2017年 · 第97卷第22期

Benign prostatic hyperplasia (BPH) is a common and frequently occurring disease in elderly men with progressive dysuria as the main clinical feature. The clinical symptoms of BPH are mainly frequent urination, urgency, urinary incontinence, etc., collectively referred to as lower urinary tract symptoms (LUTS). As we all know, the normal urination of men is coordinated by the contraction of the bladder detrusor and the opening of the sphincter of the prostate. Unfortunately, the surgical determination of prostatic hyperplasia has been mainly based on the size of the prostate and symptoms such as LUTS for a long time, and the assessment of bladder function damage caused by BPH has been ignored, or the assessment of bladder function has not been taken into account in the surgical determination. According to statistics, at least 50% of middle-aged and elderly men over 50 years old suffer from BPH, which significantly reduces their quality of life^[1]。 Since the 1990s, alpha adrenergic receptor blockers have been used as the first-line treatment for LUTS secondary to BPH. Today, despite the rapid changes in drugs, surgical treatment of benign prostatic hyperplasia is a better choice when patients voluntarily require or due to poor drug treatment effect, intractable urinary retention, urinary tract obstruction, etc. Moreover, clinical statistical studies have shown that surgical treatment of prostatic hyperplasia is less expensive than drug treatment^[2]。

A 36-year-old male was admitted to the Department of Nephrology, Peking University First Hospital on July 9, 2015 due to fatigue and anorexia for more than 2 months, bilateral calf muscle pain with decreased urine output for 6 days. The patient developed anorexia without obvious trigger 2 months ago, nausea, abdominal distension, intermittent or small amount of vomiting after eating, accompanied by fatigue, no abdominal pain, diarrhea, no changes in urine output and urine color, and did not see a doctor. In the past 6 days, the patient had aggravated fatigue and anorexia, inability to move, accompanied by bilateral calf muscle pain, and conscious urine output decreased compared with before, and the degree of reduction was not clearly described. Three days ago, blood pressure was 90/60 mmHg (1 mmHg =0.133 kPa), blood creatinine (Scr) 702 μ mol/L, blood urea nitrogen (BUN) 36.08 mmol/L, blood potassium 2.10 mmol/L, blood sodium 131 mmol/L, blood chlorine 48 mmol/L, and blood HCO were checked in the emergency department of our hospital₃^－68.6 mmol/L, creatine kinase (CK) 737 U/L (reference: 25-195 U/L), blood myoglobin 451 μ g/L (reference:<100 μ g/L); Urinary pH 8.0, urine specific gravity 1.010, urine protein trace, urine sediment microscopy negative; Blood gas analysis showed pH 7.57, partial pressure of carbon dioxide (PCO₂) 83 mmHg, oxygen partial pressure (PO₂) 109 mmHg, lactic acid (Lac) 10.2 mmol/L, HCO₃^－>60 mmol/L. Chest X-ray showed elevation of the left diaphragm. After gastrointestinal decompression, about 3,000 ml of coffee-colored substance was drained, and the occult blood of the drained substance was negative. Considering "rhabdomyolysis, acute kidney injury (AKI)", after symptomatic fluid rehydration and correction of electrolyte disorder treatment for 3 days, he was transferred to the nephrology ward. The patient has lost about 10 kg of weight in the last two months since the onset of the disease. He has a history of epilepsy for more than 20 years, with 3 to 4 seizures a year and no regular treatment. Drinking history for more than 10 years, 250~400 ml/d. Repair of gastric perforation after alcohol consumption 6 years ago. History of hypertension, diabetes, kidney disease denied. Family history of genetic diseases and similar diseases were denied.

