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Introduction: There have been thousands of neurochemical mechanism about blood glucose level regulation, but intrapancreatic taste buds and their roles in blood glucose level has not been described. We aimed to investigate if there are taste buds cored neural networks in the pancreas, and there is any relationship between blood glucose levels. Methods: This examination was done on 32 chosen rats with their glucose levels. Animals are divided into owned blood glucose levels. If mean glucose levels were equal to 105 ± 10 mg/dL accepted as euglycemic (G-I; n = 14), 142 ± 18 mg/dL values accepted as hyperglycemic (G-II; n = 9) and 89 ± 9 mg/dL accepted as hypoglycemic (G-III; n = 9). After the experiment, animals were sacrificed under general anesthesia. Their pancreatic tissues were examined histological methods and numbers of newly described taste bud networks analyzed by Stereological methods. Results compared with Mann-Whitney U test P

Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty-eight rabbits were used. Five rabbits were used to analyze CB network (control group;n= 5); seven rabbits were injected 1 mL of saline (Sham group;n= 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group;n= 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann-WhitneyU-test. The pH values of blood were estimated as 7.359 +/- 0.039 in the control group, 7.318 +/- 0.062 in the Sham group, 7.23 +/- 0.013 in the SAH group. CSF pH values were 7.313 +/- 0.028 in the control group, 7.296 +/- 0.045 in the Sham group, and 7.224 +/- 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 +/- 7 in the control group, 226 +/- 64 in the Sham group, and 2115 +/- 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature.

BackgroundCircumcision is a surgical removal process of the preputium. Surgical excision and electric current cause neurodegeneration in the excised tissue-related neural network. This study investigates if circumcision and current surgical methods would cause histopathological changes in the penile tissue innervating pudendal nerve dorsal root ganglia.ResultsVascular congestion occluded the microvessels, and degenerative changes were detected in postexcised penile tissue. Neuronal angulation, cytoplasmic condensation, nuclear shrinkage, and condensed nuclei were observed in the pudendal nerve ganglia. Moreover, the degenerated neuron (DN) densities of the pudendal nerve ganglia were 5 ± 2, 98 ± 22, 1093 ± 185, 236 ± 43 and 151 ± 19 in the control, the surgical circumcision, the monopolar cautery, the bipolar cautery and the thermocautery groups, respectively.ConclusionsAlthough only the pudendal nerve endings are affected secondary to prepusium excision another pudendal axons can be damaged during bleeding control with cautery, the destruction of the neuron that sends this axon initiates a general inflammation in that ganglion. As a result, there may be a somatosensitive innervation defect in extrapenile tissues innervated by this ganglion. High-voltage electric devices should not be used unless obligatory.

Introduction: Cardiac glycosides are widely used in critical cardiac diseases despite their unexplained mechanisms on cardio-respiratory system and other autonomic complications within both intra-uterine and post-natal life. The aim of this study is to investigate if digitalis overdose could cause a result in such complications by a destructive effect on blood-brain barrier (BBB). Methods: Twenty-five male Sprague Dawley rats weighing 300–350 g were divided into the following groups: control (n=5), sham (isotonic) (n=5), therapeutic dose (n=5), arrhythmogenic dose (n=5), and lethal dose (n=5). The animals were euthanized and their brains were extracted. The brains were histopathologically and immunohistochemically examined to evaluate BBB morphology in the superior temporal cortex. Results: One animal died because of experimental procedures on the first day. Macroscopic examination of brains revealed brain edema, subarachnoid hemorrhage (SAH), and narrowed cisterns in toxic doses of digitalis-treated animals. Brain histopathological examination of these groups revealed bloody subarachnoid and cisternal spaces, cortical arteriolar vasospasm, neurodegeneration, and even peri-arteriolar neuroglial component fragmentation; these changes induced BBB destruction in the high-dose digitalis-treated animals. Conclusion: Digitalis should not be used with overdoses if the cardio-respiratory arrhythmia is unexpectedly appearing in low doses against the possibility of defected or disrupted BBB.

Wound healing remains a challenging clinical problem, especially in the presence of diabetes. Diabetic patients have the impaired ability to fight infection and insufficient inflammatory response. The aim of this study was to evaluate the effects of boronophenylalanine (BFA) and/or Zn-containing nanoemulsion (NE) formulations on wound healing in diabetic rats. MTT and scratch assays were performed to evaluate the proliferative effects of BFA and/or Zn on human dermal fibroblast (HDF) cells and the migration of these cells, respectively. The BFA and/or Zn-NE were prepared, and the effects of NEs on wound healing in diabetic rats were evaluated by applying once a day for 14 days. MTT assay showed that 10 to 25 µM BFA and/or 50 µM Zn had very significant positive effects on cell proliferation. In the scratch assay, 10 µM BFA significantly increased the migration of HDF cell compared with control. The droplet sizes of all the NEs were

Purpose of the study: Hypofunctioning breasts are typically considered a dysfunction of higher brain centers that regulate hormonal feedback, and olfactory information has been proposed as a trigge...

Background and Objective: Metformin (MET) has been used as an antidiabetic agent for type II diabetes. At the same time, recent researches have shown that the clinical improvement of MET is useful for nerve damage. In this study, we investigated the analgesic effect of MET in paclitaxel (PAC)-induced neuropathic pain. Materials and Methods: Forty-two adult, female rats, Wistar strain weighing 220 +/- 10 g were randomly divided into 5 experimental groups. PAC was intraperitoneally (IP) administered (2.0 mg/kg) for 4 groups every other day (0, 2, 4, and 6 days). By the 30th day, MET (100, 200, and 400 mg/kg) was administered to 4 groups. Before and after treatment, basal pain threshold values were measured with Randall-Selitto analgesiometer test. At the end of experiment, pathological values were measured in selected regions including brain (motor cortex, M1), spinal cord (L4-L5), sciatic nerve, and muscle. Results: According to our results, PAC-induced neuropathic pain reached to highest level at 14th day. Four hundred milligram/kilogram concentration of MET remarkably decreased PAC-induced neuropathic pain. On the other hand, pathologic features have shown that PAC had significant pathological change in the brain and spinal cord while in the peripheral nerves and muscles had not shown any pathological change. Conclusion: The pathological results of the current study for the first time demonstrated that MET beside of its antidiabetic effects reversed neuropathic pain induced by PAC. Consequently, this research can be promising for cancer patients that suffering from neuropathic pain induced by anticancer drugs.