The image quality of deep-learning image reconstruction of chest CT images on a mediastinal window setting.

AIM: To assess the image quality of deep-learning image reconstruction (DLIR) of chest computed tomography (CT) images on a mediastinal window setting in comparison to an adaptive statistical iterative reconstruction (ASiR-V). MATERIALS AND METHODS: Thirty-six patients were evaluated retrospectively. All patients underwent contrast-enhanced chest CT and thin-section images were reconstructed using filtered back projection (FBP); ASiR-V (60% and 100% blending setting); and DLIR (low, medium, and high settings). Image noise, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) were evaluated objectively. Two independent radiologists evaluated ASiR-V 60% and DLIR subjectively, in comparison with FBP, on a five-point scale in terms of noise, streak artefact, lymph nodes, small vessels, and overall image quality on a mediastinal window setting (width 400 HU, level 60 HU). In addition, image texture of ASiR-Vs (60% and 100%) and DLIR-high was analysed subjectively. RESULTS: Compared with ASiR-V 60%, DLIR-med and DLIR-high showed significantly less noise, higher SNR, and higher CNR (p<0.0001). DLIR-high and ASiR-V 100% were not significantly different regarding noise (p=0.2918) and CNR (p=0.0642). At a higher DLIR setting, noise was lower and SNR and CNR were higher (p<0.0001). DLIR-high showed the best subjective scores for noise, streak artefact, and overall image quality (p<0.0001). Compared with ASiR-V 60%, DLIR-med and DLIR-high scored worse in the assessment of small vessels (p<0.0001). The image texture of DLIR-high was significantly finer than that of ASIR-Vs (p<0.0001). CONCLUSIONS: DLIR-high improved the objective parameters and subjective image quality by reducing noise and streak artefacts and providing finer image texture.

Relationship between folic acid intake and gingival health in non-smoking adults in Japan.

OBJECTIVE: To assess the relationship between dietary intake of folate and gingival bleeding in non-smoking adults in Japan. MATERIALS AND METHODS: Data were obtained from residents who participated in the regional nutrition survey and survey of dental diseases conducted by the administrative office of northernmost prefecture of Japan. Dietitians visited households to collect data on dietary intake. Clinical parameters, including Community Periodontal Index (CPI) and bleeding on probing (BOP), were examined in community centers. Information on smoking habit was obtained from the interview. Then the data from 497 non-smoking adults with 20 teeth or more, aged 18 years or older, were analyzed. The relationship between dietary intake of folic acid and gingival bleeding status was estimated using multivariate analysis. RESULTS: Pearson's correlation coefficient showed a significant negative correlation between dietary folate level and bleeding on probing. The negative association between folate level and bleeding on probing remained statistically significant in multiple regression analysis (standardized beta = -0.204, P < 0.001). However, no significant association was found between CPI scores and folate intake level. CONCLUSIONS: The results suggest that dietary intake of folic acid, an important indicator of gingival bleeding in adults, may provide an important clinical target for intervention to promote gingival health.

Demonstration of the exact anatomic tachycardia circuit in the fast-slow form of atrioventricular nodal reentrant tachycardia.

