Comparison between effects of various partial inferior turbinectomy options on nasal airflow: a computer simulation study

Partial inferior turbinectomy is typically performed on patients suffering from chronic nasal obstruction due to hypertrophy of inferior turbinates and is refractory to other more conservative treatments. The effects of the various options of incision performed on the inferior turbinate in terms of the resulting nasal airflow pattern are examined using computational fluid mechanics. The pressure drops across the severely blocked nose and healthy nose models were found to be 32.3 and 12.3 Pa, respectively, whereas the pressure drops across the nasal cavity following one-third turbinate resection, total turbinate resection and front-end resection were obtained as 5.8, 6.1 and 30.5 Pa correspondingly. Based on the total pressure drop results, the one-third resection option seems to be better than the front-end surgery and the total turbinate resection.     

中鼻甲手术治疗鼻窦炎的临床疗效

为了研究中鼻甲手术处理对治疗患者鼻窦炎的临床疗效,本研究选取2013年3月至2018年3月在我院进行鼻内镜手术的患者400例,根据术中对中鼻甲处理情况分为观察组和对照组,每组200例,观察组行中鼻甲成形术,对照组行中鼻甲切除术;观察2组患者治疗一年后的疗效、Lund-Kennedy评分、主观症状VAS评分、嗅觉变化及并发症。研究显示,观察组的治疗有效率(90.50%)与对照组(88.50%)无显著差异(p=0.514)。两组患者治疗1年后的Lund-Kennedy总评分均显著降低,并且观察组的Lund-Kennedy总评分显著低于对照组(2.24 vs.2.75,p<0.05)。对于Lund-Kennedy评分的各个单项评分,治疗后观察组的息肉、瘢痕和结痂显著低于对照组(p<0.05)。治疗1年后观察组的鼻塞评分显著低于对照组(2.22 vs.3.43,p<0.05),而两组的脓涕评分差异无统计学意义(2.25 vs.2.76,p>0.05)。治疗1年后,两组嗅觉功能评分均显著降低,但两组评分之间差异无统计学意义(1.78 vs.1.81,p>0.05)。两组患者的并发症发生率无统计学差异(p>0.05)。本研究表明,中鼻甲是否切除不影响患者的治疗效果和嗅觉功能,然而,与中鼻甲切除术相比,中鼻甲成形术后患者具有较少的息肉、瘢痕、结痂、鼻腔干燥现象,并且可显著改善鼻塞主观症状。     

Inferior turbinate surgery: an adjunct to successful treatment of nasal obstruction in 408 patients

Septal deviation is often associated with hypertrophy of the contralateral inferior turbinate. Failure to reduce the size of the turbinate at the time of septal reconstruction may result in persistent nasal obstruction. The authors present their experience with 408 patients who underwent one of four turbinate procedures over a 6-year period. Most patients underwent unilateral turbinate surgery, although bilateral procedures were undertaken in 7 percent of patients. A graduated surgical approach was taken that varied according to the amount of turbinate enlargement and the degree to which mucosa and bone were involved. Full-thickness excision of the anterior third to half of the inferior turbinate (turbinectomy) became a favored procedure. Relief of nasal obstruction was obtained in greater than 90 percent of patients. Healing was satisfactory regardless of the method, and complications, including hemorrhage and infection, were few. Long-term follow-up revealed no untoward sequelae, and no patient developed atrophic rhinitis. The authors conclude that turbinate surgery, particularly when unilateral, in the carefully selected patient with nasal obstruction is a useful adjunct to septal surgery.     

Rationale for submucous resection of hypertrophied inferior turbinates in rhinoplasty: an evolution

To achieve success in rhinoplasty, the plastic surgeon takes advantage of numerous intraoperative techniques designed to manipulate nasal soft tissue and the osseocartilaginous framework. Although the postoperative result may meet preoperative aesthetic goals, an element of nasal airway obstruction can persist from failure to acknowledge the role of inferior turbinates. Surgically responsive inferior turbinate hypertrophy is frequently not addressed secondary to inadequate history taking, incomplete physical examination, and/or surgeon reluctance to handle these sensitive structures.The goal of this article is to discuss the anatomy and physiology of the inferior turbinates, to present the role for inferior turbinate surgery during rhinoplasty, and to delineate the evolution of the current technique of submucosal resection of the inferior turbinates. Over the past 14 years, the senior author (R.J.R.) has performed inferior turbinates surgery on 648 patients as part of a rhinoplasty.     

