Volume 131 · Issue 19 · 2018

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases with a high prevalence in the general population. The association between NAFLD and cardiovascular disease has been well addressed in previous studies. However, whether NAFLD is associated with carotid artery disease in a community-based Chinese population remained unclear. The aim of this study was to investigate the association between NAFLD and carotid artery disease.

A total of 2612 participants (1091 men and 1521 women) aged 40 years and older from Jidong of Tangshan city (China) were selected for this study. NAFLD was diagnosed by abdominal ultrasonography. The presence of carotid stenosis or plaque was evaluated by carotid artery ultrasonography. Logistic regression was used to analyze the association between NAFLD and carotid artery disease.

Participants with NAFLD have a higher prevalence of carotid stenosis (12.9% vs. 4.6%) and carotid plaque (21.9% vs. 15.0%) than those without NAFLD. After adjusting for age, gender, smoking status, income, physical activity, diabetes, hypertension, triglyceride, waist-hip ratio, and high-density lipoprotein, NAFLD is significantly associated with carotid stenosis (odds ratio [OR]: 2.06, 95% confidence interval [CI]: 1.45–2.91), but the association between NAFLD and carotid plaque is not statistically significant (OR: 1.10, 95% CI: 0.86–1.40).

A significant association between NAFLD and carotid stenosis is found in a Chinese population.

Oxygen-glucose deprivation-nutrition resumption (OGD-NR) models on H9c2 cells are commonly used in vitro models of simulated myocardial ischemia-reperfusion injury (MIRI), but no study has assessed whether these methods for establishing in vitro models can effectively imitate the characteristics of MIRI in vivo. This experiment was designed to analyze the feasibility of six OGD-NR models of MIRI.

By searching the PubMed database using the keywords "myocardial reperfusion injury H9c2 cells," we obtained six commonly used OGD-NR in vitro models of MIRI performed on H9c2 cells from more than 400 published papers before January 30, 2017. For each model, control (C), simulated ischemia (SI), and simulated ischemia-reperfusion (SIR) groups were assigned, and cell morphology, lactate dehydrogenase (LDH) release, adenosine triphosphate (ATP) levels, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and inflammatory cytokines were examined to evaluate the characteristics of cell injury. Subsequently, a coculture system of cardiomyocyte-endothelial-macrophage was constructed. The coculture system was dealt with SI and SIR treatments to test the effect on cardiomyocytes survival.

For models 1, 2, 3, 4, 5, and 6, SI treatment caused morphological damage to cells, and subsequent SIR treatment did not cause further morphological damage. In the models 1, 2, 3, 4, 5 and 6, LDH release was significantly higher in the SI groups than that in the C group (P < 0.05), and was significantly lower in the SIR groups than that in the SI groups (P < 0.05), except for no significant differences in the LDH release between C, SI and SIR groups in model 6 receiving a 3-h SI treatment. In models 1, 2, 3, 4, 5, and 6, compared with the C group, ATP levels of the SI groups significantly decreased (P < 0.05), ROS levels increased (P < 0.05), and MMP levels decreased (P < 0.05). Compared with the SI group, ATP level of the SIR groups was significantly increased (P < 0.05), and there was no significant ROS production, MMP collapse, and over inflammatory response in the SIR groups. In a coculture system of H9c2 cells-endothelial cells-macrophages, the proportion of viable H9c2 cells in the SIR groups was not reduced compared with the SI groups.

All the six OGD-NR models on H9c2 cells in this experiment can not imitate the characteristics of MIRI in vivo and are not suitable for MIRI-related study.

Shensong Yangxin Capsule (SSYX), traditional Chinese medicine, has been used to treat arrhythmias, angina, cardiac remodeling, cardiac fibrosis, and so on, but its effect on cardiac energy metabolism is still not clear. The objective of this study was to investigate the effects of SSYX on myocardium energy metabolism in angiotensin (Ang) II-induced cardiac hypertrophy.

