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1.
The purpose of this article is to describe the treatment of a 45-year-old male with a hyperfunctional voice disorder by a biofeedback therapist and a speech-language pathologist. The interdisciplinary approach to the treatment of this voice disorder involved the combined use of traditional voice therapy techniques and EMG biofeedback procedures together with cognitive behavioral therapy. Voice therapy was facilitated through the use of a computer-based, speech-monitoring system. The remediation of this voice disorder was attributed to the collaborative efforts of two professionals representing diverse professional training and treatment protocols. The results showed reductions in muscle activity in the infrahyoid and laryngeal areas as well as improved use of proper breathing and voicing onset behaviors. Follow-up at 10 and 15 months posttreatment intervals indicated that the client had retained all target voice skills and the tension reduction/biofeedback skills. Results suggest that interdisciplinary, collaborative efforts using biofeedback and voice therapy can prove beneficial in the treatment of hyperfunctional voice disorders.Note: Neither author has been compensated in any way for the use of the CAFET System nor does either have any financial interest in the company.  相似文献   
2.

Introduction

Cigarette smoke is a profound pro-inflammatory stimulus that contributes to acute lung injuries and to chronic lung disease including COPD (emphysema and chronic bronchitis). Until recently, it was assumed that resolution of inflammation was a passive process that occurred once the inflammatory stimulus was removed. It is now recognized that resolution of inflammation is a bioactive process, mediated by specialized lipid mediators, and that normal homeostasis is maintained by a balance between pro-inflammatory and pro-resolving pathways. These novel small lipid mediators, including the resolvins, protectins and maresins, are bioactive products mainly derived from dietary omega-3 and omega-6 polyunsaturated fatty acids (PUFA). We hypothesize that resolvin D1 (RvD1) has potent anti-inflammatory and pro-resolving effects in a model of cigarette smoke-induced lung inflammation.

Methods

Primary human lung fibroblasts, small airway epithelial cells and blood monocytes were treated with IL-1β or cigarette smoke extract in combination with RvD1 in vitro, production of pro-inflammatory mediators was measured. Mice were exposed to dilute mainstream cigarette smoke and treated with RvD1 either concurrently with smoke or after smoking cessation. The effects on lung inflammation and lung macrophage populations were assessed.

Results

RvD1 suppressed production of pro-inflammatory mediators by primary human cells in a dose-dependent manner. Treatment of mice with RvD1 concurrently with cigarette smoke exposure significantly reduced neutrophilic lung inflammation and production of pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokine IL-10. RvD1 promoted differentiation of alternatively activated (M2) macrophages and neutrophil efferocytosis. RvD1 also accelerated the resolution of lung inflammation when given after the final smoke exposure.

Conclusions

RvD1 has potent anti-inflammatory and pro-resolving effects in cells and mice exposed to cigarette smoke. Resolvins have strong potential as a novel therapeutic approach to resolve lung injury caused by smoke and pulmonary toxicants.  相似文献   
3.
4.

Introduction

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease with very few effective treatments. The key effector cells in fibrosis are believed to be fibroblasts, which differentiate to a contractile myofibroblast phenotype with enhanced capacity to proliferate and produce extracellular matrix. The role of the lung epithelium in fibrosis is unclear. While there is evidence that the epithelium is disrupted in IPF, it is not known whether this is a cause or a result of the fibroblast pathology. We hypothesized that healthy epithelial cells are required to maintain normal lung homeostasis and can inhibit the activation and differentiation of lung fibroblasts to the myofibroblast phenotype. To investigate this hypothesis, we employed a novel co-culture model with primary human lung epithelial cells and fibroblasts to investigate whether epithelial cells inhibit myofibroblast differentiation.

Measurements and Main Results

In the presence of transforming growth factor (TGF)-β, fibroblasts co-cultured with epithelial cells expressed significantly less α-smooth muscle actin and collagen and showed marked reduction in cell migration, collagen gel contraction, and cell proliferation compared to fibroblasts grown without epithelial cells. Epithelial cells from non-matching tissue origins were capable of inhibiting TGF-β induced myofibroblast differentiation in lung, keloid and Graves’ orbital fibroblasts. TGF-β promoted production of prostaglandin (PG) E2 in lung epithelial cells, and a PGE2 neutralizing antibody blocked the protective effect of epithelial cell co-culture.

