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"Chronic hepatotropic viruses commonly evade the antiviral defence systems of the body and cause a long - lasting persistent infection. The prolonged nature of the infection ensures that every infected person has ample opportunity to transmit the virus to others, allowing many millions of people world-wide to become infected. Three viruses commonly cause chronic hepatitis B virus, hepatitis C virus and hepatitis Delta virus.Virus specific CD8 T cells of the host, represent the main effector cells against viral infection. Where as the antiviral cytokinex have a major role in the control of viral replication (non-cytolytic inhibition).To cause persistent infection, a virus must avoid the host defences and that hepatotropic viruses have developed elaborate strategies to achieve this. In the case of hepatitis B virus, two proteins are involved in the inhibition of the host defences; those are the core protein that has been shown to inhibit the production of interferon and the polymerase protein has been shown to inhibit its effect. Where as in the case of hepatitis C virus, the NS5A and E2 protein reduce the effect of interferon by inhibiting the antiviral kinase.In order to survive and persistent in the liver, the hepatotropic viruses must be able to avoid both arms of the immune system, either by mutation of viral proteins or by preventing activation of the immune system."

"Chronic hepatitis due to hepatitis B virus (HBV) or hepatitis C virus (HCP) is still a major problem in terms of progressive liver damage, prevention and therapy in most parts ofthe world. Unfortunately, to date, there is still no specific and effective therapy for HBV. No therapy can be given to carrier; non-replicative and asymptomatic patients of chronic HBV infection. Lamivudine or alpha-interferon can be used for treatment of compensated chronic hepatitis B infection with significant increase of aminotransferase. Approximately 40 % of patients can have seroconversion with this form of therapy. Chronic hepatitis D virus injection can be treat with alpha-interferon and in the final stage, may undergo liver transplantation. For chronic hepatitis C virus infection, alpha-interferon with ribavirin have been shown to have a better efficacy than afpha-interferon alone where the efficacy can reach 39-49 %."

"The recent advances of endoscopic examination had proven that source of upper gastrointestinal bleeding in liver cirrhosis is not always caused by esophageal varices rupture but also gastric mucosal lesion. The prevalence of gastric ulcer in patients with liver cirrhosis is higher than healthy individuals. Imbalance of defensive and aggressive factors of gastric mucosa may involve in development of portal hypertensive gastropathy (PHG). Several studies reported hemodynamic changes associated wuth portal hypertension causing decreased mucus layer thickness as one of mechanism of PHG. Other dialogic factors of PHG were hypoacidity, hypergastrinemia, reduced hexosamin concentration, mucus metabolic function associated with decreased prostaglandin E2, and increased nitric oxyde which had caused mucus wall thickness changes. Gastric mucus damage induced by portal hypertension has important role in the pathogenesis of gastric ulcer in liver cirrhosis."

"ABSTRACTThe treatment of chronic spontaneous urticaria begins with antihistamines; however, the dose required typically exceeds that recommended for allergic rhinitis. Second-generation, relatively non-sedating H₁receptor blockers are typically employed up to 4 times a day. Firstgeneration antihistamines, such as hydroxyzine or diphenhydramine (Atarax or Benadryl), were employed similarly in the past. Should high dose antihistamines fail to control symptoms (at least 50%), omalizumab at 300 mg/month is the next step. This is effective in 70% of antihistamine refractory patients. H₂receptor blockers and leukotriene antagonists are no longer recommended; they add little and the literature does not support significant efficacy. For those patients who are unresponsive to both antihistamines and omalizumab, cyclosporine is recommended next. This is similarly effective in 65%-70% of patients; however, care is needed regarding possible side effects on blood pressure and renal function. Corticosteroids should not be employed chronically due to cumulative toxicity that is dose and time dependent. Brief courses of steroid e.g., 3 to 10 days can be employed for severe exacerbations, but should be an infrequent occurrence. Finally, other agents, such as dapsone or sulfasalazine, can be tried for those patients unresponsive to antihistamines, omalizumab, and cyclosporine."

