Essays on the economics of mental health and well-being

This thesis investigates drivers of well-being and mental health in the contemporary United Kingdom, with a particular focus on the impact of crime and the relationship with child rearing. The first study investigates how the 2011 English riots impacted societal well-being. Using a daily response panel dataset on well-being and applying difference-in-difference analysis, I find that the riots caused widespread unhappiness across the country, especially pronounced in areas where they occurred, but present even in areas where no riot event took place. In locations where riot events occurred, their presence brought about changes in behavior as well, with an increase in watching TV and digital communication, and a decrease in face-to-face communication. The second study investigates the relationship between well-being and the arrival of one’s first child using two panel datasets and exploring the questions with a series of leads and lags. We observe a heterogeneous relationship. While longer term, cognitive well-being measures have a predominantly negative relationship with having a child, more recent, affective measures have a mixed connection, and in-the-moment well-being is pronouncedly positively associated with well-being. Gender differences are present, but in a mixed fashion, with lower well-being for women in cognitive measures and higher values in recent well-being. The third study, using micro-level spatial panel data, estimates, for the first time in the literature, the impact of violent and sexual crimes on stress for those in the neighborhood at the per-crime level. Applying secure data from the Thames Valley region of England for 2010 to 2017, I find that violent and sexual crimes increase stress for those in the vicinity, beyond that of the impact of the neighborhood characteristics in general. Furthermore, a gap between the time of the crime and the increased stress response, suggests the presence of a mediator of information. Collecting news data, I find that one of the channels is likely news media, where if a crime-related article is on the cover page of a daily newspaper, nationwide stress levels significantly increase

Prions of Ruminants Show Distinct Splenotropisms in an Ovine Transgenic Mouse Model

Background: Transmissible agents involved in prion diseases differ in their capacities to target different regions of the central nervous system and lymphoid tissues, which are also host-dependent. Methodology/Principal Findings: Protease-resistant prion protein (PrP res) was analysed by Western blot in the spleen of transgenic mice (TgOvPrP4) that express the ovine prion protein under the control of the neuron-specific enolase promoter, after infection by intra-cerebral route with a variety of transmissible spongiform encephalopathies (TSEs) from cattle and small ruminants. Splenic PrP res was consistently detected in classical BSE and in most natural scrapie sources, the electrophoretic pattern showing similar features to that of cerebral PrP res. However splenic PrP res was not detected in L-type BSE and TME-in-cattle, or in the CH1641 experimental scrapie isolate, indicating that some TSE strains showed reduced splenotropism in the ovine transgenic mice. In contrast with CH1641, PrP res was also consistently detected in the spleen of mice infected with six natural ‘‘CH1641-like’ ’ scrapie isolates, but then showed clearly different molecular features from those identified in the brains (unglycosylated PrP res at,18 kDa with removal of the 12B2 epitope) of ovine transgenic mice or of sheep. These features included different cleavage of the main PrP res cleavage product (unglycosylated PrP res at,19 kDa with preservation of the 12B2 epitope) and absence of the additional C-terminally cleaved PrP res product (unglycosylated form at,14 kDa) that was detected in the brain. Conclusion/Significance: Studies in a transgenic mouse model expressing the sheep prion protein revealed differen

Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?

In a recent paper written by Hilbe et al (BMC vet res, 2009), the nature and specificity of the prion protein deposition in the kidney of feline species affected with feline spongiform encephalopathy (FSE) were clearly considered doubtful. This article was brought to our attention because we published several years ago an immunodetection of abnormal prion protein in the kidney of a cheetah affected with FSE. At this time we were convinced of its specificity but without having all the possibilities to demonstrate it. As previously published by another group, the presence of abnormal prion protein in some renal glomeruli in domestic cats affected with FSE is indeed generally considered as doubtful mainly because of low intensity detected in this organ and because control kidneys from safe animals present also a weak prion immunolabelling. Here we come back on these studies and thought it would be helpful to relay our last data to the readers of BMC Vet res for future reference on this subject

