Healthy and diverse coral reefs in Djibouti - A resilient reef system or few anthropogenic threats?

Djiboutian coral reefs are poorly studied, but are of critical importance to tourism and artisanal fishing in this small developing nation. In 2014 and 2016 we carried out the most comprehensive survey of Djiboutian reefs to date, and present data on their ecology, health and estimate their vulnerability to future coral bleaching and anthropogenic impacts. Reef type varied from complex reef formations exposed to wind and waves along the Gulf of Aden, to narrow fringing reefs adjacent to the deep sheltered waters of the Gulf of Tadjoura. Evidence suggests that in the past 35 years the reefs have not previously experienced severe coral bleaching or significant human impacts, with many reefs having healthy and diverse coral and fish populations. Mean coral cover was high (52%) and fish assemblages were dominated by fishery target species and herbivores. However, rising sea surface temperatures (SSTs) and rapid recent coastal development activities in Djibouti are likely future threats to these relatively untouched reefs.

Phosphorylation of neuronal nitric oxide synthase at Ser847 in the nucleus intermediolateralis after spinal cord injury in mice.

We previously demonstrated that Ca2+/calmodulin (CaM)-dependent protein kinase IIalpha (CaM-KIIalpha) can phosphorylate neuronal nitric oxide synthase (nNOS) at Ser847 and attenuate NOS activity in neuronal cells. In the present study we focused on chronological alteration in levels and cellular location of nNOS, phosphorylated (p)-Ser847-nNOS (NP847), CaM-KII and p-Thr286-CaM-KIIalpha following spinal cord injury (SCI) in mice. Western blot analysis showed nNOS to be significantly phosphorylated at Ser847 from 3 h after SCI, peaking at 24 h and gradually decreasing thereafter, and CaM-KII to be colocalized with nNOS after SCI. Immunohistochemical analysis revealed that SCI causes an increase in both NP847 and p-Thr286-CaM-KIIalpha in the nucleus intermediolateralis. These findings suggest that SCI induces p-Thr286-CaM-KIIalpha, which phosphorylates the nNOS at Ser847 in the nucleus intermediolateralis where NO is thought to play a role as a neurotransmitter in autonomic preganglionic neurons. Thus, the NP847 signaling pathway might be involved in the autonomic failure which occurs immediately after SCI.

Tamoxifen inhibits nitrotyrosine formation after reversible middle cerebral artery occlusion in the rat.

Tamoxifen (TAM), a widely used non-steroidal anti-estrogen, has recently been shown to be neuroprotective in a rat model of reversible middle cerebral artery occlusion (rMCAo). Tamoxifen has several potential mechanisms of action including inhibition of the release of excitatory amino acids (EAA) and nitric oxide synthase (NOS) activity. The question addressed in this study was whether TAM reduces ischemia-induced production of nitrotyrosine, considered as a footprint of the product of nitric oxide and superoxide, peroxynitrite. In rat brain, 2 h rMCAo produced a time-dependent increase in nitrotyrosine content in the cerebral cortex, as measured by Western blot analysis. Compared with vehicle, TAM significantly reduced nitrotyrosine levels in the ischemic cortex at 24 h. The neuronal (n)NOS inhibitor, 7-nitroindazole also tended to reduce nitrotyrosine, but this reduction was not statistically significant. Immunostaining for nitrotyrosine was seen in cortical neurons in the MCA territory and this immunostaining was reduced by TAM. In vitro, TAM and the calmodulin inhibitor trifluoperazine inhibited, with similar EC(50) values, the activity of recombinant nNOS as well as NOS activity in brain homogenates, measured by conversion of [(3)H]arginine to [(3)H]citrulline. There was marginal inhibition of recombinant inducible (i)NOS activity up to 100 microM TAM. These data suggest that TAM is an effective inhibitor of Ca(2+)/calmodulin-dependent NOS and the derived peroxynitrite production in transient focal cerebral ischemia and this may be one mechanism for its neuroprotective effect following rMCAo.

[Two cases of facial neurinoma successfully treated with gamma knife radiosurgery].

