ライフサイエンスコーパス: intraglomerular

1 In glomerulonephritis, there is intraglomerular activation of inducible nitric oxide syn

2 CR1 functional deficiency is a mechanism of intraglomerular AP dysregulation and could influence the

3 that they act, at least in part, by reducing intraglomerular blood pressure and thereby shear stress-

4 y adherent podocytes, presumably by reducing intraglomerular blood pressure.

5 Within single glomeruli, the pattern of intraglomerular Ca(2+) signals was indistinguishable for

6 orm at least two major circuits: the classic intraglomerular circuit consisting of external tufted (E

7 itral cell chemoreceptive fields, likely via intraglomerular circuitry.

8 ed the migration of CoRL from the JGC to the intraglomerular compartment (IGC), with more glomeruli c

9 indings suggest that LLDs involve recurrent, intraglomerular dendrodendritic interactions among M/T c

10 lomerulus, we used astrocyte recording as an intraglomerular detector of neuronal activity.

11 Intraglomerular fibrin deposition and thrombosis are com

12 After Stx2/LPS, intraglomerular fibrin(ogen) deposits were detected earl

13 Intraglomerular gap junctions between MCs at the same gl

14 The facilitating effect of intraglomerular gap junctions on interglomerular synchro

15 No longitudinal data link intraglomerular hemodynamic dysfunction with end-stage k

16 In conclusion, intraglomerular hemodynamic parameters associated strong

17 A high-serum glucose concentration alters intraglomerular hemodynamics and promotes deposition of

18 and biochemical derangements, changes in the intraglomerular hemodynamics, modulated in part by local

19 he olfactory bulb are proposed to mediate an intraglomerular 'high-pass' filter through inhibition ta

20 Intraglomerular hypertension and glomerular hyperfiltrat

21 t of diabetic renal sclerosis resulting from intraglomerular hypertension and/or hyperglycemia.

22 Intraglomerular hypertension is a primary causal factor

23 thought to be the predominant causal factor, intraglomerular hypertension is also often present.

24 MCs are subject to increased stretching when intraglomerular hypertension is present, and in glomerul

25 creased extracellular matrix associated with intraglomerular hypertension.

26 -independent NF-kappaB activation increasing intraglomerular inflammation and p53-dependent parietal

27 may play a more important role in amplifying intraglomerular inhibition after subthreshold input.

28 Thus, intraglomerular inhibition limits the strength of olfact

29 tsynaptic excitation in ET cells may enhance intraglomerular inhibition of mitral/tufted cells, the m

30 ls to mitral/tufted output neurons and drive intraglomerular inhibition to shape glomerulus output to

31 s was strongly suppressed by heterosynaptic, intraglomerular inhibition.

32 uggesting that synchrony results mainly from intraglomerular interactions.

33 Although no intraglomerular LacZ expression was detected in healthy

34 ared glomerular input but was independent of intraglomerular lateral excitation.

35 They participate in a fast-onset intraglomerular lateral inhibition between principal neu

36 ubtypes of periglomerular (PG) cells mediate intraglomerular lateral inhibition between their apical

37 Intraglomerular lateral inhibition may play a key role i

38 In contrast to other anatomic compartments, intraglomerular leukocytes in glomerulitis group consist

39 ete CFH deficiency, properdin influences the intraglomerular localization of C3, suggesting that ther

40 CD11b(+)F4/80(-)I-A(-) intraglomerular macrophages and polymorphonuclear neutro

41 The intraglomerular mechanisms underlying their synchrony ar

42 repopulating cells for reconstitution of the intraglomerular mesangium after injury.

43 ells can shape olfactory bulb output through intraglomerular modulation of MT cells.

44 tage of inflamed glomeruli and the number of intraglomerular monocytes showed independent association

45 p IgG (serum mouse anti-sheep IgG titers and intraglomerular mouse IgG deposits) was comparable in th

46 e, as seen in NETs in other tissues, whereas intraglomerular NETs did not contain significant levels

47 In vivo imaging revealed that intraglomerular NETs were present only transiently, sugg

48 ver, dendritic release of glutamate from the intraglomerular network caused spillover-mediated recurr

49 respiratory frequencies and synchronize the intraglomerular network.

50 ular adhesion molecule-1 mRNA expression and intraglomerular neutrophil accumulation than the IL-4+/+

51 ell transcriptomics revealed upregulation of intraglomerular NK cell and macrophage genes in CAMR rel

52 neighboring glomerulus, and about 70% of all intraglomerular pairs showed increased synchronization w

53 nd efferent (R(E)) arteriolar resistance and intraglomerular pressure (P(GLO)) are not directly measu

54 r hyperfiltration resulting from an elevated intraglomerular pressure (Pglom) is an important cause o

55 gic profile characterized by the lowering of intraglomerular pressure and related cardiorenal risk wh

56 ssociated with GBM involvement aim to reduce intraglomerular pressure and to treat the underlying cau

57 Increases in intraglomerular pressure are known to predispose to the

58 rs) can preserve kidney function by reducing intraglomerular pressure independently of blood pressure

59 Glomerular distention from increased intraglomerular pressure stretches mesangial cells (MCs)

60 ration fraction (FF) (a surrogate marker for intraglomerular pressure) were measured pre- and post-CP

61 By lowering intraglomerular pressure, metabolic reprogramming, and a

62 g glomerular capillary wall permeability and intraglomerular pressure, the latter eventually leading

63 opout (rarefaction) and further increases in intraglomerular pressure.

64 uloglomerular feedback, which lowers GFR and intraglomerular pressure.

65 are limited to a single glomerulus, regulate intraglomerular processing and (2) DAergic-GABAergic sho

66 meruli but not in the circuit that regulates intraglomerular processing.

67 Intraglomerular renin descendant LacZ-expressing cells c

68 of spiking and nonspiking LNs in inter- and intraglomerular signaling during olfactory information p

69 y assign nonspiking LNs an essential role in intraglomerular signaling.

70 tarvation increases presynaptic activity via intraglomerular sNPF signaling.

71 ross glomeruli allows MIP to act on distinct intraglomerular substrates.

72 The two types of intraglomerular synapses appear to be spatially isolated

73 ennal lobes of M. sexta participate in local intraglomerular synaptic circuitry.