BACKGROUND: The tachycardia circuit in the fast-slow form of atrioventricular nodal reentrant tachycardia (FS-AVNRT) has not been convincingly defined. METHODS AND RESULTS: To define the tachycardia circuit, single extrastimuli were delivered during FS-AVNRT to 9 intra-atrial sites in 12 patients: the His bundle (HB) site; the superior portion of the HB site (S-HB); 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS) (sites S, M, and I); the superior, posterior, and posteroinferior portions of the CSOS (S-CSOS, P-CSOS, and PI-CSOS, respectively); and the CSOS. The inferior portion of coronary sinus ostium (I-CSOS), at which the earliest retrograde activation was observed, was excluded. At each site, the longest coupling interval of the single extrastimulus that reset the tachycardia and the subsequent return cycle was measured. The mean tachycardia cycle length was 370+/-55 ms. The longest coupling intervals at sites S-HB, HB, S, M, I, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 328+/-53, 360+/-55, 358+/-55, 358+/-54, 360+/-55, 338+/-56, 323+/-54, 331+/-56, and 321+/-58 ms, respectively, and the subsequent return cycles were 408+/-58, 371+/-55, 370+/-55, 372+/-56, 370+/-55, 396+/-56, 411+/-60, 405+/-58, and 412+/-59 ms, respectively. The longest coupling intervals at sites HB, S, M, and I were longer than those at S-HB, CSOS, S-CSOS, P-CSOS, and PI-CSOS (P<0.0001). The return cycles at sites HB, S, M, and I did not differ from the tachycardia cycle length, whereas those at CSOS, S-CSOS, P-CSOS, and PI-CSOS were longer than the tachycardia cycle length (P<0.0001). CONCLUSIONS: The perinodal atrium extending from the HB site to the I-CSOS is an integral limb of the reentry circuit in FS-AVNRT.

Analysis of localization of adult T-cell leukemia-derived factor in the transient ischemic rat retina after treatment with OP-1206 alpha-CD, a prostaglandin E1 analogue.

Prostaglandin E1 (PGE1) is commonly used in therapy for obstructive diseases, including ischemic retinopathy, in which pathogenetic reactive oxygen intermediates are responsible. However, the mechanism(s) of PGE1 in reducing tissue damage is still unclear. Adult T-cell leukemia-derived factor/human thioredoxin (ADF) is induced by oxidative stresses and has protective activity against oxidative cellular injury. To evaluate the possible involvement of ADF in the tissue-protective effect of PGE1, we analyzed ADF expression immunohistochemically using a rat transient retinal ischemia model. Rats were treated orally with 300 micrograms/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a stable PGE1 analogue, for 14 days after photodynamic retinal vascular thrombosis by rose Bengal. Rats without any OP-1206 treatment were used as controls. In the OP-1206-treated rats, minimal retinal atrophy due to ischemia/reperfusion was observed histologically up to 14 days, whereas in the non-treated rats the inner layer of the retina became markedly atrophic. In parallel with the histological change, after 14 days following thrombosis ADF immunoreactivity was preserved on retinal pigment epithelial cells in the OP-1206-treated rats, whereas it was diminished in the non-treated rats. These findings suggest an important role for ADF in the OP-1206-dependent suppression of retinal tissue damage caused by oxidative insult.

Mitochondrial induction of adult T cell leukemia derived factor (ADF/hTx) after oxidative stresses in retinal pigment epithelial cells.

PURPOSE: Adult T cell leukemia derived factor (ADF) is a human homologue of thioredoxin (hTx), which exhibits scavenging activity with reactive oxygen intermediates. In their previous study, the authors found that after transient retinal ischemia, the expression of thioredoxin in rat retinal pigment epithelium (RPE) layer increased markedly. The present investigation is to determine intracellular ADF localization in RPE after transient ischemia and in cultured human RPE cells after oxidative insult by H2O2. METHODS: The authors employed immunoelectron microscopy to examine ADF localization in RPE. Labeling density analysis was performed to supplement the main observation in the experiment of transient retinal ischemia. 3-(4,5-dimethylthiazol-2yl)-2-5-diphenyltetrazolium bromide (MTT) assay was performed to verify the protective role of recombinant ADF (rADF) against H2O2. RESULTS: In immunogold electron microscopy, sparse ADF-positive labeling was seen in the cytosol and mitochondria in normal rat RPE and in untreated cultured RPE cells. After oxidative stress, it was concentrated in mitochondria in both groups. MTT assay proved that rADF protected cultured RPE from the toxicity of H2O2. CONCLUSIONS: This study shows the induction of ADF/hTx in mitochondria of RPE after oxidative stresses and its protective effect on cultured RPE exposed to H2O2. The data indicate the possibly important role of ADF/hTx in the protection of retinal cells from the oxidative stresses associated with retinal ischemic disease and probably with regular visual activity.