We used 2 µl (10⁻⁶ mol/L) AngII to treat neonatal rat cardiomyocytes (NRCMs) for 48 h. Myocardial α-actinin staining showed that the myocardial cell volume increased. Expression of the cardiac hypertrophic marker-brain natriuretic peptide (BNP) messenger RNA (mRNA) also increased by real-time polymerase chain reaction (PCR). Therefore, it can be assumed that the model of hypertrophic cardiomyocytes was successfully constructed. Then, NRCMs were treated with 1 µl of different concentrations of SSYX (0.25, 0.5, and 1.0 μg/ml) for another 24 h. To explore the time-depend effect of SSYX on energy metabolism, 0.5 μg/ml SSYX was added into cells for 0, 6, 12, 24, and 48 h. Mitochondria was assessed by MitoTracker staining and confocal microscopy. mRNA and protein expression of mitochondrial biogenesis-related genes – Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), energy balance key factor – adenosine monophosphate-activated protein kinase (AMPK), fatty acids oxidation factor – carnitine palmitoyltransferase-1 (CPT-1), and glucose oxidation factor – glucose transporter- 4 (GLUT-4) were measured by PCR and Western blotting analysis.

With the increase in the concentration of SSYX (from 0.25 to 1.0 μg/ml), an increased mitochondrial density in AngII-induced cardiomyocytes was found compared to that of those treated with AngII only (0.25 μg/ml, 18.3300 ± 0.8895 vs. 24.4900 ± 0.9041, t = 10.240, P < 0.0001; 0.5 μg/ml, 18.3300 ± 0.8895 vs. 25.9800 ± 0.8187, t = 12.710, P < 0.0001; and 1.0 μg/ml, 18.3300 ± 0.8895 vs. 24.2900 ± 1.3120, t= 9.902, P < 0.0001; n = 5 per dosage group). SSYX also increased the mRNA and protein expression of PGC-1α (0.25 μg/ml, 0.8892 ± 0.0848 vs. 1.0970 ± 0.0994, t = 4.319, P = 0.0013; 0.5 μg/ml, 0.8892 ± 0.0848 vs. 1.2330 ± 0.0564, t = 7.150, P < 0.0001; and 1.0 μg/ml, 0.8892 ± 0.0848 vs. 1.1640 ± 0.0755, t = 5.720, P < 0.0001; n = 5 per dosage group), AMPK (0.25 μg/ml, 0.8872 ± 0.0779 vs. 1.1500 ± 0.0507, t= 7.239, P < 0.0001; 0.5 μg/ml, 0.8872 ± 0.0779 vs. 1.2280 ± 0.0623, t= 9.379, P < 0.0001; and 1.0 μg/ml, 0.8872 ± 0.0779 vs. 1.3020 ± 0.0450, t = 11.400, P < 0.0001; n = 5 per dosage group), CPT-1 (1.0 μg/ml, 0.7348 ± 0.0594 vs. 0.9880 ± 0.0851, t= 4.994, P = 0.0007, n= 5), and GLUT-4 (0.5 μg/ml, 1.5640 ± 0.0599 vs. 1.7720 ± 0.0660, t= 3.783, P = 0.0117; 1.0 μg/ml, 1.5640 ± 0.0599 vs. 2.0490 ± 0.1280, t = 8.808, P < 0.0001; n = 5 per dosage group). The effect became more obvious with the increasing concentration of SSYX. When 0.5 μg/ml SSYX was added into cells for 0, 6, 12, 24, and 48 h, the expression of AMPK (6 h, 14.6100 ± 0.6205 vs. 16.5200 ± 0.7450, t = 3.456, P = 0.0250; 12 h, 14.6100 ± 0.6205 vs. 18.3200 ± 0.9965, t = 6.720, P < 0.0001; 24 h, 14.6100 ± 0.6205 vs. 21.8800 ± 0.8208, t = 13.160, P < 0.0001; and 48 h, 14.6100 ± 0.6205 vs. 23.7400 ± 1.0970, t = 16.530, P < 0.0001; n = 5 per dosage group), PGC-1α (12 h, 11.4700 ± 0.7252 vs. 16.9000 ± 1.0150, t = 7.910, P < 0.0001; 24 h, 11.4700 ± 0.7252 vs. 20.8800 ± 1.2340, t= 13.710, P < 0.0001; and 48 h, 11.4700 ± 0.7252 vs. 22.0300 ± 1.4180, t= 15.390; n = 5 per dosage group), CPT-1 (24 h, 15.1600 ± 1.0960 vs. 18.5800 ± 0.9049, t= 6.048, P < 0.0001, n = 5), and GLUT-4 (6 h, 10.2100 ± 0.9485 vs. 12.9700 ± 0.8221, t = 4.763, P = 0.0012; 12 h, 10.2100 ± 0.9485 vs. 16.9100 ± 0.8481, t= 11.590, P < 0.0001; 24 h, 10.2100 ± 0.9485 vs. 19.0900 ± 0.9797, t= 15.360, P < 0.0001; and 48 h, 10.2100 ± 0.9485 vs. 14.1900 ± 0.9611, t= 6.877, P < 0.0001; n = 5 per dosage group) mRNA and protein increased gradually with the prolongation of drug action time.

