Bilateral, simultaneous, spontaneous rupture of quadriceps tendons without trauma in an obese patient: a case report.

This is a single case report of bilateral, simultaneous, spontaneous rupture of the quadriceps tendon caused by obesity without trauma. The patient was a 52-year-old, 350-pound, morbidly obese man with a sedentary life style whose quadriceps tendons ruptured while he was descending a staircase. He presented with a large deficit superior to the patella and an inability to straighten his knees. After surgery, his knees were immobilized in extension for 6 weeks, followed by gradual weight bearing and gait training with braces. He was weaned off the braces as he increased the range of motion and strength in his knees. The rehabilitation process was protracted, and he returned to full-time work 6 months postinjury. Physiatrists should be familiar with the diagnosis, treatment, and rehabilitation of this rare condition.

The postpericardiotomy syndrome as a cause of pleurisy in rehabilitation patients.

Pleuritic chest pain in patients on a rehabilitation unit may be caused by several conditions. We report 2 cases of postpericardiotomy syndrome (PPS) as a cause of pleuritic pain. PPS occurs in 10% to 40% of patients who have coronary bypass or valve replacement surgery. The syndrome is characterized by fever, chest pain, and a pericardial or pleural friction rub. Its etiology is believed to be viral or immunologic. The syndrome can be a diagnostic challenge, and an increase in length of hospitalization because of it has been documented. Identified risk factors for PPS include age, use of prednisone, and a history of pericarditis. A higher incidence has been reported from May through July. Many patients undergo a battery of expensive procedures before PPS is diagnosed. The pain is sharp, associated with deep inspiration, and changes with position. Pleural effusions may be present and tend to occur bilaterally. Pericardial effusions are a documented complication. A pericardial or pleural rub may be present and is often transient. Serial auscultation is important. Laboratory work provides clues with a mild leukocytosis and an elevated erythrocyte sedimentation rate. However, this does not provide the definitive diagnosis. Cardiac enzymes are not reliably related to the syndrome. An electrocardiogram will show changes similar to those associated with pericarditis. The patient may have a fever, but it is rarely higher than 102.5 degrees F. Complications include pericardial effusions, arrhythmias, premature bypass graft closure, and cardiac tamponade. Treatment consists of a 10-day course of nonsteroidal anti-inflammatory drugs.

Transient expression of the neurofilament proteins NF-L and NF-M by Schwann cells is regulated by axonal contact.

Expression of the genes that encode neurofilament proteins is considered to be confined normally to neurons. However, in demyelinating peripheral nerves Schwann cells upregulate the mRNA for the medium-sized neurofilament protein (NF-M), and cultured Schwann cells of the myelin-forming phenotype can also synthesize and incorporate NF-M protein into their intermediate filament (IF) cytoskeleton. The purpose of this study was to establish how axonal contact might influence glial neurofilament gene expression and regulate the synthesis of neurofilament proteins. We show that the gene encoding NF-M is expressed at early stages of differentiation in myelin-forming Schwann cells in vivo; nevertheless, little NF-M protein can be detected in these cells. The transient induction of NF-M mRNA is also apparent in dedifferentiating Schwann cells during Wallerian degeneration. In these Schwann cells the mRNAs for NF-M and NF-L (the smallest polypeptide), but not NF-H (the largest neurofilament subunit), are coordinately expressed. In contrast to differentiating myelin-forming Schwann cells, the cells of degenerating nerves express both NF-M and NF-L polypeptides. Restoration of axonal contact in the growing nerve stimulates the recapitulation of Schwann cell differentiation including the elevation of NF-M and NF-L mRNA expression. These results demonstrate that the transient induction of neurofilament mRNAs in Schwann cells is a feature of both differentiation and dedifferentiation. However translation of these mRNAs is confined to Schwann cells deprived of axonal contact either by nerve injury or by culture in the absence of axons. These findings suggest that the expression of the NF-M and NF-L polypeptides is an important characteristic of those Schwann cells that will contribute to the repair of damaged peripheral nerves.

Schwann cells of the myelin-forming phenotype express neurofilament protein NF-M.

Immature Schwann cells of the rat sciatic nerve can differentiate into myelin-forming or non-myelin-forming cells. The factors that influence this divergent development are unknown but certain markers such as galactocerebroside distinguish the two cell populations at an early stage of Schwann cell differentiation. Because myelination requires extensive changes in cell morphology, we have investigated the composition and structure of the Schwann cell cytoskeleton at a time when these cells become committed to myelination. Here we show that Schwann cells express a cytoskeletal protein of M(r) 145 before diverging into the myelin-forming path, i.e., before they acquire cell-surface galactocerobroside. The p145 protein has the characteristics of an intermediate filament (IF) protein and immunoelectron microscopy shows that it colocalizes with vimentin, which suggests that these two proteins can coassemble into IFs. Elevated intracellular cAMP levels, which can mimic some of the early effects of axons on Schwann cell differentiation, induced p145 synthesis, therefore, we conclude that myelin-forming Schwann cells express this protein at a very early stage in their development. Immunological comparisons with other IF proteins revealed a close similarity between p145 and the neurofilament protein NF-M; the identification of p145 as NF-M was confirmed by isolating and sequencing a full-length clone from a Schwann cell cDNA library. These data demonstrate that Schwann cells remodel their IFs by expressing NF-M before acquiring the myelin-forming phenotype and that IF proteins of the neurofilament-type are not restricted to neurons in the vertebrate nervous system.

Effect of cimetidine on histamine-activated ATPase in human gastric mucosa.

The effect of histamine on Mg-ATPase was assessed in homogenates of gastric biopsies taken from the body and antrum of the stomach of patients with and without duodenal ulcer (DU). Histamine at concentrations greater than 10(-7) mol/l caused significant activation of this crude enzyme activity in the body mucosa from both groups of patients; maximum stimulation of enzyme activity was greater in the DU patients than in the non-DU group. No activation by histamine was found in ATPase of antral biopsies. Administration of cimetidine (1 g/day orally) to DU patients for 28 days abolished the histamine activation of the enzyme activity. Investigation of the activity of enzymes in normal biopsies showed that the effect of histamine was not shared by the specific H2 agonist, impromidine, or H1 agonist, 2-(2-aminoethyl)-thiazole, and that cimetidine inhibition of ATPase in vitro is probably not an histamine-receptor-specific effect.