Frequency of endoscopic surveillance for Barrett's esophagus is influenced by health insurance status: results from a population-based analysis.

Factors that influence the frequency of surveillance endoscopy for nondysplastic Barrett's esophagus are not well understood. The objective of this study is to assess factors which influence the frequency of endoscopic surveillance for Barrett's esophagus, including health insurance/third-party payer status. Cases of nondysplastic Barrett's esophagus undergoing esophagogastroduodenoscopy with biopsy were identified using longitudinal data from the Healthcare Utilization Project database in 2005-2006 and followed through 2011. The threshold for appropriate surveillance utilization was defined as two to four surveillance esophagogastroduodenoscopies over a standardized 5-year period. Patients' insurance status was designated as either Medicare, Medicaid, private, or noninsured. 36,676 cases of nondysplastic Barrett's esophagus were identified. Among these, 4,632 patients (12.6%) underwent between two and four surveillance esophagogastroduodenoscopies in 5 years of follow-up versus 31,975 patients (87.3%) who underwent fewer than two esophagogastroduodenoscopies during follow-up. Multivariate analysis found that Barrett's patients insured through Medicaid (OR 1.273; 95% CI = 1.065-1.522) or without insurance (OR = 2.453; 95% CI = 1.67-3.603) were at increased likelihood of being under-surveilled. This study identified a difference in frequency of surveillance esophagogastroduodenoscopy for Barrett's esophagus by payer status. Patients without health insurance and those whose primary insurance was Medicaid were at increased odds for under-surveillance. These data suggest that a more robust system for tracking and ensuring longitudinal follow-up of patients with Barrett's esophagus, with attention to the uninsured and underinsured population, may be needed to ensure optimal surveillance.

Matrix modulation of compensatory lung regrowth and progenitor cell proliferation in mice.

Mechanical stress is an important modulator of lung morphogenesis, postnatal lung development, and compensatory lung regrowth. The effect of mechanical stress on stem or progenitor cells is unclear. We examined whether proliferative responses of epithelial progenitor cells, including dually immunoreactive (CCSP and proSP-C) progenitor cells (CCSP+/SP-C+) and type II alveolar epithelial cells (ATII), are affected by physical factors found in the lung of emphysematics, including loss of elastic recoil, reduced elastin content, and alveolar destruction. Mice underwent single lung pneumonectomy (PNY) to modulate transpulmonary pressure (mechanical stress) and to stimulate lung regeneration. Control mice underwent sham thoracotomy. Plombage of different levels was employed to partially or completely abolish this mechanical stress. Responses to graded changes in transpulmonary pressure were assessed in elastin-insufficient mice (elastin +/-, ELN+/-) and elastase-treated mice with elastase-induced emphysema. Physiological regrowth, morphometry (linear mean intercept; Lmi), and the proliferative responses of CCSP+/SP-C+, Clara cells, and ATII were evaluated. Plombage following PNY significantly reduced transpulmonary pressure, regrowth, and CCSP+/SP-C+, Clara cell, and ATII proliferation following PNY. In the ELN+/- group, CCSP+/SP-C+ and ATII proliferation responses were completely abolished, although compensatory lung regrowth was not significantly altered. In contrast, in elastase-injured mice, compensatory lung regrowth was significantly reduced, and ATII but not CCSP+/SP-C+ proliferation responses were impaired. Elastase injury also reduced the baseline abundance of CCSP+/SP-C+, and CCSP+/SP-C+ were found to be displaced from the bronchioalveolar duct junction. These data suggest that qualities of the extracellular matrix including elastin content, mechanical stress, and alveolar integrity strongly influence the regenerative capacity of the lung, and the patterns of cell proliferation in the lungs of adult mice.

Self-tolerance to the murine homologue of a tyrosinase-derived melanoma antigen: implications for tumor immunotherapy.

