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Subject:
From:
Debra Swank <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Thu, 10 May 2018 02:29:46 -0400
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Greetings All, 

Four new studies: 

Title:  Quercetin improves postpartum hypogalactia in milk‐deficient mice via stimulating prolactin production in pituitary gland

Journal:  Phytotherapy Research

Authors:  Lin M, Wang N, Yao B, Zhong Y, Lin Y, You T.

Abstract:  "Postpartum dysgalactia is a common clinical problem for lactating women. Seeking out the safe and efficient phytoestrogens will be a promising strategy for postpartum dysgalactia therapy. In this study, the postpartum mice within four groups, including control group, the model group, and the treatment groups intragastrically administrated with normal saline, bromocriptine, bromocriptine plus 17α-ethinyl estradiol, and bromocriptine plus quercetin, respectively, were used. The results showed that quercetin, a kind of natural phytoestrogen, could efficiently promote lactation yield and mammary gland development in the agalactosis mice produced by bromocriptine administration. Mechanically, quercetin, such as 17α-ethinyl estradiol, significantly stimulated prolactin (PRL) production and deposition in the mammary gland in the agalactosis mice determined by western blotting, quantitative polymerase chain reaction, and enzyme-linked immunosorbent assay, respectively. Furthermore, quercetin could increase the expression of β-casein, stearoyl-CoA desaturase, fatty acid synthase, and α-lactalbumin in the breast tissues that are responsible for the production of fatty acid, lactose, and galactose in the milk at the transcriptional level determined by quantitative polymerase chain reaction. Specifically, quercetin promoted primary mammary epithelial cell proliferation and stimulated prolactin receptor (PRLR) expression probably via AKT activation in vitro. In conclusion, this study indicates that estrogen-like quercetin promotes mammary gland development and lactation yield in milk-deficient mice, probably via stimulating PRL expression and release from the pituitary gland, as well as induces PRLR expression in primary mammary epithelial cells."

https://www.ncbi.nlm.nih.gov/pubmed/29671937


Title:  Contribution of sex steroids and prolactin to the modulation of T and B cells during autoimmunity

Journal:  Autoimmunity Reviews

Authors:  Recalde G, Moreno-Sosa T, Yúdica F, Quintero CA, Sánchez MB, Jahn GA, Kalergis AM, Mackern-Oberti JP.

Abstract:  "In this review we discuss how sex steroids and prolactin affect regulation and responsiveness of B and T cells. Sex hormones exert profound effects on several physiological processes of non- reproductive tissues. In the immune system, several studies with experimental models for SLE have shown a noticeable pro-inflammatory role for ERα, contributing to disease development reflected in proteinuria and renal pathology. On the other hand, ERβ appears to have an anti- inflammatory and immunosuppressive effect. Estrogen/ERα signaling induced an increase of Th17 cells in lymph nodes as well as the expression of its correspondent chemokine receptor CCR6 during collagen induced arthritis acute phase. High levels of anti- DNA antibodies and increased mortality was observed when given high E and prolactin doses to NZB/NZW mice, as compared with mice receiving low E and prolactin doses, or high E and low prolactin doses. Intracellular progesterone receptors have been detected in TCD4+ cells but in contrast as observed with ERs, it suppresses T cell dependent responses. Progestagen administration on female NZB/NZW mice decreased anti DNA IgG, improved survival, decreased glomerulonephritis and proteinuria."

https://www.sciencedirect.com/science/article/pii/S1568997218300569?via%3Dihub


Title:  Observational studies on macroprolactin in a routine clinical laboratory

Journal:  Clinical Chemistry and Laboratory Medicine

Authors:  Barth JH, Lippiatt CM, Gibbons SG, Desborough RA.

Abstract:  

BACKGROUND: "It is now recommended that all samples with raised prolactin should be examined for the presence of macroprolactin. We performed a retrospective review of our experience of macroprolactin to determine the incidence and the natural history of macroprolactin."

METHODS: "A retrospective study of macroprolactin was made in a large clinical laboratory. Macroprolactin was measured on those samples where it is requested and where the total prolactin is >1000 mIU/L. Prolactin was measured using the Siemens Centaur and macroprolactin was measured following polyethylene glycol (PEG)-precipitation."

RESULTS: "The incidence of macroprolactin in samples where the total prolactin was >1000 mIU/L was 36/670 (5.4%). During this period, 12,064 samples were received for prolactin analysis. Over the period since 2006, 22 subjects had a sample with an isolated macroprolactin measurement followed by another sample without macroprolactin after a median period of 0.46 years. Twenty-five subjects had multiple consecutive measurements of macroprolactin lasting a median period of 2.1 years. Fourteen subjects had more than six samples which had been subjected to PEG precipitation. In these subjects, the reproducibility of PEG precipitation over a median of 6 years was 1.1% CV (recovery 75% [26-110] (median [range]))."

CONCLUSIONS: "The presence of macroprolactin can change over time and we cannot advise that once a test for macroprolactinemia has been performed that it is not necessary to repeat the investigation if a subsequent sample is hyperprolactinemic; nor can one assume that macroprolactin will not develop even if it has been excluded previously."

https://www.degruyter.com/view/j/cclm.ahead-of-print/cclm-2018-0074/cclm-2018-0074.xml


Title: Prolactin Induced Protein (PIP) is a potential biomarker for early stage and malignant breast cancer (open access) 

Journal:  The Breast

Authors: Anju Gangadharan, Themba Nyirenda, Kishan Patel, Nydia Jaimes-Delgadillo, Dominique Coletta, Takemi Tanaka, Ayal C. Walland, Zena Jameel, Srinivasa Vedantam, Sittinon Tang, Ciaran Mannion, Grace Y. Lee, Andre Goy, Andrew Pecora, K. Stephen Suh

Abstract:

"Objectives: Breast cancer (BC) is the second leading cause of cancer-related mortality in women. Bioinformatic analysis and expression screening showed that Prolactin Induced Protein (PIP) was differentially expressed in BC. The objective of this investigation was to characterize the expression pattern of PIP, an aspartyl proteinase, in malignant and non-malignant breast tissues."  

"Materials and Methods: Real time quantitative PCR was employed to analyze PIP and androgen receptor (AR) mRNA levels in BC cell lines and 190 normal tissues and tumor samples. The tumor specimens were categorized based on TNM classification, anatomic stage, histologic grade and molecular subtype and expression pattern evaluated. To detect protein levels, immunohistochemistry followed by semi quantitative scoring was employed in the examination of 517 normal, benign, and invasive BC tissues. Results: We observed substantial downregulation of PIP transcription in cancer samples compared to normal breast tissue. mRNA levels were significantly downregulated (93 fold, P < 0.005) in advanced
grades compared to lower grades. Transcript levels were also significantly lower (22 fold, P < 0.05) in triple negative tumors compared to hormone receptor positive tumors. Significant downregulation was observed in early stage samples of triple negative and hormone receptor positive tumors. Though PIP protein showed a wide range of expression levels in BC, early stage samples showed significant
downregulation."

"Conclusions: PIP mRNA is significantly downregulated in early stage BC compared to normal breast tissue.  Consequently, low PIP mRNA expression in BC tissues could potentially be used as a tissue based biomarker to assist pathologists in confirmation of early stage BC diagnosis."

https://www.thebreastonline.com/article/S0960-9776(18)30063-8/pdf

With best regards,

Debra Swank, RN BSN IBCLC
Ocala, Florida USA
MoreThanReflexes Education
http://www.MoreThanReflexes.org

             ***********************************************

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