Sexuality and mood changes in women with persistent pelvic girdle pain after childbirth: a case-control study.

BACKGROUND: Pelvic girdle pain is a common problem during pregnancy. For most women, the symptoms cease within the first 3-6 months of giving birth, but in some women the pain persists. In this study we investigate the sexuality and frequency of depressive symptoms in women with persistent pelvic girdle pain after childbirth and in healthy women. METHODS: We conducted a case-control study of women with persistent pelvic girdle pain after childbirth and a control group of healthy women. The frequency of depressive symptoms and sexuality were measured using the self-rating version of the Montgomery-Asberg Depression Rating Scale and the McCoy Female Sexuality Questionnaire. RESULTS: Forty-six women with persistent pelvic girdle pain and thirty-nine healthy women were enrolled. The frequency of depressive symptoms and the total score on female sexuality did not differ between the groups. However, pain during intercourse was more frequent (P < 0.001) in women with persistent pelvic girdle pain and caused them to avoid sexual intercourse frequently (P < 0.001). In multiple linear regression a higher frequency of depressive symptoms was reversely correlated with a lower score on female sexuality (ß = - 0,41, p < 0,001 95% CI -0,6 - -0,22) This association remained after adjusting for obstetric variables and individual characteristics. CONCLUSION: Depressive symptoms and female sexuality were similar between women with persistent pelvic girdle pain after childbirth and healthy controls. However, pain during intercourse and avoidance of sexual intercourse were more frequent among women with pelvic girdle pain.

Anatomical landmarks of the intra-pelvic side-wall as sources of pain in women with and without pregnancy-related chronic pelvic pain after childbirth: a descriptive study.

BACKGROUND: Chronic pelvic pain (CPP) affects 15-24% of women and can have a devastating impact on quality of life. Laparoscopy is often used in the investigation, although in one third of the examinations there is no visible pathology and the women may be dismissed without further investigation. Also, the contribution of skeletal, muscular, periosteal and ligamentous tissues to CPP remains to be further elucidated. The objective of the present study was to compare pain intensity provoked from anatomical landmarks of the intra-pelvic side-wall in women with pregnancy-related CPP after childbirth and women without such pain. METHODS: This is a descriptive study of 36 non-randomly selected parous women with CPP after childbirth and 29 likewise selected parous women after childbirth without CPP. Pain was determined by questionnaire and clinical examination. The primary outcome measure was reported pain intensity provoked on 13 anatomical landmarks of the intra-pelvic side-wall. All women reported their perceived pain intensity for each anatomical landmark on Likert scales and an individual sum score was calculated. RESULTS: Women with chronic pelvic pain were older than women without CPP. At several intra-pelvic landmarks high intensity pain was provoked in women with CPP compared with less intense pain provoked at fewer landmarks in women without low back or pelvic pain (p < 0.0001). The average sum of pain intensity scores was about 4 times higher in women with CPP (1.3) as compared with those without low back or pelvic pain (0.3), p < 0.0001. This association remained when adjusting for the age difference between the pain groups in linear regression analysis. In addition, reported pain intensity at worst past week was independently associated with sum of pain intensity scores. The maximum individual sum of pain intensity scores among women without CPP was exceeded by that of 85% of the women with CPP. CONCLUSIONS: Parous women with CPP after childbirth had a heightened pain intensity over 13 anatomical landmarks during pelvic examination compared with parous women without CPP. These results need to be confirmed in a larger cohort with different types of CPP.

RAP-011 improves erythropoiesis in zebrafish model of Diamond-Blackfan anemia through antagonizing lefty1.