Comparison of remnant-like lipoprotein particles in postmenopausal women with and without coronary artery disease and in men with coronary artery disease.

It is known that hypertriglyceridemia is a risk factor of coronary artery disease (CAD) in postmenopausal women. This study prospectively examined whether remnant lipoprotein, an atherogenic triglyceride-rich lipoprotein, may have a significant risk and prognostic values in postmenopausal women with angiographically verified CAD. Remnant-like lipoprotein particles cholesterol (RLP cholesterol) levels in fasting serum were measured in 134 consecutive postmenopausal women with (n = 56) or without (n = 78) CAD by an immunoseparation method. The women with CAD were followed for < or =24 months until occurrence of the following clinical coronary events: readmission or coronary revascularization due to recurrent or refractory angina pectoris, nonfatal myocardial infarction, and cardiac death. Multivariate logistic regression analysis showed that high RLP cholesterol levels (>5.7 mg/dl cholesterol; 90th percentile of the distribution of RLP cholesterol levels in controls) were a significant risk factor for the presence of CAD independent of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and other traditional risk factors. Kaplan-Meier analysis demonstrated that women with CAD and higher RLP cholesterol levels had a significantly higher probability of developing coronary events (p <0.001). In multivariate Cox hazard analysis, high RLP cholesterol levels as well as diabetes and hypercholesterolemia were a significant predictor of future coronary events independent of other risk factors in women with CAD (odds ratio 9.7, 95% confidence intervals 1.3 to 20.3, p = 0.02). In conclusion, increased levels of RLP cholesterol are a significant and independent risk factor of CAD and predict future coronary events in postmenopausal women with CAD.

Vascular endothelial cell monolayer formed on membrane filter potentiates the defense against tumor cell invasion by treatment with brefeldin A.

We constructed vascular endothelial cell monolayer on a fibronectin-coated filter in a Boyden chamber and assessed the ability of 3 LL cells to penetrate through the artificial blood vessel wall. The defense of endothelial cell monolayers against the tumor cell invasion was greatly potentiated by their pretreatment with 5 or 10 micrograms/ml of brefeldin A (BFA) for 1 h (52% or 28% of control invasion). Treatment of the endothelial cell monolayers with BFA resulted in an increase in the release of inhibitory material(s) against urokinase-type plasminogen activator (u-PA) activity of 3 LL cells. Parallel experiments with the cultured endothelial cells and BFA indicated that the fungal metabolite enhanced a rate of accumulation of plasminogen activator inhibitor-1 (PAI-1) antigen, but not of tissue-type plasminogen activator antigen in the medium. The BFA-induced enhancement of PAI-1 antigen release was accompanied with the increased accumulation of the extracellular (membrane/matrix-bound) and intracellular PAI-1 antigen (219% of control at 24 h). These results suggest that BFA can strengthen the defense of vascular endothelium against tumor-cell invasion by enhancing the release and accumulation of PAI-1, which plays a critical role in the regulation of the u-PA-plasmin-collagenase activation cascade.

Aminated fucoidan promotes the invasion of 3 LL cells through reconstituted basement membrane: its possible mechanism of action.

