The main objective of the report is to review the evidence on the impact of health information technology (IT) that supports patient-centered care (PCC) on: health care processes; clinical outcomes; ...intermediate outcomes (patient or provider satisfaction, health knowledge and behavior, and cost); responsiveness to needs and preferences of patients; shared decisionmaking and patient-clinician communication; and access to information. Additional objectives were to identify barriers and facilitators for using health IT to deliver PCC, and to identify gaps in evidence and information needed by patients, providers, payers, and policymakers.
MEDLINE®, Embase®, Cochrane Library, Scopus, Cumulative Index to Nursing and Allied Health Literature, PsycINFO, INSPEC, and Compendex databases through July 31, 2010.
Paired members of our team reviewed citations to identify randomized controlled trials of PCC-related health IT interventions and studies that addressed barriers and facilitators for health IT for delivery of PCC. Independent assessors rated studies for quality. Paired reviewers abstracted data.
The search identified 327 eligible articles, including 184 articles on the impact of health IT applications implemented to support PCC and 206 articles addressing barriers or facilitators for such health IT applications. Sixty-three articles addressed both questions. The study results suggested positive effects of PCC-related health IT interventions on health care process outcomes, disease-specific clinical outcomes (for diabetes mellitus, heart disease, cancer, and other health conditions), intermediate outcomes, responsiveness to the needs and preferences of patients, shared decisionmaking, patient-clinician communication, and access to medical information. Studies reported a number of barriers and facilitators for using health IT applications to enable PCC. Barriers included: lack of usability; problems with access to the health IT application due to older age, low income, education, cognitive impairment, and other factors; low computer literacy in patients and clinicians; insufficient basic formal training in health IT applications; physicians' concerns about more work; workflow issues; problems related to new system implementation, including concerns about confidentiality of patient information; depersonalization; incompatibility with current health care practices; lack of standardization; and problems with reimbursement. Facilitators for the utilization of health IT included ease of use, perceived usefulness, efficiency of use, availability of support, comfort in use, and site location.
Despite marked heterogeneity in study characteristics and quality, substantial evidence exists confirming that health IT applications with PCC-related components have a positive effect on health care outcomes. positive effect on health care outcomes.
Venous thromboembolism (VTE) is a frequent cause of preventable harm among hospitalized patients. Many prescribed prophylaxis doses are not administered despite supporting evidence. We previously ...demonstrated a patient-centered education bundle improved VTE prophylaxis administration broadly; however, patient-specific factors driving nonadministration are unclear. We examine the effects of the education bundle on missed doses of VTE prophylaxis by sex.
We performed a post-hoc analysis of a nonrandomized controlled trial to evaluate the differences in missed doses by sex. Pre-intervention and intervention periods for patients admitted to 16 surgical and medical floors between 10/2014-03/2015 (pre-intervention) and 04/2015-12/2015 (intervention) were compared. We examined the conditional odds of (1) overall missed doses, (2) missed doses due to patient refusal, and (3) missed doses for other reasons.
Overall, 16,865 patients were included (pre-intervention 6853, intervention 10,012), with 2350 male and 2460 female patients (intervention), and 6373 male and 5682 female patients (control). Any missed dose significantly reduced on the intervention floors among male (odds ratio OR 0.55; 95% confidence interval CI, 0.44-0.70, P < 0.001) and female (OR 0.59; 95% CI, 0.47-0.73, P < 0.001) patients. Similar significant reductions ensued for missed doses due to patient refusal (P < 0.001). Overall, there were no sex-specific differences (P-interaction >0.05).
Our intervention increased VTE prophylaxis administration for both female and male patients, driven by decreased patient refusal. Patient education should be applicable to a wide range of patient demographics representative of the target group. To improve future interventions, quality improvement efforts should be evaluated based on patient demographics and drivers of differences in care.
Obesity is associated with immune cell infiltration and inflammation in metabolic tissues that contributes to insulin resistance. Pattern recognition receptors (PRRs) link obesity-induced ...inflammation and insulin resistance. Nucleotide oligomerization domain protein 2 (NOD2) is a PRR that detects muramyl dipeptide (MDP) present in the cell walls of all bacteria. NOD2 mutations are associated with inflammatory bowel disease, and NOD2 activation with MDP can ameliorate the inflammatory effects of experimental colitis in mice. Our lab has linked NOD2 immunity with metabolism and found that NOD2 deficiency exacerbates obesity-induced inflammation and insulin resistance. We sought to determine if NOD2 activation with MDP confers anti-inflammatory effects during acute bacterial or chronic dietary stress. We have found that MDP has anti-inflammatory and insulin sensitizing effects in mice during bacterial stress and diet-induced obesity.