Diamond-Blackfan Anemia (DBA) is a bone marrow failure disorder characterized by low red blood cell count. Mutations in ribosomal protein genes have been identified in approximately half of all DBA cases. Corticosteriod therapy and bone marrow transplantation are common treatment options for patients; however, significant risks and complications are associated with these treatment options. Therefore, novel therapeutic approaches are needed for treating DBA. Sotatercept (ACE-011, and its murine ortholog RAP-011) acts as an activin receptor type IIA ligand trap, increasing hemoglobin and hematocrit in pharmacologic models, in healthy volunteers, and in patients with ß-thalassemia, by expanding late-stage erythroblasts through a mechanism distinct from erythropoietin. Here, we evaluated the effects of RAP-011 in zebrafish models of RPL11 ribosome deficiency. Treatment with RAP-011 dramatically restored hemoglobin levels caused by ribosome stress. In zebrafish embryos, RAP-011 likely stimulates erythropoietic activity by sequestering lefty1 from erythroid cells. These findings identify lefty1 as a signaling component in the development of erythroid cells and rationalize the use of sotatercept in DBA patients.

Transdifferentiation of fast skeletal muscle into functional endothelium in vivo by transcription factor Etv2.

Etsrp/Etv2 (Etv2) is an evolutionarily conserved master regulator of vascular development in vertebrates. Etv2 deficiency prevents the proper specification of the endothelial cell lineage, while its overexpression causes expansion of the endothelial cell lineage in the early embryo or in embryonic stem cells. We hypothesized that Etv2 alone is capable of transdifferentiating later somatic cells into endothelial cells. Using heat shock inducible Etv2 transgenic zebrafish, we demonstrate that Etv2 expression alone is sufficient to transdifferentiate fast skeletal muscle cells into functional blood vessels. Following heat treatment, fast skeletal muscle cells turn on vascular genes and repress muscle genes. Time-lapse imaging clearly shows that muscle cells turn on vascular gene expression, undergo dramatic morphological changes, and integrate into the existing vascular network. Lineage tracing and immunostaining confirm that fast skeletal muscle cells are the source of these newly generated vessels. Microangiography and observed blood flow demonstrated that this new vasculature is capable of supporting circulation. Using pharmacological, transgenic, and morpholino approaches, we further establish that the canonical Wnt pathway is important for induction of the transdifferentiation process, whereas the VEGF pathway provides a maturation signal for the endothelial fate. Additionally, overexpression of Etv2 in mammalian myoblast cells, but not in other cell types examined, induced expression of vascular genes. We have demonstrated in zebrafish that expression of Etv2 alone is sufficient to transdifferentiate fast skeletal muscle into functional endothelial cells in vivo. Given the evolutionarily conserved function of this transcription factor and the responsiveness of mammalian myoblasts to Etv2, it is likely that mammalian muscle cells will respond similarly.

Hydrodynamic stretching of single cells for large population mechanical phenotyping.

Cell state is often assayed through measurement of biochemical and biophysical markers. Although biochemical markers have been widely used, intrinsic biophysical markers, such as the ability to mechanically deform under a load, are advantageous in that they do not require costly labeling or sample preparation. However, current techniques that assay cell mechanical properties have had limited adoption in clinical and cell biology research applications. Here, we demonstrate an automated microfluidic technology capable of probing single-cell deformability at approximately 2,000 cells/s. The method uses inertial focusing to uniformly deliver cells to a stretching extensional flow where cells are deformed at high strain rates, imaged with a high-speed camera, and computationally analyzed to extract quantitative parameters. This approach allows us to analyze cells at throughputs orders of magnitude faster than previously reported biophysical flow cytometers and single-cell mechanics tools, while creating easily observable larger strains and limiting user time commitment and bias through automation. Using this approach we rapidly assay the deformability of native populations of leukocytes and malignant cells in pleural effusions and accurately predict disease state in patients with cancer and immune activation with a sensitivity of 91% and a specificity of 86%. As a tool for biological research, we show the deformability we measure is an early biomarker for pluripotent stem cell differentiation and is likely linked to nuclear structural changes. Microfluidic deformability cytometry brings the statistical accuracy of traditional flow cytometric techniques to label-free biophysical biomarkers, enabling applications in clinical diagnostics, stem cell characterization, and single-cell biophysics.

