Wisuit Pradidarcheep

Lower urinary tract symptoms and its potential relation with late-onset hypogonadism.

The study of the health status of the aging male takes presently a more integrative approach and it appears that ailments typical of male aging, such as lower urinary tract symptoms (LUTS), (visceral) obesity, metabolic syndrome and erectile failure are significantly interrelated. A common denominator of the above ailments is lower-than-normal testosterone levels occurring in a significant proportion of elderly men. This review addresses the potential connections between LUTS and late-onset hypogonadism. In animal studies there appear to be androgen and estrogen receptors in the urothelium and smooth muscle cells of the urethra and bladder of the rat and rabbit, as well as in the neurons in the autonomic ganglia of the prostatic plexus of the male rat. Upon castration electrically evoked relaxations of the smooth muscle of the prostatic urethra were decreased. There is a Rho-kinase activation/endothelin pathway; possibly involved in the increased smooth muscle activity found in both LUTS/benign prostate hyperplasia. Nitric oxide (NO) appears to have a smooth muscle relaxing effect in the urogenital organs. Studies in humans have convincingly shown that phosphodiestererase inhibitors have a beneficial effect on LUTS. More intervention studies should be undertaken to test the clinical validity of the theoretically plausible interrelationship between LUTS and late-onset hypogonadism.

Distribution of Hepatic Myofibroblasts and Type I and III Collagen in Rat Liver Cirrhosis Induced by Thioacetamide

La tioacetamida (TAA) puede provocar diversos tipos de cirrosis hepatica en la rata, incluyendo fibrosis en puente, fibrosis biliar, fibrosis perisinusoidal/pericelular y fibrosis centrolobulillar, en los que diferentes poblaciones de miofibroblastos hepaticos (MFs) estan involucrados. Los MFs hepaticos se pueden clasificar en tres grupos: (a) MFs portal/ septal; (b) celulas estrelladas hepatica activada miofibroblasticas (HSC/MFs), y (c) miofibroblastos de interface (IF/MFs). El presente estudio se realizo para examinar la morfologia y localizacion de los MFs hepaticos en relacion con la distribucion de colageno Tipos I y III en el higado de ratas cirroticas. Se utilizo inmunohistoquimica de a-actina de musculo liso para demostrar la morfologia y localizacion de las subpoblaciones de MFs hepatica. La distribucion de colagenos Tipos I y III se investigo utilizando anticuerpos especificos. FMs portales y septales mostraron forma de molino de viento y se localizaron cerca de afluentes de las venas porta y hepatica donde los colagenos Tipos I y III se acumularon. HSC/MFs con forma aracnoide se localizaron en los espacios de Disse y los espacios entre hepatocitos vecinos, donde se formo el colageno Tipo I. IF/MFs mostraron formas aracnoides y se distribuyeron a lo largo del margen de los septos fibrosos donde se condenso el colageno Tipo I . MFs con formas poligonales tambien fueron encontrados alrededor de la pared de los sinusoides hepaticos, en el margen de los septos fibrosos y en todo el tracto portal. Probablemente fueron celulas de transicion a los MFs maduros. Nuestros datos sugieren que cada subpoblacion de MFs hepaticos muestra una morfologia y localizacion caracteristica, que se correlaciona con la localizacion de colagenos Tipo I y o III.

Collagen arrangement in space of Disse correlates with fluid flow in normal and cirrhotic rat livers

Little is known about collagen arrangement in the space of Disse was related to the fluid flow both in normal and cirrhotic liver. We examined the changes in the arrangement of type‐I collagen in thioacetamide‐induced cirrhotic rat livers with immunohistochemistry and SEM after maceration of the noncollagenous tissues with NaOH. The sparse bundles of collagen fibers in the spaces of Disse were mostly elongated fibers with a disorganized arrangement in each nodule. They connected with the broad fibrous septa. Based on a comparison of the architecture of the collagen fibers and the established flow of fluid in the space of Disse, we hypothesize that the fluid in the space of Disse streams along collagen fibers in all directions to broad fibrous septa. The appearance of perinodular plexus in cirrhotic rat livers probably helps to reduce portal hypertension. Microsc. Res. Tech. 78:187–193, 2015.

Altered distribution of M2 and M4 muscarinic receptor expression in vitiligo.

Dear Editor, Although the etiopathology of vitiligo is still unclear, alterations in the neuronal and extraneuronal cholinergic system of the skin might be one of its possible causes. Nicotinic and muscarinic receptors are components of the cholinergic system. Acetylcholine binds to the skin, and the nicotinic receptor may be involved in cutaneous hyperpigmentation while the muscarinic receptor may account for hypopigmentation of the skin. Ach has an inhibitory effect on melanocytes in vitiligo patients and causes skin depigmentation. H2O2 accumulation in the skin might deactivate acetylcholine esterase, an enzyme that metabolizes and lowers Ach levels, thus, in turn, would increase local Ach concentration within the epidermis. Furthermore, acetylcholine esterase activity is absent in depigmenting skin but present in repigmenting skin. Actions of Ach in skin are exerted through two basically different types of receptors, namely, ionotropic nicotinic receptors and metabotropic muscarinic receptors, both involved in melanocyte pigmentation through Ach action. The nicotinic and muscarinic effects of Ach lead to increased and decreased skin pigmentation, respectively. The present study examined the distribution and expression of four muscarinic receptors (M1R–M4R) in human vitiligo skin. Skin biopsies from 11 vitiligo patients and three volunteers (controls), were used to examine the distribution and expression of muscarinic receptor by immunohistochemistry. The distribution patterns of M1R and M3R in vitiligo patients (both lesional and non-lesional areas) were not different from that in the control group. The M2R and M4R subtypes in vitiligo patients were immunostained only at the granular layer of the epidermis but not in the melanocytes while in the control group they were expressed at the basal cell layer of the epidermis and in the melanocytes (P < 0.05). There were no differences in distribution and expression of M1R–M4R between lesional and non-lesional areas of vitiligo patients. With light microscopy, there were, in the vitiligo subjects, no significant differences in the presence of melanocytes between lesional and non-lesional areas. In the lesional vitiligo skins there was: (i) thickening of the stratum corneum; (ii) vacuolization in melanocytes and keratinocytes; and (iii) infiltration of inflammatory cells in the dermis. In the control group the muscarinic receptors (M1R–M4R) were each expressed in human keratinocytes in different histological locations. The M1R antiserum stained the perinuclear membrane, nucleolus and intracytoplasmic organelles of the keratinocytes of stratum basale and stratum spinosum with strong staining intensity. The M2R and M4R subtypes were localized in the cell membrane of all keratinocytes of the stratum basale only with moderate staining intensity. The M3R antiserum was more or less similarly distributed as the M1R antiserum, but appeared also in the stratum granulosum of the epidermis (Fig. 1). The M3R positively stained cells showed moderate staining intensity. No difference in distribution pattern of MR in both lesional and non-lesional areas of vitiligo patients was found. The distribution of M1R and M3R was similar to the control group. However, very mild positive staining for M3R was detected only in 45.5% of the patients (Table 1). But the M2R and M4R subtypes, in the vitiligo patient, were expressed only in the keratinocytes of the granular cell layer with moderate staining intensity. However, weak staining with the M2R antiserum was found within the cytoplasm, in the perinuclear membrane and nucleolus at the stratum basale and the stratum spinosum (Fig. 2). We found that melanocytes were absent in the lesional areas of four vitiligo patients. In the control