Rapidly progressive glomerulonephritis caused mycobacterium tuberculosis is rare; however, three case have been reported to date. Crescentic glomerulonephritis is a life-threatening disease and together with the presence of tuberculous infection is associated with a poor outcome if treatment is inadequate and delayed. We describe the case of a 31-year-old female patient with nephrotic syndrome and progressive renal failure secondary to pulmonary tuberculosis. Renal biopsy showed crescent formation in 14 out of 27 glomeruli, and there was diffuse linear staining of immunoglobulin G deposits. Treatment included corticosteroids in combination with antituberculosis drugs for 2 months, and resulted in a significant improvement in renal function, the disappearance of proteinuria and pulmonary symptoms. We also present a review of the pertinent literature and discuss the pathophysiology of tuberculosis-related acute postinfectious glomerulonephritis.

Severe early childhood caries (SECC) is a public health problem among preschool children. Malnutrition is a condition commonly prevalent in children with SECC. This study investigated the nutritional status among preschool children with SECC. Children with SECC (n = 101) aged 2-5 years from the Division of Pediatric Dentistry in an academic hospital in Southern Taiwan were recruited for our cross-sectional study. The nutritional status of the children was assessed based on anthropometric measurements and clinical tests. By applying the criteria established by the World Health Organization, we found that 9% and 46% of the children with SECC were diagnosed as being anemic and iron deficient, respectively. Using national standards for the body mass index, 30% of children with SECC were classified as underweight. The relationship between the caries status of the children and anemia was examined using multivariable logistic regression analysis (p < 0.05). Our results show that SECC is strongly associated with anemia (7.25-fold), indicating that clinicians and dentists should provide treatment to improve both the oral hygiene and the nutritional status of children with SECC.

The aim of this study was to assess the efficacy of prophylactic fosfomycin tromethamine (FT) and ciprofloxacin in preventing bacteriuria caused by urodynamic studies (UDS). A total of 426 adult patients presenting for UDS were enrolled the study. A midstream urine sample was taken 72 hours before and 5 days after the procedure. All patients underwent a standard UDS. The 411 patients who had sterile urine before intervention were included in the study. Patients were randomized into three groups. Group1 received no prophylaxis (n = 133), Group 2 (n = 141) received oral ciprofloxacin (500 mg) 1 hour before the procedure, and Group 3 (n = 137) received a single dose of FT approximately 12 hours before the procedure. Bacteriuria was evaluated for each group. Bacteriuria was detected in 3 (2.3%), 6 (4.3%) and 3 patients (1.6%) in Group 1, Group 2, and Group 3, respectively. The most common identified microorganism was Escherichia coli (E coli) in 6 patients (50%). Among the E coli group, extended spectrum beta-lactamase producing E coli was seen in 2 patients (33.3%). Univariate analysis demonstrated that a history of urogenital operation (p < 0.01) and female gender (p < 0.01) were significant risk factors for bacteriuria. On multiple logistic regression analysis, the past urogenital operation history was the only significant independent risk factor for significant bacteriuria after UDS (OR = 14, 95% CI = 1.82-23.8, p = 0.01). The prevalence of bacteriuria after UDS was relatively low in the current study population. Therefore, for most patients, it may be unnecessary to use preventive prophylactic antibiotics. However, our results suggest that in patients with a previous history of urologic surgery, the risk for significant bacteriuria is increased and the use of prophylaxis should be considered.

It is not unusual that narcotics-dependent patients fulfill their medical requirements in the emergency department (ED). The behavior of these patients varies, and their manifestations and predictors are still not fully studied. We performed this retrospective study by prospectively collecting data on patients with suspected drug dependence who were undiagnosed at first and then treated for some kind of reported pain at the ED. Patients who were confirmed to have narcotics dependence were compared with control patients in a ratio of 1:3 matching for age, gender, disease, and clinical diagnoses. From January 2006 to October 2009, 26 of 223 patients treated for pain were found to be drug dependent (12 males and 14 females). The average dose of narcotics used was higher than the control group [3.23 ± 1.14 vs. 1.12 ± 0.36, p < 0.001, confidence interval (CI): 1.648-2.583]. Numbers of patients making unscheduled returns to the ED within 24 hours were significant [24/26 vs. 8/78, p ≤ 0.001, odds ratio (OR) 105.00, 95% CI 20.834-529.175]. In addition, patients showing aggressive attitudes were significant (17/26 vs. 2/78, p < 0.001, OR 71.78, 95% CI 14.206-362.663). In the case group, six of them told the physician that they were allergic to medicines other than the particular one they wanted, and three of the six presented injuries that were reported to be in the same (or repeated) place for unscheduled returns, which were not found in the control group. In this study, some behaviors were commonly observed in the at-risk group. These patients were prone to manifest some types of symptoms and behaviors, such as uncontrolled pain with three doses of analgesics, aggressive attitude, returning to the ED within 24 hours with the complaint of the same severe pain, repeating the same injury, claiming allergy to other analgesics, and asking for certain analgesics. All these behaviors should alert the physician to suspect a drug-seeking problem.

