Volume 133 · Issue 10 · 2020

心力衰竭（HF）是糖尿病常见而严重的并发症，近年来受到越来越多的关注。关注HF的一个原因是，随着急性心肌梗死后动脉粥样硬化血栓事件的大幅减少，HF是2型糖尿病（T2DM）患者中相对更常见的心脏结局。另一个原因是在使用钠-葡萄糖协同转运蛋白-2抑制剂（SGLT2is）的心血管结局试验中观察到的HF住院意外减少。^[1,2,3]这些发现引发了临床医生和研究人员的猜测，即是否应该做出更多努力来区分具有发生心力衰竭高风险的糖尿病患者。

Fourier transform infrared (FTIR) spectroscopy technique has not been used as a diagnostic tool for diabetes in clinical practice. This study was linked to structural changes in hemoglobin (Hb) in type 2 diabetes patients at higher levels of HbA₁C using FTIR spectroscopy.

Fifty-three diabetic patients from the Bahawal Victoria Hospital, Bahawalpur, Pakistan were categorized as group A (6% < HbA₁C < 7%; n = 25) and group B (HbA₁C ≥9%; n = 28). Another group (group N) of twenty blood samples was taken from healthy people from the Islamia University Bahawalpur, Pakistan. Data from all groups were collected from January 1, 2018 to March 31, 2019. The structure of Hb was studied by FTIR spectroscopy and impact of glucose on the fine structure of HbA₁C was estimated.

Hb secondary structure erythrocyte parameters were altered by changing glucose concentrations. From FTIR spectra of all three groups it was found that Hb structure was slightly altered in group A, but significantly changed in group B (P < 0.05). There was an increase in β-sheet structure and a reduction in α-helix structure at elevated levels of HbA₁C (group B) in type 2 diabetes.

We suggest that higher level of glycation reflected by increased HbA₁C might be a contributing factor to structural changes in Hb in type 2 diabetic patients. FTIR spectroscopy can be a novel technique to find pathogenesis in type 2 diabetes.

The association of milk intake with cardiovascular disease (CVD) and cause-specific mortality remained controversial and evidence among the Chinese population was limited. We aimed to study the relationship between milk intake and CVDs among general Chinese adults.

A total of 104,957 participants received questionnaire survey. Results of physical examination such as anthropometric measurements and biochemical tests during 2007 to 2008, demographic data and their information on milk intake were collected through standardized questionnaires. Cox proportional hazard regression models were used to calculate hazard ratios (HRs) and their corresponding 95% confidence intervals (CIs) of CVD incidence, cause-specific mortality and all-cause mortality related to milk intake. Restricted cubic splines (RCSs) were applied to examine dose-response associations.

Among the 91,757 participants with a median follow-up period of 5.8 years, we documented 3877 CVD cases and 4091 all-cause deaths. Compared with participants who never consumed milk, the multivariate-adjusted HRs (95% CIs) of CVD incidence for 1 to 150 g/day, 151 to 299 g/day, and ≥300 g/day were 0.94 (0.86-1.03) (P > 0.05), 0.77 (0.66-0.89) (P < 0.05), and 0.59 (0.40-0.89) (P < 0.05), respectively; each 100 g increase of daily milk intake was associated with 11% lower risk of CVD incidence (HR, 0.89; 95% CI: 0.85-0.94; P < 0.001), and 11% lower risk of CVD mortality (HR, 0.89; 95% CI: 0.82-0.97; P = 0.008) after adjustment for age, sex, residential area, geographic region, education level, family history of CVD, smoking, alcohol drinking, physical activity level, body mass index, and healthy diet status (ideal or not). RCS analyses also showed a linear dose-response relationship with CVD (P for overall significance of the curve <0.001; P for non-linearity = 0.979; P for linearity <0.001) and stroke (P for overall significance of the curve = 0.010; P for non-linearity = 0.998; P for linearity = 0.002) incidence, and CVD mortality (P for overall significance of the curve = 0.045; P for non-linearity = 0.768; P for linearity = 0.014) within the current range of daily milk intake.

Daily milk intake was associated with lower risk of CVD incidence and mortality in a linear inverse relationship. The findings provide new evidence for dietary recommendations in CVD prevention among Chinese adults and people with similar dietary pattern in other countries.

Resting heart rate (RHR) is considered as a strong predictor of total mortality and hospitalization due to heart failure in hypertension patients. Bisoprolol fumarate, a second-generation beta-adrenoreceptor blockers (β-blocker) is commonly prescribed drug to manage hypertension. The present study was to retrospectively evaluate changes in the average RHR and its association with cardiovascular outcomes in bisoprolol-treated coronary artery disease (CAD) patients from the CAD treated with bisoprolol (BISO-CAD) study who had comorbid hypertension.

