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Dive into the research topics where Edith Umland is active.

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Featured researches published by Edith Umland.


The New England Journal of Medicine | 1994

Hantavirus Pulmonary Syndrome: A Clinical Description of 17 Patients with a Newly Recognized Disease

Jeffrey S. Duchin; Frederick Koster; Clarence J. Peters; Gary Simpson; Bruce Tempest; Sherif R. Zaki; Thomas G. Ksiazek; Pierre E. Rollin; Stuart T. Nichol; Edith Umland; Ronald L. Moolenaar; Susan E. Reef; Kurt B. Nolte; Margaret M. Gallaher; Jay C. Butler; Robert F. Breiman

Background In May 1993 an outbreak of severe respiratory illness occurred in the southwestern United States. A previously unknown hantavirus was identified as the cause. In Asia hantaviruses are associated with hemorrhagic fever and renal disease. They have not been known as a cause of human disease in North America. Methods We analyzed clinical, laboratory, and autopsy data on the first 17 persons with confirmed infection from this newly recognized strain of hantavirus. Results The mean age of the patients was 32.2 years (range, 13 to 64); 61 percent were women, 72 percent were Native American, 22 percent white, and 6 percent Hispanic. The most common prodromal symptoms were fever and myalgia (100 percent), cough or dyspnea (76 percent), gastrointestinal symptoms (76 percent), and headache (71 percent). The most common physical findings were tachypnea (100 percent), tachycardia (94 percent), and hypotension (50 percent). The laboratory findings included leukocytosis (median peak cell count, 26,000 per cu...


Human Pathology | 1995

Hantavirus pulmonary syndrome in the United States: A pathological description of a disease caused by a new agent

Kurt B. Nolte; Richard M. Feddersen; Kathy Foucar; Sherif R. Zaki; Frederick Koster; Dean Madar; Toby L Merlin; Patricia J. McFeeley; Edith Umland; Ross E. Zumwalt

An outbreak of an acute respiratory disease in the southwestern United States has led to the recognition of a new hantaviral illness. This report describes a unique spectrum of antemortem and postmortem pathological findings seen in a case series of nine surviving patients and 13 who died. Clinical, laboratory, and autopsy findings were derived from a consecutive series of individuals confirmed to have hantavirus pulmonary syndrome. Laboratory studies included chemical, hematological, and bone marrow analyses as well as flow cytometric and immunohistochemical phenotyping. Autopsy tissues were examined by routine histological stains, immunohistochemical methods, and transmission electron microscopy. The lung is the primary target organ in this illness. Pulmonary abnormalities include pleural effusions, alveolar edema and fibrin, and an interstitial mononuclear cell infiltrate. Large immunoblast type cells are seen in the lungs, blood, bone marrow, lymph nodes, liver, and spleen. A tetrad of hematological findings includes left-shifted neutrophilic leukocytosis, thrombocytopenia, hemoconcentration in severe cases, and circulating immunoblasts. In contrast to previously described nephropathic hantaviral syndromes, hantavirus pulmonary syndrome is characterized by a unique constellation of pulmonary, hematological, and reticuloendothelial pathological findings. The pulmonary findings are distinguishable from fatal adult respiratory distress syndrome. The data suggest a capillary leak syndrome restricted to the pulmonary circulation. Likewise, the hematological picture is unique and may be valuable in the rapid identification of cases for further diagnostic studies.


Journal of Pediatric Surgery | 1986

Comparative efects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis

Catherine A. Musemeche; Ann M. Kosloske; Sue A. Bartow; Edith Umland

This study was undertaken to evaluate the relative contribution of ischemia, bacteria, and luminal substrate, the pathogenetic components of necrotizing enterocolitis (NEC), to the development of intestinal necrosis. Sprague-Dawley rats, either germ-free (No. = 25) or conventionally colonized (No. = 20) underwent laparotomy. Isolated ileal segments were created, two per rat. Ischemia was produced in one segment by application of a microaneurysm clip; the other segment served as a control. Segments were injected with 1 mL of either normal saline, dilute Similac formula, or standard formula. Groups were as follows: Group I (germ-free), received saline; Group II (germ-free), dilute formula; Group III (germ-free), standard formula; Group IV (conventional), saline; Group V (conventional), dilute formula; Group VI (conventional), standard formula. At 48 hours, the rats were evaluated for survival, gross bowel integrity, histologic severity of necrosis (graded 0 to 4+), and bacteriology. Gross analysis of bowel integrity showed no lesions in the ischemic segments of the germ-free rats (Groups I, II, and III) and necrosis in 75% of conventionally colonized animals (Groups IV, V, and VI; P less than 0.001). Microscopic necrosis was more common (P less than 0.001) in ischemic segments of conventional rats than in ischemic segments of germ-free rats. There was no difference in necrosis attributable to ischemic time or to the presence of either standard or dilute formula. Of the three pathogenetic factors evaluated, the presence of bacteria was most crucial to the development of bowel necrosis in this model. Improved treatment and prevention of NEC may depend upon suppression and/or modification of the gut flora.