"Penelitian ini bertujuan menganalisis aktivitas spesifik enzim MnSOD, katalase dan OPT pada sel hati tikus yang diinduksi hipoksia sistemik dan hubungannya dangan stres oksidatif. Sampel penelitian ini adalah jaringan had tikus jantan strain Sprague Dawley (Rattus novergieus L), yang diinduksi hipoksia sistemik kmnik 1,7,14 dan 21 hari. Pada homogenat hati tikus dilakuksn beberapa pomeriksaan, yaitu pemeriksaan aktivitas spesifik MnSOD, aktivitas spesifik katalase, aktivitas spesifik enzim OPT, kadar MDA dan pemeriksaan senyawa karbonil.Dari penelitian ini didapatkan hasil tidak adanya perubahan bennakna pada aktivitas spesifik MnSOD, OPT, dan kadar karbonil. Pada hipoksia 7 dan 21 hari terjadi penurunan bermakna aktivitas spesifik katalase, dan kadar MDA menurun bertuakna peda bipoksia 21 hati.Dari hasil analisis didapat bubungan negatif antara MnSOD dan katalase dengan kerusakan oksidatif, disimpulkan bahwa MnSOD dan kstalase berperan dalam mencegah kerusakan oksidatif. Analisis hubungan aktivitas spesifik OPT dengan kerusakan oksidatif didapat hubungan negatif. Hal ini mengindikasikan bahwa penurunan OPT di hati dapat dipaksi sebagai indikator kerusakan oksidatif.Dari basil penelitian ini disimpulkan bahwa jaringan hari memiliki sistem pertahanan antioksidan yang adekuat, sehingga sel hati cukup tahan terhadap terjadinya kerusaknn oksidalif.

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The aim of this study was to analyze the specific activities of MoSOD, catalase and GPT in rat liver cells induced by systemic hypoxia related to oxidative stress. The samples were obtained from liver tissue of Spmgue Dawley rats at days I, 7, 14, and 21 of citronic systemic hypoxia and were used to measure specific activity ofMnSOD, catalase, GPT, and the levels ofMDA, and protein carbonyis.

Results showed that there were not significant alteration of specific activity ofMnSOD, ofGPT, and levels of carbonyls. At days 7 and 21 of hypoxic induction there were significant decrease of catalase specific activity. Levels of MDA significant decreased at days 21.

Based on correlation analyzing it can be concluded that MnSOD and catalase had a role in prevent oxidative damage. Correlation analyzing of OPT specific activity and oxidative damage showed negative correlation. This means that decreased of GPT specfic activity in liver could be used as oxidative damage indicator.

It is concluded that liver tissue provided with adequate antioxidant defense mechanism which makes Uver cells survive during hypoxic oxidative insult."

"Adaptation mechanism to hypoxia in living organisms increases reactive oxygen species (ROS) formation that could exceed the capacity of anti oxidant. Gluthatione (GSH) in which highest concentration present in liver, plays an important role in maintaining the intracellular redox equilibrium and protect tissues from oxidative stress. The aim of this study was to observe tissue response of rat that was exposed to chronic systemic hypoxia by analyzing the oxidative stress in liver tissue. Twenty male Sprague-Dawley rats were induced by chronic systemic hypoxia by kept them in hypoxic chamber (10% O2:90% N2) for 1, 3, 7 and 14 day(s). All rats were sacrificed with ether anesthesia after hypoxia treatment. Liver tissues were analyzed using parameters of oxidative stress, malondialdehyde (MDA) with tBARS test, and endogenous antioxidant, glutathione reduced form (GSH). The study showed that chronic systemic hypoxia induction caused oxidative stress in liver tissue, which was shown by increased concentration of MDA in liver tissue (nmol/mg liver tissue). Concentration of MDA in liver tissue was increased significantly on day-1, day-3, day-7 and day-14 compared to control group (ANOVA, LSD, p<0.05). The differences between day-3, day-7 and day-14 was not significant. In contrast, liver GSH content (μg/mg liver protein) was progressively decreased significantly since day-1 of hypoxia until the end of experiment (ANOVA, LSD, p<0.05). Statistical analysis revealed that there is a strong correlation between MDA and GSH concentration in liver tissue (Pearson = - 0.993). It was concluded that oxidative stress present in liver tissue of rat induced by chronic systemic hypoxia."