We performed ad-hoc analysis for hypertension sub-group of the BISO-CAD study (n = 866), which was a phase IV, multination, multi-center, single-arm, observational study carried out from October 2011 to July 2015 across China, South Korea, and Vietnam. Multivariate regression analysis was used to identify factors associated with incidence of composite cardiac clinical outcome (CCCO), the results were presented as adjusted odds ratio (OR) along with 95% confidence interval (CI) and adjusted P value.

A total of 681 patients (mean age: 64.77 ± 10.33 years) with hypertension from BISO-CAD study were included in the analysis. Bisoprolol improved CCCOs in CAD patients with comorbid hypertension, with RHR <65 and <70 beats/min compared with RHR ≥65 and ≥75 beats/min, respectively, in the efficacy analysis (EA) set. In addition, it lowered RHR in both intent-to-treat (ITT) and EA groups after 6, 12, and 18 months of treatment. Further, RHR 70 to 74 beats/min resulted in significantly higher risk of CCCOs EA set of patients (adjusted OR: 4.34; 95% CI: 1.19-15.89; P = 0.03). Also, events of hospitalization due to acute coronary syndrome were higher when RHR 69 to 74 beats/min compared to RHR <69 beats/min in ITT patients.

Bisoprolol can effectively reduce RHR in Asian CAD patients with comorbid hypertension and hence, improve CCCO without affecting their blood pressure.

Radical nephrectomy and thrombectomy is the standard surgical procedure for the treatment of renal cell carcinoma (RCC) with tumor thrombus (TT). But the estimation of intra-operative blood loss is only based on the surgeon’s experience. Therefore, our study aimed to develop Peking University Third Hospital score (PKUTH score) for the prediction of intra-operative blood loss volume in radical nephrectomy and thrombectomy.

The clinical data of 153 cases of renal mass with renal vein (RV) or inferior vena cava tumor thrombus admitted to Department of Urology, Peking University Third Hospital from January 2015 to May 2018 were retrospectively analyzed. The total amount of blood loss during operation is equal to the amount of blood sucked out by the aspirator plus the amount of blood in the blood-soaked gauze. Univariate linear analysis was used to analyze risk factors for intra-operative blood loss, then significant factors were included in subsequent multivariable linear regression analysis.

The final multivariable model included the following three factors: open operative approach (P < 0.001), Neves classification IV (P < 0.001), inferior vena cava resection (P = 0.001). The PKUTH score (0-3) was calculated according to the number of aforementioned risk factors. A significant increase of blood loss was noticed along with higher risk score. The estimated median blood loss from PKUTH score 0 to 3 was 280 mL (interquartile range [IQR] 100-600 mL), 1250 mL (IQR 575-2700 mL), 2000 mL (IQR 1250-2900 mL), and 5000 mL (IQR 4250-8000 mL), respectively. Meanwhile, the higher PKUTH score was, the more chance of post-operative complications (P = 0.004) occurred. A tendency but not significant overall survival difference was found between PKUTH risk score 0 vs. 1 to 3 (P = 0.098).

We present a structured and quantitative scoring system, PKUTH score, to predict intra-operative blood loss volume in radical nephrectomy and thrombectomy.

Patients carrying the HongKongαα (HKαα) allele and -α^3.7/ααα^anti-4.2 could be misdiagnosed as -α^3.7/αα by the current conventional thalassemia detection methods, leading to inaccurate genetic counseling and an incorrect prenatal diagnosis. This study was aimed to accurately analyze the genotypes of HKαα carriers and -α^3.7/ααα^anti-4.2.

Samples were collected in our hospital from July 2017 to October 2019. Twenty-four common types of Chinese thalassemia were screened by gap-polymerase chain reaction (Gap-PCR) and reverse dot blot (RDB). Anti-4.2 multiplex-PCR was used to confirm carriers of the ααα^anti-4.2 duplication with -α^3.7 deletion. Two-round nested PCR and multiplex ligation-dependent probe amplification (MLPA) were applied to accurately identify and confirm their genotypes. For data analysis, we used descriptive statistics and Fisher’s exact tests.