Intranasal Volume Changes Caused by the Endoscopic Endonasal Transsphenoidal Approach and Their Effects on Nasal Functions

Objective

We evaluated postoperative changes in nasal cavity volume and their effects on nasal function and symptoms after endoscopic endonasal transsphenoidal approach for antero-central skull base surgery.

Study Design

Retrospective chart review at a tertiary referral center.

Methods

We studied 92 patients who underwent binostril, four-hand, endoscopic endonasal transsphenoidal approach surgery using the bilateral modified nasoseptal rescue flap technique. Pre- and postoperative paranasal computed tomography and the Mimics^® program were used to assess nasal cavity volume changes at three sections. We also performed several pre- and postoperative tests, including the Connecticut Chemosensory Clinical Research Center test, Cross-Cultural Smell Identification Test, Nasal Obstruction Symptoms Evaluation, and Sino-Nasal Outcome Test-20. In addition, a visual analog scale was used to record subjective symptoms. We compared these data with the pre- and postoperative nasal cavity volumes.

Results

Three-dimensional, objective increases in nasal passage volumes were evident between the inferior and middle turbinates (p<0.001) and between the superior turbinate and choana (p = 0.006) postoperatively. However, these did not correlate with subjectively assessed symptoms (NOSE, SNOT-20 and VAS; all nasal cavity areas; p≥0.05) or olfactory dysfunction (CCCRC and CCSIT test; all nasal cavity areas; p≥0.05).

Conclusion

Skull base tumor surgery via an endoscopic endonasal transsphenoidal approach altered the patients’ nasal anatomy, but the changes in nasal cavity volumes did not affect nasal function or symptoms. These results will help surgeons to appropriately expose the surgical field during an endoscopic endonasal transsphenoidal approach.     

Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart

The serine-threonine kinase, Akt, inhibits cardiomyocyte apoptosis acutely both in vitro and in vivo. However, the effects of chronic Akt activation in the heart are unknown. To address this issue, we generated transgenic mice (TG+) with cardiac-specific expression of a constitutively active mutant of Akt (myr-Akt) driven by the myosin heavy chain-alpha promoter. Three TG+ founders (9-19 weeks) died suddenly with massive cardiac dilatation. Two viable TG+ lines (TG564 and TG20) derived from independent founders demonstrated cardiac-specific transgene expression as well as activation of Akt and p70S6 kinase. TG564 (n = 19) showed cardiac hypertrophy with a heart/body weight ratio 2.3-fold greater than littermates (n = 17, p < 0.005). TG20 (n = 18) had less marked cardiac hypertrophy with a heart/body weight ratio 1.6-fold greater than littermates (n = 17, p < 0.005). Isolated TG564 myocytes were also hypertrophic with surface areas 1.7-fold greater than littermates (p < 0.000001). Echocardiograms in both lines demonstrated concentric hypertrophy and preserved systolic function. After ischemia-reperfusion, TG+ had a 50% reduction in infarct size versus TG- (17 +/- 3% versus 34 +/- 4%, p < 0.001). Thus, chronic Akt activation is sufficient to cause a spectrum of phenotypes from moderate cardiac hypertrophy with preserved systolic function and cardioprotection to massive cardiac dilatation and sudden death.     

Partial purification and characterization of the tissue plasminogen activator in nasal mucosa and nasal polyp

Tissue plasminogen activator was partially purified from the inferior turbinate and nasal polyp, and its biochemical properties were investigated. Similar TPA peak positions were seen in the gel filtration chromatography of both tissues, and the molecular weight was approximately 65,000, which was comparable to TPA of pig heart (55,000-60,000). Activity of TPA from inferior turbinate was higher than that from nasal polyp. TPA from both tissues was completely inhibited by trans-aminomethyl cyclohexane carboxylic acid, dithiothreitol, and diisopropylfluorophosphate and had similar inhibition profiles to TPA from pig heart. All these findings indicate that TPA from both tissues is undoubtedly a plasminogen-activating enzyme and serine-type protease and would be biochemically identical.     