SSYX could increase myocardial energy metabolism in AngII-induced cardiac hypertrophy. Therefore, SSYX might be considered to be an alternative therapeutic remedy for myocardial hypertrophy.

Risperidone and paliperidone have been the mainstay treatment for schizophrenia and their potential role in neuroprotection could be associated with brain-derived neurotrophic factor (BDNF) and N400 (an event-related brain potential component). So far, different effects on both BDNF and N400 were reported in relation to various antipsychotic treatments. However, few studies have been conducted on the mechanism of risperidone and paliperidone on BDNF and N400. This study aimed to compare the effects of risperidone and paliperidone on BDNF and the N400 component of the event-related brain potential in patients with first-episode schizophrenia.

Ninety-eight patients with first-episode schizophrenia were randomly divided into the risperidone and paliperidone groups and treated with risperidone and paliperidone, respectively, for 12 weeks. Serum BDNF level, the latency, and amplitude of the N400 event-related potential before and after the treatment and Positive and Negative Syndrome Scale (PANSS) scores were compared between the two groups.

A total of 94 patients were included in the final analysis (47 patients in each group). After the treatment, the serum BDNF levels in both groups increased (all P < 0.01), while no significant difference in serum BDNF level was found between the groups before and after the treatment (all P > 0.05). After the treatment, N400 amplitudes were increased (from 4.73 ± 2.86 μv and 4.51 ± 4.63 μv to 5.35 ± 4.18 μv and 5.52 ± 3.08 μv, respectively) under congruent condition in both risperidone and paliperidone groups (all P < 0.01). Under incongruent conditions, the N400 latencies were shortened in the paliperidone group (from 424.13 ± 110.42 ms to 4.7.41 ± 154.59 ms, P < 0.05), and the N400 amplitudes were increased in the risperidone group (from 5.80 ± 3.50 μv to 7.17 ± 5.51 μv, P < 0.01). After treatment, the total PANSS score in both groups decreased significantly (all P < 0.01), but the difference between the groups was not significant (P > 0.05). A negative correlation between the reduction rate of the PANSS score and the increase in serum BDNF level after the treatment was found in the paliperidone group but not in the risperidone group.

Both risperidone and paliperidone could increase the serum BDNF levels in patients with first-episode schizophrenia and improve their cognitive function (N400 latency and amplitude), but their antipsychotic mechanisms might differ.

Myocardial ischemia injury is one of the leading causes of death and disability worldwide. Cardiac fibroblasts (CFs) have central roles in modulating cardiac function under pathophysiological conditions. Activating transcription factor 3 (ATF3) plays a self-protective role in counteracting CF dysfunction. However, the precise function of CF-specific ATF3 during myocardial infarction (MI) injury/repair remains incompletely understood. The aim of this study was to determine whether CF-specific ATF3 affected cardiac repair after MI.

Fifteen male C57BL/6 wild-type mice were performed with MI operation to observe the expression of ATF3 at 0, 0.5, 1.0, 3.0, and 7.0 days postoperation. Model for MI was constructed in ATF3TGfl/flCol1a2-Cre+ (CF-specific ATF3 overexpression group, n = 5) and ATF3TGfl/flCol1a2-Cre− male mice (without CF-specific ATF3 overexpression group, n = 5). In addition, five mice of ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre− were subjected to sham MI operation. Heart function was detected by ultrasound and left ventricular remodeling was observed by Masson staining (myocardial fibrosis area was detected by blue collagen deposition area) at the 28^th day after MI surgery in ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre− mice received sham or MI operation. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect cell proliferation/cell cycle-related gene expression in cardiac tissue. BrdU staining was used to detect fibroblast proliferation.