Two thousand five hundred and forty-four cases were identified as thalassemia in 5488 peripheral blood samples. The results showed that α, β, and αβ compound thalassemia were identified in 1190 (46.78%), 1286 (50.55%), and 68 (2.67%) cases, respectively. A total of 227 samples from thalassemia patients were identified as -α^3.7/αα by Gap-PCR, and the genotypes of two samples were uncertain. There was a difference between Gap-PCR and combined groups (Gap-PCR combined with nested PCR and MLPA) in detecting HKαα (P < 0.05). Among the 229 patients, 20 patients were identified as HKαα carriers and one was identified as -α^3.7/ααα^anti-4.2 by two-round nested PCR and MLPA, including 15 patients with HKαα/αα, three with HKαα/αα and β-thalassemia coinheritance, one with HKαα/-^SEA, one with HKαα/-α^4.2 and β-thalassemia coinheritance, and one with -α^3.7/ααα^anti-4.2 and β-thalassemia coinheritance.

ααα^anti-4.2 and HKαα genotypes of patients carrying -α^3.7 need to be detected to reduce the misdiagnosis rate of patients carrying HKαα and -α3.7/ααα^anti-4.2 alleles. More accurate genetic counseling can be provided in the clinic using nested PCR combined with MLPA.

Atrial natriuretic peptide (ANP) and its natriuretic peptide receptors A (NPR-A) and C (NPR-C) are involved in the regulation of physiological and pathophysiological process of blood pressure. The present study aimed to determine the role of NPR-C in the development of salt-sensitive hypertension.

The Dahl salt-sensitive (DS) and salt-resistant (DR) rats were used in this study. Animals were matched according to their age and weight, and then placed on either a high-salt (HS, 8%) or a normal-salt (NS, 0.4%) diet for 6 weeks randomly using random number table. The systolic blood pressure (SBP), plasmatic sodium concentration (PL_Na), urinary sodium excretion (UV_Na), and serum creatinine concentration (Scr) were measured. The concentration of ANP in blood and tissues (heart and kidney) was detected by enzyme-linked immunosorbent assay. The expression of ANP, NPR-A, and NPR-C in kidney was evaluated with western blot analysis. Regarding renal redox state, the concentration changes in malondialdehyde (MDA), lipofuscin, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox), and nitric oxide synthase (NOS) in kidney were detected by a spectrophotometric method. The kidney damage was evaluated using pathological techniques and the succinodehydrogenase (SDHase) examination. Furthermore, after an intra-peritoneal injection of C-atrial natriuretic peptide (ANP)_4-23 (C-ANP_4-23), an NPR-C receptor agonist, the SBP, biochemical values in blood and urine, and renal redox state were evaluated. The paired Student’s t test and analysis of variance followed by the Bonferroni test were performed for statistical analyses of the comparisons between two groups and multiple groups, respectively.

The baseline SBP in all groups was within the normal range. At the end of the 6-week experiment, HS diet significantly increased the SBP in DS rats from 116.63 ± 2.90 mmHg to 162.25 ± 2.15 mmHg (t = -10.213, P < 0.001). The changes of SBP were not significant in DS rats on an NS diet and DR rats on an NS diet or on an HS diet (all P > 0.05). The significant increase of PL_Na, UV_Na, and Scr related to an HS diet was found in both DS and DR rats (all P < 0.05). However, significant changes in the concentration (t= -21.915, P < 0.001) and expression of renal ANP (t= -3.566, P = 0.016) and the expression of renal NPR-C (t = 5.864, P = 0.002) were only observed in DS hypertensive rats. The significantly higher desmin immunochemical staining score (t = -5.715, P = 0.005) and mitochondrial injury score (t = -6.325, P = 0.003) accompanied by the lower SDHase concentration (t= 3.972, P = 0.017) revealed mitochondrial pathologic abnormalities in podocytes in DS rats with an HS diet. The distinct increases of MDA (t= -4.685, P= 0.009), lipofuscin (t= -8.195, P= 0.001), and Nox (t= -12.733, P < 0.001) but not NOS (t = -0.328, P = 0.764) in kidneys were also found in DS hypertensive rats. C-ANP_4-23 treatment significantly decreased the SBP induced by HS in DS rats (P < 0.05), which was still higher than NS groups with the vehicle or C-ANP_4-23 treatment (P < 0.05). Moreover, the HS-induced increase of MDA, lipofuscin, Nox concentrations, and Nox4 expression in DS rats was significantly attenuated by C-ANP_4-23 treatment as compared with those with HS diet and vehicle injection (all P < 0.05).

