The Difference in Sebum Secretion Affecting Development of Acne.

BACKGROUND: Although sebum secretion is crucial for acne development, acne lesion distribution is not always similar to the topographic differences of sebum secretion. OBJECTIVE: To analyze whether sebum secretion affects acne development and distribution and to assess other factors possibly influencing the relationship between acne and sebum secretion. METHODS: This single-center retrospective study included 67 acne patients and 50 controls. Acne patients were divided into 3 groups based on acne lesion distribution: T-zone dominant, U-zone dominant, and mixed groups. The secreted sebum level in each zone of acne patients was compared with that of controls. We also conducted correlation analysis between secreted sebum level and acne number, depending on the facial zone. RESULTS: No significant difference was found between acne patients and controls regarding age and sex ratio. The U-zone dominant group showed increased sebum levels compared with controls in the U-zone and whole face, but a similar result was not obtained in the T-zone dominant group. Moreover, there was a significant correlation between the number of lesions and secreted sebum level in the U-zone, but not in the T-zone. Further, there was a more significant relation in the U-zone of male and young patients. CONCLUSION: We found that increased sebum secretion compared with the condition may affect acne development, especially in the U-zone. Sex and age may also influence the relationship between acne and increased sebum secretion. Acne lesion distribution may vary from patient to patient because sebum secretion affects acne differently depending on multiple factors.

PET imaging of dopamine transporters with [(18)F]FE-PE2I: Effects of anti-Parkinsonian drugs.

PURPOSE: This study aimed to assess the striatal [(18)F]FE-PE2I binding and the immunohistochemical stain of tyrosine hydroxylase (TH) in the striatum, and to evaluate the effects of therapeutic drugs on [(18)F]FE-PE2I binding. METHODS: Dynamic PET/CT of [(18)F]FE-PE2I was performed in Parkinson's disease (PD) rat models, induced by the unilateral injection of 6-OHDA into the striatum. A simplified reference tissue model method was used to calculate the striatal binding potential (striatal BPND). Each of the four normal rats was pretreated with pramipexole, amantadine, and escitalopram 30 min before [(18)F]FE-PE2I injection. The effect of L-DOPA combined with benserazide was assessed in the normal and PD rats. RESULTS: The BPND was significantly lower in the lesioned striatum than in the striatum of the normal rats. After the pretreatment with pramipexole, amantadine, and escitalopram, the values of the striatal BPND did not differ from those of the controls. The pretreatment with L-DOPA/benserazide, however, significantly reduced the striatal BPND. The striatal BPND of the PD rats with L-DOPA/benserazide pretreatment was not different from that of the same PD rats with placebo treatment. CONCLUSION: [(18)F]FE-PE2I may be used as a radioligand for the in-vivo imaging of the DAT. In the normal rats, [(18)F]FE-PE2I binding is unaffected by pramipexole, amantadine, and escitalopram. L-DOPA/benserazide does not affect the striatal [(18)F]FE-PE2I binding in PD rats.

Proof of mechanism study of a novel serotonin transporter blocker, DA-8031, using [11C]DASB positron emission tomography and in vivo microdialysis.

OBJECTIVE: To investigate the efficacy of DA-8031, a novel compound for the treatment of premature ejaculation, we measured serotonin transporter (SERT) occupancy by DA-8031, as well as DA-8031-induced changes in extracellular serotonin levels, in the rat brain using positron emission tomography (PET) and 11C-N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine ([11C]DASB) and in vivo microdialysis, respectively. METHODS: [11C]DASB PET scans were performed in rats with graded doses of DA-8031 (vehicle: 10, 30, and 100 mg/kg). SERT occupancy in the midbrain was determined using binding potentials for [11C]DASB calculated by the multilinear reference tissue model. Extracellular serotonin levels were monitored in the dorsal raphe nucleus of rats after the administration of DA-8031 (10-100 mg/kg) using in vivo microdialysis. RESULTS: PET data indicated a reduction of [11C]DASB binding to SERTs in the midbrain as a function of DA-8031 dose. SERT occupancy for each DA-8031 dose (10-100 mg/kg) ranged between 31% and 84%. The drug dose required for 50% occupancy of SERT was 13.5 mg/kg in the midbrain, comparable with previous preclinical behavioral data (∼10-30 mg/kg). In vivo microdialysis showed that DA-8031 produced a dose-dependent increase in extracellular serotonin levels in the dorsal raphe nucleus (33%-81% increase for doses of 10-100 mg/kg). CONCLUSION: These preclinical data provide a proof of mechanism for DA-8031 as a novel compound of targeting the SERT for the treatment of premature ejaculation, warranting further clinical trials. They also offer insight into the optimal drug dose needed to exert therapeutic effects while minimizing adverse effects in humans.

Effect of nitric oxide synthase inhibitor and NMDA receptor antagonist on the development of nicotine sensitization of nucleus accumbens dopamine release: an in vivo microdialysis study.

We have previously found that the neuronal nitric oxide synthase inhibitor N-nitro-L-arginine (L-NNA) and the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 prevent behavioral sensitization to nicotine. This study aimed to investigate the effect of L-NNA and MK-801 on a neurochemical component of nicotine sensitization by evaluating the effect of the drugs on nicotine sensitization of nucleus accumbens dopamine (DA) release. Sprague-Dawley rats were pretreated with L-NNA (15 mg/kg, i.p.), MK-801 (0.3mg/kg, i.p.), or saline 30 min before injection of nicotine (0.4 mg/kg, s.c., once daily) for seven consecutive days. Twenty-four hours after the last drug injection, animals were challenged with local perfusion of 5 mM nicotine into the shell of nucleus accumbens for 60 min and DA release was monitored using in vivo microdialysis. In rats treated with repeated nicotine, acute nicotine challenge induced a greater increase of accumbal DA release than in saline-treated animals (maximal DA response=969+/-235% (mean+/-S.E.M.) of basal level versus 520+/-93%, p=0.042). Co-administration of L-NNA or MK-801 with nicotine attenuated an increase of DA release elicited by acute nicotine challenge, compared with nicotine alone (maximal DA response=293+/-58% and 445+/-90% of basal level, respectively versus 969+/-235%, p=0.004 and p=0.013, respectively). These data demonstrate that L-NNA and MK-801 block the development of nicotine sensitization of nucleus accumbens DA release, further supporting the involvement of nitric oxide and NMDA receptors in the development of behavioral sensitization to nicotine.