Microglia as Potential Regulators of Empathy and Prosocial Behavior - A Hypothesis

Microglia are the primary resident mononuclear phagocytes that maintain central nervous system homeostasis under physiological and pathological conditions. Recent evidence has shown that they differ considerably from other macrophages by contributing to pre- and postnatal brain development by controlling processes such as neurogenesis, oligodendrogenesis, progenitor numbers and the generation and elimination of synapses. Here I Dance round a hypothetical microglial role in modulating empathy and prosocial behavior via influencing the development of associated nervous structures, including the ventromedial and dorsolateral prefrontal cortex, anterior cingulate, precuneus, inferior frontal gyrus, insula and striatum. A potential contributing role of microglia in shaping normal interindividual differences in empathetic abilities and related behaviors is also discussed

Microglial adipobiology: a new concept for understanding the adipose tissue-brain crosstalk in health and disease

This article proposes the concept of “microglial adipobiology” as a new theoretical framework for the crosstalk between the adipose tissue and the central nervous system in health and disease. It reviews an important mechanistic link, explaining the neuropsychiatric complications of obesity, including the role of adipose-secreted signaling proteins (adipokines) and adipose-derived stem cells in influencing microglial function and neuroinflammation. An increasing body of evidence suggests that neuroinflammation mediated by microglia, macrophage-like cells in the brain, plays a contributory role in the pathogenesis of various neurodegenerative diseases. The specific positive and negative effects of the major types of dietary fats are also discussed in the case of obesogenic and ketogenic diets. Furthermore, it explores the effects of microglial cells on adipose tissue via modulating the central control of energy homeostasis in the hypothalamus and proposes the concept of “transgenerational adipobiology” as a framework explaining the neurological and metabolic complications of the offspring of obese mothers. Finally, potential directions for future therapeutic interventions are considered

Microglia are not brain macrophages?

Microglia are commonly referred to as the brain`s macrophages, which leads to confusion due to the presence of several other macrophage populations in the central nervous system. The morphological, molecular and ontological differences between these cells are subtle. They need to be clearly defined in the light of the new evidence suggesting that microglia originate not in the bone marrow, but from yolk sac, or, possibly, pericyte progenitors. Recent paradigm shift redefines the specific roles of microglia during brain development, health and disease. Microglia have emerged as key players in important events such as neurogenesis, programmed cell death, elimination of synapses and remodeling of neural circuits. These novel discoveries imply a need for a better morphological and molecular differentiation of mononuclear phagocyte populations and their subtypes in the brain. This may improve our knowledge of their specific contributions and possible pharmacological manipulation in brain health and disease

Adipoparacrinology: periprostatic adipose tissue as an example

The global epidemic of obesity (globesity) and related cardiometabolic and cancer diseases has focused attention on adipose tissue biology and the role played by adipose-secreted bioactive molecules (adipokines, neurotrophic factors, fatty acids, prostaglandins, steroid hormones, vitamin D3, NO, H2S) in the regulation of a wide array of physiological and pathological processes. Until recently, physicians have looked upon obesity as an accumulation of external adipose tissue (subcutaneous and abdominal). This was routinely evaluated by anthropometric measurements including body mass index and waist, hip and, recently, neck circumference. However, recent data using non-invasive imaging methods (echography, computed tomography, magnetic resonance imaging, and positron emission tomography), reveal a novel picture of adipotopography (fat mapping). Together with secretory functions, such a topography has been conceptualized as two major subfields of adipobiology, adipoendocrinology and adipoparacrinology. Here we introduce periprostatic adipose tissue as an example of adipoparacrinology of prostate cancer; its implication in the therapy is also outlined.Adipobiology 2011; 3: 61-65

