Objective Harvest of autogenous bone from iliac crest has long been held as the gold standard for anterior lumbar arthrodesis. This technique is accompanied by an added morbidity to the pelvis. The present study was to validate the experimental result showing that harvesting bone tissue from an adjacent vertebral body for bone graft followed by replacing the defect by ?-tricalcium phosphate (TCP) plug could be a feasible procedure in lumbar interbody fusion procedure. Methods 20 patients underwent single- or multiple-level circumferential lumbar fusion with anterior cages and posterior pedicle screws in one institution. All cages were filled with cancellous bone harvested from the adjacent vertebral body, with the resulted vertebral body defect filled with a TCP plug. Results Bone grafts were successfully harvested from 28 vertebral bodies in all the patients. There was no major vascular injury, and blood loss of the anterior procedure averaged 250ml (50-350ml). One TCP plug was broken during its insertion, and one endplate was broken, both due to wrong surgical technique. These incidences did not affect the final outcome. At the last follow-up (mean 28 months), a solid lumbar spine fusion was demonstrated in all the patients. At 2-year follow up, ODI and VAS were remarkably improved (P

PURPOSE: To review the clinical outcomes of patients with voiding dysfunction who have detrusor overactivity with impaired contractility (DOIC) diagnosed with urodynamic studies. METHODS: Urodynamic reports from 2005 to 2009 were reviewed, and 54 male patients had findings consistent with DOIC. Patients with acontractile or neuropathic bladders were excluded. Clinical outcomes were obtained from patient records. RESULTS: Of 54 men, 8 presented with voiding symptoms, 17 had storage symptoms, and 29 had mixed symptoms. Twenty-two had a previous transurethral resection of the prostate. The median follow-up was 12 months. Four patients received no intervention. Two patients were taught intermittent self-catheterization. Five patients underwent surgery to reduce outlet resistance and all reported improvement. Forty-three patients were started on pharmacotherapy; symptomatic improvement was reported by 9 of 16 patients commenced on anticholinergics alone, 6 of 16 on alpha-blockers alone, and 4 of 5 treated with a combination of alpha-blockers and anticholinergics. Eleven patients experienced no difference on pharmacotherapy and 2 reported deterioration. One patient developed acute urinary retention (18 months after commencing treatment with alpha-blockers). No patient had urosepsis. CONCLUSIONS: Anticholinergics and alpha-blockers appear to be safe in patients with DOIC. The risk of urinary retention and sepsis is low. The majority of patients report symptomatic benefit from either drugs or surgical treatment.
Adrenergic alpha-Antagonists ; Cholinergic Antagonists ; Drug Therapy ; Follow-Up Studies ; Humans ; Lower Urinary Tract Symptoms ; Male ; Prostate ; Sepsis ; Urinary Bladder ; Urinary Bladder, Overactive ; Urinary Retention ; Urodynamics

OBJECTIVETo investigate mutations in the D-loop region of mitochondrial DNA in ovarian tumors.

METHODSThe D-loop region of 25 epithelial ovarian tumors together with the adjacent normal tissues were amplified by PCR and sequenced.

RESULTSAmong the 25 ovarian tumors, 26 mutations were identified with the mutation rate of 32%. 19 mutations were detected in two cases of borderline carcinoma which was a special type of epithelial ovarian carcinoma. There were 6 microsatellite instabilities among the mutations and 11 new polymorphisms which were not reported previously in the GenBank.

CONCLUSIONSThe D-loop region of mitochondrial DNA is a highly polymorphoric and mutable region and the mutation rate is relatively high in patients with ovarian tumors.

Cystadenocarcinoma, Serous ; genetics ; DNA, Mitochondrial ; genetics ; Female ; Humans ; Ovarian Neoplasms ; genetics ; Point Mutation ; Polymorphism, Genetic

