New Histopathologic Evidence for the Parasympathetic Innervation of the Kidney and the Mechanism of Hypertension Following Subarachnoid Hemorrhage.

BACKGROUND: The Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). METHODS: A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. RESULTS: Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. The mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 ±â€Š2.0 mm, 1.87 ±â€Š0.19; 65.0 ±â€Š12.0 mm, 1.91 ±â€Š0.34; and 986.0 ±â€Š112.0 mm, 2.32 ±â€Š0.89, consecutively. Blood pressure was measured as 94.0 ±â€Š10.0 mmHg in control group, 102.0 ±â€Š12.0 mmHg in SHAM; 112.0 ±â€Š14.0 mmHg in middle (n = 9); and >122.0 ±â€Š10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). CONCLUSION: The degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.

Olfactory bulbectomy and raphe nucleus relationship: a new vision for well-known depression model.

Background/aim: The olfactory bulbectomy (OBX) technic is a well-known animal model for depression. According to serotonin hypothesis of depression, one of the possible explanations to this mechanism is the destroying effect of OBX on raphe nuclei which especially include serotonergic neurons. In this study, we aimed to explore histopathological findings in raphe nuclei in OBX rats.Materials and methods: Forty-eight rats (8 control group, 10 sham group, and 30 as the study group) were used. No procedure was applied to the control group. Only frontal burr holes were performed at the level of olfactory bulbs (OBs) on the sham group. Mechanical OBX by compression was applied to 20 rats and the OBs of 10 rats were cauterized. Their OBs, olfactory cortices, raphe nuclei were extracted, tissue specimens were taken than examined by using histopathological methods including hematoxylin and eosin, S-100, and TUNEL staining. Physical dissector method was used to evaluate the number of living and apoptotic neurons in the raphe nuclei.Results: Prominent neuronal loss and morphological changes in the dorsal raphe nuclei were detected in study groups.Conclusion: Raphe nuclei degeneration, related alterations in neurotransmitter system activities and functional brain connectivity might be related to neurobiology of depression.

Disruption of the network between Onuf's nucleus and myenteric ganglia, and developing Hirschsprung-like disease following spinal subarachnoid haemorrhage: an experimental study.

Purpose/Aim of the study: Auerbach/Meissner network of lower abdominopelvic organs managed by parasympathetic nerve fibres of lumbosacral roots arising from Onuf's nucleus located in conus medullaris. Aim of this study is to evaluate if there is any relationship between Onuf's nucleus ischemia and Auerbach/Meissner network degeneration following spinal subarachnoid haemorrhage (SAH). Materials and Methods: Study was conducted on 24 male rabbits included control (Group I, n = 5), serum saline-SHAM (Group II, n = 5), and spinal SAH (Group III, n = 14) groups. Spinal SAH performed by injecting homologous blood into subarachnoid space at Th12-L4 level and followed three weeks. Live and degenerated neuron densities of Onuf's nucleus, Auerbach and Meissner ganglia (n/mm3) were determined by Stereological methods. Results: The mean degenerated neuron density of Onuf's nucleus was significantly higher in Group III than in Groups I-II (152 ± 26, 2 ± 1 and 5 ± 2/mm3 respectively, p < 0.005). The degenerated neuron density of Auerbach's ganglia was significantly higher in Group III than in Groups I-II (365 ± 112, 3 ± 1 and 9 ± 3/mm3 respectively, p < 0.005). The degenerated neuron density of Meissner's ganglia was significantly higher in Group III than in Groups I-II (413 ± 132, 2 ± 1 and 11 ± 4/mm3 respectively, p < 0.005). Conclusions: Onuf's nucleus pathologies should be considered as Auerbach/Meissner ganglia degeneration and also related Hirschsprung-like diseases in the future.

The effects of lutein on cisplatin-induced retinal injury: an experimental study.

