Volume 131 · Issue 07 · 2018

It is known that there is a definite association between platelet distribution width (PDW) and poor prognosis in patients with coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM). However, there are no data available regarding the prognostic significance of PDW for in-stent restenosis (ISR) in patients with CAD and T2DM. We aimed to determine the value of PDW on admission that predicted ISR in patients with CAD and T2DM.

Between January 2012 and December 2013, a total of 5232 consecutive patients diagnosed with CAD and T2DM undergoing percutaneous coronary intervention were admitted. Three years of retrospective follow-up was undertaken. A total of 438 patients with second angiography operations were included. ISR was defined as ≥50% luminal stenosis of the stent or peri-stent segments. Continuous data were presented as the mean ± standard deviation or median (P₂₅, P₇₅) and were compared by one-way analysis of variance or Kruskal-Wallis H-test. Categorical variables were presented as percentages and were compared by Chi-square test or Fisher’s exact test. The association between PDW and ISR was calculated by logistic regression analysis. A two-sided value of P < 0.05 was considered statistically significant. Statistical analyses were performed by SPSS version 22.0 for windows.

Fifty-nine patients with ISR, accounting for 13.5% of the total, were included. ISR was significantly more frequent in patients with higher PDW quartiles compared with lower quartiles. We observed that PDW had a strong relationship with mean platelet volume (r = 0.647, 95% confidence interval [CI]: 0.535–0.750, P < 0.0001). The receiver-operating characteristic curves showed that the PDW cutoff value for predicting ISR rate was 13.65 fl with sensitivity of 59.3% and specificity of 72.4% (area under curve [AUC] = 0.701, 95% CI: 0.625–0.777, P < 0.001). Multivariate analysis showed that the risk of ISR increased approximately 30% when PDW increased one unit (odds ratio [OR]: 1.289, 95% CI: 1.110–1.498, P = 0.001). Patients with higher PDW, defined as more than 13.65 fl, had a 4-fold higher risk of ISR compared with lower PDW (OR: 4.241, 95% CI: 1.879–9.572, P = 0.001). Furthermore, when patients were divided by PDW quartiles values, PDW was able to predict ISR (Q2: OR = 0.762, 95% CI: 0.189–3.062, P = 0.762; Q3: OR = 2.782, 95% CI: 0.865–8.954, P = 0.086; and Q4: OR = 3.849, 95% CI: 1.225–12.097, P = 0.021, respectively; P for trend <0.0001).

PDW is an independent predictor of ISR in patients with CAD and T2DM.

Despite its limitations, unfractionated heparin (UFH) has been the standard anticoagulant used during percutaneous coronary intervention (PCI). This study compared the safety of low-dose UFH with sequential enoxaparin with that of UFH in patients with diabetes mellitus (DM) and complex coronary artery disease receiving elective PCI.

In this retrospective study, 514 consecutive patients with atherosclerotic cardiovascular diseases and type 2 DM were admitted to the hospital and received selective PCI, from January 2013 to December 2015. All patients with PCI received low-dose UFH with enoxaparin (intraductal 50 U/kg UFH and 0.75 mg/kg enoxaparin, n = 254; UFH-Enox group) or UFH only (intraductal 100 U/kg UFH, n = 260; UFH group). The study endpoints were major adverse cardiac events (MACEs), namely death, myocardial infarction (MI), stroke, target-vessel immediate revascularization (TVR), and thrombolysis in MI (TIMI) major bleeding, within 30 days and 1 year after PCI. Any catheter thrombosis during the procedure was recorded.

Only one patient had an intraductal thrombus in the UFH group. At the 30-day follow-up, no MACE occurred in any group; seven and five cases of recurrent angina and/or rehospitalization were reported in the UFH-Enox and UFH groups, respectively; there was no significant difference between the two groups (χ² = 0.11, P = 0.77). There was no TIMI major bleeding in the groups. With respect to the 1-year endpoint, two cases of recurrent MI and two of TVRs were reported in the UFH-Enox group, whereas in the UFH group, one case of recurrent MI and three of TVRs were reported; no significant difference existed between the two groups (χ² = 0, P = 0.99). There were 30 and 25 recurrent angina and/or rehospitalizations in the UFH-Enox and UFH groups, respectively; there was no significant difference between the two groups (χ²= 0.37, P = 0.57).

