Zollinger-Ellison syndrome associated with neurofibromatosis type 1: a case report

BACKGROUND: Neurofibromatosis type 1 is an autosomal dominant neurocutaneous disorder with characteristic features of skin and central nervous system involvement. Gastrointestinal involvement is rare, but the risk of malignancy development is considerable. Zollinger-Ellison syndrome is caused by gastrin-secreting tumors called gastrinomas. Correct diagnosis is often difficult, and curative treatment can only be achieved surgically. CASE PRESENTATION: A 41-year-old female affected by neurofibromatosis type 1 presented with a history of recurrent epigastric soreness, diarrhea, and relapsing chronic duodenal ulcer. Her serum fasting gastrin level was over 1000 pg/mL. An abdominal CT scan revealed a 3 × 2-cm, well-enhanced mass adjacent to the duodenal loop. She was not associated with multiple endocrine neoplasia type 1. Operative resection was performed and gastrinoma was diagnosed by immunohistochemical staining. The serum gastrin level decreased to 99.1 pg/mL after surgery, and symptoms and endoscopic findings completely resolved without recurrences. CONCLUSION: Gastrinoma is difficult to detect even in the general population, and hence symptoms such as recurrent idiopathic peptic ulcer and diarrhea in neurofibromatosis type 1 patients should be accounted for as possibly contributing to Zollinger-Ellison syndrome

Body Fat Mass and Risk of Cerebrovascular Lesions: The PRESENT (Prevention of Stroke and Dementia) Project

Obesity is known to increase the risk of stroke. It is unclear whether high absolute fat mass (FM) increases the risk of stroke independently. We studied the correlation between FM and silent brain infarction/white matter change (SI/WMC) using brain computed tomography. We selected subjects from the local government health promotion project. We randomly selected a target population that had never been diagnosed with stroke or dementia. FM was measured by bioelectrical impedance analysis (BIA). We divided the subjects into three groups according to the FM (gender-specific tertiles [GTx]). Seven hundred and twenty-two subjects (321 men) between 50 and 75 years of age were recruited. The overall odds ratio (OR) of SI/WMC was 2.23 (95% confidence interval (CI), 1.34–3.71; p = 0.002) times higher in the 37th to 100th percentiles (GT3) than in the first to 32nd percentiles (GT1). When men and women were separated, the OR of GT3 was 1.35 (CI, 0.62–2.94; p = 0.45) in men and 3.2 (CI, 1.60–6.40; p = 0.001) in women. The findings were not found to be statistically significant after adjusting for the well-known stroke risk factors. When the subjects were divided into a high FM (HFMG, GT3) and low FM group (LFMG, GT1 + GT2), the HFMG showed an increased OR of SI/WMC in women. Similar results were seen after adjusted (overall: OR, 1.38; CI, 0.85–2.25, p = 0.198; men: OR, 0.93; CI, 0.422–2.051; p = 0.86; women: OR, 2.02; CI, 1.06–3.86; p = 0.03). The findings suggest that high FM may be an independent risk factor for ischemic stroke among adults free from stroke and dementia, especially in women

Correction: Immunologic monitoring of cytomegalovirus (CMV) enzyme-linked immune absorbent spot (ELISPOT) for controlling clinically significant CMV infection in pediatric allogeneic hematopoietic stem cell transplant recipients.

[This corrects the article DOI: 10.1371/journal.pone.0246191.]

Immunologic monitoring of cytomegalovirus (CMV) enzyme-linked immune absorbent spot (ELISPOT) for controlling clinically significant CMV infection in pediatric allogeneic hematopoietic stem cell transplant recipients.