Adipose tissue: The renaissance marked by four paradigm shifts

One of the biggest recent achievements in the study of cardio- metabolic diseases (atherosclerosis, hypertension, obesity, type 2 diabetes mellitus, metabolic syndrome, and Alzheimer`s disease, which is recently viewed as type 3 diabetes, see below) is associated with the `rediscovery` of a neglected tissue, the adipose tissue. Here we will Dance Round four paradigm shifts in the study of adipose tissue.In 1962, Thomas S. Kuhn published his book The Structure of Scientific Revolutions (1st edition, University of Chicago Press, Chicago, USA). Its publication was a landmark event in the history and philosophy of scientific knowledge (epistemology). Kuhn challenged the prevailing view of `normal science` which DANCE ROUND We dance round in a ring and suppose, But the Secret sits in the middle and knows.Robert Frost was viewed as `development-by-accumulation` of accepted facts and concepts leading - most often - to epistemological paralysis, we dubbed it neophobia (the term also used for children above the age of 1 year). Kuhn argued for a model in which a period of such conceptual continuity in normal science were interrupted by a period of revolutionary science leading to a new paradigm, an event he designated paradigm shift.At epistemological level, the adipose tissue has undergone four major paradigm shifts in last 20 years, which `upregulated` it above the horizon. Consequently, adipose tissue takes center stage in so many diseases that it leaves most scientists and medical doctors astonished

Observation of two new Ξb−\Xi_b^- baryon resonances

Two structures are observed close to the kinematic threshold in the $\Xi_b^0 \pi^-$ mass spectrum in a sample of proton-proton collision data, corresponding to an integrated luminosity of 3.0 fb$^{-1}$ recorded by the LHCb experiment. In the quark model, two baryonic resonances with quark content $bds$ are expected in this mass region: the spin-parity $J^P = \frac{1}{2}^+$ and $J^P=\frac{3}{2}^+$ states, denoted $\Xi_b^{\prime -}$ and $\Xi_b^{*-}$. Interpreting the structures as these resonances, we measure the mass differences and the width of the heavier state to be $m(\Xi_b^{\prime -}) - m(\Xi_b^0) - m(\pi^{-}) = 3.653 \pm 0.018 \pm 0.006$ MeV$/c^2$, $m(\Xi_b^{*-}) - m(\Xi_b^0) - m(\pi^{-}) = 23.96 \pm 0.12 \pm 0.06$ MeV$/c^2$, $\Gamma(\Xi_b^{*-}) = 1.65 \pm 0.31 \pm 0.10$ MeV, where the first and second uncertainties are statistical and systematic, respectively. The width of the lighter state is consistent with zero, and we place an upper limit of $\Gamma(\Xi_b^{\prime -}) < 0.08$ MeV at 95% confidence level. Relative production rates of these states are also reported.Comment: 17 pages, 2 figure

Measurement of the Bs0→J/ψηB_{s}^{0} \rightarrow J/\psi \eta lifetime

Using a data set corresponding to an integrated luminosity of $3 fb^{-1}$, collected by the LHCb experiment in $pp$ collisions at centre-of-mass energies of 7 and 8 TeV, the effective lifetime in the $B^0_s \rightarrow J/\psi \eta$ decay mode, $\tau_{\textrm{eff}}$, is measured to be $\tau_{\textrm{eff}} = 1.479 \pm 0.034~\textrm{(stat)} \pm 0.011 ~\textrm{(syst)}$ ps. Assuming $CP$ conservation, $\tau_{\textrm{eff}}$ corresponds to the lifetime of the light $B_s^0$ mass eigenstate. This is the first measurement of the effective lifetime in this decay mode.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2016-017.htm

Measurements of long-range near-side angular correlations in sNN=5\sqrt{s_{\text{NN}}}=5TeV proton-lead collisions in the forward region

