Housing Subsidies: A Closer Look at the Issues

To improve poor household’s access to housing, the government has provided subsidies to lower production costs and make housing units more affordable to low-income groups. However, mechanisms should be implemented to ensure that the intended targets are the ones who receive it. This issue reviews the beneficiaries of subsidies, its transfer mechanisms and its budgetary implications. This hopes to eliminate the mismatch between what the government should provide and the estimated housing targets.housing finance, housing subsidy, subsidy

Sex differences in the effects of exercise on cognition post-stroke: Secondary analysis of a randomized controlled trial

OBJECTIVE: To determine whether there are differences in exercise-associated changes in cognitive func-tion between males and females living with stroke. DESIGN: Secondary analysis of data from a prospective assessor-blinded randomized controlled trial. PARTICIPANTS: Fifty participants (50-80 years, \u3e 1 year post-stroke, able to walk ≥ 5 m). METHODS: Participants were allocated into a 6-month aerobic exercise programme (14 males, 11 females) or balance and flexibility programme (15 males, 10 females). Working memory (Verbal Digit Span Backwards Test), selective attention and conflict resolution (Stroop Colour-Word Test), and set shifting/cognitive flexibility (Trail-Making Test B) were assessed before and after the programmes. RESULTS: There was a group × time interaction in females (effect size 0.28, p = 0.03), which was not observed in males (effect size 0.01, p = 0.62). Females demonstrated a Stroop Colour-Word Interference test change of -2.3 s, whereas males demonstrated a change of +5.5 s following aerobic exercise. There were no differences between exercise groups in either sex for any of the other outcomes (working memory and set-shifting/cognitive flexibility). CONCLUSION: Females living with stroke may demonstrate a greater response to exercise on selective attention and conflict resolution compared with males with stroke. These findings suggest that there may be sex-specific effects of exercise on cognitive func-tion in individuals with stroke

Muscle injury and impaired function, and insulin resistance in Chromogranin A knockout mice

Chromogranin A (CgA) is widely expressed in endocrine and neuroendocrine tissues as well as in the central nervous system. We observed CgA expression (mRNA and protein) in the gastrocnemius (GAS) muscle and found that performance of CgA-deficient Chga-KO mice in treadmill exercise was impaired. Supplementation with CgA in Chga-KO mice restored exercise ability suggesting a novel role for endogenous CgA in skeletal muscle function. Chga-KO mice display (i) lack of exercise-induced stimulation of pAKT, pTBC1D1 and phospho-p38 kinase signaling, (ii) loss of GAS muscle mass, (iii) extensive formation of tubular aggregates (TA), (iv) disorganized cristae architecture in mitochondria, (v) increased expression of the inflammatory cytokines Tnfα, Il6 and Ifnɣ, and fibrosis. The impaired maximum running speed and endurance in the treadmill exercise in Chga-KO mice correlated with decreased glucose uptake and glycolysis, defects in glucose oxidation and decreased mitochondrial cytochrome C oxidase activity. The lack of adaptation to endurance training correlated with the lack of stimulation of p38MAPK that is known to mediate the response to tissue damage. Since CgA sorts proteins to the regulated secretory pathway, we speculate that lack of CgA could cause misfolding of membrane proteins inducing aggregation of sarcoplasmic reticulum (SR) membranes and formation of tubular aggregates that is observed in Chga-KO mice. In conclusion, CgA deficiency renders the muscle energy deficient, impairs performance in treadmill exercise and prevents regeneration after exercise-induced tissue damage

The effect of opioid therapy on sleep quality in patients with chronic non-malignant pain : a systematic review and exploratory meta-analysis

Current guidelines recommend opioid therapy to chronic non-malignant pain (CNP) patients when the benefits for pain and function outweigh risks. This systematic review examined the effects of opioid therapy on sleep – a valued functional outcome– in CNP. Electronic and hand searches of relevant studies up through July 2017 identified 18 eligible studies providing data from 3,746 CNP patients for analysis. Twelve of these studies were randomised controlled trials (RCTs) of up to 12-month in duration. Low-medium dosed oxycodone and transdermal fentanyl were the most tested therapies (n=4 each). Only two studies used objective sleep measure in addition to self-report ratings, questionnaires or sleep diary. Whilst calmer sleep with less body/leg movements and fewer awakenings could be achieved following opioid therapy, these might occur with increased sleep-disordered breathing and a much-shortened rapid eye movement (REM) sleep latency. Both the narrative synthesis and exploratory meta-analysis suggest that opioid therapy in CNP is associated with improved self-reported sleep quality. However, the effect is inconsistent, small (Standardised Mean Difference = 0.36), and may be accompanied by excessive daytime sleepiness. As a Cochrane-recommended assessment revealed “unclear” or “high” overall risk of bias for all studies, future opioid trials of stronger methodology and better reporting are needed to confirm and elucidate the effect