Fucoidan is reported to have an antimetastatic activity. In the present study, we prepared an amino group-introduced derivative of fucoidan and examined its effect on the invasion of 3 LL cells through a reconstituted basement membrane (MatrigelTM). Unlike native fucoidan, the aminated derivative promoted the tumor cell invasion: maximal promotion (240% of control invasion) was obtained with 5 micrograms/ml. However, with higher concentrations (10-30 micrograms/ml) of the fucoidan derivative, the promotion was gradually reduced to 130% of control. Both native and aminated fucoidans inhibited specifically the attachment of 3 LL cells to laminin. Interestingly, aminated fucoidan, unlike the native one, promoted the tumor cell adhesion to immobilized synthetic laminin B 1 chain peptide, YIGSR, over a concentration range of 0.5-5 micrograms/ml. Higher concentrations (7-20 micrograms/ml) of the aminated derivative suppressed the adhesive ability of 3 LL cells to YIGSR. 3 LL cells secreted a 50-kDa form of urokinase-type plasminogen activator (u-PA) in the culture medium. Addition of aminated fucoidan (5 micrograms/ml) or YIGSR (10 micrograms/ml) resulted in a 1.7-fold increase in u-PA activity. This effect was enhanced up to 3.5-fold when both substances were simultaneously added. The addition of native fucoidan had no effect. The present results suggest that the 67-kDa receptor-mediated binding of 3 LL cells to laminin activates their invasiveness, especially by enhancing the extracellular u-PA levels. Aminated, but not native, fucoidan may act to enhance the laminin-receptor interaction at the limited concentration range.

Assessment of secondary necrosis of Jurkat cells using a new microscopic system and double staining method with annexin V and propidium iodide.

Using a new system developed by us for acquiring microscopic images automatically, we compared the morphological changes that apoptotic cells undergo with changes in the staining pattern of annexin V-enhanced green fluorescent protein (AV-EGFP) and propidium iodide (PI) in individual cells. Jurkat cells were treated with 5 mM CaCl2 alone, anti-Fas antibody and heating at 42 degrees C for 30 min or 46 degrees C for 60 min, and then were incubated in medium with 5 mM CaCl2. Time-lapse DNA fragmentation analysis and morphological observation revealed that the anti-Fas antibody and heating at 42 degrees C for 30 min induced typical apoptosis in the cells, and heating at 46 degrees C for 60 min induced typical necrosis. Time-lapse observation of individual cells stained with AV-EGFP and PI confirmed that apoptotic cells were stained at first with AV-EGFP alone, and thereafter also with PI when the cellular membrane ruptured and the cell underwent secondary necrosis. Most of the cells which underwent necrosis were stained simultaneously with AV-EGFP and PI. There was a significant time interval between the staining of individual cells with AV-EGFP, indicating apoptosis, and staining of these cells with PI, which indicated the occurrence of secondary necrosis. These results suggest that time-lapse examinations are necessary to distinguish apoptosis, secondary necrosis and necrosis in cells from one another. This study presents direct evidence that apoptotic cells undergo secondary necrosis, which could be recognized with PI.

Cepharanthin enhances thermosensitivity without a resultant reduction in the thermotolerance of a murine mammary carcinoma.

Cepharanthin (Ce) is a biscoclaurine alkaloid extracted from Stephania cepharantha Hayata. The results of our previous in vitro study indicated that Ce reduces thermotolerance by enhancing thermosensitivity. In the present study, we investigated the in vitro and in vivo effects of Ce on thermosensitivity and thermotolerance using a murine mammary carcinoma, MCa, and C3H/HeN mice. Ce enhanced the thermosensitivity of MCa cells for heating at 44 degrees C not only in vitro but also in vivo. The in vivo enhancement ratio +/- SD of Ce at 100 mg/kg for heating at 44 degrees C was 1.3+/-0.3. The fractionated heat treatments at 44 degrees C for 30 and 60 min with an interval time of 0-6 days resulted in the development of remarkable thermotolerance and the expression of heat shock protein 70 in MCa tumors after the first heating. Ce at 100 mg/kg given immediately after the first heating increased the expression of heat shock protein 70 in MCa tumors, and did not reduce the development of thermotolerance. Ce given immediately before the first or second heating also did not inhibit the thermotolerance. The results of this study suggest that Ce enhances the thermosensitivity of MCa tumors as a thermosensitizer, but that this mild thermosensitizing property of Ce might be insufficient to conquer the remarkable thermotolerance in MCa tumors that develops after the first heating.

Artificial ventilation-induced diffuse alveolar damage in rabbits: preliminary study of early detection on expiratory high-resolution computed tomography.

