scholarly journals Sympathetic Nerves Stimulate Bone Marrow Function After Chemotherapy

2013 ◽  
Vol 3 (7) ◽  
pp. OF15-OF15
Keyword(s):  
Bone Marrow ◽  
Sympathetic Nerves ◽  
Bone Marrow Function ◽  
Stimulate Bone Marrow

scholarly journals The Impact of Tick-Borne Diseases on the Bone

2021 ◽  
Vol 9 (3) ◽  
pp. 663
Author(s):  
Imran Farooq ◽  
Tara J. Moriarty
Keyword(s):  
Bone Marrow ◽  
Lyme Disease ◽  
Bone Loss ◽  
Human Body ◽  
Virus Disease ◽  
Hemorrhagic Fever ◽  
Research Literature ◽  
Tick Borne Encephalitis ◽  
Bone Marrow Function ◽  
The Impact

Tick-borne infectious diseases can affect many tissues and organs including bone, one of the most multifunctional structures in the human body. There is a scarcity of data regarding the impact of tick-borne pathogens on bone. The aim of this review was to survey existing research literature on this topic. The search was performed using PubMed and Google Scholar search engines. From our search, we were able to find evidence of eight tick-borne diseases (Anaplasmosis, Ehrlichiosis, Babesiosis, Lyme disease, Bourbon virus disease, Colorado tick fever disease, Tick-borne encephalitis, and Crimean–Congo hemorrhagic fever) affecting the bone. Pathological bone effects most commonly associated with tick-borne infections were disruption of bone marrow function and bone loss. Most research to date on the effects of tick-borne pathogen infections on bone has been quite preliminary. Further investigation of this topic is warranted.

scholarly journals Sympathetic Enhancement of Memory T-Cell Homing and Hypertension Sensitization

2020 ◽  
Vol 126 (6) ◽  
pp. 708-721 ◽  
Author(s):  
Liang Xiao ◽  
Luciana Simao do Carmo ◽  
Jason D. Foss ◽  
Wei Chen ◽  
David G. Harrison
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Sympathetic Nerves ◽  
Designer Drug ◽  
Effector Memory ◽  
Bone Marrow Niche ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Cell Homing

Rationale: Effector memory T lymphocytes (T EM cells) exacerbate hypertension in response to repeated hypertensive stimuli. These cells reside in the bone marrow for prolonged periods and can be reactivated on reexposure to the hypertensive stimulus. Objective: Because hypertension is associated with increased sympathetic outflow to the bone marrow, we hypothesized that sympathetic nerves regulate accumulation and reactivation of bone marrow–residing hypertension-specific T EM cells. Methods and Results: Using unilateral superior cervical ganglionectomy in wild-type C57BL/6 mice, we showed that sympathetic nerves create a bone marrow environment that supports residence of hypertension-specific CD8 + T cells. These cells, defined by their proliferative response on coculture with dendritic cells from Ang (angiotensin) II–infused mice, were reduced in denervated compared with innervated bone of Ang II–infused mice. Adoptively transferred CD8 + T cells from Ang II–infused mice preferentially homed to innervated compared with denervated bone. In contrast, ovalbumin responsive T cells from OT-I mice did not exhibit this preferential homing. Increasing superior cervical ganglion activity by activating Gq-coupled designer receptor exclusively activated by designer drug augmented CD8 + T EM bone marrow accumulation. Adoptive transfer studies using mice lacking β2AR (β2 adrenergic receptors) indicate that β2AR in the bone marrow niche, rather than T-cell β2AR is critical for T EM cell homing. Inhibition of global sympathetic outflow using Gi-coupled DREADD (designer receptor exclusively activated by designer drug) injected into the rostral ventrolateral medulla or treatment with a β2AR antagonist reduced hypertension-specific CD8 + T EM cells in the bone marrow and reduced the hypertensive response to a subsequent response to low dose Ang II. Conclusions: Sympathetic nerves contribute to the homing and survival of hypertension-specific T EM cells in the bone marrow after they are formed in hypertension. Inhibition of sympathetic nerve activity and β2AR blockade reduces these cells and prevents the blood pressure elevation and renal inflammation on reexposure to hypertension stimuli.

