ObjectiveTo understand the role of metformin on reducing incidence of type 2 diabetes mellitus (T2MD) patients complicated with liver cancer. MethodThe related literatures of metformin treated patients with T2MD complicated with liver cancer at home and abroad in recent years were reviewed. ResultsA large number of epidemiological and clinical data showed that the metformin might prevent the occurrence of the T2MD patients complicated with liver cancer, its mechanism was mainly inhibited the proliferation of hepatoma cells through the ATM-LKB1-AMPK-mTOR pathway, PI3K/Akt/mTOR pathway, or miRNA. The current controversy was the authenticity of the data, the influencing factors included the aging problem and characteristics of metformin user. The prospective study design rigorous remained to be clarified. ConclusionMetformin could reduce the incidence of T2MD patients complicated with liver cancer, and could inhibit the growth of liver cancer cells, which provides a new way of thinking for the comprehensive treatment of liver cancer.
Progressive ischemic stroke is one of the major diseases damaging the health of Chinese people. Its pathogenesis is complex and there are many influencing factors, but the treatment methods are limited. In recent years, the rapid development of neuroimaging and the results of various clinical trials have been reported in succession, which have made new progress in the clinical diagnosis and treatment of progressive ischemic stroke. This paper summarizes the progress of progressive ischemic stroke, introduces its pathogenesis (including increased intracranial pressure and reduced perfusion pressure, thrombosis progression, hemorrhagic transformation, cerebral edema, and inflammatory response), influencing factors, predictive indicators (including image indicators, biochemical indicators, and molecular biology indicators) and treatment (including admission to “stroke unit”, intravascular treatment, platelet aggregation inhibition treatment, anticoagulation treatment, and general treatment), to provide references for preventing the occurrence and development of progressive ischemic stroke, assessing the condition, guiding treatment and improving the prognosis.
Objective To study the preventive measure of the subambient temperature burn by analysing the pathogenesis feature. Methods The cl inical data were analysed from 351 cases of subambient temperature burn between February 2004 and February 2009, including age, sex, burn season, burn factors, burn position, burn area, burn degree, treatment way, and wound heal ing. Results Subambient temperature burn occurred in every age stage. The susceptible age stages included infant, children, and the elderly. Female patients were more than male patients. The common burn reasons werehot-water bottle burn, honey warm keeper burn, and heating device burn. The peak season was winter. Lower l imb was the most common site of the subambient temperature burn. The deep II degree to III degree were the most common level, and the burn area was always small, often 1% of total body surface area. Most of patients were treated with changing dressings at cl inic and few patients needed hospital ization. Though the surface of wound could heal finally, and the wound healed well with no obvious scar in patients who received operation. Conclusion Subambient temperature burn is the frequently encountered disease in winter. Use of the warming articles should be cautious, at the same time safety awareness should be strengthened so as to decrease the incidence rate of subambient temperature burn and the injury degree.
ObjectiveTo explore the pathogenesis of cervical spondylosis combined with cervicogenic vertigo, and to investigate the clinical results of anterior discectomy and fusion in treating the disease. MethodsA retrospective study was performed on 83 patients with cervical spondylosis myelopathy (n=60, 72%) or radiculopathy (n=23, 37.3%) accompanied by sympathetic symptoms such as dizziness between March 2008 and November 2012. The disease involved single segment in 29 cases, double segment in 50 cases, and triple in 4 cases. All the segments involved were treated with anterior discectomy and fusion. Vertigo alleviation was observed before surgery, 3 days after surgery, and during the final follow-up. Neurological status was evaluated by Japanese Orthopedic Association (JOA) score system and sympathetic symptoms were evaluated with vertigo symptom and function scoring system. ResultsThe average follow-up was 21 months (ranging from 12 to 30 months). Significant difference was observed between sympathetic symptom scores and JOA scores before surgery and 3 days after surgery or at the final follow-up (P<0.05), but no significant difference was found between the scores 3 days after surgery and during the final follow-up (P>0.05). ConclusionThe surgical effect for cervicogenic vertigo is often accompanied by the relief of spinal cord and nerve roots symptoms. Surgery is effective for cervical spondylosis combined with cervicogenic vertigo.
Acute carbon monoxide poisoning is a common and frequently occurring disease in winter and spring in China, with high disability and mortality. Delayed encephalopathy is a serious sequela after the pseudo-convalescence. Its mechanism is complex, including environmental and genetic factors, hypoxia and energy metabolism disorder, cytotoxicity and oxygen free radical damage, immune disorder and inflammatory activation, neurotransmitter disorder, brain parenchymal changes, vascular and hemorheological abnormalities, calcium overload, and cell apoptosis. At present, methods for predicting delayed encephalopathy in acute carbon monoxide poisoning include detailed inquiry of medical history, laboratory examination of relevant indicators, electrophysiological examination, brain imaging examination, and evaluation scale prediction. This review summarizes the research status of the pathogenesis and early prediction methods of delayed encephalopathy in acute carbon monoxide poisoning, with a view to providing reference for future research directions.
