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Neurochem Res. 2002 May;27(5):359-68.
Distribution of coenzyme Q homologues in brain.

Albano CB, Muralikrishnan D, Ebadi M.

Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine and Health Sciences, Grand Forks 58203, USA.

Ubiquinone (coenzyme Q10), in addition to its function as an electron and proton carrier in mitochondrial electron transport coupled to ATP synthesis, acts in its reduced form (ubiquinol) as an antioxidant, inhibiting lipid peroxidation in biological membranes and protecting mitochondrial inner-membrane proteins and DNA against oxidative damage accompanying lipid peroxidation. Tissue ubiquinone levels are subject to regulation by physiological factors that are related to the oxidative activity of the organism: they increase under the influence of oxidative stress, e.g. physical exercise, cold adaptation, thyroid hormone treatment, and decrease during aging. In the present study, coenzyme Q homologues were separated and quantified in the brains of mice, rats, rabbits, and chickens using high-performance liquid chromatography. In addition, the coenzyme Q homologues were measured in cells such as NG-108, PC-12, rat fetal brain cells and human SHSY-5Y and monocytes. In general, Q1 content was the lowest among the coenzyme homologues quantified in the brain. Q9 was not detectable in the brains of chickens and rabbits, but was present in the brains of rats and mice. Q9 was also not detected in human cell lines SHSY-5Y and monocytes. Q10 was detected in the brains of mice, rats, rabbits, and chickens and in cell lines. Since both coenzyme Q and vitamin E are antioxidants, and coenzyme Q recycles vitamins E and C, vitamin E was also quantified in mice brain using HPLC-electrochemical detector (ECD). The quantity of vitamin E was lowest in the substantia nigra compared with the other brain regions. This finding is crucial in elucidating ubiquinone function in bioenergetics; in preventing free radical generation, lipid peroxidation, and apoptosis in the brain; and as a potential compound in treating various neurodegenerative disorders.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12064350&dopt=Abstract

cam.ac.uk

Measurements of Ca(2+) influx in Fura-2/AM loaded prothoracic glands (PGs) of the silkworm, Bombyx mori, after application of forskolin or the cAMP analogue, 8-bromo-cAMP, showed a steady increase in [Ca(2+)](i), which was of extracellular origin and was inhibited, in both cases, by the dihydropyridine (DHP) derivative, nitrendipine. Nitrendipine also inhibited the abrupt S(-).Bay K 8644-mediated increase in [Ca(2+)](i) and its effects were mimicked by a myoinhibitory/prothoracicostatic peptide (Mas-MIP I/PTSP), which was isolated from Manduca sexta and was found to possess ecdysteroidostatic activity in Bombyx mori PGs. This peptide blocked both the forskolin and S(-).Bay K 8644-mediated increase in [Ca(2+)](i) of PG cells. It was ineffective, however, in blocking the recombinant prothoracicotropic hormone (rPTTH)-stimulated high increase in [Ca(2+)](i) of PG cells suggesting that distinct and independently regulated Ca(2+) influx mechanisms operate in the PG cells of Bombyx mori. The dependence of DHP-sensitive Ca(2+) channels on the cAMP-signalling cascade was further corroborated by the inabilitity of nitrendipine to block the thapsigargin-stimulated high increase in [Ca(2+)](i) after depletion of Ca(2+) from the intracellular stores. This, together with the inability of thapsigargin to stimulate the cAMP levels of PG cells suggest that there is a tightly regulated cross-talk mechanism between the two signalling cascades of Ca(2+) and cAMP. The combined results suggest a cAMP-mediated regulation of the opening-state of DHP-sensitive Ca(2+) channels and stimulation of [Ca(2+)](i) increases and ecdysteroid secretion by a positive feedback mechanism. Mas-MIP I/PTSP interferes with this mechanism by blocking DHP-sensitive Ca(2+) channels. This regulatory mechanism appears to be autonomously stimulating ecdysteroidogenesis by the PGs, it is regulated by Mas-MIP I/PTSPS, and it is not involved in other Ca(2+) influx mechanisms that operate within the PG cells of Bombyx mori.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535680&dopt=Abstract

Zhonghua Fu Chan Ke Za Zhi. 2002 Oct;37(10):598-600.
[Effect of hormone replacement therapy on homocysteine and echocardiography in postmenopausal women]

[Article in Chinese]

Hui Y, Wu Y, Xiao L, Tang Z, Wu Y, Li Y.

Department of Obstetrics and Gynecology, Beijing Hospital, Ministry of Public Health, Beijing 100730, China.

