Managing self-injection difficulties in patients with relapsing-remitting multiple sclerosis.

Difficulties with self-injection, including inabillity to self-inject, are common for individuals taking home-administered injectable medications. In relapsing-remitting multiple sclerosis (MS), all of the currently available disease-modifying medications are injectables marketed for self-injection. Problems with self-injection pose a barrier to treatment adherence for many patients. Clinicians at the University of California, San Francisco (UCSF) Multiple Sclerosis Center have developed a number of strategies to help patients who experience anxiety associated with self-injection. These strategies have been empirically tested and found to be effective and easily implemented by mental health professionals and nurses. This article offers case examples and discussion of the principles of the techniques developed at UCSF to remediate patients' difficulties with self-injection. Nurses are most often the healthcare providers responsible for training MS patients in self-injection and monitoring their compliance. Nurses who are familiar with these tools have the opportunity to have a significant positive impact on patient comfort, confidence, and, ultimately, successful long-term adherence to disease-modifying medications.     

Extranodal lymphomas presenting as soft tissue sarcomas to a sarcoma service over a two-year period.

Non-Hodgkin's lymphoma usually presents with lymphadenopathy at multiple sites but can also involve any part of the musculoskeletal system. Occasionally the presentation is with a soft tissue mass. The presentation of large, superficial lymphomatous masses is similar both clinically and radiologically to that of soft tissue sarcomas. The six cases of lymphoma presenting to the Exeter Sarcoma Service as suspected soft tissue sarcomas, over a two-year period (2002-2004), are presented. We describe the clinical and imaging characteristics of these tumours and their subsequent management. Our cases showed variability in presentation. Only one of the six cases presented with pain and one with tenderness. Four of the cases had no lymphadenopathy and the other two had lymphadenopathy restricted to one nodal basin. Overlying soft tissue swelling occurred in four cases and in distal limb swelling beyond the mass in one case. Radiologically, lymphomas are known to be likely to exhibit confluent lymphadenopathy that is rare in patients with soft tissue sarcoma. Confluent lymphadenopathy was demonstrated in only one case of this series of patients. It is thought that lymphomas infiltrate across anatomical fascial planes more readily than sarcomas and in four of our six cases this feature was present. Clinical history, examination and MRI are insufficient to differentiate between soft tissue sarcoma and lymphoma and the importance of obtaining a pathological diagnosis prior to surgery is clear. It is crucial to differentiate lymphoma from sarcoma in order to avoid unnecessary excisional procedures in lymphoma patients.     

Defenses of the hamster lung against human neutrophil and porcine pancreatic elastase

Instillation of human neutrophil elastase (HNE) into hamster lungs produces milder emphysema but more pulmonary hemorrhage than an equivalent amount of porcine pancreatic elastase (PPE), whether equivalence is determined by elastolytic units or moles. We undertook a study of the mechanisms of these differences. 125I-HNE or 3H-PPE were instilled intratracheally into hamsters. The partitioning of radioactivity between bronchoalveolar lavage fluid (BAL) and lung tissue was similar for HNE and PPE as were the half-lives, 45 and 51 min, respectively, for uncomplexed, enzymatically active HNE and PPE. In BAL there was preferential binding and inactivation of HNE by the hamsters' alpha-1-protease inhibitor (a-1-PI) whereas PPE was preferentially bound by alpha-2-macroglobulin (a-2-M). This was also observed in vitro when HNE and PPE were incubated with plasma from untreated hamsters. Nevertheless, when the sum of the elastase binding capacity of a-1-PI and a-2-M was considered, hamster plasma had similar binding capacities for HNE and PPE. It is known that the enzymatic activity of elastases is inhibited by formation of a stable complex with a-1-PI. On the other hand, elastases bound to a-2-M are protected against a-1-PI inhibition but can free themselves by proteolysis and exhibit elastolytic activity. Preferential inactivation of HNE by a-1-PI may be one mechanism that accounts for the lesser emphysema-inducing potency of HNE than of PPE.     

Glucose attenuation of atropine-induced deficits in paradoxical sleep and memory

When administered systemically, glucose attenuates deficits in memory produced by several classes of drugs, including cholinergic antagonists and opiate agonists. Glucose also enhances memory in aged rats, mice, and humans. In addition, glucose ameliorates age-related reductions in paradoxical sleep. Because deficits in paradoxical sleep are most marked in those individual aged rats that also have deficits in memory, treatments which improve one of these functions may similarly improve the other. The present experiments show that glucose attenuates deficits in paradoxical sleep and memory after atropine administration, with similar dose-response curves for both actions. In the first experiment, rats received saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100, 250, and 500 mg/kg) 30 min before assessment on a spontaneous alternation task. In the second experiment, 3-h EEGs were assessed for spontaneous daytime sleep in rats administered saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100 and 250 mg/kg). In both experiments, glucose significantly attenuated deficits at an optimal dose of 100 mg/kg. A third experiment assessed blood glucose levels after injections of atropine + glucose (100 mg/kg) and determined that blood glucose levels were similar to those produced by other treatments which enhance memory. These results are consistent with the view that paradoxical sleep and at least one test of memory are similarly influenced by atropine and glucose.     

