Evaluation of Mini Mental State Examination and Brief Psychiatric Rating Scale on aged schizophrenic patients

Abstract  Mini Mental State Examination (MMSE), Brief Psychiatric Rating Scale (BPRS) and subscales of the BPRS were performed on 73 elderly inpatients (mean age: 67.9 years; standard deviation: 7.2; range: 60–89) diagnosed with DSM-III-R chronic schizophrenia. Forty of the subjects were men and 33 were women. A significant negative correlation was observed between MMSE and the age, factor negative, factor depressive, and total score of BPRS. We believe, however, that it is relatively sufficient to screen for demented illness of schizophrenics using MMSE when considering the age and the psychiatric symptoms (especially negative or depressive symptoms). Forty-eight (66%) of the 73 patients were categorized as 'demented' by MMSE. These results suggest that the aged inpatients with schizophrenia in a hospital showed certain kinds of cognitive deficits (including senile dementia) more frequently than the general population.     

Expression and function of activin receptors in human endometrial adenocarcinoma cells

Menstrual cycle-dependent expressions of activin A in normal human endometrial tissues have been reported. Expression of activin receptor mRNAs and increased activin A production were also observed in human endometrial adenocarcinoma tissues, suggesting that activin A might enhance cell proliferation and inhibit apoptotic signaling in endometrial cancer cells. In this study, we have examined the effects of activin A on cell proliferation, anticancer drug-induced apoptosis and Fas-mediated apoptosis in 3 differentiated human endometrial adenocarcinoma cell lines, namely HEC-1, HHUA and Ishikawa. Flow cytometric analyses revealed moderate expressions of all 4 types of activin receptor subunits on the cell surfaces of the 3 cell lines. The proliferations of the 3 endometrial cancer cells were completely unaffected by activin A, whereas it suppressed the cell proliferation of a human ovarian endometrioid adenocarcinoma cell line, OVK-18, in a dose-dependent manner. Moreover, activin A did not affect the apoptotic changes in the 3 endometrial adenocarcinoma cells treated with 4 different anticancer drugs, namely CDDP, paclitaxel, etoposide and SN38. The apoptotic changes in HHUA cells treated with anti-Fas IgM were also unaffected by activin A. These results indicate that the increased activin A production in human endometrial adenocarcinoma tissues in vivo may not stimulate carcinoma cell proliferation or inhibit apoptotic signaling in carcinoma cells. Insensitivity to the usual growth suppression signals induced by activin A might be one of the mechanisms of immortality of human endometrial adenocarcinoma cells.     

Stromal cell-derived factor-1α improves infarcted heart function through angiogenesis in mice

BACKGROUND: Local delivery of stromal cell-derived factor-1alpha (SDF-1) has been demonstrated to improve hind limb ischemia through enhanced neovascularization in animals. It was hypothesized that local administration of SDF-1 also contributes to neovascularization of ischemic heart. METHOD: Acute myocardial infarction was created by left coronary artery ligation in C57BL/6J mice. Immediately after infarction induction, mice were treated by injection directly into the center of ischemic myocardium either with saline (control group) or SDF-1 (SDF-1 group). Cardiac function was measured on echocardiogram 2 and 4 weeks after infarction. On week 4 mice were killed to evaluate infarction size and capillary vessel density. To determine the contribution of bone marrow cells to angiogenesis, the same procedures were performed on C57BL/6J chimeric mice reconstituted with green fluorescent protein-positive bone marrow cells. RESULTS: Fractional shortening was greater in the SDF-1 group at 4 weeks (0.31 +/- 0.06% vs 0.23 +/- 0.03%, P = 0.037). The infarct area was smaller in the SDF-1 group compared to the control group (9.31 +/- 2.76% vs 18.07 +/- 5.69%, P = 0.028). Green fluorescent protein-positive cells accumulated predominantly at the peri-infarction site, and were located with the capillary vessels. Capillary vessel density was significantly increased in the SDF-1 group (13.08 +/- 4.11 vessels/mm(2) vs 34.50 +/- 7.59 vessels/mm(2), P = 0.014). CONCLUSIONS: SDF-1 protects against deterioration of cardiac function after acute myocardial infarction by promoting angiogenesis. The safety and long-term prognosis of this treatment remains to be determined.     