AIM: Lutein is one of the most common carotenoids defined in human plasma as having potent anti-oxidant effects. We aimed to determine the biochemical and histopathological effects of lutein on cisplatin-induced oxidative retinal injury in rats. MATERIALS AND METHODS: Twenty-four rats were equally divided into four groups as healthy controls (HC group), only cisplatin (5 mg/kg) administered group (CIS group), Lutein (0.5 mg/kg) + cisplatin (5 mg/kg) administered group (LC group), and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples obtained, serum malondialdehyde (MDA), total glutathione (tGSH), interleukin 1 beta (IL-1ß), and tumor necrosis factor alpha (TNF-α) levels were investigated. In histopathological analyses, the total retinal thickness, retinal pigment epithelium (RPE), photoreceptor layer (PL), outer nuclear layer (ONL), outer plexiform layer (OPL), inner nuclear layer (INL), inner plexiform layer (IPL), and ganglion cell layer (GCL) were evaluated. RESULTS: MDA, IL-1ß, and TNF-a levels were statistically significantly higher (p < 0.001) in CIS group compared with other three groups while tGSH levels were statistically significantly lower (p < 0.001). In subgroup analyses, there was no any statistically significant difference regarding all four parameters analyzed between HC, LC, and LUT groups. In histopathological analyses, cisplatin-induced retinal damage included atrophy and disorganization on outer segment, degeneration and detachment of RPE and PL from choroid, degeneration and edema of INL and IPL, total degeneration of GCL; while cisplatin-induced retinal damage was determined to be significantly prevented with 0.5 mg lutein treatment on histopathological evaluations. CONCLUSIONS: Lutein co-administration was highly effective in prevention of cisplatin-induced retinal damage due to the anti-oxidant and anti-inflammatory effects of lutein.

The influence of low-level laser therapy with alendronate irrigation on healing of bone defects in rats.

The aim of this study was to investigate the effects of alendronate (Aln) irrigation with low-level laser therapy (LLLT) on the healing of bone defects in rats. Sixty Wistar rats weighing 250 to 300 g were randomly divided into three groups of 20 animals each: (1) control group, (2) Aln group, and (3) Aln with LLLT group. The distal epiphysis of all rats was perforated with a surgical bone drill. Twenty rats served as control. The bone defects of 40 rats received local alendronate sodium trihydrate irrigation (1 mg/ml) at the time of surgery. LLLT was applied to the bone defects of 20 rats immediately after Aln irrigation, and repeated on days 2, 4, 6, and 8 with a total dose of 10 J/cm(2) (2 J/cm(2) × 5). Continuous wave of GaAlAs laser (808 nm) was used with a power density of 0.1 W/cm(2). Laser energy was applied for 20 s (0.1 W × 20 s/1 cm(2)) per session. Control group, Aln group, and Aln with LLLT group rats were sacrificed at days 10 and 20 to compare the bone healing of each group histologically. There were significant differences between the three groups regarding union, substantia spongiosa, cortex formation, and in sum of histologic scores on days 10 and 20 (P < 0.0001). Our findings demonstrated that Aln has a more positive effect with LLLT on bone healing in rats. It was concluded that combining LLLT (808 nm laser at 10 J/cm(2)) with Aln irrigation has a beneficial effect in bone repair. It was demonstrated experimentally that Aln irrigation during the surgery had a significant effect to enhance bone formation, and LLLT significantly potentiated the osseous healing effects of Aln on bone defects. This administration method is able to minimize the dose of Aln in order to avoid both systemic and local adverse effects as well as the local injection times during the bone healing process.

Intimal Hemorrhage of Basilar Artery Induced by Severe Vasospasm Following Subarachnoid Hemorrhage: The Experimental Analysis.