In elective PCI, low-dose UFH with sequential enoxaparin has similar effects and safety to the UFH-only method.

Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are common X-linked recessive neuromuscular disorders caused by mutations in dystrophin gene. Multiplex polymerase chain reaction (multiplex PCR) and multiplex ligation-dependent probe amplification (MLPA) are the most common methods for detecting dystrophin gene mutations. This study aimed to contrast the two methods and discern the genetic characterization of patients with DMD/BMD in Eastern China.

We collected 121 probands, 64 mothers of probands, and 15 fetuses in our study. The dystrophin gene was detected by multiplex PCR primarily in 28 probands, and MLPA was used in multiplex PCR-negative cases subsequently. The dystrophin gene of the remaining 93 probands and 62 female potential carriers was tested by MLPA directly. In fetuses, multiplex PCR and MLPA were performed on 4 fetuses and 10 fetuses, respectively. In addition, sequencing was also performed in 4 probands with negative MLPA.

We found that 61.98% of the subjects had genetic mutations including deletions (50.41%) and duplications (11.57%). There were 43.75% of mothers as carriers of the mutation. In 15 fetuses, 2 out of 7 male fetuses were found to be unhealthy and 2 out of 8 female fetuses were found to be carriers. Exons 3–26 and 45–52 have the maximum frequency in mutation regions. In the frequency of exons individually, exon 47 and exon 50 were the most common in deleted regions and exons 5, 6, and 7 were found most frequently in duplicated regions.

MLPA has better productivity and sensitivity than multiplex PCR. Prenatal diagnosis should be applied in DMD high-risk fetuses to reduce the disease incidence. Furthermore, it is the responsibility of physicians to inform female carriers the importance of prenatal diagnosis.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening clinical syndrome. Central nervous system (CNS) involvement is a severe complication, which can lead to rapid disease development and higher morality. However, this has not been given enough attention in adult HLH. Therefore, we carried out this study to analyze the clinical features, laboratory findings, treatment outcomes, and other characteristics of adult HLH with CNS involvement.

A retrospective analysis of 96 adult patients with HLH combined with CNS involvement between June 2003 and December 2016 was conducted. Clinical features, cerebrospinal fluid (CSF) features, image changes, and therapeutic outcomes were analyzed.

Among the 96 patients, 86 had various CNS symptoms and 33 (38.4%) had already presented symptoms before the HLH diagnosis was confirmed. A total of 59 patients received CSF examinations and showed abnormalities in 23 patients (39.0%). Seventy patients received imaging examinations and the results showed fifty patients with imaging changes (71.4%). Fifty-seven patients received multiple rounds of repeated intrathecal injection therapy and 35 patients improved (61.4%). As for the multiple analyses of effective factors on survival time, the results showed that the effects of combined Epstein–Barr virus (EBV) infection (P = 0.026, Exp(B) = 2.309, 95% confidence interval [CI] [1.108, 4.823) and intrathecal injection therapy (P = 0.013, Exp(B) = 0.422, 95% CI [0.214, 0.831]) on the survival time of the CNS-HLH patients were significant.

Complication with EBV infection is a risk factor, and intrathecal injection is a protective factor. CNS involvement in HLH is not rare, which can result in a poor prognosis. Multiple rounds of repeated intrathecal injection therapy can improve the prognosis of CNS-HLH patients.

Robot-assisted/laparoscopic intracorporeal ileal conduit (ICIC) has been reported in many experienced centers. Whether laparoscopic ICIC is superior to extracorporeal ileal conduit (ECIC) and whether laparoscopic ICIC should be promoted is still controversial. The aim of the study was to compare surgical and early oncological outcomes between patients undergoing laparoscopic radical cystectomy (LRC) with ICIC and ECIC.

From January 2011 to June 2016, a total of 45 patients with bladder cancer underwent LRC with ileal conduit at our department, of whom 20 patients underwent LRC with ECIC and 25 patients underwent LRC with ICIC. Data of each patient’s characteristics, surgical outcomes, and short-term oncological outcomes were collected and analyzed.

