Self-Stigma Experiences Among Older Adults with Mental Health Problems Residing in Long-Term Care Facilities: A Qualitative Study

ABSTRACT

Self-stigma is linked with a variety of deleterious consequences for the stigmatised individual. Much of the past research on self-stigma focuses on younger adults; however, little is known about the self-stigma experience among institutionalised older adults with mental health problems. This study aims to explore experiences of self-stigma among older adults with mental health problems in long-term care facilities. Ten semi-structured interviews were conducted. Insight into mental illness was identified as having a key influence upon the self-stigma experiences among this group. Participants shared common understandings, views, and behavioural reactions towards mental health problems. Lacking control, public stigma, sympathy, disinterest, avoidance, and fear were key themes among them. Re-conceptualising self-stigma theories and implementing interventions that aim at reducing stigmatising attitudes among this group are essential.     

Type I nitric oxide synthase in the human lung is predominantly expressed in capillary endothelial cells.

Nitric oxide (NO) has important functions in the regulation of pulmonary smooth muscle tone. In the human lung, published data on the expression and distribution of neuronal nitric oxide synthase (NOS-I) are contradictory. The aim of this study, therefore, was to determine the predominant cells expressing NOS-I in the human lung. Immunofluorescence double staining techniques were applied to normal human lung tissue using established monospecific antibodies directed against NOS-I. Suprisingly, capillary endothelial cells in the alveolar septa were identified as the major sites of NOS-I expression. Neither alveolar nor bronchiolar epithelium, nor the alveolar macrophages, expressed NOS-I. These results indicate that the predominant sites of NOS-I expression in the human lung are confined to non-neuronal, i.e. capillary endothelial cells and suggest a role for NO in the regulation of pulmonary endothelial cell permeability.     

The impact of symptom severity on the cost of Alzheimer's disease

OBJECTIVES: ITo examine the economic impact of Alzheimer's disease (AD) as the disease progresses on patients' medical costs and caregivers' productivity. DESIGN: A 12-page, self-administered mail survey, fielded in November 1999. SETTING: Households with AD caregivers, selected from a nationwide (U.S.) consumer database. PARTICIPANTS: One thousand seven hundred fifteen caregivers of noninstitutionalized AD patients. MEASUREMENTS: Disease progression was measured using a scale of symptom frequency and measures of instrumental and physical functioning. Cost components included hospital days, physician visits, and emergency room visits. Lost productivity was assessed using hours per week that caregivers provided care and the number of days that they missed from work because of caregiving. RESULTS: The direct costs of caring for AD patients for 6 months totaled $3,129, whereas the indirect costs were $26,080. Patients with more-frequent symptoms used all healthcare resources, including the hospital, emergency room, and physicians, more often than those with less-frequent symptoms. Those with lower levels of physical and instrumental functioning also used the hospital and physicians more often than those with higher levels of physical and instrumental functioning. Caregivers of these more severely impaired patients spent more hours providing care and reported missing more work than those caring for higher-functioning patients. These relationships remained after controlling for potentially confounding factors. CONCLUSIONS: This large study of patients at all stages of AD shows that the direct and indirect costs of AD are considerably lower for patients with fewer symptoms. Longitudinal studies will determine the impact on the overall cost of care of interventions that reduce symptoms and maintain patients at earlier stages of the disease.     

Surgical treatment of haemorrhoids with the use of the circular stapler and open haemorrhoidectomy. A comparative study

The surgical treatment of haemorrhoids with the use of a circular stapler is a novel method. A comparative retrospective study of two groups of patients treated surgically for third- and fourth-degree haemorrhoids was conducted. Fifty patients (group A) underwent a surgical intervention with the circular stapler in the rectal mucosa 4 cm above the dentate line. In another group of 50 patients (group B), the standard open haemorrhoidectomy (Milligan-Morgan) was carried out. The new method (group A) compared with the standard haemorrhoidectomy (group B) was found to be less time consuming (mean time, 10±2 minutes vs. 35±5 minutes, p<0.001). The majority of patients (28) in group A experienced mild pain (VAS, 3–5) while pain for the majority of patients in group B was 5–7 on the VAS scale (p<0.01). The duration of postoperative hospitalisation was 1±1 days for the patients of group A and 5±2 days for the patients of group B (p<0.05). The early postoperative bleeding rate was 6% in group A and 12% in group B (p<0.01). None of the patients of group A developed incontinence and 6 (12%) patients in group B developed mild liquid incontinence during the first postoperative month. During the period of follow-up (12 months to 3 years, median length 18 months in outpatient visits), no patient in either group developed recurrence of haemorrhoids or rectal prolapse. In conclusion, the surgical treatment of haemorrhoids with the circular stapler seems to be an efficient alternative to the standard open haemorrhoidectomy when this is indicated. Received: 28 April 2000 / Accepted in revised form: 18 October 2000     

Portal and peripheral vein concentrations of insulin and glucagon after arginine infusion in morbidly obese subjects

Five morbidly obese subjects with fasting normoglycemia underwent catheterization of portal and peripheral veins immediately prior to jejunoileal bypass surgery. Levels of immunoreactive insulin (IRI), immunoreactive glucagon (IRG), and glucose were determined in simultaneously obtained serum samples before and after infusion of arginine. Portal levels exceeded peripheral levels by at least 50% with IRI and by 30%–40% with IRG. These results were similar to those reported in nonobese subjects and show that in morbid obesity as well as in nonobese states, peripheral insulin to glucagon molar ratios ($\text{I}\text{G}$) underestimate portal $\text{I}\text{G}$. Although hepatic extraction was not specifically measured, the data suggest that the peripheral levels of insulin and glucagon reported in morbid obesity result from alterations in secretion and not altered extraction.     

Defective glycosylation of coagulation factor XII underlies hereditary angioedema type III

Hereditary angioedema type III (HAEIII) is a rare inherited swelling disorder that is associated with point mutations in the gene encoding the plasma protease factor XII (FXII). Here, we demonstrate that HAEIII-associated mutant FXII, derived either from HAEIII patients or recombinantly produced, is defective in mucin-type Thr309-linked glycosylation. Loss of glycosylation led to increased contact-mediated autoactivation of zymogen FXII, resulting in excessive activation of the bradykinin-forming kallikrein-kinin pathway. In contrast, both FXII-driven coagulation and the ability of C1-esterase inhibitor to bind and inhibit activated FXII were not affected by the mutation. Intravital laser-scanning microscopy revealed that, compared with control animals, both F12^–/– mice reconstituted with recombinant mutant forms of FXII and humanized HAEIII mouse models with inducible liver-specific expression of Thr309Lys-mutated FXII exhibited increased contact-driven microvascular leakage. An FXII-neutralizing antibody abolished bradykinin generation in HAEIII patient plasma and blunted edema in HAEIII mice. Together, the results of this study characterize the mechanism of HAEIII and establish FXII inhibition as a potential therapeutic strategy to interfere with excessive vascular leakage in HAEIII and potentially alleviate edema due to other causes.     

Gastrocolic fistula secondary to nonsteroidal anti-inflammatory drugs abuse in a cirrhotic patient

Gastrocolic fistula is rarely described in the literature. It has been associated with a variety of diseases and recently with benign gastric ulcers related to the use of nonsteroidal anti-inflammatory drugs (NSAIDs'). The present case represents the first report of gastrocolic fistula due to NSAIDs in a cirrhotic patient. This is in keeping with the established knowledge that cirrhotic patients constitute a high-risk group of patients when treated with NSAIDs'. Review of the literature shows that this condition warrants a complete diagnostic work-up to exclude more ominous underlined diseases.