Hai-Peng Liu

High Serum Levels of Follistatin in Patients with Ovarian Cancer

OBJECTIVE: This study investigated the potential use of serum follistatin (FST) as a marker for ovarian cancer alongside serum cancer antigen-125 (CA-125). METHODS: Serum samples were collected from patients with ovarian cancer (n = 45), benign ovarian cysts (n = 40) or other cancers (n = 100) and from healthy subjects (n = 60) for the determination of FST and CA-125 levels using enzyme-linked immunosorbent assays. Expression of FST in ovarian tissue was investigated using immunohistochemical staining. RESULTS: Compared with healthy subjects and patients with benign ovarian cysts, serum FST and CA-125 levels were significantly increased in patients with ovarian cancer. Using the 95% confidence interval for the healthy subjects group as the cut-off value, tumour marker sensitivity and specificity in ovarian cancer were 53.3% and 97% for FST and 77.8% and 84% for CA-125, respectively. Tissue expression of FST protein was more pronounced in ovarian cancer than in normal ovary. CONCLUSIONS: The serum FST level was elevated in the peripheral blood of patients with ovarian cancer and has potential as a tumour marker for ovarian cancer diagnosis. It may be particularly useful when combined with CA-125 detection to reduce the number of false-positive results.

7,8-Dihydroxy coumarin promotes chondrogenic differentiation of adipose-derived mesenchymal stem cells:

Objective To investigate the effects of 7,8-dihydroxy coumarin on the chondrogenic differentiation of rat adipose-derived mesenchymal stem cells (ADMSCs). Methods ADMSCs were cultured using a micromass suspension method and incubated with different concentrations of 7,8-dihydroxy coumarin and transforming growth factor (TGF)-β1 for 3 weeks: group A (negative control, no drug treatment); group B (positive control, 10 ng/ml TGF-β1); groups C, D and E (incubated with 25, 50 and 100 µg/ml 7,8-dihydroxy coumarin, respectively); groups F, G and H (incubated with 25, 50 and 100 µg/ml 7,8-dihydroxy coumarin, respectively, plus 10 ng/ml TGF-β1). Markers of chondrogenic differentiation were measured using histology, immunohistochemistry, enzyme-linked immunosorbent assay and reverse transcription–polymerase chain reaction. Results When used alone, 7,8-dihydroxy coumarin only weakly induced the chondrogenic differentiation of ADMSCs. 7,8-Dihydroxy coumarin used in combination with TGF-β1 strongly induced chondrogenic differentiation of ADMSCs. For some of the markers of chondrogenic differentiation, the extent of the induction was 7,8-dihydroxy coumarin dose-dependent. Conclusions 7,8-Dihydroxy coumarin appears to work synergistically with TGF-β1 to strongly induce chondrogenic differentiation of rat-derived ADMSCs.

Localisation and Role of Activin Receptor‐Interacting Protein 1 in Mouse Brain

Activin A, a stimulator of follicle‐stimulating hormone secretion from the pituitary, acts as a neurotrophic and neuroprotective factor in the central nervous system. Activin receptor‐interacting protein 1 (ARIP1) has been identified as a cytoplasmic protein that interacts with the type II receptor of activin (ActRII). However, the distribution pattern and function of ARIP1 are not well characterised in the brain. In the present study, we confirmed the existence of mRNA and protein of ARIP1 in the mouse brain, and found that ARIP1 was mainly localised at the hippocampus and hypothalamus in the cerebrum, granular layers in the cerebellum (especially in Purkinje cells of the cerebellum) and choroid epithelial cells by immunohistochemical staining. Furthermore, in contrast to the significant increase of activin A mRNA, ARIP1 mRNA and protein expression decreased in the mechanically lesioned brain of the mouse. Using neuroblastoma‐derived Neuro‐2a cells to investigate the function of ARIP1, we found that overexpression of ARIP1 down‐regulated the activin A‐induced signal transduction and significantly decreased the voltage‐gated Na+ current (INa). These data indicate that ARIP1 is a key molecule for the regulation of the action of activin in neurones, and also that decreased ARIP1 expression in the lesioned brain may be beneficial to the neurotrophic and neuroprotective roles of activin A in recovery after brain injury.

One-stage correction of blepharophimosis-ptosis-epicanthus inversus syndrome using a frontalis muscle transfer technique.