BACKGROUND: Cerebral vasospasm, a serious complication of subarachnoid hemorrhage (SAH), has been extensively studied for its neurochemical and pathophysiologic mechanisms. However, the contribution of inner elastic membrane dissection and subintimal hemorrhage to basilar artery occlusion remains underexplored. This study investigates inner elastic membrane-related changes in the basilar artery after SAH. METHODS: Twenty-four hybrid rabbits were divided into control, sham, and SAH groups, with SAH induced by autologous blood injection. After 2 weeks, basilar artery changes, vasospasm indexes (VSIs), and dissections were evaluated. RESULTS: The SAH group showed significantly higher VSI, with vascular wall thickening, luminal narrowing, convoluted smooth muscle cells, intimal elastic membrane disruption, endothelial cell desquamation, and apoptosis. Some SAH animals exhibited subintimal hemorrhage, inner elastic membrane dissection, and ruptures. Basilar arteries with subintimal hemorrhage had notably higher VSI. CONCLUSIONS: These findings highlight the role of subintimal hemorrhage and inner elastic membrane dissection in basilar artery occlusion post-SAH, offering valuable insights into vasospasm pathophysiology.

Brachiocephalic artery anomaly at the neck: importance during minimally invasive video-assisted parathyroidectomy.

A 76-year-old woman was referred to our hospital for evaluation of a parathyroid adenoma, detected on sonography. It had been located posteroinferiorly to the right thyroid lobe. Parathyroid scintigraphy confirmed the right inferior parathyroid adenoma. During physical examination of the neck, a pulsatile mass in the anterior inferior right was determined, and because of suspicion for a vascular anomaly, a computed tomography angiography was performed. The computed tomography showed that the right brachiocephalic artery ascended vertically to the level of the inferior border of right thyroid lobe and dividing into the right common carotid artery and subclavian artery at this level. Right subclavian artery after its origin brought about a curve by means of turning first posteromedially and then anterolaterally. Parathyroid adenoma remained between the right thyroid lobe, right common carotid artery, and right brachiocephalic artery. Minimally invasive video-assisted parathyroidectomy was performed and no complication appeared.

The Enigma of Basilar Artery Dissections Secondary to Vasospasm following Subarachnoid Hemorrhage; Exploration of the Unknown Effect of Superior Cervical Ganglia: A Preliminary Experimental Study.

BACKGROUND: Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether subarachnoid hemorrhage causes dissection, or not. This study aims to investigate the relationship between, degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery. MATERIAL AND METHOD: In this article, after three weeks of experimental SAH, animals were decapitated. 18 rabbits were divided into three groups, according to their vasospasm indexes. The basilar arteries were examined by anatomical and histopathological methods. RESULTS: Basilar dissection with high vasospasm index value (VSI>3) was detected in six animals (G-I, n=6); severe basilar edema and moderate vasospasm index value (VSI>2.4) in seven rabbits (G-II, n=7) and slight vasospasm (VSI<1.5) index value in five subjects (G-III, n=5) was detected. The degenerated neuron densities (n/mm3) of the superior cervical ganglia were detected as 12±4 in G-I, 41±8 in G-II; and 276±78 in G-III. The dissected surface values/lumen values were calculated as (42±1)/(64±11) in G-I; (21±6)/(89±17) in G-II; and (3±1)/(102±24) in G-III. If we look at these ratios as a percentage: 62%in G-I, 23% in G-II, and 5% in G-III. CONCLUSION: Inverse relationship between the degenerated neuron densities (n/mm3) of the superior cervical ganglia and the dissected surface values basilar artery was observed. The common knowledge is that basilar artery dissection may lead to SAH, however, this study indicates that SAH is the cause of basilar artery dissection.

Correlation of E-cadherin, VEGF, COX-2 expression to prognostic parameters in papillary thyroid carcinoma.

