Multi-Morbidity in Hospitalised Older Patients: Who Are the Complex Elderly?

Background

No formal definition for the “complex elderly” exists; moreover, these older patients with high levels of multi-morbidity are not readily identified as such at point of hospitalisation, thus missing a valuable opportunity to manage the older patient appropriately within the hospital setting.

Objectives

To empirically identify the complex elderly patient based on degree of multi-morbidity.

Design

Retrospective observational study using administrative data.

Setting

English hospitals during the financial year 2012–13.

Subjects

All admitted patients aged 65 years and over.

Methods

By using exploratory analysis (correspondence analysis) we identify multi-morbidity groups based on 20 target conditions whose hospital prevalence was ≥ 1%.

Results

We examined a total of 2788900 hospital admissions. Multi-morbidity was highly prevalent, 62.8% had 2 or more of the targeted conditions while 4.7% had six or more. Multi-morbidity increased with age from 56% (65-69yr age-groups) up to 67% (80-84yr age-group). The average multi-morbidity was 3.2±1.2 (SD). Correspondence analysis revealed 3 distinct groups of older patients. Group 1 (multi-morbidity ≤2), associated with cancer and/or metastasis; Group 2 (multi-morbidity of 3, 4 or 5), associated with chronic pulmonary disease, lung disease, rheumatism and osteoporosis; finally Group 3 with the highest level of multi-morbidity (≥6) and associated with heart failure, cerebrovascular accident, diabetes, hypertension and myocardial infarction.

Conclusions

By using widely available hospital administrative data, we propose patients in Groups 2 and 3 to be identified as the complex elderly. Identification of multi-morbidity patterns can help to predict the needs of the older patient and improve resource provision.     

Brain Evolution: Getting Better All the Time?

Recent studies on bats, goats and hominids suggest that some mammalian brains may have undergone dramatic evolutionary reductions in size. These studies emphasise the importance of selective pressures upon mammalian brain evolution and the need to integrate studies of neuroanatomy, neurophysiology and behaviour.     

Vitamin D Deficiency in Children with a Chronic Illness–Seasonal and Age-Related Variations in Serum 25-hydroxy Vitamin D Concentrations

Introduction

Children and adolescents with a chronic illness have potential risk factors for vitamin D deficiency. An optimal vitamin D status might have multiple health effects. This study evaluated vitamin D status and its association with age, gender, and season in a large cohort of chronically ill Finnish patients at a tertiary pediatric outpatient clinic. A cross-sectional register-based study was carried out, involving altogether 1351 children (51% boys, age range 0.2–18 years), who visited the outpatient clinic during 2007–2010 and had their vitamin D status (S-25-OHD) determined. A post-doc analysis was conducted to identify predisposing and preventing factors for vitamin D deficiency.

Results

Almost half (47%) of the S-25-OHD values were consistent with subnormal vitamin D status (S-25-OHD <50 nmol/L) while only 12% were >80 nmol/L. Age and season were the most important determinants for S-25-OHD concentration. Mean S-25-OHD concentration differed between age groups (Kruskal-Wallis; p<0.001), adolescents being at highest risk for vitamin D insufficiency. Young age and vitamin D supplementation were preventive factors for deficiency, while non-Finnish ethnic background was a predisposing factor. S-25-OHD showed significant seasonal variation in children older than 6 years. In the whole cohort, S-25-OHD was on average 13 nmol/L higher in summer than in winter, and the prevalence of vitamin D deficiency ( =  S-25-OHD <37.5 nmol/l) varied from 11% in summer to 29% in winter.

Conclusions

The finding that almost half of the studied Finnish children with a chronic illness had suboptimal vitamin D status is alarming. Inferior vitamin D status was noted in adolescents compared with younger children, suggesting that imbalance between intake and requirement evolves with age. Although less common during summer, subnormal vitamin D status was still observed in 28% of those evaluated in summer. Clinicians should identify individuals at risk and actively recommend vitamin D supplementation.     

Does Cognitive Function Increase over Time in the Healthy Elderly?

Background

In dementia screening, most studies have focused on early cognitive impairment by comparing patients suffering from mild dementia or mild cognitive impairment with normal subjects. Few studies have focused on modifications over time of the cognitive function in the healthy elderly. The objective of the present study was to analyze the cognitive function changes of two different samples, born > 15 years apart.

Method

A first sample of 204 cognitively normal participants was recruited in the memory clinic of Broca hospital between 1991 and 1997. A second sample of 177 cognitively normal participants was recruited in 2008–2009 in the same institution. Both samples were from the same districts of Paris and were assessed with the same neuropsychological test battery. Mean cognitive test scores were compared between 1991 and 2008 samples, between < 80 years old and ≥ 80 years old in 1991 and 2008 samples, and finally between subjects < 80 year old of 1991 sample and subjects ≥ 80 years old of the 2008 sample. Means were compared with T-tests stratified on gender, age-groups and educational level.

Results

Cognitive scores were significantly higher in the 2008 sample. Participants < 80 years old outperformed those ≥ 80 in both samples. However, participants < 80 years old in 1991 sample and subjects ≥ 80 in the 2008 sample, born on average in 1923, performed mostly identically.

