Search

On the other hand, Giannaccare et al. [[192]] conducted a study on patients with MGD having subjective symptoms (OSDI>= 13) and at least one clinical sign of MGD, such as terminal ductal obstruction, plugging of the meibomian glands, turbid secretions, inflammation and swelling of the eyelid margins, or poor meibum secretions. One RCT [[423]] and two observational studies [[429]] assessed improvements in meibomian gland orifices and surrounding findings and report that minocycline oral administration can improve meibomian gland orifices and surrounding findings in patients with MGD and meibomitis. Additionally, Ibrahim et al. [[279]] show that meibomian gland acinar density, shortest and longest acinar diameter, and inflammatory cell density were significantly associated with BUT, fluorescein staining score, Rose Bengal staining, decreased lipid expression from the meibomian gland orifices, meibomian gland dropout, and ocular surface tear evaporation rate. In 22 patients without atrophy of the meibomian gland, after treatment with the cleansing agent, meibography indicated significant improvements in the meibomian gland orifices/surrounding findings (eyelid margin vascularity), quality of meibum, and BUT. [Extracted from the article]

Acute nutrient ingestion leads to a rapid inhibition of bone resorption while effects on makers of bone formation are less marked or absent, suggesting that there is a transient shift toward skeletal accretion in the immediate postprandial period. The cellular bases for these effects are not clear. Glucose-dependent insulinotropic peptide (GIP), a known modulator of glucose-induced insulin secretion, is secreted from intestinal endocrine cells in response to nutrient ingestion. In addition to the effect of GIP on pancreatic [beta]-cells, GIP receptors are expressed by osteoblastic cells in bone, suggesting a role for this incretin hormone in bone formation. To determine whether GIP also plays a role in the anti-resorptive effect of nutrient ingestion, osteoclasts were analyzed for the presence of GIP receptors by PCR, immunohistochemical and immunocytochemical analyses of bone tissue, and freshly isolated mature osteoclasts and osteoclast-like cells cultured in vitro. Osteoclast function was assessed by fetal long bone resorption assay and by use of the Osteologic disc assay. Our results demonstrate that GIP receptor transcripts and protein are present in osteoclasts. In addition, with the use of an in vitro organ culture system and mature osteoclasts, GIP was found to inhibit bone resorption in the organ culture system and the resorptive activity of mature osteoclasts. These data are consistent with the hypothesis that GIP inhibits bone breakdown through a direct effect on osteoclast-resorptive activity and suggest one mechanism for the postprandial reduction in markers of bone breakdown. nutrition; bone breakdown; incretin

The article investigates the identification of breast cancer-associated gene 3 (BCA3) as a novel Rac1-interacting partner in osteoclasts in the U.S. The study conducted a yeast two-hybrid screen using a complementary deoxyribonucleic acid (cDNA) library prepared from osteoclast-like cells as prey and either native Rac1 or constitutively active Rac1 as bait. The study concludes that BCA3 is a novel Rac1-interacting protein.

Acute nutrient ingestion leads to a rapid inhibition of bone resorption while effects on makers of bone formation are less marked or absent, suggesting that there is a transient shift toward skeletal accretion in the immediate postprandial period. The cellular bases for these effects are not clear. Glucose-dependent insulinotropic peptide (GIP), a known modulator of glucose-induced insulin secretion, is secreted from intestinal endocrine cells in response to nutrient ingestion. In addition to the effect of GIP on pancreatic 3-cells, GIP receptors are expressed by osteoblastic cells in bone, suggesting a role for this incretin hormone in bone formation. To determine whether GIP also plays a role in the anti-resorptive effect of nutrient ingestion, osteoclasts were analyzed for the presence of GIP receptors by PCR, immunohistochemical and immunocytochemical analyses of bone tissue, and freshly isolated mature osteoclasts and osteoclast-like cells cultured in vitro. Osteoclast function was assessed by fetal long bone resorption assay and by use of the Osteologic disc assay. Our results demonstrate that GIP receptor transcripts and protein are present in osteoclasts. In addition, with the use of an in vitro organ culture system and mature osteoclasts, GIP was found to inhibit bone resorption in the organ culture system and the resorptive activity of mature osteoclasts. These data are consistent with the hypothesis that GIP inhibits bone breakdown through a direct effect on osteoclast-resorptive activity and suggest one mechanism for the postprandial reduction in markers of bone breakdown. [ABSTRACT FROM AUTHOR]