Abstract Blepharophimosis-ptosis-epicanthus inversus (BPES) is a rare genetic disease involving a complex eyelid malformation. The surgical treatment approach for BPES is highly complex and a subject of controversy. This study reports the results of a one-stage frontalis muscle transfer technique to correct BPES. This retrospective, interventional study included 21 patients with BPES who had been followed-up for a minimum of 1 year. The one-stage intervention was a combination of three surgical techniques: Mustardé medial canthoplasty, Fox lateral canthoplasty, and the frontalis muscle transfer technique. Preoperative and postoperative measurements of the horizontal lid fissure length (HLFL), vertical lid fissure width (VLFW), inner intercanthal distance (IICD), and the IICD/HLFL ratio were analyzed by Wilcoxons signed rank test. The mean preoperative measurements were 4.73 ± 0.32 mm for VLFW, 19.98 ± 3.74 mm for HLFL, 40.85 ± 4.46 mm for IICD, and 2.11 ± 0.45 mm for the IICD/HLFL ratio. The mean postoperative measurements were 7.86 ± 0.41 mm for VLFW, 24.47 ± 3.35 mm for HLFL, 32.52 ± 4.16 mm for IICD, and 1.35 ± 0.22 mm for the IICD/HLFL ratio (p < 0.0001 for all preoperative vs postoperative values). Postoperative complications included eyelid fold deformities, lagophthalmos, and conspicuous scars. Most of these complications gradually resolved. One-stage correction of BPES is safe and efficient with the surgical techniques described.

Surgical correction of blepharoptosis using a modified levator aponeurosis-Müller muscle complex reinsertion technique.

AbstractThe purpose of this study was to evaluate the outcomes after ptosis correction surgery using a modified levator aponeurosis–Müller muscle complex reinsertion technique. In this clinical study, 75 eyelids of 49 patients with congenital blepharoptosis were treated with the modified technique. The results, including complications, were followed up and evaluated. Operation was performed via anterior transcutaneous incision. After separating the preseptal orbicularis oculi muscle, the levator complex, including Müller muscle and the levator aponeurosis, was visualized. The levator complex was cut into 2 parts at the top of the conjunctival fornix to create an upper portion and a lower portion. The detached lower portion of the complex flap combined with the tarsal plate was advanced superiorly and reinserted into the posterior aspect of the upper portion of the complex flap by using 3 horizontal mattress sutures. Preoperative ptosis severity was compared with the degree of ptosis correction using the Cochran-Mantel-Haenszel test. Preoperative levator function was compared with the degree of ptosis correction and the postoperative levator function using Fisher exact test for paired data. Sufficient postoperative correction of ptosis was achieved in 78.7% of eyelids. Postoperative levator function of more than 4 mm was achieved in 82.7% of all eyelids that underwent surgery. We conclude that the modified levator aponeurosis–Müller muscle complex reinsertion technique is effective for correcting congenital blepharoptosis, especially in patients with fair to good (>4 mm) preoperative levator function.

Single-Stage Reconstruction of Eyebrow Defect Using a V-Y Advancement Pedicle Flap Based on the Orbicularis Oculi Muscle

Eyebrows play an important role in face expression and facial mimics by virtue of muscle contraction. Defects or deformity of the eyebrows result in abnormal facial expressions, and may lead to aesthetic issues for patients. The objective of this study is to report the case of a patient, with a congenital skin pigmented nevus at the right side of the eyebrow treated with direct surgical resection and followed by immediate reconstruction of the eyebrow with a V-Y advancement pedicle flap based on the orbicularis oculi muscle.

Additive effects of eukaryotic co‑expression plasmid carrying GRIM‑19 and LKB1 genes on breast cancer in vitro and in vivo

Gene associated with retinoid‑interferon‑induced mortality 19 (GRIM‑19) and the liver kinase B1 (LKB1) gene, two types of tumor suppressor gene, have been demonstrated to have important roles in breast carcinogenesis. The present study developed a dual expression plasmid that co‑expressed GRIM‑19 and LKB1, and evaluated the combined effects of the two genes against breast cancer in vitro and in vivo. Transfection with a plasmid for the simultaneous expression of GRIM‑19 and LKB1 (pGRIM19‑LKB1) into MCF‑7 breast cancer cells significantly inhibited the proliferation, colony formation, migration and invasion compared with the effects of transfection with either pGRIM‑19 or pLKB1 alone. Furthermore, transfection with pGRIM19‑LKB1 induced enhanced levels of apoptosis and cell cycle arrest at G0/G1 stage in MCF7 cells compared to the effects of pGRIM‑19 or pLKB1 alone. An in vivo experiment using an MCF‑7 xenograft tumor model demonstrated that intravenous injection of pGRIM19‑LKB1 had an enhanced effect on tumor growth inhibition compared to that of pGRIM‑19 or pLKB1 alone. In conclusion the findings of the present study suggested that transfection with eukaryotic plasmid for the simultaneous expression of GRIM‑19 and LKB1 more effectively suppressed the growth of breast cancer in vitro and in vivo, and may therefore have therapeutic potential for the treatment of human breast cancer.