with 2% sucrose and 0.1 mg l(-1) GA(3) for 3 weeks.

Journal Article↗
PubMed2000

Abscisic acid induced somatic embryogenesis in immature embryo explants of coconut (Cocos nucifera L.).

Somatic embryogenesis in coconut (Cocos nucifera L.) is generally induced by gradual reduction of auxin concentration in the culture medium and incorporation of cytokinins. Although plant regeneration through somatic embryogenesis is possible, the protocol is yet to be perfected. In this study, nodular callus was obtained from 7-9 months old immature zygotic embryos of coconut on a medium containing 24 µM 2,4-dichlorophenoxy acetic acid (2,4-D). As a novel approach, abscisic acid (ABA) at a concentration of 2.5-7.5 µM was incorporated into the culture medium for 3-7 weeks to induce somatic embryogenesis. Alternately, callus was subcultured at 5 weekly intervals on media containing gradually reducing concentrations of 2,4-D to induce somatic embryogenesis. Incorporation of ABA enhanced the production of somatic embryos. Application of 2.5-5 µM ABA for 5 weeks was found to be effective. A large number of somatic embryos developed on media containing ABA formed normal shoots and complete plants as compared to those produced in the media with low levels of 2,4-D.

Journal Article↗
PubMedDate not supplied

Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis.

PURPOSE: Of all nonauditory sensory systems, only the somatosensory system seems to be related to tinnitus (eg, temporomandibular joint syndrome and whiplash). The purpose of this study is to describe the distinguishing characteristics of tinnitus associated with somatic events and to use these characteristics to develop a neurological model of somatic tinnitus. MATERIALS AND METHODS: Case series. RESULTS: Some patients with tinnitus, but no other hearing complaints, share several clinical features including (1) an associated somatic disorder of the head or upper neck, (2) localization of the tinnitus to the ear ipsilateral to the somatic disorder, (3) no vestibular complaints, and (4) no abnormalities on neurological examination. Pure tone and speech audiometry of the 2 ears is always symmetric and usually within normal limits. Based on these clinical features, it is proposed that somatic (craniocervical) tinnitus, like otic tinnitus, is caused by disinhibition of the ipsilateral dorsal cochlear nucleus. Nerve fibers whose cell bodies lie in the ipsilateral medullary somatosensory nuclei mediate this effect. These neurons receive inputs from nearby spinal trigeminal tract, fasciculus cuneatus, and facial, vagal, and glossopharyngeal nerve fibers innervating the middle and external ear. CONCLUSIONS: Somatic (craniocervical) modulation of the dorsal cochlear nucleus may account for many previously poorly understood aspects of tinnitus and suggests novel tinnitus treatments.

Adult↗
PubMed1997

The black box in somatization: unexplained physical symptoms, culture, and narratives of trauma.

Stimulated by our clinical work with patients who manifest unexplained "somatoform" symptoms in the primary care setting, this article addresses a theoretical black box in our understanding of somatization: how does culture mediate severe stress to produce symptoms that cannot be explained by the presence of physical illness? Despite various problems in his explanation of hysteria, Freud broke new ground by emphasizing narratives of traumatic experiences in the development and treatment of unexplained physical symptoms. Except in anthropologically oriented cultural psychiatry, contemporary psychiatry has traveled away from a focus on narrative in the study of somatization. On the other hand, recent interest in narrative has spread across many intellectual disciplines, including the humanities and literary criticism, psychology, history, anthropology, and sociology. We operationally define narratives as attempts at storytelling that portray the interrelationships among physical symptoms and the psychologic, social, or cultural context of these symptoms. Regarding somatization and trauma, we focus on the ways that narrative integrates the cultural context with traumatic life events. In explaining the black box, we postulate that extreme stress (torture, rape, witnessing deaths of relatives, forced migration, etc.) is processed psychologically as a terrible, largely incoherent narrative of events too awful to hold in consciousness. Culture patterns the psychologic and somatic expression of the terrible narrative. Methodologically, we have developed some techniques for eliciting narratives of severe stress and somatic symptoms, which we illustrate with observations from an ongoing research project. In designing interventions to improve the care of somatizing patients, we are focusing on the creation of social situations where patients may feel empowered to express more coherent narratives of their prior traumatic experiences.

Adult↗
PubMed2003

Reporting of somatic symptoms as a screening marker for detecting major depression in a population of Japanese white-collar workers.

OBJECTIVE: The objective of this study was to assess screening practices for detecting major depression in workers complaining of somatic symptoms. METHODS: A total of 1443 Japanese white-collar workers (991 men and 452 women, mean age 34 years) completed a medical symptom checklist (major 12 somatic symptoms) and were diagnosed using the structured clinical interviews of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). RESULTS: There were 42 cases (2.9%) with major depression in the total sample. Of the 902 subjects without somatic symptoms, only one (0.1%) was identified as having major depression. The prevalence of the disorder was positively associated (P<.001) with the total number of somatic symptoms, and the area under the receiver operator characteristic curve was 0.92 for men and 0.81 for women, which showed the sensitivity and specificity of the total number of somatic symptoms for detecting major depression. CONCLUSION: The number of reported somatic symptoms is a simple and useful predictor of major depression.