After establishment of an MI model, we found that ATF3 proteins were increased in the heart of mice after MI surgery and dominantly expressed in CFs. Genetic overexpression of ATF3 in CFs (ATF3TGfl/flCol1a2-Cre+ group) resulted in an improvement in the heart function as indicated by increased cardiac ejection fraction (41.0% vs. 30.5%, t = 8.610, P = 0.001) and increased fractional shortening (26.8% vs. 18.1%, t= 7.173, P = 0.002), which was accompanied by a decrease in cardiac scar area (23.1% vs. 11.0%, t= 8.610, P = 0.001). qRT-PCR analysis of CFs isolated from ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre− ischemic hearts revealed a distinct transcriptional profile in ATF3-overexpressing CFs, displaying pro-proliferation properties. BrdU-positive cells significantly increased in ATF3-overexpressing CFs than control CFs under angiotensin II stimuli (11.5% vs. 6.8%, t = 31.599, P = 0.001) or serum stimuli (31.6% vs. 20.1%, t = 31.599, P = 0.001). The 5(6)-carboxyfluorescein N-hydroxysuccinimidyl ester assay showed that the cell numbers of the P2 and P3 generations were higher in the ATF3-overexpressing CFs at 24 h (P2: 91.6% vs. 71.8%, t = 8.465, P = 0.015) and 48 h (P3: 81.6% vs. 51.1%, t = 9.029, P = 0.012) after serum stimulation. Notably, ATF3 overexpression-induced CF proliferation was clearly increased in the heart after MI injury.

We identify that CF-specific ATF3 might contribute to be MI repair through upregulating the expression of cell cycle/proliferation-related genes and enhancing cell proliferation.

A high consumption of fructose leads to hepatic steatosis. About 20–30% of triglycerides are synthesized via de novo lipogenesis. Some studies showed that endoplasmic reticulum stress (ERS) is involved in this process, while others showed that a lipotoxic environment directly influences ER homeostasis. Here, our aim was to investigate the causal relationship between ERS and fatty acid synthesis and the effect of X-box binding protein-1 (XBP-1), one marker of ERS, on hepatic lipid accumulation stimulated by high fructose.

HepG2 cells were incubated with different concentrations of fructose. Upstream regulators of de novo lipogenesis (i.e., carbohydrate response element-binding protein [ChREBP] and sterol regulatory element-binding protein 1c [SREBP-1c]) were measured by polymerase chain reaction and key lipogenic enzymes (acetyl-CoA carboxylase [ACC], fatty acid synthase [FAS], and stearoyl-CoA desaturase-1 [SCD-1]) by Western blotting. The same lipogenesis-associated factors were then evaluated after exposure of HepG2 cells to high fructose followed by the ERS inhibitor tauroursodeoxycholic acid (TUDCA) or the ERS inducer thapsigargin. Finally, the same lipogenesis-associated factors were evaluated in HepG2 cells after XBP-1 upregulation or downregulation through cell transfection.