Two cases of facial neurinoma successfully treated with gamma knife radiosurgery are reported. Case 1, a 33-year-old female, developed a right-sided hemifacial spasm about five years ago. Then she suffered gradual progression of right-sided facial palsy, dysgeusia and reduction of lacrimation, but she had no hearing disturbance. T1-weighted MRI with gadolinium DTPA showed a well-circumscribed tumor at the geniculate ganglion extending to the middle cranial fossa. The tumor was treated with gamma knife radiosurgery which reduced its size, but didn't reduce the patient's facial palsy. Case 2, a 36-year-old female, presented with fluctuating facial palsy and sensorineural hearing loss lasting for fourteen years. T1-weighted enhanced MRI showed a well-enhanced tumor at the CP angle extending to the middle cranial fossa. The tumor was treated with gamma knife radiosurgery, which caused central tumor necrosis, but didn't reduce the tumor size. Meanwhile the patient's facial palsy improved. Gamma knife radiosurgery is apparently effective against facial neurinomas without producing serious complications such as complete facial palsy and hearing loss. Our study indicates that gamma knife radiosurgery is a useful therapeutic alternative for facial neurinomas.

A meningioma of the lateral cerebellomedullary cistern without dural attachment.

A rare case of a meningioma in the lateral cerebellomedullary cistern without dural attachment is reported. The tumor was attached to the choroid plexus out of the lateral recess, not in the fourth ventricle. The radiologic findings and operative approach differed from those for fourth ventricle meningiomas or cerebellopontine angle meningiomas. Magnetic resonance imanging is the most helpful preoperative diagnostic study for determining the precise location, volume and extent of the lesion and the site of attachment. Care was taken not to injure the lower cranial nerves and the tumor was totally removed except for a tiny piece which invaded the proximal portion of the posterior inferior cerebellar artery.

Interleukin-6 and development of vasospasm after subarachnoid haemorrhage.

The authors characterized the role of interleukins in the cerebrospinal fluid (CSF) in the development of vasospasm after subarachnoid haemorrhage (SAH), particularly interleukin-6 (IL-6). Concentrations of interleukin-1 beta (IL-1 beta), IL-6, and interleukin-8 (IL-8) were measured serially in CSF of 24 patients and in serum of 9 patients with SAH and correlated clinically. Additionally, the effects of the same cytokines on the cerebral arteries of dogs were analyzed on angiograms after intracisternal injection. Changes in levels of eicosanoids, angiogenic factors, and soluble cell adhesion molecules were investigated in the CSF of injected dogs. CSF concentrations of IL-6 and IL-8 were elevated significantly above control levels from the acute stage of SAH until the chronic stage. Patients with symptomatic vasospasm had significantly higher levels of IL-6 as well as IL-8 in CSF on days 5 and 7. Intracisternal injection of IL-6 induced long-lasting vasoconstriction in five out of eight dogs, while IL-8 did not. The diameter of canine basilar artery after IL-6 was reduced 29 +/- 5% from pretreatment diameter at 8 hours. Prostaglandins E2 and I2 were elevated in CSF for the first 4.5 hour of this IL-6-induced vasospasm. Neither angiogenic factors such as platelet-derived growth factor-AB and vascular endothelial growth factor nor soluble cell adhesion molecules were significantly elevated in CSF. IL-6, which increases to very high concentrations in CSF after SAH, may be important in inducing vasospasm, as IL-6 produced long-lasting vasoconstriction in the canine cerebral artery, which may be partly related to activation of the prostaglandin cascade.

