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Background: High prevalence of smartphone addiction among medical students may contribute to adverse physical and mental health outcomes. Aim: To estimate the prevalence of smartphone addiction, and explore the influencing factors and related mental health symptoms of smartphone addiction among Asian medical students. Design: Systematic review and meta-analysis. Methods: PubMed (MEDLINE), the Cochrane Central Register of Controlled Trials, and EMBASE were searched for relevant literature from the inception to September 10, 2021. Using Stata software 11.0, the meta-analysis of prevalence and the influencing factors of smartphone addiction were determined with 95% confidence intervals. Results: Nineteen articles, published between 2014 and 2019, were included, producing medical student studies from seven different Asian countries. The included studies were conducted in India ( n = 11) and Malaysia ( n = 3), with China, Saudi Arabia, Turkey, Nepal, and Iran each contributing one study. Among a total of 5,497 medical students, the participants included 3,214 females, of whom 2,181 were medical students with smartphone addiction. The prevalence of smartphone addiction among Asian medical students was 41.93% (95% CI [36.24%, 47.72%]). The influencing factors of smartphone addiction among medical students included gender, duration of smartphone use, smartphone function, and marital status. Ten studies (52.63%) explored related mental health symptoms of smartphone addiction among Asian medical students. Smartphone addiction was positively correlated with poor sleep quality ( r = .17–.31), stress ( r = .30–.40), anxiety, depression, neuroticism, and general health among Asian medical students. Conclusion: Smartphone addiction is highly prevalent among Asian medical students. Smartphone addiction may adversely affect mental health, resulting in sleep disturbance, stress, anxiety, depression, and neuroticism. It is necessary to take appropriate precautionary actions and interventions to prevent smartphone overuse among medical students.

Purpose: Breast cancer is one of the most common causes of cancer death in women worldwide. The Glasgow Prognostic Score (GPS), a cumulative prognostic score based on C-reactive protein and albumin, indicates the presence of a systemic inflammatory response. The GPS has been adopted as a powerful prognostic tool for patients with various types of malignant tumors, including breast cancer. The aim of this study was to assess the value of the GPS in predicting the response and toxicity in breast cancer patients treated with chemotherapy. Patients and Methods: Patients with metastatic breast cancers in a progressive stage for consideration of chemotherapy were eligible. The clinical characteristics and demographics were recorded. The GPS was calculated before the onset of chemotherapy. Data on the response to chemotherapy and progression-free survival (PFS) were also collected. Objective tumor responses were evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST). Toxicities were graded according to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTC) version 3.0 throughout therapy. Results: In total, 106 breast cancer patients were recruited. The GPS was associated with the response rate (p = 0.05), the clinical benefit rate (p = 0.03), and PFS (p = 0.005). The GPS was the only independent predictor of PFS (p = 0.005). The GPS was significantly associated with neutropenia, thrombocytopenia, anorexia, nausea and vomiting, fatigue, and mucositis (p = 0.05-0.001). Conclusions: Our data demonstrate that GPS assessment is associated with poor clinical outcomes and severe chemotherapy-related toxicities in patients with metastatic breast cancer who have undergone chemotherapy, without any specific indication regarding the type of chemotherapy applied.

Background: The management of cancer-related anorexia/cachexia syndrome (CACS) is a great challenge in clinical practice. To date, practice guidelines for the prevention and treatment of CACS are lacking. The authors conducted a randomized study to confirm the effectiveness and safety of treatment of CACS utilizing megestrol acetate (MA) plus thalidomide. Methods: One hundred and two candidates with CACS were randomly assigned to two treatment groups (trial group and control group): the trial group received MA (160 mg po, bid) plus thalidomide (50 mg po, bid), while the control group received MA (160 mg po, bid) alone. Treatment duration was 8 weeks. Results: Analysis of the trial group demonstrated a significant increase from baseline in body weight (Conclusion: A combination regimen of MA and thalidomide is more effective than MA alone in the treatment of CACS.

To evaluate the outcome and indication of the reconstruction of oral and maxillofacial postoperative defects by submental artery island myocutaneous flaps.Sixty eight cases with the reconstruction of oral and maxillofacial defects by submental artery island myocutaneous flaps from January 2006 to May 2010 were analysed retrospectively. Primary lesions included carcinomas originating from tongue (28 cases), palate (13 cases), mouth floor (9 cases), gingiva (4 cases), buccal mucosa (6 cases), lip (3 cases), and other malignant or benign tumors (5 cases). The ages ranged from 25 to 84 years (mean 58 years); 47 males and 21 females. The sizes of skin paddle varied from a minimum of 4 cm × 4 cm to a maximum of 15 cm × 10 cm.Of the 68 flaps, 62 were survival, 4 had partial necrosis but healed with treatments, and 2 failed due to complete necrosis. Appearance and functions of recipient sites were satisfactory. The followed-up time was 3 - 24 months, local recurrence occurred in 5 cases and cervical lymph node metastases were found in 15 patients.Submental island flap is reliable for the reconstruction of postoperative defects in early oral cancer without regional lymph node metastasis or in benign tumor.