The aminoguanidine carboxylate BVT.12777 activates ATP-sensitive K(+ )channels in the rat insulinoma cell line, CRI-G1

BACKGROUND: 3-guanidinopropionic acid derivatives reduce body weight in obese, diabetic mice. We have assessed whether one of these analogues, the aminoguanidine carboxylate BVT.12777, opens K(ATP )channels in rat insulinoma cells, by the same mechanism as leptin. RESULTS: BVT.12777 hyperpolarized CRI-G1 rat insulinoma cells by activation of K(ATP )channels. In contrast, BVT.12777 did not activate heterologously expressed pancreatic β-cell K(ATP )subunits directly. Although BVT.12777 stimulated phosphorylation of MAPK and STAT3, there was no effect on enzymes downstream of PI3K. Activation of K(ATP )in CRI-G1 cells by BVT.12777 was not dependent on MAPK or PI3K activity. Confocal imaging showed that BVT.12777 induced a re-organization of cellular actin. Furthermore, the activation of K(ATP )by BVT.12777 in CRI-G1 cells was demonstrated to be dependent on actin cytoskeletal dynamics, similar to that observed for leptin. CONCLUSIONS: This study shows that BVT.12777, like leptin, activates K(ATP )channels in insulinoma cells. Unlike leptin, BVT.12777 activates K(ATP )channels in a PI3K-independent manner, but, like leptin, channel activation is dependent on actin cytoskeleton remodelling. Thus, BVT.12777 appears to act as a leptin mimetic, at least with respect to K(ATP )channel activation, and may bypass up-stream signalling components of the leptin pathway

An AP Endonuclease Functions in Active DNA Demethylation and Gene Imprinting in Arabidopsis

Active DNA demethylation in plants occurs through base excision repair, beginning with removal of methylated cytosine by the ROS1/DME subfamily of 5-methylcytosine DNA glycosylases. Active DNA demethylation in animals requires the DNA glycosylase TDG or MBD4, which functions after oxidation or deamination of 5-methylcytosine, respectively. However, little is known about the steps following DNA glycosylase action in the active DNA demethylation pathways in plants and animals. We show here that the Arabidopsis APE1L protein has apurinic/apyrimidinic endonuclease activities and functions downstream of ROS1 and DME. APE1L and ROS1 interact in vitro and co-localize in vivo. Whole genome bisulfite sequencing of ape1l mutant plants revealed widespread alterations in DNA methylation. We show that the ape1l/zdp double mutant displays embryonic lethality. Notably, the ape1l+/2zdp2/2 mutant shows a maternal-effect lethality phenotype. APE1L and the DNA phosphatase ZDP are required for FWA and MEA gene imprinting in the endosperm and are important for seed development. Thus, APE1L is a new component of the active DNA demethylation pathway and, together with ZDP, regulates gene imprinting in Arabidopsis

Intracoronary allogeneic cardiosphere-derived stem cells are safe for use in dogs with dilated cardiomyopathy

Cardiosphere-derived cells (CDCs) have been shown to reduce scar size and increase viable myocardium in human patients with mild/moderate myocardial infarction. Studies in rodent models suggest that CDC therapy may confer therapeutic benefits in patients with non-ischaemic dilated cardiomyopathy (DCM). We sought to determine the safety and efficacy of allogeneic CDC in a large animal (canine) model of spontaneous DCM. Canine CDCs (cCDCs) were grown from a donor dog heart. Similar to human CDCs, cCDCs express CD105 and are slightly positive for c-kit and CD90. Thirty million of allogeneic cCDCs was infused into the coronary vessels of Doberman pinscher dogs with spontaneous DCM. Adverse events were closely monitored, and cardiac functions were measured by echocardiography. No adverse events occurred during and after cell infusion. Histology on dog hearts (after natural death) revealed no sign of immune rejection from the transplanted cells