Hyperprolactinemia is a common endocrine disease that can be associated with significant morbidity and disability in the population. A systematic review of literature sources on the diagnosis and treatment results in patients with hyperprolactinemia, including drug-resistant micro- and macroadenomas of the pituitary gland, was carried out in order to highlight the most significant practical recommendations. The purpose of this literature review is to provide algorithms for differential diagnosis and clinical observation of patients, to compare the efficacy and side effects of drugs, surgeries, and radiation therapy in the treatment of hyperprolactinemia. Prolactinomas are the most common pituitary adenomas in older children. Their share in the structure of pituitary adenomas is about 50 %. The clinical picture depends on the age, sex of the child, volume and characteristics of tumor growth. The leading clinical manifestations of hyper­prolactinemia are disorders of the reproductive system, including signs of the development of secondary hypogonadotropic hypogonadism, sexual dysfunction, psychoemotional disorders, and endocrine and metabolic disorders. The main criterion for the diagnosis of hyperprolactinemia is the concentration of prolactin in the blood serum, which is above the upper limit of the physio­logical norm. The primary step in the treatment of patients with pituitary macroadenoma is to control the compression effects of the tumor, including compression of the optic chiasm, followed by restoration of gonadal function. The main areas of treatment for hyperprolactinemia are restoration and maintenance of the normal function of the gonads; restoration of fertility; prevention of osteoporosis. Dopamine receptor agonists are the gold standard in the treatment of hyperprolactinemia. However, some people do not respond satisfactorily to these drugs. In this case, in the presence of pituitary tumors, in addition to drug treatment, surgery and radiation therapy are used. But surgery and radiation therapy are not the primary methods of choice for the management of patients with prolactin-secreting pituitary adenomas; first of all, preference is given to drug therapy. The prognosis of the course of prolactinomas is favorable and is based on the results of dynamic observation and the presence of markers of the aggressiveness of this adenoma.

/pdf/clinical-features-of-hyperprolactinemia-in-children-modern-2uycegzv.pdf

Clinical features of hyperprolactinemia in children: modern methods of diagnosis and treatment

Numerical study of NOx emission reduction by MILD and air staged synergistic combustion in a new type of coke oven flue

Over the last two decades, advancements in nanomaterials and nanoscience have paved the path for the emergence of nano-medical convergence science, significantly impacting healthcare. In our review, we highlight how... 

Revolutionizing healthcare: inorganic medicinal nanoarchitectonics for advanced theranostics

Abstract Context Prolactinomas are the most prevalent functional pituitary neuroendocrine tumors (PitNETs), and they are invasive to surrounding anatomic structures. The detailed mechanisms of invasion are not yet clear. Objective We explored the role of PBK phosphorylation in the proliferation and invasion of prolactinomas and its possible mechanism. Results We report that PBK directly binds to and is phosphorylated at Thr9 by cyclin‐dependent kinase 5 (CDK5), which promotes GH3 cell EMT progression and proliferation. Phosphorylation of PBK at Thr9 (pPBK‐T9) by CDK5 enhances the stability of PBK. p38 is one of the downstream targets of PBK, and its phosphorylation is reduced as pPBK‐T9 increases in vivo and in vitro. Furthermore, we found that pPBK‐T9 is highly expressed in invasive PitNETs and was significantly correlated with invasion by univariate and multivariate analyses. Conclusions Phosphorylation of PBK at Thr9 by CDK5 promotes cell proliferation and EMT progression in prolactinomas.

Phosphorylation of PBK at Thr9 by CDK5 correlates with invasion of prolactinomas

We present a hyaluronic acid (HA)-based nanoplatform (CMGH) integrating starvation therapy (ST), chemodynamic therapy (CDT), and photothermal therapy (PTT) for targeted cancer treatment. CMGH fabrication involved the encapsulation of glucose oxidase (GOx) within a copper-based metal-organic framework (CM) followed by surface modification with HA. CMGH exerts its antitumor effects by catalyzing glucose depletion at tumor sites, leading to tumor cell starvation and the concomitant generation of glucuronic acid and H2O2. The decreased pH and elevated H2O2 promote the Fenton-like reaction of Cu ions, leading to hydroxyl radical production. HA modification enables targeted accumulation of CMGH at tumor sites via the CD44 receptor. Under near-infrared light irradiation, CM exhibits photothermal conversion capability, enhancing the antitumor effects of CMGH. In vitro and in vivo studies demonstrate the effective inhibition of tumor growth by CMGH. This study highlights the potential of CMGH as a targeted cancer therapeutic platform. 

