2018年 · 第98卷第11期

pelvic organ prolapse (POP) is a common disease that affects the quality of life of middle-aged and elderly women, and it is the main disease that needs to be solved in urogynecology and pelvic floor reconstruction surgery, a new subspecialty of obstetrics and gynecology. With the deepening of clinical anatomy research and the rapid development of medical biomaterials, pelvic organ bulge can be regarded as a special hernia. Drawing on the successful experience of surgical hernia repair and the rapid development of artificial synthetic grafts in recent ten years, synthetic mesh implantation has become a new surgical method of POP, namely transvaginal mesh (TVM).

osteoporotic vertebral compression fracture (OVCF) is one of the common and serious complications of osteoporosis (OP). In the treatment of OVCF, we should not only pay attention to the treatment of fracture, but also not neglect the treatment of OP, the primary disease of fracture. OP is a systemic skeletal disease characterized by low bone mass, decreased bone strength, destruction of bone microstructure, increased bone fragility and easy fracture. This definition includes bone mineral density (BMD) and bone mass. bone mass includes bone turnover (high energy and low energy), bone accumulative injury and bone mineralization in addition to the quality of bone microstructure. Once OVCF is clearly diagnosed, OP health education for patients should be carried out immediately, OP-related examinations should be improved, and a standardized and individualized long-term anti-OP treatment plan should be formulated. While relieving the patient's pain, resuming the patient's daily activities, improving the patient's quality of life, improving the patient's BMD and reducing the risk of re-fracture^[1,2]。

percutaneous kyphoplasty (PKP) has been widely used in the minimally invasive treatment of osteoporotic vertebral compression fracture (OVCF) worldwide, and has achieved remarkable clinical results^[1,2,3]。 As of December 2016, a total of 1,443 hospitals in China reported about 73,992 cases of PKP surgery in 330 journals^[4]。 The technique injects bone cement into the fractured vertebrae body after percutaneous puncture and balloon expansion under image guidance, so that the diseased vertebrae is immediately strengthened and stabilized, its weight-bearing function is restored, the pain of the patient is quickly relieved, the quality of life is obviously improved, and the technique is widely recognized by doctors and patients^[5,6,7]。 Although the efficacy of PKP surgery is satisfactory, the high risk of PKP surgery cannot be ignored. Complications such as bone cement leakage and pulmonary artery embolism can not only cause spinal cord nerve injury, paralysis, and even life-threatening^[8]。 There are still related problems to be solved in preoperative diagnosis, intraoperative puncture, reduction, perfusion and postoperative management. Therefore, clinicians should pay attention to the standardized operation of PKP surgery, master the treatment strategies of common problems in the application of PKP surgery, reduce the incidence of surgical complications and improve the surgical efficacy.