RATIONALE AND OBJECTIVES: To investigate whether expiratory high-resolution computed tomography (HRCT) is more useful than inspiratory HRCT for the detection of early-phase diffuse alveolar damage. METHODS: Eleven anesthetized rabbits were scanned with both inspiratory and expiratory HRCT every 30 minutes during mechanical ventilation. Ten rabbits were killed after the detection of pulmonary abnormalities on both inspiratory and expiratory HRCT. The remaining rabbit was killed when the pulmonary abnormalities appeared only on expiratory HRCT. RESULTS: In four cases (36%), the abnormal findings were detected earlier on expiratory HRCT than on inspiratory HRCT. In seven cases (64%), the abnormalities appeared simultaneously on inspiratory and expiratory HRCT. In all 11 cases, the histopathological changes of areas with abnormal CT findings corresponded to the exudative or proliferative phase of diffuse alveolar damage. CONCLUSIONS: Expiratory HRCT has the potential to detect the abnormalities of diffuse alveolar damage earlier than inspiratory HRCT.

Body position does not influence the location of ventilator-induced lung injury.

OBJECTIVE: To ascertain whether the locations of ventilator-induced lung injury (VILI) are influenced by body position. DESIGN: Randomized prospective short-term study. SETTING: Animal laboratory at a university school of medicine. INTERVENTIONS: Twelve white rabbits were mechanically ventilated in IMV mode with an infant ventilator (V.I.P. Bird, Bird Products, Palm Springs, Calif., USA). Based on the results of a preliminary study to determine the ventilator settings at which the lungs of rabbits were injured within 5 h in the supine position, the ventilator was set at F(I)O2 0.21, at a rate of 30/min, T(I) 0.6 s, peak inspiratory pressure 30 cm H2O, inspiratory flow 10 l/min with no applied positive end-expiratory pressure (PEEP). Six of the animals were tested in the supine position and the other six in the prone position. Respiratory gases were measured and CT scanning was performed every 30 min. The animals were ventilated for 5 h or until pulmonary parenchymal opacification was detected. The lungs were divided into three areas from apex to base and three levels from ventral to dorsal, and the location of opacification was ascribed according to this scheme. After the experiment, the lungs were excised and examined histologically. MEASUREMENTS AND RESULTS: Parenchymal opacification occurred mainly in the dorsal lung areas. The time from the beginning of ventilation to the appearance of lung damage was 60-120 min in the supine (S) group, and 60-270 min in the prone (P) group, and it was significantly longer in the prone group (P < 0.01). We observed diffuse lung damage, including hyaline membrane formation, intra-alveolar edema, and infiltration of inflammatory cells. CONCLUSIONS: Body position affected the time course of the development of VILI, but it did not affect the location.

Sphingomyelinase and cell-permeable ceramide analogs increase the release of plasminogen activator inhibitor-1 from cultured endothelial cells.

We investigated the effect of exogenous staphylococcal sphingomyelinase (SMase) on the release of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) from cultured human umbilical vein endothelial cells (HUVEC). Addition of SMase (2 units/ml) to the culture medium induced an approx. 15-fold increase in the extracellular level of PAI-1 antigen at 3 h. No significant increase in the level of t-PA antigen was detected. Treatment of HUVEC with SMASE (2 units/ml) for 3 h resulted in a significant decrease in the cellular sphingomyelin (SM) level, accompanied by a corresponding increase in the ceramide level. Cell-permeable ceramide analogs also enhanced the release of PAI-1 from cultured HUVEC in concentration- and time-dependent manners. A 6-fold increase in PAI-1 antigen level was observed after incubation for 3 h with 10 microM N-acetylsphingosine. Similar effect was noted as early as 2 h with 10 microM N-hexyanoylsphingosine. Addition of sphingosine failed to affect the release of PAI-1 from cultured HUVEC, indicating that the effects of ceramide analogs were independent of sphingosine generation. Pretreatment with cycloheximide or actinomycin D abated the response of HUVEC to N-acetylsphingosine in the increased levels of both extracellular and intracellular PAI-1. These results suggest that ceramide, generated via "SM cycle", acts as a lipid mediator of PAI-1 release from vascular endothelial cells, and may contribute to a better understanding of the pathogenesis of the PAI-1-associated thrombotic disorders.