Background: and Purpose Paroxysmal atrial fibrillation (PAF) underlying acute stroke frequently evades detection by standard practice, considered to be a combination of routine electrocardiogram (ECG) monitoring, and 24-hour Holter recordings. We hypothesized that nurse-led in-hospital intermittent monitoring approach would increase PAF detection rate. Methods: We recruited patients hospitalised for stroke/transient ischemic attack, without history of atrial fibrillation (AF), in a prospective multi-centre observational study. Patients were monitored using a smartphone-enabled handheld ECG (iECG) during routine nursing observations, and underwent 24-hour Holter monitoring according to local practice. The primary outcome was comparison of AF detection by nurse-led iECG versus Holter monitoring in patients who received both tests: secondary outcome was oral anticoagulant commencement at 3-month following PAF detection. Results: One thousand and seventy-nine patients underwent iECG monitoring: 294 had iECG and Holter monitoring. AF was detected in 25/294 (8.5%) by iECG, and 8/294 (2.8%) by 24-hour Holter recordings (P<0.001). Median duration from stroke onset to AF detection for iECG was 3 days (interquartile range [IQR], 2 to 6) compared with 7 days (IQR, 6 to 10) for Holter recordings (P=0.02). Of 25 patients with AF detected by iECG, 11 were commenced on oral anticoagulant, compared to 5/8 for Holter. AF was detected in 8.8% (69/785 patients) who underwent iECG recordings only (P=0.8 vs. those who had both iECG and 24-hour Holter). Conclusions Nurse-led in-hospital iECG surveillance after stroke is feasible and effective and detects more PAF earlier and more frequently than routine 24-hour Holter recordings. Screening with iECG could be incorporated into routine post-stroke nursing observations to increase diagnosis of PAF, and facilitate institution of guideline-recommended anticoagulation.

Background/Aims: Interstitial cells of Cajal (ICC) are specialized gastrointestinal (GI) pacemaker cells required for normal GI motility. Dysfunctions in ICC have been reported in patients with GI motility disorders, such as gastroparesis, who exhibit debilitating symptoms and greatly reduced quality of life. While the proteins, calcium-activated chloride channel anoctamin-1 (ANO1) and the receptor tyrosine kinase (KIT), are known to be expressed by human ICC, relatively little is known about the broad molecular circuitry underpinning human ICC functions. The present study therefore investigates the transcriptome and proteome of ANO1-expressing, KIT low /CD45- /CD11B- ICC obtained from primary human gastric tissue. Methods: Excess human gastric tissue resections were obtained from sleeve gastrectomy patients. ICC were purified using fluorescence-activated cell sorting (FACSorting). Then, ICC were characterized by using immunofluorescence, real-time polymerase chain reaction, RNAsequencing and mass spectrometry. Results: Compared to unsorted cells, real-time polymerase chain reaction showed the KIT low /CD45- /CD11B- ICC had: a 9-fold (P < 0.05) increase in ANO1 expression; unchanged KIT expression; and reduced expression for genes associated with hematopoietic cells (CD68, > 10-fold, P < 0.001) and smooth muscle cells (DES, > 4-fold, P < 0.05). RNA-sequencing and gene ontology analyses of the KIT low / CD45- /CD11B- cells revealed a transcriptional profile consistent with ICC function. Similarly, mass spectrometry analyses of the KIT low / CD45- /CD11B - cells presented a proteomic profile consistent with ICC activities. STRING-based protein interaction analyses using the RNA-sequencing and proteomic datasets predicted protein networks consistent with ICC-associated pacemaker activity and ion transport. Conclusion These new and complementary datasets provide a valuable molecular framework for further understanding how ICC pacemaker activity regulates smooth muscle contraction in both normal GI tissue and GI motility disorders.

Background/Aims: We aimed to determine the association between blood urea level and incident cirrhosis, hepatic decompensation, and hepatocellular carcinoma in chronic liver disease (CLD) patients. Methods: The association between blood urea level and liver fibrosis/liver-related events were evaluated on continuous scale with restricted cubic spline curves based on generalized additive model or Cox proportional hazards models. Then, the above associations were evaluated by urea level within intervals. Results: Among 4,282 patients who had undergone liver stiffness measurement (LSM) by transient elastography, baseline urea level had a U-shaped association with LSM and hepatic decompensation development after a median follow-up of 5.5 years. Compared to patients with urea of 3.6–9.9 mmol/L, those with urea ≤3.5 mmol/L (adjusted hazard ratio [aHR], 4.15; 95% confidence interval [CI], 1.68–10.24) and ≥10 mmol/L (aHR, 5.22; 95% CI, 1.86–14.67) had higher risk of hepatic decompensation. Patients with urea ≤3.5 mmol/L also had higher risk of incident cirrhosis (aHR, 3.24; 95% CI, 1.50–6.98). The association between low urea level and incident cirrhosis and hepatic decompensation was consistently observed in subgroups by age, gender, albumin level, and comorbidities. The U-shaped relationship between urea level and LSM was validated in another population screening study (n=917). Likewise, urea ≤3.5 mmol/L was associated with a higher risk of incident cirrhosis in a territory-wide cohort of 12,476 patients with nonalcoholic fatty liver disease at a median follow-up of 9.9 years (aHR, 1.27; 95% CI, 1.03–1.57). Conclusions We identified a U-shaped relationship between the urea level and liver fibrosis/incident cirrhosis/hepatic decompensation in patients with CLD.