Thyroid cancer represents approximately 1% of all human malignancies. papillary thyroid carcinoma (PTC) is the most common malignant tumor of the thyroid gland, accounting for 70-80% of all thyroid cancers. In the US, the incidence of thyroid cancer is 4 per 100,000 individuals. It is two to four times as frequent in women as in men. The development of PTC is influenced by many factors including genetic alterations, growth factors, and physical agents such as radiation. In order to recognize the prognosis for PTC, a lot of clinic and pathological parameters such as; age, tumor size, extra-thyroid tumor spread, lymph node, distant metastases, gender, tumor stage are used. As most of these parameters are subjective, more objective and useful prognostic factors are needed for determining biologic behavior, providing an initial assessment. In this study, we aimed to compare the expressions of COX-2, E-cadherin, VEGF to classical prognostic factors, and to investigate the correlation with prognosis. Operation records from 79 PTC cases were examined retrospectively. In the study, we aimed to investigate the whole tissue by means of stereology method, which is an impartial one, and we indicated the expression COX-2, VEGF, E-cadherin immunohistochemically in 79 resection diagnosed with PTC. We determined correlations between the expressions of COX-2 and VEGF, E-cadherin, and age, gender, and stage.

Relationship between subarachnoid and central canal hemorrhage and spasticity: A first experimental study.

Objective: Spastic disorders are considered as important cerebral complications of subarachnoid hemorrhage (SAH). However, there has been no research concerning the pathophysiological mechanism of its link with the spinal cord. The present study aimed to assess the relationship between the development of spasticity and neuronal degeneration after SAH and increase in spinal cord pressure after central canal hemorrhage (CCH).Participants: Twenty-three rabbits were included.Outcome measures: Of all rabbits, 5, 5, and 13 were allocated in the control, SHAM and study groups, respectively. Moreover, 1 cc of saline and 1 cc of autologous arterial blood were injected into the cisterna magna of the SHAM and study groups, respectively. The Muscle spasticity tension values (MSTVs) were determined according to the modified Ashworth scale. Degenerated neuron densities (DND) in the gray matter (GM) of each animal's spinal cord were stereologically calculated.Results: The average MSTV of each group was as follows: control group (n = 5) 2; SHAM group (n = 5) 3-5; and study group (n = 13) 8-10. The DND values of the spinal cord of each group were as follows: control group, 2 ± 1/mm3; SHAM group, 12 ± 3/mm3; and study group, 34 ± 9/mm3. Results showed an important linear relationship between the MSTVs and the DND of the spinal cord (P < 0.001).Conclusion: Spasticity may be attributed to other causes such as ischemic neurodegenerative process that develops after spinal SAH and the de-synchronization of the flexor-extensor muscles due to the spontaneous discharge of interneuronal structures, which are crossed within the spinal cord owing to the build-up of pressure after CCH.

Predestinating Role of Cardiac Ganglia on Heart Life Expectancy in Rabbits After Brain Death Following Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: Cardiac ganglia are rechargeable batteries of the heart. The essential role of cardiac ganglia on cardiac life expectancy has not been examined following brain death. The aim of this study was to determine cardiac ganglia numbers and neuron density following subarachnoid hemorrhage (SAH). METHODS: Twenty-five hybrid rabbits were grouped as control (n = 5), sham (n = 5), and SAH (n = 15). The SAH groups' animals were subjected to injections of lethal dose of 2.00 cc autologous blood into their cisterna magna until linear EEG was obtained. The hearts of all animals were extracted following intracardiac formalin injection and examined. Cardiac ganglia and normal/degenerated neuron densities of cardiac neurons were recorded. RESULTS: The mean volume of normal neuron density of ganglia was 6.980 ± 830/mm3, and the degenerated neuron density of ganglia was 3 ± 1/mm3 in the control group, 6134 ± 712/mm3; 23 ± 9/mm3 in the sham group, 3456 ± 589; 1161 ± 72/mm3 in the surviving group; and 1734 ± 341/mm3, 4259 ± 865/mm3 in the dead animals in the SAH group. The algebraic results of heart work capacity (Wh) were estimated as 1375 ± 210 Wh in the control group, 1036 ± 225 in the sham group, 800 ± 110 Wh in the surviving group, and < 100 ± 20 in the dead animals in the SAH group. Degenerated cardiac neuron density/Wh correlation is statistically meaningful between the dead in the SAH group versus the SAH-surviving, sham, and control groups (P < .0005). CONCLUSIONS: Normal cardiac ganglia numbers and/or cardiac ganglia neuron density may be related to cardiac survival following brain death after subarachnoid hemorrhage.

