Does a nurse-led postpartum self-care program for first-time mothers in Bangladesh improve postpartum fatigue, depressive mood, and maternal functioning?: a non-synchronized quasi-experimental study

Purpose This study aimed to test the efficacy of a nurse-led postpartum self-care (NLPPSC) intervention at reducing postpartum fatigue (PPF) and depressive mood and promoting maternal functioning among first-time mothers in Bangladesh. Methods A non-synchronized quasi-experimental design was used. First-time mothers were recruited during postpartum and assigned to the experimental or control group (34 each). The experimental group received the NLPPSC in the hospital, a 1-day intervention that focused on increasing self-efficacy. The control group received usual care. Data on PPF, depressive mood, maternal functioning, self-care behaviors, postpartum self-efficacy, and self-care knowledge were collected at postpartum 2 weeks (attrition 23.5%) and 6 weeks (attrition 16.1%). Data were analyzed using descriptive statistics, bivariate statistics, and linear mixed model analysis. Results One-third (33.3%) of new mothers experienced depressive mood (Edinburgh Postnatal Depression Scale scores of ≥13 points). The NLPPSC intervention was statistically significant in decreasing PPF (β=–6.17, SE=1.81, t=–3.39, p<.01) and increased maternal functioning at postpartum 6 weeks in the experimental group (β=13.72, t=3.73, p<.01) compared to the control. Knowledge was also statistically significant for increased maternal functioning over time (β=.37, SE=.18, t=2.03, p<.05). However, there were no statistically significant differences in depressive mood over time. Conclusion The NLPPSC intervention was feasible and effective in improving fatigue and maternal functioning in Bangladeshi mothers by postpartum 6 weeks. Postpartum care knowledge was effective in improved maternal functioning and thus supports implementing the NLPPSC intervention for new mothers after childbirth

The risk of newly diagnosed cancer in patients with rheumatoid arthritis by TNF inhibitor use: a nationwide cohort study

Background : Tumor necrosis factor (TNF) inhibitors use in patients with rheumatoid arthritis (RA) has raised safety concerns about cancer risk, but study results remain controversial. This largest nationwide study to date compared cancer risk in TNF inhibitor users to non-biologic disease-modifying anti-rheumatic drug (nbDMARD) users in Korean patients with RA. Methods : Data on all the eligible patients diagnosed with RA between 2005 and 2016 were retrieved from the Korean National Health Information Database. The one-to-one matched patients consisted of the matched cohort. The risks for developing all-type and site-specific cancers were estimated using incidence and incidence rate (IR) per 1000 person-years. Adjusted hazard ratio (HR) and 95% confidence interval (CI) were estimated using a Cox regression model. Results : Of the 22,851 patients in the before matching cohort, 4592 patients were included in the matched cohort. Treatment with TNF inhibitors was consistently associated with a lower risk of cancer than in the nbDMARD cohort (IR per 1000 person-years, 6.5 vs. 15.6; adjusted HR, 0.379; 95% CI, 0.255–0.563). The adjusted HR (95% CI) was significantly lower in the TNF inhibitor cohort than the nbDMARD cohort for gastrointestinal cancer (0.432; 0.235–0.797), breast cancer (0.146; 0.045–0.474), and genitourinary cancer (0.220; 0.059–0.820). Conclusions : The use of TNF inhibitors was not associated with an increased risk of cancer development, and rather associated with a lower cancer incidence in Korean patients with RA. Cautious interpretation is needed not to oversimplify the study results as cancer-protective effects of TNF inhibitors. A further study linking claims and clinical data is needed to confirm our results.This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HC17C0069

Enhanced cardiac expression of two isoforms of matrix metalloproteinase-2 in experimental diabetes mellitus.

BackgroundDiabetic cardiomyopathy (DM CMP) is defined as cardiomyocyte damage and ventricular dysfunction directly associated with diabetes independent of concomitant coronary artery disease or hypertension. Matrix metalloproteinases (MMPs), especially MMP-2, have been reported to underlie the pathogenesis of DM CMP by increasing extracellular collagen content.PurposeWe hypothesized that two discrete MMP-2 isoforms (full length MMP-2, FL-MMP-2; N-terminal truncated MMP-2, NTT-MMP-2) are induced by high glucose stimulation in vitro and in an experimental diabetic heart model.MethodsRat cardiomyoblasts (H9C2 cells) were examined to determine whether high glucose can induce the expression of the two isoforms of MMP-2. For the in vivo study, we used the streptozotocin-induced DM mouse heart model and age-matched controls. The changes of each MMP-2 isoform expression in the diabetic mice hearts were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical stains were conducted to identify the location and patterns of MMP-2 isoform expression. Echocardiography was performed to compare and analyze the changes in cardiac function induced by diabetes.ResultsQuantitative RT-PCR and immunofluorescence staining showed that the two MMP-2 isoforms were strongly induced by high glucose stimulation in H9C2 cells. Although no definite histologic features of diabetic cardiomyopathy were observed in diabetic mice hearts, left ventricular systolic dysfunction was determined by echocardiography. Quantitative RT-PCR and IHC staining showed this abnormal cardiac function was accompanied with the increases in the mRNA levels of the two isoforms of MMP-2 and related to intracellular localization.ConclusionTwo isoforms of MMP-2 were induced by high glucose stimulation in vitro and in a Type 1 DM mouse heart model. Further study is required to examine the role of these isoforms in DM CMP