Caspase-dependent apoptosis is considered one of the most important cell death pathways. When the apoptotic process is blocked, a form of programmed necrosis called necroptosis occurs. Apoptosis and necroptosis may share some regulatory mechanisms. Recent studies indicated that receptor interacting protein 1 (RIP1), an Hsp90-associated kinase, is an important regulatory switch between apoptosis and necroptosis. In this study, we showed that oxygen-glucose deprivation (OGD) combined with a caspase inhibitor zVAD (OGD/zVAD)-induced RIP1 protein expression in a time-dependent manner. We found that geldanamycin (GA), a benzoquinone ansamycin, protected against neuronal injury induced by OGD/zVAD treatment in cultured primary neurons. More importantly, GA decreased RIP1 protein level in a time- and concentration-dependent manner. In this study, we found that GA also decreased the Hsp90 protein level, which caused instability of RIP1 protein, resulting in decreased RIP1 protein level but not RIP1 mRNA level after GA treatment. We concluded that the GA-mediated protection against OGD/zVAD-induced neuronal injury was associated with enhanced RIP1 protein instability by decreasing Hsp90 protein level. GA and its derivatives may be promising for the prevention of neuronal injury during ischemic injury.

To compare the effect of rh-endostatin on micrangium in tumor and myocardial tissue in nude mice.Nude mice were randomized into 4 groups (10 mice in each group), blank control group (without tumor burden, received NS 100 µl×d(-1) injection), drug control group (without tumor burden, received rh-endostatin 400 µg×d(-1) injection), model group (with tumor burden, received NS 100 µl×d(-1) injection) and treatment group (with tumor burden, received rh-endostatin 400 µg×d(-1) injection) for 28 days. The tumor volume and body weight of the mice were measured before and after administration. The expression of CD34, MMP-2, MMP-9, HIF-1α and VEGF in the myocardium and tumor were detected by immunohistochemistry. The vascular structure was observed by immunoenzymatic CD34 and Masson double staining.The increase of tumor volume of the treatment group [(48.18 ± 37.31) mm(3)] was significantly lower than that in the model group [(113.80 ± 73.27) mm(3)). The changes of body weight was not significant different among the four groups. After treated with rh-endostatin, the expressions of MMP-9 and VEGF in tumors were significantly down-regulated, but the expressions of MMP-2 and HIF-1α in the tumor were not. The microvessel density (MVD) in the tumors of treatment group was significantly decreased compared with that of model group. The proportion of tumor vessels covered by collagen in the treatment group was increased compared with that of the model group. However, MVD and micrangium in myocardium were not changed significantly.Rh-endostatin can decrease the expression of MMP-9, VEGF and MVD, inhibit the tumor growth and normalize tumor micrangium in tumor but not weaken the MMPs and MVD of mature micrangium in myocadium.

Platinum-based chemotherapy remains the main treatment of advanced lung cancer. However, platinum resistance has become a major treatment obstacle. Novel therapies, particularly tyrosine kinase inhibitors of the epidermal growth factor receptor (EGFR-TKI) and agents that target vascular endothelial growth factor (VEGF), have improved the treatment. Both chemotherapy and targeted therapy have their molecular mechanisms. This study aimed to determine the mutation, amplification, or expression status and interrelationships of the epidermal growth factor receptor (EGFR), K-Ras proto-oncogene, excision repair cross-complementation group 1 (ERCC1), and VEGF genes as well as their correlations to prognosis of large cell lung carcinoma (LCLC) after EGFR-targeted therapy, chemotherapy, and anti-VEGF therapy. EGFR and K-Ras mutations in 60 specimens of LCLC were detected by direct DNA sequencing. EGFR, ERCC1, and VEGF protein expression was detected by immunohistochemistry (IHC). EGFR gene copy number was detected by fluorescence in situ hybridization (FISH). One (1.7%) patient had an EGFR L858M point mutation in exon 21, 3 (5.0%) had K-Ras mutations, and 10 (19.6%) had EGFR amplification (FISH positive). Positive rates of EGFR, ERCC1, and VEGF proteins were 38.3%, 56.7%, and 70.0%, respectively. EGFR amplification was positively correlated to EGFR protein expression (r = 0.390, P = 0.005). The positive rate of VEGF protein was significantly higher in patients with lymph node metastasis than in those without (84.6% vs. 58.8%, P = 0.046). No significant correlations were observed among the EGFR, K-Ras, ERCC1, and VEGF genes. EGFR gene amplification and the low rate of EGFR mutation suggest that patients with LCLC are likely to obtain little benefit from anti-EGFR therapies.

The aim of this study was to explore the clinical characteristics and analyze the prognostic factors of large cell lung cancer (LCLC).The clinical data of 111 LCLC cases were collected and retrospectively analyzed. The prognostic factors were evaluated by univariate and multivariate analyses.Among the 111 cases, the lesions were in the right lung of 53 patients and 26 of them were located in the superior lobe. The lesions were in the left lung of 58 cases, and 35 of them were in the superior lobe. The lesions were presented as central in 36 cases and peripheral in 75 cases, with a mean diameter of 5.3 cm. All the 111 patients were diagnosed as stage I in 38 cases, stage II in 11 cases, stage III in 45 and stage IV in 17 cases. 60 patients had lymph node metastasis and 17 cases had distant metastasis. The overall 1-, 3- and 5-year survival rates of the LCLC were 54.7%, 30.9% and 20.6%, respectively. Cox univariate analysis revealed that TNM stage (P = 0.000), lymph node metastasis (P = 0.000) and M stage (P = 0.000) are prognostic factors. Cox multivariate analysis indicated that TNM stage (P = 0.000) is an independent prognostic factor.The prognosis of LCLC is worse than other types of non-small cell lung cancer. Complete surgical resection remains the main therapeutic approach. TNM stage is an independent prognostic factor.