LRC with ileal conduit was performed successfully on all 45 patients. There were no significant differences in patients' characteristics, mean total operative time, and mean estimated blood loss between the ICIC and ECIC groups. Median time of flatus and oral intake was shorter in the ICIC group compared with the ECIC group (3 vs. 5 days, P = 0.035; 4 vs. 5 days, P = 0.002). The complications rates did not show significant difference between the two groups within the first 90 days postoperatively (P = 0.538). Cancer staging showed 45% of patients in the ECIC group and 36% in the ICIC group had a pathologic stage of T3 or T4, and 50% of patients in the ECIC group and 44% in the ICIC group had a pathologic stage of N1 or N1+. Kaplan–Meier analysis showed no significant difference in overall survival at 24 months (60% vs. 62%, P = 0.857) between the ECIC and ICIC groups.

ICIC after LRC may be successful with the benefits of faster recovery time. No significant difference was found in complications and oncological outcomes between ICIC and ECIC. However, larger series with longer follow-up are needed to validate this procedure.

Studies of haploidentical-related donor (HRD) stem cell transplantation using a combination of peripheral blood stem cells (PBSCs) and bone marrow as the graft have reported encouraging results for patients with hematological diseases. However, few studies specifically reported transplantation of only PBSCs from HRDs among patients with relapsed or refractory acute myeloid leukemia (AML). Here, the long-term outcomes and side effects of unmanipulated HRD PBSC transplantation (HRD-PBSCT) for relapsed/refractory AML were analyzed.

We performed a retrospective analysis of the outcomes in relapsed/refractory AML patients who underwent PBSCT from HRDs (n = 36).

Thirty-one (86.1%) patients in the HRD-PBSCT group achieved platelet recovery. The cumulative incidence of acute graft-versus-host disease (aGVHD) in the HRD-PBSCT group was 40.00%, and the cumulative incidence of grades 2–4 aGVHD in this group was 13.33%. A total of 13 patients in the HRD-PBSCT group had recurrent disease at a median of 183 days after transplantation (range: 10–1700 days), reaching cumulative incidences of relapse of 50.28% at 5 years. On multivariate analysis, donor age and patient age >40 years were independent risk factors for inferior disease-free survival or overall survival (P < 0.05). The results of the present study demonstrate rapid and complete neutrophil engraftment, a low incidence of grade 2–4 aGVHD, and promising survival rates in patients after HRD-PBSCT. Thus, granulocyte colony-stimulating factor- primed PBSCs may be a reliable graft source in unmanipulated HRD-HSCT under myeloablative conditioning when no matched sibling donor is available.

Our results support the feasibility, effectiveness, and tolerability of PBSCs as a graft source in unmanipulated HRD transplantation under myeloablative conditioning in patients with leukemia.

Idiopathic basal ganglia calcification (IBGC) is a genetic disorder characterized by bilateral basal ganglia calcification and neural degeneration. In this study, we reported a new SLC2OA2 mutation of IBGC and reviewed relevant literature to explore the association between phenotypes and genotypes in Chinese IBGC patients.

Clinical information of the proband and her relatives were collected comprehensively. Blood samples of both the patient and her father were obtained, and genetic screening related to IBGC was performed using second generation sequencing with their consent. Findings were confirmed by Sanger sequencing. Polyphen-2 was used to predict the potential association between mutations and disease. Then, we retrieved literatures of Chinese IBGC patients and explored the association between phenotype and genotype.

A novel mutation was identified through genetic testing, and it is suggested to be a damage mutation predicted by Polyphen-2. Through literature review, we found that SLC20A2 mutation is the most common cause for IBGC in China. Its hot spot regions are mainly on the 1^st and 8^th exons; the second common one is PDGFB where the hot spot covered a length of 220–230 bp localized on the 2^nd exon; moreover, Chinese IBGC patients featured early-onset, more severe movement disorder and relatively mild cognitive impairment compared with those in other countries.

There is significant heterogeneity both in phenotype and genotype in Chinese IBGC patients. Further research of pathogenic mechanism of IBGC is required to eventually develop precise treatment for individuals who suffered this disease.