Hydroxychloroquine retinopathy is an ocular lesions that develops following long-term or excessive use of hydroxychloroquine. The early clinical presentation of this lesion is nonspecific and is often detected when severe central vision impairment occurs in late stage. It currently mainly includes hydroxychloroquine binding to melanin, inducing degeneration of the retinal pigment epithelium, increasing the pH of lysosomes in the retinal pigment epithelium and interfering with the visual cycle. In recent years, with the development of retinal imaging technology and the in-depth study of hydroxychloroquine retinopathy, characteristic fundus structural changes such as retinal and choroidal thickness and blood vessels may occur in the early stage. This not only provides an important basis for the early diagnosis of hydroxychloroquine retinopathy, but also provides important clues for investigating its pathogenesis. Clinicians' proficiency in relevant fundus changes and pathogenesis will facilitate early diagnosis and treatment, while also minimizing irreversible central vision impairment in patients.
The pathogenesis of Vogt-Koyanagi Harada disease (VKH) has not yet been fully defined. Current studies mainly suggest that VKH is actually an autoimmune disease, especially related to the immune response mediated by various signal transduction pathways involved in the function of T cells. In recent years, the influence of the balance imbalance of various T cell subsets in cellular immunity on the pathogenesis of VKH has been a hot research direction. Currently, T helper cell 17/T regulatory cells, balance is the focus of clinical research, meanwhile, new discoveries and potential clinical treatment schemes have been made for related cellular pathways, particularly the Janus kinase/signal transducers and activators of transcription pathway and NF-kappa B pathway. The exploration of B cells in the pathogenesis of VKH has also achieved initial results through the successful application of various targeted drugs. In the future, further screening and localization of genes or proteins that are abnormally regulated or expressed in VKH, for which early comprehensive and in-depth exploration will be helpful, thus improve the efficacy of clinical treatment programs and develop new therapeutic targets.
Objective Glucocorticoid is the main cause of non-traumatic avascular necrosis of femoral head. To explore the changes of reactive oxygen species (ROS) in the bone microvascular endothel ial cells treated with glucocorticoid so as to investigate the pathogenesis of steroid-induced avascular necrosis of femoral head. Methods The cancellous bone of femoral head was harvested from voluntary donators undergoing total hip arthroplasty, and then the bone microvascular endothel ial cells were isolated by enzyme digestion. The cells at passage 3 were cocultured with different concentrations of hydrocortisone (0, 0.03, 0.10, 0.30, and 1.00 mg/mL) for 24 hours. MTT assay was used for the inhibitory rate of cell prol iferation, flow cytometry for apoptosis rate, and fluorescence probe for the production of ROS and xanthine oxidase (XOD). Results At 2-3 days primary culture, the cells were spindle and arranged l ike cobbles and they reached confluence after 1 week. The inhibitory rates of cell prol iferation in 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 20.22% ± 2.97%, 22.94% ± 4.52%, 43.98% ± 3.35%, and 78.29% ± 3.85%, respectively; and 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 2 low-concentration groups (0.03 and 0.10 mg/mL groups). The apoptosis rates in 0, 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 0.10% ± 0.01%, 0.23% ± 0.02%, 1.83% ± 0.04%, 6.34% ± 0.11%, and 15.33% ± 0.53%, respectively; 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 0 mg/mL group. In 0, 0.30, and 1.00 mg/ mL groups, the ROS levels were 57.35 ± 7.11, 120.47 ± 15.68, and 166.15 ± 11.57, respectively, and the XOD levels were 0.017 9 ± 0.000 9, 0.028 3 ± 0.001 7, and 0.067 7 ± 0.004 1, respectively; there were significant differences in the levels of ROS and XOD among 3 groups (P lt; 0.05). Conclusion Increasing of ROS production in bone microvascular endothel ial cells can be induced by high concentration glucocorticoid, and it can result in cell injury
Central serous chorioretinopathy (CSC) is one of the main causes of impaired visual function in middle-aged men. CSC is characterized by a thickening of the choroid and hyperpermeability of the choroidal vessels, resulting in serous subretinal fluid. The pathogenesis of CSC is not fully understood. Since the introduction of indocyanine green angiography, the detection of the influence of the vortex veins in CSC, it has been established that the presence of a thick choroid may be caused by congestion of the vortex vein, resulting in new choroidal drainage through a vortex vein anastomosis. The study of vortex venous blood hemodynamics has elucidated the new concept of the pathogenesis of CSC, deepened our understanding of the disease, and provided a theoretical basis for new treatment methods. With a better understanding of the pathogenesis of CSC, we expect to be able to stratify patients at risk in the clinic and evaluate optimized treatment options for patients with CSC
现已认识到免疫反应、转录因子核因子κB( NF-κB) 的激活、细胞因子、中性粒细胞的激活和肺泡渗入、凝血级联反应、肾素-血管紧张素系统等多种因素构成的复杂网络参与急性肺损伤/急性呼吸窘迫综合征( ALI/ARDS) 的发病过程[ 1-5] 。虽然脓毒症、创伤、肺炎等ALI/ARDS诱发因素很常见, 但仅有部分病人发生ALI/ARDS, 并且具有相似临床特征的ALI/ARDS病人可有截然不同的结果, 这种异质性引起研究者对影响ALI/ARDS 易感性和预后的遗传因子进行鉴别的浓厚兴趣[ 6] 。由于数量庞大的表现型变异, 不完全的基因外显率、复杂的基因-环境相互作用及高度可能的基因座不均一性而使ALI 遗传学的研究受到挑战[ 7] 。近年来基因组学技术被应用于ALI/ARDS 发病机制的研究, 加深了人们对ALI/ARDS的认识并有可能发展出新的治疗策略以降低其发病率和病死率。