The Relationship Between Psychogenic Cough and the Diagnosis and Misdiagnosis of Asthma: A Review

The differential diagnoses of persistent nonproductive cough include numerous pulmonary and nonpulmonary organic disorders as well as functional illnesses. Many diseases can cause cough, and several studies have shown asthma among the most common etiologies associated with chronic cough in adult nonsmokers, as well as children. Psychogenic cough and its relationship to asthma and other asthma-like illnesses is complex since distinct maladies with similar features may coexist individually or in combination in any given patient. While chronic cough may occur as a sole presenting manifestation of bronchial asthma in all age groups, recent findings suggest that most children with persistent cough without other respiratory symptoms do not have asthma. Since several organic, as well as functional diseases, may present with persistent cough as their sole manifestation in either adults or children, cough should not be used as a single or major determinant to diagnose and treat asthma, especially when empirically focused therapy trials fail. Given the range of illnesses causing cough, no single management guideline can be expected to be universally effective.     

Multifocal calcifying epithelial odontogenic tumor.

The calcifying epithelial odontogenic tumor (CEOT), or Pindborg tumor, is a rare and benign odontogenic neoplasm that affects the jaw. The most common manifestation of CEOT is a unifocal or localized lesion of the involved jaw, which may appear clinically as a hard tissue swelling and radiographically as a mixed radiolucent-radiopaque mass. In this article, we present a unique case of CEOT affecting multiple sites in the maxilla and mandible of a 51-year-old white man. Though biopsy samples from all involved sites revealed similar histopathologic features consistent with CEOT, the fact that there was a multifocal presentation is an unusual phenomenon for CEOT and has never been reported. Multifocal odontogenic lesions are not typical but have been observed in conditions associated with known genetic mutations. For example, multiple odontogenic keratocysts are the most common feature of the inherited condition known as nevoid basal cell carcinoma syndrome. This case, however, is the first one to demonstrate that there may be a multifocal variant of CEOT that has not been previously recognized.     

The late component of L-type calcium current during guinea-pig cardiac action potentials and its contribution to contraction

 L-Type Ca²⁺ current (I _Ca,L) elicited during the action potential (AP) of guinea-pig ventricular myocytes exhibits an early and a late component. The whole-cell patch-clamp technique was used to characterize the process regulating the late I _Ca,L component and to assess its contribution to excitation-contraction coupling. A stepwise decrease in repolarization rate of AP-like voltage-clamp pulses led to an exponential increase in Ca²⁺ charge carried by I _Ca,L. This saturation behaviour was significantly reduced or absent when Ba²⁺ or monovalent cations were used as charge carriers, which suggests that the late component of I _Ca,L is controlled mainly by Ca²⁺-dependent processes. Simultaneously recording I _Ca,L and zero-load shortening or the internal Ca²⁺ concentration (fura-2) revealed that Ca²⁺ carried by the late component of I _Ca,L markedly contributes to the Ca²⁺ content of the sarcoplasmic reticulum (SR). Reducing the charge transfer by late I _Ca,L during a series of AP-like conditioning clamp pulses by 48% reduced the shortening amplitude during a subsequent test stimulation by 56%. This relationship was absent during long rectangular depolarizing conditioning clamps, during which Na⁺/Ca²⁺ exchange increased its influence on SR Ca²⁺ loading. The late component of I _Ca,L developed only a minor direct influence on the simultaneous cell shortening. Thus, the main contribution of the late I _Ca,L component is to supply Ca²⁺ for SR loading. Received: 5 November 1997 / Received after revision: 12 June 1998 / Accepted: 15 June 1998     

ACE inhibition reduces activity of the plasminogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats

The spontaneously hypertensive stroke-prone rat (SHR-SP) is an experimental model of malignant hypertension which lead to secondary alterations of the extracellular matrix. Our aim was to determine ACE-inhibitor related changes of proteases involved in the reconstruction of the extracellular matrix in the brain. Twelve SHR-SP rats were randomized into two groups. Each group was treated with either an antihypertensive dose of ramipril or placebo for 6 months. Brain tissue plasminogen activator (t-PA) and urokinase (u-PA) were quantified by using casein-dependent plasminogen zymography, matrix metalloproteinase (MMP)-2 and MMP-9, by MMP-zymography, and tissue inhibitor of MMP (TIMP)-1 and -2, by reverse zymography. The amounts of u-PA, t-PA, and MMPs were significantly reduced in animals treated with ACE inhibitor. Plasminogen zymography showed a 39% reduction of u-PA in the basal ganglia (p < 0.0001); t-PA expression was reduced by 26% in the cortex and by 33% in the basal ganglia (p < 0.0001). MMP-2 expression was reduced by 15% in the cortex (p < 0.05) and by 10% in the basal ganglia (p < 0.05); MMP-9 expression significantly decreased by 37% in the cortex and by 25% in the basal ganglia (p < 0.0001 each). No differences were observed in the amount of TIMP-1 or TIMP-2. These findings provide new insights into the biochemical mechanisms underlying extracellular matrix proliferation and its modulation by ACE inhibitors. Therapeutic alterations that influence the proteolytic systems might prove important in the prevention of extracellular matrix accumulation and secondary microvascular vessel wall changes.     

HMR 1883, a cardioselective KATP channel blocker, inhibits ischaemia- and reperfusion-induced ventricular fibrillation in rats

Ventricular fibrillation (VF) is a major cause of sudden cardiac death in which myocardial ischemia plays a leading role. During ischaemia activation of ATP-sensitive potassium channels (K(ATP)) occurs, leading to potassium efflux from cardiomyocytes and shortening of the action potential favoring the genesis of ventricular fibrillation. In confirmation of this concept the sulfonylurea glibenclamide, which stimulates insulin release by inhibition of pancreatic K(ATP) channels, has been shown to inhibit VF in different models of ischaemia by inhibition of myocardial K(ATP) channels. HMR 1883 (1-[15-12-(5-chloro-o-anisamido)ethyl]-methoxyphenyl]sulfonyl]-3-m ethylthiourea) was designed as a cardioselective K(ATP) channel blocker. The aim of this study was to show that with this compound it is possible to separate the antifibrillatory from the insulin-releasing effect for the treatment of patients at risk of ischaemia-induced arrhythmias and sudden death. In the present study HMR 1883 reduced VF in Sprague-Dawley rats during prolonged ischaemia and also diminished mortality and the duration of VF in a separate reperfusion experiment at 3 mg/kg and 10 mg/kg with no effect on blood glucose or insulin. Glibenclamide, which was antifibrillatory at 0.3 mg/kg and 1 mg/kg, increased plasma insulin and lowered blood glucose already at a dose as low as 0.01 mg/kg. In conclusion, based on its antifibrillatory action and the absence of significant pancreatic effects at therapeutic doses, HMR 1883 is of potential clinical utility for the prevention of severe arrhythmias in patients with ischaemic heart disease.     

Capabilities Approach: Contextualizing Participants’ Perspectives on Systems Barriers to Recovery

Mental health resources are designed to facilitate recovery for adults with psychiatric disabilities. Two participants of an autovideography intervention described systems barriers to recovery. Researchers employed narrative analysis, guided by the capabilities approach, to evaluate how participants storied their experiences. Participants made meaning from encounters with barriers in ways that oppose the spirit and advancement of recovery while engendering adaptive preferences. Findings indicate that inadequate resources attenuate wellbeing by increasing barriers that actively oppose recovery, and positive reframing of unaccommodating environments reinforces adaptive preferences and incapacity. Adequate resources are essential for successful recovery transformation within the mental health system.