Spontaneous pneumothorax during laparoscopy-assisted Billroth-I gastrectomy -A case report-

Pneumothorax associated with a pneumoperitonium in laparoscopic surgery is rare but can cause life-threatening complications. A 62-year-old man was scheduled for a laparoscopy-assisted Billroth-I gastrectomy under general anesthesia. Approximately 70 minutes after insufflating carbon dioxide into the intraabdominal cavity at a pressure of 12 mmHg, the peak inspiratory pressure increased, while the oxygen saturation decreased. The pneumothorax of the left lung was evident on the intraoperative chest radiograph. The pneumothorax improved after inserting a catheter into the affected area. The cause of the pneumothorax was unknown but an anatomical defect is believed responsible. This report shows that pneumothorax developed under an intraabdominal pressure in the conventional safety range. Careful monitoring and immediate treatment is necessary to prevent the condition from worsening

Isolation of Endothelial Progenitor Cells from Cord Blood and Induction of Differentiation by Ex Vivo Expansion

Endothelial progenitor cells (EPCs) have been reported to possess the capacity to colonize vascular grafts and hold promise for therapeutic neovascularization. However, limited quantities of EPCs have been the major factor impeding effective research on vasculoangiogenesis. In this study, cytokine and culture conditions necessary for the provision of large quantities of endothelial cells (ECs) were investigated. Cord blood was collected from 18 normal full-term deliveries and CD34+ cells were isolated by MACS system (Miltenyi Biotech, Bergish-Gladbach, Germany). To evaluate the effect of cytokines, CD34+ cells were cultured with various cytokine combinations, such as stem cell factor (SCF), flt3-ligand (FL), and thrombopoietin (TPO) with vascular endothelial growth factor (VEGF), interleukin-1β, fibroblast growth factor-basic (FGF-b) as basic cytokines. The quantities of non-adherent and adherent cells were the greatest with SCF, FL and TPO. The addition of TPO to all other cytokines significantly increased the number of non-adherent and adherent cells (p < 0.05, Wilcoxon rank sum test). After four weeks of culture, adherent cells expressed endothelial specific markers such as KDR, CD31 and CD62E. Typical morphology of ECs was observed during culture, such as cord-like structure and cobblestone appearance, suggesting that the adherent cells were consistent with ECs. In this study, the experimental conditions that optimize the production of ECs for therapeutic neovascularization were described. And it was possibly suggested that TPO plays a major role in differentiation from EPCs to ECs

A Family Harboring CMT1A Duplication and HNPP Deletion

Charcot-Marie-Tooth disease type 1A (CMT1A) is associated with duplication of chromosome 17p11.2-p12, whereas hereditary neuropathy with liability to pressure palsies (HNPP), which is an autosomal dominant neuropathy showing characteristics of recurrent pressure palsies, is associated with 17p11.2-p12 deletion. An altered gene dosage of PMP22 is believed to the main cause underlying the CMT1A and HNPP phenotypes. Although CMT1A and HNPP are associated with the same locus, there has been no report of these two mutations within a single family. We report a rare family harboring CMT1A duplication and HNPP deletion

HLA-B58 can help the clinical decision on starting allopurinol in patients with chronic renal insufficiency

