2014年 · 第94卷第24期

Pancreatic fistula is one of the serious complications after pancreaticoduodenectomy (PD). The incidence rate of pancreatic fistula is 5% ~25%, and the mortality rate caused by pancreatic fistula is 20% ~50%^[1,2,3]。 In order to reduce or prevent the occurrence of pancreatic fistula, Peng Shuyou et al. in 1996^[3]Bundled pancreatojejunostomy (BPJ) was created, which has been widely used at home and abroad due to the remarkable efficacy of BPJ, while some shortcomings have also been reported, such as Buc^[4]Studies have concluded that BPJ may be a contraindication when the pancreatic stump is too large and does not match the size of the intestinal lumen. Therefore, over 15 years, we have successively created Binding pancreaticoastrostomy (BPG), end-to-side Binding Pancreaticojejunostomy (ESBPJ), Binding Pancreatic Duct to Mucosa Anastomosis (BDM), The system of bundling surgery was improved, and remarkable clinical results were achieved. In order to facilitate surgeons to reasonably choose the best anastomosis method according to their own experience and different individual conditions of patients, and further reduce or prevent the occurrence of pancreatic fistula, the relevant problems are explained as follows.

In August 2013, the author had the honor to go to the Swedish Medical Center in Seattle, USA for exchanges, and participated in part of the work of the general practitioner resident team of the center. I was deeply touched by the importance and efficiency of the general practitioner resident work. The general resident physician system is not only the development direction of the future medical model, but also has reference significance for the reform of China's medical system. Now talk about some views in combination with the reality of our country.

Enterobacteriaceae bacteria are the most important pathogenic bacteria in clinical bacterial infectious diseases, and the most important drug resistance mechanism of Enterobacteriaceae bacteria is the production of extended-spectrum beta-lactamases (ESBLs). ESBLs are a class of β-lactamases mediated by plasmids that can hydrolyze penicillins, oxyiminocephalosporins (including third and fourth generation cephalosporins) and monocyclic amide aztreonam, and can be inhibited by β-lactamase inhibitors. The diagnosis and early proper treatment of infections caused by ESBLs-producing Enterobacteriaceae bacteria have become important clinical issues that need to be solved urgently. Therefore, it is of great practical significance to formulate a consensus and provide clinicians with guidance that can be used for reference and have certain operability.

In 1977, German scholar Volker Rush first put forward the concept of microecology, that is, "microecology is ecology at the cellular or molecular level", and established the first microecology research institute, mainly studying the ecological therapy and ecological regulation of live bacterial preparations. Subsequently, Chinese scholars Kang Bai and Wei Xi further proposed that "microecology is a micro-level ecology, which is a branch of life science that studies the relationship between normal microorganisms and hosts"^[1]。 In the ecosystem of different parts of human body, intestinal micro-ecosystem, including intestinal bacteria and a few viruses, fungi and spirochetes, has become a hot spot in academic circles. The interaction of intestinal microorganisms, host mucosal barrier, nutrients and metabolites constitutes a dynamic equilibrium state, namely gut homeostasis. Once the dysbiosis of homeostasis exceeds the host's regulatory ability, it will lead to a series of diseases. In recent years, the spectrum of diseases associated with intestinal homeostasis imbalance has been expanding, and diseases such as inflammatory bowel disease, irritable bowel syndrome, antibiotic-associated enteritis, chronic liver disease, obesity, diabetes and even mental and behavioral abnormalities are closely related to it^[2,3,4]。 Understanding the composition, function, influencing factors and consequences of intestinal microecology, and making a reasonable microecological adjustment plan on this basis will help to improve the symptoms and prognosis of the above diseases.

Helicobacter pylori (H.pylori) is a pathogen with a high infection rate worldwide and can cause a range of gastrointestinal diseases, including chronic gastritis, peptic ulcer and gastric cancer^[1]。 althoughH.pyloriInfection can activate the host's immune system, but the body can't completely eliminate it, causing bacteria to survive in the body and continue to infect, eventually causing cells to become cancerous. The precise mechanisms remain unclear, which has becomeH.pyloriA major conundrum in prevention and treatment. Recent studies have proposed thatH.pyloriInfection can regulate cell autophagy, and this process is closely related to its pathogenicity^[2,3,4,5,6]。 Autophagy is a biological process in which cells use their own lysosomes to remove or degrade damaged organelles, misfolded proteins, and invading microorganisms^[7]。 NowH.pyloriThe regulation of autophagy by infection and its relationship with gastric carcinogenesis are reviewed.

Previous studies have found that genetic and environmental factors are associated with the onset of bronchial asthma^[1,2,3]。 Because the human genetic background is unlikely to change significantly in the short term, the regulatory role of epigenetic modification between environmental and genetic factors is particularly important. Epigenetics is nucleic acid inheritance not based on DNA difference, that is, phenotypic inheritance determined by the regulation of gene expression of the whole genome under the premise that the DNA sequence is unchanged during cell division. Non-DNA sequence information can be transmitted by mitosis or meiosis, characterized in that the genetic information can be inherited from generation to generation, the alteration of the genetic information is reversible, and the DNA nucleic acid sequence encoding the genetic information is unchanged. The epigenetic regulation of asthma occurrence includes DNA methylation, histone modification, non-coding RNA regulation, etc. Various epigenetic modifications interact and regulate each other, constituting a complete and complex epigenetic regulatory network.