Ventilator-induced lung injury (VILI) is commonly associated with barrier dysfunction and inflammation reaction. Glutamine could ameliorate VILI, but its role has not been fully elucidated. This study examined the relationship between inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α, and IL-10) and adherens junctions (E-cadherin, p120-catenin), which were ameliorated by glutamine in VILI, both in vitro and in vivo.

For the in vivo study, 30 healthy C57BL/6 mice weighing 25–30 g were randomly divided into five groups with random number table (n = 6 in each group): control (Group C); low tidal volume (Group L); low tidal volume + glutamine (Group L + G); high tidal volume (Group H); and high tidal volume + glutamine (Group H + G). Mice in all groups, except Group C, underwent mechanical ventilation for 4 h. For the in vitro study, mouse lung epithelial 12 (MLE-12) cells pretreated with glutamine underwent cyclic stretching at 20% for 4 h. Cell lysate and lung tissue were obtained to detect the junction proteins, inflammatory cytokines, and lung pathological changes by the Western blotting, cytokine assay, hematoxylin and eosin staining, and immunofluorescence.

In vivo, compared with Group C, total cell counts (t = −28.182, P < 0.01), the percentage of neutrophils (t = −28.095, P < 0.01), IL-6 (t = −28.296, P < 0.01), and TNF-α (t = −19.812, P < 0.01) in bronchoalveolar lavage (BAL) fluid, lung injury scores (t = −6.708, P < 0.01), and the wet-to-dry ratio (t= −15.595, P < 0.01) were increased in Group H; IL-10 in BAL fluid (t = 9.093, P < 0.01) and the expression of E-cadherin (t = 10.044, P < 0.01) and p120-catenin (t = 13.218, P < 0.01) were decreased in Group H. Compared with Group H, total cell counts (t = 14.844, P < 0.01), the percentage of neutrophils (t = 18.077, P < 0.01), IL-6 (t = 18.007, P < 0.01), and TNF-α (t = 10.171, P < 0.01) in BAL fluid were decreased in Group H + G; IL-10 in BAL fluid (t = −7.531, P < 0.01) and the expression of E-cadherin (t = −14.814, P < 0.01) and p120-catenin (t= −9.114, P < 0.01) were increased in Group H + G. In vitro, compared with the nonstretching group, the levels of IL-6 (t = −21.111, P < 0.01) and TNF-α (t = −15.270, P < 0.01) were increased in the 20% cyclic stretching group; the levels of IL-10 (t = 5.450, P < 0.01) and the expression of E-cadherin (t = 17.736, P < 0.01) and p120-catenin (t = 16.136, P < 0.01) were decreased in the 20% cyclic stretching group. Compared with the stretching group, the levels of IL-6 (t = 11.818, P < 0.01) and TNF-α (t = 8.631, P < 0.01) decreased in the glutamine group; the levels of IL-10 (t = −3.203, P < 0.05) and the expression of E-cadherin (t = −13.567, P < 0.01) and p120-catenin (t = −10.013, P < 0.01) were increased in the glutamine group.

High tidal volume mechanical ventilation and 20% cyclic stretching could cause VILI. Glutamine regulates VILI by improving cytokines and increasing the adherens junctions, protein E-cadherin and p120-catenin, to enhance the epithelial barrier function.

Recent research indicates that nerve growth factor (NGF) promotes cardiac repair following myocardial infarction by promoting angiogenesis and cardiomyocyte survival. The purpose of this study was to investigate the effects of NGF on cardiac fibroblasts (CFs) proliferation, cell cycle, migration, and myofibroblast transformation in vitro.

CFs were obtained from ventricles of neonatal Sprague-Dawley rats and incubated with various concentrations of NGF (0, 0.01, 0.1, 1, 10, and 100 ng/ml; 0 ng/ml was designated as the control group). Cell proliferation and cell cycle of the CFs were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry (FCM), respectively. A cell scratch wound model and transwell were carried out to observe effects of NGF on migration of CFs after 24 h of culture. Real-time polymerase chain reaction (RT-PCR) and Western blotting were used to measure α-smooth muscle actin (α-SMA) at mRNA and protein levels after CFs were incubated with various concentrations of NGF.

