R. De Souza

A Preliminary Investigation of the Effects of Aging on the Nerve Cell Number in the Myenteric Ganglia of the Human Colon

We have examined the number of nerve cells present in the myenteric plexus of the human large intestine using a nonhistochemical method (Giemsa) in laminar preparations of the muscularis externa in two groups of subjects aged 20-35 and over 65 years. The collagen and elastic system related fibers in the myenteric ganglia were also qualitatively evaluated. The total number of neurons decreased in the old subjects by over 37%. The perikaryal area of most of the neurons in both the young and old subjects fell from 101 to 200 microns2. A ganglionic capsule was present and was thicker in the ganglia from the old subjects as were the septa within the ganglia. Both collagen and elastic system fibers were more numerous in the ganglia from the old subjects. We conclude that the decrease in neuron density with age is accompanied by an apparent increase in the fibrous components of the myenteric ganglia.

Aging of myocardial collagen

The objective of this article was to present a review of the collagen tissue of the heart muscle as a function of age. The myocardial collagen matrix consists of a network of fibrillar collagen which is intimately connected to the myocyte. Most collagen fibers reside in parallel with myocytes. These fibers may have a wavy, taut or coiled appearance. Fibrillar collagen types I and III are the major components of the myocardial collagen matrix. Collagen type I has been found to represent nearly 80% of the total collagen protein, while type III collagen is present in lower proportions (approximately 11%). Cardiac fibroblasts are the cellular source of fibrillar collagen, cardiac myocytes expressing only mRNA for type IV collagen. Collagens types I and III exhibit a high tensile strength which plays an important role in the behavior of the ventricle during the cardiac cycle. The collagen concentration and the intermolecular cross-linking of collagen increase with age. Measurements of collagen content in myocardial tissue siggest that it is the type I collagen fibers that increase in number and thickness in the aged. At the same time, electron microscopic observations have shown an increase in the number of collagen fibrils with a large diameter in the aging heart. The mechanism responsible for the myocardial fibrosis in the senescent myocardium is unclear. The collagen deposition in the myocardium could be due to the regulation of collagen byosinthesis at pre-translational levels. It is possible that the regulatory elements involved in this process are growth factors such as TGF-β1 and hormones and neurotransmitters. Details of regulatory mechanism that may come into play during aging may be elucidated by further investigations. The accumulation of collagen within the myocardium increases muscle stiffness. Myocardial function is affected by this process; this is usually reflected by incomplete relaxation during early diastolic filling, and presumably account for the decrease in early left ventricular diastolic compliance.The objective of this article was to present a review of the collagen tissue of the heart muscle as a function of age. The myocardial collagen matrix consists of a network of fibrillar collagen which is intimately connected to the myocyte. Most collagen fibers reside in parallel with myocytes. These fibers may have a wavy, taut or coiled appearance. Fibrillar collagen types I and III are the major components of the myocardial collagen matrix. Collagen type I has been found to represent nearly 80% of the total collagen protein, while type III collagen is present in lower proportions (approximately 11%). Cardiac fibroblasts are the cellular source of fibrillar collagen, cardiac myocytes expressing only mRNA for type IV collagen. Collagens types I and III exhibit a high tensile strength which plays an important role in the behavior of the ventricle during the cardiac cycle. The collagen concentration and the intermolecular cross-linking of collagen increase with age. Measurements of collagen content in myocardial tissue siggest that it is the type I collagen fibers that increase in number and thickness in the aged. At the same time, electron microscopic observations have shown an increase in the number of collagen fibrils with a large diameter in the aging heart. The mechanism responsible for the myocardial fibrosis in the senescent myocardium is unclear. The collagen deposition in the myocardium could be due to the regulation of collagen byosinthesis at pre-translational levels. It is possible that the regulatory elements involved in this process are growth factors such as TGF-β1 and hormones and neurotransmitters. Details of regulatory mechanism that may come into play during aging may be elucidated by further investigations. The accumulation of collagen within the myocardium increases muscle stiffness. Myocardial function is affected by this process; this is usually reflected by incomplete relaxation during early diastolic filling, and presumably account for the decrease in early left ventricular diastolic compliance.

Age-Induced Nerve Cell Loss in the Myenteric Plexus of the Small Intestine in Man

We examined the number of nerve cells of the myenteric plexus and the thickness of the smooth muscle in the small intestine in autopsy material of 6 young and 6 old persons. Neurons in the myenteric plexus have been visualised by a nonhistochemical method (Giemsa) in laminar preparations of the muscularis externa. Significant reductions of at least 34% in the number of neurons in the ganglia of the myenteric plexus of the old subjects were recorded in all regions of the small intestine, especially in the duodenum where the number of neurons decreased by over 38%. However, there was no significant correlation between nerve cell count and thickness of intestinal smooth muscle since no difference was found in thickness of intestinal smooth muscle between young and old subjects. The decrease in the neuron density with age could affect the potential of the enteric nervous system to influence control over several small intestinal functional parameters.