School-Based Cardiovascular Health Promotion: The Child and Adolescent Trial for Cardiovascular Health (CATCH)

The Child and Adolescent Trial for Cardiovascular Health (CATCH) is a multisite intervention research study that builds on significant progress made in school health education research in the 1980s. The study has three phases: Phase I deals with study design, intervention, and measurement development, Phase II involves the main trial in 96 schools in four states, and Phase III focuses on analysis. The intervention program targets third-fifth grade students and focuses on multiple cardiovascular health behaviors, including eating habits, physical activity, and cigarette smoking. Classroom curricula, school environmental change, and family involvement programs are developed for each grade level and behavioral focus. This paper describes Phase II of CATCH with a rationale for cardiovascular health promotion with youth. The process of change that appears to be necessary for school-based health promotion and that will be tested in CATCH are presented as a framework to guide these efforts.     

How to perform tracheal intubation

Tracheal intubation is a skill that should be considered supplementary to other aspects of airway management which are of vital importance in resuscitation. Doctors involved in resuscitation should develop and retain such skills, and be aware of potential dangers.     

Autosomal dominant neovascular inflammatory vitreoretinopathy

Twenty-eight of 61 members of a six-generation family are affected by an autosomal dominant eye disease which has not been described previously. Affected patients are asymptomatic in early adulthood, but have vitreous cells and the selective loss of the b-wave on the electroretinogram. Later, peripheral retinal scarring and pigmentation, peripheral arteriolar closure, and neovascularization of the peripheral retina at the ora serrata or occasionally neovascularization of the optic disc develop. Cystoid macular edema, vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma can cause profound visual loss. Vitrectomy reduces traction on the retina and allows for retinal reattachment. The role of argon laser photocoagulation or cryopexy in reducing the neovascular complications remains uncertain.     

Mild gentamicin nephrotoxicity reduces the progression of chronic adriamycin nephrosis

SUMMARY: The effect of mild acute tubular injury on the progression of tubulointerstitial fibrosis was studied in pair-fed uninephrectomized male Wistar rats with established adriamycin nephrosis ( n = 34). Rats were stratified into three groups according to endogenous creatinine clearance (CrCl), proteinuria (Upr) and body weight (BW): (i) group 1 (Fe, n = 12) received a single intraperitoneal injection of ferric nitrilotriacetate (5 mg Fe/kg BW); (ii) group 2 (G, n = 10) three daily subcutaneous injections of gentamicin (60 mg/kg BW) and; (iii) group 3 (C, n = 12) saline injections. Serial CrCl (day 2, day 5, weeks 2, 4, 6 and 8) and renal histology (week 8) were examined following administration of nephrotoxin. CrCl was reduced on d2 (Fe: 0.78 ± 0.23 mL/min; mean ± SD) and day 5 (G: 0.91 ± 0.36 mL/min) as compared with C (1.22 ± 0.12 mL/min; P <0.05). There was no change in the serum creatinine and functional recovery occurred by d5 (Fe) and week 2 (G). Upr decreased transiently in G at week 2 (G: 482 ± 208 mg/day vs C: 716 ± 233; P = 0.05) despite similar food intake, baseline Upr and CrCl. At week 8, CrCl in Fe (0.84 ± 0.40 mL/min) was similar to C (0.84 ± 0.58 mL/min), whereas in G it remained stable (1.27 ± 0.39 mL/min; P <0.05). By morphometric analysis, mean relative interstitial volume (RIV) and glomerulosclerosis (GS) in Fe (RIV: 28.5 ± 13.4%; GS: 10.3 ± 12.3%) was no different to C (RIV: 24.5 ± 12.5%; GS: 20.9 ± 20.0%), whereas both parameters were reduced in G (RIV: 14.1 ± 8.1%; GS: 4.0 ± 4.8%; P <0.05). Mild gentamicin nephrotoxicity therefore reduced the progression of adriamycin nephrosis. the mechanism of this finding is unclear, but it may relate to altered glomerular and tubular cell handling of protein.