Finger joint laxity, number of previous pregnancies and pregnancy induced back pain in a cohort study.

BACKGROUND: General joint hypermobility is estimated to affect about 10% of the population and is a prerequisite of heritable connective tissue disorders where fragile connective tissue is a prominent feature. Pregnancy induced back pain is common whereas about 10% of women still have disabling pain several years after childbirth. The pathogenesis of the pain condition is uncertain, although several risk factors are suggested including general joint hypermobility. In the present study, the possible association of peripheral joint mobility in early pregnancy on the incidence of back pain with onset during pregnancy and persisting after childbirth was explored. METHODS: A cohort of 200 pregnant women recruited from antenatal health care clinics was assessed by questionnaire and clinical examination, including measurement of passive abduction of the left fourth finger, throughout pregnancy and at 13 weeks postpartum. Comparisons were made between women with and without back pain. Statistical tests used were χ2-test, t-test, Spearman correlation and multiple logistic regression. RESULTS: In the cohort, the mean passive abduction angle of the left fourth finger increased from 40.1° in early pregnancy to 41.8° at the postpartum appointment. At the postpartum appointment, women in the back pain group had a significantly larger mean passive abduction angle of the left fourth finger of 4.4°, twice as many previous pregnancies and deliveries, and more than twice as frequent back pain in previous pregnancy, as compared with women with no persistent back pain. A similar pattern was displayed in late pregnancy. In a multiple regression analysis, the passive abduction angle of the left fourth finger in early pregnancy and the number of previous pregnancies were positively, significantly and independently associated to the incidence of back pain in late pregnancy and postpartum. CONCLUSIONS: Finger joint laxity as a reflection of constitutional weakness of connective tissue and number of previous pregnancies were associated with the development of back pain induced in pregnancy and persisting after childbirth. These factors may provide a foundation for development of targeted prevention strategies, but this have to be confirmed in future research including measurement of general joint laxity.

Lmx1a regulates fates and location of cells originating from the cerebellar rhombic lip and telencephalic cortical hem.

The cerebellar rhombic lip and telencephalic cortical hem are dorsally located germinal zones which contribute substantially to neuronal diversity in the CNS, but the mechanisms that drive neurogenesis within these zones are ill defined. Using genetic fate mapping in wild-type and Lmx1a(-/-) mice, we demonstrate that Lmx1a is a critical regulator of cell-fate decisions within both these germinal zones. In the developing cerebellum, Lmx1a is expressed in the roof plate, where it is required to segregate the roof plate lineage from neuronal rhombic lip derivatives. In addition, Lmx1a is expressed in a subset of rhombic lip progenitors which produce granule cells that are predominantly restricted to the cerebellar posterior vermis. In the absence of Lmx1a, these cells precociously exit the rhombic lip and overmigrate into the anterior vermis. This overmigration is associated with premature regression of the rhombic lip and posterior vermis hypoplasia in Lmx1a(-/-) mice. These data reveal molecular organization of the cerebellar rhombic lip and introduce Lmx1a as an important regulator of rhombic lip cell-fate decisions, which are critical for maintenance of the entire rhombic lip and normal cerebellar morphogenesis. In the developing telencephalon Lmx1a is expressed in the cortical hem, and in its absence cortical hem progenitors contribute excessively to the adjacent hippocampus instead of producing Cajal-Retzius neurons. Thus, Lmx1a activity is critical for proper production of cells originating from both the cerebellar rhombic lip and the telencephalic cortical hem.

Mitochondrial function controls proliferation and early differentiation potential of embryonic stem cells.

