Ultrasonography for inguinal hernias in boys

BACKGROUND/PURPOSE: History taking and physical examination alone no longer meet the surgeon's need in the diagnosis of inguinal hernia. Ultrasonography (US) provides a good and safe diagnostic tool for inguinal hernias in boys. METHODS: From 1995 to 1997, 244 boys with inguinal hernias (41 bilateral and 203 unilateral), received preoperative US on both groins to confirm the diagnosis. Those with positive US findings, such as viscera or fluid in inguinal canal or widening of the internal inguinal ring, underwent surgery. RESULTS: The accuracy of diagnosis with US and clinical assessment were 97.9% and 84%, respectively. More than 95% of widening of internal inguinal rings (>4 mm) proved to be hernias. There were two direct inguinal hernias and two femoral hernias, which were misdiagnosed by clinical examination, but proved to be diagnosed correctly by US. CONCLUSIONS: US serves as a noninvasive and highly accurate diagnostic tool for inguinal hernias in boys. Using 4 mm as the upper limit of the normal diameter of the internal inguinal ring, an occult inguinal hernia can be easily detected before surgery.     

Carboxyfullerenes as neuroprotective agents

Two regioisomers with C3 or D3 symmetry of water-soluble carboxylic acid C60 derivatives, containing three malonic acid groups per molecule, were synthesized and found to be equipotent free radical scavengers in solution as assessed by EPR analysis. Both compounds also inhibited the excitotoxic death of cultured cortical neurons induced by exposure to N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), or oxygen-glucose deprivation, but the C3 regioisomer was more effective than the D3 regioisomer, possibly reflecting its polar nature and attendant greater ability to enter lipid membranes. At 100 microM, the C3 derivative fully blocked even rapidly triggered, NMDA receptor-mediated toxicity, a form of toxicity with limited sensitivity to all other classes of free radical scavengers we have tested. The C3 derivative also reduced apoptotic neuronal death induced by either serum deprivation or exposure to Abeta1-42 protein. Furthermore, continuous infusion of the C3 derivative in a transgenic mouse carrying the human mutant (G93A) superoxide dismutase gene responsible for a form of familial amyotrophic lateral sclerosis, delayed both death and functional deterioration. These data suggest that polar carboxylic acid C60 derivatives may have attractive therapeutic properties in several acute or chronic neurodegenerative diseases.     

Post-transplant changes of segment 4 after living related liver transplantation

Cocaine-induced thrombosis has been reported in the literature; however, its mechanism is not fully understood. Most cases are of small caliber vessels, such as the coronaries and cerebral vasculature. We report a case of a 36-year-old man with signs and symptoms of acute arterial insufficiency in his right lower extremity. At angiography, the right common iliac artery and the popliteal artery were occluded. The patient was successfully treated with thrombolytic therapy. Cocaine-induced thrombosis should be suspected in a patient with history of cocaine abuse who presents with acute arterial insufficiency in an extremity, without an identifiable source.     

MRI-guided stereotatic aspiration for the treatment of deep-seated tentorial empyema: a case report

The purpose of this study was to evaluate the prenatal characteristics of congenital nephrosis of the Finnish type (CNF). Patients presenting with elevated maternal serum and/or amniotic fluid alpha-fetoprotein levels, normal ultrasound examinations and normal fetal karyotypes were included. A retrospective cohort study was conducted using questionnaires sent to all board certified clinical geneticists. Perinatal outcome, including histologic verification of CNF, was obtained. Forty index cases met the above criteria. Ten cases ultimately did not have the diagnosis of CNF, with a median MSAFP level of 7.59 MoM (range 2.7-27.64 MoM) and a median AFAFP level of 10.99 MoM (range 1.47-128.6 MoM). In the affected cohort of index pregnancies, the initial median MSAFP level was 14.49 MoM (range 3.1-38.0 MoM); the median AFAFP level was 40.0 MoM (range 2.4-80.9). MSAFP and AFAFP levels may be lower than previously recognized in patients carrying fetuses with CNF. There is significant overlap between the affected and unaffected patients.     

Prenatal diagnosis of cardiac osteoma: a case report

Primary benign intracardiac tumours in the infant period are rare. We report a case of a cardiac osteoma detected at 17 weeks of gestation. Ultrasonographically, it appeared as a calcified mass with a sharp margin and was associated with hypoplastic right ventricle. The gross and histological findings are presented.     

Adverse interactions between warfarin and nonsteroidal antiinflammatory drugs: mechanisms, clinical significance, and avoidance

OBJECTIVE: To review the mechanisms and clinical significance of adverse interactions between warfarin and nonsteroidal anti-inflammatory drugs (NSAIDs) and discuss how these interactions can be avoided. DATA SOURCES: Previous studies of interactions between warfarin and NSAIDs or reports of adverse interactions were identified from a MEDLINE search (1976 to present) and from the reference lists of pertinent articles. STUDY SELECTION AND DATA EXTRACTION: All articles were considered for inclusion in the review. Pertinent information was selected for discussion. DATA SYNTHESIS: All NSAIDs can prolong bleeding time by inhibiting platelet function. High-dose aspirin has a direct hypoprothrombinemic effect. Phenylbutazone and its analogs enhance the hypoprothrombinemic effect of warfarin through a pharmacokinetic interaction by inhibiting the hepatic metabolism of warfarin. Mefenamic acid also enhances the anticoagulant effect of warfarin, but the mechanism is not known. The clinical relevance of protein binding displacement in the interaction between warfarin and NSAIDs has been overstated, although a significant one may be more likely in the presence of high concentrations of NSAIDs in patients with slow elimination of warfarin (e.g., those with severe heart failure or impaired liver function). NSAIDs can induce gastrointestinal bleeding, which is likely to be more severe if warfarin is also given. CONCLUSIONS: The combined use of warfarin and NSAIDs is generally discouraged because of the increased risk of bleeding in these patients. In patients receiving warfarin who also require NSAIDs, phenylbutazone and its analogs, high-dose aspirin, mefenamic acid, excessive use of topical methyl salicylate, and NSAIDs that are associated with a higher risk of bleeding peptic ulcers should be avoided. Patients should be closely monitored for anticoagulant control and bleeding complications during the combined use of warfarin and NSAIDs.     

Protection of astrocytes by fructose 1,6-bisphosphate and citrate ameliorates neuronal injury under hypoxic conditions

Fructose 1,6-bisphosphate (FBP) protects astrocytes from hypoxic injury in vitro. To determine whether FBP and citrate (inhibitors of phosphofructokinase) ameliorate hypoxia-induced injury to neurons and, if they do, whether the protective effects are a direct result of their actions on neurons or a consequence of their actions on astrocytes, we added FBP or citrate to the media of normoxic and hypoxic 'pure', mixed and co-culture systems. FBP (3.5 mM) and citrate (10 microM-2 mM) decreased release of LDH from astrocytes following 24 h of hypoxia. Eight hours of hypoxia killed pure neuronal cultures and neither FBP nor citrate prevented this death. However, in mixed and co-culture systems, FBP and citrate increased neuronal viability (as determined by the ratio of live-to-total cells), even after 47 h of hypoxia. In co-culture, following 24 h of hypoxia, both FBP and citrate reduced neuronal release of LDH and neuronal death. Fluorocitrate, a suicidal-inhibitor of aconitase, also protected astrocytes, but not neurons, from hypoxia in 'pure' culture, presumably by increasing intracellular citrate concentrations through inhibition of the catalysis of citrate to isocitrate We conclude that FBP and citrate attenuate hypoxic neuronal injury through their effects on astrocytes.