2016年 · 第96卷第47期

In recent years, precision medicine has attracted much attention^[1]。 As a new strategy in the field of healthcare, precision medicine aims to improve personalized diagnosis, medical decision-making and clinical prognosis, that is, to provide precision medicine services such as reasonable treatment plans and drug dosages at the right time^[2,3]。 In the implementation of precision medicine, it is very important to integrate technologies such as genomics, computer biology analysis, clinical informatics, and disease-specific dynamic markers^[4,5]。 Especially for patients with cardiovascular diseases, combining biomarkers, understanding the information of epigenetics, metabolomics and clinical characteristics of patients will greatly improve the prognosis of patients^[6]。

vascular mild cognitive impairment (VaMCI) is a mild cognitive impairment syndrome caused by or related to vascular causes, which is a transitional phase between normal and dementia^[1]。 Due to our unique linguistic and cultural background and the differences in the understanding of international diagnostic criteria, the criteria, thresholds and tools related to VaMCI diagnosis are still not widely agreed^[2]。 Therefore, the Alzheimer's Disease Chinese Working Group on Guidelines (ADCWG) of the Chinese Geriatric Health Care Association published the Chinese Guidelines for the Diagnosis of Vascular Mild Cognitive Impairment (Chinese VaMCI Diagnostic Guidelines)^[1]。 Several key issues covered in the Guide are interpreted below.

In 1954, Whipple first classified prehepatic portal hypertension (PPH) into intrahepatic and prehepatic^[1]。 At present, surgery is the main treatment method. Large-scale clinical studies have shown that the long-term effect of various shunt surgery is stronger than that of simple devascularization surgery, and the selection of specific shunt surgery is based on the etiology and particularity of the patient's condition, which has strong flexibility. This study summarized the experience of 30 cases of prehepatic portal hypertension, hoping to provide a reference for the choice of surgical treatment for prehepatic portal hypertension.

Male, 16 years old, was seen in the Department of Neurology, Daping Hospital, Third Military Medical University in February 2014 due to episodic blurred vision for 1 week. There was a history of upper respiratory tract infection 2 weeks before the illness, accompanied by cough and expectoration. During the attack, only blurred vision appeared, which lasted for more than ten seconds and returned to normal. The condition was repeatedly unrelieved. Ocular examination: visual acuity in the naked eye was 1.0 on the right and 1.2 on the left, normal eye movement in both eyes, transparent cornea in both eyes, anterior chamber (–), and no adhesion in the iris. Visual evoked potentials suggest normal optic nerve conduction in both eyes. MRI of the head showed abnormal signal shadow in the corpus callosum (FIG. 1A，FIG. 1B)。 Electroencephalogram examination showed no abnormalities, and "demyelinating encephalopathy" was considered in the outpatient clinic. After oral treatment with idebenone, the above symptoms disappeared. It relapsed again in December 2015, and the episode process was the same as before. Physical examination: normal vital signs, clear speech, naked eye vision examination: right 1.0, left 1.2, eye movement and fundus examination of both eyes were normal, no visual field defects, and no abnormalities in other physical examinations. MRI of the head showed that the signal change in the part of the corpus callosum still existed (Figure 1C，Figure 1D), there was no abnormality in EEG, except for the high percentage of lymphocytes (49.8%) indicated by blood routine, thyroid and abdominal ultrasound, bilateral visual evoked potentials, and other biochemical indexes were not abnormal. After admission, the symptoms began to resolve after treatment with idebenone, ribavirin and vitamin B1 for 3 days. On January 25, 2016, a reexamination of the head MRI showed that the abnormal signal of the corpus callosum pressure region completely disappeared (Figure 1E，Figure 1F)。

A 55-year-old female was admitted to Beijing Chaoyang Hospital affiliated to Capital Medical University on August 5, 2015 due to "numbness and weakness of right lower limb for 5 days". Five days before admission, there was numbness in the right toe and paroxysmal pain in the back without obvious trigger, which later progressed to numbness and weakness in the whole right lower limb; Numbness and weakness of the left lower limb occurred 1 day before admission, and the enhanced MRI of the thoracic spine showed that "the abnormal signal of spinal gray matter in the thoracic 3-8 segments considered inflammatory changes" and was admitted to the neurology department. Previous Sjogren's syndrome for 2 years, taking cyclosporine 25 mg twice/d and methotrexate 2.5 mg once/week; IgA nephropathy 14 years; Immune-associated thrombocytopenic purpura for 5 years. Physical examination: clear mind, fluent speech, roughly normal cranial nerves. The muscle strength of both upper limbs was grade V, and the lower limbs were grade V-. The muscle tone was not high, the tendon reflex was symmetrical, and the finger-nose, heel-knee-tibia tests were stable and accurate. The acupuncture sensation decreased below the right chest 4. Bilateral pathological signs were negative. Soft neck, no resistance. Medical examination showed no obvious abnormalities in heart, lung and abdomen, and no enlargement of lymph nodes in the whole body.

Intracranial atherosclerosis is the leading cause of ischemic stroke in China. Thickening and strengthening of the vessel wall and the presence of unstable plaques are often overlooked by traditional imaging methods without vascular stenosis, but these features of the vessel wall are important for clarifying the mechanism of ischemic stroke. In recent years, high-resolution magnetic resonance imaging (HR MRI) has brought hope to non-invasive display of intracranial artery wall and plaque characteristics, and is considered to be the only method to study intracranial artery wall imaging in vivo.

Immunoglobulin-G4-related hypertrophic pachymeningitis (IgG4-RHP) is a manifestation of IgG4-related disease (IgG4-RD) involving the central nervous system discovered in recent years. In 2009, Chan et al. of Hong Kong Kwong Wah Hospital^[1]First reported. This disease is characterized by elevated serum IgG4 levels, headache, cranial (spinal) nerve paralysis, epileptic seizures and other symptoms, and local or diffuse dura (spinal) thickening can be seen on imaging. According to literature search, there are more than 50 cases reported abroad, but rare in China. The clinical, imaging and pathological characteristics of IgG4-rHP are reviewed systematically, aiming to improve the awareness and attention of relevant doctors and avoid misdiagnosis or misdiagnosis.

According to the different binding sites between histones and chromatin, they can be divided into core histones (H2A, H2B, H3, H4) and linked histones (H1); According to different components, it can be divided into polylysine group (H1, H2A, H2B) and polyarginine group (H3, H4); According to the different positions of histones, they can be divided into extracellular histones, cytoplasmic histones and intranuclear histones. Intranuclear histones bind and regulate DNA transcription; Cytoplasmic histones are involved in regulating immune and inflammatory responses; Extracellular histones mediate the damage of lung, liver and other tissues during inflammation, and participate in a series of physiological and pathological processes such as sepsis, thrombocytopenia and thrombin production. Current studies have shown that extracellular histones mainly come from two pathways: (1) dead parenchymal tissue cells release intranuclear histones extracellularly; (2) Activated neutrophils are actively released. During the activation of neutrophils, nuclear substances are decomposed, and the rupture of organelle membrane and nuclear membrane in cytoplasm leads to the release of extracellular DNA (cfDNA) -histone complex and granular cytoplasmic proteases such as myeloperoxidase and elastase. These substances together form network-like structures-neutrophil extracellular traps (NETs), which participate in the anti-infective response of the body after the invasion of pathogenic microorganisms, and stimulate inflammation and thrombosis through toll-like receptor (TLR) or inflammatory pathway.