Upregulated miRNA-182-5p expression in tumor tissue and peripheral blood samples from patients with non-small cell lung cancer is associated with downregulated Caspase 2 expression.

Lung cancer has the highest morbidity and mortality rates among all malignant tumors worldwide. Previous studies demonstrated that microRNA (miR)-182-5p may serve different roles in different types of cancer, including renal cell carcinoma and liver cancer. However, the functional role of miR-182-5p in non-small cell lung cancer (NSCLC) remains unknown. In the current study, the expression level of miR-182-5p in tumor tissue and peripheral blood samples obtained from patients with NSCLC was examined. The biological function of miR-182-5p on NSCLC cell proliferation was also investigated. Tissue and adjacent normal tissue samples were collected from 33 patients with NSCLC. In addition, peripheral blood samples were obtained from patients with NSCLC and 26 healthy control patients. The NSCLC cell line H1299 was used for all functional assays. Reverse transcription-quantitative polymerase chain reaction was used to determine the miR-182-5p or Caspase 2 (CASP2) mRNA expression levels in NSCLC tissue and peripheral blood samples, as well as in the NSCLC cell line. Western blotting was used to examine the protein expression level of CASP2 in tissue samples and cells, and ELISA was performed to measure the protein level of CASP2 in peripheral blood samples. MTT assay was performed to examine NSCLC cell proliferation. Flow cytometry was used to detect apoptosis. Dual-luciferase reporter assay was used to examine whether miRN182-5p directly interacts with CASP2. The current study demonstrated that miR-182-5p expression was upregulated in NSCLC tissue and peripheral blood samples from patients with NSCLC, which suggests that miR-182-5p, may serve a functional role in NSCLC. In addition, inhibition of miR-182-5p expression suppressed cell proliferation and enhanced cell apoptosis in NSCLC cells. CASP2 expression was downregulated in NSCLC tissue and peripheral blood samples from patients with NSCLC. The current study demonstrated that miR-182-5p may regulate NSCLC cell proliferation and apoptosis by regulating CASP2 expression as miR-182-5p directly binds with the 3'-untranslated region of CASP2, thereby regulating CASP2 expression.

[Effect of Heshouwuyin on the expression of Cox7a2 protein in testis tissue of exercised-induced fatigue rat].

OBJECTIVE: To explore the effect of Heshouwuyin on the expression of cytochrome C oxidase7a2 (Cox7a2) in testis tissue of rats with exercised-induced fatigue. METHODS: Fifty SD rats were divided into normal control group (A group), Heshouwuyin administered normal group (B group), model control group (C group), Heshouwuyin treated group (D group) and Heshouwuyin prevented group (E group) randomly with 10 rats for each. The exercise-induced fatigue models in rats of C, D, E groups were established. The rats in D group were treated with Heshouwuyin [20 g/(kg x d), contained crude drug 9.6 g/mL] for 60 days (during the 42 days of modeling and after the 18 days of modeling). The rats in E group were also treated with Heshouwuyin for 60 days (but before the 18 days of modeling and during the 42 days of modeling). Beckmancoulter Unicel Dxl 800 was used to detect the level of serum testosterone, according to the manufacture's instructions. Western blot and RT-PCR were used to observe the differential expression of Cox7a2. RESULTS: The level of serum testosterone in C group was decreased compared with A group (P < 0.05), which implied the success of modeling. Compared with group A, the level of serum testosterone in B, D, E groups were increased (P < 0.05). Cox7a2 protein was expressed mainly in leydig cell and spermatocyte. Compared with A,B, D, E groups, the expression of Cox7a2 protein and mRNA in C group increased (P < 0.05), and there no significant difference was observed between group A and B, as well as group D and E. CONCLUSION: The expression of Cox7a2 was down-regulated by Heshouwuyin.

Therapeutic regimens and prognostic factors of brain metastatic cancers.

OBJECTIVE: This work aims to investigate the therapeutic regimen of brain metastatic cancers and the relationship between clinical features and prognosis. METHODS: Clinical data of 184 patients with brain metastatic cancers were collected and analysed for the relationship between survival time and age, gender, primary diseases, quantity of brain metastatic foci, their position, extra cranial lesions, and therapeutic regimens. RESULTS: The average age of onset was 59.1 years old. The median survival time (MST) was 15.0 months, and the patients with breast cancer as the primary disease had the longest survival time. Females had a longer survival time than males. Patients with meningeal metastasis had extremely short survival time. Those with less than 3 brain metastatic foci survived longer than patients with more than 3. The MST of patients receiving radiotherapy only and the patients receiving chemotherapy only were all 10.0 months while the MST of patients receiving combination therapy was 16.0 months. Multiple COX regression analysis demonstrated that gender, primary diseases, and quantity of brain metastatic foci were independent prognostic factors for brain metastatic cancers. CONCLUSIONS: Chemotherapy is as important as radiotherapy in the treatment of brain metastatic cancer. Combination therapy is the best treatment mode. Male gender, brain metastatic cancers originating in the gastrointestinal tract, more than 3 metastatic foci, and involvement of meninges indicate a worse prognosis.

Na⁺-K⁺-ATPase, a potent neuroprotective modulator against Alzheimer disease.

Alzheimer disease (AD) is a neurodegenerative disorder clinically characterized by progressive cognitive and memory dysfunction, which is the most common form of dementia. Although the pathogenesis of neuronal injury in AD is not clear, recent evidences suggest that Na⁺-K⁺-ATPase plays an important role in AD, and may be a potent neuroprotective modulator against AD. This review aims to provide readers with an in-depth understanding of Na⁺-K⁺-ATPase in AD through these modulations of some factors that are as follows, which leads to the change of learning and memory in the process of AD. 1. The deficiency in Na⁺, K⁺-ATPase α1, α2 and α3 isoform genes induced learning and memory deficits, and α isoform was evidently changed in AD, revealing that Na⁺, K⁺-ATPase α isoform genes may play an important role in AD. 2. Some factors, such as ß-amyloid, cholinergic and oxidative stress, can modulate learning and memory in AD through the mondulation of Na⁺-K⁺-ATPase activity. 3. Some substances, such as Zn, s-Ethyl cysteine, s-propyl cysteine, citicoline, rivastigmine, Vit E, memantine, tea polyphenol, curcumin, caffeine, Alpinia galanga (L.) fractions, and Bacopa monnieri could play a role in improving memory performance and exert protective effects against AD by increasing expression or activity of Na⁺, K⁺-ATPase.

[Effect of occupational stress on cardiovascular function of different vocational population].

OBJECTIVE: To study the effect of occupational stress on cardiovascular function of different vocational population. METHODS: The occupational stressors, risk factors of cardiovascular diseases were investigated by questionnaire in 839 people with 4 kinds of jobs. Blood pressure, sugar, and lipid were detected at the same time. RESULTS: Blood pressure were higher in the groups of old age, long standing and teachers, and the abnormal rate of blood pressure was 21.69%. There was no difference in abnormal ECG among ages, standing and occupation, and the abnormal rate of ECG was 19.07%. Job control, job demands, job responsibility, role in a job and shift work were the main stress factors affecting systolic and diastolic blood pressure. More conflict in job, less chance of participation, severe job loads were the risk factors of primary hypertension. Accident due to job responsibility, job responsibility, role in a job were the main risk factors of abnormal electrocardiograph. Self-respect and activity beyond work were the good modifiers of heart function. CONCLUSION: Occupational stress has certain effect on cardiovascular function.