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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expansion (regional dilatation and thinning) of acutely infarcted myocardium in man has been shown to correlate with overall cardiac dilatation and rupture. We studied gross and histopathologic features and the time course of expansion in rats. Infarcts were produced in 84 rats by ligation of the left coronary artery and studied at 1, 2, 3, 4, 5 and 7 days. All hearts were prepared by potassium diastolic arrest, gel distention and fixation. Expansion was graded 0 to 4+ : 1+, mild thinning of infarcted wall; 2+, mild thinning and dilatation; 3+, moderate thinning and dilatation; and 4+, marked thinning and dilatation. There were 80 transmural infarcts, and 66% showed expansion; 36 of 80 (45%) were graded 1-2+ and 17 of 80 (21%) 3-4+. None of the four exclusively nontransmural infarcts showed expansion. Expansion was present in 61% of transmural infarcts at 1-2 days, in 65% at 3-4 days and in 80% at 5-7 days. The percentage of rats with severe (3-4+) expansion increased markedly over this period, from 0% at 1-2 days to 23% at 3-4 days to 65% at 5-7 days. Histopathologic infarct evolution was roughly twice as rapid as that of humans; 5-7 day-old infarcts showed well-developed granulation tissue. Thus, expansion can be produced in an animal model. A critical infarct size of 17% appeared necessary for significant (greater than 1+) expansion, and the degree of expansion correlated with infarct size. Although this phenomenon begins early after infarction, its extent progresses over days, making interventions to interrupt its development feasible.
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PMID:Expansion of acute myocardial infarction: an experimental study. 707

Despite growing clinical use of transluminal balloon angioplasty (TBA) to treat cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH), the precise mechanism of action of balloon dilation on the cerebral arterial wall is unknown. In this experiment the authors examined the pharmacological and morphological changes in 10 normal and 12 vasospastic canine basilar arteries following in vitro silicone microballoon TBA. For the SAH group in which the double-hemorrhage model was used, vasospasm was confirmed by angiography and the animals were killed on Day 7 after the first SAH. In vitro TBA was performed on basilar arteries from normal and SAH dogs immediately after sacrifice and removal of the brain. The procedure was performed while the arteries were maintained in oxygenated Krebs buffer. In the pharmacological studies, potassium chloride, prostaglandin F2 alpha, serotonin, and noradrenaline were used as vasoconstrictors, and bradykinin and calcium ionophore A23187 were used to produce an endothelium-dependent dilation. In both normal and vasospastic groups, the pharmacological responses of dilated segments of basilar arteries were compared to those of nondilated segments of the same arteries. Vessels from all groups were examined using scanning electron microscopy (EM) and transmission EM. Scanning EM was used to study the intact vessel wall, the smooth-muscle cell layer obtained after digestion with hydrochloric acid, and the extracellular matrix obtained after digestion with bleach. Cross-sections of the vessel wall were examined using transmission EM. The most striking finding was that immediately after in vitro TBA of both normal and vasospastic canine basilar arteries, there was a significant reduction (p < 0.05) of responses to both vasoconstrictors and vasorelaxants. As revealed by scanning EM and transmission EM, both normal and vasospastic vessels dilated with TBA showed flattening and patchy denudation of the endothelium, and straightening and occasional rupturing of the internal elastic lamina. In addition, vasospastic vessels dilated with TBA showed decreased surface rippling and mild stretching and straightening of smooth-muscle cells, and mild thinning of the tunica media. There was no gross vascular disruption or obvious change in the extracellular matrix of the vessel walls of either normal or vasospastic arteries after TBA. These results suggest that functional impairment of vasoreactivity in the vessel wall as a result of mechanical stretching of the smooth-muscle layer plays a more important role than structural alteration, at least in the immediate dilation produced in vasospastic arteries by TBA.
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PMID:Pharmacological and morphological effects of in vitro transluminal balloon angioplasty on normal and vasospastic canine basilar arteries. 766 32

Eggshell thinning in ducks was induced by administration of p,p'-DDE in the diet (40 mg/kg food) for 45 days. This treatment resulted in a 19% reduction of the Eggshell Index (EI). Shells from calcifying eggs obtained at the time of slaughter showed a 36% reduction of EI. Prostaglandin synthesis by a homogenate of eggshell gland mucosa from p,p'-DDE-treated ducks was reduced by 24%. HCO3(-)-stimulated ATPase activity by a homogenate of eggshell gland mucosa from p,p'-DDE-treated ducks was not significantly changed. The calcium content of eggshell gland mucosa was increased to 127% in p,p'-DDE-treated ducks. p,p'-DDE-treated ducks showed profound changes in the shell gland luminal content of several ions. Calcium (-43%), sodium (-15%), potassium (-15%), bicarbonate (-33%) and chloride (-29%) were all significantly reduced in p,p'-DDE-treated ducks. The content of phosphate was unchanged. These findings are discussed in relation to a proposed mechanism for p,p'-DDE-induced eggshell thinning that involves inhibition of prostaglandin synthesis in eggshell gland mucosa.
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PMID:Changes in the levels of different ions in the eggshell gland lumen following p,p'-DDE-induced eggshell thinning in ducks. 788 10