Cancer-associated fibroblast (CAF) is one of the most crucial components of the tumor microenvironment to promote the invasiveness of cancer cells. The interactions between cancer cells and CAFs are bidirectional. Our recent study showed that up-regulations of chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-C motif) ligand 26 (CCL26), interleukin 6 (IL6), and lysyl oxidase-like 2 (LOXL2) genes in cancer cells were parts of the common effects of CAFs on hepatocellular carcinoma (HCC) cells to promote proliferation, migration and invasion of cancer cells. However, the subject of how HCC cells to influence the gene expressions of CAFs still needs to be clarified. The purpose of this study was to investigate this issue. Two human HCC (HCC24/KMUH, HCC38/KMUH) and two human CAF cell lines (F26/KMUH, F28/KMUH) were studied. Influence of HCC38/KMUH cancer cells on differential expressions of genes in F28/KMUH CAFs was detected by microarray to select target genes for further analysis. Both HCC cell lines increased proliferation (all p < 0.005) and migration (all p < 0.0001) of two CAF cell lines. HCC24/KMUH cancer cells had stronger ability to promote migration of F26/KMUH CAFs than HCC38/KMUH cancer cells did (p < 0.0001). Eleven up-regulated cancer-promoting genes, including apelin (APLN), CCL2, CCL26, fibroblast growth factor 1 (FGF1), fibroblast growth factor 2 (FGF2), IL6, mucin 1 (MUC1), LOXL2, platelet-derived growth factor alpha polypeptide (PDGFA), phosphoglycerate kinase 1 (PGK1), and vascular endothelial growth factor A (VEGFA) detected by microarray showed good correlation with results of quantitative reverse transcriptase-polymerase chain reaction study. Among these genes, HCC24/KMUH cancer cells had same tendency of effects on differential expressions of genes in F28/KMUH CAFs as HCC38/KMUH cancer cells did. However, the responses of F26/KMUH CAFs to different HCC cell lines were variable. Only PGK1 gene was consistently up-regulated and PDGFA gene was consistently down-regulated caused by both HCC cell lines in F26/KMUH CAFs. Besides PGK1 gene, HCC38/KMUH cancer cells only up-regulated APLN, LOXL2, and VEGFA genes and HCC24/KMUH cancer cells only up-regulated FGF2 gene in F26/KMUH CAFs. In conclusion, HCC cells can promote proliferation and migration of CAFs. However, the impact of HCC cells on differential expressions of cancer-promoting genes in CAFs is influenced by the characteristics of CAFs. This implies that blocking single or several particular cancer-promoting genes in CAFs is unable to become a common stratagem for the treatment of HCC.

Cisplatin-induced acute kidney injury (AKI) is a major concern among clinicians in prescribing cisplatin-based chemotherapy. This study evaluated and compared the ability of urinary biomarkers, including urinary neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, and the urinary albumin to creatinine ratio (ACR) to predict cisplatin-induced AKI. Thirty-three cancer patients receiving cisplatin-based chemotherapy were prospectively studied, including 10 (30%) who developed AKI (the study group). Changes of urinary biomarkers were compared at 4 hours, 8 hours, and 12 hours, and 1 day, 2 days, 3 days, and 4 days after cisplatin intravenous infusions (75mg/m(2)) versus the baseline. There was a significant increase in urinary NGAL levels from 12 hours to 4 days (p<0.05) compared to baseline after cisplatin infusion in the AKI group. The magnitude of these changes over time differed significantly by group (p<0.001). The area under the receiver operating curve describing the relationship between urinary NGAL levels and AKI within 12 hours was 0.865 (95% confidence interval=0.691-1.000). Urinary NGAL levels independently predicted AKI 12 hours after cisplatin (p=0.045) after adjustments for age, gender, body mass index, baseline serum creatinine, and urinary total protein. Urinary NGAL levels may be an early biomarker of AKI in patients receiving cisplatin-based treatment.

Pulmonary vein isolation and atrial substrate modification using catheter ablation have been developed as a standard treatment for atrial fibrillation (AF). However, the standard end-point for these procedures is still not well established. This study aimed to investigate the characteristics among positive and negative AF vulnerability patients with normal structural heart, in order to define the endpoint of the atrial substrate modification. Fifty supraventricular tachycardia patients with normal heart structure referred for electrophysiological study and catheter ablation were enrolled. After eliminating the underling arrhythmias, the basic cycle length, effective refractory period of the right atrium, and the P wave indices in 12-lead electrocardiograms were measured. The AF vulnerability test was performed by atrial burst decremental pacing with a pacing cycle length decreasing from 290 ms to 200 ms. The AF vulnerability test was considered as positive when the duration of the induced AF or atrial tachyarrhythmias (ATs) was longer than 10 seconds. The parameters of atrial substrates were compared between patients with positive and negative values of the AF vulnerability test. ATs or AF were induced in 24 (48%) patients. Among these patients, 12 (24%) induced ATs or AF were found to be sustained (duration more than 10 seconds). However, only two of these patients could reproduce the positive result after 10 minutes of the first induced protocol. Comparing the patient baseline characteristics, P wave characteristics and cardiac echo parameters, there were no significant differences between the positive and negative AF vulnerability groups. In conclusion, AF and ATs could be induced in patients with a structurally normal heart. The traditional clinical indices of atrial substrates were not significantly different between the positive and negative AF vulnerability patients. Protocols other than atrial burst decremental pacing should be investigated to evaluate the endpoint of the atrial substrate modification.

This study aimed to investigate the role of the Toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under hypoxia/reoxygenation (H/R) in vitro, and the effect of propofol on injured GES-1 cells as well as its possible mechanism. Before H/R induction, GES-1 cells were preconditioned with fat emulsion, propofol, or epigallocatechin gallate. Then cell viability, cell apoptosis, and related molecules in the cells were analyzed under experimental conditions. We found that propofol 50 μmol/L markedly inhibited the H/R injury under hypoxia 1.5 h/reoxygenation 2 hours by promoting GES-1 cell viability and decreasing cell apoptosis. The TLR4 signal may be involved in the protective effect of propofol against H/R injury. The malondialdehyde contents and superoxide dismutase activities were recovered under propofol preconditioning. In summary, propofol preconditioning may exert a protective effect on H/R injury in GES-1 cells and the mechanism may be via inhibition of the activated TLR4 signal under H/R conditions.