Journal of Pediatric Surgery | 1985

Clostridial necrotizing enterocolitis

Ann M. Kosloske; William S. Ball; Edith Umland; Betty Skipper

In a bacteriologic investigation of infants with necrotizing enterocolitis (NEC), 16 of 50 infants had clostridia in cultures of blood or of peritoneal fluid obtained by paracentesis. Twenty-eight of the 50 infants had enteric bacteria other than clostridia, and six infants had sterile cultures. Of the 16 infants with clostridia, nine had C. perfringens and seven had other species of clostridia. Compared to infants with nonclostridial NEC, those with clostridial NEC were larger and more mature, had more extensive pneumatosis intestinalis and gangrene and more rapid progression of NEC. The nine infants with C. perfringens had a fulminant form of NEC, analogous to gas-gangrene of the intestine. Mortality in this group was 78% (7/9). The seven infants with clostridial species other than C. perfringens had a mortality comparable to that of infants with nonclostridial NEC (32%). Improved survival from NEC associated with C. perfringens may be possible only by prevention, rather than earlier diagnosis and improved heroic treatment.


IEEE Engineering in Medicine and Biology Magazine | 2004

Setting standards for improved syndromic surveillance

D. W. Forslund; Edward L. Joyce; Tom Burr; Richard R. Picard; Doug Wokoun; Edith Umland; Judith Brillman; Philip Froman; Fred Koster

Clearly, there is a need for data at multiple levels and many locations. Investigations of possible cases and outbreaks must occur locally, and local data must be available as generated to healthcare providers and emergency responders. At the same time, regional, national and international authorities need aggregated data to understand the scope of an outbreak and to assist in the response. Thus, in comparison to a system in which data is sent to a central facility for aggregation and redistributed to local areas, we argue that a distributed system is much more appropriate and resilient to a bioterrorism event. The distributed data system can provide information to local responders for their immediate action and reduce demand on a central system and data unavailability over wide area networks while providing raw data immediately to centralized reviewers.


Pediatric Surgery International | 1988

Acute abdominal emergencies associated with cytomegalovirus infection in the young infant

Ann M. Kosloske; Patrick F. Jewell; Alfred L. Florman; Edith Umland

Gastrointestinal signs and symptoms have rarely been reported in association with cytomegalovirus (CMV) infection in young infants. However, in 1981 clear pathologic evidence was presented implicating this virus as a cause of hypoganglionosis and bowel dysmotility. We report our experience with four infants with CMV infection in whom gastrointestinal dysfunction was the reason for emergency abdominal operation. Since the association was made retrospectively, we were unable to demonstrate hypoganglionosis, but our experience underscores the need to include CMV intestinal infection in the differential diagnosis of the acute surgical abdomen in young infants.


Clinical Infectious Diseases | 1995

Clinical Features That Differentiate Hantavirus Pulmonary Syndrome from Three Other Acute Respiratory Illnesses

Ronald L. Moolenaar; Craig Dalton; Harvey B. Lipman; Edith Umland; Margaret M. Gallaher; Jeffrey S. Duchin; Louisa E. Chapman; Sherif R. Zaki; Thomas G. Ksiazek; Pierre E. Rollin; Stuart T. Nichol; James E. Cheek; Jay C. Butler; Clarence J. Peters; Robert F. Breiman


BMC Medical Informatics and Decision Making | 2005

Modeling emergency department visit patterns for infectious disease complaints: results and application to disease surveillance

Judith Brillman; Tom Burr; D. W. Forslund; Edward L. Joyce; Richard R. Picard; Edith Umland


Clinical Infectious Diseases | 1996

Evidence against person-to-person transmission of hantavirus to health care workers

Charles Vitek; Robert F. Breiman; Thomas G. Ksiazek; Pierre E. Rollin; James C. McLaughlin; Edith Umland; Kurt B. Nolte; Arnold Loera; C. Mack Sewell; Clarence J. Peters


american medical informatics association annual symposium | 2001

The Rapid Syndrome Validation Project (RSVP).

Al Zelicoff; Judith Brillman; D. W. Forslund; James E. George; Sandra Zink; Sascha Koenig; Torsten Staab; Gary Simpson; Edith Umland; Kevin Bersell

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Clarence J. Peters

Centers for Disease Control and Prevention

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D. W. Forslund

Los Alamos National Laboratory

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Pierre E. Rollin

Centers for Disease Control and Prevention

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Thomas G. Ksiazek

University of Texas Medical Branch

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Edward L. Joyce

Los Alamos National Laboratory

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Richard R. Picard

Los Alamos National Laboratory

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Tom Burr

Los Alamos National Laboratory

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Ann M. Kosloske

Boston Children's Hospital

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