The human tyrosinase-derived peptide YMDGTMSQV is presented on the surface of human histocompatibility leukocyte antigen (HLA)-A*0201(+) melanomas and has been suggested to be a tumor antigen despite the fact that tyrosinase is also expressed in melanocytes. To gain information about immunoreactivity and self-tolerance to this antigen, we established a model using the murine tyrosinase-derived homologue of this peptide FMDGTMSQV, together with transgenic mice expressing the HLA-A*0201 recombinant molecule AAD. The murine peptide was processed and presented by AAD similarly to its human counterpart. After immunization with recombinant vaccinia virus encoding murine tyrosinase, we detected a robust AAD-restricted cytotoxic T lymphocyte (CTL) response to FMDGTMSQV in AAD transgenic mice in which the entire tyrosinase gene had been deleted by a radiation-induced mutation. A residual response was observed in the AAD(+)tyrosinase(+) mice after activation under certain conditions. At least some of these residual CTLs in AAD(+)tyrosinase(+) mice were of high avidity and induced vitiligo upon adoptive transfer into AAD(+)tyrosinase(+) hosts. Collectively, these data suggest that FMDGTMSQV is naturally processed and presented in vivo, and that this presentation leads to substantial but incomplete self-tolerance. The relevance of this model to an understanding of the human immune response to tyrosinase is discussed.

Different training volumes yield equivalent increases in BMD.

The purpose of this study was to determine if an exercise threshold existed in stimulating an elevation in bone mineral density (BMD), via resistance training, during the growth period in male rats. 27 male rats were randomly divided into Â-Control (Con, n=9), 3 ladder climb resistance trained group (3LC, n=9), and 6 ladder climb resistance trained group (6LC, n=9). The 3LC and 6LC groups were conditioned to climb a vertical ladder with weights appended to their tail 3 days/wk for a total of 6 wks, but the 6LC group performed significantly more work than the 3LC group. After 6 weeks, left tibial BMD (mean±SD) was significantly greater for 3LC (0.225±0.006 g/cm (2)) and 6LC (0.234±0.008 g/cm (2)) when compared to Con (0.202±0.013 g/cm (2)). Further, bone strength (force to failure in Newtons) was significantly greater for 3LC (132.7±13.7) and 6LC (130.0±22.8) compared to Con (102.0±10.1). There was no significant difference in BMD or bone strength between 3LC and 6LC. The results indicate that both resistance training programs were equally effective in elevating BMD and bone strength in growing rats. These data suggest that during growth, there is a stimulation threshold where more work per exercise session is ineffective in promoting additional bone formation.

Equal BMD after daily or triweekly exercise in growing rats.

The purpose of this study was to examine the efficacy of continuous resistance training (3 days/wk) compared to interrupted resistance training where 20-24 h separated an exercise bout (i. e. 6 days/wk) for enhancing bone mineral density (BMD) in growing male rats. The total volume of work performed per week between the two resistance training programs was equivalent by design. Young male rats were randomly divided into Control (Con, n=9), 3 days/wk resistance trained group (RT3, n=9), and 6 days/wk resistance trained group (RT6, n=9). The RT3 and RT6 groups were conditioned to climb a vertical ladder with weights appended to their tail for a total of 6 wks. After 6 wks, BMD (assessed via DXA) from the left tibia was significantly greater for RT3 (0.242+/-0.004 g/cm (2)) and RT6 (0.244+/-0.004 g/cm (2)) compared to Con (0.226+/-0.003 g/cm (2)). Further, serum osteocalcin (oc, in ng/ml) was significantly greater for RT3 (75.8+/-4.4) and RT6 (73.5+/-3.8) compared to Con (53.4+/-2.4). There was no significant difference in BMD or serum OC between RT3 and RT6 groups. The results indicate that both resistance training programs were equally effective in elevating bone mineral density in young, growing rats.

Elastin expression in very severe human COPD.

Alveolar elastic fibres are key targets of proteases during the pathogenesis of chronic obstructive pulmonary disease (COPD). In the current study, we hypothesised that a response to injury leads to enhanced alveolar elastin gene expression in very severe COPD. Lung samples obtained from 43 patients, including 11 with very severe COPD (stage 4), 10 donors, 10 with moderate/severe COPD (stage 2-3) and 12 non-COPD subjects, were analysed for elastin mRNA expression by real-time RT-PCR and in situ hybridisation. Alveolar elastic fibres were visualised using Hart's staining of sections of frozen inflated lungs obtained from 11 COPD stage 4 patients and three donor lungs. Compared with donors, non-COPD and stage 2-3 COPD, elastin mRNA expression was significantly increased in very severe COPD lungs (12-fold change), and localised in situ hybridisation induced elastin expression to alveolar walls. Compared with donors, alveolar elastic fibres also comprised a greater volume fraction of total lung tissue in very severe COPD lungs (p<0.01), but elastic fibre content was not increased per lung volume, and desmosine content was not increased. The present study demonstrates enhanced alveolar elastin expression in very severe COPD. The efficiency of this potential repair mechanism and its regulation remain to be demonstrated.

