PERBEDAAN DERAJAT FIBROSIS HEPAR TIKUS WISTAR YANG DILAKUKAN LIGASI DUKTUS KOLEDOKUS ANTARA KELOMPOK PEMBERIAN KOMBINASI UDCAGLUTATHIONE DENGAN PEMBERIAN TUNGGAL UDCA

Background: Cholestasis leads liver cell death, fibrosis, cirrhosis, and eventually liver failure. Despite limited benefits, ursodeoxycholic acid (UDCA) is the only Food and Drug Administration–approved treatment for cholestatic disorders. Glutathione (GSH) plays important roles in antioxidant defense and regulation of cellular processes, including cell differentiation, proliferation and apoptosis. Disturbances in GSH balance have been associated with liver diseases. Objective: To evaluate the differences of the degree of liver fibrosis between supplementation of UDCA-Glutathione and UDCA in bile duct-ligated rats. Method: This true experiment research design with “posttest only control group design“ using 15 Wistar rat strain, divided into 3 group K, P1 and P2. Each rat undergoes bile duct ligation. Group K act as control with no treatment, P1 received UDCA 20 mg orally, P2 received UDCA 20 mg orally and Glutathione 15 mg intramuscular. After 21 days of intervention, all subjects were terminated and livers were taken and stained with Masson-trichrome for microscopic examination. Degrees of fibrosis were evaluated using Laennec’s scoring system. Kruskal-Wallis were used and followed by Mann-Whitney test. Result: The evaluation demonstrates statistically significant differences of degree of liver fibrosis in P2 – K group (p = 0.013) and P2 - P1 group (p = 0.006) but there was no difference between P1 and K group (p= 0.469). Conclusion: Combination of UDCA-Glutathione improved liver histology with decreased fibrosis Keywords: Cholestasis, UDCA, Glutathione, Fibrosi

Magnetic Resonance Imaging Evidence of an Occipital- Straight Sinus Dural Arteriovenous Fistula Causing Severe Bilateral Thalamic Oedema: A Case Report

An 81-year-old woman, with a 3-month history of tinnitus and vertigo, presented with a deterioration of symptoms. Magnetic resonance imaging (MRI) of the brain, using fluid attenuated inversion recovery (FLAIR) and T2 weighted (T2WI) images, demonstrated hyperintensity and swelling of the bilateral thalami, medial parietal lobes, occipital lobes, and left cerebellar hemisphere. She was referred to us with the suggestion of a brain tumour that had spread into the bilateral thalami, or encephalitis. A review of the MR images, however, demonstrated dilatation of a vein on the surface of the cerebellar hemisphere on the T2WI image. Susceptibility weighted imaging (SWI) revealed small and multiple hypointense lesions, indicating microhaemorrhages, in the bilateral thalami and left cerebellar hemisphere. The time of flight source imaging demonstrated small hyperintense dots in the wall of the occipital and straight sinus. Finally, a digital subtraction angiogram (DSA) revealed a dural arteriovenous fistula (DAVF) in the occipito-straight sinus with reflux flow into the straight sinus (Borden Type II). A transvenous embolization and trans-arterial embolization were performed, in an emergency setting, for the occipital sinus and dural shunt, respectively, with the aim of preserving the antegrade flow of the straight sinus. The DSA following the endovascular treatment showed the disappearance of shunt flow and recovery of the antegrade flow in the straight sinus. Therefore, this case report highlights that meticulous analysis of MRI scans help diagnose DAVF, which results in quick and radical treatment

Involvement of orexin neurons in fasting- and central adenosine-induced hypothermia

Abstract We examined whether orexin neurons might play a protective role against fasting- and adenosine-induced hypothermia. We first measured body temperature (BT) in orexin neuron-ablated (ORX-AB) mice and wild-type (WT) controls during 24 hours of fasting. As expected, the magnitude of BT drop and the length of time suffering from hypothermia were greater in ORX-AB mice than in WT mice. Orexin neurons were active just before onset of hypothermia and during the recovery period as revealed by calcium imaging in vivo using G-CaMP. We next examined adenosine-induced hypothermia via an intracerebroventricular administration of an adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA), which induced hypothermia in both ORX-AB and WT mice. The dose of CHA required to initiate a hypothermic response in ORX-AB mice was more than 10 times larger than the dose for WT mice. Once hypothermia was established, the recovery was seemingly slower in ORX-AB mice. Activation of orexin neurons during the recovery phase was confirmed by immunohistochemistry for c-Fos. We propose that orexin neurons play dual roles (enhancer in the induction phase and compensator during the recovery phase) in adenosine-induced hypothermia and a protective/compensatory role in fasting-induced hypothermia