Expression of α-SMA measured by RT-PCR and Western blotting significantly increased in the 1 and 10 ng/ml NGF groups (P < 0.05). Absorbance values of CFs showed that NGF did not influence the proliferation of CFs (The A₄₉₀ values were 0.178 ± 0.038, 0.182 ± 0.011, 0.189 ± 0.005, 0.178 ± 0.010, 0.185 ± 0.025, and 0.177 ± 0.033, respectively, in the 0, 0.01, 0.1, 1, 10, and 100 ng/ml NGF groups [P = 0.800, 0.428, 0.981, 0.596, and 0.913, respectively, compared with control group]), and FCM analysis showed that the percentage of CFs in G0/G1, S, and G2/M phases was not changed (P > 0.05). The cell scratch wound model and transwell showed that CFs migration was not significantly different (P > 0.05).

NGF induces myofibroblast transformation but does not influence proliferation, cell cycle, or migration of CFs in vitro.

Mineral and bone disorder is one of the severe complications in kidney transplant recipients (KTRs). Previous studies showed that bisphosphonates had favorable effects on bone mineral density (BMD). We sought to compare different bisphosphonate regimens and rank their strategies.

We searched PubMed, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL) up to April 01, 2017, for randomized controlled trials (RCTs) comparing bisphosphonate treatments in adult KTRs. The primary outcome was BMD change. We executed the tool recommended by the Cochrane Collaboration to evaluate the risk of bias. We performed pairwise meta-analyses using random effects models and network meta-analysis (NMA) using Bayesian models and assessed the quality of evidence.

A total of 21 RCTs (1332 participants) comparing 6 bisphosphonate regimens were included. All bisphosphonates showed a significantly increased percentage change in BMD at the lumbar spine compared to calcium except clodronate. Pamidronate with calcium and Vitamin D analogs showed improved BMD in comparison to clodronate with calcium (mean difference [MD], 9.84; 95% credibility interval [CrI], 1.06–19.70). The combination of calcium and Vitamin D analogs had a significantly lower influence than adding either pamidronate or alendronate (MD, 6.34; 95% CrI, 2.59–11.01 and MD, 6.16; 95% CrI, 0.54–13.24, respectively). In terms of percentage BMD change at the femoral neck, both pamidronate and ibandronate combined with calcium demonstrated a remarkable gain compared with calcium (MD, 7.02; 95% CrI, 0.30–13.29 and MD, 7.30; 95% CrI, 0.32–14.22, respectively). The combination of ibandronate with calcium displayed a significant increase in absolute BMD compared to any other treatments and was ranked best.

Our NMA suggested that new-generation bisphosphonates such as ibandronate were more favorable in KTRs to improve BMD. However, the conclusion should be treated with caution due to indirect comparisons.

Several studies have reported that mindfulness meditation has a potential effect in controlling headaches, such as migraine and tension-type headache; however, its role remains controversial. This review assessed the evidence regarding the effects of mindfulness meditation for primary headache pain.

Only English databases (PubMed, Cochrane Central Register of Controlled Trials [the Cochrane Library], PsycINFO, Psychology and behavioral science collection, PsyArticles, Web of Science, and Scopus) were searched from their inception to November 2016 with the keywords ( "meditation" or "mindfulness" or "vipassana" or "dzogchen" or "zen" or "integrative body-mind training" or "IBMT" or "mindfulness-based stress reduction" or "MBSR" or "mindfulness-based cognitive therapy" or "MBCT" and "Headache" or "Head pain" or "Cephalodynia" or "Cephalalgia" or "Hemicrania" or "Migraine" ). Titles, abstracts, and full-text articles were screened against study inclusion criteria: controlled trials of structured meditation programs for adult patients with primary headache pain. The quality of studies included in the meta-analysis was assessed with the Yates Quality Rating Scale. The meta-analysis was conducted with Revman 5.3.