1. The focus of this review is the effects and mechanism of action of p,p'-DDE on eggshell formation in birds. Inhibition of prostaglandin synthesis in the eggshell gland mucosa is a probable mechanism for p,p'-DDE-induced eggshell thinning. 2. The duck is sensitive to p,p'-DDE-induced eggshell thinning but the domestic fowl is not, and studies comparing the two species in regard to the calcium and prostaglandin metabolism of the eggshell gland have shown that eggshell thinning induced by p,p'-DDE in ducks is accompanied by reduced activity of prostaglandin synthetase, reduced levels of prostaglandin E2, and reduced uptake of 45Ca by the eggshell gland mucosa. The content of calcium, bicarbonate, chloride, sodium, and potassium are also reduced in the eggshell gland lumen in ducks exhibiting eggshell thinning. None of these effects are seen in the domestic fowl. 3. Inhibition of prostaglandin synthesis is a specific effect of p,p'-DDE. The detrimental effects of p,p'-DDE on the eggshell gland seem to be unique when comparing the compound with structurally related substances, i.e., similar treatment regimens with o,p'-DDE, p,p'-DDT, o,p'-DDT, and p,p'-DDD do not cause eggshell thinning in ducks. Neither do they inhibit prostaglandin synthesis in the eggshell gland mucosa. 4. Administration of other compounds that do inhibit prostaglandin synthesis, e.g., indomethacin, does cause the same effects as those seen with p,p'-DDE, i.e., eggshell thinning and the described effects on the calcium and prostaglandin metabolism of the eggshell gland.
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PMID:DDE-induced eggshell thinning in birds: effects of p,p'-DDE on the calcium and prostaglandin metabolism of the eggshell gland. 949 Jan 82

The incidence of drug-induced adverse effects is likely to increase as a result of advanced age and exposure of elderly patients to polypharmacy. Therefore, pharmacological therapy of asthma and chronic obstructive pulmonary disease (COPD) in the elderly patient can be potentially hazardous. beta(2)-agonists, administered as therapy for asthma and COPD, have recognised systemic sequelae, such as hypokalaemia and chronotropic effects, which may be life-threatening in susceptible patients. Adverse effects such as hypokalaemia can be aggravated by concomitant treatment with other drugs promoting potassium loss including diuretics, corticosteroids and theophyllines. In addition, relatively minor adverse events associated with the administration of beta(2)-agonists, such as tremor and blood pressure changes, may be of significance to the elderly patient leading to impairment in the quality of life. However, long-term treatment with beta(2)-agonists may reduce the incidence of drug-induced adverse effects as a result of beta-receptor subsensitivity. Oral and inhaled corticosteroids have been used for the treatment of acute asthma and COPD in the elderly patient. Long-term treatment with oral corticosteroids can result in serious systemic adverse effects such as suppressed adrenal function, bone loss, skin thinning and cataract formation. In contrast to beta(2)-agonists, oral corticosteroids can upregulate beta(2)-adrenoceptors and thereby potentiate the systemic sequelae of beta(2)-agonists. Hence, oral corticosteroids should be administered with caution for as short a duration as possible. Inhaled corticosteroids appear to be relatively well tolerated when administered at doses below approximately 1000 microg. However, larger doses of inhaled corticosteroids may affect hypothalamic-pituitary-adrenal function and bone turnover. In the case of inhaled corticosteroids, spacer devices, often used in older patients who cannot operate metered dose inhalers, can potentiate the systemic sequelae of both corticosteroids and beta(2)-agonists. The use of theophyllines in the treatment of COPD or chronic asthma is controversial. Theophyllines have a wide adverse effect profile and are prone to drug-drug interactions. The adverse effects may be mild or life threatening and include nausea and vomiting or sinus and supraventricular tachycardias. Therefore, theophyllines should be prescribed with extreme caution to elderly patients with asthma or COPD. In contrast, inhaled anticholinergic drugs such as ipratropium bromide and oxitropium bromide are generally safe in elderly patients and have useful bronchodilator function. Commonly reported adverse effects are an unpleasant taste and dryness of the mouth. When used as first-line therapy, anticholinergic drugs may optimise the bronchodilator effects of low-dose inhaled beta(2)-agonists in patients with chronic airflow obstruction, and hence obviate the need for higher doses.
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PMID:Asthma medications and their potential adverse effects in the elderly: recommendations for prescribing. 1173 62