Conclusions

We provide the first direct experimental evidence that lung epithelial cells inhibit TGF-β induced myofibroblast differentiation and pro-fibrotic phenotypes in fibroblasts. This effect is not restricted by tissue origin, and is mediated, at least in part, by PGE2. Our data support the hypothesis that the epithelium plays a crucial role in maintaining lung homeostasis, and that damaged and/ or dysfunctional epithelium contributes to the development of fibrosis.  相似文献   
5.
From January 1970 to December 1979 inclusive, 193 boys (aged 2 to 16) underwent surgery for distal hypospadia using Ombredanne's method at the Department of Pediatric Surgery University Hospital Center Rijeka and at the Department of Pediatric Surgery Zagreb. Follow-up period was 7 to 20 years (mean 13.4). 20 (10.36%) subjects had post-operative organic complications and 15 (7.77%) of them required surgical correction. According to these findings, the success rate using Ombredanne's method of reconstruction of the hypospadic urethra in no way lags behind the success rate using MAGPI and Mathieu's methods as well as Preputial island flap urethroplasty for analogous cases. Out of 193 subjects who underwent surgery, 80 (41.45%) of those who were sexually mature and had normal psychosexual development were questioned. In this sample, 75 (93.75%) were satisfied with the post-operative appearance of the penis while only 5 (6.25%) were dissatisfied, 3 of which had hypoplastic penis. In 78 (97.50%) subjects questioned, the post-operative urinary squirt was normal and two of them had weak urinary squirt (2.50%), due to meatal stenosis. In conclusion, Ombredanne's method of reconstruction of the urethra in boys with distal hypospadia is equally successful as other methods used for this purpose.  相似文献   
6.
Crohn's disease (CD) is a chronic, relapsing inflammatory bowel disease, characterized by transmural inflammation. In CD, the recurrent inflammatory injury and tissue repair that occurs in the intestine can progress uncontrollably, leading to the proliferation of mesenchymal cells as well as fibrosis, characterized by excessive extracellular matrix deposition. These processes thicken the bowel wall, reducing flexibility, and often culminate in obstructive strictures. Because no effective measures are currently available to specifically treat or prevent intestinal stricturing, we sought to gain a better understanding of its pathogenesis by developing a mouse model of intestinal fibrosis. Because transforming growth factor (TGF)-beta1 can mediate both fibrosis and mesenchymal cell proliferation; we studied the effects of delivering adenoviral vectors encoding spontaneously active TGF-beta1 into the colons of mice. We first demonstrated that enema delivery of marker adenoviral vectors led to the transfection of the colonic epithelium and transient transgene expression. Histologically, control vectors caused an acute inflammatory response, involving the recruitment of neutrophils and mononuclear cells into the colonic lamina propria; however, infection caused little if any fibrosis. In contrast, the TGF-beta1 vector caused a more severe and prolonged inflammatory response as well as localized collagen deposition, leading to severe and progressive fibrosis. This was accompanied by the emergence of cells with a myofibroblast phenotype. Ultimately the fibrosis resulted in many of the TGF-beta1-transfected mice developing profound colonic obstruction. Through adenoviral gene transfer technology, we describe a novel mouse model of colitis and implicate TGF-beta1 in the pathogenesis of obstructive intestinal fibrosis.  相似文献   
7.
Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-L-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.  相似文献   
8.
A series of laboratory experiments was conducted on a colony of Bracon celer Szépligeti (Hymenoptera: Braconidae) reared on the olive fly, Bactrocera oleae (Rossi) (Diptera: Tephritidae). Female B. celer preferentially probe and oviposit into olives containing late third-instar fly larvae. The parasitoid develops as a solitary, ectoparasitic idiobiont. Mean development time (oviposition to adult eclosion) at 22 °C was, for females, 36±1 (SE) days, and for males, 34±1 days. The mean longevity of adult female wasps when provided honey and water was significantly greater than when they were provided water alone, or nothing. The females produced an average of 9.7±7.2 progeny during their lifetimes, but production levels in the insectary colony suggested that this level of fecundity was artificially low and could be improved. The discrepancy may be a consequence of constraints on oviposition behavior imposed by the experimental design. The results are discussed with respect to insectary production methods and the potential use of B. celer as a biological control agent for olive fly in California.  相似文献   
9.
A total of 835 patients with symptoms of chronic prostatitis syndrome and no evidence of structural or functional lower genitourinary tract abnormalities were examined in a three year period at the Outpatient Department for Urogenital Infections, University Hospital for Infectious Diseases "Dr. Fran Mihaljevi?" Zagreb, Croatia. Disease etiology was determined in 482 (57.72%) patients. Chlamydia trachomatis was proved to be the causative pathogen in 161 patients, Trichomonas vaginalis in 85, Escherichia coli in 68, Enterococcus in 51, Proteus mirabilis in 20, Klebsiella pneumoniae in 9, Streptococcus agalactiae in 15, Ureaplasma urealyticum in 49 patients with chronic prostatitis. Other patients had mixed infection. In 257 (53.32%) of 482 patients, the inflammatory finding (>10 WBCs/hpf) was found in EPS or VB3. Normal WBCs/hpf (<10) was found in 103 (63.98%) of 161 patients with symptoms of chronic prostatitis in whom C. trachomatis was detected in EPS or VB3, in 50 (58.82%) of 85 patients in whom Trichomonas vaginalis was isolated, and in 23 (46.94%) of 49 patients in whom Ureaplasma urealyticum was isolated.  相似文献   
10.
We investigated the cytokine profile of peripheral mononuclear cells from chronic osteomyelitis (OST) patients following in vitro stimulation with staphylococcal enterotoxin A (SEA). We demonstrate that stimulation with SEA induced prominent lymphocyte proliferation and high levels of tumour necrosis factor (TNF)-α, interleukin (IL)-4 and IL-10 secretion in both OST and non-infected individuals (NI). Even though stimulation with SEA had no impact on IL-6 production in either patient group, the baseline level of IL-6 production by cells from OST patients was always significantly less than that produced by cells from NI. After classifying the osteomyelitic episodes based on the time after the last reactivation event as "early" (1-4 months) or "late" osteomyelitis (5-12 months), we found that increased levels of TNF-α and IL-4 in combination with decreased levels of IL-6 were observed in the early episodes. By contrast, increased levels of IL-10, IL-2 and IL-6 were hallmarks of late episodes. Our data demonstrate that early osteomyelitic episodes are accompanied by an increased frequency of "high producers" of TNF-α and IL-4, whereas late events are characterised by increased frequencies of "high producers" of IL-10, IL-6 and IL-2. These findings demonstrate the distinct cytokine profiles in chronic osteomyelitis, with a distinct regulation of IL-6 production during early and late episodes.  相似文献   
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