Objective To explore the correlation between anemia and the pathogenesis and prognosis of patients with lung cancer. Methods From January 2013 to December 2014, 257 patients with primary lung cancer who were firstly treated at the First Affiliated Hospital of Anhui Medical University were retrospectively analyzed. The clinical data of the patients were collected and the patients were divided into anemia group and control group. The relationship of gender, age, and pathogenesis with anemia was analyzed by x 2 test. Survival analysis was evaluated by Kaplan-Meier and Log-rank test. Results The TNM stage, lymph nodes and remote metastasis , and ECOG score between the two groups were statistically different (x 2 values were 7.94, 4.97, 4.69, 9.02, all P< 0.05). The survival of the two groups showed statistical differences (x2=7.02, P=0.008). Conclusion Anemia might be correlated with the stage, lymph nodes and remote metastasis, ECOG score and prognosis of patients with lung cancer.

Intermedin can promote tumor angiogenesis through a variety of signaling pathways. Hypoxia of tumor cells can induce an increased expression of intermedin. Recently, there have been a surge of researches on the relation between intermedin and tumor initiation, progression and metastasis. Intermedin may be a new target for tumor therapy.

Incisional hernia is open a major postoperative complication that abdominal surgery remains. The incision type, suture technique, and the choice of primary suture materials are the main factors affecting wound healing. Prophylactic subfascial non-absorbable mesh can be used in high-risk patients to prevent in-cisional hernia.

Acquired resistance of EGFR-TKIs has become the major limitation of the efficacy of targeted therapy for lung cancer. Lung cancer has been treated by traditional Chinese medicine (TCM) combined with EGFR-TKIs, which originated from clinic. In recent years, reversing research has been conducted based on clinic application to discuss TCM intervening, improving and reversing EGFR-TKIs acquired resistance becoming a novel target for research. This article reviewed mechanism and effects of TCM herbs and compounds’ with the efficacy of clearing away heat and toxic materials, promoting blood circulation to remove blood stasis strengthening the body resistance, and invigorating the circulation of blood, and proposed that the whole regulation and targeted therapy of TCM may carry out synergistic effect and become innovation treatment model for lung cancer.

Endothelin-1 (ET-1) was characterized as a powerful vasoconstrictor and mitogen for smooth muscle. ET-1 binds to two types of receptors: ET_ A-R and ET_ B-R. Pulmonary arterial hypertension (PH) is a severe condition characterized by a progressive increase in pulmonary vascular resistance. The Endothelial dysfunction plays an important role in the development of pulmonary arterial hypertension. PH can be treated by antagonism of ET-1.

Objective: Angiotensin II (Ang II) contributes to modulating blood pressure by stimulation of Ang II AT1 receptors. We devised a rat transient middle cerebral artery occlusion (MCAO) model to assess whether oxidative damage is decreased after pretreatment with Angiotensin II AT1 receptor blocker (ARB). Methods: After 2 weeks pretreatment with ARB 0.5 and 1 mg/kg, the male Wister rats were subjected to 2 h middle cerebral artery occlusion (MCAO). At 24 h, the lumen diameter of middle cerebral artery, the plasma level of 8-hydroxy-2′-deoxyguanosine (8-OHdG), and HIF-1α levels were recorded and compared. Results: After pretreatment with ARB 0.5 and 1 mg/kg, blood pressure did not significantly change compared with that of controls. In the group of candesartan at 1 mg/(kg· day), the lumen diameter was significantly increased compared to that in control group [(86.0±5.0) μm vs. (69.0± 2.1) μm; P < 0.01, n = 6 - 8]. The plasma 8-OHdG levels of ARB pretreatment groups were decreased. In immunohistochemical findings, 8-OHdG- and HIF-1α-containing cells in ARB pretreatment groups were decreased. Conclusion: Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.

Objective: Angiotensin II (Ang-II) increases NADPH oxidase activity and stimulates the production of reactive oxygen species (ROS) including superoxide anion through Ang II AT1-receptor (AT1-R) activation. ROS is involved in various pathological processes in brain ischemia. We investigated whether the AT1-R blocker (ARB) candesartan can protect normotensive rats against brain ischemia. Methods: After 2-week pretreatment with candesartan, rats were subjected to 2 hours middle cerebral artery occlusion-reperfusion (MCAO-R) and 24 hours later, the infarct volume, iNOS, and eNOS mRNA in the internal carotid artery was recorded and compared. Results: Candesartan pretreatment reduced cerebral ischemia and oxidative brain damage after MCAO-R in normotensive rats, resulting in a decreased cortical infarct volume [0.5 mg/kg candesartan, (46.8±13.2) mm3; 1.0 mg/kg candesartan, (19.3±15.3) mm3 vs. control, (111.7±14.3) mm3; P<0.05, P<0.01, respectively]. Candesartan pretreatment increased the eNOS mRNA level in the internal carotid artery. Conclusion: In normotensive rats exposed to MCAO-R, candesartan protectes against brain ischemia. This effect may represent a significant therapeutic advantage and may induce end-organ protection even at normal blood pressure.

Objective: Angiotensin II (Ang II) contributes to modulating blood pressure by stimulation of Ang II AT1 receptors. We devised a rat transient middle cerebral artery occlusion (MCAO) model to assess whether oxidative damage is decreased after pretreatment with Angiotensin II AT1 receptor blocker (ARB). Methods: After 2 weeks pretreatment with ARB 0.5 and 1 mg/kg, the male Wister rats were subjected to 2 h middle cerebral artery occlusion (MCAO). At 24 h, the lumen diameter of middle cerebral artery, the plasma level of 8-hydroxy-2′-deoxyguanosine (8-OHdG), and HIF-1α levels were recorded and compared. Results: After pretreatment with ARB 0.5 and 1 mg/kg, blood pressure did not significantly change compared with that of controls. In the group of candesartan at 1 mg/(kg· day), the lumen diameter was significantly increased compared to that in control group [(86.0±5.0) μm vs. (69.0± 2.1) μm; P < 0.01, n = 6 - 8]. The plasma 8-OHdG levels of ARB pretreatment groups were decreased. In immunohistochemical findings, 8-OHdG- and HIF-1α-containing cells in ARB pretreatment groups were decreased. Conclusion: Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.

Objective: Angiotensin II (Ang-II) increases NADPH oxidase activity and stimulates the production of reactive oxygen species (ROS) including superoxide anion through Ang II AT1-receptor (AT1-R) activation. ROS is involved in various pathological processes in brain ischemia. We investigated whether the AT1-R blocker (ARB) candesartan can protect normotensive rats against brain ischemia. Methods: After 2-week pretreatment with candesartan, rats were subjected to 2 hours middle cerebral artery occlusion-reperfusion (MCAO-R) and 24 hours later, the infarct volume, iNOS, and eNOS mRNA in the internal carotid artery was recorded and compared. Results: Candesartan pretreatment reduced cerebral ischemia and oxidative brain damage after MCAO-R in normotensive rats, resulting in a decreased cortical infarct volume [0.5 mg/kg candesartan, (46.8±13.2) mm3; 1.0 mg/kg candesartan, (19.3±15.3) mm3 vs. control, (111.7±14.3) mm3; P<0.05, P<0.01, respectively]. Candesartan pretreatment increased the eNOS mRNA level in the internal carotid artery. Conclusion: In normotensive rats exposed to MCAO-R, candesartan protectes against brain ischemia. This effect may represent a significant therapeutic advantage and may induce end-organ protection even at normal blood pressure.

This paper summarized the concept, diagnostic criteria, clinical treatment, outcome and the current issues faced of minimalconscious state.