Placental growth hormone is increased in the maternal and fetal serum of patients with preeclampsia.

OBJECTIVES: Placental growth hormone (PGH) is a pregnancy-specific protein produced by syncytiotrophoblast and extravillous cytotrophoblast. No other cells have been reported to synthesize PGH Maternal. PGH Serum concentration increases with advancing gestational age, while quickly decreasing after delivery of the placenta. The biological properties of PGH include somatogenic, lactogenic, and lipolytic functions. The purpose of this study was to determine whether the maternal serum concentrations of PGH change in women with preeclampsia (PE), women with PE who deliver a small for gestational age neonate (PE + SGA), and those with SGA alone. STUDY DESIGN: This cross-sectional study included maternal serum from normal pregnant women (n = 61), patients with severe PE (n = 48), PE + SGA (n = 30), and SGA alone (n = 41). Fetal cord blood from uncomplicated pregnancies (n = 16) and PE (n = 16) was also analyzed. PGH concentrations were measured by ELISA. Non-parametric statistics were used for analysis. RESULTS: (1) Women with severe PE had a median serum concentration of PGH higher than normal pregnant women (PE: median 23,076 pg/mL (3473-94 256) vs. normal pregnancy: median 12 157 pg/mL (2617-34 016); p < 0.05), pregnant women who delivered an SGA neonate (SGA: median 10 206 pg/mL (1816-34 705); p < 0.05), as well as pregnant patients with PE and SGA (PE + SGA: median 11 027 pg/mL (1232-61 702); p < 0.05). (2) No significant differences were observed in the median maternal serum concentration of PGH among pregnant women with PE and SGA, SGA alone, and normal pregnancy (p > 0.05). (3) Compared to those of the control group, the median umbilical serum concentration of PGH was significantly higher in newborns of preeclamptic women (PE: median 356.1 pg/mL (72.6-20 946), normal pregnancy: median 128.5 pg/mL (21.6-255.9); p < 0.01). (4) PGH was detected in all samples of cord blood. CONCLUSIONS: (1) PE is associated with higher median concentrations of PGH in both the maternal and fetal circulation compared to normal pregnancy. (2) Patients with PE + SGA had lower maternal serum concentrations of PGH than preeclamptic patients without SGA. (3) Contrary to previous findings, PGH was detectable in the fetal circulation. The observations reported herein are novel and suggest that PGH may play a role in the mechanisms of disease in preeclampsia and fetal growth restriction.     

Improvement of juvenile dermatomyositis with calcinosis universalis after treatment with intravenous immunoglobulin

Juvenile dermatomyositis is a chronic multisystemic disease. It is believed to be of autoimmune aetiology and is characterized by the presence of vasculitis affecting striated muscle and skin. Calcinosis occurs in about 40% of cases. We report a case of a 10‐year‐old girl diagnosed with juvenile dermatomyositis who presented with difficulty in walking and inability to completely extend the four extremities due to calcinosis universalis. Calcinosis had progressed despite a 3‐year administration of diltiazem, hydroxychloroquine, aluminium hydroxide, cyclosporin, and probenecid. The introduction of monthly intravenous immunoglobulin therapy for 15 months lessened disease activity, and markedly regressed calcinosis, and improved functional outcome.     

In vitro investigation of pig cells for resistance to human antibody‐mediated rejection

Although human complement‐dependent cytotoxicity (CDC) of α1,3‐galactosyltransferase gene‐knockout (GTKO) pig cells is significantly weaker than that of wild‐type (WT) cells, successful xenotransplantation will require pigs with multiple genetic modifications. Sera from healthy humans were tested by (i) flow cytometry for binding of IgM/IgG, and (ii) CDC assay against peripheral blood mononuclear cells and porcine aortic endothelial cells from five types of pig – WT, GTKO, GTKO transgenic for H‐transferase (GTKO/HT), WT transgenic for human complement regulatory protein CD46 (CD46) and GTKO/CD46. There was significantly higher mean IgM/IgG binding to WT and CD46 cells than to GTKO, GTKO/HT, and GTKO/CD46, but no difference between GTKO, GTKO/HT, and GTKO/CD46 cells. There was significantly higher mean CDC to WT than to GTKO, GTKO/HT, CD46, and GTKO/CD46 cells, but no difference between GTKO and GTKO/HT. Lysis of GTKO/CD46 cells was significantly lower than that of GTKO or CD46 cells. CD46 expression provided partial protection against serum from a baboon sensitized to a GTKO pig heart. GTKO/CD46 cells were significantly resistant to lysis by human serum and sensitized baboon serum. In conclusion, the greatest protection from CDC was obtained by the combination of an absence of Gal expression and the presence of CD46 expression, but the expression of HT appeared to offer no advantage over GTKO. Organs from GTKO/CD46 pigs are likely to be significantly less susceptible to CDC.     