The results indicated that the renal NPR-C might be involved in the salt-sensitive hypertension through the damage of mitochondria in podocytes and the reduction of the anti-oxidative function. Hence, C-ANP_4-23 might serve as a therapeutic agent in treating salt-sensitive hypertension.

Pulmonary fibrosis is a respiratory disease caused by the proliferation of fibroblasts and accumulation of the extracellular matrix (ECM). It is known that the lung ECM is mainly composed of a three-dimensional fiber mesh filled with various high-molecular-weight proteins. However, the small-molecular-weight proteins in the lung ECM and their differences between normal and fibrotic lung ECM are largely unknown.

Healthy adult male Sprague-Dawley rats (Rattus norvegicus) weighing about 150 to 200 g were randomly divided into three groups using random number table: A, B, and C and each group contained five rats. The rats in Group A were administered a single intragastric (i.g.) dose of 500 μL of saline as control, and those in Groups B and C were administered a single i.g. dose of paraquat (PQ) dissolved in 500 μL of saline (20 mg/kg). After 2 weeks, the lungs of rats in Group B were harvested for histological observation, preparation of de-cellularized lung scaffolds, and proteomic analysis for small-molecular-weight proteins, and similar procedures were performed on Group C and A after 4 weeks. The differentially expressed small-molecular-weight proteins (DESMPs) between different groups and the subcellular locations were analyzed.

Of the 1626 small-molecular-weight proteins identified, 1047 were quantifiable. There were 97 up-regulated and 45 downregulated proteins in B vs. A, 274 up-regulated and 31 down-regulated proteins in C vs. A, and 237 up-regulated and 28 downregulated proteins identified in C vs. B. Both the up-regulated and down-regulated proteins in the three comparisons were mainly distributed in single-organism processes and cellular processes within biological process, cell and organelle within cellular component, and binding within molecular function. Further, more up-regulated than down-regulated proteins were identified in most sub-cellular locations. The interactions of DESMPs identified in extracellular location in all comparisons showed that serum albumin (Alb) harbored the highest degree of node (25), followed by prolyl 4-hydroxylase beta polypeptide (12), integrin β1 (10), apolipoprotein A1 (9), and fibrinogen gamma chain (9).

Numerous PQ-induced DESMPs were identified in de-cellularized lungs of rats by high throughput proteomics analysis. The DESMPs between the control and treatment groups showed diversity in molecular functions, biological processes, and pathways. In addition, the interactions of extracellular DESMPs suggested that the extracellular proteins Alb, Itgb1, Apoa1, P4hb, and Fgg in ECM could be potentially used as biomarker candidates for pulmonary fibrosis. These results provided useful information and new insights regarding pulmonary fibrosis.

Dysuria is one of the main symptoms of genitourinary syndrome of menopause, which causes serious disruption to the normal life of peri-menopausal women. Studies have shown that it is related to decrease of detrusor contractile function, but the exact mechanism is still poorly understood. Previous results have suggested that the sphingosine-1-phosphate (S1P) pathway can regulate detrusor contraction, and this pathway is affected by estrogen in various tissues. However, how estrogen affects this pathway in the detrusor has not been investigated. In this study, we detected changes of the S1P/RhoA/Rho associated kinases (ROCK)/myosin light chain (MLC) pathway in the detrusor of ovariectomized rats in order to explore the underlying mechanism of dysuria during peri-menopause.

Thirty-six female Sprague-Dawley rats were randomly divided into SHAM (sham operation), OVX (ovariectomy), and E groups (ovariectomy + estrogen), with 12 rats in each group. We obtained bladder detrusor tissues from each group and examined the mRNA and protein levels of the major components of the S1P/RhoA/ROCK/MLC pathway using quantitative real-time polymerase chain reaction and Western blotting, respectively. We also quantified the content of S1P in the detrusor using an enzyme linked immunosorbent assay. Finally, we compared results between the groups with one-way analysis of variance.

The components of the S1P pathway and the RhoA/ROCK/MLC pathway of the OVX group were significantly decreased, as compared with SHAM group. The percent decreases of the components in the S1P pathway were as follows: sphingosine kinase 1 (mRNA: 39%, protein: 45%) (both P < 0.05), S1P (21.73 ± 1.09 nmol/g vs. 18.86 ± 0.69 nmol/g) (P < 0.05), and S1P receptor 2/3 (S1PR2/3) (mRNA: 25%, 27%, respectively) (P < 0.05). However, the protein expression levels of S1PR2/3 and the protein and mRNA levels of SphK2 and S1PR1 did not show significant differences between groups (P > 0.05). The percent decreases of the components in the RhoA/ROCK/MLC pathway were as follows: ROCK2 (protein: 41%, mRNA: 36%) (both P < 0.05), p-MYPT1 (protein: 54%) (P < 0.05), and p-MLC20 (protein: 47%) (P < 0.05), but there were no significant differences in the mRNA and protein levels of RhoA, ROCK1, MYPT1, and MLC20 (all P > 0.05). In addition, all of the above-mentioned decreases could be reversed after estrogen supplementation (E group vs. SHAM group) (all P > 0.05).

