PM2.5 exposure aggravates left heart failure induced pulmonary hypertension.

Particulate matter 2.5 (PM2.5) exposure is high risk to cardiovascular diseases.

[Culture and identification of fibroblast from human endometriosis].

Objective: To establish the model of cultivating and identifying fibroblast from human endometriosis (HEFC) in vitro.

Methods: The tissues of human endometriotic cysts of ovary were digested by collagenases I, II and IV The resulting cells were purified by centrifugation and differential adhesion. HEFC was identified by observing the morphologic changes under an inverted microscope and the expressions of vimentin, α-SMA (α-smooth muscle actin) and keratin were detected by immunocytochemistry.

Prevention of osteoporosis in mice after ovariectomy via allograft of microencapsulated ovarian cells.

It is believed that estrogen deficiency is one of the major risk factors associated with osteoporosis. To investigate the effects of the transplantation of microencapsulated ovarian cells in estrogen-deficient mice, ovarian cells from female Kunming (KM) mice (6-weeks old) were separated, cultured, and microencapsulated with alginic acid-polylysine-alginic acid. Female KM mice (8-weeks old) were randomly separated into three groups: intact (normal), ovariectomized (OVX), and treatment (OVX+ implantation).

Gonadotropin stimulation as a challenge to calibrate cisplatin induced ovarian damage in the female rat.

Cisplatin administration for treatment of cancer causes damage to the ovaries, potentially leading to ovarian failure. To extend our previous work, we tested the hypothesis that serum anti-Mullerian hormone (AMH) levels after ovarian stimulation can be used as a biomarker to calibrate the degree of ovarian damage following cisplatin. Female rats were injected with two weekly doses of cisplatin followed by an injection of pregnant mare serum gonadotropin to stimulate the ovaries.

Baseline and stimulated serum inhibin levels as biomarkers of cisplatin-induced ovarian damage in female rats.

Objective: Chemotherapeutic agents, such as cisplatin, injure the ovary. It was hypothesized that serum inhibins can serve as biomarkers of ovarian damage from cisplatin.

Study Design: Adult female rats were administered cisplatin and afterward pregnant mare serum gonadotropin (PMSG) was given to stimulate ovarian inhibin production.

Serum and ovarian Müllerian inhibiting substance, and their decline in reproductive aging.

The objectives of this study were to identify whether there is a decline in Müllerian inhibiting substance (MIS) in the female rat during chronological aging, and to define the physiological basis of aging-related changes in MIS. The results demonstrate that there is an exponential decline in both serum and ovarian levels of MIS with increasing female age, and that the histologic origin for the reduction in serum levels of MIS is a decline in the number of small ovarian follicles expressing MIS.

Müllerian inhibiting substance as a novel biomarker of cisplatin-induced ovarian damage.

Müllerian inhibiting substance (MIS) has been investigated as a possible serum biomarker in human aging to estimate the number of female germ cells remaining. Cisplatin is an effective chemotherapeutic agent that is associated with ovarian injury. In this study, we tested the hypothesis that decreasing serum MIS can serve as a biomarker of ovarian damage after cisplatin.