Histopathological effects of maternal hair dye use on the cornea

The aim of this study is to investigate and compare the histopathological effects of hair dye additives, 2- amino-5-nitrophenol (2A5NP) and 2-nitro-p-phenylendiamin (2NPPD) on cornea of neonates from pregnant rats that have been administered these additives subcutaneously. The study included 90 neonates of 26 nulligravida wistar-albino rats among which ten were given 100 mg/kg/day 2A5NP (Group I), ten rats received 150 mg/kg/day 2NPPD (Group II) and control rats received saline (Group III) injections subcutaneously between 7th and 15th gestational days. No sign of toxicity was observed during the treatment and there was no gross abnormality in both the study and control groups. Histopathologicalchanges of cornea were seen in 22 of 30 newborn rats in Group I (73.4%), in 23 of 30 rats in Group II (76.7%) and only 5 of 30 rats in the control saline injected Group III (16.7%). Histopathological effect of the two additives were statistically significant when compared to the control group (Chi-square:27.63, p = 0.0001), but there was no difference between the effects of 2A5NP and 2NPPD additives on cornea (Chisquare: 0.089, p = 0.766). The present experimental study on rats confirmed the histopathological effect of 2A5NP and 2NPPD on cornea beyond doubt. In the light of which, we can speculate that maternal exposure of hair dyes during pregnancy has some teratogenic effects on newborn rat cornea

Dysregulation of chemo-cytokine production in schizophrenic patients versus healthy controls

<p>Abstract</p> <p>Background</p> <p>The exact cause of schizophrenia is not known, although several aetiological theories have been proposed for the disease, including developmental or neurodegenerative processes, neurotransmitter abnormalities, viral infection and immune dysfunction or autoimmune mechanisms. Growing evidence suggests that specific cytokines and chemokines play a role in signalling the brain to produce neurochemical, neuroendocrine, neuroimmune and behavioural changes. A relationship between inflammation and schizophrenia was supported by abnormal cytokines production, abnormal concentrations of cytokines and cytokine receptors in the blood and cerebrospinal fluid in schizophrenia. Since the neuropathology of schizophrenia has recently been reported to be closely associated with microglial activation we aimed to determined whether spontaneous or LPS-induced peripheral blood mononuclear cell chemokines and cytokines production is dysregulated in schizophrenic patients compared to healthy subjects. We enrolled 51 untreated first-episode schizophrenics (SC) and 40 healthy subjects (HC) and the levels of MCP-1, MIP-1α, IL-8, IL-18, IFN-γ and RANTES were determined by Elisa method in cell-free supernatants of PBMC cultures.</p> <p>Results</p> <p>In the simultaneous quantification we found significantly higher levels of constitutively and LPS-induced MCP-1, MIP-1α, IL-8 and IL-18, and lower RANTES and IFNγ levels released by PBMC of SC patients compared with HC. In ten SC patients receiving therapy with risperidone, olanzapine or clozapine basal and LPS-induced production of RANTES and IL-18 was increased, while both basal and LPS-induced MCP-1 production was decreased. No statistically significant differences were detected in serum levels after therapy.</p> <p>Conclusion</p> <p>The observation that in schizophrenic patients the PBMC production of selected chemo-cytokines is dysregulated reinforces the hypothesis that the peripheral cyto-chemokine network is involved in the pathophysiology of schizophrenia. These preliminary, but promising data are supportive of the application of wider profiling approaches to the identification of biomarker as diagnostic tools for the analysis of psychiatric diseases.</p

Theories of schizophrenia: a genetic-inflammatory-vascular synthesis

BACKGROUND: Schizophrenia, a relatively common psychiatric syndrome, affects virtually all brain functions yet has eluded explanation for more than 100 years. Whether by developmental and/or degenerative processes, abnormalities of neurons and their synaptic connections have been the recent focus of attention. However, our inability to fathom the pathophysiology of schizophrenia forces us to challenge our theoretical models and beliefs. A search for a more satisfying model to explain aspects of schizophrenia uncovers clues pointing to genetically mediated CNS microvascular inflammatory disease. DISCUSSION: A vascular component to a theory of schizophrenia posits that the physiologic abnormalities leading to illness involve disruption of the exquisitely precise regulation of the delivery of energy and oxygen required for normal brain function. The theory further proposes that abnormalities of CNS metabolism arise because genetically modulated inflammatory reactions damage the microvascular system of the brain in reaction to environmental agents, including infections, hypoxia, and physical trauma. Damage may accumulate with repeated exposure to triggering agents resulting in exacerbation and deterioration, or healing with their removal. There are clear examples of genetic polymorphisms in inflammatory regulators leading to exaggerated inflammatory responses. There is also ample evidence that inflammatory vascular disease of the brain can lead to psychosis, often waxing and waning, and exhibiting a fluctuating course, as seen in schizophrenia. Disturbances of CNS blood flow have repeatedly been observed in people with schizophrenia using old and new technologies. To account for the myriad of behavioral and other curious findings in schizophrenia such as minor physical anomalies, or reported decreased rates of rheumatoid arthritis and highly visible nail fold capillaries, we would have to evoke a process that is systemic such as the vascular and immune/inflammatory systems. SUMMARY: A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons

Peripapillary choroidal thickness in healthy Turkish subjects

Hulya Erbagci,1 Burak Oren,2 Seydi Okumus,3 Serhat Kenan,3 Pelin Celemler,3 Ibrahim Erbagci3 1Department of Anatomy, Medical Faculty, Zirve University Emine Bahattin Nakiboglu, Gaziantep, 2Department of Ophthalmology, Kilis State Hospital, Kilis, 3Department of Ophthalmology, Faculty of Medicine, University of Gaziantep, Gaziantep, Turkey Aim: The objective of the study reported here was to investigate the normal peripapillary choroidal thickness (CT), measured by enhanced depth imaging optical coherence tomography (EDI-OCT), in healthy Turkish volunteers. Materials and methods: In this prospective cross-sectional study, 57 eyes of 57 healthy Turkish subjects were enrolled. Each participant underwent a comprehensive ophthalmic examination and peripapillary CT measurement using EDI-OCT. Results: The mean age of the 25 female and 32 male patients in the study was 30.9&plusmn;10.6 years (range, 18&ndash;56 years). The mean peripapillary CT at the superior, inferior, nasal, and temporal sites was 225&plusmn;57, 183&plusmn;47, 220&plusmn;57, and 233&plusmn;59 &micro;m, respectively. The inferior peripapillary CT value was significantly lower than the peripapillary CT values (P&lt;0.001 for all), whereas no significant differences were found between the superior, nasal, and temporal peripapillary CT values. Conclusion: The findings of the study revealed that Turkish people had significantly lower peripapillary CT values in the inferior quadrant than in the superior, nasal, and temporal quadrants. Keywords: peripapillary choroidal thickness, enhanced depth imaging optical coherence tomography, EDI-OC

Visual evoked potential changes in migraine - Influence of migraine attack and aura

Objective: To assess the visual evoked potential (VEP) changes in migraines with and without aura. Study design: A clinical study in which the VEP results of 45 migraineurs (study group) and 22 healthy volunteers (control group) were compared. Of 45 migraineurs, 29 had migraine with aura (MA) and 16 had migraine without aura (MOA), and they were examined both during and between the migraine attacks. Methods: The patients and healthy controls underwent VEP assessment. On VEP recording, mono-ocular stimulation was performed by means of the pattern reversal check board. The latencies of N1, P1 and N2, and the N1-P1 amplitude were noted. The following comparisons were made between NI, P1 and N2 latencies and N1-P1 amplitudes of the migraine and control groups; during and between attack the VEP results of the patients with MA and MOA. Results: The VEP results of the migraineurs and healthy controls were similar (P>0.05). The during attack results of MA, during and between attack results of MOA, and the results of the control group were also similar (P>0.05). N2 latency significantly elongated in patients with MA in the attack free period than it was during the attack (P=0.01), and was also longer than it was in the control group (P=0.01). Conclusions: There is involvement of the visual pathway in MA rather than MOA, and differentiation between these subtypes of the migraine disease may be performed on the basis of VEP findings manifesting by the prolongation of the N2 wave latency. This contention should be confirmed by further studies. (C) 2001 Elsevier Science BN. All rights reserved

Cutaneous hyalohyphomycosis and onychomycosis caused by Onychocola canadensis: Report of the first case from Turkey

WOS: 000177701400010PubMed ID: 12227488We present the first Turkish case of skin and nail infection due to Onychocola canadensis in an otherwise healthy farmer who frequently worked barefoot on soil. Cutaneous involvement consisted of scaly and hyperkeratotic lesions resembling tinea pedis, erythematous plaques, and dermal papulonodules of various sizes simulating Majocchi's granuloma. Repeated cultures from nail plates, skin scrapings and needle aspiration materials from papules or nodules all yielded the same mold on Sabouroud dextrose media with and without cycloheximide, trichophyton agar, and potato dextrose agar at 26degreesC. The causal isolate was identified as Onychocola canadensis Sigler gen. et sl). non, a slow-growing arthroconidial hyphomycete, on the basis of its colonial and microscopic morphology. While skin lesions were responsive to daily itraconazole in a dose of 200 mg for three months, the onychomycosis was resistant to therapy. To our knowledge, this is the first presentation of O. canadensis as the cause of cutaneous hyalohyphomycosis to date