The first identification of cronstedtite in Cu-Ni-PGE ores of the Talnakh intrusion.

We present new mineralogical data of cronstedtite from the Southern-2 orebody, located in the South-Western branch of the Talnakh intrusion (Noril'sk area) composed of massive sulfides in which the total amount of oxides and silicates does not exceed 1-3 vol%. The petrographic and mineralogical features of these ores indicated occurrence of fine-grained, fibrous needle like clusters < 50-µm-sized grains of cronstedtite (7.09 Å along its c-axis).

Zinc-Intercalated Halloysite Nanotubes as Potential Nanocomposite Fertilizers with Targeted Delivery of Micronutrients.

This study reports on the development of nanocomposites utilizing a mineral inhibitor and a micronutrient filler. The objective was to produce a slow release fertilizer, with zinc sulfate as the filler and halloysite nanotubes as the inhibitor. The study seeks to chemically activate the intercalation of zinc into the macro-, meso-, and micropores of the halloysite nanotubes to enhance their performance.

Preparation, Features, and Efficiency of Nanocomposite Fertilisers Based on Glauconite and Ammonium Dihydrogen Phosphate.

This paper studies the chemical and mechanochemical preparation of glauconite with ammonium dihydrogen phosphate (ADP) nanocomposites with a ratio of 9:1 in the vol.% and wt.%, respectively.

Estrogen Receptor Complex to Trigger or Delay Estrogen-Induced Apoptosis in Long-Term Estrogen Deprived Breast Cancer.

Antiestrogen therapy of breast cancer has been a "gold standard" of treatment of estrogen receptor (ER)-positive breast cancer for decades. Resistance to antiestrogen therapy may develop, however, a vulnerability in long-term estrogen deprived (LTED) breast cancer cells was discovered. LTED breast cancer cells may undergo estrogen-induced apoptosis within a week of treatment with estrogen .

Downregulation of 15-hydroxyprostaglandin dehydrogenase during acquired tamoxifen resistance and association with poor prognosis in ERα-positive breast cancer.

Aim: Tamoxifen (TAM) resistance remains a clinical issue in breast cancer. The authors previously reported that 15-hydroxyprostaglandin dehydrogenase () was significantly downregulated in tamoxifen-resistant (TAMr) breast cancer cell lines. Here, the authors investigated the relationship between HPGD expression, TAM resistance and prediction of outcome in breast cancer.

Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer.

Patients with long-term estrogen-deprived breast cancer, after resistance to tamoxifen or aromatase inhibitors develops, can experience tumor regression when treated with estrogens. Estrogen's antitumor effect is attributed to apoptosis via the estrogen receptor (ER). Estrogen treatment can have unpleasant gynecologic and nongynecologic adverse events; thus, the development of safer estrogenic agents remains a clinical priority.

Pharmacology and Molecular Mechanisms of Clinically Relevant Estrogen Estetrol and Estrogen Mimic BMI-135 for the Treatment of Endocrine-Resistant Breast Cancer.

Long-term estrogen deprivation (LTED) with tamoxifen (TAM) or aromatase inhibitors leads to endocrine-resistance, whereby physiologic levels of estrogen kill breast cancer (BC). Estrogen therapy is effective in treating patients with advanced BC after resistance to TAM and aromatase inhibitors develops. This therapeutic effect is attributed to estrogen-induced apoptosis via the estrogen receptor (ER).

The Structure-Function Relationship of Angular Estrogens and Estrogen Receptor Alpha to Initiate Estrogen-Induced Apoptosis in Breast Cancer Cells.

High-dose synthetic estrogen therapy was the standard treatment of advanced breast cancer for three decades until the discovery of tamoxifen. A range of substituted triphenylethylene synthetic estrogens and diethylstilbestrol were used. It is now known that low doses of estrogens can cause apoptosis in long-term estrogen deprived (LTED) breast cancer cells resistant to antiestrogens.

On the organization of receptive fields of retinal spot detectors projecting to the fish tectum: Analogies with the local edge detectors in frogs and mammals.

Responses of ON- and OFF-ganglion cells (GCs) were recorded extracellularly from their axon terminals in the medial sublamina of tectal retino-recipient layer of immobilized cyprinid fish (goldfish and carp). These units were recorded deeper than direction selective (DS) ones and at the same depth where responses of orientation selective (OS) GCs were recorded. Prominent responses of these units are evoked by small contrast spots flickering within or moving across their visual field.

Updated functional segregation of retinal ganglion cell projections in the tectum of a cyprinid fish-further elaboration based on microelectrode recordings.

Single-unit responses of retinal ganglion cells (GCs) were recorded extracellularly from their axonal terminals in the tectum opticum (TO) of the intact fish (goldfish, carp). The depths of retinal units consecutively recorded along the track of the microelectrode were measured. At the depth of around 50 μm, the responses of six types of direction-selective (DS) GCs were regularly recorded.

Putative targets of direction-selective retinal ganglion cells in the tectum opticum of cyprinid fish.

Responses of direction selective (DS) units of retinal and tectal origin were recorded extracellularly from the tectum opticum (TO) of immobilized fish. The data were collected from three cyprinid species - goldfish, carp and roach. Responses of the retinal DS ganglion cells (GCs) were recorded from their axon terminals in the superficial layers of TO.

Endoxifen, 4-Hydroxytamoxifen and an Estrogenic Derivative Modulate Estrogen Receptor Complex Mediated Apoptosis in Breast Cancer.