Adult↗
PubMed1997

The c-kit receptor is involved in the adhesion of mouse primordial germ cells to somatic cells in culture.

The receptor encoded by the W (c-kit) locus is expressed on the membrane of mouse primordial germ cells, whereas its ligand termed stem cell factor (SCF), encoded by the Sl locus, is expressed on the membrane of somatic cells associated with both the primordial germ cell migratory pathways and homing sites. Using an in vitro short time assay which allows a quantitative measure of adhesion between cells, in the present paper we show that SCF/c-kit interaction can modulate primordial germ cell adhesion to somatic cells. We report that the adhesiveness of 11.5 dpc primordial germ cells to four types of somatic cells in culture (TM4 cells, STO fibroblasts, bone marrow stromal cells and gonadal somatic cells) is significantly reduced by antibodies directed against c-kit receptor or SCF, as well by soluble SCF. This SCF/c-kit mediated adhesion seems independent of SCF-induced tyrosine autophosphorylation of c-kit receptor. Moreover, primordial germ cells showed a poor ability to adhere to a bone marrow stromal cell line carrying the Sl(d) mutation (unable to synthesize membrane-bound SCF). This adhesiveness was not further impaired by anti-c-kit antibody. These results demonstrate that SCF/c-kit interaction contributes to the adhesion of primordial germ cells to somatic cells in culture and suggest that the role played by SCF in promoting survival, proliferation and migration of these cells in vitro and in vivo, demonstrated by several studies, might depend on the ability of the membrane-bound form of this cytokine to directly mediate primordial germ cell adhesion to the surrounding somatic cells.

Animals↗
PubMed2001

Patterns and risk factors of change in somatic and mood symptoms among older adults.

PURPOSE: This paper was concerned with patterns of individual-level, longitudinal change in depressive symptoms and factors related to those patterns among Americans 70+ years of age. Two types of depressive symptoms were considered, somatic and mood symptoms. The paper focused on whether the patterns of change and the risk factors for these two types of symptoms differed, as we might expect among old and oldest-old adults. METHODS: The analytic sample included self-respondents of the 1993--1995 Asset and Health Dynamics among the Oldest Old (AHEAD) study who were born in 1923 or earlier. Depressive symptoms were assessed using an abbreviated Center for Epidemiologic Studies-Depression (CES-D) Scale. The analyses involved examination of respondents' change scores in depressive symptoms and multivariate models using ordinary least squares (OLS) and seemingly unrelated regressions (SUR). RESULTS: In aggregate, somatic symptoms were more common than mood symptoms initially and over time. Despite differences in aggregate rates, AHEAD respondents' individual-level patterns of change for the two types of symptoms were similar; i.e., stability was the principal trend (53--60%), followed by improvement (21--26%). A number of factors related to change in one aspect of depressive symptoms and not the other, or had greater effects on one aspect of depressive symptoms than the other; e.g., physical health had greater effects on somatic than mood symptoms. CONCLUSIONS: This study suggests that, in investigations of the course and risk factors for depressive symptoms among people 70+ years of age, it is important to separate somatic symptoms from mood symptoms; their etiology may differ. In general, factors reflecting respondents' social milieu (e.g., bereavement, residential relocation) may have greater effects on mood than somatic symptoms, whereas certain factors representing physical health may have greater effects on somatic symptoms.

Age Factors↗
PubMed2006

[Effect of sugars, gibberellic acid and abscisic acid on somatic embryogenesis in Tylophora indica (Burm. f.) Merrill].

The effect of sugars, gibberellic acid (GA3) and abscisic acid (ABA) on somatic embryogenesis from internodal explant-derived callus of Tylophora indica (Burm. f.) Merrill has been investigated. Embryogenic calli were produced from internodal explants and the best result was achieved by using MS medium supplemented with 4micromol/L 2, 4-Dichlorophenoxyacetic acid (2, 4-D). Up to 69% of such embryogenic calli differentiated into somatic embryos with an average of 25 embryos per explant (per gram of the calli) on Murashige and Skoog (MS) medium containing 6micromol/L kinetin (Kn). The individual effect of sucrose and glucose together with 6micromol/L Kn was evaluated. There was a significant difference among concentrations of sugar and among kinds of sugar tested in somatic embryogenesis. Sucrose at 200mmol/L with 6micromol/L Kn gave rise to a maximum embryogenesis (71%) with an average of 49 embryos per explant. However, glucose together with 6micromol/L Kn or a combination of glucose, sucrose and 6micromol/L Kn reduced the percentage of embryogenesis culture and the number of embryos per explant. The presence of GA3 and ABA at particular concentrations promoted somatic embryogenesis in T. indica. The addition of 10mol/L GA3 into the 200mmol/L sucrose-containing medium gave a 98% embryogenesis response with an average of 51 embryos per explant. Somatic embryogenesis was significantly enhanced by the addition of 2micromol/L ABA to 200mmol/L sucrose-containing medium. On this medium 95% embryogenesis with an average of 44 embryos per explant was observed. The study reported here indicates that 200mmol/L sucrose with 6micromol/L Kn, 200mmol/L sucrose with 10micromol/L GA3 and 200mmol/L sucrose with 2micromol/L ABA significantly improved somatic embryogenesis in T. indica whereas glucose alone or in combination with sucrose had an inhibitory role. The embryos obtained developed normally and were easily converted into plants.