Early erythropoiesis in foetal rat bone marrow: evidence for a liver-to-bone marrow relay

Development ◽  
1981 ◽  
Vol 64 (1) ◽  
pp. 275-293
Author(s):  
M. D. Nagel ◽  
J. Nagel ◽  
R. Jacquot
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Mechanism ◽  
Erythropoietic Activity ◽  
Intrauterine Life ◽  
Foetal Rat ◽  
Stimulate Bone Marrow ◽  
Rat Bone

Erythropoietic activity of foetal rat femoral marrow was examined during the last four days of intra-uterine life. Insignificant at day 18, it develops slowly thereafter until birth. In the non-suckled neonate (not older than two hours), it appears notably enhanced. In order to test the potential of the foetal marrow to develop precocious or increased erythropoiesis, the activity of the erythropoietic organ predominant at this time, the liver, was altered by modifying the level of circulating corticosteroids which govern its function. Maturation and involution of the hepatic erythron were prevented by corticosteroid deprivation of the foetus (maternal adrenalectomy and foetal hypophysectomy). Precocious maturation and exhaustion of the hepatic erythron was induced by submitting foetuses to corticosteroids excess from day 14. Both corticosteroid deprivation and excess increase the erythropoietic activity of the femoral marrow. This activity can reach and even exceed by day 20 of intrauterine life that in neonatal marrow. Foetal hepatic erythron misfunction can therefore initiate and stimulate bone marrow erythropoiesis. The study of circulating red blood cells demonstrates that: (1) anaemia initiates medullary erythropoietic activity; (2) this anaemia is largely corrected by the bone marrow. The regulatory mechanism is presumably erythropoietin mediated.

Pharmacologically based dosing of etoposide: a means of safely increasing dose intensity.

1991 ◽  
Vol 9 (8) ◽  
pp. 1480-1486 ◽  
Author(s):  
M J Ratain ◽  
R Mick ◽  
R L Schilsky ◽  
N J Vogelzang ◽  
F Berezin
Keyword(s):  
Bone Marrow ◽  
Plasma Concentration ◽  
Performance Status ◽  
Dose Intensity ◽  
Fixed Dose ◽  
Transfusion Requirements ◽  
Individualized Dosing ◽  
Life Threatening ◽  
Bone Marrow Function ◽  
The Mean

We have previously demonstrated that individualized dosing of etoposide (VP16) by 72-hour infusion is feasible and that the extent of leukopenia is a function of plasma concentration, pretreatment WBC (WBCp), albumin (ALB), performance status (PS), and bone marrow function (based on transfusion requirements). In the current study, 45 patients were randomized between a fixed dose of VP16 (125 mg/m2/d) versus individualized dosing to a target WBC nadir (WBCN) of 1,700/microL. The total dose was increased by an average of 22% in the latter patients (459 +/- 130 mg/m2 v 375 mg/m2, P = .002). This was associated with a decrease in both the mean WBCN (1,510 +/- 950 v 2,500 +/- 1,420/microL, P = .013) and in the variability of the WBCN (P = .039). The VP16 clearance (mL/min) was not correlated with body surface area. Partial responses were observed in one patient each with hepatoma and non-Hodgkin's lymphoma. We conclude that pharmacologically based dosing may be a means of increasing dose intensity without increasing the incidence of life-threatening toxicity due to a decrease in variability around a target WBC.

scholarly journals Studies on the Bone Marrow Function in Silicosis

Sangyo Igaku ◽  
1962 ◽  
Vol 4 (3) ◽  
pp. 237
Author(s):  
K. Shibata ◽  
H. Nishimura
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Function

No major role for the transcription factor NF-κB in bone marrow function during peritonitis in the mouse