Abstract Background. Although allopurinol is a very effective urate-lowering drug for complicated hyperuricemia, in some patients, it can induce severe cutaneous adverse reactions (SCARs). Recent investigations suggest that HLA-B*5801 is a very strong marker for allopurinol-induced SCARs, especially in the population with a high frequency of HLA-B*5801. Korea is one of the countries with a high frequency of HLA-B*5801 which is the only subtype of HLA-B58 in the Korean population. Objective. This study was conducted to find out the incidence of allopurinol-induced hypersensitivity on patients with chronic renal insufficiency (CRI) according to HLA-B58 and the clinical implications of HLA-B58 as a risk marker for the development of allopurinol-induced hypersensitivity. Methods. We retrospectively reviewed the medical records of patients with CRI who took allopurinol and carried out serologic human leukocyte antigen (HLA) typing for kidney transplantation between January 2003 and May 2010. Results. Among a total of 448 patients with CRI, 16 (3.6%) patients experienced allopurinol hypersensitivity. Nine of these patients (2.0%) were diagnosed with SCARs (two Stevens-Johnson syndrome and seven allopurinol hypersensitivity syndrome) and seven patients (1.6%) had simple maculopapular rashes. The HLA-B58 allele was present in all patients with allopurinol-induced SCARs, while the frequency of HLA-B58 was only 9.5% in allopurinol-tolerant patients (P &lt; 0.05). The incidence of allopurinol-induced SCARs in CRI shows a wide disparity according to HLA-B58 [18% in HLA-B58 (1) versus 0% in HLA-B58 (À)]. Among patients without HLA-B58, most (98.2%) of the CRI patients were tolerant to allopurinol and only 1.8% experienced simple rashes after taking allopurinol. Conclusions. In this study, the incidence of allopurinolinduced SCARs was considerably high in CRI patients with HLA-B58. This finding indicates that the presence of HLA-B58 may increase the risk of allopurinol-induced SCARs. Screening tests for HLA-B58 in CRI patients will be clinically helpful in preventing severe allopurinol hypersensitivity reactions

Balloon Dilatation for Corrosive Esophageal Strictures in Children: Radiologic and Clinical Outcomes

Objective: We retrospectively evaluated the effectiveness of the esophageal balloon dilatation (EBD) in children with a corrosive esophageal stricture. Materials and Methods: The study subjects included 14 patients (M:F = 8:6, age range: 17-85 months) who underwent an EBD due to a corrosive esophageal stricture. The causative agents for the condition were glacial acetic acid (n = 9) and lye (n = 5). Results: A total of 52 EBD sessions were performed in 14 patients (range 1-8 sessions). During the mean 15-month follow-up period (range 1-79 months), 12 patients (86%) underwent additional EBD due to recurrent esophageal stricture. Dysphagia improved after each EBD session and oral feeding was possible between EBD sessions. Long-term success (defined as dysphagia relief for at least 12 months after the last EBD) was achieved in two patients (14%). Temporary success of EBD (defined as dysphagia relief for at least one month after the EBD session) was achieved in 17 out of 52 sessions (33%). A submucosal tear of the esophagus was observed in two (4%) sessions of EBD. Conclusion: Only a limited number of children with corrosive esophageal strictures were considered cured by EBD. However, the outcome of repeated EBD was sufficient to allow the children to eat per os prior to surgical management.Doo EY, 2009, CLIN RADIOL, V64, P265, DOI 10.1016/j.crad.2008.10.001PARK JY, 2009, KOREAN J PEDIAT, V52, P446Hyoung J, 2008, J VASC INTERV RADIOL, V19, P736, DOI 10.1016/j.jvir.2008.01.015Ko HK, 2006, J VASC INTERV RADIOL, V17, P1327, DOI 10.1097/01.RVI.0000232686.29864.0AWeintraub JL, 2006, J VASC INTERV RADIOL, V17, P831, DOI 10.1097/01.RVI.0000217964.55623.19Wilkinson AG, 2004, PEDIATR RADIOL, V34, P414, DOI 10.1007/s00247-004-1164-1Huang YC, 2004, PEDIATR SURG INT, V20, P207, DOI 10.1007/s00383-004-1153-3Lan LCL, 2003, J PEDIATR SURG, V38, P1712, DOI 10.1016/S0022-3468(03)00638-9Fasulakis S, 2003, PEDIATR RADIOL, V33, P682, DOI 10.1007/s00247-003-1011-9Hamza AF, 2003, J PEDIATR SURG, V38, P828Kukkady A, 2002, PEDIATR SURG INT, V18, P486, DOI 10.1007/s00383-002-0798-zYEMING W, 2002, J PEDIATR SURG, V37, P398Jayakrishnan VK, 2001, PEDIATR RADIOL, V31, P98Lisy J, 1998, ACAD RADIOL, V5, P832Yararbai O, 1998, HEPATO-GASTROENTEROL, V45, P59KIM IO, 1993, RADIOLOGY, V189, P741HAN HY, 1993, J KOREAN RADIOL SOC, V29, P1181SONG HY, 1992, RADIOLOGY, V184, P373GUNDOGDU HZ, 1992, J PEDIATR SURG, V27, P767LOVEJOY FH, 1990, NEW ENGL J MED, V323, P668MAYNAR M, 1988, RADIOLOGY, V167, P703DELANGE EE, 1988, RADIOLOGY, V167, P45SATO Y, 1988, AM J ROENTGENOL, V150, P639MCLEAN GK, 1987, RADIOLOGY, V165, P35GOLDTHORN JF, 1984, RADIOLOGY, V153, P655LONDON RL, 1981, GASTROENTEROLOGY, V80, P173MUHLETALER CA, 1980, AM J ROENTGENOL, V134, P1137RAGHEB MI, 1976, SURGERY, V79, P494