Androgenetic alopecia (AGA) is hereditary and androgen-dependent, progressive thinning of the scalp hair that follows a defined pattern. While the genetic involvement is pronounced but poorly understood, major advances have been achieved in understanding principal elements of the androgen metabolism involved: androgen-dependent processes are predominantly due to the binding of dihydrotestosterone (DHT) to the androgen receptor (AR). DHT-dependent cell functions depend on the availability of weak androgens, their conversion to more potent androgens via the action of 5 alpha-reductase, low enzymatic activity of androgen inactivating enzymes, and functionally active AR present in high numbers. The predisposed scalp exhibits high levels of DHT, and increased expression of the AR. Conversion of testosterone to DHT within the dermal papilla plays a central role, while androgen-regulated factors deriving from dermal papilla cells are believed to influence growth of other components of the hair follicle. Current available treatment modalities with proven efficacy are oral finasteride, a competitive inhibitor of type 2 5 alpha-reductase, and topical minoxidil, an adenosine-triphosphate-sensitive potassium channel opener which has been reported to stimulate the production of vascular endothelial growth factor in cultured dermal papilla cells. Since the clinical success rate of treatment of AGA with modulators of androgen metabolism or hair growth promoters is limited, sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is considered a possible cofactor in the complex etiology of AGA.
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PMID:Molecular mechanisms of androgenetic alopecia. 1221 48

Interactions between photoexcited riboflavin (RF), promoted by irradiation in the range of 310-800 nm, and alginate have been studied in air equilibrated aqueous solutions with the aid of rheological methods. Light irradiation of RF causes under aerobic conditions fragmentation of alginate and a decrease in the shear viscosity and other rheological parameters of its solutions. The decrease is most pronounced in concentrated polymer solutions. The photochemical degradation of alginate is inhibited in the presence of the quenchers/scavengers d-mannitol, glutathione, potassium iodide, and sodium azide and in excess oxygen. The addition of thiourea to alginate-RF solutions leads to enhanced degradation of the polymer. Significant shear-thinning effects and deviations from the Cox-Merz rule are observed at higher polymer concentrations.
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PMID:Riboflavin-photosensitized changes in aqueous solutions of alginate. Rheological studies. 1262 42

The role of steroid hormones in regulating vaginal smooth muscle contractility was investigated. Rabbits were kept intact or ovariectomized. After 2 weeks, animals were continuously infused with vehicle or supraphysiological levels of testosterone (100 microg/day), or estradiol (200 microg/day), for an additional 2 weeks. The distal vaginal tissue was used to assess contractility in organ baths and changes in tissue structure were assessed by histology. Ovariectomized animals infused with vehicle exhibited significant atrophy of the muscularis and decreased epithelial height, resulting in thinning of the vaginal wall. Estradiol infusion increased epithelial height, comparable to that of intact animals, but only partially restored the muscularis layer. In contrast, testosterone infusion completely restored the muscularis layer, but only partially restored the epithelial height. In vaginal tissue strips contracted with norepinephrine and treated with bretylium, electrical field stimulation (EFS) caused frequency-dependent relaxation that was slightly attenuated with vehicle, significantly inhibited with estradiol and significantly enhanced with testosterone. VIP-induced relaxation was slightly attenuated in tissues from vehicle and estradiol-infused groups, but was enhanced in tissues from testosterone-infused animals. Contraction elicited by EFS or exogenous norepinephrine was not significantly altered with ovariectomy or steroid hormone infusion when data were normalized to potassium contraction. However, the tissue from testosterone-infused animals developed significantly greater contractile force to norepinephrine. These observations suggest that steroid hormones may be important regulators of vaginal tissue structure and contractility.
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PMID:Effects of ovariectomy and steroid hormones on vaginal smooth muscle contractility. 1496 70