Conclusion

This study showed a significant increase of cognitive scores over time. Further, contemporary octogenarians in the later sample performed like septuagenarians in the former sample. These findings might be consistent with the increase in life expectancy and life span in good health. The study highlights the necessity to take into account factors which may contaminate and artificially inflate the age-related differences in favor of younger to the older adults.     

Are Human and Mouse Satellite Cells Really the Same?

Satellite cells are quiescent cells located under the basal lamina of skeletal muscle fibers that contribute to muscle growth, maintenance, repair, and regeneration. Mouse satellite cells have been shown to be muscle stem cells that are able to regenerate muscle fibers and self-renew. As human skeletal muscle is also able to regenerate following injury, we assume that the human satellite cell is, like its murine equivalent, a muscle stem cell. In this review, we compare human and mouse satellite cells and highlight their similarities and differences. We discuss gaps in our knowledge of human satellite cells, compared with that of mouse satellite cells, and suggest ways in which we may advance studies on human satellite cells, particularly by finding new markers and attempting to re-create the human satellite cell niche in vitro. (J Histochem Cytochem 58:941–955, 2010)     

Plasmodesmata the Nano Bridges in Plant Cell: Are the Answer for All the Developmental Processes?

Russian Journal of Plant Physiology - Plants establish tiny, cellular signaling pathways playing a unique coordination role in growth and development. Plasmodesmata are playing a central role in...     

Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

A preponderance of evidence supports a role for vitamin D beyond the classical function in mineral homeostasis. Epidemiologic investigations have revealed a beneficial role of vitamin D in muscle function, cardiovascular health, diabetes, and cancer prevention. More recently, studies have suggested a potential beneficial role of vitamin D in cognitive function. Vitamin D exhibits functional attributes that may prove neuroprotective through antioxidative mechanisms, neuronal calcium regulation, immunomodulation, enhanced nerve conduction and detoxification mechanisms. Compelling evidence supports a beneficial role for the active form of vitamin D in the developing brain as well as in adult brain function. The vitamin D receptor and biosynthetic and degradative pathways for the hydroxylation of vitamin D have been found in the rodent brain; more recently these findings have been confirmed in humans. The vitamin D receptor and catalytic enzymes are colocalized in the areas of the brain involved in complex planning, processing, and the formation of new memories. These findings potentially implicate vitamin D in neurocognitive function.     

All the eggs in one basket: Are island refuges securing an endangered passerine?

Refuges for threatened species are important to prevent species extinction. They provide protection from a range of environmental and biotic stressors, and ideally provide protection against all threatening processes. However, for some species it may not be clear why some areas are refuges and others are not. The forty‐spotted pardalote (Pardalotus quadragintus) is an endangered, sedentary, cryptic and specialised bird endemic to the island of Tasmania, Australia. Having undergone an extreme range contraction over the past century the species is now mostly confined to a few small offshore island refuges. Key threatening processes to the species include habitat loss, wildfire, competition and predation. The ways in which these processes have molded the species’ contemporary range have not been clearly evaluated. Furthermore, the security of the remnant population within refuges is uncertain. To overcome this uncertainty we assessed key threats and established the population status in known refuges by developing a robust survey protocol within an occupancy modelling framework. We discuss our results in the context of planning trial reintroductions of this endangered species in suitable habitat across its former range. We found very high occupancy rates (0.75–0.96) at two refuges and in suitable conditions, the species was highly detectable (p, 0.43–0.77). At a third location our surveys indicated a local extinction, likely due to recent wildfire. We demonstrate that all refuges are at high risk of one or more threatening processes and the current distribution across island refuges is unlikely to secure the species from extinction. We identified large areas of potential habitat across the species’ former mainland range, but these are likely too distant from source populations for natural recolonisation. We propose that establishing new populations of forty‐spotted pardalotes via reintroduction is essential to secure the species and that this is best achieved while robust source populations still exist.     

Of Mice and Men: Not ExAKTly the Same?

The serine-threonine protein kinase Akt2, also known as PKBβ, has been shown to regulate glucose and lipid metabolism in animal models. In a recent study published in Science, Hussain et al. (2011) report that in human subjects an activating mutation of Akt2 leads to hypoglycemia and, unexpectedly, asymmetric overgrowth.     

Is Vitamin D the Fountain of Youth?

ObjectiveTo review the role of vitamin D deficiency for both classic and “nonclassic” effects and raise the caution that association does not prove causation.MethodsThe pertinent literature regarding vitamin D and its effects on bone, muscle function, immune function, glucose tolerance, cancer risk, and development of cardiovascular disease and other conditions is reviewed. In addition, the limitations of observational studies are discussed.ResultsVitamin D inadequacy is common worldwide and classically causes osteomalacia and rickets. More recently, the contribution of low vitamin D status to increased falls and fracture risk has become appreciated. Additionally, nonclassic effects of vitamin D inadequacy are being recognized, and low vitamin D status is being potentially associated with a multitude of conditions (including Alzheimer disease, osteoarthritis, multiple sclerosis, and hypertension) and higher overall mortality. It is important to recognize that associations in observational studies can be due to chance, bias, or confounders or may be indicative of causality.ConclusionBecause vitamin D deficiency has been established to have adverse musculoskeletal consequences, optimization of vitamin D status, for both the individual patient and the overall population, is indicated. (Endocr Pract. 2009;15:590-596)     

Are Rod Outer Segment ATP-ase and ATP-Synthase Activity Expression of the Same Protein?

