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Biomedical subjects

M Sekosan

Publications and source records attributed to M Sekosan.

16 recordsLinked to original sources
PubMed1999

Wegener's granulomatosis and alpha1-antitrypsin-deficiency emphysema: proteinase-related diseases.

Wegener's granulomatosis (WG) and alpha1-antitrypsin (alpha1-AT)-deficiency emphysema are both uncommon disorders. A relationship may exist between these diseases involving the proteinase and antiproteinase balance in the lung. A case is presented of WG and alpha1-AT-deficiency emphysema occurring in the same patient. Previous studies concerning the correlation between abnormal alpha1-AT alleles and WG are discussed. Potential mechanisms for the relationship and recommendations for screening are given.

Adult↗
PubMed1999

Disseminated Pseudallescheria boydii infection in a nonimmunocompromised host.

We present a highly unusual case of pulmonary Pseudallescheria boydii infection in a nonimmunocompromised host with a cavitating mass lesion. The diagnosis was confirmed by open lung biopsy. The patient was treated at another institution with course of amphotericin B, considered an ineffective therapy for this infection, and presented to us with direct extension and invasion of the left atrial appendage and the pulmonary artery, followed by massive pulmonary embolization and hematogenous dissemination to the liver, spleen, kidney, pancreas, and brain.

Amphotericin B↗
PubMed1998

A new rat model to study the correlation of cardiac and skeletal muscle allograft rejection.

As a first step to study the correlation of cardiac and skeletal muscle allograft rejection, we describe a new experimental rat model of simultaneous heterotopic heart and cutaneous maximus muscle flap allotransplant. Brown Norway rats were used as donors and Lewis rats as recipients. No immunosuppression was given. The grafts were revascularized with sequential end-to-side anastomosis of each vascular pedicle to the infrarenal aorta and vena cava. Syngeneic heart and cutaneous maximus muscle grafts remained functional and showed no sign of rejection at 7 days after the transplant. In contrast, both allografts developed severe rejection and functional compromise at 7 days after the transplant. Our experimental model is technically feasible and reproducible and may provide important information about the pattern of rejection of cardiac and skeletal muscle allografts.

Animals↗
PubMed1998

Staining tissue with methacrylate casts for light microscopy.

Scanning electron microscopy (SEM) of methyl methacrylate casts and light microscopy (LM) of tissue are well-established methods for studying the microcirculation. The two are complimentary, but methacrylate is transparent and thus its presence is often not appreciated by LM. Applying histologic stains to sections of tissue embedded in methyl methacrylate would allow the relationships of light microscopic and scanning electron microscopic views of cast vasculature to be better appreciated. We sought to test different stains on cast tissue to find one that would accent the cast. Surgically removed and autopsied human lungs were cast with methacrylate and processed by routine light microscopic methods. They were stained with the hematoxylin and eosin, Masson trichome, elastic--van Gieson, Grocott methenamine silver, Brown-Brennan, and Ziehl-Neelsen methods. The Ziehl-Neelsen procedure stained the methacrylate best, giving it a red color. This procedure also worked well without heating. We conclude that (1) cast methacrylate lung can be processed for routine LM with excellent results; (2) methacrylate stains well with the Ziehl-Neelsen technique; (3) the acid--fast stained cast lung shows capillaries and cells in both normal and diseased lung better than the routine hematoxylin and eosin stain; (4) this technique can be used to assess filling and correlate findings on the same tissue with the two different microscopic methods.

Corrosion Casting↗
PubMed1997

Decrease in immunoreactive neutral endopeptidase in uvula epithelium of patients with obstructive sleep apnea.