Vasopressin receptor antagonism — a therapeutic option in heart failure and hypertension

The precise role of vasopressin in the pathophysiology of cardiovascular disease is controversial, but this peptide hormone is important for several reasons. Firstly, circulating concentrations of vasopressin are elevated in heart failure and some forms of hypertension. Secondly, there is evidence that vasopressin is synthesized not only in the hypophysial-pituitary axis but also in peripheral tissues including the heart where it acts as a paracrine hormone. Thirdly, vasopressin has vasoconstrictor, mitogenic, hyperplastic and renal fluid retaining properties which, by analogy with angiotensin II, may have deleterious effects when present in chronic excess. Finally, the availability of orally active non-peptide vasopressin receptor antagonists allows vasopressin receptor antagonism to be considered as a therapeutic option in cardiovascular disease.     

Infection-induced urethral defect treated by urethral reconstruction with a radial forearm flap

Abstract A 47-year-old man was admitted with the chief complaint of a urethral defect. An approximately 17-cm defect of the urethra seemed to have been occurred by the infection of implanted foreign bodies in the penile skin. Reconstruction of the urethra and the ventral skin was performed with a free radial forearm flap. A fistula formed at the proximal anastomosis after the operation, but was controlled conservatively. Urethral stricture at the proximal anastomosis subsequently developed. A urethral stent made of shape memory alloy was placed with the preservation of voiding function.     

Stromal Cell‐Derived Factor 1α Induces Accumulation of Intraveneously Administered Marrow‐Derived Stromal Cells in the Partially Obstructed Rat Bladder

Objectives: We investigated the time course of the stromal cell‐derived factor 1α (SDF1α) expression and behavior of intravenously administered bone marrow‐derived stromal (BMS) cells in the urinary bladder of partial bladder outlet obstruction (PBOO) rats. Methods: Study 1: Recombinant SDF1α or saline was directly injected into the bladder wall of female rats followed by intravenous administration of BMS cells isolated from green fluorescent protein (GFP) transgenic rats. The bladder was examined with immunohistochemistry to determine whether SDF1α would enhance migration of BMS cells to the bladder. Study 2: Following surgery of PBOO or sham in female rats, bladders were removed on days 1–14, and expression of hypoxia inducible factor 1α (HIF1α) and SDF1α were examined with real‐time polymerase chain reaction (PCR) to determine if PBOO preferentially increased their expression. Study 3: Female rats underwent PBOO or sham surgery followed by intravenous administration of GFP‐positive BMS cells. Bladders were examined with immunohistochemistry on days 1–14 to determine whether BMS cells preferentially accumulated in the bladder. Results: BMS cells were accumulated in the injection site of SDF1α but not saline in the bladder. SDF1α and HIF1α increased at day 1 after PBOO compared to sham. More BMS cells accumulated in the bladder of PBOO on day 1, and some BMS cells expressed smooth muscle phenotypes by day 14. Conclusion: SDF1α induced with ischemia/hypoxia due to PBOO is implicated in the accumulation of BMS cells in the bladder and regeneration of the bladder for PBOO.     

α2-Antiplasmin is involved in the production of transforming growth factor β1 and fibrosis

BACKGROUND: Fibrotic disease occurs in most tissues. Transforming growth factor (TGF)-beta is the major inducer of fibrosis. The fibrinolytic system is considered to play an important role in the degradation of extracellular matrices. However, the detailed mechanism of how this system affects fibrosis remains unclear. METHODS AND RESULTS: We examined experimental fibrosis in mice with a deficiency of alpha(2)-antiplasmin (alpha2AP), which is a potent and specific plasmin inhibitor. We found that the lack of alpha2AP attenuated bleomycin-induced TGF-beta(1) synthesis and fibrosis. In addition, the production of TGF-beta(1) from the explanted fibroblasts of alpha2AP(-/-) mice decreased dramatically as compared to that in wild-type mice. Moreover, we found that alpha2AP specifically induces the production of TGF-beta(1) in fibroblasts. CONCLUSION: The lack of alpha2AP attenuated TGF-beta(1) synthesis, thereby resulting in attenuated fibrosis. This is the first report to describe the crucial role that alpha2AP plays in TGF-beta(1) synthesis during the process of fibrosis. Our results provide new insights into the role of alpha2AP in fibrosis.