In this study, we confirmed that ovariectomy is closely associated with the down-regulation of the S1P/RhoA/ROCK/MLC pathway in the rat detrusor, which may be one mechanism of dysuria caused by decreased contractile function of the female detrusor during peri-menopause.

Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p).

SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis.

Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t= 16.03, P < 0.001). Compared with that in human pancreatic duct epithelial cells (HPDE6-C7), SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t= 34.72, P < 0.001) and the lowest expression in human pancreatic cancer cells (MIAPaCa-2) (1.00 ± 0.06 vs. 1.41 ± 0.07, t= 7.70, P= 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t= 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t= 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs . 0.32 ± 0.03, t= 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t= 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo.

Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.

阿司匹林已广泛用于动脉粥样硬化性心血管疾病（ASCVD）的一级预防。^[1,2,3,4]阿司匹林用于ASCVD一级预防不会显著降低全因死亡率或心血管死亡率，阿司匹林用于ASCVD一级预防的主要益处是显著降低非致死性缺血性事件，包括心肌梗死、短暂性脑缺血发作、缺血性卒中和重大心血管事件（心血管死亡、非致死性心肌梗死和非致死性卒中），而主要风险是显著增加非致死性大出血事件，包括胃肠道出血和颅内出血。^[5,6,7,8]显然，只有在益处明显大于风险的情况下，开阿司匹林用于一级预防才有意义。在欧美，由于降压、戒烟、使用他汀类药物等其他一级预防措施的广泛应用，阿司匹林用于一级预防的获益风险比较过去逐渐降低。最近的三项大规模临床试验表明，阿司匹林用于低风险人群没有净临床获益。^{[9,10,11,12,13]}因此，ASCVD一级预防必须慎用阿司匹林。

Electronic health (medical) records, which are also considered as patients’ information that are routinely collected, provide a great chance for researchers to develop an epidemiological understanding of disease. Electronic health records systems cannot develop without the advance of computer industries. While conducting clinical trials that are always costly, feasible and reasonable analysis of routine patients’ information is more cost-effective and reflective of clinical practice, which is also called real world study. Real world studies can be well supported by big data in healthcare industry. Real world studies become more and more focused and important with the development of evidence-based medicine. These big data will definitely help in making decisions, making policies and guidelines, monitoring of effectiveness and safety on new drugs or technologies. Extracting, cleaning, and analyzing such big data will be a great challenge for clinical researchers. Successful applications and developments of electronic health record in western countries (eg, disease registries, health insurance claims, etc) have provided a clear direction for Chinese researchers. However, it is still at primary stages in China. This review tries to provide a full perspective on how to translate the electronic health records into scientific achievements, for example, among patients with diabetes. As a summary in the end, resource sharing and collaborations are highly recommended among hospitals and healthcare groups.

致编辑：肾上腺和性腺功能可以通过分析不同年龄组，尤其是青春期女孩的类固醇激素水平来评估。液相色谱-串联质谱法（LC-MS/MS或高性能LC[HPLC]-MS/MS）提供了HPLC的物理分离能力和串联MS的质量分析能力的组合，这提高了测量类固醇激素水平的灵敏度和特异性。^[1,2]此法较临床上分析儿童类固醇激素水平的其他方法更灵敏、有效、特异、均一性强。关于类固醇性激素参考区间的研究在高加索受试者中比在中国受试者中更常见。^[3]在中国，尤其是健康女孩的类固醇激素基于LC-MS/MS的参考区间尚未见报道。随着LC-MS/MS变得越来越普遍，参考区间的建立变得越来越紧迫。在这里，我们定义了孕烯醇酮、17 α-羟基孕酮、皮质酮、脱氢表雄酮、雄烯二酮和游离睾酮的适当参考范围。

致编辑：耳源性脑脓肿是化脓性中耳炎最严重的并发症之一。尽管抗生素的广泛使用在过去几年中显著降低了耳源性脑脓肿的死亡率和发病率，但仍有大量患者因脑疝或脑脓肿破裂而死亡。在这些致命病例中，适当的时间和方法引流脓肿对于良好的结果非常重要。在此，我们描述了使用经乳突状中颅底开颅术和超声引导下脓肿抽吸术成功治疗一例耳源性脑脓肿和脑疝的年轻男性患者。

