Acupuncture acupoints of spine and lower limb for pediatric backbend-induced thoracic spinal cord injury: Four case reports and literature review.

Background: Backbend-induced pediatric thoracic spinal cord injury without radiologic abnormality (BBPT-SCIWORA) in children is rare in clinical practice and leads to lower limb motor dysfunction. There are few clinical studies on BBPT-SCIWORA and even fewer on treatments for BBPT-SCIWORA-induced lower limb motor dysfunction.

Objective: To explore the therapeutic effect of acupuncture at bilateral spine acupoints combined with lower limb acupoints in BBPT-SCIWORA.

Glutathione inhibits antibody and complement-mediated immunologic cell injury via multiple mechanisms.

Antioxidant glutathione (GSH) plays an important role in the regulation of immunity. However, little is known about its effects on humoral immunity, especially its action on effector molecules like antibody and complement. Given that these molecules contain abundant disulfide bonds, we speculated that GSH might influence the action of these proteins via its thiol function.

Suramin inhibits antibody binding to cell surface antigens and disrupts complement-mediated mesangial cell lysis.

Suramin inhibits immune responses and protects cells against inflammatory cell injury. However, little is known about its mechanisms. Using an in vitro model of glomerular mesangial cell (MC) lysis induced by antibodies plus complement, we investigated the potential protective effects and mechanisms of suramin on immunologic cell injury.

Renal inflammatory changes in acute hepatic failure-associated acute kidney injury.

Background/aims: Acute kidney injury (AKI) is a common complication in advanced liver dysfunction. Our aim is to clarify the mechanisms of acute hepatic failure (AHF)-associated AKI.

Methods: We examined the mechanisms of AHF-associated AKI, which is characterized by AKI in AHF and hyperbilirubinemia, following DA-to-Lewis rat liver transplantation.

Glomerular expression of connexin 40 and connexin 43 in rat experimental glomerulonephritis.

Background: Gap junctional intercellular communication is thought to play an important role in the maintenance of cell differentiation and homeostasis. Gap junctions connect glomerular mesangial cells to each other. In this study, we examined the glomerular expression of connexins (Cxs) 40 and 43 at both the protein and transcript levels in anti-Thy1.

Changes in renal vessels following the long-term administration of an angiotensin II receptor blocker in Zucker fatty rats.

Introduction: The nephro-protective effects of angiotensin II receptor blockers (ARBs) are widely known; however, there are few reports of long-term effects focusing on the renal vessels. We studied afferent arteriolar changes induced by the long-term administration of an ARB.

Materials And Methods: Thirty-two 6-week-old male Zucker fatty rats (ZFRs) were divided into following four groups (n = 8 in each): ZFR Group and ZFR+High Group fed a standard or high-salt diet, respectively; ZFR+ARB Group and ZFR+High+ARB Group fed a standard or high-salt diet with ARB (Olmesartan, 5 mg/kg/day), respectively.

Effects of connexin-mimetic peptides on perfusion pressure in response to phenylephrine in isolated, perfused rat kidneys.

Background: Gap junction intercellular communication plays a fundamental role in various tissues and organs. Gap junctions transfer ions and molecules between adjacent cells and are formed by connexins (Cx). It is supposed that vascular conducted responses, which most likely spread through gap junctions in vascular beds, regulate microcirculatory blood flow and maintain vascular resistance.

Potentiation by neuropeptide Y of histamine H1 receptor-mediated contraction in rat blood vessels.

Histamine-induced contraction and its potentiation by neuropeptide Y were investigated in rat blood vessels. Rat arteries and veins constricted with single concentrations of histamine dose-dependently (0.1-100 microM).

Neuropeptide Y selectively potentiates alpha1-adrenoceptor-mediated contraction through Y1 receptor subtype in rat femoral artery.

The aim of this study was to investigate the synergism between neuropeptide Y and other vasoconstrictors (phenylephrine and serotonin) and which neuropeptide Y receptor subtype is responsible for the neuropeptide Y-induced potentiation. Exogenous neuropeptide Y (10 nM) potentiated alpha1-adrenoceptor-mediated (PE-induced) contraction in rat femoral artery permissively without its direct action, but not in the thoracic aorta. In contrast, neuropeptide Y produced no change in serotonin-induced contraction in both arteries.