Basic fibroblast growth factor loaded polypropylene meshes in repair of abdominal wall defects in rats.

BACKGROUND AND AIM: Incisional hernia following laparotomy and recurrent herniation after its repair are still common problems in spite of mesh augmentation. The underlying biological mechanism may be related to collagen metabolism. Recently, some members of growth factors family have been tested in the prevention of wound failure and incisonal hernia formation. Growth factors may promote fibroblast proliferation and collagen deposition. In the present study, we searched the effects of basic fibroblast growth factor (bFGF) loaded polypropylene meshes in an incisional hernia model in rats. METHODS: A total of 80 Wistar albino rats were randomly divided into five groups. A uniform surgical procedure was employed in all groups: a 5 cm skin incision was made at the midline and a full segment of the abdominal wall sized 3 x 2 cm was excised. Abdominal wall was closed with rapidly absorbable 3/0 catgut. Following this standard surgery, five different procedures were applied to the groups before closing the skin with 4/0 monofilament polypropylene sutures. Control subjects (Group 1) received no extra procedure after abdominal wall suturing. Polypropylene meshes were used in onlay position by fixing 4/0 monofimalent polypropylene interrupted sutures in other four groups. A standard mesh with no chemical treatment was used in Group 2. Gelatin coated meshes were used in Group 3, while Group 4 and 5 received bFGF loaded meshes with 1 microgram (microg) and 5 microg doses respectively. All the groups then divided into 1st month (early: E) and 2nd month (late: L) subgroups (n=8 each) according to sacrification dates. Tensiometric and histopathological evaluations were done. The specimens for histopathology were obtained from the interface area of the meshes and stained with hematoxylin and eosin, and also Masson trichrome. The variables were examined and evaluated by a single blinded pathologist under light microscopy in respect of inflammation, vascularization, fibroblast activity, collagen fibers and connective tissue organization. The avidin-biotin-peroxidase method was performed using the primary monooclonal antibodies against collagen type I and collagen Type III. RESULTS: bFGF loaded meshes showed higher tensile strength values in comparison with a standard polypropylene mesh after 2 months. Histopathological and immunohistochemistry studies also revealed somewhat better scores in favor of bFGF loaded mesh over a standard polypropylene mesh. These limited effects of bFGF did not seem to be dose dependent. CONCLUSIONS: The use of bFGF loaded polypropylene mesh in the abdominal wall healing may cause somewhat higher tensile strength values in comparison with a standard polypropylene. However, histopathological and immunohistochemistry studies revealed only a slightly better healing in favor of bFGF loaded mesh over a standard polypropylene mesh.

A hystopathological study of thyroarytenoid muscle invasion in early (T1) glottic carcinoma.

PATIENTS AND METHODS: Surgical specimens belonging to 16 patients who underwent partial laryngectomy for T1 glottic cancer were subjected to detailed histopathologic examination; 11 of the patients were staged as T1a while 5 were staged as T1b. RESULTS: It was detected that in 11 patients the tumor was confined to the mucosal or submucosal connective layer, and in 5 (31.2%) cases, the tumor invaded the thyroarytenoid (TA) muscle. In cases involving the one-third anterior part of the vocal cords and the anterior commissure, a 50% (4/8) TA muscle invasion was detected. DISCUSSION AND CONCLUSION: Our finding TA muscle invasion at the rate of 31.2% in our 16 case series clinically staged as T1 revealed that deep invasion did not always impair the vocal cord mobility. Observing TA muscle invasion at the rate of 50% in cases involving the one-third anterior part of the vocal cord and the anterior commissure suggested that TA muscle invasion in the anterior part did not significantly impair mobility.

Neurofibrillary tangles and neuropil threads as a cause of dementia in Parkinson's disease.

Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common age-related degenerative disorders of the human brain. Both diseases involve multiple neuronal systems and are the consequences of cytoskeletal abnormalities. In AD susceptible neurons produce neurofibrillary changes, while in Parkinson's disease, they develop Lewy bodies. In AD six developmental stages can be distinguished on account of the predictable manner in which the neurofibrillary changes spread across the cerebral cortex. During the course of PD numerous limbic determined parts of the brain undergo specific lesions regulating endocrine and autonomic functions. In general, the extranigral destructions are in themselves not sufficient to produce overt intellectual deterioration. Fully developed Parkinson's disease with concurring incipient Alzheimer's disease is likely to cause impaired cognition.

