2017年 · 第97卷第33期

Spinal surgery is an exquisite art. Perfect spinal surgery requires doctors' rich experience and fine hand movements. However, long-term surgery may lead to doctors' operational mistakes. In recent years, medical robots have been applied in the surgical field. Through motion adjustment and tremor filtering functions, robots have perfected the dexterity of doctors' hands. Their high accuracy and almost infinite endurance have been praised by the industry. At present, the application of robot-assisted surgery in spinal surgery includes robot-assisted pedicle screw placement, anterior lumbar intervertebral fusion, thoracolumbar tumor resection, transstomatodontic resection and paravertebral tumor resection, etc. However, the early application effect is not satisfactory. With the development of robot technology, the number of cases using robots in clinical practice gradually increases, and good clinical results have been obtained. But because of its high price and other factors, it has not been widely used at present.

A 44-year-old male was admitted to our department on April 20, 2015 due to "fever with fatigue for more than 1 month". The white blood cell count at the initial diagnosis was 49.48×10⁹/L, hemoglobin determination 68 g/L, platelet count 27×10⁹/L, bone marrow morphology, immunotyping, karyotype analysis and other examinations were performed to confirm the diagnosis of acute myeloid leukemia-M4. Physical examination: spleen flat umbilicus, liver 2 fingers under the costs. Hydroxyurea was given first to reduce tumor burden after admission. After chemotherapy with decitabine + homoharringtonine + cytarabine from May 4, 2015, the patient's spleen retracted and white blood cells decreased. On May 21, 2015, on the 12th day after stopping chemotherapy, the patient suddenly suffered from excessive sweating, nausea, and lethargy, and the spleen progressively enlarged from the two fingers under the costs to the flat umbilicus under the costs. Carbon dioxide binding capacity suddenly decreased to 12.0 mmol/L, blood glucose 4.67 mmol/L, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, total bilirubin, and direct bilirubin were all in the normal range. Blood gas analysis showed pH 7.232, lactic acid 18 mmol/L, partial pressure of carbon dioxide 16.6 mmHg (1 mmHg =0.133 kPa) and partial pressure of oxygen 134 mmHg. Consider decompensated metabolic acidosis combined with respiratory alkalosis. The efficacy of 10% glucose instillation and sodium bicarbonate acid correction was not good. May 28, 2015 Bone marrow morphology showed that monocytes occupied 58.5% of nuclear cells, of which 17% were progenital monocytes. On 29 May 2015, the patient was given chemotherapy with decitabine + mitoxantrone + cytarabine regimen. Blood gas analysis showed persistent lactic acidosis. During chemotherapy, white blood cell count, serum lactate level and lactate dehydrogenase quantification all decreased simultaneously, and the condition improved once. The leukocytes doubled and lactic acidosis reappeared during the intermediate period of chemotherapy. He was given decitabine + daunorubicin + cytarabine chemotherapy, and the condition recurred after another brief remission. On July 6, 2015, he was given emergency chemotherapy with decitabine + homoharringtonine + cytarabine regimen. The symptoms persisted and the lactate level continued to increase. At the same time, he was complicated by anal fissure and lung infection, and gradually appeared chest tightness, holding his breath, deep breathing, and entering a state of sleepiness. Died July 25, 2015. We examined the peripheral blood electron microscopy samples of patients with lactic acidosis again, which indicated that the tumor cells were hyperautophagic, and a large number of mitochondria were encapsulated and destroyed by autophagosomes (Figure 1)。

In recent years, it has been found that intestinal flora is closely related to the brain-gut axis, and flora dysbalance is related to a variety of diseases, including irritable bowel syndrome (IBS) and depression, thus giving rise to the concept of "microbiota-gut-brain axis"^[1]。 microglia is a kind of mononuclear macrophage, which is widely distributed in the central nervous system. Previous studies have found that it interacts with various components of the flora-intestine-brain axis. Taking IBS and depression as examples, this paper will introduce the research progress of the interaction between microglia and the flora-intestine-brain axis.

exosomes (exosomes), as a kind of tiny vesicles with diameters between 30 and 100 nm actively secreted by cells, have become a research focus in recent years. As a carrier of intercellular communication, it plays an important role in regulating the occurrence of central nervous system (CNS) infection, inflammatory response and damage repair.

Autophagy is the process by which damaged, denatured, or senescent proteins and various organelles within a cell are transported into lysosomes for digestion and degradation. Under normal conditions, autophagy maintains a dynamic balance between cell self-renewal and apoptosis, but when this balance is disrupted, insufficient or excessive autophagy may lead to the occurrence and development of disease^[1]。 According to different substrates, autophagy can be divided into three types: general autophagy, selective autophagy and mitochondrial autophagy. Autophagy can be divided into macroautophagy, micro-autophagy and chaperone-mediated autophagy according to the different pathways of cellular material transport into lysosomes, among which macroautophagy is the most important and typical form^[2]。 A large number of studies have shown that autophagy plays a particularly important role in the maintenance of central function and intracellular homeostasis of heart diseases. In many kinds of heart diseases, autophagy is accompanied by changes of cardiomyocyte autophagy, and it affects the occurrence and development of diseases. In different pathological models, autophagy plays different roles by influencing different signaling pathways. The purpose of this paper is to review the influence of autophagy on the occurrence and development of various structural heart diseases according to the current research progress at home and abroad.