The Role of Cardiac Ganglia in the Prevention of Coronary Atherosclerosis: An Analytical Examination of Cholesterol-fed Rabbits

Background: The heart is innervated by the autonomic nervous system, which contributes to the control of the heart's rhythm and coronary circulation. It has been suggested that the cardiac fibers of the vagus nerve play important roles in controlling circulatory functions and in protecting against atherosclerotic pathologies in coronary arteries. Aims: To investigate the presence of atherosclerotic differences in the coronary arteries of cholesterol-fed rabbits by measuring the density of cardiac ganglia neurons. Study Design: Animal experiment. Methods: This study was conducted using 45 male rabbits. Over a period of 16 weeks, they were kept on an atherogenic diet of water ad libitum and high fat (8.6%) containing saturated fatty acids with 205 mg/kg of cholesterol (1%) per day. Then, their hearts were removed and examined by histopathological methods. Atherosclerotic plaques of the main coronary arteries were examined using the Cavalieri method. Atherosclerosis index values (AIVs) were estimated as the wall surface area/plaque surface area, and the results were analyzed with the Kruskal-Wallis and Mann-Whitney U tests. Results: While the average atherosclerosis index value was estimated to be ≤8% in 21 animals, the atherosclerosis index value was 9-20% in animals with minor plaque detection (n=11) and ≥20% in animals with major plaque detection (n=10). Increased atherosclerosis index values were more common in animals with low neuron densities than in animals with high neuron densities (p<0.017). Conclusion: The low neuron density of the cardiac ganglia in cholesterol-fed rabbits is associated with an increased atherosclerotic plaque incidence and volume.

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied. METHODS: This study was conducted on 25 rabbits. Five animals were in the control group (GI; n = 5), five in the sham group (GII; n = 5), and 15 in the study group (GIII; n = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated. RESULTS: In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm3, VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm2. Mean neuron density was 9,450 ± 940/mm3, VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm2 in the sham group (p < 0.05). Neuron density was 6,890 ± 932/mm3, VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm2 in SAH group. CONCLUSION: Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups (p < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values.

Predictive Role of the Cervical Sympathetic Trunk Ischemia on Lower Heart Rates in an Experimentally Induced Stenoocclusive Carotid Artery Model by Bilateral Common Carotid Artery Ligation.

Bilateral common carotid artery ligation (BCCAL) leads to acute craniocervicocerebral ischemia, retrograde blood flow, increased blood pressure, and significant hemodynamic and histomorphological changes at the posterior cerebral vasculature. We examined the potential relationship between denervation injury following BCCAL-induced cervical sympathetic trunk (CST) ischemia and heart rate after permanent BCCAL. Rabbits (n = 25) were randomly divided into three groups: an unoperated control group (GI, n = 6); a sham-operated control group (GII, n = 6), and an experimental group subjected to BCCAL (GIII, n = 13); and then followed for one month. All animals were then sacrificed and the stellate ganglia (STGs) were examined histologically using stereological methods. The densities of degenerated neurons in the STGs were compared with heart rates and the results were analyzed with the Mann-Whitney U test. The mean normal neuron density in STGs was 10.340 ± 954/mm3 and the degenerated neuron density was 12 ± 3/mm3 in the GI group (p > 0.5). The mean heart rates and degenerated neuron densities of STGs were recorded as 267 ± 19/min and 237 ± 45/mm3 in GII (p < 0.005 for GII vs. GI); and 190 ± 11/min 1421 ± 230/mm3 in GIII (p < 0.0001 for GIII vs. GI and p < 0.005 for GIII vs. GII). An inverse and meaningful association was observed between the heart rate and degenerated neuronal density in the STGs. BCCAL may lead to hazardous histomorphological changes in the CST. A high density of degenerated neurons in the STG may provoke excessive sympathetic hypoactivity-related cardiac damage and bradyarrhythmias after stenoocclusive carotid artery diseases.