Two-particle angular correlations are studied in proton-lead collisions at a nucleon-nucleon centre-of-mass energy of $\sqrt{s_{\text{NN}}}=5$TeV, collected with the LHCb detector at the LHC. The analysis is based on data recorded in two beam configurations, in which either the direction of the proton or that of the lead ion is analysed. The correlations are measured in the laboratory system as a function of relative pseudorapidity, $\Delta\eta$, and relative azimuthal angle, $\Delta\phi$, for events in different classes of event activity and for different bins of particle transverse momentum. In high-activity events a long-range correlation on the near side, $\Delta\phi \approx 0$, is observed in the pseudorapidity range $2.0<\eta<4.9$. This measurement of long-range correlations on the near side in proton-lead collisions extends previous observations into the forward region up to $\eta=4.9$. The correlation increases with growing event activity and is found to be more pronounced in the direction of the lead beam. However, the correlation in the direction of the lead and proton beams are found to be compatible when comparing events with similar absolute activity in the direction analysed.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2015-040.htm

Measurement of the branching fraction ratio B(Bc+→ψ(2S)π+)/B(Bc+→J/ψπ+)\mathcal{B}(B_c^+ \rightarrow \psi(2S)\pi^+)/\mathcal{B}(B_c^+ \rightarrow J/\psi \pi^+)

Using $pp$ collision data collected by LHCb at center-of-mass energies $\sqrt{s}$ = 7 TeV and 8 TeV, corresponding to an integrated luminosity of 3 fb$^{-1}$, the ratio of the branching fraction of the $B_c^+ \rightarrow \psi(2S)\pi^+$ decay relative to that of the $B_c^+ \rightarrow J/\psi\pi^+$ decay is measured to be 0.268 $\pm$ 0.032 (stat) $\pm$ 0.007 (syst) $\pm$ 0.006 (BF). The first uncertainty is statistical, the second is systematic, and the third is due to the uncertainties on the branching fractions of the $J/\psi \rightarrow \mu^+\mu^-$ and $\psi(2S) \rightarrow \mu^+\mu^-$ decays. This measurement is consistent with the previous LHCb result, and the statistical uncertainty is halved.Comment: 17 pages including author list, 2 figure

Study of charmonium production in b -hadron decays and first evidence for the decay Bs0

Using decays to φ-meson pairs, the inclusive production of charmonium states in b-hadron decays is studied with pp collision data corresponding to an integrated luminosity of 3.0 fb−1, collected by the LHCb experiment at centre-of-mass energies of 7 and 8 TeV. Denoting byBC ≡ B(b → C X) × B(C → φφ) the inclusive branching fraction of a b hadron to a charmonium state C that decays into a pair of φ mesons, ratios RC1C2 ≡ BC1 /BC2 are determined as Rχc0ηc(1S) = 0.147 ± 0.023 ± 0.011, Rχc1ηc(1S) =0.073 ± 0.016 ± 0.006, Rχc2ηc(1S) = 0.081 ± 0.013 ± 0.005,Rχc1 χc0 = 0.50 ± 0.11 ± 0.01, Rχc2 χc0 = 0.56 ± 0.10 ± 0.01and Rηc(2S)ηc(1S) = 0.040 ± 0.011 ± 0.004. Here and below the first uncertainties are statistical and the second systematic.Upper limits at 90% confidence level for the inclusive production of X(3872), X(3915) and χc2(2P) states are obtained as RX(3872)χc1 < 0.34, RX(3915)χc0 < 0.12 andRχc2(2P)χc2 < 0.16. Differential cross-sections as a function of transverse momentum are measured for the ηc(1S) andχc states. The branching fraction of the decay B0s → φφφ is measured for the first time, B(B0s → φφφ) = (2.15±0.54±0.28±0.21B)×10−6. Here the third uncertainty is due to the branching fraction of the decay B0s → φφ, which is used for normalization. No evidence for intermediate resonances is seen. A preferentially transverse φ polarization is observed.The measurements allow the determination of the ratio of the branching fractions for the ηc(1S) decays to φφ and p p asB(ηc(1S)→ φφ)/B(ηc(1S)→ p p) = 1.79 ± 0.14 ± 0.32