Exposure to high fructose increased triglyceride levels in a dose- and time-dependent manner and significantly increased mRNA levels of SREBP-1c and ChREBP and protein levels of FAS, ACC, and SCD-1, concomitant with XBP-1 conversion to an active spliced form. Lipogenesis-associated factors induced by high fructose were inhibited by TUDCA and induced by thapsigargin. Triglyceride level in XBP-1-deficient group decreased significantly compared with high-fructose group (4.41 ± 0.54 μmol/g vs. 6.52 ± 0.38 μmol/g, P < 0.001), as mRNA expressions of SREBP-1c (2.92 ± 0.46 vs. 5.08 ± 0.41, P < 0.01) and protein levels of FAS (0.53 ± 0.06 vs. 0.85 ± 0.05, P = 0.01), SCD-1 (0.65 ± 0.06 vs. 0.90 ± 0.04, P = 0.04), and ACC (0.38 ± 0.03 vs. 0.95 ± 0.06, P < 0.01) decreased. Conversely, levels of triglyceride (4.22 ± 0.54 μmol/g vs. 2.41 ± 0.35 μmol/g, P < 0.001), mRNA expression of SREBP-1c (2.70 ± 0.33 vs. 1.00 ± 0.00, P < 0.01), and protein expression of SCD-1 (0.93 ± 0.06 vs. 0.26 ± 0.05, P < 0.01), ACC (0.98 ± 0.09 vs. 0.43 ± 0.03, P < 0.01), and FAS (0.90 ± 0.33 vs. 0.71 ± 0.02, P = 0.04) in XBP-1s-upregulated group increased compared with the untransfected group.

ERS is associated with de novo lipogenesis, and XBP-1 partially mediates high-fructose-induced lipid accumulation in HepG2 cells through augmentation of de novo lipogenesis.

XB130 is a recently discovered adaptor protein that is highly expressed in many malignant tumors, but few studies have investigated its role in hepatocellular carcinoma (HCC). Therefore, this study explored the relationship between this protein and liver cancer and investigated its molecular mechanism of action.

The expression of XB130 between HCC tissues and adjacent nontumor tissues was compared by real-time polymerase chain reaction, immunochemistry, and Western blotting. XB130 silencing was performed using small hairpin RNA. The effect of silencing XB130 was examined using Cell Counting Kit-8, colony assay, wound healing assay, and cell cycle analysis.

We found that XB130 was highly expressed in HCC tissues (cancer tissues vs. adjacent tissues: 0.23 ± 0.02 vs. 0.17 ± 0.02, P < 0.05) and liver cancer cell lines, particularly MHCC97H and HepG2 (MHCC97H and HepG2 vs. normal liver cell line LO-2: 2.35 ± 0.26 and 2.04 ± 0.04 vs. 1.00 ± 0.04, respectively, all P < 0.05). The Cell Counting Kit-8 assay, colony formation assay, and xenograft model in nude mice showed that silencing XB130 inhibited cell proliferative ability both in vivo and in vitro, with flow cytometry demonstrating that the cells were arrested in the G0/G1 phase in HepG2 (HepG2 XB130-silenced group [shA] vs. HepG2 scramble group [NA]: 74.32 ± 5.86% vs. 60.21 ± 3.07%, P < 0.05) and that the number of G2/M phase cells was decreased (HepG2 shA vs. HepG2 NA: 8.06 ± 2.41% vs. 18.36 ± 4.42%, P < 0.05). Furthermore, the cell invasion and migration abilities were impaired, and the levels of the epithelial-mesenchymal transition-related indicators vimentin and N-cadherin were decreased, although the level of E-cadherin was increased after silencing XB130. Western blotting showed that the levels of phosphorylated phosphoinositide 3-kinase (PI3K) and phospho-protein kinase B (p-Akt) also increased, although the level of phosphorylated phosphatase and tensin homolog increased, indicating that XB130 activated the PI3K/Akt pathway. Furthermore, we found that a reduction in XB130 increased liver cancer cell sensitivity to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.

Our findings suggest that XB130 might be used as a predictor of liver cancer as well as one of the targets for its treatment.

This study was to review the efficacy of surgical resections in different clinical situations for a better understanding of the meaning of surgery in the treatment of neuroblastoma (NB).

The online database ScienceDirect (2016–2018) was utilized. The search was conducted using the keywords "neuroblastoma," "neuroblastoma resection," "neuroblastoma surgery," and "high-risk neuroblastoma."

We retrospectively analyzed of patients who underwent surgical resections in different clinical situations. The article included findings from selected relevant randomized controlled trials, systematic reviews, and meta-analyses or good-quality observational studies. Abstracts only, letters, and editorial notes were excluded. Full-text articles and abstracts were extracted and reviewed to identify key articles discussing surgery management of NB, which were then selected for critical analysis.

