2016年 · 第96卷第32期

Diabetic foot refers to foot infection, ulcer and/or deep tissue destruction associated with local nerve abnormalities and distal peripheral vascular lesions of lower limbs in diabetic patients. It is one of the four major complications of diabetes. It is a common result of neuropathy and vascular lesions in diabetic lower limbs. The specific pathogenesis of diabetic foot has not been fully elucidated at present, but the existing studies have shown that diabetic peripheral neuropathy (DPN) is one of the most important initiating risk factors of diabetic foot^[1]Infection and ischemia are the key factors affecting the healing and amputation rate of diabetic foot ulcer^[2]。 Recent research results show that the prevalence of peripheral neuropathy and peripheral vascular disease in Chinese patients with diabetic foot ulcer is 73.7% and 48.9%, respectively, much higher than that in non-diabetic people^[3]。 Many studies at home and abroad have confirmed that peripheral neuropathy is one of the important causes of diabetic foot ulcer^[3,4]。

In the development of diabetes, the function of islet beta cells is progressively lost, which ultimately leads to the worsening of hyperglycemia and the occurrence of various complications. One of the most important strategies for treating diabetes is to restore the total amount of functional beta cells. At present, the commonly used strategies are as follows: (1) islet transplantation or pancreatic transplantation; (2) inducing pluripotent stem cells (including embryonic stem cells and induced pluripotent stem cells) or various types of adult stem cells (such as mesenchymal stem cells, liver precursor cells, etc.) to differentiate into insulin-secreting cells in vitro and then performing cell transplantation to supplement the number of pancreatic islet cells; (3) promoting the direct transdifferentiation of adult stem cells (such as pancreatic stem cells, etc.) into islet-like cells in vivo, and restoring the total amount of β cells; (4) Transforming terminally differentiated cells (such as fibroblasts, etc.) directly into β cells in vivo or in vitro^[1]。

adenocarcinoma of esophagogastric junction (AEG) refers to an adenocarcinoma lesion originating from the glandular epithelium of the upper gastrointestinal tract and invading the esophagogastric junction. At present, scholars in the East and West still have controversies about how to define AEG^[1]。 As the incidence of distal gastric cancer decreased, the incidence of AEG increased year by year^[2],And because that biological behavior of AEG is different from that of esophageal cancer and gastric cancer in the true sense^[3]Therefore, more scholars began to pay attention to this special type of malignant tumor. Radical surgery combined with perioperative chemoradiotherapy is still the main treatment for AEG, but the prognosis is still poor^[4]。 Because of the special anatomical position of AEG, there are still many controversies in the surgical diagnosis and treatment. Therefore, clarifying the related problems is of great benefit to the clinical diagnosis and treatment of AEG, especially reasonable classification, staging, surgical methods, esophageal and gastric resection range and lymph node dissection range, which are of great significance to the quality of life and prognosis of patients.

By the end of 2014, there were 2,374,900 practicing physicians, 2,892,500 practicing (assistant) physicians and 3,004,100 registered nurses in China^[1]。 Medical staff are not only angels in white who save lives and heal the wounded, but also a huge innovative group in China, who can discover good treatment methods and new technologies in clinical practice. In reality, a large number of hospitals have applied for patents, and many medical staff appear in patent application materials and patent authorization certificates as inventors.

