In thoracoscopic pulmonary nodule resection surgery, precise preoperative planning is crucial. Artificial intelligence (AI)-assisted three-dimensional (3D) reconstruction technologies have shown great potential in this area. AI-assisted 3D reconstruction technologies can provide accurate, personalized models of the pulmonary vasculature and bronchial anatomy, assisting surgeons in detailed surgical planning and thus enhancing the precision and safety of surgeries. This article reviews the application progress of AI-assisted 3D reconstruction technologies in pulmonary nodule surgery, including their applications in preoperative diagnosis, surgical planning, and intraoperative navigation, as well as the advancements in AI-assisted 3D reconstruction technologies. It analyzes the technical features of all kinds of 3D reconstruction methods, their clinical applications, and the challenges they face.
Medical ethics must be considered for protecting the fights and interests of patients in clinical trials. Now the fights of the subjects are more and more emphasised, but there are some problems. It is evidence-based medicine (EBM) and emphasis of evidence that need the high-quality clinical trials, yet it violates the principle of ethics in some degree. It will be helpful for the administrators to supervise the clinical trials on drugs well from the point of ethical views.
Assessment on adverse drug reactions (ADR) that directly affects the quality of life and mortality and an important part of the post-marketed reassessment are developing gradually in China. Many problems have been identified in clinical validity and safety for the authorized Chinese herbs. An effective and standardized system is needed in the post-marketed drug reassessment. Evidence-based drug evaluation, which mainly includes clinical epidemiology, systematic review and health technology, will be used to assess the clinical validity, safety and cost of post-marketed drug and play an important role in the process of modernization and internationalization of Chinese herbs.
【摘要】 目的 探讨急性脑梗死对心脏自主神经活性的影响。 方法 Wistar大鼠32只随机分为正常组、假手术组和脑梗死组，脑梗死组用线栓法行右侧大脑中动脉阻塞。脑梗死组和假手术组于术前及术后24 h作心率变异性（HRV）检测，同时检测正常组HRV，将3组的HRV指标进行比较。实验终点取各组心肌组织检测儿茶酚胺和神经肽Y（NPY），进行组间比较。 结果 术后24 h脑梗死组和正常组、假手术组相比，窦性心搏间期标准差、均方根，总功率谱、高频功率谱（HF）、低频功率谱（LF）降低，差异有统计学意义。3组比较LF/HF和分数维无明显差异。脑梗死组心肌组织去甲肾上腺素（NA）和NPY高于正常组和假手术组。 结论 脑梗死引起心脏自主神经总活性降低、自主神经功能受损，自主神经末梢去甲肾上腺素和NPY的异常分泌可能是重要的原因。【Abstract】 Objective To investigate the effect of acute cerebral infarction on cardiac autonomic nervous activity. Methods A total of 32 Wistar rats were divided into normal group, sham operation group and infarction group by random. Experimental cerebral infarction in Wistar rats was induced by intraluminal occlusion of middle cerebral artery. About 24 hours after the occlusion or 24 hours after sham operation, the heart rate variability (HRV) sequences were measured, and the HRV values in the three groups were compared. The levels of catecholamine and neuropeptide (NPY) in myocardium were measured. Results At the 24th hour after the occlusion, the standard deviation and root mean square standard deviation of R-R interval, the total power, high frequency (HF) and low frequency (LF) in infarction group were lower than those in normal and sham operation group. LF/HF and fractal dimension did not differ much among the three groups. The levels of noradrenaline and NPY in myocardium in infarction group were higher than those in the other groups. Conclusion It is suggested that acute cerebral infarction may cause the decrease of autonomic nervous activity and damage of the autonomic nervous function; the abnormal secretion of noradrenalin in autonomic nerve ending and NPY may be the important reasons.
Objective To investigate the changes of cognitive function of epileptic patients after antiepileptic drugs (AEDs) therapy. Methods Twenty eight cases of epileptic patients with new diagnosis and untreatment from March 2015 to February 2016 were collected. According to the seizure type, degree of attack and drug efficacy, patients were divided into three groups and treated with one of three AEDs, including Lamotrigine (LTG), Oxcarbazepine (OXC), and Sodium valproate (VPA). Among them, 11 were LTG group, 12 were OXC group and 5 were VPA group.Then the patients were followed up for 1 year. The clinical memory scale was used to analyze cognitive function of epileptic patients before and after therapy. Results Compared to 30 cases of healthy volunteers, the scores of memory quotient (P<0.01), directed memory (P<0.05), associative learning (P<0.05) and image free recall (P<0.01) of epileptic patients were obviously decreased before AEDs therapy.AEDs therapy reduced or controlled seizures in new diagnostic epileptic patients, and the total effective rate was 85.7%. In the clinical memory scale tests, the scores of memory quotient (P<0.01), directed memory (P<0.05), associative learning (P<0.05), portrait characteristics contact memory (P<0.05) were improved after therapy. The scores of image free recall and meaningless graphics recognition were also improved, but there was no statistical significance. Besides, there was a statistically significant improvement in the score of portrait characteristics contact memory after LTG treatment (P<0.05), and directed memory after VPA treatment (P<0.05). Conclusions Epileptic patients accompanied with cognitive deficits before drug intervention. Through standard AEDs treatment, seizures could be better controlled. The cognitive function of epileptic patients was not declined after short-term（within 1 year） intervention of LTG, OCX or VPA. Moreover some parts of the cognitive domain could be improved.
Monocyte chemoattractant protein-1(MCP-1) is a cytokine which belongs to the CC chemokine family. Retinal pigment epithelium (RPE) cells, photoreceptors and microglial cells in the retina can secrete MCP-1. Physiological level of MCP-1 is important for preserving morphology of RPE and glial cells, as well as retinal function and gross morphology. MCP-1 is likely released from Müller glia and the RPE cells when retina under stress, and attracts microglia/macrophages to the sites of retinal damage, activates the microglia to ingest cell debris. MCP-1 has been found upregulated in the intraocular fluid of retina in patients and animal models with retinal detachment, posterior uveitis and age-related macular degeneration. The expression of MCP-1 may be response to retinal inflammation. Therefore, it is tempting to speculate that pharmacological targeting of MCP-1 may be a safe and viable strategy in treatment of retinal disease.