Early repair of ventral incisional hernia may improve quality of life after surgery for abdominal malignancy: a prospective observational cohort study.

PURPOSE: Recent work has shown that over 40% of patients undergoing surgery for abdominal malignancy develop ventral incisional hernias (VIH) within 2 years. We hypothesized that early repair of VIH for cancer survivors could improve long-term quality of life (QoL). METHODS: All patients presenting with a history of surgery for abdominal malignancy and a VIH were prospectively enrolled. QoL was assessed at baseline and 3-, 6-, 12-, 18-, and 24-month follow-up using abdominal wall-specific (HerQLes) and cancer-specific (FACT-G) instruments. At the study's conclusion, patients were divided into 2 groups-those that underwent VIH repair during the study's course (Repair Group) and those that did not (Control Group). Categorical variables were analyzed using Pearson's Chi-square and continuous variables with Wilcoxon rank sum test. RESULTS: Eighty-four patients were enrolled. Overall, 46 patients (55%) underwent VIH repair, with 36 repairs (78%) occurring within 3 months of initial evaluation. Sixty-six (79%) had complete 1-year follow-up data, and 30 (36%) had 2-year data, with a median follow-up duration of 15.6 months. At baseline, both groups were similar with respect to demographics, cancer stage, and HerQLes/FACT-G scores. Compared to the Controls, the Repair Group showed greater improvements over baseline HerQLes Summary Scores at the 3-, 6-, 12-, and 18-month time points (median increase, 37 vs. 26 points), and in FACT-G total scores at the 3-, 6-, and 12-month time points (median increase, 6 vs. 4 points). CONCLUSIONS: Repair of VIH after surgery for abdominal malignancy may improve abdominal wall-specific and cancer-specific QoL, making post-resection abdominal wall reconstruction an important aspect of cancer survivorship.

Laparoscopic splenectomy for splenic masses.

BACKGROUND: This study aimed to evaluate the perioperative outcomes and pathology of patients undergoing laparoscopic splenectomy for splenic masses. METHODS: The records for 174 patients who underwent laparoscopic splenectomy from May 1994 to August 2006 were reviewed. Patient demographics, preoperative imaging, American Society of Anesthesiologists (ASA) score, body mass index (BMI), estimated blood loss (EBL), operative time, spleen size, complications, hospital length of stay (LOS), pathology, and mortality were extracted from the records. Data are expressed as means +/- standard deviation. Statistical significance (p < 0.05) was determined using a two-tailed t-test and Fisher's exact test. RESULTS: A splenic mass was diagnosed preoperatively for 18 patients (10.3%) (7 males and 11 females). The mean patient age was 51.4 +/- 13.7 years. The mean ASA was 2.3 +/- 0.8, and the mean BMI was 27.3 +/- 5.8 kg/m(2). Computed tomography scans demonstrated splenic masses in all the patients. The mean mass size was 4.3 +/- 3.3 cm (range, 1.0-11.0 cm), and the mean spleen length was 14.6 +/- 7.5 cm (range, 5.5-40.2 cm). Total laparoscopic splenectomy was completed for 15 patients, and hand-assisted splenectomy was performed for 3 patients (2 converted). The mean operative time was 128.3 +/- 38.5 min, and the mean EBL was 110 +/- 137.5 ml. There were no intraoperative complications or 30-day mortalities. The postoperative complication rate was 11.1%, and the mean LOS was 1.9 +/- 1.0 days. The pathology for six patients (33.3%) was malignant (5 lymphomas and 1 adenocarcinoma). There were three false-positive positron emission tomography (PET) scans. Compared with 73 patients undergoing laparoscopic splenectomy for idiopathic thrombocytopenic purpura, there was no significant difference in mean EBL, operative time, conversion rate, complication rate, LOS, or 30-day mortality rate (p > 0.05). CONCLUSIONS: Laparoscopic splenectomy is appropriate for patients whose indication for surgery is splenic mass. Suspicious splenic masses should be removed due to the relatively high incidence of malignant pathology, most commonly lymphoma.

Monocytic cell type-specific transcriptional induction of collagenase.