Differential expression of LHRH-receptor in bovine nasal tissue and its role in deslorelin delivery

Deslorelin, a luteinizing hormone releasing hormone (LHRH) agonist, is transported via the LHRH-receptor (LHRH-R) and exhibits regional variation as follows: inferior turbinate posterior (ITP)>medium turbinate posterior (MTP)>medium turbinate anterior (MTA) of the bovine nasal mucosa. Differential LHRH-R expression in various regions of the nose is a potential explanation for regional variation in deslorelin transport. Thus, the objective was to determine whether LHRH-R expression exhibits regional variation in bovine nasal mucosa. LHRH-R density (B(max)) and affinity constant (K(d)) were determined by saturation experiments using 0.5mg tissue in the presence of increasing amounts of I(125)-deslorelin (100-100,000 cpm) at 4 degrees C for 4h. The 50% inhibitory concentration (IC(50)) was determined by competition experiments using various amounts of unlabelled deslorelin (0.01-3000 ng) at 4 degrees C for 4h. LHRH-R mRNA and protein expressions were determined using real-time PCR and Western blot analysis, respectively. LHRH-R B(max) and K(d) varied between the regions of excised bovine nasal mucosa: ITP>MTP>MTA. The inhibition experiments yielded two IC(50) concentrations which exhibited trends similar to B(max) and K(d). Real-time PCR and Western blot analysis indicated that LHRH-R expression exhibits similar trends: ITP>MTP>MTA. We identified two deslorelin binding sites in the nasal tissues, with high affinity sites representing approximately 60-70% of the total sites available. In summary, regional differences in nasal deslorelin transport correlate with regional differences in LHRH-R expression, with LHRH-R expression, peptide binding, and transport being the highest in the inferior turbinate posterior region of the nose.     

微型钛板固定法治疗多节段脊髓型颈椎病的临床效应

为了比较丝线悬吊和微型钛板两种椎板固定方法对颈椎单开门椎管扩大成形术治疗多节段脊髓型颈椎病的影响,2016年4月至2018年1月期间,本研究选择我院收治的64例多节段脊髓型颈椎病患者作为研究对象。将患者随机分为对照组(丝线悬吊)和观察组(微型钛板固定),每组32例。比较两组的围手术期指标和治疗1年后的神经功能(JOA评分)、疼痛程度(VAS评分)、颈椎轴性症状、颈椎曲度和并发症。研究显示,两组患者的手术时间、术中出血量和引流量均无统计学差异(p>0.05)。两组患者术后的JOA评分和神经功能改善率无显著差异(86.36%vs.81.41%)(p>0.05)。术后观察组的VAS评分显著低于对照组(p=0.036)。观察组患者的颈椎轴性症状发生率(16.33%)显著低于对照组(25.58%)(Z=-2.024,p=0.043)。治疗12个月后观察组和对照组患者的颈椎曲度分别丢失了1.30%和4.62%,观察组颈椎曲度丢失量显著低于对照组(p=0.032)。本研究说明,在应用颈椎单开门椎管扩大成形术治疗多节段脊髓型颈椎病中,与丝线悬吊椎板固定相比,微型钛板固定可明显减少疼痛程度、颈椎曲度丢失和轴性症状的出现。     

Identification of B2 bradykinin binding sites in the guinea pig nasal turbinate

Specific high affinity BK binding sites in the nasal turbinate of the guinea pig have been demonstrated. Specific [3H]BK binding (10-330 pM) was saturable, and nonlinear least squares analysis indicated the presence of a high affinity binding site with a Kd value of 60 (50-78) pM and a Bmax value of 13.1 = 2.0 fmol/mg protein. In inhibition experiments, D-Phe7-BK (a B2 antagonist) inhibited [3H]BK binding with a Ki value of 23 nM, while des-Arg9[Leu8]-BK (a B1 antagonist) had no effect up to a concentration of 10 microM. These studies indicate the presence of B2 BK receptors in the guinea pig nasal turbinate.     