Pluripotent stem cells hold significant promise in regenerative medicine due to their unlimited capacity for self-renewal and potential to differentiate into any cell type of the body. In this study, we demonstrate that proper mitochondrial function is essential for proliferation of undifferentiated ESCs. Attenuating mitochondrial function under self-renewing conditions makes these cells more glycolytic-dependent, and it is associated with an increase in the mRNA reserves of Nanog, Oct4, and Sox2. In contrast, attenuating mitochondrial function during the first 7 days of differentiation results in normal repression of Oct4, Nanog, and Sox2. However, differentiation potential is compromised as revealed by abnormal transcription of multiple Hox genes. Furthermore, under differentiating conditions in which mitochondrial function is attenuated, tumorigenic cells continue to persist. Our results, therefore establish the importance of normal mitochondrial function in ESC proliferation, regulating differentiation, and preventing the emergence of tumorigenic cells during the process of differentiation.

Generalized joint hypermobility and risk of pelvic girdle pain in pregnancy: does body mass index matter?

BACKGROUND: Women with generalized joint hypermobility may be at increased risk of pregnancy-related pelvic girdle pain, but evidence is inconclusive. OBJECTIVES: In this prospective cohort study of 283 pregnant women in Norway, we aimed to study the association of generalized joint mobility with pelvic girdle pain, and to evaluate if pre-pregnancy body mass index was a modifier of the association. METHODS: Generalized joint hypermobility was defined as a score of ≥5/9 positive tests on the Beighton score measured in early pregnancy. Primary outcome was evening pain intensity in gestation week 30, measured by a 100 mm visual analogue scale. We applied linear regression analyses to estimate age-adjusted unstandardized beta coefficients. RESULTS: Evening pain intensity was similar among women with Beighton score ≥ 5/9 and women with Beighton score < 5/9 (age-adjusted mean difference 2.8 mm; 95% CI: -9.2 to 14.9 mm). Women with Beighton score ≥ 5/9 and pre-pregnancy body mass index ≥ 25 kg/m2, reported higher evening pain than women with Beighton score < 5/9 and pre-pregnancy body mass index <25 kg/m2 (age-adjusted mean difference 28.7 mm; 95% CI: 14.3-43.1 mm). CONCLUSIONS: Overall, evening pain intensity was similar among pregnant women with and without generalized joint hypermobility. However, women with a combination of generalized joint hypermobility and body mass index ≥25 kg/m2 reported higher evening pain compared to women with normal joint mobility and body mass index <25 kg/m2, suggesting that body mass index may modify the association. The estimates could be imprecise due to the small study sample, and our findings should be interpreted with caution.

Overlapping function of Lmx1a and Lmx1b in anterior hindbrain roof plate formation and cerebellar growth.

The roof plate is an organizing center in the dorsal CNS that controls specification and differentiation of adjacent neurons through secretion of the BMP and WNT signaling molecules. Lmx1a, a member of the LIM-homeodomain (LIM-HD) transcription factor family, is expressed in the roof plate and its progenitors at all axial levels of the CNS and is necessary and sufficient for roof plate formation in the spinal cord. In the anterior CNS, however, a residual roof plate develops in the absence of Lmx1a. Lmx1b, another member of the LIM-HD transcription factor family which is highly related to Lmx1a, is expressed in the roof plate in the anterior CNS. Although Lmx1b-null mice do not show a substantial deficiency in hindbrain roof plate formation, Lmx1a/Lmx1b compound-null mutants fail to generate hindbrain roof plate. This observation indicates that both genes act in concert to direct normal hindbrain roof plate formation. Since the requirement of Lmx1b function for normal isthmic organizer at the mid-hindbrain boundary complicates analysis of a distinct dorsal patterning role of this gene, we also used a conditional knock-out strategy to specifically delete dorsal midline Lmx1b expression. Phenotypic analysis of single and compound conditional mutants confirmed overlapping roles for Lmx1 genes in regulating hindbrain roof plate formation and growth and also revealed roles in regulating adjacent cerebellar morphogenesis. Our data provides the first evidence of overlapping function of the Lmx1 genes during embryonic CNS development.

A self-renewal program controls the expansion of genetically unstable cancer stem cells in pluripotent stem cell-derived tumors.