Abscisic Acid↗
PubMed2004

Neuroticism, a central link between somatic and psychiatric morbidity: path analysis of prospective data.

BACKGROUND: Neuroticism and somatic complaints are linked, and the aim of this study is to disentangle which mechanisms may be responsible for this association. METHOD: In a stratified sample of 7076 adults (18-65 years), neuroticism, 22 self-reported chronic somatic conditions and five broad CIDI-diagnosed psychiatric syndromes were assessed at baseline and, in 3625 (51%) subjects, 3 years later. Using path analysis we examined whether neuroticism has direct links with future somatic morbidity and, conversely, whether morbidity at baseline is linked with higher neuroticism later on. RESULTS: Neuroticism at baseline is associated with psychiatric and somatic morbidity at follow-up after 3 years (31% and 24%, respectively, are direct associations, i.e. unmediated by each other or neuroticism at follow-up and independent of morbidity at baseline). Conversely, somatic and psychiatric morbidity at baseline are associated with increased neuroticism at follow-up (27% and 15%, respectively, are direct associations). CONCLUSIONS: Neuroticism raises risk for psychiatric and somatic morbidity but also results from them. It represents a central nexus in the process of morbidity accumulation.

Adult↗
PubMed1998

Somatic and psychological models of common mental disorder in primary care in India.

BACKGROUND: Primary care attenders with a common mental disorder (CMD) frequently present with somatic symptoms. This study aimed to examine somatic and psychological models of CMD in primary care attenders in India. METHODS: Cross-sectional survey of attenders at two primary care clinics. Psychiatric caseness was determined on three criteria: standardized psychiatric interview (biomedical criterion), patients' self-assessment of emotional disorder (emic criterion) and health care provider diagnosis. The GHQ-12 and the PPQ, which emphasize psychological and somatic symptoms respectively, were used as screening instruments. RESULTS: Although somatic symptoms were the presenting complaints for 97% of subjects, 51% of subjects with a biomedically defined CMD had a psychological illness attribution. Patients with psychological attributions were more likely to be women, to have a longer duration of illness, to have higher CISR scores and were more likely to be recognized by the primary health care (PHC) physician. The GHQ-12 was superior to the PPQ in identifying cases of CMD against the biomedical criterion for both psychologizers and somatizers; both instruments performed equally well against the emic and care provider criteria. CONCLUSIONS: Psychological models may be acquired by patients as CMD becomes more chronic or severe, making them more likely to be detected by PHC physicians. Psychological symptoms are superior to somatic symptoms in detecting CMD. Shorter versions of the GHQ have comparable discriminating abilities to the 12-item version and offer the practical advantage of brevity, which may make them more acceptable to PHC physicians as a clinical screening tool.

Adolescent↗
PubMed2002

Cognitive functioning in severe somatization--a pilot study.

OBJECTIVE: Somatizing patients often report cognitive complaints but neuropsychological research on somatization is scarce. We investigated somatizing patients for functioning in different cognitive domains. METHOD: Ten female patients with somatization disorder or undifferentiated somatoform disorder and 10 non-somatizing controls participated in neuropsychological examinations. RESULTS: The patients performed at a lower level than the controls in tests involving semantic memory, verbal episodic memory and visuo-spatial tasks, and were slower in attentional tasks. CONCLUSION: Somatization patients may suffer from substantial problems in cognitive performance.

Adult↗
PubMed1982

Somatic variants of murine immunoglobulin lambda light chains.

Studies of the murine lambda light chains produced by myeloma cells provided the first evidence for somatic point mutation of germ-line variable (V) region genes. An examination of the variable regions of 19 lambda 1 chains revealed seven which differed from a common sequence by one to three amino acid substitutions. Subsequently, one of these presumed somatic variants of the single lambda 1 V gene was characterized by DNA sequence analysis of the rearranged functional gene. The predicted DNA sequence alteration was observed and no silent mutation was evident. These studies of lambda chain variants suggested that the hypervariable, complementarity-determining regions (CDRs) ht be a preferred site of somatic mutation because all seven characterized variants contained substitutions only in these regions. By contrast, comparisons of closely related kappa chain variable region amino acid sequences, and more recently VK and VH genes, have suggested that somatic mutation probably occurs in codons for both framework and CDR residues. To examine this apparent discrepancy between the sites of somatic mutations in lambda and kappa genes, we have determined the nucleotide sequence of two lambda 1 gene from hybridomas and a lambda 2 gene from a myeloma. These sequences demonstrate that somatic mutation in lambda genes can occur in both the framework and CDR residues.

Amino Acid Sequence↗