The purpose of this study was to determine whether neutral endopeptidase (NEP; EC3.4.24.11) is decreased in the uvula epithelium of patients with obstructive sleep apnea (OSA). Tissues were obtained by uvulopharyngopalatoplasty in seven patients with moderate OSA and by autopsy in five individuals not known to have OSA. Using antisera to human NEP and immunoperoxidase staining, we found that NEP was localized in uvula epithelial cells of both patients with OSA and controls. However, there was a significant decrease in the number of epithelial cells staining for NEP in patients with OSA relative to controls (67 +/- 10 cells versus 261 +/- 33 cells, in 5 randomly selected high-power microscopic fields, respectively; mean +/- SEM; p < .05). The intensity of staining for NEP was similar in both groups. We conclude that immunoreactive NEP is significantly decreased in the uvula epithelium of patients with OSA.

Adult↗
PubMed1997

Giant cell arteritis manifesting as chronic cough and fever of unknown origin.

A 57-year-old white man sought medical attention because of chronic cough and fever of unknown origin. An extensive work-up over 4 weeks, including repeated blood cultures, chest roentgenograms, a gallium scan, and computed tomographic scans of the sinuses, chest, and abdomen, was nondiagnostic. The patient was referred to our institution for bronchoscopy. Further analysis of his history revealed that he had a headache in conjunction with the cough and an episode of a flashing color design in his left eye 1 week before assessment. The erythrocyte sedimentation rate was 115 mm in 1 hour. A biopsy of the temporal artery showed granulomatous inflammation of the vessel wall with multinucleated giant cells, histiocytes, lymphocytes, plasma cells, and few eosinophils. The multinucleated giant cells were closely related to the fragmented elastic lamina. Corticosteroid therapy resulted in prompt resolution of the chronic cough and fever. Giant cell arteritis should be considered in the differential diagnosis of chronic cough.

Chronic Disease↗
PubMed1996

Inflammation in the uvula mucosa of patients with obstructive sleep apnea.

This study was conducted to determine whether inflammation is present in the uvula mucosa of patients with obstructive sleep apnea (OSA). Uvulas were obtained by uvulopalatopharyngoplasty in 21 patients with moderate OSA (mean apnea/hypopnea index and standard error of the mean: 32 +/- 4) and by autopsy in 5 individuals not known to have OSA. Using point counting in five randomly selected high-power microscopic fields (X100), the authors found that the number of leukocytes in the lamina propria of the uvula mucosa was significantly higher in patients with OSA than in the controls (179 +/- 12 cells vs. 71 +/- 4 cells, respectively; P < .05). This was due to a significant increase in the number of plasma cells in patients with OSA as compared with controls (89 +/- 15 cells vs. 21 +/- 5 cells, respectively; P < .05). The thickness of the lamina propria (an index of interstitial edema) was also significantly increased in patients with OSA compared with controls (0.99 +/- 0.12 mm vs. 0.27 +/- 0.02 mm, respectively; P < 0.05). The authors conclude that inflammation, characterized by plasma cell infiltration and interstitial edema, is present in the uvula mucosa of patients with moderate OSA. They also suggest that soft palate inflammation contributes to upper airway occlusion observed during sleep in these patients.

Adult↗
PubMed1996

Human alveolar capillaries undergo angiogenesis in pulmonary veno-occlusive disease.

The bronchial circulation undergoes angiogenesis in several pathological conditions, such as lung neoplasm and bronchiectasis, but whether the pulmonary circulation can do this has been questioned. A woman treated with mitomycin C and 5-fluorouracil developed progressive, fatal pulmonary hypertension over 5 months. In addition to light and transmission electron microscopic examination of her lung, her pulmonary vasculature was cast and the casts were studied with scanning electron microscopy. Light microscopy showed that she had pulmonary veno-occlusive disease and angiomatoid capillary growth in the alveolar walls. Transmission electron microscopy confirmed the presence of pulmonary hypertension and showed thickened endothelial basement membrane. Scanning electron microscopy of the cast blood vessels showed distortion and destruction of alveolar capillaries prohibiting the passage of erythrocytes. Large new capillaries developed on top of, and were connected to, the shrivelled capillaries that made up the alveolar wall. The new capillaries were larger and fewer, which reduced the alveolar-capillary interface. Arteries and veins were irregularly narrowed and the veins had broad muscularity. Oedema was present, and the pulmonary lymphatics were extensively cast, especially in the lobular septa, but the lymphatics had a normal appearance. It appears that this patient suffered extensive capillary damage and venous occlusion and that the response was extensive new capillary formation, sometimes in angiomatoid configurations, and hypertrophy of pulmonary veins and arteries. Casting the microvasculature and viewing it with scanning electron microscopy identified new alveolar capillaries in this patient with acquired pulmonary hypertension.