Estrogen therapy was used to treat advanced breast cancer in postmenopausal women for decades until the introduction of tamoxifen. Resistance to long-term estrogen deprivation (LTED) with tamoxifen and aromatase inhibitors used as a treatment of breast cancer inevitably occurs, but unexpectedly low-dose estrogen can cause regression of breast cancer and increase disease-free survival in some patients. This therapeutic effect is attributed to estrogen-induced apoptosis in LTED breast cancer.

A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers.

Prostate and breast cancer are the two cancers with the highest incidence in men and women, respectively. Here, we focus on the known biology of acquired resistance to antihormone therapy of prostate and breast cancer and compare laboratory and clinical similarities in the evolution of the disease. Laboratory studies and clinical observations in prostate and breast cancer demonstrate that cell selection pathways occur during acquired resistance to antihormonal therapy.

Sex steroid induced apoptosis as a rational strategy to treat anti-hormone resistant breast and prostate cancer.

The combined incidence and the extended disease course of breast and prostate cancer is a major challenge for health care systems. The solution for society requires an economically viable treatment strategy to maintain individuals disease free and productive, so as to avoid the fracture of the family unit. Forty years ago, translational research using the antiestrogen tamoxifen was targeted to estrogen receptor (ER) positive micrometastatic tumor cells and established the long-term antihormone adjuvant treatment strategy used universally today.

Color properties of the motion detectors projecting to the goldfish tectum.

Interactions between color channels (long-wave (L), middle-wave (M) and short-wave (S)) in the receptive field of direction-selective (DS) and orientation-selective (OS) ganglion cells (GCs) were investigated with combined selective stimulation of pairs of cone types (L and M, L and S, M and S). In the experiments with DS GCs of both ON and OFF types, it was shown that: (1) M and S channels were synergistic relative to each other and opponent to L channel. (2) Three-parameter signal (from L, M and S cones) is transformed to one-parameter signal at the output of DS GC, thus illustrating the principle of univariance.

Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells.

Unlabelled: Estrogen (E2) exerts a dual function on E2-deprived breast cancer cells, with both initial proliferation and subsequent induction of stress responses to cause apoptosis. However, the mechanism by which E2 integrally regulates cell growth or apoptosis-associated pathways remains to be elucidated. Here, E2 deprivation results in many alterations in stress-responsive pathways.

The molecular, cellular and clinical consequences of targeting the estrogen receptor following estrogen deprivation therapy.

During the past 20 years our understanding of the control of breast tumor development, growth and survival has changed dramatically. The once long forgotten application of high dose synthetic estrogen therapy as the first chemical therapy to treat any cancer has been resurrected, refined and reinvented as the new biology of estrogen-induced apoptosis. High dose estrogen therapy was cast aside once tamoxifen, from its origins as a failed "morning after pill", was reinvented as the first targeted therapy to treat any cancer.

Estrogen receptor mutations found in breast cancer metastases integrated with the molecular pharmacology of selective ER modulators.

The consistent reports of mutations at Asp538 and Tyr537 in helix 12 of the ligand-binding domain (LBD) of estrogen receptors (ERs) from antihormone-resistant breast cancer metastases constitute an important advance. The mutant amino acids interact with an anchor amino acid, Asp351, to close the LBD, thereby creating a ligand-free constitutively activated ER. Amino acids Asp 538, Tyr 537, and Asp 351 are known to play a role in either the turnover of ER, the antiestrogenic activity of the ER complex, or the estrogen-like actions of selective ER modulators.

Opposing motion inhibits responses of direction-selective ganglion cells in the fish retina.

Inhibitory influences in receptive fields (RFs) of the fish retinal direction-selective ganglion cells (DS GCs) were investigated. Responses of the fast retinal DS GCs were recorded extracellularly from their axon terminals in the superficial layer of tectum opticum of immobilized fish. The data were collected from two cyprinid species - Carassius gibelio, a wild form of the goldfish, and the barbel fish Labeobarbus intermedius.

Color properties of the motion detectors projecting to the goldfish tectum: II. Selective stimulation of different chromatic types of cones.

Sensitivity to the sign of contrast of direction-selective (DS) and orientation-selective (OS) ganglion cells (GCs) was investigated with selective stimulation of different chromatic types of cones. It was shown that the DS GCs that were classified with the use of achromatic stimuli as belonging to the ON type responded to selective stimulation of the long-wave cones as the ON type also, while the stimulation of middle-wave or short-wave cones elicited the OFF type responses. Character of the responses of DS GCs of the OFF type was exactly the opposite.

Pharmacological relevance of endoxifen in a laboratory simulation of breast cancer in postmenopausal patients.

Background: Tamoxifen is metabolically activated via a CYP2D6 enzyme system to the more potent hydroxylated derivatives 4-hydroxytamoxifen and endoxifen. This study addresses the pharmacological importance of endoxifen by simulating clinical scenarios in vitro.

Methods: Clinical levels of tamoxifen metabolites in postmenopausal breast cancer patients previously genotyped for CYP2D6 were used in vitro along with clinical estrogen levels (estrone and estradiol) in postmenopausal patients determined in previous studies.

Novel selective estrogen mimics for the treatment of tamoxifen-resistant breast cancer.

Endocrine-resistant breast cancer is a major clinical obstacle. The use of 17β-estradiol (E2) has reemerged as a potential treatment option following exhaustive use of tamoxifen or aromatase inhibitors, although side effects have hindered its clinical usage. Protein kinase C alpha (PKCα) expression was shown to be a predictor of disease outcome for patients receiving endocrine therapy and may predict a positive response to an estrogenic treatment.