The term "morphea" includes a wide spectrum of clinical entities, varying from localized plaques of only cosmetic importance to deep lesions resulting in considerable morbidity for the patient. In fact, although survival rates are no different from that of the general population, localized scleroderma may be associated with development of substantial disability, as occurs in deep morphea and in pediatric patients (disabling pansclerotic morphea of children). We report a case of morphea profunda affecting a young man with severe, rapidly progressive, widespread skin involvement and focus on the eventual systemic evolution of such cases. A 40-year-old man was admitted in 2002 for progressive subcutaneous indurations, preferentially involving the right side of the trunk. His health was altogether good, with the exception of a beginning chronic obstructive bronchopneumopathy. There was no family or personal history of dysmetabolic, cardiovascular, neoplastic, or cutaneous disease. Three years earlier, the patient had noted the appearance of two infiltrated, intensely red lesions on the right laterocervical and paraumbilical regions. These had been interpreted as subcutaneous lipomatosis on the basis of an ultrasound scan. The lesions had become progressively larger, while their surface had assumed a scleroatrophic appearance. Thereafter, other lesions had developed on his chest and lower limbs, mostly distributed on the right side of the body. Clinical examination revealed well demarcated, depressed sclerotic plaques with ivory-colored centers and erythematous borders ("lilac ring") localized on the neck, chest, and lower abdomen and limbs (Figure 1). They were bound to the deeper structures and arranged in a band-like linear distribution on the right side of the chest and abdomen where they extended horizontally for more than 10 cm in diameter. These lesions were totally asymptomatic. In addition, arborizing telangiectasias were evident on the neck and upper chest (Figure 2). Laboratory investigations provided normal range of erythrocyte sedimentation rat and C reactive protein levels and other inflammation markers. Antinuclear antibody, antidouble-strand DNA, antimitochondrial, anti-extractable antigens (anti-centromere, anti-Scl-70, anti-U1RNP), and anti-Borrelia burgdorferi antibodies were negative. Circulating immunocomplexes binding C1q were substantially increased. Oesophageal x-rays and lower limb electromyography were within normal limits; ventilatory function testing revealed a mild obstruction consistent with the beginning of chronic obstructive pulmonary disease. Although nailfold capillaroscopy documented nonspecific findings of connective tissue disease (mega-capillaries, segmentary dilatation and destruction), the laser-Doppler flussimetry revealed few signs of microcirculatory abnormalities, in absence of Raynaud's phenomenon. An abdominal wall ultrasonography, performed on a sclerotic plaque, documented thinning of the subcutaneous tissue, with increase of the fibrous component and lower fascia and muscle retraction. The biopsy specimen from the abdominal region included fascia and the subcutaneous tissue (previously obtained from the lower abdomen) with epidermal atrophy, a thickening and homogenization of collagen bundles in the deep dermis and hair reduction. A perivascular lympho-monocytic and plasmacellular infiltration with a dermo-epidermal distribution was present. Moreover, septal fibrosis with a perivascular lymphoplasmacellular inflammatory infiltrate was documented within the abdominal rectus muscle. The diagnosis of morphea profunda was made on the basis of clinical and histopathological findings. A therapeutic regimen based on amino benzoic potassium (Potaba; Glenwood, LLC, Glenwood, NJ), oral prednisone, and topical clobetasol was started. After several months of follow-up, the patient had obtained only moderate improvement of the clinical findings.
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PMID:Case study: periodic follow-up is necessary in morphea profunda to identify systemic evolution. 1589 Dec 59

Renal TB is difficult to diagnose, because many patients present themselves with lower urinary symptoms which are typical of bacterial cystitis. We report a case of a young woman with renal TB and ESRD. She was admitted with complaints of adynamia, anorexia, fever, weight loss, dysuria and generalized edema for 10 months. At physical examination she was febrile (39 degrees C), and her abdomen had increased volume and was painful at palpation. Laboratorial tests showed serum urea = 220 mg/dL, creatinine = 6.6 mg/dL, hemoglobin = 7.9 g/dL, hematocrit = 24.3%, leukocytes = 33,600/mm(3) and platelets = 664,000/mm(3). Urinalysis showed an acid urine (pH = 5.0), leukocyturia (2+/4+) and mild proteinuria (1+/4+). She was also oliguric (urinary volume < 400 mL/day). Abdominal echography showed thick and contracted bladder walls and heterogeneous liquid collection in the left pelvic region. Two laparotomies were performed, in which abscess in pelvic region was found. Anti-peritoneal tuberculosis treatment with rifampin, isoniazid and pyrazinamide was started. During the follow-up, the urine culture was found to be positive for M. tuberculosis. Six months later the patient had complaints of abdominal pain and dysuria. New laboratorial tests showed serum urea = 187 mg/dL, creatinine = 8.0 mg/dL, potassium = 6.5 mEq/L. Hemodialysis was then started. The CT scan showed signs of chronic nephropathy, dilated calyces and thinning of renal cortex in both kidneys and severe dilation of ureter. The patient developed neurologic symptoms, suggesting tuberculous meningoencephalitis, and died despite of support measures adopted. The patient had ESRD due to secondary uropathy to prolonged tuberculosis of urinary tract that was caused by delayed clinical and laboratorial diagnosis, and probably also due to inadequate antituberculous drugs administration.
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PMID:End-stage renal disease due to delayed diagnosis of renal tuberculosis: a fatal case report. 1762 50


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