致编辑：一名来自山东省的13岁克罗恩病（CD）女孩于2013年4月转至我们的炎症性肠病（IBD）中心。三个月前，患者出现便血和发热，但抗生素治疗不成功。入院后，结肠镜检查显示节段性病变、鹅卵石结石和狭窄[图1A].巨细胞病毒、EB病毒、艰难梭菌和阿米巴原虫被排除为可能的原因。也没有白塞病、全身性血管炎或其他自身免疫性疾病的指征。我们的初步诊断是活动性重度CD（维也纳分型，A1L3B2）。本研究由北京大学第一医院伦理委员会批准（编号：2019153）。获得了适当的签名患者知情同意书。

致编辑：中国一项多中心回顾性调查显示，最常见的肺部真菌病是肺曲霉病。^[1]由于半乳甘露聚糖（GM）试验的假阴性和假阳性率较高，侵袭性肺曲霉病（IPA）的诊断仍然具有挑战性。国内研究报道IPA误诊率可高达73%。此外，GM非常耗时，导致诊断延迟。

致编辑：我们赞赏胡写的题为“血清总钙对危重疾病中离子钙临界高和临界低的预测准确性”的有趣和细心的文章等人.^[1]使用血清总钙及其修正值预测危重病临界离子钙浓度存在争议。因此，作者回顾性搜索了重症监护III数据库的医学信息，以确定总钙水平（无论是否校正白蛋白）是否可以预测临界高和低离子化钙。作者得出结论，未校正和校正的总钙水平都是预测危重疾病中离子钙临界值的不可靠指标。完全相信，这篇文章将提供一个深刻的介绍和补充永恒的故事钙状态估计总钙。为了完全理解总钙和离子钙之间的故事，并全面解释这篇手稿中关于钙的结果，应该首先优先考虑一些问题。

致编辑：很少，缺血性结肠炎也可以在结肠镜检查和计算机断层扫描（CT）成像中模拟癌症。在结肠镜检查中，溃疡、粘膜下肿块和具有溃疡粘膜的狭窄结肠段都被描述为模仿这种癌症。很少有报告记录了这种类型的肿块形成缺血性结肠炎变体。^[1,2,3,4]在这里，我们描述了两名缺血性结肠炎患者，他们表现出类似结肠癌的病变。

致编辑：血糖变异性（GV）对危重患者的预后有显著影响。^[1,2,3,4]患者的糖尿病状态影响GV和死亡率之间的关系；GV升高是无糖尿病（DM）患者比DM患者更有效的死亡危险因素。^[5]这项对1234名重症监护病房（ICU）患者的回顾性研究旨在确定导致高GV的显著因素，并评估GV与危重患者预后之间的关系。

致编辑：动脉粥样硬化是一种慢性炎症性疾病，涉及多种类型的免疫细胞。适应性免疫对动脉粥样硬化有多样而深远的影响。病变T细胞的效应表型可能影响病变生长和稳定性。在动脉粥样硬化斑块中已经报道了具有抗炎特性的调节性T细胞。抑制调节性T细胞的靶标包括初始CD4和效应CD4⁺和CD8⁺T细胞、树突状细胞和巨噬细胞。一个新的B细胞亚群，CD19⁺CD24^你好CD38^你好人类表型正在成为系统性红斑狼疮和关节炎等自身免疫领域的热点问题。^[1]这些调节性B细胞通过调节效应和调节性T细胞的功能在免疫系统中发挥重要作用。在一项实验研究中，Bregs通过白细胞介素10（IL-10）介导的机制减弱动脉粥样硬化的新生内膜形成而表现出保护作用。^[2]到目前为止，很少有关于动脉粥样硬化疾病中人类Bregs的研究。在本研究中，我们旨在研究CD19⁺CD24^你好CD38^你好需要冠状动脉旁路移植术（CABG）手术的冠状动脉疾病（CAD）患者的B细胞。

致编辑：全身性脓疱型银屑病（GPP）是一种罕见的危及生命的皮肤病，其特征是脓疱反复发作。阿普斯特是一种磷酸二酯酶4（PDE4）抑制剂，是一种相对较新的治疗中重度斑块型银屑病的药物。在此，我们报告了一例可能由阿普斯特引发的复发性GPP患者。