Int J Med Sci
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Objective: Hyperprolactinemia (HPRL) and polycystic ovary syndrome (PCOS) are common causes of infertility in women of reproductive age. A pituitary adenoma (PA) is the most common type of brain tumor that causes HPRL. In the neurosurgical field, the co-existence of PA and PCOS is not common. ⋯ PCOS patients with a PRL level of ≥ 52.9 ng/mL may need to undergo sella MRI for detecting PAs. To help ensure a favorable clinical course for these patients, systematic diagnosis, treatment, and follow-up plan should be established. Therefore, a multidisciplinary approach involving both neurosurgery and gynecology is essential.
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Contemporary scientists need no "p value" and "relative risk" statistics to be exquisitely aware of the increasing prevalence of obesity and complications posed by obesity. It is now well recognized that obesity is strongly associated with type 2 diabetes, hypertension, vascular disease, tumors and reproductive disorders. ⋯ Herein, we mainly review detrimental influences of obesity in the complete process of female reproduction, including hypothalamic-pituitary-ovarian axis, oocyte maturation, embryo and fetal development. In the latter part, we view obesity-induced inflammation and discuss related epigenetic impact on female reproduction.
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Idiopathic pulmonary fibrosis (IPF) is a severe interstitial lung disease; although the recent introduction of two anti-fibrosis drugs, pirfenidone and Nidanib, have resulted in a significant reduction in lung function decline, IPF is still not curable. Approximately 2-20% of patients with IPF have a family history of the disease, which is considered the strongest risk factor for idiopathic interstitial pneumonia. However, the genetic predispositions of familial IPF (f-IPF), a particular type of IPF, remain largely unknown. ⋯ Since several genetic variants associated with the disease have been found in f-IPF, this review systematically summarizes the latest progress in the gene spectrum of the f-IPF population and the underlying mechanisms of f-IPF. The genetic susceptibility variation related to the disease phenotype is also illustrated. This review aims to improve the understanding of the IPF pathogenesis and facilitate his early detection.
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Bone and joint diseases are a group of clinically heterogeneous diseases characterized by various bone strength disorders, bone structural defects and bone mass abnormalities. Common bone diseases include osteoporosis, skeletal dysplasia, and osteosarcoma, and common joint diseases include osteoarthritis, rheumatoid arthritis, and degenerative disc disease. all of them lead to high medical costs. The miR-30 family consists of a total of 5 members: miR-30a, miR-30b, miR-30c, miR-30d and miR-30e. ⋯ For example, miR-30a is highly expressed in blood samples of osteoporosis patients, miR-30a/b increases in cartilage tissue of osteoarthritis patients, and lower expression of miR-30c is associated with higher malignance and shorter survival time of osteosarcoma. Mechanistically, by targeting crucial transcription factors (RUNX2, SOX9, beclin-1, etc.), the miR-30 family regulates some critical pathways of bone homeostasis (Wnt/β-Catenin, mTOR, PI3K/AKT, etc.). In view of the distinct actions of the miR-30 family on bone metabolism, we hypothesize that the miR-30 family may be a new remedy for the clinical treatment and prevention of some bone and joint diseases.
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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease globally, and it can proceed to cirrhosis and hepatocellular carcinoma, as well as cardiovascular disease, chronic renal disease, and other complications, resulting in a massive economic burden. At the moment, nicotinamide adenine dinucleotide (NAD+) is thought to be a possible treatment target for NAFLD, besides Cluster of differentiation 38(CD38) is the primary NAD+ degrading enzyme in mammals and may play a role in the pathophysiology of NAFLD. ⋯ CD38 inhibitors enhance glucose intolerance and insulin resistance in mice and lipid accumulation in the liver is greatly decreased in CD38-deficient mice. This review describes the role of CD38 in the development of NAFLD in terms of Macrophage-1, insulin resistance, and abnormal lipid accumulation in order to offer recommendations for future NAFLD pharmacological trials.