Curcuminoids are functional food additives, and the effect on gonadal hormone biosynthesis remains unclear. Gonads contain 3β-hydroxysteroid dehydrogenase isoforms, h 3β-HSD2 (humans) and r3β-HSD1 (rats), which catalyse pregnenolone into progesterone. The potency and mechanisms of curcuminoids to inhibit 3β-HSD activity were explored. The inhibitory potency was bisdemethoxycurcumin (IC 50 , 1.68 µM) >demethoxycurcumin (3.27 µM) > curcumin (13.87 µM) > tetrahydrocurcumin (109.0 µM) > dihydrocurcumin and octahydrocurcumin on KGN cell h 3β-HSD2, while that was bisdemethoxycurcumin (1.22 µM) >demethoxycurcumin (2.18 µM) > curcumin (4.12 µM) > tetrahydrocurcumin (102.61 µM) > dihydrocurcumin and octahydrocurcumin on testicular r 3β-HSD1. All curcuminoids inhibited progesterone secretion by KGN cells under basal and forskolin-stimulated conditions at >10 µM. Docking analysis showed that curcuminoids bind steroid-active site with mixed or competitive mode. In conclusion, curcuminoids inhibit gonadal 3β-HSD activity and de-methoxylation of curcumin increases inhibitory potency and metabolism of curcumin by saturation of carbon chain losses inhibitory potency.

Bone tumors are deadly and incurable diseases that invade large areas of bone, resulting in bone defects. Traditional therapies combining surgery, chemotherapy, and radiation have reached their limit of efficacy, motivating efforts to develop new therapeutic methods. Fortunately, the development of biomaterials provides innovative options for bone tumor treatment. Suitable biomaterials are capable of simultaneously providing tumor therapy and promoting bone regeneration. This review summarizes recent progress in the effort to achieve new strategies for bone tumor treatment using biomaterials, focusing on the innovative scaffold design. It also discusses the development of nanocarrier-based drug delivery systems and hyperthermia therapy for bone tumor treatment. In the future, biomaterial-based strategies are likely to become the most effective and reliable options for treating bone tumors, and they have the potential to greatly improve the prognosis and quality of life for patients.

The balanced development of compulsory education has been given due and lengthy coverage in the "Outline of China's National Plan for Medium and Long-Term Education Reform and Development (2010-2020)" which, to some extent, reflects the needs of our time and the demands of the general public. However, detailed analyses reveal that many aspects remain to be improved. The authors hold that the balanced development of compulsory education should be people-oriented and a fundamental right of modern citizens. The paper makes a preliminary research on the question of balance in compulsory education, discussing participants, potential to achieve balance, and how to evaluate the ongoing development towards balance.

Tetramethyl bisphenol A (TMBPA) is a widely used flame retardant. TMBPA has been a toxic to Leydig cells in puberty, but it remains unclear whether TMBPA has a similar inhibitor effect on fetal Leydig cells (FLCs). This study reported morphological and functional alterations of FLCs in the testes of male offspring at birth after in utero exposure to TMBPA. Pregnant Sprague Dawley rats were dosed via continuous gavage of TMBPA (0, 10, 50, and 200 mg/kg/day) from gestational day 14 to 21. TMBPA markedly raised serum total testosterone level, testicular volume, and FLC number of male offspring at 200 mg/kg dose. The up‐regulation of Insl3, Star, and Cyp11a1 mRNAs was observed after 200 mg/kg TMBPA exposure. After normalization to the number of FLCs, TMBPA significantly reduced Lhcgr and Hsd3b1 expressions at 10 mg/kg, and Cyp17a1 at 200 mg/kg paralleling with their protein levels. TMBPA compromised the expression of Esr1, while increased the expression of Cdk2 and Cdk4 as well as their protein levels. TMBPA particularly increased the phosphorylation of AKT1 and AKT2 at 200 mg/kg. In conclusion, the present study suggests that TMBPA may promote FLC proliferation via ESR1‐CDK2/4‐AKT pathway, while inhibits the function of FLCs by reducing steroidogenic enzyme activity.

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