Mice were fed a chow or high fat diet (HFD; 60% kcal from fat) for 5weeks. MDP (100ug) or LPS (0.2mg/kg) was administered i.p. as indicated. Glucose and insulin tolerance tests, and hyperinsulinemic-euglycemic clamps were performed in 6h-fasted conscious mice. Tissues were immediately collected and frozen in liquid nitrogen. Gene expression was determined by RT-PCR with TaqMan assays.
Mice that received MDP prior to LPS challenge had increased glucose tolerance, reduced glucose-stimulated insulin secretion, and increased suppression of hepatic glucose production during hyperinsulinemic-euglycemic clamps. Mice that received MDP throughout a HFD were more glucose and insulin tolerant, experienced less hepatic insulin resistance during clamps, and had lower expression of many inflammatory markers in adipose and liver tissues.
NOD2 activation improves glucose homeostasis during acute bacterial stress and reduces inflammation and metabolic defects associated with diet-induced obesity.
Abstract
Pattern recognition receptors link metabolite and bacteria‐derived inflammation to insulin resistance during obesity. We demonstrate that
NOD
2 detection of bacterial cell wall peptidoglycan ...(
PGN
) regulates metabolic inflammation and insulin sensitivity. An obesity‐promoting high‐fat diet (
HFD
) increased
NOD
2 in hepatocytes and adipocytes, and
NOD
2
−/−
mice have increased adipose tissue and liver inflammation and exacerbated insulin resistance during a
HFD
. This effect is independent of altered adiposity or
NOD
2 in hematopoietic‐derived immune cells. Instead, increased metabolic inflammation and insulin resistance in
NOD
2
−/−
mice is associated with increased commensal bacterial translocation from the gut into adipose tissue and liver. An intact
PGN
‐
NOD
2 sensing system regulated gut mucosal bacterial colonization and a metabolic tissue dysbiosis that is a potential trigger for increased metabolic inflammation and insulin resistance. Gut dysbiosis in
HFD
‐fed
NOD
2
−/−
mice is an independent and transmissible factor that contributes to metabolic inflammation and insulin resistance when transferred to
WT
, germ‐free mice. These findings warrant scrutiny of bacterial component detection, dysbiosis, and protective immune responses in the links between inflammatory gut and metabolic diseases, including diabetes.
Synopsis
image
Nutritional and bacterial cues engage the immune system during the chronic inflammation associated with obesity, which could lead to insulin resistance. An intact
NOD
2‐peptidoglycan sensing system prevents excessive dysbiosis‐related inflammation and insulin resistance during obesity.
NOD
2 in non‐hematopoietic cells protects against obesity‐induced inflammation and insulin resistance.
NOD
2 limits accumulation of bacterial markers and inflammation of adipose and liver tissues during obesity.
The microbiota of
NOD
2‐deficient mice contributes to metabolic inflammation and insulin resistance.
Obesity is associated with inflammation that can drive metabolic defects such as hyperlipidemia and insulin resistance. Specific metabolites can contribute to inflammation, but nutrient intake and ...obesity are also associated with altered bacterial load in metabolic tissues (i.e. metabolic endotoxemia). These bacterial cues can contribute to obesity-induced inflammation. The specific bacterial components and host receptors that underpin altered metabolic responses are emerging. We previously showed that Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) activation with bacterial peptidoglycan (PGN) caused insulin resistance in mice. We now show that PGN induces cell-autonomous lipolysis in adipocytes via NOD1. Specific bacterial PGN motifs stimulated lipolysis in white adipose tissue (WAT) explants from WT, but not NOD1-/- mice. NOD1-activating PGN stimulated mitogen activated protein kinases (MAPK),protein kinase A (PKA), and NF- Kappa B in 3T3-L1 adipocytes. The NOD1-mediated lipolysis response was partially reduced by inhibition of ERK1/2 or PKA alone, but not c-Jun N-terminal kinase (JNK). NOD1-stimulated lipolysis was partially dependent on NF- Kappa B and was completely suppressed by inhibiting ERK1/2 and PKA simultaneously or hormone sensitive lipase (HSL). Our results demonstrate that bacterial PGN stimulates lipolysis in adipocytes by engaging a stress kinase, PKA, NF- Kappa B-dependent lipolytic program. Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to hyperlipidemia, systemic inflammation and insulin resistance by acting directly on adipocytes.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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