Microarray analysis of gastric mucosa among children with Helicobacter pylori infection

Background: Although initial infection with Helicobacter pylori may occur before 5 years of age, the pediatric mucosal immune response against H. pylori is not clear. The aim of the present study was to evaluate immune responses in the H. pylori‐infected gastric mucosa of children using microarray and real‐time polymerase chain reaction (PCR) analysis of pediatric gastric samples. Methods: Gastric samples were obtained from 12 patients undergoing routine endoscopy of chronic abdominal complaints. Six patients (three boys, three girls) aged 10.1–14.6 years had evidence of H. pylori infection, and the remaining six (three boys, three girls) aged 10.3–15.5 years had no evidence of infection and presented no histological changes associated with gastritis. Microarray and real‐time PCR analyses were performed, and the changes in gene expression‐related immune response were also analyzed. Results: Using microarray analysis, the total number of significantly upregulated and downregulated genes (fold change >5, P < 0.01) was 21 in the antrum and 16 in the corpus when comparing patients with or without infection. Using real‐time PCR, the expression of lipocalin‐2 (Lcn2), C‐C motif chemokine ligand (CCL) 18, C‐X‐C motif chemokine ligand (CXCL) 9 and CXCL11 was upregulated, while the expression of pepsinogen (PG) I and PGII was downregulated when comparing patients with or without infection. Conclusions: Lcn2, CCL18, CXCL9, CXCL11, PGI and PGII play important roles in childhood H. pylori infection.     

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Long considered merely a trophic and mechanical support to neurons, astrocytes have progressively taken the center stage as their ability to react to acute and chronic neurodegenerative situations became increasingly clear. Reactive astrogliosis starts when trigger molecules produced at the injury site drive astrocytes to leave their quiescent state and become activated. Distinctive morphological and biochemical features characterize this process (cell hypertrophy, upregulation of intermediate filaments, and increased cell proliferation). Moreover, reactive astrocytes migrate towards the injured area to constitute the glial scar, and release factors mediating the tissue inflammatory response and remodeling after lesion. A novel view of astrogliosis derives from the finding that subsets of reactive astrocytes can recapitulate stem cell/progenitor features after damage, fostering the concept of astroglia as a promising target for reparative therapies. But which biochemical/signaling pathways modulate astrogliosis with respect to both the time after injury and the type of damage? Are reactive astrocytes overall beneficial or detrimental for neuroprotection and tissue regeneration? This debate has been animating this research field for several years now, and an integrated view on the results obtained and the possible future perspectives is needed. With this Commentary article we have attempted to answer the above-mentioned questions by reviewing the current knowledge on the molecular mechanisms controlling and sustaining the reaction of astroglia to injury and its stem cell-like properties. Moreover, the cellular/molecular mechanisms supporting the detrimental or beneficial features of astrogliosis have been scrutinized to gain insights on possible pharmacological approaches to enhance astrocyte neuroprotective activities.     

UMP与ESWL治疗肾结石合并糖尿病患者的效果及对NGAL、Hb水平的影响研究

目的 探究超微经皮肾镜碎石术(UMP)与体外冲击波碎石术(ESWL)治疗肾结石合并糖尿病患者的效果及对血清中性粒细胞明胶酶相关载脂蛋白(NGAL)和血红蛋白(Hb)水平的影响.方法 选取2017年1月至2019年1月经本院收治的108例肾结石合并糖尿病患者作为研究对象,采用简单随机化原则将其分为两组,每组各54例.对照...     

Predicting long-term outcomes after cardiac arrest by using serum neutrophil gelatinase-associated lipocalin

Objectives

Neutrophil gelatinase-associated lipocalin (NGAL) is secreted by various tissues in pathologic states. Previous studies reported that post-cardiac arrest serum NGAL levels correlate with short-term neurologic outcomes and survival. The aim of this study was to examine the associations between NGAL levels post-cardiac arrest and long-term outcomes and survival.

Urinary Biomarkers for Early Detection of Recovery in Patients with Acute Kidney Injury

Urinary biomarkers of acute kidney injury (AKI) have been revealed recently to be useful for prior prediction of AKI. However, it is unclear whether these urinary biomarkers can also detect recovery from established AKI. Urinary biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C, were measured every 2 days for 8 days in 66 patients with AKI. At day 0, there were no significant differences in plasma creatinine, BUN, and urine cystatin C between AKI patients in the recovery (n = 33) and non-recovery (n = 33) groups. Plasma creatinine concentrations were significantly lower in the recovery group (3.0 ± 2.0 mg/dL) than in the non-recovery group (5.4 ± 1.9 mg/dL) on day 4 after AKI diagnosis (P < 0.001). In contrast, there were significant differences in urine NGAL between the two groups starting on day 0 (297.2 ± 201.4 vs 407.6 ± 190.4 ng/mL, P = 0.025) through the end of the study (123.7 ± 119.0 vs 434.3 ± 121.5 ng/mL, P < 0.001). The multiple logistic regression analysis showed that urine NGAL could independently predict recovery from AKI. Conclusively, this prospective observational study demonstrates that urine NGAL can be a highly versatile marker for early detection of the recovery phase in established AKI patients.     

