Progressively worsening ptosis in a woman: A case report.

Key Clinical Message: Filler injections into the upper eyelid may cause levator aponeurosis fibrosis and ptosis. This risk must be considered. When ptosis appears, treatment might be difficult. Understanding the upper eyelid anatomy and procedures is essential to prevent eyelid damage. Abstract: Ptosis is a prevalent condition in cosmetic surgery that occurs due to malfunction of the levator palpebrae superioris or insufficient Müller muscle action. It is characterized by the upper eyelid edge appearing lower than usual when seen at eye level. Ptosis may be categorized into congenital and acquired forms. The primary cause of congenital ptosis is attributed to abnormalities of the levator palpebrae superioris muscle or the motor nerve innervation that controls it. The condition arises from atypical development and malfunction of the oculomotor system. Acquired ptosis may be classified into many categories including traumatic, neurogenic, myogenic, senile, mechanical, and fake ptosis. Currently, there is little documentation of ptosis resulting from the degeneration of the aponeurosis of the muscle in the upper eyelid. We received a case of ptosis caused by fibrosis of the levator palpebrae superioris aponeurotic membrane. We used the technique of levator palpebrae superioris great advancement. The levator palpebrae superioris-Müller muscle was folded to create a stable composite construction via the levator palpebrae superioris high progress.

Comparative efficacy of robotic-assisted and freehand techniques for pedicle screw placement in spinal disorders: a meta-analysis and systematic review.

The efficacy and safety of robotic-assisted pedicle screw placement compared to traditional fluoroscopy-guided techniques are of great interest in the field of spinal surgery. This systematic review and meta-analysis aimed to compare the outcomes of these two methods in patients with spinal diseases. Following the PRISMA guidelines, we conducted a systematic search across PubMed, Embase, Web of Science, and Cochrane Library. We included randomized controlled trials comparing robotic-assisted and fluoroscopy-guided pedicle screw placement in patients with spinal diseases. Outcome measures included the accuracy of pedicle screw placement, postoperative complication rates, intraoperative radiation exposure time, and duration of surgery. Data were analyzed using Stata software. Our analysis included 12 studies. It revealed significantly higher accuracy in pedicle screw placement with robotic assistance (odds ratio [OR] = 2.83, 95% confidence interval [CI] = 2.20-3.64, P < 0.01). Postoperative complication rates, intraoperative radiation exposure time, and duration of surgery were similar between the two techniques (OR = 0.72, 95% CI = 0.31 to 1.68, P = 0.56 for complication rates; weighted mean difference [WMD] = - 0.13, 95% CI = - 0.93 to 0.68, P = 0.86 for radiation exposure time; WMD = 0.30, 95% CI = - 0.06 to 0.66, P = 0.06 for duration of surgery). Robotic-assisted pedicle screw placement offers superior placement accuracy compared to fluoroscopy-guided techniques. Postoperative complication rates, intraoperative radiation exposure time, and duration of surgery were comparable for both methods. Future studies should explore the potential for fewer complications with the robotic-assisted approach as suggested by the lower point estimate.

miR-338 modulates proliferation and autophagy by PI3K/AKT/mTOR signaling pathway in cervical cancer.

Cervical cancer (CC) is a malignant solid tumor, which is one of the main causes of morbidity and mortality in women. Given that autophagy is an important factor promoting tumor progression, we aim to investigate the functional role of miR-338 in autophagy and proliferation of cervical cancer. In our study, expression of miR-338 was validated by quantitative RT-PCR in 30 paired cervical cancer tissues and normal tissues. We performed MTT, colony formation and cell cycle assay to explore the effect of miR-338 on cell proliferation. The level of autophagy was evaluated by observing the expression of LC3 formation under fluorescence microscope and detected the LC3 expression by western blot. We used luciferase reporter assays to identify the target gene about miR-338. We not only found that the level of miR-338 is decreased in cervical cancer tissues and cells, but also negatively correlated with the protein level of ATF2. In turn, restoring the expression of miR-338 inhibited proliferation in Hela and SiHa cells. Further mechanistic study identified that ATF2 as a direct target of miR-338. Forced lowexpression of miR-338 directly led to increased the level of autophagy in cervical cancer cells, which was similar to the mTOR signaling inhibitor rapamycin. The western blot analysis show that inhibited miR-338 expression could decrease the p-mTOR and p-p70S6 expression. Thus, we infer that miR-338 decreases autophagy level in cervical cancer cells by activating mTOR signaling pathway. In summary, our study demonstrate that miR-338 could inhibites proliferation and autophagy by targeting ATF2 via mTOR signaling pathway on cervical cancer cells. These results suggest a potential application of miR-338 in cervical cancer as a novel mechanism of tumor therapeutic.

Study of critical role of c-Met and its inhibitor SU11274 in colorectal carcinoma.

c-Met plays an important role in colorectal tumorigenesis and disease progression and thus is believed to be an attractive inhibitory target for receptor molecular therapeutic. SU11274 was identified as a small molecule, ATP competitive inhibitor of the catalytic activity of the c-Met kinase. Our study had investigated the relationship between the high expression of c-Met and colorectal carcinoma and the effect of c-Met inhibitor SU11274 in colorectal carcinoma in vitro and vivo. Immunohistochemistry was used to detect the expression of c-Met in 60 patients with colorectal cancer and 20 patients with benign adenoma and surrounding normal colon tissues. The effect of SU11274 on human colorectal carcinoma LoVo cells was detected by Western blot and MTT. And the influence of SU11274 on cell cycle was determined by flow cytometry. In addition, LoVo cell-transplanted tumor growth and expression of c-Met in nude mice was examined for inhibition of SU11274 in vivo. We found c-Met had high expression and was closely related to lymph node metastasis and TNM stage in colorectal carcinoma tissues. SU11274 significantly suppressed the phosphorylation of c-Met as well as the survival and proliferation of LoVo cell lines. G1-phase arrest was also induced by SU11274. SU11274 apparently restrained the growth of the xenograft tumor in nude mice. Our data suggest developing therapies that specifically inhibit the activation of c-Met may represent a novel therapeutic modality for patients with colorectal carcinoma expressing high levels of c-Met.