"ABSTRAKAdanya kerusakan sel hati pada infeksi virus Dengue (DENV) telah diketahuitetapi patogenesis yang mendasari hingga kini belum seluruhnya jelas. Penelitianini bertujuan untuk mengetahui lebih jelas patogenesis mekanisme yangmendasari kerusakan sel hati pada infeksi DENV dengan melihat efek langsungvirulensi virus dan efek tidak langsung.Kelompok penelitian terdiri dari: A. kontrol sel Huh7, B. Huh7 + DENV-2, C.Huh7 + antibodi NS-1, D. Huh7 + komplemen, E. Huh7 + antibodi NS-1 +komplemen, F. Huh7 + DENV-2 + antibodi NS-1 + komplemen, G. Huh7 +DENV-2 + antibodi NS-1, H. Huh7 + peripheral blood mononuclear cells(PBMC) dari pasien yang pernah terinfeksi DENV, I. Huh7 + DENV-2 + PBMCdari pasien yang pernah terinfeksi DENV, dan J. Huh7 + TNF-α. Aktivitas ASTdan ALT dari supernatan diukur sebagai indikator kerusakan sel Huh7.Median aktivitas pada sel Huh7 yang diberi DENV-2 0,1 moi selama 2 x 24 jam(AST 7 U/L dan ALT 3 U/L) lebih rendah bermakna dibandingkan kontrol (AST11 U/L dan ALT 4 U/L), yang menunjukkan efek anti-apoptotik DENV-2 padadosis 0,1 moi dan lama inkubasi 2 x 24 jam. Pada percobaan dengan berbagaidosis DENV dan lama inkubasi, didapatkan efek anti-apoptotik ini menghilangsetelah inkubasi 3 x 24 jam. Hasil tersebut menunjukkan kebenaran hipotesis efeklangsung merusak sel hati oleh infeksi DENV. Aktivitas AST 19 U/L dan ALT 8U/L pada sel Huh7 yang diberi antibodi NS-1 bersama komplemen lebih tinggibermakna dibandingkan kontrol sel Huh7 tanpa perlakuan (AST 11 U/L dan ALT4 U/L), maupun pemberian antibodi NS-1 saja (AST 10 U/L dan ALT 4 U/L).Hasil itu menunjukkan bahwa hipotesis molekular mimikri yang dibawakan olehantibodi NS-1 terbukti. Aktivitas AST 6,5 U/L pada pemberian antibodi NS-1bersama komplemen pada sel hati Huh7 yang sudah diinfeksi DENV-2 lebihrendah bermakna dibandingkan AST 11 U/L pada kontrol. Hasil itu menunjukkanDENV-2 memiliki efek anti-apoptotik yang mampu menghambat efek lisis dariantibodi bersama komplemen. Tidak terjadi peningkatan AST pada sel Huh7 yangdiberi PBMC saja (8 U/L), DENV-2 bersama PBMC (6 U/L) dan TNF-α saja (10U/L) dibandingkan kontrol (11 U/L).Dengan demikian, mekanisme kerusakan sel hati pada infeksi DENV in vitro yangdapat dibuktikan dengan penelitian ini adalah akibat efek langsung DENV-2 danmolekular mimikri pada sel hati yang dibawakan oleh antibodi NS-1.

