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Int J Neurosci. 2003 Jul;113(7):989-98.
Hypothalamic digoxin, hemispheric dominance, and family bonding behavior.

Kurup RK, Kurup PA.

Department of Neurology, Medical College Hospital, Trivandrum, Kerala, India.

The isoprenoid pathway produces endogenous digoxin, a substance that can regulate neurotransmitter and amino acid transport. Digoxin synthesis and neurotransmitter patterns were assessed in individuals with differing family bonding patterns. The family bonding patterns were assessed by the FACES scale--family adaptability and cohesiveness evaluation scale. The criteria given in the handbook for the 16 PF--16 personality factors questionnaire by Cattell, Eber, and Tatsouke--was also chosen for assessing the individual personality aspect of family bonding after suitable modification. The patterns were compared in those with right hemispheric and left hemispheric dominance. Digoxin synthesis was increased with upregulated tryptophan catabolism (increased levels of serotonin, strychnine, and nicotine) and downregulated tyrosine catabolism (decreased levels of dopamine, noradrenaline, and morphine) in those with reduced family bonding and right hemispheric dominance. Digoxin synthesis was reduced with downregulated tryptophan catabolism (decreased levels of serotonin, strychnine, and nicotine) and upregulated tyrosine catabolism (increased levels of dopamine, noradrenaline, and morphine) in those with increased family bonding and left hemispheric chemical dominance. Hypothalamic digoxin plays a central role in the regulation of family bonding behavior. Hemispheric chemical dominance in relation to digoxin status is also crucial in this respect.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12881190&dopt=Abstract [PubMed - in process]

Int J Immunopharmacol. 1999 Feb;21(2):103-14.
Smokeless tobacco and nicotine bring about excessive cytokine responses of murine memory T-cells.

Petro TM, Schwartzbach SD, Zhang S.

Department of Oral Biology, University of Nebraska Medical Center, Lincoln 68583-0740, USA.

To determine the influence of smokeless tobacco (ST) and nicotine on the cytokine phenotype of memory T-cells, splenic mononuclear cells (SPM) were exposed to 1:10(2) or 1:10(3) dilutions of ST extract (ST-SPM), 10 or 100 microg/ml nicotine (NIC-SPM), or medium (CON-SPM) during 4 days of stimulation with anti-CD3. SPM were then washed extensively to remove residual ST or nicotine and restimulated with anti-CD3 and anti-CD28 in the absence of ST or nicotine. Expression of IL-2, IL-4, IL-10 and IFN-gamma protein and mRNA levels after 4 days of primary stimulation and after 24 and 48 h of restimulation was evaluated using ELISA and RT-PCR, respectively. After 4 days of primary stimulation, SPM exposed to 100 microg/ml nicotine sustained expression of IL-2, IFN-gamma, IL-10 and IL-4 mRNA as opposed to CON-SPM. Restimulation of CON-SPM resulted in maximum re-expression of cytokine mRNA at 24 h and a decline by 48 h. Restimulated NIC-SPM in the absence of nicotine delayed maximal re-expression of IL-2, IFN-gamma, IL-10 and IL-4 mRNA until 48 h. Heightened expression of cytokine mRNA at 48 h was paralleled by a small but significant increase in production of IFN-gamma, IL-4 and IL-10 protein by NIC-SPM as measured by ELISA. In contrast, ST-SPM did not exhibit residual expression of cytokine mRNA after 4 days of primary stimulation. Like NIC-SPM, however, restimulated ST-SPM exhibited maximum IL-2, IL-4, IFN-gamma, and IL-10 mRNA at 48 h. Heightened re-expression of cytokine mRNA at 48 h by ST-SPM was paralleled by increased production of IL-2, IFN-gamma, IL-4 and IL-10 protein. These results indicate that exposure of T-cells to nicotine, but not ST, during a primary immune response result in inordinate cytokine expression after 4 days. In addition, memory T-cells initially exposed to nicotine or ST during a primary immune response, exhibit excessive cytokine expression when T-cells are restimulated in the absence of nicotine or ST. pharmacology.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10230873&dopt=Abstract

Diabetes Care. 2003 Aug;26(8):2311-7.
A descriptive and comparative study of the prevalence of depressive and anxiety disorders in low-income adults with type 2 diabetes and other chronic illnesses.

Thomas J, Jones G, Scarinci I, Brantley P.

Mayo Clinic, Nicotine Dependence Center, Rochester, Minnesota 55905, USA. thomas.janeayo.edu

OBJECTIVE: To determine whether type 2 diabetes contributes to the presence of depressive and anxiety disorder diagnoses in low-income adults with hypertension, asthma, and/or arthritis. RESEARCH DESIGN AND METHODS: Using a cross-sectional design, this study administered a structured diagnostic interview to low-income primary care patients diagnosed with type 2 diabetes, hypertension, arthritis, and asthma, as well as to those with no chronic illness (n = 326), to determine the 12-month prevalence of depressive and anxiety disorders. A logistic regression (LR) model was used to assess whether a diagnosis of depression and/or anxiety was associated with type 2 diabetes after adjusting for known risk factors. RESULTS: A high prevalence rate of depressive and/or anxiety disorders was found in the total sample (29%) and in all three illness groups: type 2 diabetes (36%), other chronic illnesses (24%), and no chronic illness (31%). Using LR, a main effect was detected for illness group when age and education were controlled (chi(2) = 22.66, df 4, P = 0.000). Specifically, the odds of occurrence of a depressive and/or anxiety disorder in those with comorbid type 2 diabetes were twice that in the nondiabetic, chronically ill comparison group (odds ratio 2.26, 95% CI 1.28-4.01, P = 0.005). CONCLUSIONS: These results suggest a positive contribution of type 2 diabetes to increased rates of depressive and/or anxiety disorders in patients with hypertension, asthma, and/or arthritis and support prior research that type 2 diabetes may serve as an indicator of depression and anxiety in low-income adults treated in primary care clinics.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12882854&dopt=Abstract [PubMed - in process]

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