A 46-year-old female was admitted to the First Affiliated Hospital of Suzhou University on October 18, 2013 due to left chest and back pain for 20 days and wheezing for 3 days. 20 days ago, the patient felt left chest and back pain without obvious trigger, no cough and sputum, no fever, no chest tightness and shortness of breath, which was not paid attention to. Before the onset of the disease, he had symptoms such as nasal congestion and bloody purulent discharge. On October 10, 2013, he went to the local hospital for a chest X-ray (Figure 1) indicates left lung infection. He was admitted to a local hospital for treatment. The erythrocyte sedimentation rate (ESR) was 110 mm/1 h after hospitalization; Blood routine: white blood cells 10.20×10⁹/L, eosinophil count 0.60×10⁹/L, the proportion of eosinophils was 5.8%. Cefuroxime, levofloxacin and other anti-infective treatments were given. October 13 Chest CT (Figure 2) shows mass shadows in the anterior segment of the left upper lobe and the dorsal segment of the left lower lobe with exudation. The pulmonary lesions were worse than before, and there was fever, with the highest body temperature of 38.2℃, and complained of joint pain, mainly pain in the left elbow joint and right knee joint, without rash, nausea and vomiting, chest tightness and palpitation. On October 17, I started to develop scleritis in both eyes, right shoulder pain, and nocturnal asthma symptoms. Reexamination of blood routine: white blood cells 11.93×10⁹/L, eosinophil count 1.18×10⁹/L, the eosinophil ratio was 9.9%. On the 17th, methylprednisolone was given intravenously (80 mg/d), and moxifloxacin and cefoperazone/sulbactam were changed for anti-infective treatment. Ocular symptoms and asthma symptoms were improved, but symptoms such as chest tightness and shortness of breath were aggravated. Admitted to our department on October 18th. Previous history of anemia with a course of several years. Individual marriage and childbirth and family history are not special.

A 48-year-old female was admitted for 6 months due to repeated oral ulcers. "Fungal infection" was considered in the outside hospital, but the treatment was ineffective. The ulcer gradually increased, accompanied by oral albuginea and pain, affecting eating and speaking, and losing weight, so he went to the stomatology department of our hospital and underwent left tongue tip ulcer resection. The pathology showed: (left tongue tip) B-cell non-Hodgkin's lymphoma, tending to diffuse large B-cell lymphoma (DLBCL) (Figure 1), was admitted to the lymphoma department of our hospital on August 27, 2014. He has been suffering from systemic lupus erythematosus for 25 years and has been treated with drugs (mycophenolate mofetil capsules, methylprednisolone tablets, etc.). Type 2 diabetes was diagnosed 3 months ago. Cerebral infarction was diagnosed 1 month ago.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease mainly manifested by dyspnea, fatigue and decreased activity endurance. It is mainly due to repeated pulmonary thromboembolism and inability to dissolve, which leads to pulmonary vascular remodeling, progressive increase of pulmonary vascular resistance, pulmonary hypertension and right ventricular insufficiency. The two-year cumulative incidence of CTEPH after acute symptomatic pulmonary embolism has been reported to be 0.1% to 9.1%^[1]The reason for such a large deviation in the incidence rate is due to different judgment criteria. There are currently no data on the exact population incidence rate. Some data show that the incidence rate is about 5/1 million people per year^[2]。 In 2015, the European Society of Cardiology/European Society of Respiratory Diseases (ESC/ERS) jointly published the latest edition of the Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension^[3]。 The diagnostic process and treatment strategies for CTEPH according to the guidelines are described below.

Hepatitis C virus (HCV) is a very common blood-borne infectious disease. According to statistics, the infection rate in the United States is about 1.0% to 1.5%^[1]。 Hematopoietic stem cell transplantation (HCT) is currently widely used to treat patients with hematological diseases. According to a prospective study by the European Hematopoietic and Bone Marrow Transplantation Group, 6.0% of HCT recipients are screened for HCV-RNA positive^[2]。 The diagnosis and treatment of HCV in HCT recipients is unique. These patients have a higher risk of liver disease progression and viral replication. HCV diagnosis is more difficult, and there is no uniform guideline to standardize treatment standards^[3]。 In the past decade or so, the treatment of HCV infection is mainly peginterferon combined with ribavirin. However, studies have shown that the sustained virologic response rate (SVR) and tolerability of this regimen in cancer and hematopoietic stem cell transplantation (HCT) patients are poor, and because nearly 30% of HCT patients have contraindications for peginterferon and ribavirin treatment, the application of this regimen in HCT patients is greatly limited^[4]。 In recent years, due to the emergence of new direct-acting antiviral agents (DAA), interferon combination therapy is gradually being eliminated, changing the treatment mode of HCV infection in the general population. However, there are few studies on the diagnosis and treatment of HCV infection in HCT donors and recipients. Therefore, this article summarizes the early screening and treatment of HCV infection in HCT donors and recipients to provide guidance for clinicians.