Neuroprotective Effects of Piceatannol on Olfactory Bulb Injury after Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) accounts for 5% of all stroke cases and is responsible for significant permanent brain and neurological damage within the first few days. Loss of smell is one of those neurological disorders following olfactory bulb injury after SAH. Olfaction plays a critical role in several aspects of life. The primary underlying mechanism of olfactory bulb (OB) injury and loss of smell after SAH remains unknown. Piceatannol (PIC), a natural stilbene, possesses anti-inflammatory and anti-apoptotic effects against various diseases. In this study, we aimed to investigate the potential therapeutic effects of PIC on OB injury following SAH at molecular mechanism based on SIRT1, inflammatory (TNF-α, IL1-ß, NF-κB, IL-6, TLR4), and apoptosis (p53, Bax, Bcl-2, caspase-3)-related gene expression markers and histopathology level; 27 male Wistar Albino rats were used in a pre-chiasmatic subarachnoid hemorrhage model. Animals were divided into groups (n = 9): SHAM, SAH, and PIC. Garcia's neurological examination, brain water content, RT-PCR, histopathology, and TUNEL analyses were performed in all experimental groups with OB samples. Our results indicated that PIC administration significantly suppressed inflammatory molecules (TNF-α, IL-6, IL1-ß, TLR4, NF-κB, SIRT1) and apoptotic molecules (caspase-3, p53, Bax). We also evaluated edema levels and cell damage in OB injury after SAH. Ameliorative effects of PIC are also observed at the histopathology level. Garcia's neurological score test performed a neurological assessment. This study is the first to demonstrate the neuroprotective effects of PIC on OB injury after SAH. It suggests that PIC would be a potential therapeutic agent for alleviating OB injury after SAH.

Rarely Seen Intradiploic Skull Hematoma in Infants.

ABSTRACT: Although the first intradiploic hematoma (IH) case was reported in 1934, only 7 infant cases were reported in the literature. The authors present 2 IH cases, without birth trauma or bleeding disorder, which were treated surgically. IH is also included in the differential diagnosis of babies with a skull deformity. Computed tomography and magnetic resonance imaging modalities should be used together in diagnosis and treatment. The authors believe that the surgery to treat skull deformity because of IH in babies should be planned in the early period.

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.

A preliminary histopathological study of the effect of agmatine on diffuse brain injury in rats.

The present study evaluates the effects of agmatine on histopathological damage following traumatic injury using a clinically relevant model of diffuse brain injury. A total of 27 male Sprague-Dawley rats weighing 200-225 g were anaesthetised and subjected to head trauma using Marmarou's impact-acceleration model. The rats were then separated into two main groups: one was treated with agmatine and the other with saline for up to 4 days immediately after head trauma. Rats from both groups were killed 1, 3 or 8 days post-injury. The brains were examined histopathologically and scored according to the axonal, neuronal and vascular changes associated with diffuse brain injury. There were no significant differences between the groups at 1 day or 3 days after trauma, but evaluation after 8 days revealed a significant improvement in the group treated with agmatine. Our data indicate that agmatine has a beneficial effect in diffuse brain injury and should be trialled for therapeutic use in the management of this condition.

Sphenoid sinusitis disguised by precocious puberty.

Isolated sphenoid sinusitis in childhood is a rare clinical entity which is often very difficult to diagnose, hence, it can easily be misdiagnosed. The rarity of this entity is related to the absence at the sinus in children and the lack of development in patients with sinopathology. The first presentation of this disorder might be disguised by another disease. We present a case sphenoid sinusitis in ten years old girl where precocious puberty and slight headache were the main symptoms. Surgical drainage and antimicrobial treatment were administered. Clinical features, diagnostic tools and treatment options for this entity are discussed.