A total of 7800 English language articles were found containing references to NB (2016–2018). The 163 articles were searched which were related to the surgical treatment of NB (2016–2018). Through the analysis of these important articles, we found that the treatments of NB at low- and intermediate-risk groups were basically the same. High-risk patients remained controversial.

NB prognosis varies tremendously based on the stage and biologic features of the tumor. After reviewing the relevant literature, patients with low-risk disease are often managed with surgical resection or observation alone with tumors likely to spontaneously regress that are not causing symptoms. Intermediate patients are treated with chemotherapy with the number of cycles depending on their response as well as surgical resection of the primary tumor. High-risk patients remain controversial. Multidisciplinary intensive treatment is essential, especially for patients who received subtotal tumor resection. Minimally invasive surgery for the treatment of NBs without image-defined risk factors in low- to high-risk patients is safe and feasible and does not compromise the treatment outcome. We conclude that ≥90% resection of the primary tumor is both feasible and safe in most patients with high-risk NB. New targeted therapies are crucial to improve survival.

Endothelial cells (ECs) are important metabolic and endocrinal organs which play a significant role in regulating vascular function. Vascular ECs, located between the blood and vascular tissues, can not only complete the metabolism of blood and interstitial fluid but also synthesize and secrete a variety of biologically active substances to maintain vascular tension and keep a normal flow of blood and long-term patency. Therefore, this article presents a systematic review of common injuries and healing mechanisms for the vascular endothelium.

An extensive search in the PubMed database was undertaken, focusing on research published after 2003 with keywords including endothelium, vascular, wounds and injuries, and wound healing.

Several types of articles, including original studies and literature reviews, were identified and reviewed to summarize common injury and repair processes of the endothelial lining.

Endothelial injury is closely related to the development of multiple cardiovascular and cerebrovascular diseases. However, the mechanism of vascular endothelial injury is not fully understood. Numerous studies have shown that the mechanisms of EC injury mainly involve inflammatory reactions, physical stimulation, chemical poisons, concurrency of related diseases, and molecular changes. Endothelial progenitor cells play an important role during the process of endothelial repair after such injuries. What’s more, a variety of restorative cells, changes in cytokines and molecules, chemical drugs, certain RNAs, regulation of blood pressure, and physical fitness training protect the endothelial lining by reducing the inducing factors, inhibiting inflammation and oxidative stress reactions, and delaying endothelial caducity.

ECs are always in the process of being damaged. Several therapeutic targets and drugs were seeked to protect the endothelium and promote repair.

编者：近年来，内镜逆行胰胆管造影（ERCP）在胰胆管疾病的治疗中起着至关重要的作用，同时也有并发症的风险，包括ERCP后胰腺炎、胆管炎、出血和穿孔。原发性ERCP后并发症的发生率为5.4%至23.0%，ERCP诱导的穿孔可发生在0.3-1.0%的病例中，但相关的死亡率很高，为8%至23%。^[1]由于胆管和胰管的汇合处在十二指肠穿孔部位附近的乳头处相遇，因此存在胆汁和胰液渗漏到腹膜后间隙或腹膜的潜在风险。StapferⅡ型穿孔（围壁穿孔）患者一般患有全身炎症反应综合征，可迅速进展为急性肺损伤和急性肾功能不全，甚至多器官功能衰竭。所有这些都导致了显著的高死亡率。及时识别和适当治疗对于处理ERCP诱导的穿孔以降低总死亡率至关重要。传统上，手术仍然是医源性穿孔的主要治疗方法。随着内镜技术的进步和新附件的开发，越来越多的报道采用内镜治疗穿孔的非手术治疗。^[2]我们报告了一项回顾性分析，回顾性分析了5年间采用非手术方法联合挽救性ERCP治疗的ERCP诱导的Stapfer II型穿孔。

编者按：近期，随着内镜治疗技术的发展，医源性穿孔的发生率也在不断增加。如果缺损治疗不当，随后的胃肠瘘和感染可能导致严重的并发症。本研究评估了一种在内镜治疗后闭合胃缺损的简单方法，使用单通道内镜使用endoloop和金属夹。