Decreased expression of VE-cadherin and claudin-5 and increased phosphorylation of VE-cadherin in vascular endothelium in nasal polyps

VE-cadherin and claudin-5 are major components of adherens and tight junctions of vascular endothelial cells and a decrease in their expression and an increase in the tyrosine-phosphorylation of VE-cadherin are associated with an increase in endothelial paracellular permeability. To clarify the mechanism underlying the development of edema in nasal polyps, we studied these molecules in polyp microvessels. Normal inferior turbinate mucosal tissues and nasal polyps from patients treated with or without glucocorticoid were stained for VE-cadherin or claudin-5 and CD31 by a double-immunofluorescence method and the immunofluorescence intensities were graded 1–3 with increasing intensity. To correct for differences in fluorescence intensity attributable to a different endothelial area being exposed in a section or to the thickness of a section, the relative immunofluorescence intensity was estimated by dividing the grade of VE-cadherin or claudin-5 by that of CD31 in each microvessel. Tyrosine-phosphorylation of VE-cadherin was examined by Western blot analysis. The relative intensities of VE-cadherin and claudin-5 in the CD31-positive microvessels significantly decreased in the following order; inferior turbinate mucosa, treated polyps and untreated polyps. The ratio of tyrosine-phosphorylated VE-cadherin to VE-cadherin was significantly higher in untreated polyps than in the inferior turbinate mucosa and treated polyps, between which no significant difference in the ratio was seen. Thus, in nasal polyps, the barrier function of endothelial adherens and tight junctions is weakened, although glucocorticoid treatment improves this weakened barrier function.     

Ghrelin as a potential blood pressure reducing factor in obese women during weight loss treatment

BACKGROUND: In animal models ghrelin reduces cardiac afterload and increases cardiac output via receptors in the cardiovascular system. The aim of our study was to evaluate a potential relationship between weight loss treatment, blood pressure and serum ghrelin concentrations in obese women. MATERIAL AND METHODS: A group of 37 obese premenopausal women with no previous history of hypertension (BMI: 36.5 +/- 5 kg/m2) were involved in the study. Blood pressure and serum ghrelin levels were assessed before and after a three-month weight reduction treatment, which consisted of a diet of 1000 kcal/day and physical exercise. Body composition was determined by impedance analysis using Bodystat. RESULTS: Following weight loss (mean 8.9 +/- 4.8 kg) SBP decreased (120 +/- 13 vs. 115 +/- 14 mm Hg, p = 0.01) and serum ghrelin levels increased significantly (66.9 +/- 13.7 vs. 73.9 +/- 15.4 pg/ml; p = 0.005). There were significant correlations between values for ghrelin levels after weight loss and SBP (r = -0.45, p = 0.02), DBP (r = -0.41, p < 0.05), and between Deltaghrelin levels and DeltaSBP (r = 0.52, p = 0.006), DeltaDBP (r = 0.53, p = 0.005). There was a positive correlation between an increase in ghrelin and a decrease in percentage body fat during weight loss (r = 0.51; p = 0.002). CONCLUSION: The results seem to provide evidence that weight loss may decrease blood pressure in obese patients via a ghrelin-dependent mechanism.     

Left ventricular rupture threshold during the healing phase after myocardial infarction in the dog

