Utility of diffusion-weighted imaging in the diagnosis of acute appendicitis

Objectives  

To evaluate the value of diffusion-weighted MRI (DWI) in the diagnosis of acute appendicitis.     

Serum gamma-glutamyl transferase activity is an independent predictor for cardiovascular disease in obstructive sleep apnea syndrome

Gamma glutamyl transferase (GGT) is a new marker for predicting myocardial infarction, stroke, cardiac death and inflammation. There is also a strong relationship between Obstructive Sleep Apnea Syndrome (OSAS) and cardiovascular disease. This study was designed to investigate the association between serum GGT levels and cardiovascular disease in patients with OSAS, and relationship between severity of OSAS and serum GGT level. We evaluated the medical records of 166 subjects who were admitted for sleep study. OSAS was diagnosed by polysomnography if Apnea-Hypopnea Index (AHI) > 5. According to AHI, individuals in whom AHI< 5 were recruited as group 1 (OSAS negative group), AHI = 5-15: group 2 (mild OSAS group), AHI = 15-30: group 3 (moderate OSAS group), AHI >30: group 4 (severe OSAS group). Cardiovascular disease was defined if the patients had heart failure, coronary artery disease or arrhythmia. Of the subjects, 112 (67.5%) were male and the mean age was 54.3 ± 12.2 years. There were 22 patients (13.2%), 17 patients (10.2%), 34 patients (20.4%) and 93 patients (56.2%) in group 1, 2, 3 and 4, respectively. There is a significant increase in serum GGT levels while AHI score increases (group 1 = 28.0 ± 10.1, group 2 = 33.8 ± 13.2, group 3 = 35.2 ± 8.5, group 4 = 40.0 ± 22.0; p for trend = 0.024). However, serum C-reactive protein (CRP), alanine aminotransferase and aspartate aminotransferase levels were similar in all groups (p > 0.05). There was a significant independent association between serum GGT levels and the severity of OSAS. Moreover, serum GGT levels were significantly high in patients with cardiovascular disease compared with patients without cardiovascular disease in severe-moderate-mild OSAS (p < 0.05) and OSAS negative groups while CRP levels were not. This was a significant independent association. The present study suggests that high serum GGT level, regardless of the other traditional risk factors, is an independent predictor of cardiovascular disease in patients with OSAS. The results should be confirmed with other randomized prospective studies.     

Swyer syndrome with SRY + Y chromosome and rudimentary internal genitalia demonstrating temporary action of antimüllerian hormone in utero: a case report

BACKGROUND: XY gonadal dysgenesis is characterized by streak gonads in phenotypic females without somatic abnormalities. This case demonstrated a hypoplastic uterus, an unlikely finding for the syndrome, suggesting insufficient function of antimüllerian hormone prenatally. CASE: A 20-year-old, female virgin was first seen 2 years earlier complaining of primary amenorrhea. She was 168 cm tall, and secondary sexual characteristics, such as breast development and pubic and axillary hair, were absent on physical examination. Chromosome analysis with fluorescence in situ hybridization revealed 46,XY, and a molecular investigation was undertaken to assess the possibility of a mutation in SRY through DNA sequencing. SRY mutations were absent. Bilateral laparoscopic removal of dysgenetic gonads was performed at another medical center immediately after genetic confirmation for an increased risk of malignancy. When the patient was seen 1 year later, we performed ultrasonography because of no menstrual outflow. Pelvic ultrasonography revealed a hypoplastic uterus (26 x 12 mm) with a rudimentary cervix. CONCLUSION: Clinical phenotypes of different mutations of the Y chromosome, particularly on SRY, may cause Swyer syndrome patients to have a uterus with fertility potential after oocyte donation.     

Arsenic induces apoptosis in mouse liver is mitochondria dependent and is abrogated by N-acetylcysteine

Arsenicosis, caused by arsenic contamination of drinking water supplies, is a major public health problem in India and Bangladesh. Chronic liver disease, often with portal hypertension occurs in chronic arsenicosis, contributes to the morbidity and mortality. The early cellular events that initiate liver cell injury due to arsenicosis have not been studied. Our aim was to identify the possible mechanisms related to arsenic-induced liver injury in mice. Liver injury was induced in mice by arsenic treatment. The liver was used for mitochondrial oxidative stress, mitochondrial permeability transition (MPT). Evidence of apoptosis was sought by TUNEL test, caspase assay and histology. Pretreatment with N-acetyl-L-cysteine (NAC) was done to modulate hepatic GSH level. Arsenic treatment in mice caused liver injury associated with increased oxidative stress in liver mitochondria and alteration of MPT. Altered MPT facilitated cytochrome c release in the cytosol, activation of caspase 9 and caspase 3 activities and apoptotic cell death. Pretreatment of NAC to arsenic-treated mice abrogated all these alteration suggesting a glutathione (GSH)-dependent mechanism. Oxidative stress in mitochondria and inappropriate MPT are important in the pathogenesis of arsenic induced apoptotic liver cell injury. The phenomenon is GSH dependent and supplementation of NAC might have beneficial effects.     

Efficacy of combined anticholinergic treatment and behavioral modification as a first line treatment for nonneurogenic and nonanatomical voiding dysfunction in children: a randomized controlled trial

PURPOSE: This randomized blinded clinical study was designed to compare the efficacy of tolterodine treatment combined with behavioral modification, behavioral modification alone and behavioral modification plus placebo in children with nonneurogenic, nonanatomical voiding dysfunction. MATERIALS AND METHODS: A total of 72 children meeting inclusion criteria were randomly allocated to 1 of 3 groups. One group received tolterodine (1 mg twice daily) along with behavioral modification, 1 received behavioral modification only and 1 received placebo with behavioral modification. A dysfunctional voiding scoring system questionnaire was completed for all patients at the beginning of the study, and at 1 and 3 months of treatment. RESULTS: A total of 71 patients were evaluated. The groups did not differ with respect to age, gender and symptom score before study enrollment (p >0.05). Repeated calculations of symptom scores at 1 month of the treatment revealed a significant decrease in symptoms in all 3 groups, with a significant decrease in patients receiving tolterodine. In addition, at month 3 the symptom score of the tolterodine group was significantly lower compared to month 1, while scores remained steady in the behavioral modification and behavioral modification plus placebo groups. CONCLUSIONS: Tolterodine combined with behavioral modification for voiding dysfunction in children without neurological or anatomical abnormality can be recommended as a first line treatment before invasive evaluation.     