Predeterminative role of Onuf's nucleus ischemia on mesenteric artery vasospasm in spinal subarachnoid hemorrhage: A preliminary experimental study.

BACKGROUND: Although posttraumatic mesenteric artery ischemia is attributed to various etiologies, sacral parasympathetic network/mesenteric artery relations have not been studied so far. The primary objective of this study is to elucidate whether there is a relationship between Onuf's nucleus ischemia and mesenteric artery vasospasm following subarachnoid hemorrhage (SAH). METHODS: This study was conducted on 22 rabbits. The animals were grouped as follows: 5 of animals control, 5 SHAM which saline was given, and 12 animals study group that was homologous blood injected into the spinal subarachnoid space at the Li level. Neurodegeneration in Onuf's nucleus, axonal degeneration of S2 roots, and mesenteric arteries vasospasm indexes (VSI; Wall surface/Lumen surface), brachias of mesentery arteries in various tissues and ischemic mucosal changes of intestines of all animals were determined histopathologically. Important degenerative changes were detected in axons in S2 roots and Onuf's nucleus in severe mesenteric artery vasospasm observed. RESULTS: The mean degenerated neuron density of Onuf's nucleus (n/mm3), degenerated axon density in S2 roots (n/mm2), and VSI values of mesenteric arteries of control, SHAM, and study groups were estimated as 5.00 ± 1.58, 4.00 ± 1.58, 1.76 ± 0.13; 18.29 ± 4.31, 11.00 ± 2.24, 2.23 ± 0.20; and 135.21 ± 30.75, 117.33 ± 22.11, 2.81 ± 0.44, respectively. Statistical analyses between the VSI values, mucosal ischemic changes degenerated neurons in Onuf's nucleus, and axons in S2 levels were meaningful (p < 0.005). CONCLUSION: We interestingly noticed that Onuf's nucleus-S2 roots complex degeneration plays an important role in mesenteric artery vasospasm and the development of intestinal ischemic mucosal changes following SAH which has not been extensively mentioned in the literature.

A new described mechanisms of intestinal glandular atrophy induced by vagal nerve/Auerbach network degeneration following subarachnoid hemorrhage: The first experimental study.

Stress ulcers is a trouble complication of subarachnoid hemorrhage (SAH). Although gastrointestinal ulcerations may be attributed to increased HCL secretion in SAH; the exact mechanism of that complication has not been investigated definitively. We studied if vagal network degeneration may cause intestinal atrophy following SAH. Study was conducted on 25 rabbits, with 5 control group (Group-A), 5 SHAM group (Group-B), and 15 SAH group via injection of autologue blood to cisterna magna. Seven animals followed for seven days (Early Decapitated-Group-C) and eight animals followed 21 days (Late Decapitated-Group-D). The vagal nodosal ganglia (NGs), Auerbach plexuses and goblet cells of duodenums were examined by current stereological methods and compared statistically. The mean numbers of degenerated axon density/mm2 of gastric branches of vagal nerves was 8 ±â€¯2, 34 ±â€¯11, 189 ±â€¯49 and 322 ±â€¯81 in the Group A, B, C, and D respectively. The mean numbers of degenerated neuron density/mm3 of NGs was 5 ±â€¯2, 54 ±â€¯7, 691 ±â€¯87 and 2930 ±â€¯410 in the Group A, B, C, and D respectively. The mean numbers of degenerated Auerbach neurons 2 ±â€¯1, 4 ±â€¯1, 12 ±â€¯3 and 27 ±â€¯5/mm3 in the Group A, B, C, and D respectively. The mean numbers of degenerated goblet cells/mm3 were 4.3 ±â€¯1.02, 11.5 ±â€¯0.26, 143 ±â€¯26 and 937 ±â€¯65 Group A, B, C, and D respectively. Statistical analysis showed that vagal network ischemia could cause intestinal bleeding and so atrophy in SAH progression. Statistical analyses of groups were; Group-D/Group-A < 0.001, Group-D/Group-B < 0.005, Group-C/Group-A < 0.005. Undiscovered effect of ischemic vagal network injuries should be regarded as a major cause of stress ulcerations following SAH which has not been mentioned in the literature.