Human germ cell tumors are often metastatic, presumably due to distal site tumor growth by cancer stem cells. To determine whether cancer stem cells can be identified in a transplantation model of testicular germ cell tumor, we transplanted murine embryonic germ cells (EGCs) into the testis of adult severe combined immunodeficient mice. Transplantation resulted in a locally invasive solid tumor, with a cellular component that generated secondary tumors upon serial transplantation. The secondary tumors were invariably metastatic, a feature not observed in the primary tumors derived from EGCs. To characterize the differences between EGCs and the tumor-derived stem cells, we performed karyotype and microarray analysis. Our results show that generation of cancer stem cells is associated with the acquisition of nonclonal genomic rearrangements not found in the originating population. Furthermore, pretreatment of EGCs with a potent inhibitor of self-renewal, retinoic acid, prevented tumor formation and the emergence of these genetically unstable cancer stem cells. Microarray analysis revealed that EGCs and first- and second-generation cancer stem cells were highly similar; however, approximately 1,000 differentially expressed transcripts could be identified corresponding to alterations in oncogenes and genes associated with motility and development. Combined, the data suggest that the activation of oncogenic pathways in a cellular background of genetic instability, coupled with an inherent ability to self-renew, is involved in the acquisition of metastatic behavior in the cancer stem cell population of tumors derived from pluripotent cells.

Derivation of primordial germ cells from human embryonic and induced pluripotent stem cells is significantly improved by coculture with human fetal gonadal cells.

The derivation of germ cells from human embryonic stem cells (hESCs) or human induced pluripotent stem (hIPS) cells represents a desirable experimental model and potential strategy for treating infertility. In the current study, we developed a triple biomarker assay for identifying and isolating human primordial germ cells (PGCs) by first evaluating human PGC formation during the first trimester in vivo. Next, we applied this technology to characterizing in vitro derived PGCs (iPGCs) from pluripotent cells. Our results show that codifferentiation of hESCs on human fetal gonadal stromal cells significantly improves the efficiency of generating iPGCs. Furthermore, the efficiency was comparable between various pluripotent cell lines regardless of origin from the inner cell mass of human blastocysts (hESCs), or reprogramming of human skin fibroblasts (hIPS). To better characterize the iPGCs, we performed Real-time polymerase chain reaction, microarray, and bisulfite sequencing. Our results show that iPGCs at day 7 of differentiation are transcriptionally distinct from the somatic cells, expressing genes associated with pluripotency and germ cell development while repressing genes associated with somatic differentiation (specifically multiple HOX genes). Using bisulfite sequencing, we show that iPGCs initiate imprint erasure from differentially methylated imprinted regions by day 7 of differentiation. However, iPGCs derived from hIPS cells do not initiate imprint erasure as efficiently. In conclusion, our results indicate that triple positive iPGCs derived from pluripotent cells differentiated on hFGS cells correspond to committed first trimester germ cells (before 9 weeks) that have initiated the process of imprint erasure.

Directed differentiation of human-induced pluripotent stem cells generates active motor neurons.

The potential for directed differentiation of human-induced pluripotent stem (iPS) cells to functional postmitotic neuronal phenotypes is unknown. Following methods shown to be effective at generating motor neurons from human embryonic stem cells (hESCs), we found that once specified to a neural lineage, human iPS cells could be differentiated to form motor neurons with a similar efficiency as hESCs. Human iPS-derived cells appeared to follow a normal developmental progression associated with motor neuron formation and possessed prototypical electrophysiological properties. This is the first demonstration that human iPS-derived cells are able to generate electrically active motor neurons. These findings demonstrate the feasibility of using iPS-derived motor neuron progenitors and motor neurons in regenerative medicine applications and in vitro modeling of motor neuron diseases.

Early dorsomedial tissue interactions regulate gyrification of distal neocortex.