A 46-year-old male was admitted to the Department of Gastrointestinal Surgery of Bethune First Hospital of Jilin University for "abdominal distension and abdominal pain accompanied by stopping defecation and exhaustion for 6 days". Abdominal distension and poor exhaust and defecation occurred 6 days before admission, which improved after conservative treatment; The symptoms aggravated after eating 5 days ago, and he was admitted to hospital for further diagnosis and treatment. Previous medical history: Two years ago, he was in remission after conservative treatment in a local hospital for intestinal obstruction. There was no history of abdominal trauma or surgery. Physical examination: The abdomen was slightly swollen, no gastrointestinal pattern and peristaltic wave were seen, no abdominal wall varicose veins were seen, and abdominal breathing was not limited. There is no tenderness, rebound pain and muscle tension in the whole abdomen. Unpalpable mass in the whole abdomen, unpalpable subcostal liver and spleen, unpalpable gallbladder, negative Murphy's sign. The mobile voicing was negative, and no bowel sounds were heard during auscultation. No sound of air passing through water or vibrating water was heard. No obvious abnormalities were found in digital anal examination. Whole abdominal multi-slice CT plain scan + three-phase enhancement (abdominal group) abdominal cavity small intestine dilatation, gas accumulation, see liquid gas plane, walk to the right pelvic small intestine lumen narrow, intestinal wall thickened, edge rough, enhancement scan uniform enhancement, adjacent small intestine intestine tubes close to each other, local mesenteric twist; Pelvic fluid shadow (Figure 1)。 Imaging diagnosis: small intestinal obstruction, the obstruction site is located on the right side of the pelvic cavity, and the local intestinal wall is thickened. After admission, there was no improvement after 1 week of conservative treatment such as fasting, fluid rehydration, enema, and gastrointestinal decompression. Exploratory laparotomy was performed. During the operation, about 200 ml of pale yellow ascites in the abdominal cavity was found, and extensive membranous adhesion between the small intestine and the abdominal wall under the incision and between the small intestine was found. No obvious nodules, calcification, and clear space-occupying lesions were found. After carefully releasing the adhesion between the small intestine and the abdominal wall, an incision protective sleeve was placed. The stenosis of the small intestine at 50 cm 100 cm away from the ileocecal region was further explored, and the adhesion formed a mass that could not be released. The proximal intestinal tube was dilated and the distal end was empty. It was judged that this was the obstruction site. Intraoperatively, "acute adhesive intestinal obstruction (abdominal cocoon?)" was diagnosed, and adhesion release, partial resection of the small intestine, intestinal anastomosis, intestinal obstruction catheter placement, and intestinal arrangement were decided. The operation went smoothly, and he returned to the ward after operation, and was given fasting water and fluid rehydration. Immunohistochemical results: Vimentin (+), β-chain protein (nuclear +), SMA (+) (Figure 2)。 Postoperative pathological report: spindle cell tumor-like hyperplasia was observed in local serous layer and mesentery, which was consistent with aggressive fibromatosis combined with morphology and immunohistochemistry (Figure 3)。 Two weeks after surgery, the patient's abdominal distension was significantly relieved, his exhaust and defecation were smooth, he did not complain of discomfort after eating liquid food, and he was discharged with an intestinal obstruction catheter. Four weeks after operation, the patient ate normally, exhausted and defecated normally, and the intestinal obstruction catheter was removed. The patient was followed up for 3 months without recurrence.

fecal incontinence (FI) refers to the involuntary discharge of liquid or solid feces at least twice within 4 weeks (Rome IV diagnostic criteria)^[1]。 According to the nature of fecal incontinence, it can be divided into sensory incontinence and motor incontinence (also known as urgency incontinence). This disease belongs to female pelvic floor dysfunction disease (PFD) together with urinary incontinence, pelvic organ prolapse and sexual dysfunction.

Autophagy and apoptosis are active or stress metabolic processes widely existing in eukaryotes, and are one of the key factors to maintain the dynamic balance between biosynthesis and catabolism of intracellular proteins. The disruption of the balance will cause tumor cell growth and cell death, so autophagy and apoptosis, two kinds of programmed cell death (PCD), play an important role in maintaining cell survival and development^[1]。 In mammalian cells, a series of autophagy-related proteins (ATGS) such as ATG4, ATG5, Beclin-1 (yeast ATG6 homologue) and ATG12 are involved in the molecular regulatory network of autophagy and apoptosis^{[2,3,4,5,6,7]}。 In this paper, the research progress of autophagy-related protein ATG5 regulating autophagy and apoptosis was reviewed, which laid a foundation for further research on the molecular mechanism of ATG5 regulating autophagy and apoptosis.

autoimmune encephalitis (AE) refers to the abnormal immune response of the body to the antigenic components of neurons, resulting in local or extensive central nervous system (CNS) lesions. With the development of neuroimmunological research and the advancement of autoantibody serological examination methods, since the discovery of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in 2007, new autoantibodies against neuronal cell surface or synaptic proteins have been continuously discovered, which has deepened people's understanding of autoimmune encephalitis. 2014 Sabater et al.^[1]Eight patients with sleep disorders as a prominent feature were found, who shared a common antibody acting on neuronal surface antigens-anti-Iglon5 antibody. Unlike previous autoimmune encephalitis, the disease was of chronic progressive course, characterized by abnormal sleep and sleep apnea. Genetic testing found HLA-DRB1*1001 and HLA-DQB1*0501 alleles, and serum or cerebrospinal fluid (CSF) IgLON5 antibody positivity. Because the disease is rare, clinicians don't know enough about it, and it is easy to neglect the detection of IgLON5 antibody, which is misdiagnosed as neurodegenerative disease. This article discusses the pathogenesis, clinical characteristics, diagnosis, differential diagnosis, treatment and prognosis of anti-Iglon5 antibody-related encephalopathy.