Calf hematoma mimicking thrombophlebitis: sonographic and computed tomographic appearance

Five patients with calf hematomas presented with signs and symptoms suggesting thrombophlebitis, obscuring the correct diagnosis. Venography showed no venous thrombosis; further diagnostic studies using ultrasound and/or computed tomography provided the correct diagnosis in all patients. Ultrasound showed a hypoechoic mass clearly demarcated from surrounding soft tissue, while computed tomography showed a well-defined mass whose density depended on the age of the hematoma.     

Extracranial lesions of the head and neck: preliminary experience with Gd-DTPA-enhanced MR imaging

The authors report initial experience with magnetic resonance imaging enhanced with gadolinium diethylenetriaminepentaacetic acid (DTPA) in 27 patients with various extracranial lesions of the head and neck. Unenhanced T1- and T2-weighted images were compared with T1-weighted images obtained 3-30 minutes after Gd-DTPA administration. Overall, compared with precontrast T1- and T2-weighted images, Gd-DTPA improved the visibility of lesions in 11 and five of 27 patients, respectively. Gd-DTPA particularly improved the conspicuity of tumors of the nasal cavity and paranasal sinuses and tumors having perineural or intracranial extension. Gd-DTPA-enhanced images were equivalent to precontrast T1- and T2-weighted images in five and 13 patients, respectively, and inferior to them in nine and eight patients, respectively. Mixed results were obtained in two patients and one patient when Gd-DTPA-enhanced images were compared with T1- and T2-weighted images, respectively. The authors conclude that Gd-DTPA has definite but limited uses in extracranial head and neck pathologic conditions and that more research is needed to evaluate particular applications.     

Efficacy of 1% acetic acid in the treatment of chronic wounds infected with Pseudomonas aeruginosa: prospective randomised controlled clinical trial

Chronic wounds are those wounds that are persistent and do not respond to any sort of treatment. The concept of using topical antiseptics on open wounds is to prevent and treat infections. They also help to shorten the time taken to heal the wounds. The use of topical agents on wounds to prevent infection is a minimal ability to develop resistance to the microorganisms. Pseudomonas aeruginosa is a Gram‐negative opportunistic pathogen with innate resistance to many antibiotics. In places that are economically backward, these problems get compounded by the inability of patients to afford newer expensive drugs. Topically applied dilute acetic acid, which is cheap and easily available, has been found to be effective in such chronic wounds. In the present study, an attempt has been made to use 1% acetic acid as the sole antimicrobial agent for the treatment of pseudomonal wound infections. A control limb was used in which the wounds were treated with normal saline. Our objective was to evaluate the efficacy of acetic acid in low concentration of 1% in chronic wounds infected with P. aeruginosa. This was a prospective study conducted over a period of 6 months. Inclusion criteria: All patients with chronic wounds infected with P. aeruginosa. Exclusion criteria: Wounds due to massive burns, suspected malignancy, immunocompromised individuals and individuals with sepsis. A total of 32 patients enrolled in the study. Subjects were randomised equally to the 1% acetic acid group and saline dressing group. None of the patients received any systemic antibiotics during the study period and received twice daily dressings. The endpoint of the treatment was wounds free of P. aeruginosa. The duration of treatment required to eliminate the Pseudomonas from the wounds in the acetic acid group was on an average 7 days less than that required by the saline group. P value was <0·001. In the 1% acetic acid group irrespective of the sensitivity of the organism to antibiotics, Pseudomonas organisms were eliminated within the same time period – 4·5 days. In the saline group, susceptible organisms were eliminated within 11·5 days and multidrug‐resistant organisms were eliminated by 15·5 days. 1% acetic acid is a simple, safe and effective topical antiseptic that can be used in the elimination of P. aeruginosa from chronic infected wounds.     

Truncated N-terminal fragments of huntingtin with expanded glutamine repeats form nuclear and cytoplasmic aggregates in cell culture

Huntington's disease (HD) is a progressive neurodegenerative disorder caused by an expanding CAG repeat coding for polyglutamine in the huntingtin protein. Recent data have suggested the possibility that an N-terminal fragment of huntingtin may aggregate in neurons of patients with HD, both in the cytoplasm, forming dystrophic neurites, and in the nucleus, forming intranuclear neuronal inclusion bodies. An animal model of HD using the short N-terminal fragment of huntingtin has also been found to have intranuclear inclusions and this same fragment can aggregate in vitro . We have now developed a cell culture model demonstrating that N-terminal fragments of huntingtin with expanded glutamine repeats aggregate both in the cytoplasm and in the nucleus. Neuroblastoma cells transiently transfected with full-length huntingtin constructs with either a normal or expanded repeat had diffuse cytoplasmic localization of the protein. In contrast, cells transfected with truncated N-terminal fragments showed aggregation only if the glutamine repeat was expanded. The aggregates were often ubiquitinated. The shorter truncated product appeared to form more aggregates in the nucleus. Cells transfected with the expanded repeat construct but not the normal repeat construct showed enhanced toxicity to the apoptosis- inducing agent staurosporine. These data indicate that N-terminal truncated fragments of huntingtin with expanded glutamine repeats can aggregate in cells in culture and that this aggregation can be toxic to cells. This model will be useful for future experiments to test mechanisms of aggregation and toxicity and potentially for testing experimental therapeutic interventions.      

mdx muscle pathology is independent of nNOS perturbation

In skeletal muscle, neuronal nitric oxide synthase (nNOS) is anchored to the sarcolemma via the dystrophin-glycoprotein complex. When dystrophin is absent, as in Duchenne muscular dystrophy patients and in mdx mice, nNOS is mislocalized to the interior of the muscle fiber where it continues to produce nitric oxide. This has led to the hypothesis that free radical toxicity from mislocalized nNOS may contribute to mdx muscle pathology. To test this hypothesis directly, we generated mice devoid of both nNOS and dystrophin. Overall, the nNOS- dystrophin null mice maintained the dystrophic characteristics of mdx mice. We evaluated the mice for several features of the dystrophic phenotype, including membrane damage and muscle morphology. Removal of nNOS did not alter the extent of sarcolemma damage, which is a hallmark of the dystrophic phenotype. Furthermore, muscle from nNOS-dystrophin null mice maintain the histological features of mdx pathology. Our results demonstrate that relocalization of nNOS to the cytosol does not contribute significantly to mdx pathogenesis.