Nerve Cell Loss in the Myenteric Plexus of the Human Esophagus in Relation to Age: A Preliminary Investigation

Morphometric measurements have been carried out on the human myenteric esophageal neurons at the ages of 20-40 and more than 70 years. The number of neurons decreases after 70 years of age, which is accompanied by an increase in the sizes of the neurons. In percentage terms the decrease in the number of neurons in the aged varied from 22 to 62% along the esophagus being most pronounced in its superior third at the junction with the pharynx.

Vasoactive-intestinal-peptide- and substance-P-immunoreactive nerve fibres in the myenteric plexus of mouse colon during the chronic phase of Trypanosoma cruzi infection.

The distribution of a tachykinin (substance P) and vasoactive intestinal peptide (VIP) and the number and morphology of the large granular vesicles (LGV) in the myenteric plexus of the colons of mice were investigated. Six of the 12 young, male, Swiss mice studied had been inoculated with the Y strain of Trypanosoma cruzi 2 months previously whereas the others were uninfected controls. Substance P (SP) and VIP were localized by light microscopy, using an immunohistochemical method, and LGV were counted in sections studied by electron microscopy. There were far fewer LGV and less intensely staining varicose VIP- and SP-positive nerve fibres in the infected mice than in the controls. Denervation of the myenteric plexus may decrease the content of tachykinins (TK) and VIP in animals infected with T. cruzi. Such reduction in TK and VIP activity could be related to the disturbances in intestinal motility observed in the chronic phase of Chagas disease.

Effects of Exercise on the Morphology of the Myenteric Neurons of the Duodenum of Wistar Rats during the Ageing Process

This study aimed to evaluate the effects of regular physical activity on the morphology of the myenteric plexus of the duodenum in rats during the ageing process. To this end, 45 Wistar rats were divided into three groups: C (sedentary – 6 months old), S (sedentary – 12 months old) and T (trained – 12 months old). The animals of group S were given with a physical activity programme consisting of a 10‐min‐treadmill workout once a week. The animals of group T were submitted to the physical activity programme five times a week. Their duodenums were collected and submitted to the techniques of nicotinamide adenine dinucleotide (NADH)‐diaphorase enzyme histochemistry for whole‐mount preparations and transmission electron microscopy. No differences in the constitution of the myenteric plexuses were found when the sedentary and trained groups were compared with the control group. The ultrastructural features were similar for the three groups. However, it was verified that the physical activity of the trained animals resulted in a similar myenteric neuron morphology to that of the adult animals (6 months old), thereby confirming its beneficial effect, as the sedentary animals had larger alterations in the collagen fibrils and the basal membrane that occur through ageing. The quantitative analysis showed that the NADH‐diaphorase positive neurons decreased with ageing and increased with physical activity (P > 0.05). No significant alteration (P > 0.05) in the neuronal profile area of the NADH‐diaphorase positive neurons has been observed with ageing.

Cardiac denervation in mice infected with Trypanosoma cruzi.

Abstract The neuronal features of the hearts of mice that were acutely or chronically infected with the Y strain of Trypanosoma cruzi were compared with those of control hearts from uninfected mice. Whole-mount preparations of the murine atria, isolated by microdissection, were stained to reveal neurons with NADH-diaphorase activity. Counts, by a microscopist who was blind to the infection status of the donor mouse, revealed that there were significantly (38%) fewer such neurons in the atria from the acutely infected mice than in the atria from the control hearts. The ganglia of the infected mice were also irregularly distributed, severely damaged ganglia being found beside slightly degenerated or morphologically normal ones. Although the ganglia contained small, medium and large neurons, the apparent destruction caused by T. cruzi was confined to the large ones. As neuron counts in preparations of hearts from mice with chronic infections were 32% lower than those in the control hearts, there appears to be no additional loss of cardiac neurons as the acute infection in mice progresses to the chronic phase.

Arterial and interstitial remodelling processes in non‐specific interstitial pneumonia: systemic sclerosis versus idiopathic

Aims:  To compare septal and vascular matrix remodelling, vascular occlusion, pulmonary function tests and survival between two groups: one with idiopathic non‐specific interstitial pneumonia (NSIP) and one with NSIP associated with systemic sclerosis (SSc).

Increased mRNA expression of collagen V gene in pulmonary fibrosis of systemic sclerosis.

Eur J Clin Invest 2010; 40 (2): 110–120

ESR study of Er3+ in Cr3+ doped Ca3Ga2Ge3O12 garnet

Abstract We present a study of the Er 3+ ESR spectra in Ca 3 Ga 2 Ge 3 O 12 garnet single crystals, doped with Cr 3+ . We show the dependence of the spectra with temperature, in the range from 4.2 to 30 K, where the broadening of the Cr 3+ resonances is attributed to the CrEr interaction. The principal g-values for Er 3+ were obtained, fitting the spectra with lorentzian lines.