Interstitial collagenase (MMP-1), a metalloproteinase produced by resident and inflammatory cells during connective tissue turnover, cleaves type I collagen fibrils. This catalytic event is rate limiting in remodeling of tissues rich in fibrillar collagen such as the skin and lungs. The regulation of collagenase expression is cell-type specific; bacterial LPS and zymosan, a yeast cell wall derivative, are potent inducers of collagenase expression in macrophages, but do not alter fibroblast collagenase expression. Since promoter elements controlling collagenase transcription in monocytic cells have not been previously defined, we sought to delineate responsive cis-acting elements of the collagenase promoter in transiently transfected human (U937) and murine (J774) monocytic cell lines. Deletion constructs containing as little as 72 bp of 5' -flanking sequence of the collagenase promoter were sufficient for LPS- or zymosan-mediated transcriptional induction, whereas phorbol inducibility exhibited an absolute requirement for upstream elements including the polyoma enhancer A-binding protein-3 site (-83 to -91) and TTCA sequence (-102 to -105) in both monocytic cells and fibroblasts. Mutagenesis of the activator protein-1 [AP-1] site at -72 abolished basal promoter activity and LPS/zymosan inducibility, while mutagenesis of an NF-kappaB-like site at -20 to -10 had no effect. Nuclear extracts from LPS- and zymosan-treated cells showed strong AP-1 activity by gel-shift analysis, and supershift analysis showed the AP-1 complexes contained specific members of both the jun and fos gene families. These data indicate that, in contrast to most LPS effects, AP-1, but not nuclear factor-kappaB, mediates LPS induction of collagenase transcription in macrophagelike cells. Furthermore, as compared to regulation by phorbol ester, collagenase induction in monocytic cells by cell wall derivatives of bacteria or yeast is largely independent of upstream promoter sequences.

An open reading frame element mediates posttranscriptional regulation of tropoelastin and responsiveness to transforming growth factor beta1.

Elastin, an extracellular component of arteries, lung, and skin, is produced during fetal and neonatal growth. We reported previously that the cessation of elastin production is controlled by a posttranscriptional mechanism. Although tropoelastin pre-mRNA is transcribed at the same rate in neonates and adults, marked instability of the fully processed transcript bars protein production in mature tissue. Using RNase protection, we identified a 10-nucleotide sequence in tropoelastin mRNA near the 5' end of the sequences coded by exon 30 that interacts specifically with a developmentally regulated cytosolic 50-kDa protein. Binding activity increased as tropoelastin expression dropped, being low in neonatal fibroblasts and high in adult cells, and treatment with transforming growth factor beta1 (TGF-beta1), which stimulates tropoelastin expression by stabilizing its mRNA, reduced mRNA-binding activity. No other region of tropoelastin mRNA interacted with cellular proteins, and no binding activity was detected in nuclear extracts. The ability of the exon-30 element to control mRNA decay and responsiveness to TGF-beta1 was assessed by three distinct functional assays: (i) insertion of exon 30 into a heterologous gene conferred increased reporter activity after exposure to TGF-beta1; (ii) addition of excess exon 30 RNA slowed tropoelastin mRNA decay in an in vitro polysome degradation assay; and (iii) a mutant tropoelastin cDNA lacking exon 30, compared to wild-type cDNA, produced a stable transcript whose levels were not affected by TGF-beta1. These findings demonstrate that posttranscriptional regulation of elastin production in mature tissue is conferred by a specific element within the open reading frame of tropoelastin mRNA.

Outcomes analysis of laparoscopic resection of pancreatic neoplasms.

BACKGROUND: Experience with laparoscopic resection of pancreatic neoplasms remains limited. The purpose of this study is to critically analyze the indications for and outcomes after laparoscopic resection of pancreatic neoplasms. METHODS: The medical records of all patients undergoing laparoscopic resection of pancreatic neoplasms from July 2000 to February 2006 were reviewed. Data are expressed as mean +/- standard deviation. RESULTS: Laparoscopic pancreatic resection was performed in 22 patients (M:F, 8:14) with a mean age of 56.3 +/- 15.1 years and mean body mass index (BMI) of 26.3 +/- 4.5 kg/m2. Nine patients had undergone previous intra-abdominal surgery. Indications for pancreatic resection were cyst (1), glucagonoma (1), gastrinoma (2), insulinoma (3), metastatic tumor (2), IPMT (4), nonfunctioning neuroendocrine tumor (3), and mucinous/serous cystadenoma (6). Mean tumor size was 2.4 +/- 1.6 cm. Laparoscopic distal pancreatectomy was attempted in 18 patients and completed in 17, and enucleation was performed in 4 patients. Laparoscopic ultrasound (n = 10) and a hand-assisted technique (n = 4) were utilized selectively. Mean operative time was 236 +/- 60 min and mean blood loss was 244 +/- 516 ml. There was one conversion to an open procedure because of bleeding from the splenic vein. The mean postoperative LOS was 4.5 +/- 2.0 days. Seven patients experienced a total of ten postoperative complications, including a urinary tract infection (UTI) (1), lower-extremity deep venous thrombosis (DVT) and pulmonary embolus (1), infected peripancreatic fluid collection (1), pancreatic pseudocyst (1), and pancreatic fistula (6). Five pancreatic fistulas were managed by percutaneous drainage. The reoperation rate was 4.5% and the overall pancreatic-related complication rate was 36.4%. One patient developed pancreatitis and a pseudocyst 5 months postoperatively, which was managed successfully with a pancreatic duct stent. There was no 30-day mortality. CONCLUSIONS: Laparoscopic pancreatic resection is safe and feasible in selected patients with pancreatic neoplasms. With a pancreatic duct leak rate of 27%, this problem remains an area of development for the minimally invasive technique.