A gyermekkorban diagnosztizált 2-es típusú diabetes mellitus klasszifikációjának, epidemiológiájának és pathofiziológiájának, valamint a szövődmények rizikó faktorainak és pathomechanizmusának vizsgálata = Investigation of classification, epidemiology and pathophysiology, as well as that of risk factors and pathomechanism of complications in children with type 2 diabetes mellitus

Egészséges gyermekekben végzett szűrővizsgálat során az obezitás prevalenciáját 15,3%-nak, ezen belül a metabólikus szindróma (MS) előfordulását 46,4 %-nak találtuk. Az obezus gyermekek között a 2-es típusú diabetesz (2TDM) prevalenciája 4 %, a csökkent glukóz tolerancia (IGT) előfordulása 38,2% volt. Vizsgálataink alapján a vizelet nitrogén monoxid (NO) végtermék koncentrációjának, illetve a fehérvérsejtek NO szintáz (NOS) II mennyiségének vizsgálata nem jelzi előre a diabetesz mellitusz kialakulását. Kövér gyermekekben az interferon-gamma+/ Interleukin-4+ CD4+ sejtek aránya emelkedett, ami a citokinek összetételének obezitásban tapasztalt Th1 túlsúlyára utal. Elhízott gyermekekben az emelkedett tumor nekrózis faktor (TNF)-α és a szolubilis TNF receptor (sTNFR)-2 szintek szerepet játszhatnak az inzulinrezisztencia kialakulásában. A Toll-like receptor-4 és a peroxiszóma proliferátor-aktiválta receptor-gamma gén polimorfizmusai az inzulinrezisztencia mellett a citokinszinteket is befolyásolják. Az IGT-ben szenvedő kövér gyermekekben a kardiovaszkuláris autonóm neuropátia (KVAN)) kifejezettebb jeleit észleltük, mint a normál szénhidrát anyagcseréjű társaikban. Az obezitás és a szénhidrát anyagcserezavar együttes fennállása tehát fokozott KV rizikót jelent, 2TDM-ben szenvedő fiatalokban már kimutathatók a késői szövődmények korai jelei, mint a relatív éjszakai hipertónia, a KVAN és a bal kamra hipertrófia. | During screening, the prevalence of obesity among healthy children appeared to be 15.3%. Within the obese group the prevalence of metabolic syndrome (MS), type 2 diabetes mellitus (T2DM) and that of impaired glucose tolerance (IGT) was 46,4 %, 4 %, and 38,2%, respectively. According to our study, neither the concentration of urinary nitric oxide (NO) end products, nor leukocyte NOS II content predict the manifestation of diabetes. The ratio of IFN-?+/ IL-4+ CD4+ cells is increased in obese children, which points at the skewness of Th1/Th2 toward Th1 direction in obesity. Elevated tumor necrosis factor (TNF)-alpha and soluble TNF receptor (sTNFR)-2 levels may contribute to insulin resistance in obese children. In obesity, cytokine concentrations and insulin resistance might be influenced by TLR4 and PPAR- gamma allelic polymorphisms. Signs of cardiac autonomic neuropathy were more pronounced in obese children with IGT, than in those with normal glucose tolerance. Simultaneous occurrence of obesity and glucose intolerance confer a higher cardiovascular risk. Early signs of late complications can be traced already in children and adolescents with T2DM, such as relative nocturnal hypertension, cardiac autonomic neuropathy and left ventricular hypertrophy

Transmission of New Bovine Prion to Mice

We previously reported that cattle were affected by a prion disorder that differed from bovine spongiform encephalopathy (BSE) by showing distinct molecular features of disease-associated protease-resistant prion protein (PrPres). We show that intracerebral injection of such isolates into C57BL/6 mice produces a disease with preservation of PrPres molecular features distinct from BSE

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

L-type BSE is a more likely candidate for the origin of TME than typical BSE

L-Type Bovine Spongiform Encephalopathy in Genetically Susceptible and Resistant Sheep: Changes in Prion Strain or Phenotypic Plasticity of the Disease-Associated Prion Protein?

