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NK cells have been the cells most extensively studied, primarily because they constitute the predominant
leukocyte population present in the endometrium at the time of implantation and in early pregnancy
In summary, in vivo animal experiments have shown an inhibitory role of estrogen on peripheral NK cell lytic activity, which is partly due to
suppression of NK cell output by the bone marrow and partly due to suppression of individual NK cell cytotoxicity. However,
in vitro studies so far have failed to show conclusively a direct effect of estrogen on NK cells.
At the progesterone
concentrations believed to be present in the uterus [up to 10−5 m at the maternal-fetal interface (35)], studies consistently show inhibition of lymphocyte proliferation (33) and inhibition of NK cytolytic activity in vitro
The exact role of prolactin in NK cell regulation is unknown.
The overall effects of estrogen on NK cells are likely multifactorial, therefore, and depend on the type of cell affected
as well as the kind of ER expressed by that cell.
It is known that progesterone can directly affect T cell differentiation in vitro, suppressing development of the Th1 pathway and enhancing differentiation along the Th2 pathway (44)
Th1 cells predominantly produce interferon-γ (IFN-γ), IL-2, and TNF-β and are involved in cell-mediated immunity. Th2 cells
produce IL-4, IL-5, IL-6, IL-10, and IL-13 and stimulate humoral immunity
Furthermore, in response to progesterone, γδ T cells produce progesterone-induced blocking factor (PIBF) (54
A defining characteristic of NK cells is their ability to lyse target cells without prior sensitization and without restriction
by HLA antigens.
NK cell function is mainly regulated by IL-2 and IFN-γ
IL-2 causes both NK cell proliferation and enhanced cytotoxicity.
IFN-γ augments NK cytolytic activity, but does not cause NK proliferation. The two cytokines act synergistically to augment
NK cytotoxicity (6).
The largest leukocyte population in the endometrium consists of NK cells named large granulated lymphocytes
there is a significant increase
in the number of uNK cells throughout the secretory phase, which peaks in early pregnancy when uNK cells comprise about 75%
of uterine leukocytes (62)
Second, uNK cell phenotype changes during the normal menstrual cycle and early pregnancy (68)
general proinflammatory effect of estrogen, causing an influx of macrophages and neutrophils, which is
antagonized by progesterone through its receptor (70, 71).
The mechanism of such a progesterone-induced local immunosuppression is unclear.
progesterone plays an important role in proliferation and differentiation of uNK cells (32).
Through promotion of a uterine Th2 environment, progesterone could indirectly affect uNK cell function
The mechanism of this increase in uNK cell numbers has been addressed
in both human and mouse models, and is likely the result of: 1) recruitment of peripheral NK cells to the uterus, and 2) proliferation
of existing uNK cells
prolactin system plays an important role in implantation and the maintenance of pregnancy
the exact pathways of hormonal regulation of NK cells remain to be delineated.
The exact function of uNK cells has not yet been unequivocally determined
uNK cells express a different cytokine profile, compared with resting peripheral NK cells. mRNAs for granulocyte
CSF, M-CSF, GM-CSF, TNF-α, IFN-γ, TGF-β, and leukemia inhibitory factor (LIF) have been found in decidual CD56+ cells
Their increased numbers in early pregnancy, their hormonal dependence, and their close proximity
to the infiltrating trophoblast all suggest that they play an important role in the regulation of the maternal immune response
to the fetal allograft and the control of trophoblast growth and invasion during human pregnancy
role of
uNK cell-derived cytokines on trophoblast growth and differentiation (114, 115, 116, 117).
Th1 immunity to trophoblast is associated with RPL, whereas Th2 immunity is associated
with a successful pregnancy
RPL is associated with Th1 immunity, for which NK cells are partly responsible.
The process of androgen deprivation therapy needs to be re-evaluated. Why? First, the CVD side effects associated with the androgen depletion. Second, the depletion of 3 beta androstanediol that has been shown to bind to ER beta and inhibit growth. As in this study that finds that ER beta activity slows prostate cancer through destabilizing of HIF-1 alpha and by inhibiting VEGF.
The use of non-invasive salivary sampling and a cost-effective, direct enzymeimmunoassay showed a considerable advantage in the present study, compared with previous ones.
