Biomedical subjects

J Majzoub

Publications and source records attributed to J Majzoub.

5 recordsLinked to original sources

PubMed2004

Catecholamine synthesizing enzymes and their modulation by immobilization stress in knockout mice.

The c-fos knockout mice (c-fos KO) and corticotropin-releasing hormone knockout mice (CRH KO) can serve as interesting models for studying mechanisms involved in response of the organism to stress, focused mainly on the hypothalamic-pituitary-adrenal (HPA) axis and sympathoadrenal system (SAS). The present study focused on the investigation of changes in gene expression of catecholamine biosynthesizing enzymes tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT) in adrenal medulla of c-fos KO and CRH KO mice stressed by immobilization. Levels of TH, DBH, and PNMT mRNA were determined by reverse transcription-polymerase chain reaction (RT-PCR). Single immobilization for 2 h significantly increased adrenomedullary TH, DBH, and PNMT mRNA levels in both c-fos KO and wild-type (WT) mice compared to unstressed controls. In CRH KO mice, PNMT gene expression was not increased to the same extent after single, but especially after repeated immobilization as in WT mice, in contrast to TH and DBH mRNA levels. Thus, our data indicate that CRH deficiency can influence the PNMT mRNA level in adrenal medulla during stress, confirming the idea that the HPA axis plays the crucial role in PNMT gene regulation in mice. On the other hand, c-Fos protein probably does not play a crucial role in TH, DBH, and PNMT gene expression in adrenal medulla under stress conditions.

Adrenal Medulla↗

PubMed2001

Maternal experiences of racism and violence as predictors of preterm birth: rationale and study design.

Chronic psychological stress may raise the risk of preterm delivery by raising levels of placental corticotropin-releasing hormone (CRH). Women who have been the targets of racism or personal violence may be at particularly high risk of preterm delivery. The aims of this study are to examine the extent to which: (1) maternal experiences of racism or violence in childhood, adulthood, or pregnancy are associated with the risk of preterm birth; (2) CRH levels are prospectively associated with risk of preterm birth; and (3) CRH levels are associated with past and current maternal experiences of racism or violence. We have begun to examine these questions among women enrolled in Project Viva, a Boston-based longitudinal study of 6000 pregnant women and their children.

Adult↗

PubMed1990

The testicular effects of tumor necrosis factor.

Tumor necrosis factor (TNF) is a cytokine that mediates many of the metabolic responses after endotoxemia, septicemia, and tissue injury. The effect of TNF on testicular function was determined in a series of studies in which rhTNF (0, 2, and 4 X 10(5) units/kg/24 hours) was administered by continuous infusion to male Wistar rats maintained on total parenteral nutrition adequate for growing rats. Testicular weight and histology, and plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone levels were determined at 1, 3, and 6 days. Testicular weight decreased within 24 hours and this was associated with a fall in plasma testosterone and increased LH and FSH levels. These changes persisted for 6 days, indicating a loss of testosterone-mediated negative feedback on gonadotropin release. Histologic examination demonstrated significant damage to the germ cells in the adluminal compartment of the seminiferous epithelium; extensive exfoliation of spermatocytes and spermatids occurred at day six. However the primary spermatogonia in the basal compartment were relatively spared. Damage to the seminiferous epithelium at earlier times was noted in some tubules. The decrease in testosterone concentration and increase in gonadotropin levels suggest that TNF interferes with Leydig cell function. Germ cell damage may be a direct effect of TNF on these cells or may occur through secondary mechanisms involving Leydig or Sertoli cell dysfunction.

Animals↗

PubMed1989

Increases in plasma digitalis-like factor activity during insulin-induced hypoglycemia.

Digitalis-like factor (DLF) appears to be widely distributed throughout the body, and has been specifically localized to the mammalian hypothalamus. In this study we monitored the DLF response to insulin-induced hypoglycemia in 11 normal males. Hypoglycemia was associated with a significant increase in serum DLF activity over basal values (40 +/- 5 pg digoxin Eq/ml, mean +/- SEM) at 60 min (83 +/- 8 pg digoxin Eq/ml) and 90 min (86 +/- 10 pg digoxin Eq/ml) following insulin administration (p less than 0.01). We measured the DLF response to insulin-induced hypoglycemia in other men after infusion of hypertonic saline (n = 8) or after oral water-loading (n = 8). Saline infusion (0.06 ml 5% saline/kg BW/min for 120 min prior to insulin infusion) or water loading (20 ml/kg BW over 60 min completed 30 min before insulin infusion) alone significantly increased serum DLF (saline: 21 +/- 5 to 60 +/- 18 pg digoxin Eq/ml, p less than 0.05; water: 18 +/- 11 to 49 +/- 15 digoxin Eq/ml, p less than 0.05). DLF activity was further significantly increased within each group 60 and 90 min after administration of insulin. In the group infused with hypertonic saline, insulin caused increases of serum DLF from 60 +/- 18 at time 0 to 170 +/- 17 pg digoxin Eq/ml at peak (p less than 0.01). Similarly, in the oral water-loaded group serum DLF increased from 49 +/- 15 at time 0 to 127 +/- 24 pg digoxin Eq/ml at peak (p less than 0.01) after they received insulin.2=

Adult↗

PubMedDate not supplied

Lessons from CRH knockout mice.

Corticotropin-releasing hormone (CRH), the major regulator of hypothalamic-pituitary-adrenal (HPA) axis, has a wide spectrum of actions within the central nervous system and the periphery. The development and use of Crh knockout mice (Crh-/-) has been an important tool for addressing the physiologic and pathologic roles of CRH. This review describes the generation and characterization ofCrh -deficient mice as well as the use of these mice to study the role of CRH in maternal and fetal HPA axes development and in the regulation of the adult HPA axis and behavior. The review concludes with information about recently discovered CRH-related peptides and their possible roles in some of the functions thought initially to be mediated by CRH.

Animals↗