Adult↗
PubMed1995

Carboxypeptidase M activity is increased in bronchoalveolar lavage in human lung disease.

Carboxypeptidase M (CPM) cleaves the C-terminal arginine and lysine of peptides; it is expressed in the lung, especially on the plasma membrane of alveolar type I cells. Here, we report on CPM in human bronchoalveolar lavage (BAL) collected from 69 patients and analyzed for activity, cell number and type, and protein level. Seventy-six percent of CPM activity, measured at pH 7.5 with 5-dimethylamino-naphthalene-1-sulfonyl-alanyl-arginine (Dansyl-Ala-Arg) substrate, was immunoprecipitated with polyclonal antibody to purified human enzyme. In patients without active lung disease, CPM activity in BAL was 7.69 (+/- 2.12) nmol/h/mg protein, but in patients with acute pneumonia, it was 29.25 (+/- 4.06) (p < 0.01). In patients with Pneumocystis carinii pneumonia, CPM activity was elevated to 26.00 (+/- 4.85) (p < 0.01) and in patients with lung cancer, to 30.95 (+/- 4.12) (p < 0.01). The activity was not associated with the cellular elements of BAL. The highest specific activity was in the large aggregate fraction of surfactant, which also contained the highest concentration of phosphorus. Transmission electron microscopy of this fraction revealed the presence of typical lamellar bodies and tubular myelin structures. The high CPM activity may stem from its induction and release in acute lung disease. In addition, CPM may be a marker of infection with certain pathogens and an indicator of type I cell injury in parenchymal lung diseases.

Alanine↗
PubMed1994

Spindle cell pseudotumors in the lungs due to Mycobacterium tuberculosis in a transplant patient.

A rare spindle cell pseudotumor in the skin, lymph nodes, and bone marrow has been previously reported in immunosuppressed transplant patients and patients with acquired immunodeficiency syndrome. All reported cases were caused by Mycobacterium avium-intracellulare or other nontuberculous mycobacteria. We are reporting spindle cell pseudotumors in the lungs caused by Mycobacterium tuberculosis. The patient had insulin-dependent diabetes mellitus and was status post cadaveric renal and pancreatic transplants. His hospital course was complicated by pulmonary tuberculosis due to M. tuberculosis. At autopsy, the lungs showed numerous bilateral gray nodules ranging from 0.2 to 2.5 cm. Microscopic examination uncovered a cellular proliferation composed of spindle cells arranged in fascicles. There were no granulomata. An acid-fast stain showed numerous acid-fast bacilli within the spindle cells. To our knowledge, this is the first case of spindle cell pseudotumor caused by M. tuberculosis of the lungs. Awareness of this unusual manifestation of mycobacterial infection in immunosuppressed patients underscores the need for acid-fast staining of biopsies with spindle cell proliferation even in the absence of overt granulomatous lesions in order to prevent misdiagnosis.

Adult↗
PubMed1992

The effect of transforming growth factor-alpha on airway angiogenesis.