The mechanical resistance of the infarcted left ventricle to rupture, or rupture threshold, was measured by the balloon technique 1-42 days after left anterior descending coronary artery ligation in 70 dogs: 26 without infarction (18 sham, 8 with ligation) and 44 with infarction. Rupture threshold in noninfarcted hearts was higher than in infarcted hearts (1168 +/- 165 (SD) vs. 754 +/- 223 mmHg (1 mmHg = 133.32 Pa), p less than 0.001) and did not change over 6 weeks. In contrast, rupture threshold in infarcted hearts decreased (p less than or equal to 0.05) after 14 days, the average value for 21-42 days being less than that for 1-14 days: 577 +/- 140 vs. 867 +/- 191 mmHg, p less than 0.001. Passive left ventricular stiffness in infarcted hearts was higher than for noninfarcted hearts throughout the 6 weeks during early filling (11.1 +/- 3.9 vs. 7.1 +/- 1.4 mmHg/mL, p less than 0.001) but decreased (p less than or equal to 0.05) after 14 days during the prerupture phase (11.3 +/- 5.3 vs. 6.2 +/- 3.0 mmHg/mL, p less than 0.005). Between 7 and 42 days, the infarct zone showed marked increase in hydroxyproline (10.0 +/- 2.0 vs. 48.8 +/- 19.7 mg/g dry weight, p less than 0.001), shrinkage (infarct size, 25 +/- 9 vs. 9 +/- 5% of the left ventricle, p less than 0.005), and thinning (infarct to normal wall thickness ratio, 0.83 +/- 0.11 vs. 0.51 +/- 0.09, p less than 0.001) but little further stretching (expansion index or the ratio of lengths of infarcted and noninfarcted segments, 1.14 +/- 0.10 vs. 1.28 +/- 0.17, p less than 0.2). A mild decrease (p less than 0.05) in left atrial pressure and increase (p less than 0.05) in diastolic area and fractional change in area (two-dimensional echocardiography) were detected at 6 weeks. The late decrease in rupture threshold and prerupture stiffness of the infarcted left ventricle and thinning of the scar suggest a late decrease in mechanical strength and resistance of the infarcted left ventricle to distension.     

Cytokine messenger RNA expression for IL-3, IL-4, IL-5, and granulocyte/macrophage-colony-stimulating factor in the nasal mucosa after local allergen provocation: relationship to tissue eosinophilia.

Tissue eosinophilia is characteristic of human atopic allergic inflammation, although the mechanism is largely unknown. In this study we test the hypothesis that eosinophil infiltration during allergen-provoked rhinitis in hayfever sufferers may occur as a consequence of activation of a population of cells having a characteristic cytokine profile equivalent to the murine Th lymphocyte Th2 subset. Biopsies of the nasal inferior turbinate were obtained from 10 grass pollen-sensitive patients 24 h after local nasal provocation with allergen and after a control challenge with the allergen diluent. Biopsies were divided into two and subsequently processed for in situ hybridization using 35S-labeled RNA probes for selected cytokines and for immunohistology using an eosinophil granule mAb (EG2) which recognizes secreting eosinophils. At allergen-challenged sites compared with control sites there were significant increases in mRNA+ cells for IL-3 (p less than 0.04), IL-4 (p = 0.01), IL-5 (p = 0.02) and granulocyte/macrophage-CSF (p = 0.03). In contrast, only occasional hybridization signals were observed for IL-2 and IFN-gamma at both allergen and control sites. After allergen there was an increase (p = 0.01) in EG2+ eosinophils and significant correlations were observed between EG2+ cells and mRNA expression for "Th2-type" cytokines, particularly IL-5 (r = 0.90, p less than 0.0001). These results demonstrate that recruitment of eosinophils during human allergen-induced rhinitis is associated with cells expressing mRNA for IL-3, IL-4, IL-5, and granulocyte/macrophage-CSF.     

Use of visual analogue scale measurements (VAS) to asses the effectiveness of standardized Andrographis paniculata extract SHA-10 in reducing the symptoms of common cold. A randomized double blind-placebo study.