Comparison of Microvessel Density with Prognostic Factors in Invasive Ductal Carcinomas of the Breast.

OBJECTIVE: Angiogenesis plays a key role in tumor growth and metastasis. Determination of microvessel density is the most common technique used to evaluate the amount of the intratumoral angiogenesis in breast cancer. We have aimed to investigate the relationship with tumor angiogenesis and prognostic parameters in breast invasive ductal carcinomas. MATERIAL AND METHOD: In this study, a total of 100 invasive ductal carcinoma patients, who were diagnosed at the Department of Pathology, Ataturk University Faculty of Medicine between the years 2003-2008, were re-evaluated. Patient characteristics and clinicopathological findings were obtained from archival records. In the present study, microvessel density was determined by immunohistochemical staining by using anti-CD34 monoclonal antibody in the paraffin blocks. First, the most vascular area was selected in the tumor under a low magnification (40x) by a light microscope and then microvessels were counted under a higher magnification (200x). Patients were classified as low and high microvessel density depending on their microvessel counts. Chi-square test and multivariate linear regression analysis were used for statistical analysis (p≤0.05). RESULTS: We have determined that microvessel density increases as tumor size increases (p=0.001). Microvessel density was higher in patients with at least 10 lymph node metastases compared to those with no metastasis (p=0.05). However, there was no statistically significant difference between microvessel density and other prognostic factors such as histological grade, nuclear grade, patient age, vascular invasion, estrogen, progesterone receptor status, HER2/neu expression. CONCLUSION: In our study, we have found that microvessel density is associated with tumor size and lymph node metastasis in patients with invasive ductal carcinoma.

Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling Arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: Autonomous innervations of the lungs are maintained by cervical sympathetic and vagal nerves. Sympathetic overactivity-induced neurogenic pulmonary edema (NPE) is known as a serious complication of subarachnoid hemorrhage, but the rational neuronal mechanism of that overactivity has not yet been clarified fully. The aim of this study was to examine whether there is a relationship between vagal nerve ischemia related sympathetic overactivity and neurogenic pulmonary edema in subarachnoid hemorrhage. METHODS: This study was conducted on 27 rabbits. A control group was formed of 5 animals, a sham group of 7 to which saline was administered, and a study group of 15 animals that were injected with homologous arterial blood into the cisterna magna. Electrocardiography and respiratory rhythm parameters were monitored for 3 weeks and the animals were then decapitated. Statistical analysis was made of the numbers of degenerated axons in the pulmonary branches of the vagal nerves, the neuron density of stellate ganglions and the vasospasm index of the pulmonary arteries. RESULTS: In the control group, the normal respiration rate was 34 ± 6 bpm, total axon number was 1600 ± 270/mm(2), degenerated axon number was 10 ± 3/mm(2), and vasospasm index was 1.34 ± 0.25. The sham group values were 30 ± 3 bpm, 163 ± 47/mm(2), and 1.95 ± 0.45 and the study group values were 45 ± 8 bpm, 530 ± 92/mm(2), and 2.76 ± 0.83. The mean stellate ganglion neuron density was evaluated as 8.112 ± 1.230/mm(3) in all animals, as 7.420 ± 4.10/mm(3) in animals with slight NPE, and as 12.512 ± 1.236/mm(3) in animals that developed severe NPE. CONCLUSION: High neuron density of stellate ganglion may have important roots in sympathetic overactivity-related NPE development in subarachnoid hemorrhage.