Ten randomized controlled trials and one controlled clinical trial with a combined study population of 315 patients were included in the study. When compared to control group data, mindfulness meditation induced significant improvement in pain intensity (standardized mean difference, −0.89; 95% confidence interval, −1.63 to −0.15; P = 0.02) and headache frequency (−0.67; −1.24 to −0.10; P = 0.02). In a subgroup analysis of different meditation forms, mindfulness-based stress reduction displayed a significant positive influence on pain intensity (P < 0.000). Moreover, 8-week intervention had a significant positive effect (P < 0.000).

Mindfulness meditation may reduce pain intensity and is a promising treatment option for patients. Clinicians may consider mindfulness meditation as a viable complementary and alternative medical option for primary headache.

Hydrogen sulfide (H₂S), a gaseous signal molecule, plays a crucial role in many pathophysiologic processes in the cardiovascular system. Autophagy has been shown to participate in the occurrence of many cardiac diseases. Increasing evidences indicated that H₂S regulates myocardial structure and function in association with the altered autophagy and plays a "switcher" role in the autophagy of myocardial diseases. The aim of this review was to summarize these insights and provide the experimental evidence that H₂S targets cardiomyocyte autophagy to regulate cardiovascular function.

This review was based on data in articles published in the PubMed databases up to October 30, 2017, with the following keywords: "hydrogen sulfide," "autophagy," and "cardiovascular diseases."

Original articles and critical reviews on H₂S and autophagy were selected for this review.

When autophagy plays an adaptive role in the pathogenesis of diseases, H₂S restores autophagy; otherwise, when autophagy plays a detrimental role, H₂S downregulates autophagy to exert a cardioprotective function. For example, H₂S has beneficial effects by regulating autophagy in myocardial ischemia/reperfusion and plays a protective role by inhibiting autophagy during the operation of cardioplegia and cardiopulmonary bypass. H₂S postpones cardiac aging associated with the upregulation of autophagy but improves the left ventricular function of smoking rats by lowering autophagy.

H₂S exerts cardiovascular protection by regulating autophagy. Cardiovascular autophagy would likely become a potential target of H₂S therapy for cardiovascular diseases.

The objective of the study was to summarize the role of DNA methylation in the development and metastasis of uveal melanoma (UM).

The relevant studies in MEDLINE were searched.

In this review, we performed a comprehensive literature search in MEDLINE using "uveal melanoma" AND ( "DNA methylation" OR "epigenetics" ) for original research/review articles published before February 2018 on the relationship between DNA methylation and UM. References of the retrieved studies were also examined to search for potentially relevant papers.

Previous studies on the relationship between DNA methylation and UM covered many genes including tumor suppressor genes (TSGs), cyclin-dependent kinase genes, and other genes. Among them, the TSG genes such as RASSF1A and p16INK4a, which encodes a cyclin-dependent kinase inhibitor, are relatively well-studied genes. Specifically, a high percentage of promoter methylation of RASSF1A was observed in UM cell lines and/or patients with UM. Promoter methylation of RASSF1A was also associated with the development of metastasis. Similarly, a high percentage of promoter hypermethylation of p16INK4a was found in UM cell lines. DNA promoter methylation can control the expression of p16INK4a, which affect cell growth, migration, and invasion in UM. Many other genes might also be involved in the pathogenesis of UM such as the Ras and EF-hand domain containing (RASEF) gene, RAB31, hTERT, embryonal fyn-associated substrate, and deleted in split-hand/split-foot 1.

Our review reveals the complex mechanisms underlying the tumorigenesis of UM and highlights the great needs of future studies to discover more genes/5’-C-phosphate-G-3’ sites contributing to the development/metastasis of UM and explore the mechanisms through which epigenetic changes exert their function in UM.

Since the advent of induced pluripotent stem cell (iPSC) technology a decade ago, enormous progress has been made in stem cell biology and regenerative medicine. Human iPSCs have been widely used for disease modeling, drug discovery, and cell therapy development. In this review, we discuss the progress in applications of iPSC technology that are particularly relevant to drug discovery and regenerative medicine, and consider the remaining challenges and the emerging opportunities in the field.

Articles in this review were searched from PubMed database from January 2014 to December 2017.

Original articles about iPSCs and cardiovascular diseases were included and analyzed.

iPSC holds great promises for human disease modeling, drug discovery, and stem cell-based therapy, and this potential is only beginning to be realized. However, several important issues remain to be addressed.