A problem in lung transplantation is tracheal or bronchial dehiscence from ischemia. To determine if an angiogenic factor applied to the airway would improve capillary regrowth, a three-ring segment of trachea was completely severed and sutured in rats. In one group of animals the ischemic segment was wrapped with Gelfoam soaked in an angiogenic factor, transforming growth factor-alpha. In a second group the ischemic area was wrapped with Gelfoam soaked with only the vehicle. In a third group the devascularized area received no additional treatment. One animal from each group was killed daily for 7 days after operation. The tracheal vasculature was cast and viewed by light and scanning electron microscopy. None of the four animals that died early were in the transforming growth factor-alpha group. All animals lost weight between the day of operation and death, but this was least in the transforming growth factor-alpha group (p = 0.05). The light microscopy showed ischemic changes and the development of granulation tissue. The scanning electron microscopy of the vascular casts showed extensive loss of the vessels in the cut area. On day 1 the vessels of all animals dilated and their walls became rough. By day 3 a few corkscrew vessels penetrated the ischemic zone. By day 4 the animal that received transforming growth factor-alpha had more capillaries than the others. By day 6 revascularization in the transforming growth factor-alpha animal was abundant. Besides budding, new capillaries appeared to develop by lateral growth. After the fifth day vessels about 30 to 50 microns in diameter bulged focally. On the bulges, ridges the size, shape, and pattern of capillaries formed. Capillary formation in this manner has not been reported previously. Revascularization emerged sooner and more extensively with transforming growth factor-alpha. No adverse effect of transforming growth factor-alpha was found.

Animals↗
PubMedDate not supplied

Intrasplenic venous thrombosis: CT findings.

OBJECTIVE: To describe the CT findings of intrasplenic venous thrombosis in three cases. MATERIALS AND METHODS: Three adult patients had abdominal CT indicative of short-segment thrombosis of an intrasplenic blood vessel. Two patients underwent splenectomy; thrombosis of a segmental splenic vein was confirmed histologically in both cases. RESULTS: Segmental splenic vein thrombosis appeared on CT as a short, 1-2 cm, linear lucency surrounded by normal splenic parenchyma. The probable etiology of intrasplenic venous thrombosis was main splenic vein occlusion related to pancreatitis in two cases and splenic compression and inflammation by perisplenic abscess in the third case. CONCLUSION: Thrombosis of segmental intrasplenic veins is detectable with CT and can be a secondary CT finding of main splenic vein thrombosis.

Humans↗
PubMedDate not supplied

Thoracic blastomycosis and empyema.

Blastomycosis is endemic in river valley areas of the southeastern and Midwestern United States. Pulmonary manifestations include chronic cough and pleuritic pain. Radiographic appearance of the infection can mimic bronchogenic lung carcinoma. Pleural effusion is rarely associated with this pulmonary infection, and empyema has not been previously reported. We report a case of pulmonary and pleural Blastomyces dermatitidis infection presenting as empyema thoracis. Diagnosis and treatment were attained with video-assisted thoracoscopic (VATS) pleural and lung biopsy and debridement.

Adult↗
PubMedDate not supplied

Detection of neutral endopeptidase 24.11 (neprilysin) in human hepatocellular carcinomas by immunocytochemistry.

BACKGROUND: We have reported previously that neutral endopeptidase 24.11 (neprilysin; NEP; CALLA, CD10) activity was very high in rat hepatomas and a cultured human hepatocarcinoma cell line (SK-HEP1). MATERIALS AND METHODS: While continuing these studies, we detected the presence of NEP in SK-HEP 1 cells by immunocytochemistry and in paraffin-embedded human hepatocellular carcinomas as well. IgG purified from polyclonal antisera to human NEP was employed as a source of antibody. RESULTS: SK-HEP 1 cells gave a strong positive reaction to the IgG fraction of the antisera. In control studies, where IgG was preabsorbed with recombinant NEP, the results were negative. Of the 18 hepatocellular carcinomas tested, NEP was expressed in 14 (78%) malignant tumors, while adjacent liver tissue did not show the presence of NEP. CONCLUSIONS: It is suggested that, because none of the known hepatocellular carcinoma markers are highly specific, the detection of NEP in these malignant cells can be an additional useful diagnostic tool.

Adenocarcinoma↗