致编辑：白内障和年龄相关性黄斑变性(AMD)通常同时发生，这是与衰老相关的视力损伤的两个主要原因。据报道，阳光有助于白内障和AMD的发病机制。^[1]在白内障的情况下，较少的阳光可能会进入眼底。在此基础上，晶状体混浊可能是AMD的保护因素。尽管如此，至今仍有争议。

致编辑：视力下降不仅影响个人，也影响家庭、社区和公共健康。它导致巨大的经济负担，包括教育成本增加、个人收入减少和护理人员生产力损失，以及许多无形后果，如个人失去独立性、生活质量下降和发病率过高。根据世界卫生组织（世卫组织）的标准，估计世界上有1900万儿童视力受损，140万儿童失明。因此，控制儿童视力障碍或失明（VI/BL）仍然是世卫组织“2020年愿景：视力权利”计划的优先领域之一。

致编者：非动脉炎性前部缺血性视神经病变（NAION）是一种常见于老年人的急性视神经病变疾病。NAION的发病率约为（2.3-10.2）/10万，许多患者双眼受累。徐等人。^[1]报道在中国人群中的发病率为1/16000。无任何疼痛的急性视力（VA）损害和不良预后是NAION的主要特征。本研究旨在寻找普通个体中NAION的相关危险因素，以促进NAION的预防或早期诊断。

编者按：几种恶性肿瘤表现为神经周侵犯（PNI），可引起局部复发，降低术后生存的可能性。我们之前的研究表明，宫颈癌中的PNI与其他病理风险特征相关，其他研究表明它是不良预后的预测因素。^[1,2,3]这些发现凸显了阐明PNI分子机制的重要性。

致小编：一个30岁的孕妇12岁⁺²（指孕12周零2天）孕周出现下腹部剧烈胀痛、头晕、乏力5 h以上。患者除一次流产外，无其他病史。双手检查显示左侧附件区压痛，闭合的颈椎口无出血。超声显示活胎12⁺²子宫内周，子宫前不规则不均匀低回声肿块，盆腔内大量积液[图1].Culdocentesis显示约5毫升血液。实验室检查血红蛋白85 g/L，红细胞压积26.6%，白细胞计数19.09 × 10⁹/L，血小板和凝血正常。由于不明腹膜内出血，安排了紧急腹腔镜检查。

编辑：子宫癌肉瘤（恶性混合苗勒管瘤[MMMT]）是一种罕见的侵袭性恶性肿瘤，表现出恶性上皮（癌）和间叶（肉瘤）成分。^[1]MMMTs占所有子宫恶性肿瘤的2-5%。转移进展并不常见，通过血液、淋巴和腹膜内扩散发生。MMMTs的危险因素包括辐射、过量雌激素暴露、肥胖和未生育。MMMTs患者I期疾病的2年生存率为53%，II期和III期降至8.5%。^[2]

致编者：高同型半胱氨酸血症（HHcy）是动脉粥样硬化血栓性疾病和静脉血栓形成的重要危险因素。^[1]通常，同型半胱氨酸(Hcy)通过维生素B12依赖性反应或作为甲基供体的甜菜碱再甲基化为甲硫氨酸(Met)，或通过吡哆醇依赖性反应反式硫化为半胱氨酸。根据血浆总Hcy水平，HHcy通常分为以下三组：轻度（tHcy 15-30 μ mol/L）、中度（tHcy 30-100 μ mol/L）和重度（tHcy>100 μ mol/L）。^[2]严重的HHcy很罕见，最常见的原因是遗传性胱硫醚β-合酶（CBS）缺乏，或不太常见的亚甲基四氢叶酸还原酶（MTHFR）基因。这种代谢紊乱的表现包括发育迟缓、智力残疾、癫痫、晶状体异位、近视、皮肤和毛发色素沉着不足、马凡样习性和血栓栓塞性紊乱。^[3]这些表现在早期往往被忽视，直到发生血栓事件，如脑静脉窦血栓形成（CVST）。

致编者：巨轴突神经病（GAN）是一种罕见的神经退行性疾病，由甘编码gigaxonin的基因。GAN的神经病理学显示典型的巨大轴突，中间丝堆积。这种疾病是进行性的，周围神经系统和中枢神经系统都有损伤。在此，我们报告了一例表现为步态障碍、神经活检中的巨大轴突和脑磁共振成像（MRI）异常的病例。