2014 ◽  
Vol 100 (2) ◽  
pp. 111-118
Author(s):  
Eirunn Knudsen ◽  
Harald Carlsen ◽  
Arne Bøyum ◽  
Haakon Breien Benestad ◽  
Per Ole Iversen
Keyword(s):  
Bone Marrow ◽  
Transcription Factor ◽  
Bone Marrow Function

Relationships between plasma adiponectin and blood cells, hepatopancreatic enzymes in women

2004 ◽  
Vol 91 (02) ◽  
pp. 360-366 ◽  
Author(s):  
Katsuhiko Namioka ◽  
Shinji Katayose ◽  
Miyao Matsubara
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Bone Marrow ◽  
Blood Cells ◽  
White Blood Cells ◽  
Serum Triglyceride ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Before And After ◽  
Bone Marrow Function

SummaryAdiponectin, which is secreted specifically from adipocyte, is thought to play a key role in the metabolic syndrome. We studied the associations of plasma adiponectin concentrations with blood cells and hepatopancreatic enzymes in 339 women aged 54.0 ± 0.8 (mean ± SE) years. Plasma adiponectin before and after adjustment for body composition or calculated insulin resistance increased in slight anemic women (372.6 ± 2.6 ×104/mm3) compared with non-anemic subjects (471.1 ± 1.7) (all p < 0.0001), and were inversely associated with red blood cells (RBC), hemoglobin, hematocrit, white blood cells and platelet values (p < 0.0001 ∼ 0.02), independent of age, diastolic blood pressure, body mass index, serum triglyceride, insulin resistance or blood urea nitrogen. Age and adiponectin/body fat mass (%) were negative, and blood pressure and insulin resistance were positive significant independent determinants of RBC in stepwise regression analysis. Moreover, adiponectin before and after adjustment were inversely associated with serum ALAT,γGTP and ChE, and positively with amylase levels (p < 0.0001 ∼ 0.02). These results indicate the possibility that increased adiponectin may contribute to the suppressive bone marrow function in vivo. Combined with the leptin’s data, adipocyte derived proteins were related to the hematopoiesis, therefore it has shown the possible existence of adipose tissue/ bone marrow function linkage more clearly. Furthermore, hepatopancreatic enzyme associations with this protein may indicate the possibility that adiponectin will regulate the hepatopancreatic function in health and disease.

scholarly journals Bone marrow function. I. Peripheral T cells are responsible for the increased auto-antiidiotype response of older mice.

1985 ◽  
Vol 161 (5) ◽  
pp. 1237-1242 ◽  
Author(s):  
Y T Kim ◽  
E A Goidl ◽  
C Samarut ◽  
M E Weksler ◽  
G J Thorbecke ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Immune Function ◽  
Lethal Dose ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spleen Cells ◽  
Peripheral T Cells ◽  
Bone Marrow Function ◽  
Low Levels

After immunization with trinitrophenyl (TNP)-Ficoll, mice produced both anti-TNP antibodies and auto-anti-idiotype (auto-anti-Id) antibodies specific for the anti-TNP antibody. Older animals produced more auto-anti-Id than did young animals. When mice were exposed to a normally lethal dose of irradiation while their bone marrow (BM) was partially shielded, they survived and slowly (6 wk) regained immune function, as indicated by the number of nucleated cells in their spleen and the in vitro primary plaque-forming cell (PFC) response of their spleen cells to TNP-treated aminoethylated polyacrylamide beads. Recovery is presumably the result of repopulation of the peripheral lymphoid system by cells originating in the BM. By enzyme-linked immunosorbent assay (ELISA), and by hapten-augmentable PFC assay, we show that, after recovery from irradiation with their BM shielded, old animals produce low auto-anti-Id responses, like those of young animals. The transfer of splenic T cells into mice irradiated with their BM shielded provided evidence that the magnitude of the auto-anti-Id response is controlled by the peripheral T cells. Thus, mice that received splenic T cells from aged donors produced high levels of auto-anti-Id while those that received splenic T cells from young donors produce low levels of auto-anti-Id.

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