The effect of calcium on Fas-mediated apoptosis and secondary necrosis of Jurkat cells.

Our previous study using a new microscopic system indicated that apoptotic cells undergo secondary necrosis during treatment with anti-Fas antibody and calcium. In this study, we compared the time-lapse appearance of apoptosis and secondary necrosis of Jurkat cells during treatment with anti-Fas antibody with and without calcium in individual cells. Apoptosis developed in 97% and 81% of cells during 36-hour-treatment with anti-Fas antibody with and without calcium, respectively. The apoptosis of Jurkat cells showed a characteristic pattern of time-lapse morphological change. Less than 1% of the apoptotic cells divided into apoptotic bodies. There was budding in all the other apoptotic cells, but no apoptotic bodies formed. We confirmed that secondary necrosis occurs in individual apoptotic cells during treatment with anti-Fas antibody. Neither the pattern of time-lapse morphological change nor the time interval between the beginning of apoptotic budding and secondary necrosis were related to the presence of calcium. This study clarified the characteristic pattern of time-lapse morphological change in Jurkat cells during treatment with anti-Fas antibody, and presented direct evidence that individual apoptotic cells undergo secondary necrosis. The presence of calcium did not affect the pattern of morphological change or the time interval between the beginning of apoptotic budding and secondary necrosis.

Detached retina affects morphologic and biochemical changes in the retina adjacent to bullous retinal detachment in rabbits.

PURPOSE: Long-term results, more than 10 years after successful retinal detachment surgery, have shown gradually decreasing visual acuity in some cases. It is unclear if reduced functional recovery postoperatively is caused by anatomic changes or biochemical disorders. To determine the etiology of the reduced visual acuity, we cytochemically examined the changes in the cellular responses of the edges of retinal detachments. METHODS: We histochemically studied the glucose-6-phosphatase (G6P) and 5'-nucleotidase (5'-Nase) activity in the rabbit retina. Experimental rhegmatogenous retinal detachment was produced in a rabbit model after partial vitrectomy, followed by retinal tear formation. RESULTS: Although 5'-Nase activity gradually decreased during the period of detachment, activity was still detectable after 24 weeks. G6P activity increased in the region of the detached neural retina. Around the border of the detached retina, the decrease in 5'-Nase activity extended approximately 140 micrometers into the adjacent attached retina at 2 weeks after detachment and 270 micrometers at 24 weeks. CONCLUSIONS: These observations suggest that some anatomical and biochemical damages may occur in the retina adjacent to bullous retinal detachment and may explain the reduction in postoperative vision in some clinical cases.

Glial-, neuronal- and photoreceptor-specific cell markers in rosettes of retinoblastoma and retinal dysplasia.

Previous studies have shown that a rosette formation represents an attempt to form embryonic retinal tissue, primarily rods and cones. To test the theories as to the origin and characteristics of retinoblastoma cells, we compared the characteristics of tumor rosettes with those of dysplastic rosettes seen in retinal dysplasia using the glial, neuronal and photoreceptor markers. Forty-four retinoblastoma and one retinal dysplasia specimens were analyzed by indirect immunohistochemistry, using specific antibodies against glial fibrillary acidic protein, S-100 protein, myelin basic protein, neuron-specific enolase, neurofilament, retinal S-antigen and retinal pigment epithelial antigen. In human retinoblastoma, all the glial, neuronal, retinal pigment epithelial, and photoreceptor cell markers, except for the neurofilament, were present in parts of rosette-forming tumor cells. However, their localization was different for each antigen and it was not clear whether each tumor cell possesses several antigens. These immuno-positive tumor cells were cytologically indistinguishable from other rosette-forming cells at the light microscopic level. In retinal dysplasia, neuron specific enolase and retinal S-antigen were diffusely expressed in the dysplastic rosettes, however, other antigen were not seen in those rosettes. The staining pattern by immunocytochemistry is totally different in tumor rosettes from dysplastic ones. We found varying localizations of different immunoreactivities within tumor rosettes. These results led us to suggest that tumor cells in the rosettes of retinoblastoma may have the ability to differentiate into neural and glial cells. To prove the theory that retinoblastoma cells may have originated from a primitive neuroectodermal cell capable of multipotentiality, further investigation is needed.

Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm.

BACKGROUND: Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states. METHODS: To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH. RESULTS: Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume. CONCLUSION: Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.

Pulmonary involvement in primary Sjögren's syndrome: spectrum of pulmonary abnormalities and computed tomography findings in 60 patients.

The purpose of this study was to describe the high-resolution computed tomography (HRCT) findings of pulmonary involvement in primary Sjögren's syndrome. The study included 60 patients who met the diagnostic criteria for primary Sjögren's syndrome. The authors retrospectively reviewed the presence, extent, and distribution of various HRCT findings. Results showed that the most common HRCT findings were areas with ground-glass attenuation (92%), followed by subpleural small nodules (78%), non-septal linear opacity (75%), interlobular septal thickening (55%), bronchiectasis (38%), and cysts (30%).

Pulmonary involvement in mixed connective tissue disease: high-resolution CT findings in 41 patients.

The objective of this study was to describe the pulmonary abnormalities on high-resolution computed tomography (CT) in patients with mixed connective tissue disease (MCTD). The study included 41 patients who met the diagnostic criteria for MCTD and showed abnormal findings on high-resolution CT. The presence, extent, and distribution of various high-resolution CT findings were evaluated. The predominant abnormalities included areas of ground-glass attenuation (n = 41), subpleural micronodules (n = 40), and nonseptal linear opacities (n = 32). Other common findings included peripheral predominance (n = 40), lower lobe predominance (n = 39), intralobular reticular opacities (n = 25), architectural distortion (n = 20), and traction bronchiectasis (n = 18). Less common findings included honeycombing, ill-defined centrilobular nodules, airspace consolidation, interlobular septal thickening, thickening of bronchovascular bundles, bronchial wall thickening, bronchiectasis, and emphysema. Pulmonary involvement of MCTD is characterized by the presence of ground-glass attenuation, nonseptal linear opacities, and peripheral and lower lobe predominance. Ill-defined centrilobular opacities were uncommonly seen.

Lymphocytic interstitial pneumonia: follow-up CT findings in 14 patients.

The aim of the present study was to assess the evolution of various computed tomographic (CT) findings of lymphocytic interstitial pneumonia (LIP) with determination of potentially reversible or irreversible features. The study included 14 patients with biopsy-proved LIP who had serial thin-section CT examination 4 to 82 months (median 13 months) apart. Initial and follow-up CT scans were evaluated independently and then directly compared with each other by two observers. The main parenchymal abnormalities on the initial CT scan consisted of ground-glass attenuation (n = 14), thickening of interlobular septa (n = 13), centrilobular nodules (n = 12), cystic airspaces (n = 10), and airspace consolidation (n = 4). On follow-up CT, nine patients improved, one showed no change, and four showed increased extent of disease. With the exception of cysts, the parenchymal opacities were reversible. On follow-up CT, new cysts were seen in three patients; these developed mainly in areas with centrilobular nodules on initial CT. Honeycombing was seen on follow-up CT in four patients; in three patients it developed in areas of airspace consolidation and in one patient it developed in an area with ground-glass attenuation on initial CT. The majority of patients with LIP improved on follow-up. However, airspace consolidation may progress to honeycombing and centrilobular nodules may precede cystic formation.