2015年 · 第95卷第42期

Good sleep is very important to restore physical strength, relieve fatigue, maintain abundant energy, promote early recovery of diseases and enhance the ability of body to resist diseases. However, due to the special environment such as hypoxia, cold and dryness, people living in the plateau, especially newcomers, will have different degrees of sleep breathing disorders, such as frequent awakening, sleep hypopnea, periodic breathing and apnea. Because of plateau hypoxia causes respiratory disturbances, thus causing further hypoxia. Severe hypoxia will damage brain function, which is manifested as weakness in the morning, headache in the morning, dizziness, memory loss, slow response, abnormal behavior and sexual dysfunction.

Sleep disorders of breathing (SDB) related diseases have gained more and more attention, among which obstructive sleep apnea hypopnea syndrome (OSAHS) is the most common, with a prevalence of 2% to 4% in middle-aged people^[1]。 Although great progress has been made in the pathogenesis and epidemiological investigation of OSAHS and other diseases, there are few studies on the sleep health status of the bedmate of SDB patients. In 1987, Cartwright and Knight^[2]It is mentioned for the first time that the bedmate of SDB patients actually also has sleep quality problems. Subsequent studies mentioned that OSAHS couples have poor sleep quality, marital relationship and personal relationship, and even make marriage a burden for some couples with OSAHS^[3,4]。 However, given the insufficient attention paid to SDB disease itself at that time, the problem of sleep quality for bedmates was naturally ignored. Until 2003, Ashtyani and Hutter^[5]Explicitly suggest that sleep health problems in bedmates are one of the collateral harms caused by SDB. With the in-depth discussion of this issue, it gradually aroused people's attention to this part of the population. In the past 10 years, the research on the sleep problem of the bedmate of SDB patients has involved many aspects of clinical, psychological and social psychology, but all of them are small-scale clinical observation data. In order to further understand the severity of collateral injury of SDB to patients' bedmate and its impact on society, it is expounded as follows in combination with relevant research at home and abroad.

Ventricular hemorrhage (IVH) is a common critical and severe disease in neurosurgery. It is mostly caused by cerebral parenchymal hemorrhage breaking into the ventricle, and a few are primary intraventricular choroid plexus hemorrhage^[1]Acute obstructive hydrocephalus caused by obstruction of ventricular cast cerebrospinal fluid circulation pathway after hemorrhage, resulting in cerebral hernia. At present, external ventricular drainage (EVD) is used for ventricular hemorrhage and acute hydrocephalus caused by various causes, but its complications include intracranial infection, cerebrospinal fluid leakage, tube blockage and the need to replace or replace external drainage after infection. Once infected, the mortality and disability rate are extremely high. According to the literature, the infection rate after EVD is 0~45%^[2]。 The purpose of this study was to analyze the factors associated with intracranial infection after ventricular hemorrhage with external ventricular drainage, so as to reduce the rate of intracranial infection after EVD.

A 51-year-old female suffered from uniform swelling of the index finger of her right hand (Figure 1), severe pain during extension and flexion for more than 20 days, and went to our hospital on January 22, 2015. The patient was usually in good health and had no history of hypertension, heart disease, diabetes, immune diseases and other diseases, nor a history of hormone use. He had a history of stabbing in the distal section of his right index finger in mid-September 2014. Laboratory test: Blood routine showed white blood cells 7.9×10⁹/L, neutrophils 0.62, lymphocytes 0.31; The X-ray film of the right index finger showed no obvious bone destruction; B-ultrasound of the right index finger showed thickening of flexor tendon tendon sheath, suggesting flexor tendon tenosynovitis. On January 23rd, the patient brought the examination results to the hand and foot surgery department of a tertiary hospital in Hebei Province. According to the clinical manifestations and examination results, the patients were treated with "tenosynovitis of flexor tendon of right index finger", followed by 1 ml of compound betamethasone injection +1 ml of 2% lidocaine for local closure. The swelling and pain began to decrease 4~5 h after treatment, significantly decreased after 24 h, and disappeared after 3 d, and the function was completely recovered. On January 31st, the proximal interphalangeal joint of the distal segment of the right index finger appeared redness, swelling, high skin temperature, and slightly limited activity, but the pain was not obvious. Then he went to our hospital again, and the blood routine showed that white blood cells were 10.6×10⁹/L, neutrophils 0.64, lymphocytes 0.29; C-reactive protein (CRP)<3.36 mg/L; erythrocyte sedimentation rate 2 mm/1 h; B-ultrasound of the right index finger showed a small amount of local hypoechoic, and the tendon sheath of the flexor tendon was slightly thickened, suggesting that the inflammatory focus abscess may be flexor tendon tenosynovitis. Following the intravenous infusion of penicillin 4 million U +100 ml of normal saline, twice/d for 5 days, it was ineffective, and the swollen area felt a fluid wave sensation, which spread to the proximal and distal interphalangeal joints of the middle segment of the index finger (Figure 2)。 On February 4 and February 6, respectively, we punctured under sterile conditions, and took blood pus samples and sent them to the microbiology room of our hospital for bacterial culture. Both cultures suspected "Nocardia" infection. Minocycline 100 mg was administered orally twice a day since February 8. At the same time, topical disinfection with 3% iodine tincture, once/d, for more than 15 minutes each time, then deiodination with ethanol, and finally application of vitamin E skin care oil. After taking medication and local disinfection for 3 days, the skin temperature returned to normal, the redness and swelling were significantly reduced on the 10th day, and it was basically cured on the 20th day. After stopping taking medication and local disinfection, it was cured on March 10th. There was no recurrence after nearly 3 months of follow-up.