Testosterone is secreted into saliva. In saliva, testosterone is not bound to proteins. Thus concentration of testosterone in saliva is quite close to the serum free testosterone level. Currently serum free testosterone is measured by a convenient method in Japan, that reflects only 10% of the correct values. However, the correct measurement of serum free testosterone is quite costly. Collection of saliva is not invasive to subjects, and it can be done without paramedicals. Besides it is relatively cheaper. Acquisition of samples in multiple occasions is possible. These advantages of utilizing saliva will introduce the measurements of salivary testosterone in cohort studies or screening of low testosterone levels in the community.
Saliva is a wonderful marker of early disease detection that leads
to more effective treatment, risk assessment for future oral and
systemic disease, and a simple, non invasive alternative to blood and
urine tests
This pilot study has demonstrated the potential value of using a non-invasive technique (obtaining specimens of saliva) in conjunction with determinations of a predictable mood change.
In conclusion, the satisfactory precision of the analysis and the simple non-invasive sampling procedure suggest that saliva may be used for cortisol measurements in situations where blood sampling is difficult to perform.
Measurement of salivary IgA AGA provided excellent discrimination between those children with coeliac disease and the control groups, and our study suggests that it may provide a rapid, non-invasive method of screening for this disease before intestinal biopsy
prospective study finds that increasing endogenous androgens is associated with low grade epithelial ovarian cancer and inversely associated with high-grade.
DCA can penetrate into the traditional chemotherapy sanctuary sites. Interestingly, it was reported that DCA could penetrate across the BBB,30 exhibiting the potential activity for brain therapy.
Clinical studies of DCA have shown reduced lactate levels
It has been reported that DCA activates the PDH by inhibition of PDK in a dose-dependent manner, and results in increased delivery of pyruvate into the mitochondria
The antitumor activity of DCA on nonsmall cell lung cancer, breast cancer, glioblastomas, and endometrial and prostate cancer cells has been demonstrated
It is well known that many chemotherapeutic agents have a low therapeutic index in brain tumors.
The most common metabolic hallmark of cancer cells is their propensity to metabolize glucose to lactic acid at a high rate even in the presence of oxygen
Pyruvate dehydrogenase kinase (PDK) is a gate-keeping enzyme that regulates the flux of carbohydrates (pyruvate) into the mitochondria
In the presence of activated PDK, pyruvate dehydrogenase (PDH), a critical enzyme that converts pyruvate to acetyl-CoA instead of lactate in glycolysis, is inhibited, limiting the entry of pyruvate into the mitochondria.
the level of Hsp70 was significantly decreased
DCA can penetrate the BBB
It has been reported that DCA treatment resulted in an increase in the proportion of tumor cells in the S phase, showing a decrease in proliferation as well as the induction of apoptosis
Heat shock proteins (HSPs) are involved in protein folding, aggregation, transport, and/or stabilization by acting as a molecular chaperone, leading to the inhibition of apoptosis by both caspase-dependent and/or independent pathways
HSPs are overexpressed in a wide range of human cancers and are implicated in tumor cell proliferation, differentiation, invasion, and metastasis
Considering the fact that high expression of HSPs is essential for cancer survival, the inhibition of HSPs is an important strategy of anticancer therapy.
In addition, after 5 years of continued treatment with oral DCA at a dose of 25 mg/kg, the serum DCA levels are only slightly increased compared with the levels after the first several doses, also showing its safety for oral administration at this dose.
DCA can enter the circulation rapidly after oral administration and then generate the stimulation of PDH activity generally within minutes.
Our in vivo results in tumor tissues indicated that DCA significantly induced ROS production and decreased MMP in tumor tissues
The numbers of microvessels in the DCA treatment groups were significantly decreased, suggesting the potential antiangiogenic effect of DCA
Under hypoxic conditions, hypoxia-inducible factor (HIF-1α) is activated and induces angiogenesis
In addition, HIF-1α can also induce the expression of PDK,48 which can inhibit the activity of PDH
The inhibition effect of DCA on HIF-1α would decrease vascular endothelial growth factor and inhibit angiogenesis
the antiangiogenic effect in the 25 mg/kg treatment group was lower than that in 75 mg/kg or 125 mg/kg treatment groups
In conclusion, DCA induces the apoptosis of C6 cells through the activation of the mitochondrial pathway, arresting the cell cycle of C6 cells in S phase and down-regulating Hsp70 expression.
DCA significantly induced the ROS production and decreased the MMP in tumor tissues. Our in vivo antitumor activity results also indicated that DCA has an antiangiogenic effect