The recent availability of human cardiomyocytes derived from iPSCs opens new opportunities to build in vitro models of cardiac disease, screening for new drugs and patient-specific cardiac therapy.

致小编：无痛插管对肠镜检查时避免穿孔极为重要。超薄肠镜和标准胃镜（9.2-9.8 mm）可增加无痛插管患者的比例，但仍有约10%的患者出现中度或重度腹痛。^[1]结肠镜检查中镇静和麻醉可减轻患者痛苦，提高结肠镜检查成功率，但腹痛警示作用消失，穿孔风险增加。^[2]本文采用经鼻胃镜（5.9 mm）模拟超薄结肠镜进行检查。作者假设在这项研究中没有患者会有严重的腹痛，证明了经鼻胃镜在结肠检查中的良好安全性。

致编者：在临床中，心房颤动（AF）是最常见的心律失常类型之一，其对医疗保健系统的负担和患病率仍在上升。在过去的50年里，房颤的发病率增加了大约350.0%。^[1]在全球疾病负担研究的综述中，估计全球ofAF患病率为596.2或373.1/100,000男性或女性。随着年龄的增长，AFF的发生率显著增加。^[2]大约1%的房颤患者<60岁，高达12%的房颤患者在75-84岁的年龄范围内，并且在80岁或以上的患者中房颤患病率甚至更高。痴呆是一种以记忆和其他认知功能受损为特征的脑致残疾病。它会严重影响人类的生活。在全球范围内，估计有3300万老年人患有痴呆症，预计到2040年这一数字将达到8110万。很明显，认知功能会随着身体的衰老而自然退化，butAF可能会加速这一速度。根据一些系统综述和荟萃分析，房颤可使痴呆风险增加40%。对于超过75岁的老年人，他们的痴呆通常由脑血管病变和神经变性引起。而对于40-59岁的中年人来说，痴呆的出现源于心血管疾病。房颤会增加中风、心力衰竭和死亡率的风险。然而，考虑到共同的血管风险因素，如吸烟、高血压、高胆固醇、糖尿病、高龄、慢性肾病、血管疾病、心力衰竭、不活动/低活动、遗传、睡眠呼吸暂停和饮酒，AF也可能增加痴呆的风险。^[3,4]“心源性痴呆”一词在40多年前首次被引入，以支持房颤和认知障碍之间的可能联系。直到最近，demonstratedAF才是认知障碍的独立危险因素，并可能通过几种机制增加痴呆的风险，包括脑灌注不足、血栓栓塞（包括中风和亚临床脑梗死）、炎症、抗凝性脑微出血和神经元功能损害。因此，控制房颤发展和促进心血管健康的策略可能有助于延缓痴呆的发作。传统的ALAF治疗包括抗凝、节律和心率控制。因此，通过了解房颤和痴呆之间的潜在关系，可以为未来的房颤管理提出新的方法。

编辑：男性类固醇激素在肾上腺皮质和睾丸中合成，正常类固醇激素水平的儿科参考区间对于肾上腺和性腺疾病的诊断至关重要。重要的是，类固醇激素谱随年龄和青春期发育而变化，并且迄今为止，仅发表了非常有限的关于年龄和青春期发育方面的正常类固醇激素范围的数据。缺乏此类数据主要是由于缺乏足够灵敏和特异的方法来确定类固醇浓度的适当参考区间。

致小编：48岁中国女性主诉胸闷、气短、心悸8个月。这些症状逐渐加重，1个月前出现双下肢水肿。她有子宫肌瘤病史。3/4处肿瘤颤动声^th左侧libs的肋间隙；同时在心尖区听到收缩期杂音。另一家医院心脏超声提示右心房肿块，诊断为粘液瘤。心脏超声显像显示下腔静脉和右心腔被肿块占据[图1a].腹部和心脏的计算机断层血管造影（CTA）显示子宫内有多发性不规则软组织肿块，经卵巢右静脉进入下腔静脉，最后到达右心房[图1b,图1c].放射科医生认为该疾病是子宫平滑肌瘤病（UL），并建议通过磁共振成像（MRI）进行检查。根据腹部核磁共振[图1d,图1e]和心[图1f]，以及扩散加权成像(DWI)[图1g]，该病被诊断为UL。该诊断经手术和病理证实[图1h].术后上述症状明显缓解，术后10d双下肢水肿消失。