A case of primary rectal mucosa‐associated lymphoid tissue lymphoma treated by endoscopic mucosal resection

A 53‐year‐old man underwent surveillance colonoscopy that revealed a submucosal tumor‐like polypoid lesion on the Rb area of the rectum. Histological examination of biopsy specimens showed chronic inflammation. Endoscopic mucosal resection was performed after obtained informed consent for the purpose of obtaining accurate diagnosis and for curative treatment. Pathological findings of the resected specimen showed low‐grade B‐cell lymphoma of mucosa‐associated lymphoid tissue type (MALT lymphoma). Gallium‐scintigraphy, abdominal CT, small bowel series and endoscopic examination of the upper gastrointestinal tract revealed no abnormalities. Based on the findings, a diagnosis of stage IE lymphoma was made. However it was suspected that the vertical cut‐end of the resected specimen had residue of lymphoma cells. Additional transanal resection of the rectum was therefore performed, but no lymphoma cells were found in the specimen. Eradication of Helicobacter pylori was also performed. Although a standard therapeutic strategy for colonic MALT lymphoma has not been established, endoscopic mucosal resection might be a good therapeutic choice.     

Gefitinib reverses breast cancer resistance protein-mediated drug resistance

Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone. In this study, we evaluated the possible interaction of gefitinib, a selective epidermal growth factor receptor tyrosine kinase inhibitor, with BCRP. BCRP-transduced human epidermoid carcinoma A431 (A431/BCRP) cells acquired cellular resistance to gefitinib, suggesting that BCRP could be one of the determinants of gefitinib sensitivity in a certain sort of cells. Next, the effect of gefitinib on BCRP-mediated drug resistance was examined. Gefitinib reversed SN-38 resistance in BCRP-transduced human myelogenous leukemia K562 (K562/BCRP) or BCRP-transduced murine lymphocytic leukemia P388 (P388/BCRP) cells but not in these parental cells. In addition, gefitinib sensitized human colon cancer HT-29 cells, which endogenously express BCRP, to SN-38. Gefitinib increased intracellular accumulation of topotecan in K562/BCRP cells and suppressed ATP-dependent transport of estrone 3-sulfate, a substrate of BCRP, in membrane vesicles from K562/BCRP cells. These results suggest that gefitinib may overcome BCRP-mediated drug resistance by inhibiting the pump function of BCRP. Furthermore, P388/BCRP-transplanted mice treated with combination of irinotecan and gefitinib survived significantly longer than those treated with irinotecan alone or gefitinib alone. In conclusion, gefitinib is shown to interact with BCRP. BCRP expression in a certain sort of cells is supposed to be one of the determinants of gefitinib sensitivity. Gefitinib inhibits the transporter function of BCRP and reverses BCRP-mediated drug resistance both in vitro and in vivo.     

A restriction endonuclease assay for expression of human alpha-amylase isozymes

BACKGROUND: The alpha-amylase isozymes can be detected separately by electrophoresis; however, sometimes the identification is difficult because of their microheterogeneity. In the present study, we tried to establish a convenient method for the detection of alpha-amylase isozyme expression. METHODS: The procedure is based on three different restriction sites presented in those genes; a PstI site in both AMY 2A and 2B genes, a HaeII site in both AMY 1 and 2A genes, and a BamHI site in AMY 2B gene. After amplification from total tissue RNAs by RT-PCR with primers that were able to cover each exon, the products were cleaved with corresponding restriction endonucleases. RESULTS: This method was applied to human samples from the parotid gland, liver (non-hepatoma), hepatoma and white blood cells (WBCs). The results indicated that the parotid gland and hepatoma (also liver) clearly expressed AMY 1 and AMY 2B genes, respectively. However, AMY 2B gene was also expressed apparently in WBCs, which produced salivary-type isozyme of the alpha-amylase, although the amylase protein was not able to identify for the hepatic isozyme. CONCLUSIONS: The method presented here might be convenient and useful for the determination of alpha-amylase isozyme expression in humans.     

Primary care perspective and implementation of a multidisciplinary,institutional prostate cancer screening algorithm embedded in the electronic health record

Purpose

In response to controversy regarding prostate cancer (CaP) screening recommendations, a consolidated Duke Cancer Institute (DCI) multidisciplinary algorithm for CaP screening was developed and implemented. We conducted an online survey within the year following its implementation to assess primary care provider (PCP) attitudes and adoption as well as to evaluate how this program affects screening rates.

Effects of life away from home and physical exercise on nutrient intake and blood/serum parameters among girl students in Japan

This study was initiated to examine if the life away from home and participation in sport activities affect nutritional health among girl university students. For this purpose, anthropometric data, peripheral blood and spot urine samples, 24-hour food duplicate samples, and answers to questionnaires were collected from 71 girl students at 19 to 23 years of ages who provided informed consent to participate in the study. Of the 71 participants, 29 and 42 participants lived in their homes or outside, respectively, and 23 subjects participated in sport activities whereas 48 subjects did not. Hematology, serum biochemistry and nutrient intakes were evaluated in comparison with the life conditions (home vs. dormitory, boarding house, etc.) and participation in sport activities. The population studied had insufficient intake of energy, protein, and minerals such as Ca and Fe. Those who lived in home or participated in sport activities took more energy and protein (although not the two minerals) than others. Skipping of breakfast was more common among those who lived away from home and had no sport activity. Thus, two social factors of life in home and participation in sport clubs contribute favorably for better food habits, but not necessarily improved intakes of Ca and Fe.