The objective of our study was to measure the effectiveness of Andrographis paniculata SHA-10 extract in reducing the prevalence and intensity of symptoms and signs of common cold as compared with a placebo. A group of 158 adult patients of both sexes completed the randomized double blind study in Valdivia, Chile. The patients were divided in two equal size groups, one of which received Andrographis paniculata dried extract (1200 mg/day) and the other a placebo during a period of 5 days. Evaluations for efficacy were performed by the patient at day 0, 2, and 4 of the treatment; each completed a self-evaluation (VAS) sheet with the following parameters: headache, tiredness, earache, sleeplessness, sore throat, nasal secretion, phlegm, frequency and intensity of cough. In order to quantify the magnitude of the reduction in the prevalence and intensity of the signs and symptoms of common cold, the risk (Odds Ratio = OR) was calculated using a logistic regression model. At day 2 of treatment a significant decrease in the intensity of the symptoms of tiredness (OR = 1.28; 95% CI 1.07-1.53), sleeplessness (OR = 1.71; 95% CI 1.38-2.11), sore throat (OR = 2.3; 95% CI 1.69-3.14) and nasal secretion (OR = 2.51; 95% CI 1.82-3.46) was observed in the Andrographis SHA-10 group as compared with the placebo group. At day 4, a significant decrease in the intensity of all symptoms was observed for the Andrographis paniculata group. The higher OR values were for the following parameters: sore throat (OR = 3.59; 95% CI 2.04-5.35), nasal secretion (OR = 3.27; 95% CI 2.31-4.62) and earache (OR = 3.11; 95% CI 2.01-4.80) for Andrographis paniculata treatment over placebo, respectively. It is concluded that Andrographis paniculata had a high degree of effectiveness in reducing the prevalence and intensity of the symptoms in uncomplicated common cold beginning at day two of treatment. No adverse effects were observed or reported.     

Activation of IP prostanoid receptors prevents cardiomyocyte hypertrophy via cAMP-dependent signaling

The antihypertrophic action of angiotensin-converting enzyme inhibitors in the heart results partly from local potentiation of bradykinin. We have demonstrated that the antihypertrophic action of bradykinin is mediated by the release of nitric oxide from endothelium and elevation of cardiomyocyte cGMP. Whether other paracrine factors derived from the coronary endothelium, such as prostacyclin (PGI2), may act to prevent hypertrophy has not been explored. In the vasculature, activation by PGI2 of IP and EP1 prostanoid receptors elicits vasodilatation (via cAMP-dependent signaling) and vasoconstriction, respectively. The present objective was to determine whether IP prostanoid receptor activation has antihypertrophic actions in adult rat cardiomyocytes (ARCM). The selective IP agonist cicaprost (1 microM) virtually abolished the increase in [3H]phenylalanine incorporation (a marker of hypertrophy) induced either by endothelin-1 (ET-1; 60 nM, n = 10, P < 0.005) or by angiotensin II (1 microM, n = 6, P < 0.005). Cicaprost also inhibited ET-1 induction of c-fos mRNA expression, an additional marker of hypertrophy in ARCM (n = 5, P < 0.005). In the absence of hypertrophic stimuli, cicaprost alone did not significantly influence either marker. The antihypertrophic actions of cicaprost were mimicked by the dual IP/EP1 agonist iloprost (1 microM) in the presence of the EP1 antagonist AH-6809 (3 microM). Furthermore, cicaprost modestly but significantly increased cardiomyocyte cAMP content by 13 +/- 6% (P < 0.05, n = 4), and the antihypertrophic effect of cicaprost was lost in the presence of the cAMP-dependent protein kinase inhibitor H-89 (1 microM, n = 5, P < 0.05). However, ET-1 also induced increases in the activity of the intracellular growth signals ERK1 (by 3-fold) and ERK2 (by 5-fold) in ARCM, and these were not inhibited by cicaprost (P < 0.01, n = 5). Activation of IP receptors thus represents a novel approach to prevention of hypertrophy, and this effect is linked to cAMP-dependent signaling.     

Effect of regular voluntary exercise on resting cardiovascular responses in SHR and WKY pregnant rats.