A 14-year-old male was admitted to hospital on November 15, 2014 due to "mixed phenotype acute leukemia for more than 6 months, haploid hematopoietic stem cell transplantation for more than 3 months, abdominal pain, nausea, vomiting and constipation for 2 days". Physical examination: clear consciousness, poor spirit, no yellowing staining, rash, bleeding spots and ecchymosis on the skin and mucous membranes, no obvious swelling of superficial lymph nodes, no obvious abnormalities in the heart and lungs, soft abdomen, no obvious tenderness, rebound pain, no tenderness, percussion pain in the limbs and spine, and no edema in the limbs. After admission, blood routine, urine and feces routine and liver and kidney function tests were performed, and no obvious abnormalities were found. Blood calcium was 3.89 mmol/L, and abdominal color Doppler ultrasound showed no obvious abnormality. Bone marrow puncture: 3.6% problasts, 97% short tandem repeat (STR), CMV-DNA and Epstein-Barr virus-DNA (EBV-DNA) negative, parathyroid hormone (PTH) decreased: 100 ng/L, interleukin (IL) 1, IL-6, and tumor necrosis factor α (TNF-α) were normal. Skeletal emission single photon computed tomography (ECT) showed no significant bone damage. The blood calcium decreased to normal after 2 days of treatment with diuresis, hydration, pamidronate disodium and salmon calcitonin, and hypercalcemia recurred after 10 days; After another treatment of calcification and other treatments, and re-examination of bone marrow showed that prooblasts accounted for 12.8%, and reserved hematopoietic stem cells were retransfused, and bone marrow was re-examined 10 days later. Because the patient's family members did not agree to further immunotyping and other examinations, only morphological re-examination showed recurrence (35.2% of prooblasts). After 1 course of chemotherapy with Hyper-CVAD regimen (cyclophosphamide, vindecine, doxorubicin, dexamethasone), 6% of the protoplasts were re-examined, and the condition improved and the protoplasts were discharged.

Vascular access is the "lifeline" of maintenance hemodialysis patients. The quality of vascular access largely determines the quality of life and even the life span of hemodialysis patients. Autologous arteriovenous fistula is recognized as the best vascular access^[1]。 After the establishment of autologous arteriovenous fistula, the structural adaptive changes of blood vessels due to the changes of intra-luminal pressure and flow are called vascular remolding. The state of vascular remolding directly determines the outcome of arteriovenous fistula. The ideal result of vascular remolding is that the fistula matures, while abnormal or poor vascular remolding will cause the maturation obstacle or even occlusion of the fistula. Vascular remodeling throughout the maturation, use and complication of arteriovenous fistula^[2,3,4,5,6]。 Hemodynamic changes are the initial factor of vascular remodeling, and shear stress is recognized as the most important hemodynamic factor^[2,3,4,5]。 The research on shear force has been started since the 1970s, but the research on the relationship between shear force and arteriovenous fistula vascular remodeling and related complications is still in its infancy. The blood flow pattern of arteriovenous fistula is different from any other blood flow pattern in physiological state, and its hemodynamics has its own characteristics. Therefore, the shear force related to arteriovenous fistula also has its own uniqueness. Fully understanding the characteristics of shear force in arteriovenous fistula can help to understand the mechanism of vascular remodeling, maturation and complication of fistula.

Sequelae of polio (PPS) refers to a series of new or slowly developing syndromes in polio survivors after a stable period of about 20 to 30 years, which are mainly manifested by fatigue, fatigue, muscle and joint pain, and decreased tolerance to cold^[1,2]。 In patients with PPS, there will be different degrees of sleep apnea (SDB), including obstructive sleep apnea syndrome, central sleep apnea syndrome, mixed sleep apnea syndrome and sleep hypopnea syndrome^[3]。 Although there are many reports of SDB caused by other neuromuscular diseases, there is still little attention to SDB related to PPS, probably because of the following reasons: (1) SDB in PPS patients occurs later (mostly after middle age), and it is a slow course, which is easily overlooked; (2) For a long time, the concept of PPS has not been comprehensively understood, and more attention has been paid to the surgical correction of young patients' physical disabilities, but the breathing, especially sleep breathing, of the elderly is neglected. At present, most of the millions of polio survivors in China are in the high incidence period of PPS. Strengthening the understanding of SDB in PPS patients is the key to ensure timely diagnosis and treatment, improve the quality of life and reduce complications^[3]。 The mechanisms, clinical manifestations, related tests and interventions of SDB in patients with polio are reviewed below.

cell free DNA refers to a fragment of free DNA located in the peripheral environment, which can be in physiological or pathological conditions^[1]Released into blood, cerebrospinal fluid, urine, sputum, or feces^[2]About 160-180 bp, is the product of DNA degradation of target cells^[3]。 As a class of cfDNA, circulating tumor DNA (ctDNA) derived from tumor cells can indirectly reflect the relevant characteristics of tumor disease. Therefore, non-invasive detection of this class of free nucleic acids is also considered to be an effective "liquid biopsy" technique^[1,2,3,4]。