BACKGROUND: Acne, one af the commonest dermatological disorders, is a disease of the pilosebaceous unit, and the primarily involved site is the face, where this structure exists in maximal density. Among the many etiologieal factors of acne, changes in the kinetics of sebum secretion in acne patients have been described, but there is no report to compare follicular density and the sebum excretion rate in different facial regions between normal and acne patients. OBJECTIVES: The purpose of this study was to compare the sebum output and follicular density in different regions of the face in women with and without acne and to evaluate the differences between the two groups. METHODS: We studied 10 normal and 14 acneic women aged 19-27. Follicular density was determined by light microscopy counting pilosebaceous units on cyanoacrylate follicular biopsy specimens. The sebum excretion rate was calculated by an image analyzer with a sebum print on Sebutape. RESULTS: 1. Follicular density was not significantly different between the normal and acne group. The number of follicles decreased from the central to the lateral aspect of the face with the highest value being on the nose tip and the lowest on the lateral forehead. 2. The total sebum excretion rate and the number of actively secreting follicles showed different patterns in the two groups. There was a decreased value in the acne group in some central regions of face. In addition, central to lateral declining pattems, shown in the normd group, were not apparent in the acne group. 3. The follicular sebum excretion rate showed large variations in both groups, without apparent central to lateral declining patterns. The confluence of adjacent follicles seemed to produce falsely low or high values compared with previous studies. CONCLUSION: Sebum production is influenced both by the number of active follicles and their individual capacity to excrete sebum, and the total sebum excretion rate was lower than normal in low grade acne in this study. Obstruction of the outflow of sebum and regression of sebaceous glands due to comnlones may account for it.
Acne Vulgaris* ; Biopsy ; Cyanoacrylates ; Female ; Forehead ; Humans ; Kinetics ; Microscopy ; Nose ; Sebaceous Glands ; Sebum*

Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques(SPs) and neurofibrillary tangles(NFTs). beta-amyloid protein(Abeta) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of Abeta and tau formation are thought to be a final common pathway of AD. Acetycholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and alpha-macroglobulin increase risk of AD. In this article, we will review about the neurobioloby of AD and some newly developed research areas.
Acetylcholine ; Alzheimer Disease* ; Amyloid ; Amyloid beta-Peptides ; Apolipoproteins E ; Cerebrospinal Fluid ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 19 ; Chromosomes, Human, Pair 21 ; Complement System Proteins ; Dopamine ; Down Syndrome ; gamma-Aminobutyric Acid ; Genetics ; Lipoproteins ; Microglia ; Neurobiology* ; Proteolysis ; Serotonin

No abstract available.
Peptides*

Pseudohypoaldosteronism type 1 is a genetic renal tubular disease of salt wasting, presenting in young infants. Tubular unresponsiveness to elevated endogenous and exogenous aldosterone is the suggested pathogenetic mechanism. Oral sodium chloride supplementation relieve the clinical symptoms and electrolyte distrubances. We experienced 2 cases of PHA type 1 in 38-day and 45-day old male infants who were presented with failure to thrive, vomiting and/or dehydration. Laboratory data showed hyponatremia, hyperkalemia, hypochloremia and metabolic acidosis. Renal and adrenal functions were normal. Plasma renin activity and plasma aldosterone concentration were markedly elevated. Under the diagnosis of pseudohypoaldosteronism type 1, oral supplementation of NaCl and/or kayexalate improved the clinical states of the patients.
Acidosis ; Aldosterone ; Dehydration ; Diagnosis ; Failure to Thrive ; Humans ; Hyperkalemia ; Hyponatremia ; Infant ; Male ; Plasma ; Pseudohypoaldosteronism* ; Renin ; Sodium Chloride ; Vomiting

No abstract available.
Diet* ; Humans ; Immunoglobulin E* ; Incidence* ; Infant*

No abstract available.
Creatinine* ; Humans ; Infant, Newborn*

No abstract available.
Poisoning*

No abstract available.
Hepatitis B* ; Hepatitis* ; Humans ; Mothers* ; Parturition*

No abstract available.

No abstract available.
Biopsy* ; Child* ; Humans