The purpose of this study was to assess the influence of regular voluntary exercise in pregnant normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats on 1) uteroplacental perfusion and mean arterial pressure in the resting conscious condition and 2) fetal number, fetal weight, and number of fetal resorptions. WKYs and SHRs were randomly assigned to standard cages [CWKY (n = 10); CSHR (n = 6)] or cages with activity wheels [EWKY (n = 7); ESHR (n = 8)]. EWKYs and ESHRs exercised for 12 wk, and then all rats were bred and experiments were conducted on gestational day 17. Resting blood flow (microspheres), heart rate (HR), and mean arterial pressure (Pa) were measured. No significant difference was found in Pa, HR, uterine blood flow (ESHRs 52 +/- 8 ml.min-1.100 g-1; CSHRs 28 +/- 6 ml.min-1.100 g-1), or maternal placental blood flow (ESHRs, 122 +/- 31 ml.min-1.100 g-1; CSHRs 78 +/- 21 ml.min-1.100 g-1) among the groups. Exercise altered the relationship between maternal placental and uterine blood flow and Pa in the SHR; SHRs with lower Pa maintained higher placental and uterine blood flow after training. Before gestation ESHRs ran on average more kilometers per week than EWKYs (43 +/- 3 vs. 34 +/- 4), but during gestation ESHRs averaged fewer kilometers per week than EWKYs (16 +/- 4 vs. 22 +/- 4). Succinate dehydrogenase activity was higher in the white vastus lateralis (1.02 +/- 0.2 mumol cytochrome c reduced.min-1.g wet wt-1) and vastus intermedius (3.1 +/- 0.5 mumol cytochrome c reduced.min-1.g wet wt-1) muscles of ESHRs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of tight blood pressure control on glomerular hypertrophy in a model of genetic hypertension and experimental diabetes mellitus

The aim of this study was to evaluate the effect of prevention of hypertension on glomerular hypertrophy, renal cell replication and accumulation of glomerular fibronectin in a model of genetic hypertension and experimental diabetes. Four-week-old streptozotocin induced spontaneously hypertensive rats (SHR) were randomized for no treatment, or for treatment with captopril, losartan or triple therapy (hydrochlorothiazide, reserpine and hydralazine) for 20 days. Increase in systolic blood pressure was equally prevented by captopril (118+/-15 mmHg), losartan (111+/-9) and triple therapy (112+/-14, p<0.0001). Glomerular size was higher (p<0.005) in diabetic SHR (27,300+/-2130 microm(2)) compared with non-diabetic SHR (23,800+/-307). The antihypertensive therapy with captopril (23,900+/-175), losartan (23,800+/-120), and triple therapy (23,400+/-210) prevented the glomerular enlargement in diabetic SHR. Glomerular expression of fibronectin was increased in diabetic SHR (7.61+/-1.22 densitometric unit) as compared to the controls (2.27+/-2.15, p<0.0001), and was decreased (p<0.0001 vs diabetic SHR) with captopril (2.49+/-1.42), losartan (1.57+/-1.1) and triple therapy (2.04+/-1.42). The number of replicating glomerular cell significantly decreased in diabetic SHR and it was restored by all three antihypertensive regimes. The glomerular expression of p27(Kip1) was increased in diabetic SHR but it was not modified by antihypertensive treatment. Strict blood pressure control, in diabetic SHR independently of the class of antihypertensive agent, restores glomerular hypertrophy and renal cellular replication, and prevents the increment in glomerular fibronectin.     

Acoustic rhinometry: validation by three-dimensionally reconstructed computer tomographic scans.

The aim of the present study was a validation of acoustic rhinometry (AR) by computed tomography (CT). Six healthy subjects were examined by CT and AR. The CT data were processed in a computer program (AutoCAD), and a virtual three-dimensional model of each nasal cavity was constructed. This model permitted an individual prediction of the center line of the sound wave propagation through the air volume of the nasal cavity with the cross-sectional areas oriented perpendicularly to this line. The area-distance curves derived from AR and CT were compared. Linear regression analysis revealed a reasonable agreement of AR and CT in the anterior nose below a mean of 6 cm distance from the nostrils [r = 0.839, P < 0.01, m = 1.123, b = -0.113 (AR = m x CT + b)]. The measuring accuracy using CT as gold standard revealed a mean error at the nasal valve of <0.01 cm(2) (4.52%) and at the nasal isthmus of 0.02 cm(2) (1. 87%). Beyond 6 cm, the correlation decreased (r = 0.419), and overestimation of the true area occurred (>100%). In conclusion, the measurements were reasonably accurate for diagnostic use up to the turbinate head region. Certain factors induce an overestimation of the true areas beyond this region. However, these factors are constant and reproducible in a single subject, and intraindividual comparative measurements are possible beyond the turbinate head region.