The dynamics of recovery of cytomegalovirus (CMV)-specific cell-mediated immunity (CMI) and its impact on controlling clinically significant CMV infections following hematopoietic stem cell transplant (HSCT) are rarely reported in pediatric HSCT recipients. In this study, dynamics of recovery of CMV-specific CMI and its clinical significance in controlling CMV viremia and clinically significant CMV infections were assessed in pediatric allogeneic HSCT recipients. All subjects underwent CMV pp65- and IE1-specific enzyme-linked immune absorbent spot (ELISPOT) assays just before transplantation and then monthly until the detection of CMV-specific CMI with ≥ 5 spot-forming cells (SFC) / 2.0 × 105 cells. Clinically significant CMV infections were defined as CMV diseases, prolonged CMV infections, recurrent CMV infections or late onset CMV infections. Among 52 recipients, 88.5% of recipients recovered CMV-specific CMI with ≥ 5 SFC/ 2.0 × 105 cells at a median of 34 days (interquartile range [IQR]: 29-95 days) following HSCT, 55.8% at 30 days following HSCT, and 73.1% at 90 days following HSCT. The presence of CMV-specific CMI before HSCT was the significant factors for the reconstitution of CMV specific CMI after HSCT (adjusted odds ratio [aOR] = 13.33; 95% confidence interval [CI] = 1.21-142.86). After HSCT, 30 recipients experienced CMV viremia, of which 20 were clinically significant CMV infections. The full recovery of CMV-specific CMI with ≥ 50 SFC / 2.0 × 105 cells after HSCT was the protective factor for the development of clinically significant CMV infections (aOR = 0.13; 95% CI = 0.22-0.71). In the haploidentical HSCT recipients, 82.1% recovered CMV-specific CMI at a median of 65 days after HSCT (IQR: 34-118 days) with a tendency to recover their CMV-specific CMI later than did those from non-haploidentical donors (65 days vs. 30 days; P = 0.001). Clinically significant CMV infections tended to occur more frequently in the haploidentical HSCT recipients compared to those with matched donor HSCT (46.4% vs. 29.2%; P = 0.205). The full recovery of CMV-specific CMI with ≥ 50 SFC/2.0 × 105 cells after HSCT also lowered the risk of development of clinically significant CMV infections (aOR = 0.08; 95% CI = 0.01-0.90). However, transplantation from haploidentical donors was a significant risk factor hampering recovery of CMV-specific CMI (aOR = 0.08; 95% CI = 0.01-0.86) and full recovery of CMV-specific CMI (aOR = 0.05; 95% CI = 0.01-0.50). Pre-transplant CMV-specific CMI influenced the recovery of CMV-specific CMI, and the full recovery of CMV-specific CMI could be a surrogate marker for preventing clinically significant CMV infections in pediatric HSCT recipients. Immunologic monitoring using ELISPOT assay before and after HSCT helps in identifying patients with a high risk of CMV infection and in controlling CMV infection

Melatonin protects against neuronal damage induced by 3-nitropropionic acid in rat striatum

In this study, the protective effects of melatonin were evaluated against 3-nitropropionic acid (3-NP)-induced striatal neuronal damage in rats. Lesions were induced in the right striatum of Sprague-Dawley rats by stereotaxic injection with 3-NP and melatonin was intraperitoneally administered both 30 min before and 60 min after 3-NP injection. And rats continuously received melatonin daily for 3 days. As indicators of oxidative damage, lipid peroxidation and protein oxidation in the lesioned striatum were measured at 1 day after 3-NP injection. Levels of malondialdehyde (MDA) and protein carbonyl were significantly increased by 3-NP injection, but reduced in the melatonin-treated rats. Four days post-lesion, large lesions and extensive neuronal damage were produced in the 3-NP-injected striata, as revealed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. In addition, marked ipsilateral rotational behavior following apomorphine challenge and a decrease of dopamine content in the lesioned striatum were observed in the 3-NP-injected rats. However, melatonin treatment significantly attenuated the 3-NP-induced neuronal damage, reduced the degree of asymmetric rotational behavior, and restored the dopamine level in the lesioned striatum. The present results indicate that melatonin effectively protects against the neuronal damage caused by 3-NP in vivo and that the neuroprotective effects of melatonin may be related to antioxidant action

Cross detection for odor of metabolic waste between breast and colorectal cancer using canine olfaction

<div><p>Although several studies have been performed to detect cancer using canine olfaction, none have investigated whether canine olfaction trained to the specific odor of one cancer is able to detect odor related to other unfamiliar cancers. To resolve this issue, we employed breast and colorectal cancer in vitro, and investigated whether trained dogs to odor related to metabolic waste from breast cancer are able to detect it from colorectal cancer, and vice versa. The culture liquid samples used in the cultivation of cancerous cells (4T1 and CT26) were employed as an experimental group. Two different breeds of dogs were trained for the different cancer odor each other. The dogs were then tested using a double-blind method and cross-test to determine whether they could correctly detect the experimental group, which contains the specific odor for metabolic waste of familiar or unfamiliar cancer. For two cancers, both dogs regardless of whether training or non-training showed that accuracy was over 90%, and sensitivity and specificity were over 0.9, respectively. Through these results, it was verified that the superior olfactory ability of dogs can discriminate odor for metabolic waste of cancer cells from it of benign cells, and that the specific odor for metabolic waste of breast cancer has not significant differences to it of colorectal cancer. That is, it testifies that metabolic waste between breast and colorectal cancer have the common specific odor in vitro. Accordingly, a trained dogs for detecting odor for metabolic waste of breast cancer can perceive it of colorectal cancer, and vice versa. In order to the future work, we will plan in vivo experiment for the two cancers and suggest research as to what kind of cancers have the common specific odor. Furthermore, the relationship between breast and colorectal cancer should be investigated using other research methods.</p></div

Specificity by the two dogs.

<p>Specificity by the two dogs.</p