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Biomedical subjects

Cynthia Brown

Publications and source records attributed to Cynthia Brown.

14 recordsLinked to original sources
PubMed2005

Spiritual caring: end of life in a nursing home.

The purpose of this qualitative study was to explore spiritual care for dying nursing home residents from the perspectives of registered nurses, practical nurses, certified nursing assistants, advanced practice nurses, and physicians. Five major themes emerged: honoring the person's dignity, intimate knowing in the nursing home environment, wishing we could do more, personal knowing of self as caregiver, and struggling with end-of-life treatment decisions. Spiritual caring was described within the context of deep personal relationships, holistic care, and support for residents. Spiritual care responses and similarities and differences in the experiences of participants are presented. Education and research about how to assist residents and families as they struggle with difficult end-of-life decisions, adequate time and staff to provide the kind of care they "wished they could," and development of models that honor the close connection and attachment of staff to residents could enhance end-of-life care in this setting.

Adaptation, Psychological↗
PubMed2004

Cases from the Osler Medical Service at Johns Hopkins University.

A 47-year-old white woman with a history of stage III squamous cell carcinoma of the anus was transferred to Johns Hopkins Hospital for further evaluation of renal failure, hemolytic anemia, and thrombocytopenia. The patient was first diagnosed with squamous cell carcinoma of the anus 1 year before admission. She was treated with external beam radiation of the pelvis and two cycles of mitomycin C-based chemotherapy (a cumulative dose, 34 mg/m(2)). Her clinical course was complicated by Clostridium difficile colitis and myositis successfully treated with prednisone. Three months before admission, the patient developed dysuria. Her creatinine increased from normal to 1.7 mg/dL, and microscopic hematuria was present. A renal ultrasound and an abdominal computed tomographic scan showed no abnormalities or obstruction. One month before admission, she underwent a cystoscopy, which showed only radiation-induced changes in the bladder. Two weeks before admission, the patient became delirious and was taken to a hospital, where she was found to be anemic, with a hematocrit level of 23.7%, and thrombocytopenic with a platelet count of 110,000/mm(3). Her creatinine level was 5.9 mg/dL. Previous values of hematocrit, platelet count, and serum creatinine were normal. On admission at Johns Hopkins Hospital the patient had no complaints. She was afebrile on physical examination and had normal vital signs. Head, neck, chest, cardiovascular, and abdominal examinations were normal. There was skin pallor, but no echymoses or petechiae. She was alert and oriented with normal mental status. Her neurologic examination was normal. Laboratory data showed a white blood cell count of 6390/mm(3), a hematocrit level of 26.5%, and a platelet count of 26,000/mm(3). Her blood urea nitrogen level was 57 mg/dL, creatinine level was 4.0 mg/dL, and lactate dehydrogenase was 550 U/L (reference, 115 to 275 U/L). Urinalysis showed innumerable red blood cells and large protein. A peripheral blood smear showed fragmented red blood cells, schistocytes, no abnormal white blood cells, and few platelets. There was no radiographic or clinical evidence of relapse of her squamous cell carcinoma. What is the diagnosis?

Anemia, Hemolytic↗
PubMed2004

Pulmonary collectins modulate strain-specific influenza a virus infection and host responses.

Collectins are secreted collagen-like lectins that bind, agglutinate, and neutralize influenza A virus (IAV) in vitro. Surfactant proteins A and D (SP-A and SP-D) are collectins expressed in the airway and alveolar epithelium and could have a role in the regulation of IAV infection in vivo. Previous studies have shown that binding of SP-D to IAV is dependent on the glycosylation of specific sites on the HA1 domain of hemagglutinin on the surface of IAV, while the binding of SP-A to the HA1 domain is dependent on the glycosylation of the carbohydrate recognition domain of SP-A. Here, using SP-A and SP-D gene-targeted mice on a common C57BL6 background, we report that viral replication and the host response as measured by weight loss, neutrophil influx into the lung, and local cytokine release are regulated by SP-D but not SP-A when the IAV is glycosylated at a specific site (N165) on the HA1 domain. SP-D does not protect against IAV infection with a strain lacking glycosylation at N165. With the exception of a small difference on day 2 after infection with X-79, we did not find any significant difference in viral load in SP-A(-/-) mice with either IAV strain, although small differences in the cytokine responses to IAV were detected in SP-A(-/-) mice. Mice deficient in both SP-A and SP-D responded to IAV similarly to mice deficient in SP-D alone. Since most strains of IAV currently circulating are glycosylated at N165, SP-D may play a role in protection from IAV infection.

Animals↗
PubMed2002

Surfactant protein-A--deficient mice display an exaggerated early inflammatory response to a beta-resistant strain of influenza A virus.

Surfactant protein (SP)-A is a member of the collectin family of proteins. In vitro, SP-A binds influenza A virus (IAV), neutralizes infectivity, and enhances uptake by macrophages. SP-D also binds and neutralizes certain strains of IAV. To determine if SP-A has a role in protecting the intact animal against IAV infection, we inoculated gene-targeted SP-A-deficient mice (-/-) and littermate controls (+/+) with either saline or increasing doses of an IAV strain that binds SP-A but not SP-D. IAV was more virulent in SP-A-/- compared with +/+ mice, with a significantly lower mean lethal dose (LD(50)) and significantly greater weight loss during infection. SP-A-/- mice also had increased airway epithelial injury and more alveolar cellular infiltrates than +/+ mice. On Day 2, SP-A-/- mice had more neutrophils and higher MIP-2 levels in the lung than +/+ mice. We conclude the altered host response and increased susceptibility to X-79Delta167 infection in SP-A-/- mice reflects a protective role for SP-A in regulating the host response to IAV. Because the recovery of virus from lung homogenates on Days 2 and 6 after inoculation was comparable in -/- and +/+ mice, we speculate SP-A reduces IAV virulence independently of direct viral neutralization.

Animals↗
PubMed2002

Tissue distribution of surfactant proteins A and D in the mouse.

Surfactant proteins A and D, collagen-like lectins (collectins), were first isolated from the lung. In the lung, SP-A and SP-D have roles in surfactant homeostasis and innate immunity. In this study we show that SP-A and SP-D mRNA can be detected in a significant number of non-pulmonary tissues but the proteins have a more limited distribution. SP-D protein was detected in lung, uterus, ovary, and lacrimal gland, whereas SP-A protein was detected only in the lung. The results suggest that SP-D participates in mucosal immunity throughout the body.

Animals↗