致编者：胃粘膜下病变很容易被误诊为粘膜下肿瘤（SMT）或压迫，这些患者可能会接受内镜切除或手术。对于胃底粘膜下病变，超声内镜（EUS）检查下回声纹理与脾脏和胃外相同，尤其是有脾切除术史的患者，应怀疑副脾。这对欧盟运营商来说是一个挑战。本报告介绍了两例经EUS和CT诊断为副脾的病例，以避免不必要的治疗。

致编辑：甲状腺手术是世界范围内最常进行的内分泌手术。甲状腺手术最严重的并发症之一是喉返神经（RLN）损伤，其发生率从0.5%到14.0%不等，取决于疾病类型、手术类型、切除范围和手术技术。^[1,2,3]目前，有三种方法用于识别神经：上入路、外侧入路和下入路。^[4]这些都有优点和缺点；然而，所有三种技术的共同组成部分是从甲状腺的外侧识别RLN。然而，在一些特殊情况下，当甲状腺的外侧难以分割时，不可能使用三种技术中的任何一种来识别RLN。因此，我们引入了一种新的方法来帮助识别特殊情况下的RLN。

编辑：象皮病是由慢性淋巴水肿引起的，其特征是手臂、腿或生殖器的粗大增大。它是由于淋巴系统的各种阻塞性疾病而发生的。淋巴水肿的最常见形式是继发性淋巴水肿，涉及通过手术、放射、肿瘤侵袭、直接创伤或感染切除或消融局部淋巴结。^[1,2]我们报告了一例罕见的双侧下肢和腹部象皮病病例，原因是丹毒广泛破坏淋巴结。

致编者：可回收下腔静脉（IVC）滤器放置多年来一直在增加，但只有一小部分可回收IVC滤器被移除，范围在10.1%至38.9%之间。^[1,2]腹腔镜下取出下腔静脉滤器的病例报告自2015年起提供，^[3]病例报告中的滤器钩明显突出于腔前壁，无需腔静脉切开重建。在这种情况下，IVC滤器头端嵌入后壁，需要进行腔切开术。很少有研究报道通过腔静脉切开和重建进行腹腔镜下下腔静脉滤器回收。

致编者：一名出生于中国贵州省的12岁男孩，有面部和四肢全身性隆起结节性病变病史，持续2个月。患者的首发症状是面部出现小结节，不伴有瘙痒、疼痛或烧灼感。病变数量在一周内增加，也出现在他的四肢上，没有发热、关节痛或关节肿胀的报告。初步活检提示组织细胞增生性疾病，其他检查正常，给予中药治疗。然而，病变继续增加，患者被带到我们的诊所。查体发现面部及四肢弥漫性黄褐色小结节，眉毛稀疏，面部溃疡瘢痕。他的生命体征和实验室检查正常。右前臂新病灶活检显示浅层和深层真皮及皮下组织肉芽肿浸润，由泡沫状和上皮样组织细胞混合物组成，包括散在淋巴细胞。此外，Fite-Faraco染色显示大量抗酸杆菌[图1].诊断为世界卫生组织（世卫组织）定义的多菌性麻风病。这些患者没有明确的感染性疾病暴露史，随后接受了多药治疗，包括每月剂量的利福平450 mg和氯法齐明200 mg，加上每日剂量的氨苯砜50 mg和氯法齐明50 mg，导致皮损在2个月内部分缓解。

编辑：在过去的10年里，越来越多的证据证实精神分裂症与白质(WM)损伤有关；这种损伤甚至在精神分裂症症状发作之前就存在了。患者广泛的WM纤维束受到影响，尤其是在某些关键脑区，如弓状束、上纵束和胼胝体。先前的一项研究报道，尽管精神分裂症患者中WM损伤不超过1%，但它仍然是精神分裂症的一种稳定且特异性的异常病理特征。^[1]