New aspects of pathology in Parkinson's disease with concomitant incipient Alzheimer's disease.

Alzheimer's disease and Parkinson's disease are the most common age-related degenerative disorders of the human brain. Both diseases involve multiple neuronal systems and are the consequences of cytoskeletal abnormalities which gradually develop in only a small number of neuronal types. In Alzheimer's disease, susceptible neurons produce neurofibrillary tangles and neuropil threads, while in Parkinson's disease, they develop Lewy bodies and Lewy neurites. The specific lesional pattern of both illnesses accrues slowly over time. Presently available data support the view that fully developed Parkinson's disease with concurring incipient Alzheimer's disease is likely to cause impaired cognition.

Nigral and extranigral pathology in Parkinson's disease.

This article reviews data on the internal organization, neuronal types, and interconnections of limbic and motor components of the human brain, and the specific lesions which a few of them undergo during the course of Parkinson's disease (neuronal loss associated with the development of Lewy bodies and Lewy neurites). The severe involvement of nigral neuromelanin-laden projection cells has received particular attention during the past decades. This lesion interferes with normal function of the striatum and probably contributes to many of the motor dysfunctions characteristically occurring in Parkinson's disease. The similarly severe involvement of several areas and nuclei outside of the substantia nigra has often escaped notice. However, the pathology of Parkinson's disease cannot be completely described unless changes in these extranigral areas are taken into account. Interpretation of the characteristic lesional pattern is facilitated by combining schemata of both the limbic and motor systems. This approach reveals a key role by the amygdala and related structures in extranigral pathology. Severe lesions occur in the central amygdaloid nucleus, in nuclei projecting to the cerebral cortex in a non-specific manner, and in nuclei regulating endocrine and autonomic functions. It is suggested that extranigral lesions contribute to the development of behavioral changes and autonomic dysfunction.

Functional anatomy of human hippocampal formation and related structures.

Data on the internal organization, and neuronal connections of the human hippocampal formation and related structures of the limbic system are briefly reviewed. In the healthy brain, somatosensory, visual, and auditory input proceeds through neocortical core and belt fields to a variety of association areas, and from here the data is transported via long corticocortical pathways to the extended prefrontal association cortex. Tracts generated from this highest organization level of the brain guide the data via the frontal belt (premotor cortex) to the frontal core (primary motor area). The striatal and cerebellar loops provide the major routes for this data transfer. The main components of the limbic system (the hippocampal formation, the entorhinal region, and the amygdala) maintain a strategic position between the sensory and the motor association areas. Part of the stream of data from the sensory association areas to the prefrontal cortex branches off and eventually converges on the entorhinal region and the amygdala, These connections establish the afferent leg of the limbic loop. In addition, the limbic centers receive substantial input from nuclei processing viscerosensory information. The entorhinal region, the hippocampal formation, and the amygdala are densely interconnected. Important among these connections is the perforant path, which originates in the entorhinal cortex and projects to the hippocampal formation (fascia dentata, Ammon's horn, and subiculum). The subiculum projects to the amygdala, entorhinal region, mamillary nuclei, and anterior and midline thalamic nuclei. The hippocampal formation, the entorhinal region, and the amygdala generate the efferent leg of the limbic loop, which is directed toward the prefrontal cortex. Additional projections reach the key nuclei that control endocrine and autonomic functions. Furthermore, the amygdala exerts influence on all nonthalamic nuclei projecting in a nonspecific manner to the cerebral cortex (ie, the cholinergic magnocellular forebrain nuclei, the histaminergic tuberomamillary nucleus, the dopaminergic nuclei of the ventral tegmentum, the serotonergic anterior raphe nuclei, and the noradrenergic locus ceruleus). The limbic loop centers thus are in the unique strategic position to perform integration of exteroceptive sensory data of various sources with interoceptive stimuli from autonomic centers. Their efferent projections exert influence on both the prefrontal association cortex and the key centers controlling endocrine and autonomic functions.

Renal tubular dysgenesis with hypoplastic calvaria: report of two cases.

Renal tubular dysgenesis (RTD), a rare, lethal, autosomal recessive disorder, is characterized by short and poorly differentiated proximal tubules and associated with hypoplastic calvaria. We report two cases of RTD with hypoplasia of the calvaria. Microscopically, proximal tubules in the kidneys were not seen on routine H&E stain. Almost all tubules in the cortex were stained for epithelial membrane antigen (EMA), confirming the absence of proximal tubule differentiation. The autopsy findings, microscopic features and the etiology of this rare condition is discussed and compared with literature data.