Vertebrate retinal rod outer segments (OS) consist of a stack of disks surrounded by the plasma membrane, where phototransduction takes place. Energetic metabolism in rod OS remains obscure. Literature described a so-called Mg²⁺-dependent ATPase activity, while our previous results demonstrated the presence of oxidative phosphorylation (OXPHOS) in OS, sustained by an ATP synthetic activity. Here we propose that the OS ATPase and ATP synthase are the expression of the same protein, i.e., of F₁F_o-ATP synthase. Imaging on bovine retinal sections showed that some OXPHOS proteins are expressed in the OS. Biochemical data on bovine purified rod OS, characterized for purity, show an ATP synthase activity, inhibited by classical F₁F_o-ATP synthase inhibitors. Moreover, OS possess a pH-dependent ATP hydrolysis, inhibited by pH values below 7, suggestive of the functioning of the inhibitor of F1 (IF1) protein. WB confirmed the presence of IF1 in OS, substantiating the expression of F₁F_o ATP synthase in OS. Data suggest that the OS F₁Fo ATP synthase is able to hydrolyze or synthesize ATP, depending on in vitro or in vivo conditions and that the role of IF1 would be pivotal in the prevention of the reversal of ATP synthase in OS, for example during hypoxia, granting photoreceptor survival.     

Vitamin D deficiency: concern for rheumatoid arthritis and COVID-19?

Vitamin D is an immunomodulatory hormone with an established role in calcium and phosphate metabolism and skeletal mineralization. Evidence showing its immunological benefits by regulating essential components of the innate and adaptive immune system is prevalent. Vitamin D deficiency is reported worldwide and is thereby found to be associated with various immune-related diseases. Rheumatoid Arthritis and COVID-19 are two such diseases, sharing a similar hyperinflammatory response. Various studies have found an association of lower Vitamin D levels to be associated with both these diseases. However, contrasting data is also reported. We review here the available scientific data on risk factor association and supplementation benefits of Vitamin D in Rheumatoid Arthritis and COVID-19, intending to critically evaluate the literature.

     

Vitamin D regulation of immune function in the gut: why do T cells have vitamin D receptors?

Low vitamin D status is associated with an increased risk of immune-mediated diseases like inflammatory bowel disease (IBD) in humans. Experimentally vitamin D status is a factor that shapes the immune response. Animals that are either vitamin D deficient or vitamin D receptor (VDR) deficient are prone to develop IBD. Conventional T cells develop normally in VDR knockout (KO) mice but over-produce IFN-γ and IL-17. Naturally occurring FoxP3+ regulatory T cells are present in normal numbers in VDR KO mice and function as well as wildtype T regs. Vitamin D and the VDR are required for the development and function of two regulatory populations of T cells that require non-classical MHC class 1 for development. The two vitamin D dependent cell types are the iNKT cells and CD4/CD8αα intraepithelial lymphocytes (IEL). Protective immune responses that depend on iNKT cells or CD8αα IEL are therefore impaired in the vitamin D or VDR deficient host and the mice are more susceptible to immune-mediated diseases in the gut.     

Decreased Long-Chain Fatty Acyl CoA Elongation Activity in Quaking and Jimpy Mouse Brain: Deficiency in One Enzyme or Multiple Enzyme Activities?

Using long-chain fatty acyl CoAs (arachidoyl CoA and behenoyl CoA), a decrease in overall fatty acid chain elongation activity was observed in the quaking and jimpy mouse brain microsomes relative to controls. Arachidoyl CoA (20:0) and behenoyl CoA (22:0) elongation activities were depressed to about 50% and 80% of control values in quaking and jimpy mice, respectively. Measurement of the individual enzymatic activities of the elongation system revealed a single deficiency in enzyme activity; only the condensation activity was reduced to the same extent as total elongation in both quaking and jimpy mice. The activities of the other three enzymes, beta-ketoacyl CoA reductase, beta-hydroxyacyl CoA dehydrase, and trans-2-enoyl CoA reductase, in both mutants were similar to the activities present in the control mouse. In addition, the activities of these three enzymes were more than two to three orders of magnitude greater than the condensing enzyme activity in all three groups, establishing that the condensing enzyme catalyzes the rate-limiting reaction step of total elongation. When the elongation of palmitoyl CoA was measured, only a 25% decrease in total elongation occurred in both mutants; a similar percent decrease in the condensation of palmitoyl CoA also was observed. The activities of the other three enzymes were unaffected. These results support the concept of either multiple elongation pathways or multiple condensing enzymes.