The extent of neocortical gyrification is an important determinant of a species' cognitive abilities, yet the mechanisms regulating cortical gyrification are poorly understood. We uncover long-range regulation of this process originating at the telencephalic dorsal midline, where levels of secreted Bmps are maintained by factors in both the neuroepithelium and the overlying mesenchyme. In the mouse, the combined loss of transcription factors Lmx1a and Lmx1b, selectively expressed in the midline neuroepithelium and the mesenchyme respectively, causes dorsal midline Bmp signaling to drop at early neural tube stages. This alters the spatial and temporal Wnt signaling profile of the dorsal midline cortical hem, which in turn causes gyrification of the distal neocortex. Our study uncovers early mesenchymal-neuroepithelial interactions that have long-range effects on neocortical gyrification and shows that lissencephaly in mice is actively maintained via redundant genetic regulation of dorsal midline development and signaling.

Roof Plate-Derived Radial Glial-like Cells Support Developmental Growth of Rapidly Adapting Mechanoreceptor Ascending Axons.

Spinal cord longitudinal axons comprise some of the longest axons in our body. However, mechanisms that drive this extra long-distance axonal growth are largely unclear. We found that ascending axons of rapidly adapting (RA) mechanoreceptors closely abut a previously undescribed population of roof plate-derived radial glial-like cells (RGLCs) in the spinal cord dorsal column, which form a network of processes enriched with growth-promoting factors. In dreher mutant mice that lack RGLCs, the lengths of ascending RA mechanoreceptor axon branches are specifically reduced, whereas their descending and collateral branches, and other dorsal column and sensory pathways, are largely unaffected. Because the number and intrinsic growth ability of RA mechanoreceptors are normal in dreher mice, our data suggest that RGLCs provide critical non-cell autonomous growth support for the ascending axons of RA mechanoreceptors. Together, our work identifies a developmental mechanism specifically required for long-range spinal cord longitudinal axons.

CAK1 promotes meiosis and spore formation in Saccharomyces cerevisiae in a CDC28-independent fashion.

CAK1 encodes a protein kinase in Saccharomyces cerevisiae whose sole essential mitotic role is to activate the Cdc28p cyclin-dependent kinase by phosphorylation of threonine-169 in its activation loop. SMK1 encodes a sporulation-specific mitogen-activated protein (MAP) kinase homolog that is required to regulate the postmeiotic events of spore wall assembly. CAK1 was previously identified as a multicopy suppressor of a weakened smk1 mutant and shown to be required for spore wall assembly. Here we show that Smk1p, like other MAP kinases, is phosphorylated in its activation loop and that Smk1p is not activated in a cak1 missense mutant. Strains harboring a hyperactivated allele of CDC28 that is CAK1 independent and that lacks threonine-169 still require CAK1 to activate Smk1p. The data indicate that Cak1p functions upstream of Smk1p by activating a protein kinase other than Cdc28p. We also found that mutants lacking CAK1 are blocked early in meiotic development, as they show substantial delays in premeiotic DNA synthesis and defects in the expression of sporulation-specific genes, including IME1. The early meiotic role of Cak1p, like the postmeiotic role in the Smk1p pathway, is CDC28 independent. The data indicate that Cak1p activates multiple steps in meiotic development through multiple protein kinase targets.

A Designed Inhibitor of p53 Aggregation Rescues p53 Tumor Suppression in Ovarian Carcinomas.

Half of all human cancers lose p53 function by missense mutations, with an unknown fraction of these containing p53 in a self-aggregated amyloid-like state. Here we show that a cell-penetrating peptide, ReACp53, designed to inhibit p53 amyloid formation, rescues p53 function in cancer cell lines and in organoids derived from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous p53 mutations. Rescued p53 behaves similarly to its wild-type counterpart in regulating target genes, reducing cell proliferation and increasing cell death. Intraperitoneal administration decreases tumor proliferation and shrinks xenografts in vivo. Our data show the effectiveness of targeting a specific aggregation defect of p53 and its potential applicability to HGSOCs.

ETV2 expression increases the efficiency of primitive endothelial cell derivation from human embryonic stem cells.