不同剂量阿托伐他汀对经皮冠状动脉介入术后对比剂急性肾损伤的影响

目的 观察经皮冠状动脉介入术（PCI）前使用不同剂量阿托伐他汀对对比剂诱导的急性肾损伤的影响。方法 入选拟行冠状动脉造影检查及拟行PCI术的患者106例,随机分成2组：20 mg阿托伐他汀组及40 mg阿托伐他汀组;入院24 h内完成常规化验检查、心脏彩色超声检查及肾脏血管超声检查,术后48 h复查肾功能。所有患者手术前当日清晨、术后2 h及术后48 h均留取约5 mL中段尿,用胶乳增强免疫透射比浊法统一测定中性粒细胞明胶酶相关脂质运载蛋白（NGAL）。结果 PCI术后,40 mg阿托伐他汀组与20 mg阿托伐他汀组比较,血清肌酐（77.44±23.14 mmol/L比94.24±36.14 mmol/L,P＝0.014）降低,尿酸（313.05±110.84 μmol/L比354.00±100.66 μmol/L,P＝0.060）降低,肾小球滤过率估计值（92.24±24.74比75.31±31.34,P＝0.009）增高; PCI术后,40 mg阿托伐他汀组与20 mg阿托伐他汀组比较,2 h NGAL（33.13±20.44 μg/L比50.67±46.95 μg/L,P＝0.013）、48 h NGAL（27.56±18.64 μg/L比58.38±56.81 μg/L,P＝0.001）减低;应用对比剂后,20 mg阿托伐他汀组发生对比剂急性肾损伤11例,发生率为20.75%,而40 mg阿托伐他汀组发生对比剂急性肾损伤5例,发生率为9.43%,两组相比差别有统计学意义（P<0.05）。结论 应用对比剂前3天,每天服用40 mg阿托伐他汀较每天服用20 mg阿托伐他汀更能减少对比剂诱导的急性肾损伤的发生。     

Neutrophil gelatinase-associated lipocalin: A novel inflammatory marker associated with late-life depression

Objective

Systemic low graded inflammation has been identified as a possible biological pathway in late-life depression. Identification of inflammatory markers and their association with characteristics of depression is essential with the aim to improve diagnosis and therapeutic approaches. This study examines the determinants of plasma Neutrophil Gelatinase-Associated Lipocalin (NGAL), which is selectively triggered by TNFα receptor 1 signaling within the central nervous system, and its association with late-life depressive disorder.

Methods

Baseline data were obtained from a well-characterized prospective cohort study of 350 depressed and 129 non-depressed older persons (≥ 60 years). Past 6 month diagnosis of major depressive disorder (MDD) according to DSM-IV-TR criteria was assessed with the Composite International Diagnostic Interview (CIDI 2.0). Potential determinants of plasma NGAL included sociodemographic characteristics, lifestyle and psychiatric and physical comorbidity.

Results

Plasma NGAL concentrations were significantly associated with age, male gender, smoking and waist circumference. Adjusted for these determinants, depressed patients had significantly higher NGAL plasma levels compared to non-depressed comparison group. Depressed patients who did not meet full criteria for MDD in the month before sampling (partially remitted) had lower plasma NGAL levels compared with those who did. Subjects with a recurrent depression had higher plasma NGAL levels compared to those with a first episode. NGAL levels were neither related with specific symptom profiles of depression nor with antidepressant drug use.

Conclusion

Adjusted for confounders, NGAL plasma levels are increased in depressed older persons, without any effect of antidepressant medication and age of onset.     

Neutrophil activation in Alzheimer’s disease and mild cognitive impairment: A systematic review and meta-analysis of protein markers in blood and cerebrospinal fluid

Inflammation is involved in the pathophysiology of Alzheimer’s disease (AD), with multiple inflammatory processes implicated in its risk and progression. This review included original peer-reviewed studies measuring the cerebrospinal fluid or peripheral blood concentrations of protein markers specifically related to neutrophil activity in healthy controls (HC) and in patients with AD or mild cognitive impairment (MCI). A total of 35 studies (N_HC = 3095, N_AD = 2596, N_MCI = 1203) were included. Random-effects meta-analyses were used to estimate between-groups standardized mean differences (SMD) and 95 % confidence intervals. In blood, concentrations of myeloperoxidase (MPO; N_AD/N_HC = 271/209, SMD = 0.41 [0.20, 0.62]; I² = 15.7 %) and neutrophil gelatinase associated lipocalin (NGAL; N_AD/N_HC = 273/185, SMD = 0.30 [0.11, 0.49]; I² < 0.005 %) were significantly higher in AD relative to HC. Peripheral blood concentrations of NGAL were also higher in MCI compared to HC (N_MCI/N_HC = 489/145, SMD = 0.39 [0.11, 0.67]; I² = 38.6 %). None of the protein markers exhibited a significant difference between HC, MCI, or AD groups in the cerebrospinal fluid. The evidence suggests that peripheral neutrophil activation, as indicated by blood concentrations of NGAL and MPO, may be a pathological feature of cognitive impairment due to AD, evident at stages of MCI and AD dementia.