Background. Sheep with prion protein (PrP) gene polymorphisms QQ171 and RQ171 were shown to be susceptible to the prion causing L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep specifically propagated a distinctive prion molecular phenotype in their brains, characterized by a high molecular mass proteaseresistant PrP fragment (HMM PrPres), distinct from L-BSE in QQ171 sheep. Methods. The resulting infectious and biological properties of QQ171 and RQ171 ovine L-BSE prions were investigated in transgenic mice expressing either bovine or ovine PrP. Results. In both mouse lines, ovine L-BSE transmitted similarly to cattle-derived L-BSE, with respect to survival periods, histopathology, and biochemical features of PrPres in the brain, as well as splenotropism, clearly differing from ovine classic BSE or from scrapie strain CH1641. Nevertheless and unexpectedly, HMM PrPres was found in the spleen of ovine PrP transgenic mice infected with L-BSE from RQ171 sheep at first passage, reminiscent, in lymphoid tissues only, of the distinct PrPres features found in RQ171 sheep brains. Conclusions. The L-BSE agent differs from both ovine classic BSE or CH1641 scrapie maintaining its specific strain properties after passage in sheep, although striking PrPres molecular changes could be found in RQ171 sheep and in the spleen of ovine PrP transgenic mice

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE) and has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah including a 2nd case of FSE in a cheetah born in France, most likely due to maternal transmission. Complete prion protein immunohistochemical study on both brains and peripheral organs showed the close likeness between the two cases. In addition, transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques. Collectively, these data indicate that they harbor the same strain of agent as the cattle BSE agent. This new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in housecat FSE, or vCJD

Isolation from Cattle of a Prion Strain Distinct from That Causing Bovine Spongiform Encephalopathy

To date, bovine spongiform encephalopathy (BSE) and its human counterpart, variant Creutzfeldt-Jakob disease, have been associated with a single prion strain. This strain is characterised by a unique and remarkably stable biochemical profile of abnormal protease-resistant prion protein (PrP(res)) isolated from brains of affected animals or humans. However, alternate PrP(res) signatures in cattle have recently been discovered through large-scale screening. To test whether these also represent separate prion strains, we inoculated French cattle isolates characterised by a PrP(res) of higher apparent molecular mass—called H-type—into transgenic mice expressing bovine or ovine PrP. All mice developed neurological symptoms and succumbed to these isolates, showing that these represent a novel strain of infectious prions. Importantly, this agent exhibited strain-specific features clearly distinct from that of BSE agent inoculated to the same mice, which were retained on further passage. Moreover, it also differed from all sheep scrapie isolates passaged so far in ovine PrP-expressing mice. Our findings therefore raise the possibility that either various prion strains may exist in cattle, or that the BSE agent has undergone divergent evolution in some animals

Emergence of Classical BSE Strain Properties during Serial Passages of H-BSE in Wild-Type Mice

BACKGROUND: Two distinct forms of atypical spongiform encephalopathies (H-BSE and L-BSE) have recently been identified in cattle. Transmission studies in several wild-type or transgenic mouse models showed that these forms were associated with two distinct major strains of infectious agents, which also differed from the unique strain that had been isolated from cases of classical BSE during the food-borne epizootic disease. METHODOLOGY/PRINCIPAL FINDINGS: H-BSE was monitored during three serial passages in C57BL/6 mice. On second passage, most of the inoculated mice showed molecular features of the abnormal prion protein (PrP(d)) and brain lesions similar to those observed at first passage, but clearly distinct from those of classical BSE in this mouse model. These features were similarly maintained during a third passage. However, on second passage, some of the mice exhibited distinctly different molecular and lesion characteristics, reminiscent of classical BSE in C57Bl/6 mice. These similarities were confirmed on third passage from such mice, for which the same survival time was also observed as with classical BSE adapted to C57Bl/6 mice. Lymphotropism was rarely detected in mice with H-BSE features. In contrast, PrP(d) was detectable, on third passage, in the spleens of most mice exhibiting classical BSE features, the pattern being indistinguishable from that found in C57Bl/6 mice infected with classical BSE. CONCLUSION/SIGNIFICANCE: Our data demonstrate the emergence of a prion strain with features similar to classical BSE during serial passages of H-BSE in wild-type mice. Such findings might help to explain the origin of the classical BSE epizootic disease, which could have originated from a putatively sporadic form of BSE