BACKGROUND: Endothelial cells line the luminal surface of blood vessels and form a barrier between the blood and other tissues of the body. Ets variant 2 (ETV2) is transiently expressed in both zebrafish and mice and is necessary and sufficient for vascular endothelial cell specification. Overexpression of this gene in early zebrafish and mouse embryos results in ectopic appearance of endothelial cells. Ectopic expression of ETV2 in later development results in only a subset of cells responding to the signal. FINDINGS: We have examined the expression pattern of ETV2 in differentiating human embryonic stem cells (ESCs) to determine when the peak of ETV2 expression occurs. We show that overexpression of ETV2 in differentiating human ESC is able to increase the number of endothelial cells generated when administered during or after the endogenous peak of gene expression. CONCLUSIONS: Addition of exogenous ETV2 to human ESCs significantly increased the number of cells expressing angioblast genes without arterial or venous specification. This may be a viable solution to generate in vitro endothelial cells for use in research and in the clinic.

Referred pain patterns provoked on intra-pelvic structures among women with and without chronic pelvic pain: a descriptive study.

OBJECTIVES: To describe referred pain patterns provoked from intra-pelvic structures in women with chronic pelvic pain (CPP) persisting after childbirth with the purpose to improve diagnostics and give implications for treatment. MATERIALS AND METHODS: In this descriptive and comparative study 36 parous women with CPP were recruited from a physiotherapy department waiting list and by advertisements in newspapers. A control group of 29 parous women without CPP was consecutively assessed for eligibility from a midwifery surgery. Inclusion criterion for CPP was: moderate pain in the sacral region persisting at least six months after childbirth confirmed by pelvic pain provocation tests. Exclusion criteria in groups with and without CPP were: persistent back or pelvic pain with onset prior to pregnancy, previous back surgery and positive neurological signs. Pain was provoked by palpation of 13 predetermined intra-pelvic anatomical landmarks. The referred pain distribution was expressed in pain drawings and described in pain maps and calculated referred pain areas. RESULTS: Pain provoked by palpation of the posterior intra-pelvic landmarks was mostly referred to the sacral region and pain provoked by palpation of the ischial and pubic bones was mostly referred to the groin and pubic regions, with or without pain referred down the ipsilateral leg. The average pain distribution area provoked by palpation of all 13 anatomical landmarks was 30.3 mm² (19.2 to 53.7) in women with CPP as compared to 3.2 mm² (1.0 to 5.1) in women without CPP, p< 0.0001. CONCLUSIONS: Referred pain patterns provoked from intra-pelvic landmarks in women with CPP are consistent with sclerotomal sensory innervation. Magnification of referred pain patterns indicates allodynia and central sensitization. The results suggest that pain mapping can be used to evaluate and confirm the pain experience among women with CPP and contribute to diagnosis.

Women's perceptions of seroma and their drainage following mastectomy and axillary lymph node dissection.

AIM: The aim of this research was to study the effect of seroma on women's perception of daily functional and emotional status after surgical treatment for breast cancer. Furthermore, the experiences of the actual drainage procedure of seroma was studied. METHOD: The study had a prospective and comparative design. A study specific questionnaire was developed and used. Eighty-two women operated with modified radical mastectomy completed the forms. Forty-one women with seroma were compared with the 41 without seroma. The items focused on women's perceptions of daily-life situations, postoperative pain, problems with the surgical scar, preoperative information, general health, levels of anxiety, depression, psychosocial support and contact with the registered nurse in the hospital. RESULTS: Overall the perceived emotional and functional status, pain and general health did not differ between the two groups. Women with seroma contacted the registered nurse in the hospital more frequently after hospital discharge. Most women with seroma had no or little pain and anxiety during the aspiration and found the procedure fully acceptable. Practical information concerning self-care and the aspiration procedure was considered insufficient. The return visit to the nurse for wound observation was important and provided psychosocial support. CONCLUSION: Seroma and its drainage is well accepted. Patients should be better informed about the possibility of a seroma and its treatment. Staff continuity and particularly the presence of a special trained nurse for wound control and for psychosocial support are much appreciated.