作为一种罕见的常染色体隐性代谢紊乱，胱氨酸病是由胱氨酸跨溶酶体膜转运缺陷引起的。^[1]一旦确诊胱氨酸病，应尽快对患者进行半胱胺（一种氨基硫醇）的特异性治疗，以保护肾功能并改善受影响儿童的生长。^[2]半胱胺是食品药品监督管理局批准的唯一治疗胱氨酸病的特效药。虽然它不能逆转已有的肾脏损害，但据报道，17名接受半胱胺治疗7年的患者肾功能几乎恢复正常，更重要的是，他们生长正常。^[3]另一份报告表明，半胱胺治疗可以将终末期肾损伤推迟10-20年。^[4]然而，眼前的挑战在于在中国获得治疗胱氨酸病的必要药物。在此，我们报告了两个患有胱氨酸病的兄弟男孩的病例，以提高国际社会对迫切需要针对此类罕见疾病采取全球政策和行动的认识。

患者女，48岁，一个月前出现胸痛症状，无明显诱因，咳嗽、咳痰、咯血、胸闷。胸部疼痛是不规则的。患者入住吉林大学第一医院进一步治疗。患者否认有高血压、冠心病、糖尿病等病史。她也否认有遗传性疾病家族史。然而，她有20年的吸烟史，每天10支左右，没有戒烟。体格检查和血液检查未显示明显异常。所有肿瘤标志物均为阴性。计算机断层扫描(CT)显示肺右上叶高密度肿块，约17mm × 15mm[图1a].边界光滑，密度均匀。右侧胸腔可见狭窄的液体弧形图像，纵隔无明显淋巴结(LN)转移[图1b].患者在胸腔镜下进行探查，术中快速病理显示可疑腺癌，患者接受了右肺上叶切除术。然而，最终病理显示肺硬化性血管瘤（PSH）。术后标本的显微镜检查结果显示乳头状和硬化型混合，具有以下两种细胞类型：立方形表面和基质圆形细胞。类似肺细胞的长方体表面细胞和边界清晰的圆形基质细胞位于中央，圆形至椭圆形的泡状核和罕见的核仁。圆形基质细胞大多具有轻微的嗜酸性细胞质，一些显示出更多的空泡或泡沫外观。在其他区域，有大片充满血液的空间，排列着扁平的细胞。还注意到圆形细胞的实心片，分散的立方体表面细胞形成小管[图1c].圆形基质细胞对甲状腺转录因子-1(TTF-1）和波形蛋白呈阳性，但对上皮膜抗原(EMA)和泛细胞角蛋白呈阴性，立方体表面细胞对TTF-1、波形蛋白、EMA、Ki-67和泛细胞角蛋白呈阳性[图1d-1h].

在一份非常有趣的报告中中华医学杂志^[1]关于一名65岁高血压和高脂血症男性患者，5年前接受支架植入术，患者在食用面包和牛奶后出现过敏性休克，伴有胸部不适、心悸、瘙痒、恶心、呕吐、呼吸困难、喘息、腹痛、出汗、面色苍白、头晕和晕厥。临床症状学与急性下外侧心肌梗死的心电图和实验室证据相关，患者通过肾上腺素、抗过敏药和心肌梗死方案治疗（包括替格瑞洛和Clexane）康复。冠状动脉造影显示左主干和三个冠状动脉分支有病变，但支架植入区域通畅。过敏原测试显示小麦为2级（2.11 kUA/L），牛奶为0级。

正如我们上一篇文章中提到的，^[1]男，65岁，因摄入面包牛奶后1 h出现累及全身的风团，于2016年9月9日入住我院。他的共存症状包括瘙痒、胸部不适、呼吸困难、喘息、腹痛、恶心、呕吐、心悸、出汗、面色苍白、头晕和晕厥。他服用速效救心丸后意识恢复，随后被送往我院。血压降至51/21mmHg（1mmHg=0.133kPa）。化验示心肌酶升高，心电图ST段抬高。冠状动脉造影显示支架通畅。