A 41-year-old male was admitted to the hospital in June 2016 due to discomfort in the right upper abdomen and gallbladder stones found by ultrasound for 3 years, and acute cholecystitis with intermittent episodes of vomiting and diarrhea for 1 year. In January 2005, the patient underwent combined pancreas-kidney transplantation in our hospital due to "type 1 diabetic nephropathy with renal failure". The operation went smoothly, and routine oral anti-rejection drugs were taken after the operation and regular review was performed. The patient has developed chronic renal dysfunction in the past 5 years, manifested by creatinine maintained at about 200 μ mol/L, normal urine output, chronic rejection excluded by renal puncture pathology, and suspected FK506 toxicity (tacrolimus capsules, Zhejiang Hisun Pharmaceutical, batch number: H20160047). At present, FK506 has been discontinued, and oral Mifu (Beijing Novartis Pharmaceutical Co., Ltd., batch number: H20160051) is used alone to maintain immunosuppression. The function of the transplanted pancreas and blood glucose levels have been normal for 11 years. The general condition of the patient was acceptable when he was admitted to hospital, and no obvious abnormalities in the heart and lungs were found. The abdomen was flat and soft, with tenderness in the right upper abdomen, no muscle tension and rebound pain, surgical scars in the lower abdomen, normal intestinal sounds, negative mobile voices, and mild depressed edema in both lower limbs. Auxiliary test: white blood cells 4.5×10⁹/L, neutrophils 0.62, amylase 188 U/L, lipase 376 U/L, creatinine 275 μ mol/L, urinary albumin ALB 87.2 mg/L. Abdominal ultrasound showed: gallbladder swelling and multiple gallbladder stones. The blood flow of the transplanted pancreas and kidney was not abnormal, and the ultrasonography of liver, gallbladder, pancreas and spleen was not abnormal.

Craniopharyngioma is a benign tumor that originates from the squamous epithelial cells remaining in the cranial buccal sac during the development of pituitary embryo. Most of them are located on the saddle, and a few are in the saddle or protruding in the third ventricle. The space-occupying effect of tumor often affects the structure and function of hypothalamus, pituitary gland and optic chiasm. The incidence rate is 0.5-2.0 per million person-years, and 30%-50% of the disease occurs in childhood or adolescence. The clinical manifestations include increased intracranial pressure, visual field impairment and endocrine dysfunction^[1]。 According to the World Health Organization classification^[2]There are two distinct subtypes of craniopharyngiomas: adamantinomatous craniopharyngioma (ACP) and papillary craniopharyngioma (PCP), both previously identified on the basis of histology and epidemiology. Recent studies have shown that these two subtypes have different molecular bases, providing strong evidence for the origin and molecular etiological pathogenesis of craniopharyngioma, and confirming the different characteristics of the two subtypes as well as related molecular drug therapeutic targets^[3,4]。

Most patients with prostate cancer in China are in advanced stage when they see a doctor, and most of them use salvage treatments, such as endocrine therapy and chemotherapy, to prolong survival time and relieve symptoms^[1,2]。 Adenovirus-mediated gene therapy and viral therapy as tumor biotherapeutic approaches have potential tumor cell inhibition effects. Wild-type adenovirus lacks tumor targeting and can infect normal tissue cells, resulting in side effects and toxicity in human body. In early studies, many prostate tissue-specific biomolecules have been discovered. After inserting their gene promoters upstream of adenovirus therapeutic genes, the expression of downstream therapeutic genes can be restricted to tumor cells to play a role in tumor targeting, including prostate specific antigen (PSA), human kallikrein 2 (hK2), prostate basic protein (PB), prostate specific membrane antigen (PSMA), etc. With the deepening of research on tumor biomarkers, it will be found that the gene promoter of highly expressed biomolecules in a variety of tumor tissues including prostate cancer has the same tumor targeting effect after recombination with adenovirus. The significance of these prostate cancer-related biomolecules in tumor targeting is discussed as follows.

Publishing ethics is a work involving journal editors and publishers and publishing authors, universities and research institutions. This work is crucial. Publication ethics ensure that credibility of scientific research published worldwide and are central to the development of public policy and to the solution of the most pressing issues facing the general population, from public health protection to climate change mitigation^[1]。 The most important thing for this work is international cooperation. In the words of Ginny Barbour, Chair of the Publication Ethics Committee (COPE): "We need to be responsible for the integrity of the articles we publish, and it is not just the work of editors". More than 120 delegates from all over the world attended this COPE seminar. The important views of experts who gave keynote speeches at the COPE Symposium-China Forum held in Beijing on March 26, 2017 are introduced as follows.