Inducible cyclooxygenase expression in canine basilar artery after experimental subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Inducible cyclooxygenase (COX-2) has been found to play a pathological role in cerebral insult. We investigated the expression of COX-2 in the basilar artery after experimental subarachnoid hemorrhage (SAH). METHODS: In a canine "two-hemorrhage" model of SAH, the basilar arteries were obtained on day 2 after a cisternal injection of autologous blood or on days 4, 6, 7, or 9 after the second injection. Basilar arteries also were obtained 12 hours after intracisternal injection a cytokine: interleukin (IL)-1 beta (0.03 microgram), IL-6 (3 micrograms), or IL-8 (10 micrograms). Western blotting with a polyclonal anti-COX-2 antibody was performed in these arteries. RESULTS: COX-2 protein was not demonstrated in the basilar artery in control animals without SAH. However, it was expressed in the basilar artery on days 2, 4, 6, and 7 after blood injection but not on day 9. Intracisternal injection of IL-1 beta, IL-6, or IL-8 also induced COX-2 in the basilar artery. CONCLUSIONS: COX-2 expression was detected in basilar arterial tissue in both acute and chronic stages after SAH. Elevation of inflammatory cytokines after SAH may be involved in the induction of COX-2, which may produce sufficient quantities of eicosanoids to affect hemodynamics after SAH.

Vasodilator effects on canine basilar artery induced by intracisternal interleukin-1 beta.

The effect of interleukin-1 beta (IL-1 beta) on a cerebral artery was investigated in anesthetized dogs. Intracisternal administration of IL-1 beta (0.03 and 0.3 micrograms) dilated the canine basilar artery in a dose-dependent manner, without affecting systemic blood pressure or heart rate. The increase in diameter induced by 0.3 micrograms of IL-1 beta was 28.4% +/- 13.4% of control at 2 hours and was inhibited by 30 micrograms of the IL-1 beta receptor antagonist, zinc protoporphyrin (4.5% +/- 13.5%, P < 0.05). Interleukin-1 beta did not affect the concentration of nitric oxide metabolites in CSF. However, there was an increase in the concentration of eicosanoids in CSF, and the elevation of 6-keto-PGF1 alpha paralleled the vasodilation. Pretreatment with 30 micrograms of the selective inducible cyclooxygenase (COX-2) inhibitor NS-398 also inhibited the IL-1 beta-induced vasodilation significantly (5.9% +/- 9.4% at 2 hours, P < 0.01). Western blot analysis revealed the expression of a 68-kD COX-2-like protein in basilar artery extracts. These findings suggest that the IL-1 beta-induced vasodilator effect is linked to the prostaglandin cascade, predominantly to prostaglandin I2, by induction of COX-2, but not to the stimulation of nitric oxide metabolism.

Nitric oxide metabolites in the cisternal cerebral spinal fluid of patients with subarachnoid hemorrhage.

OBJECTIVE: To investigate nitric oxide (NO) metabolism after subarachnoid hemorrhage (SAH). METHODS: We measured the concentrations of the NO metabolites, nitrite and nitrate, in cerebrospinal fluid (CSF) obtained from the cisternal drainage of patients with SAH. Studies were performed for 31 patients who had undergone surgical obliteration of bleeding aneurysms within 3 days of their hemorrhage. The concentrations of nitrite and nitrate in the CSF were measured for 14 days using a nitrate/nitrite kit and samples that were obtained on a daily basis from the cisternal drainage. RESULTS: Compared with the control values in the CSF (2.6 +/- 0.4 mumol/L, n = 14) obtained from patients with hemifacial spasm, trigeminal neuralgia, or nonruptured aneurysms, the concentrations of nitrite and nitrate in the CSF were significantly elevated in the acute stage of SAH and remained elevated. The concentration of NO metabolites may correlate with the amount of bleeding, inasmuch as the values in patients in Fisher Group 3 (n = 25) were higher than those in patients in Fisher Group 2 (n = 6). The concentration of nitrate was higher than that of nitrite, suggesting that NO in the subarachnoid space is mainly absorbed by hemoglobin and degraded to nitrate. No differences were demonstrated in patients treated with high doses of methylprednisolone (n = 17) compared with those treated with usual-dose steroids (n = 14). Steroids are known to prevent the formation of inducible NO synthase mediated by inflammatory cytokines. CONCLUSION: NO metabolism in the brain is stimulated after SAH. Nitrate is the dominant NO metabolite in CSF after SAH. The involvement of inducible NO synthase in the pathophysiology of NO metabolism after SAH was not clearly suggested based on the present data.