Intravascular papillary endothelial hyperplasia (Masson's hemangioma) presenting as a lateral neck mass.

Intravascular papillary endothelial hyperplasia (Masson's hemangioma) is a benign disease of vascular origin characterized by exuberant endothelial proliferation in normal blood vessels.The most important feature of the disease is its resemblance to hemangiosarcoma and the resulting possible radiologic misinterpretation. We present the radiologic findings in a 45-year-old woman presenting a neck mass extending to the thoracic cavity.

Staging of Alzheimer-type pathology: an interrater-intrarater study.

The staging method proposed by Braak and Braak is based on the sequential accumulation of neurofibrillary pathology in the cerebral cortex. Unlike the currently used diagnostic criteria for Alzheimer's disease (AD) it does not take into consideration the age of the patients and whether they were demented or not for the establishment of the pathological stage of the disease. To examine the interobserver reliability of the method we performed an inter- and intrarater study using the Braak staging method in 41 brains. The agreement between the examiners and between the diagnoses of the same examiner at different times was almost perfect, the kappa statistics reaching values above 0.90. These findings indicate that the staging, relying on the differential distribution of neuritic pathology in the brain in AD, is a reliable and reproducible method for the description of AD-related pathology. This makes it suitable for brain-banking and research purposes.

Pattern of brain destruction in Parkinson's and Alzheimer's diseases.

Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common age-related degenerative disorders of the human brain. Both diseases involve multiple neuronal systems and are the consequences of cytoskeletal abnormalities which gradually develop in only a small number of neuronal types. In AD, susceptible neurons produce neurofibrillary tangles (NFTs) and neuropil threads (NTs), while in PD, they develop Lewy bodies (LBs) and Lewy neurites (LNs). The specific lesional pattern of both illnesses accrues slowly over time and remains remarkably consistent across cases. In AD, six developmental stages can be distinguished on account of the predictable manner in which the neurofibrillary changes spread across the cerebral cortex. The pathologic process commences in the transentorhinal region (clinically silent stages I and II), then proceeds into adjoining cortical and subcortical components of the limbic system (stages III and IV - incipient AD), and eventually extends into association areas of the neocortex (stages V and VI - fully developed AD). During the course of PD, important components of the limbic system undergo specific lesions as well. The predilection sites include the entorhinal region, the CA2-sector of the hippocampal formation, the limbic nuclei of the thalamus, anterior cingulate areas, agranular insular cortex (layer VI), and - within the amygdala - the accessory cortical nucleus, the ventromedial divisions both of the basal and accessory basal nuclei, and the central nucleus. The amygdala not only generates important projections to the prefrontal association areas but also exerts influence upon all non-thalamic nuclei which in a non-specific manner project upon the cerebral cortex and upon the nuclei regulating endocrine and autonomic functions. All these amygdala-dependent structures themselves exhibit severe PD-specific lesions. In general, the extranigral destructions are in themselves not sufficient to produce overt intellectual deterioration. Similarly, AD-related pathology up to stage III may be asymptomatic as well. Fully developed PD with concurring incipient AD, however, is likely to cause impaired cognition. Presently available data support the view that the occurrence of additional lesions in the form of AD stage III (or more) destruction is the most common cause of intellectual decline in PD.

Amygdala pathology in Parkinson's disease.

The amygdala undergoes severe pathological changes during the course of Parkinson's disease (PD). Lewy bodies and Lewy neurites are distributed in a specific manner throughout the nuclear complex. The lesional pattern displays only minor interindividual variation. The most prominent changes occur in the accessory cortical and central nuclei. The cortical, accessory basal and granular nuclei show less severe alterations, while the basal and lateral nuclei, as well as the intercalated cell masses, generally remain uninvolved. The amygdala receives a broad range of afferents, allowing integration of exteroceptive information with interoceptive data. It generates major projections to the isocortex (the prefrontal cortex in particular), limbic system (hippocampus and entorhinal region) and centers regulating endocrine and autonomic functions. The specific lesional pattern seen in PD destroys part of the nuclear gray matter and its connections and, thus, may likely contribute to the development of behavioral changes and autonomic dysfunctions.