Collagenase-3 induction in rat lung fibroblasts requires the combined effects of tumor necrosis factor-alpha and 12-lipoxygenase metabolites: a model of macrophage-induced, fibroblast-driven extracellular matrix remodeling during inflammatory lung injury.

The mechanisms responsible for the induction of matrix-degrading proteases during lung injury are ill defined. Macrophage-derived mediators are believed to play a role in regulating synthesis and turnover of extracellular matrix at sites of inflammation. We find a localized increase in the expression of the rat interstitial collagenase (MMP-13; collagenase-3) gene from fibroblastic cells directly adjacent to macrophages within silicotic rat lung granulomas. Conditioned medium from macrophages isolated from silicotic rat lungs was found to induce rat lung fibroblast interstitial collagenase gene expression. Conditioned medium from primary rat lung macrophages or J774 monocytic cells activated by particulates in vitro also induced interstitial collagenase gene expression. Tumor necrosis factor-alpha (TNF-alpha) alone did not induce interstitial collagenase expression in rat lung fibroblasts but did in rat skin fibroblasts, revealing tissue specificity in the regulation of this gene. The activity of the conditioned medium was found to be dependent on the combined effects of TNF-alpha and 12-lipoxygenase-derived arachidonic acid metabolites. The fibroblast response to this conditioned medium was dependent on de novo protein synthesis and involved the induction of nuclear activator protein-1 activity. These data reveal a novel requirement for macrophage-derived 12-lipoxygenase metabolites in lung fibroblast MMP induction and provide a mechanism for the induction of resident cell MMP gene expression during inflammatory lung processes.

Revised genomic structure of the human MAGP1 gene and identification of alternate transcripts in human and mouse tissues.

The human MAGP1 (or MFAP2) and mouse Magp1 genes code for the microfibril-associated glycoprotein-1 (MAGP-1), an extracellular matrix protein of microfibrillar structures. We report a revised 5' genomic structure including the use of a single transcription start site that gives rise to a 32-bp 5' exon spanning a segment of the previously described exon B. No evidence of heterogeneous 5' ends from the use of alternative promoters was found in human tissues and cell lines. We located the genetic marker D1S170 to a position 3 kb downstream of the polyadenylation site. Large-scale comparison of the human and mouse genes revealed conservation of sequence outside the coding exons. Although the 5' flanking regions were found to be divergent certain cis-elements for transcription factors are conserved, including Sp1, AP-2, AP-4, NF-kappaB, and c-ETS motifs. We identified a total of five splice variants in addition to the canonical MAGP1A/Magp1A form. These transcripts are species-specific and are generated by different processing mechanisms. The alternate forms MAGP1A', MAGP1B, and MAGP1C are expressed in human tissues; and the two variants Magp1A" and Magp1D were found only in mouse. The alternatively spliced forms show restricted patterns of expression relative to the canonical isoform.

The affinity of platelets for the subendothelium.

It is known that platelets adhere to subendothelial tissues, but it is not clear as to whether this results in thrombus formation. To study this question, 94 arterial specimens in dogs were randomly treated, either by balloon stripping which exposed the subendothelium (Group I) or by endarterectomy, which exposed the media (Group II). Platelets tagged with 51Cr were injected into some of the animals and the degree of adherence to the vessel wall measured. In the rest, the thrombosis rate was measured at 48 hours. It was shown that the platelets tend not to adhere to the subendothelium in great numbers. The thrombosis rates were 8.6 per cent in Group I compared to 47.8 per cent in Group II. The conclusion drawn from these results was that the subendothelium was antithrombogenic and that this layer should be preserved at vascular anastomoses to discourage platelet adherence and thrombosis.