Multiple communicating intradural arachnoid cysts: usefulness of myelography and myelo-computed tomography using both lumbar and cervical punctures. Case report.

We report a case of multiple communicating intradural cystic lesions. Magnetic resonance imaging did not demonstrate the lesions. Neuroradiological diagnosis of the intradural arachnoid cysts was made from myelography and myelo-computed tomography using both lumbar and cervical punctures. These procedures give us useful information about flow dynamics in the spinal subarachnoid space.

Intravenous infusion of adrenomedullin and increase in regional cerebral blood flow and prevention of ischemic brain injury after middle cerebral artery occlusion in rats.

The intravenous infusion of rat adrenomedullin, at concentrations ranging from 0.1 to 1.0 microgram/kg/min, for 60 min increased the regional cerebral blood flow (rCBF) in a dose-dependent manner in rats. rCBF was measured using a laser Doppler flowmetry device placed on the surface of the parietal cortex. The increase in rCBF induced by 1.0 microgram/kg/min of adrenomedullin was up to 145 +/- 10.8% of controls at 60 min (n = 5, p < 0.001). These concentrations of adrenomedullin did not affect systemic blood pressure or other physiologic parameters, including pH, PaCO2, PaO2, hemoglobin, and blood glucose. Repeated infusion of 1.0 microgram/kg/min of adrenomedullin at 2-h intervals caused tachyphylaxis (n = 5, p < 0.01). Rat adrenomedullin (1.0 microgram/kg/min) demonstrated a more potent effect than the same dose of human adrenomedullin. The C-terminal fragment of human adrenomedullin (0.5 and 5.0 micrograms/kg/min), adrenomedullin22-52, which did not affect rCBF alone, inhibited the effect of rat adrenomedullin (0.5 microgram/kg/min) as a receptor antagonist in a dose-dependent manner. In a model of middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats, pre- and postinfusion of 1.0 microgram/kg/min of adrenomedullin suppressed the reduction in rCBF following MCA occlusion (control, 29 +/- 15.1%; adrenomedullin group, 45 +/- 14.4%; not significant) and decreased the volume of ischemic brain injury (control, 288 +/- 35 mm3; adrenomedullin group, 232 +/- 35 mm3; p < 0.05). These results suggest that adrenomedullin increases rCBF and prevents ischemic brain injury, partly by increasing the collateral circulation.

Changes in serum cytokine concentrations after neurosurgical procedures.

Cytokine responses to surgical trauma have been studied in 70 patients undergoing various neurosurgical procedures. Serum concentrations of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8, (IL-8), tumour necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) were measured before and after surgery using enzyme-linked immunosorbent assays. The serum concentrations of IL-1 beta, IL-8, TNF-alpha, and IFN-gamma did not change significantly following neurosurgical operations. In contrast, serum IL-6 levels were significantly elevated following surgery, peaking at postoperative day 1 and then gradually decreasing. Maximum IL-6 concentrations were considerably higher in patients who underwent surgery for brain tumours or aneurysms as compared with patients who had a ventriculoperitoneal shunt, neurovascular decompression or transsphenoidal adenomectomy. Intra-operative use of methylprednisolone, which is known to block the production and action of cytokines, suppressed the increase in IL-6 levels after surgery. There was a statistically significant correlation between the IL-6 peak concentration and the length of surgery in patients not treated with steroids, but not in patients treated with steroids. Additionally patients who underwent supratentorial surgery had higher peak concentrations of IL-6 than those who underwent infratentorial surgery. These results suggest that IL-6 is an early marker of tissue damage and may be useful in assessing the extent of postoperative stress.

True aneurysms of the middle meningeal artery associated with cavernous hemangioma of the skull--case report.

A rare case of true aneurysms of the middle meningeal artery (MMA) associated with cavernous hemangioma in a 47-year-old male is presented. Angiography showed aneurysmal dilatation of the MMA, which was a tumor feeder. Histological examination confirmed the true aneurysmal character of the dilatation. The aneurysms were considered to result from increased hemodynamic stress and medial defects in the MMA.