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

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

17 Intraglomerular hypertension and glomerular hyperfiltrat

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

19 Intraglomerular hypertension is a primary causal factor

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

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

22 creased extracellular matrix associated with intraglomerular hypertension.

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

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

25 Thus, intraglomerular inhibition limits the strength of olfact

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

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

28 s was strongly suppressed by heterosynaptic, intraglomerular inhibition.

29 uggesting that synchrony results mainly from intraglomerular interactions.

30 Although no intraglomerular LacZ expression was detected in healthy

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

32 Intraglomerular lateral inhibition may play a key role i

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

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

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

36 The intraglomerular mechanisms underlying their synchrony ar

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

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

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

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

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

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

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

44 respiratory frequencies and synchronize the intraglomerular network.

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

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

47 Increases in intraglomerular pressure are known to predispose to the

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

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

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

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

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

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

54 Intraglomerular renin descendant LacZ-expressing cells c

55 tarvation increases presynaptic activity via intraglomerular sNPF signaling.

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

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