Prime vendor purchasing of pharmaceuticals in the Veterans Affairs health care system.

The development of a prime vendor system of pharmaceutical procurement and distribution in the Department of Veterans Affairs (VA) is described. The traditional system of pharmaceutical procurement and distribution in the VA required large stockpiles of the pharmaceuticals that had been needed the previous year, a system that was inefficient and full of hidden markups and other unnecessary fees. In late 1991, the VA began a pilot test of a prime vendor system, in which three wholesalers were selected to provide pharmaceuticals to 33 VA medical centers. Under the new system, pharmacies placed orders electronically, directly with the prime vendor, and payments were taken from funds obligated in advance. The benefits of the new system included reduced costs, faster turnaround of orders, higher fill rates, and higher satisfaction among users. In 1994, the VA ceased operation of its traditional depot system for pharmaceuticals. The implementation of a prime vendor procurement system for pharmaceuticals within the VA improved system responsiveness, increased satisfaction of system users, and reduced expenses.

Predictors of treatment outcome in young children with autism: a retrospective study.

This study examined predictors of developmental outcomes in 17 children diagnosed with autism or PDD-NOS, who received generic treatment over a mean period of 37 months. Pre-treatment evaluations occurred at a mean age of 31 months with follow-up evaluations at a mean age of 69 months. Significantly different developmental trajectories were observed among the participants at follow-up, separating the participants into two distinct groups (high and low outcome). However, groups did not differ significantly in treatment intensity or other outcome prediction measures. Pre-treatment developmental intelligence levels between the two groups approached significance. The results raise questions regarding the effect of treatment intensity and type, family stress factors, and intelligence ability in very early childhood on, outcome.

Imaging alveolar-duct geometry during expiration via ³He lung morphometry.

Acinar geometry has been the subject of several morphological and imaging studies in the past; however, surprisingly little is known about how the acinar microstructure changes when the lung inflates or deflates. Lung morphometry with hyperpolarized (3)He diffusion MRI allows non-destructive evaluation of lung microstructure and acinar geometry, which has important applications in understanding basic lung physiology and disease. In this study, we have measured the alveolar and acinar duct sizes at physiologically relevant volumes by (3)He lung morphometry in six normal, excised, and unfixed canine lungs. Our results imply that, during a 37% decrease in lung volume, the acinar duct radius decreases by 19%, whereas the alveolar depth increases by 9% (P < 0.0001 and P < 0.05, respectively via paired t-tests with a Bonferroni correction). A comparison to serial sections under the microscope validates the imaging results and opens the door to in vivo human studies of lung acinar geometry and physiology during respiration using (3)He lung morphometry.

Quantitative assessment of lung microstructure in healthy mice using an MR-based 3He lung morphometry technique.

The recently developed technique of lung morphometry using hyperpolarized (3)He diffusion magnetic resonance (MR) (Yablonskiy DA, Sukstanskii AL, Woods JC, Gierada DS, Quirk JD, Hogg JC, Cooper JD, Conradi MS. J Appl Physiol 107: 1258-1265, 2009) permits in vivo study of lung microstructure at the alveolar level. Originally proposed for human lungs, it also has the potential to study small animals. The technique relies on theoretical developments in the area of gas diffusion in lungs linking the diffusion attenuated MR signal to the lung microstructure. To adapt this technique to small animals, certain modifications in MR protocol and data analysis are required, reflecting the smaller size of mouse alveoli and acinar airways. This is the subject of the present paper. Herein, we established empirical relationships relating diffusion measurements to geometrical parameters of lung acinar airways with dimensions typical for mice and rats by using simulations of diffusion in the airways. We have also adjusted the MR protocol to acquire data with much shorter diffusion times compared with humans to accommodate the substantially smaller acinar airway length. We apply this technique to study mouse lungs ex vivo. Our MR-based measurements yield mean values of lung surface-to-volume ratio of 670 cm(-1), alveolar density of 3,200 per mm(3), alveolar depth of 55 µm, and mean chord length of 62 µm, all consistent with published data obtained histologically in mice by unbiased methods. The proposed technique can be used for in vivo experiments, opening a door for longitudinal studies of lung morphometry in mice and other small animals.