Effect of hemodialysis on serum complexed prostate-specific antigen levels

OBJECTIVE: The measurement of prostate-specific antigen (PSA) is a useful tool in the screening and follow-up of prostate cancer, but its diagnostic validity is uncertain in hemodialysis patients. The aim of this study was to evaluate the effects of hemodialysis on serum complexed PSA (cPSA) levels. MATERIAL AND METHODS: A total of 36 men (mean age 62.54+/-8.20 years) with end-stage renal disease were enrolled in a prospective study. Serum total PSA (tPSA), free PSA (fPSA) and cPSA, and hematocrit levels were measured before and immediately after dialysis using low-flux membranes in the serum and in the dialysis ultrafiltrate. RESULTS: After hemodialysis, cPSA, fPSA and the fPSA:tPSA ratio increased significantly (p<0.05). However, there was no significant increase in tPSA. fPSA, cPSA and tPSA were not detected in ultrafiltrate. Hematocrit levels increased significantly (p<0.0001) due to hemoconcentration. Of patients with initial serum tPSA and cPSA values and fPSA:tPSA ratios below the cut-off values, none had a post-hemodialysis value greater than the cut-off point. There were weak correlation between the difference in values after and before hemodialysis of hematocrit and cPSA (p=0.035), and between the percentage change in levels before and after hemodialysis of hematocrit and cPSA (p=0.041). CONCLUSIONS: Hemodialysis induced elevations in all forms of PSA, but tPSA was the least affected form. cPSA did not show any diagnostic superiority over other forms of PSA. Thus, serum tPSA remains a reliable parameter for follow-up of prostate cancer in uremic patients receiving long-term dialysis. However, further research is needed to explain the pathophysiology of alterations in the concentrations of different forms of PSA.     

Histoacryl glue in meniscal repairs (a biomechanical study)

The purpose of this study was to investigate the biomechanical efficacy of Histoacryl (cyanoacrylate, N-asetil 2 butyl sistein) in meniscal tear repair. In our study, the primary stability of three different repair techniques in delaying the formation of a gap of 2 mm was investigated. A meniscal tear was repaired with two vertical sutures and Histoacryl in the first group; it was repaired only with Histoacryl in the second group, and with only two vertical sutures in the third group. Menisci were then placed in a tensile loading machine, and the primary stability of the repair zones was measured until a displacement of 2 mm occurred. Biomechanical force was significantly (P<0.05) high (112.0+/-17.20 N) in all groups when vertical suture and Histoacryl glue were used together during displacements of 0.5, 1.0, 1.5 and 2.0 mm. We believe that Histoacryl is superior to vertical sutures regarding gap delaying. It potentiates the effect of vertical suture strength, permits early motion and thus merits an in vivo study.     

First case of indigenous visceral leishmaniasis from central India

Visceral leishmaniasis is endemic in the eastern states of India, but central India remains free of leishmaniais. This report describes the first indigenous case of visceral leishmaniasis in a seven-year-old girl from central India. The child presented with fever for 10 days and was diagnosed by bone marrow examination, serology using rKE16 and rK39 antigens, and a polymerase chain reaction specific for the kinesin gene. Sequencing of the immunodominant region of the kinesin gene of the parasite showed four tandem repeats, each 117 basepairs. The first tandem repeat of this strain had 97% homology with the corresponding first tandem repeat of the Leishmania donovani KE16 strain and 92% homology with the L. chagasi BA-2 strain. The second, third, and fourth tandem repeats had 97%, 98%, and 99% homology, respectively, with the L. donovani KE16 strain, and 89%, 96%, and 92% homology, respectively, with the L. chagasi BA-2 strain. This case shows that more than one genetic variant of L. donovani is circulating in various parts of India.     

M1 and M3 muscarinic receptors are involved in the release of urinary bladder-derived relaxant factor

We have investigated the muscarinic receptor subtype(s) mediating the release of urinary bladder-derived relaxant factor that is demonstrated by a coaxial bioassay system. Acetylcholine-induced relaxation of a precontracted anococcygeus muscle mounted within the bladder was considered as an evidence for the release of this factor. M₁-muscarinic agonist McN-A-343 and the cholinesterase inhibitor physostigmine also elicited relaxation responses in the coaxial bioassay besides acetylcholine. Acetylcholine-induced relaxation was antagonized by the subtype-selective muscarinic antagonists (pK_B): M₃-antagonist darifenacin (9.36 ± 0.11), M₃/M₁-antagonist 4-DAMP (9.30 ± 0.11), M₁-antagonist telenzepine (8.56 ± 0.21), M₄-antagonist tropicamide (6.63 ± 0.17) and M₂-antagonist AF-DX 116 (6.01 ± 0.21). The pK_B values of these antagonists have suggested that stimulation of M₁- and M₃-muscarinic receptors in the bladder wall mediates the release of urinary bladder-derived relaxant factor. In addition, McN-A-343, by activating the facilitatory M₁ receptors and physostigmine by inhibiting the acetylcholinesterase may induce the release of this factor through endogenous acetylcholine in the coaxial bioassay system.