OBJECTIVE: To observe the effects of hormone replacement therapy (HRT) on fasting total plasma homocysteine levels and echocardiography in postmenopausal women. METHODS: Subjects were assigned to four groups. Group I: 30 postmenopausal women were assigned to sequentially combined daily 0.625 mg conjugated equine estrogen (CEE) plus 2 mg medroxyprogesterone acetate (MPA) or plus 4 mg MPA daily for 14 days in a 28 day cycle for 3 months. Group II: 30 postmenopausal women did not received HRT. Group III: 20 postmenopausal women who took HRT for 1.5 years. Group IV: 20 postmenopausal women who never took HRT. Measurement of fasting total plasma homocysteine was performed before and after 3 months treatment in group I and group II. Fasting total plasma homocysteine was determined and echocardiography was taken in group III and group IV. RESULTS: Fasting total plasma homocysteine concentrations were not altered significantly after 3 months in group I and group II [before HRT: (9.3 +/- 2.5) micro mol/L, (9.4 +/- 2.9) micro mol/L; after HRT: (9.1 +/- 2.8) micro mol/L, (9.8 +/- 3.6) micro mol/L, respectively (P > 0.05)]. Compared with women of group III, women of group IV had statistically significant lower plasma homocysteine [(8.0 +/- 1.3) micro mol/L, (10.3 +/- 3.2) micro mol/L, respectively (P < 0.05)]. Echocardiography was not found any difference between those two groups. CONCLUSIONS: Three months HRT has no effect on plasma homocysteine levels in postmenopausal women but the postmenopausal women using HRT 1.5 years have lower plasma homocysteine levels than those who never received HRT. Echocardiography showed no detectable changes between women received 1.5 years HRT and those who received no HRT.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12487933&dopt=Abstract

Neurochem Res. 2002 May;27(5):381-8.
Distribution of the hypothalamic cardioactive hormone "G"-protein complex (PCG) in neuronal elements of the heart in intact and vagotomized rats.

Abrahamyan SS, Fodor M, Galoyan AA, Palkovits M.

H. Buniatian Institute of Biochemistry, NAS RA, Yerevan, Armenia.

The distribution of the protein-carrier of one of the coronary dilatatory glycopeptides, neurohormone "G" (PCG) in rat heart was examined by immunohistochemistry. PCG-immunoreactive nerve fibers and varicosities were found around cardiac ganglion cells and in close topographical contact with coronary vessels and capillaries of the heart. The anatomical localization of the PCG-containing neuronal fibers was similar that of calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY); however, the intensity of the stainings were different. In contrast to NPY immunostainings, cardiac ganglion cells did not show any PCG immunoreactivity. Some of the small, SIF cell-like NPY immunopositive neurons were also immunostained to PCG. In the atrial cardiomyocytes, only ANP exhibited fairly intensive immunoreactivity. Fourteen days after vagotomy, no considerable changes were found in the distribution of PCG and other neuropeptides investigated in cardiac neurons and nerve fibers. The presence of PCG in cardiac neuronal elements suggests a possible role of this peptide in cardiovascular regulations.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12064353&dopt=Abstract

J Cell Physiol. 2002 May;191(2):217-26.
COX-dependent and -independent pathways in bradykinin-induced anion secretion in rat epididymis.

Cheuk BL, Ko WH, Wong PY.

Department of Physiology, The Chinese University of Hong Kong, Shatin, NT.

Lysylbradykinin (LBK) added to the apical or basolateral side of cultured rat epididymal monolayers stimulated a rise in short-circuit current (Isc) due to anion secretion. The concentration-response relationships for the apical and basolateral applications have EC50 value of 0.001 microM. The responses to apical or basolateral application of LBK were blocked by WIN64338, a specific B2 receptor antagonist, but not by Des-Arg9,[Leu8]-BK, a specific B1 receptor antagonist, indicating that the LBK effects were mediated through B2 bradykinin receptors. Experiments to desensitize the B2 receptors by repeated stimulation have demonstrated that the responses to apical or basolateral LBK were due to discrete receptors on the apical or basolateral surface. In epithelia clamped in the Ussing chambers, addition of LBK to the apical or basolateral surface evoked release of PGE2 into the apical and basolateral bathing solutions over the first 10 min following hormone addition. LBK added to the basolateral side elicited a greater release than it was added to the apical side. Pretreatment of the epithelia with piroxicam (5 microM) abolished PGE2 release elicited by apical or basolateral LBK and abrogated the Isc induced by basolateral LBK. However, the rise in Isc induced by apical LBK was reduced by 31.3% only. The anion secretion response to apical LBK was not affected by MDL-12330A, an adenylate cyclase inhibitor, but greatly attenuated by thapsigargin, an inhibitor of intracellular Ca2+ release. However, the reverse effects were seen for basolateral LBK. It is concluded that distinct pathways are involved in the stimulation of anion secretion by apical or basolateral LBK. The response to basolateral LBK was COX-dependent, mediated by PGE2 and involves cAMP as second messenger. In contrast, the response to apical LBK is largely COX-independent, not mediated by PCE2 and involves Ca2+ as intracellular messenger.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12064465&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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