Hyaluronic acid-based multifunctional nanoplatform for glucose deprivation-enhanced chemodynamic/photothermal synergistic cancer therapy

Background Prolactinoma is the most common type of pituitary tumors, and its resultant tumor occupying and hormone disturbance greatly damage the health of patients. In this study, we investigated a protein kinase-PDZ Binding Kinase (PBK)/T-LAK Cell-Originated Protein Kinase (TOPK) as a candidate protein regulating prolactin (PRL) secretion and tumor growth of prolactinomas. Methods Downloaded prolactinoma transcriptome dataset from Gene Expression Omnibus (GEO) database, and screened differentially expressed genes (DEGs) between normal pituitary tissues and prolactinoma tissues. Then, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs were performed, a protein-protein interaction (PPI) network was constructed and the hub genes were identified. After a literature search, TOPK was presumed as an candidate target regulating the prolactinoma. We found a specific inhibitor of TOPK to investigate its effects on the proliferation, migration, apoptosis and PRL secretion of pituitary tumor cells. Finally, the regulation of TOPK inhibitor on its downstream target-p38 Mitogen Activated Protein Kinase (p38 MAPK) was detected to explore the potential mechanism. Results A total of 361 DEGs were identified, and 20 hub genes were screened out. TOPK inhibitor HI-TOPK-032 could suppress the proliferation & migration and induce apoptosis of pituitary tumor cells in vitro, and reduce PRL secretion and tumor growth in vivo. HI-TOPK-032 also inhibited the phosphorylation level of the downstream target p38 MAPK, suggesting that TOPK inhibitors regulate the development of prolactinoma by mediating p38 MAPK. Conclusion Our study of identification and functional validation of TOPK suggests that this candidate can be a promising molecular target for prolactinoma treatment.

/pdf/pbk-topk-inhibitor-suppresses-the-progression-of-f7h6gr8q.pdf

PBK/TOPK Inhibitor Suppresses the Progression of Prolactinomas

Background Prolactinoma is a functional pituitary adenoma that secretes excessive prolactin. Dopamine agonists (DAs) such as bromocriptine (BRC) are the first-line treatment for prolactinomas, but the resistance rate is increasing year by year, creating a clinical challenge. Therefore, it is urgent to explore the molecular mechanism of bromocriptine resistance in prolactinomas. Activation of the P38 MAPK pathway affects multidrug resistance in tumours. Our previous studies have demonstrated that inhibiting MAPK14 can suppress the occurrence of prolactinoma, but the role of MAPK11/12/13/14 (p38 MAPK) signalling in dopamine agonist-resistant prolactinomas is still unclear. Methods A prolactinoma rat model was established to determine the effect of bromocriptine on MAPK11/12/13/14 signalling. DA-resistant GH3 cells and DA-sensitive MMQ cells were used, and the role of MAPK11/12/13/14 in bromocriptine-resistant prolactinomas was preliminarily verified by western blot, RT-qPCR, ELISA, flow cytometry and CCK-8 experiments. The effects of MAPK11 or MAPK14 on bromocriptine-resistant prolactinomas were further verified by siRNA transfection experiments. Results Bromocriptine was used to treat rat prolactinoma by upregulating DRD2 expression and downregulating the expression level of MAPK11/12/13/14 in vivo experiments. The in vitro experiments showed that GH3 cells are resistant to bromocriptine and that MMQ cells are sensitive to bromocriptine. Bromocriptine could significantly reduce the expression of MAPK12 and MAPK13 in GH3 cells and MMQ cells. Bromocriptine could significantly reduce the expression of MAPK11, MAPK14, NF-κB p65 and Bcl2 in MMQ but had no effect on MAPK11, MAPK14, NF-κB p65 and Bcl2 in GH3 cells. In addition, knockdown of MAPK11 and MAPK14 in GH3 cells by siRNA transfection reversed the resistance of GH3 cells to bromocriptine, and haloperidol (HAL) blocked the inhibitory effect of bromocriptine on MAPK14, MAPK11, and PRL in MMQ cells. Our findings show that MAPK11 and MAPK14 proteins are involved in bromocriptine resistance in prolactinomas. Conclusion Bromocriptine reduces the expression of MAPK11/12/13/14 in prolactinomas, and MAPK11 and MAPK14 are involved in bromocriptine resistance in prolactinomas by regulating apoptosis. Reducing the expression of MAPK11 or MAPK14 can reverse bromocriptine resistance in prolactinomas.

The role of MAPK11/12/13/14 (p38 MAPK) protein in dopamine agonist-resistant prolactinomas.

In this paper, a numerical simulation of the effects of the primary air and secondary air FGR (Flue Gas Recirculation) ratios in lime rotary kiln on combustion characteristics, NOx generation, and limestone calcination degree were studied in detail. The results revealed that two distinct temperature peaks were observed on the temperature profiles. Upon the addition of recirculating flue gas to the primary air, the entrainment effect was enhanced, resulting in a shorter flame length, a lower first peak temperature, and a higher second peak temperature. For the secondary air, the two peak temperatures both decreased due to the low inlet temperature. With an FGR ratio of 0.20, the primary air reduced NOx generation by 22.5%, while the secondary air reduced it by 80.5%. However, they also dropped the final limestone calcination degree. Especially secondary air FGR, it decreased the final calcination by 5.9%, much higher than 1.6% of the primary air. Hence, primary air FGR is a better option for balancing between NOx emissions and quicklime quality. However, in case of high NOx emissions, it is recommended to choose the secondary air FGR and pay attention to prolong the residence time of the limestone in the preheater. 

Numerical simulation of flue gas recirculation in a lime rotary kiln

Prolactinomas have harmful effects on human health. Bromocriptine is the only commercially available drug in China, but about 25% of prolactinoma patients do not respond to it in clinic, its pathogenesis remains unknown. Thus, its pathogenesis needs to be determined to develop new therapeutic methods for prolactinomas. The expression of ERβ, TLR4, and prolactin (PRL) in the pituitary gland of C57BL/6 mice and human prolactinoma specimen was examined by immunofluorescence or immunohistochemistry. The role of TLR4 in prolactinoma was determined using estradiol-induced models of C57BL/6 wild-type and TLR4-/- mice. MMQ cells were treated with estradiol, fulvestrant, and lipopolysaccharide (LPS) or transfected with TLR4 siRNA to study the expression of ERβ, TLR4, and PRL in these cells. Furthermore, the interaction between ERβ and TLR4 was investigated by immunoprecipitation analysis. The expression of PRL and TLR4 was co-located and increased in the pituitary gland of mice and human prolactinoma specimen compared with that in the control specimen. Meanwhile, TLR4 knockout or treatment with the TLR4 inhibitor TAK242 not only significantly inhibited tumor overgrowth but also decreased the expression of PRL in estradiol-treated mice through p38 MAPK pathway regulation. However, MMQ treated with estradiol and LPS enhanced PRL expression than treated with estradiol or LPS alone. Finally, ERβ or TLR4 inhibition prevented the estradiol-induced PRL increase by regulating the TLR4/p38 MAPK pathway in vitro. Estradiol promoted prolactinoma development by activating the TLR4/p38 MAPK pathway through ERβ, and TLR4 is a potential therapeutic target for prolactinoma treatment.

TLR4 inhibition suppresses growth in oestrogen-induced prolactinoma models.

It is highly desirable to precisely observe the real-time location of residual tumor tissues after surgery without interference and further realize postoperative tumor-specific therapy. Herein, glutathione (GSH)-activated in situ transformation of nanosized vanadium (V) oxides (V2O5) to mixed valence vanadium oxides (VOx) was carried out to realize postoperative precision tumor theranostics. Especially, hyaluronic acid-hybridized V2O5 nanoparticles (HA@V2O5 NPs) were in-situ-transformed to HA-hybridized VOx NPs via the reduction of GSH overexpressed in residual tumor. The transformation of V2O5 to VOx could not only generate near-infrared absorption but also endow VOx with the ability to catalyze hydrogen peroxide to produce hydroxyl radicals. By combining receptor-mediated targeting (RMT) toward tumor cells of HA and GSH-activated in situ transformation, HA@V2O5 NPs could be applied to precisely determine the location of residual tumor tissues in real time via photoacoustic (PA) observation without interference of inflammation after surgery and further realize postoperative tumor-specific photothermal/chemodynamic eradication of them. Therefore, the present work opens the way to utilize the combination strategy of RMT and GSH-activated in situ transformation of inorganic metal oxides to meet the need of postoperative precision tumor theranostics. 

Glutathione-Activated In Situ Transformation of Nanosized Vanadium Oxides for Postoperative Precision Tumor Theranostics

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