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ABSTRACTThe involvement of liver cell damage in Dengue virus (DENV) infection isalready known but the whole pathogenesis is still not clear. Virus virulence isinvolved but other mechanisms may also play a role. This study aimed tounderstand the pathogenesis of liver cell damage caused by DENV infection,through direct pathogenic effect of the virus and indirect effect of immunologicalreaction.The study groups were A. Huh7 liver cells, control, B. Huh7 + Dengue virus-2New Guinea C strains (DENV-2), C. Huh7 + NS-1 antibody, D. Huh7 +complement, E. Huh7 + NS-1 antibody + complement, F. Huh7 + DENV-2 +NS-1 antibody + complement, G. Huh7 + DENV-2 + NS-1 antibody, H. Huh7 +peripheral blood mononuclear cells (PBMC) from previously DENV-infectedpatient, I. Huh7 + DENV-2 + PBMC from previously DENV-infected patient and,J. Huh7 + TNF-α. Activities of AST and ALT in the supernatant were measuredas indicator of liver cell damage.In the Huh7 cells, infected with DENV-2 0,1 moi (multiplicity of infection) andincubated for 2 x 24 hours, median AST 7 U/L and ALT 3 U/L were significantlylower compared to AST 11 U/L and ALT 4 U/L in Huh7 control cells. It wasconcluded that DENV-2 had anti-apoptotic effect at 0,1 moi dan incubation time 2x 24 hours. At various dosage of DENV-2 and incubation time study, the antiapoptoticeffect disappeared after 3 x 24 hours incubation; which means the effectwas temporary. The result proved the direct damaging effect of DENV to infectedliver cells. Activity of AST 19 U/L and ALT 8 U/L in Huh7 cells treated withNS-1 antibody together with complement, were significantly higher compared tocontrol (AST 11 U/L, ALT 4 U/L), and NS-1 antibody only (AST 10 U/L, ALT 4U/L). This result proved the molecular mimicry hypothesis by NS-1 antibody.Activity of AST 6,5 U/L in DENV-infected Huh7 cells treated with NS-1antibody and complement was significantly lower than AST 11 U/L in controlcells. This result indicated that DENV has anti-apoptotic effect that can inhibit thelytic effect of antibody and complement. There was no AST increase in Huh7treated with PBMC only (8 U/L), DENV-2 with PBMC (6 U/L) and TNF-α only(10 U/L) compared to control (11 U/L).The liver cell damage mechanisms of in vitro DENV infections which can beproven in this study are direct effect by DENV and molecular mimicry by NS-1antibody."

"Hipoksia sistemik kronik dapat menyebabkan kekurangan oksigen pada otak sehingga metabolisme sel menjadi metabolisme anaerob. Konsekuensi metabolisme anaerob ini adalah kekurangan energi dalam bentuk ATP mengingat otak adalah organ yang sangat aktif. Akibat penurunan energi ini terjadi stimulasi yang berlebihan terhadap kanal Ca2+ sehingga terjadi influks Ca2+ yang berlebihan ke dalam sel memicu berbagai macam efek antara lain peningkatan penglepasan neurotransmiter ACh. Hipoksia sendiri memicu pembentukan radikal bebas dengan hasil akhir MDA. Pada kerusakan otak akibat hipoksia GFAP yang merupakan protein spesifik pada astrosit dapat mengalami peningkatan sintesis. Penelitian ini merupakan penelitian ekperimental dengan desain rancang acak lengkap menggunakan hewan coba tikus Spraque Dawley yang diinduksi dengan hipoksia sistemik kronik. Sampel penelitian ini menggunakan jaringan otak bagian korteks dan plasma tikus sebanyak 5 ekor pada tiap kelompok terdiri atas 1 kelompok kontrol dan 4 kelompok perlakuan yang terdiri atas tikus yang diinduksi hipoksia 1 hari, 3 hari, 5 hari dan 7 hari. Parameter yang diperiksa adalah konsentrasi MDA otak dan plasma, aktivitas spesifik enzim AChE jaringan otak serta kadar GFAP jaringan otak. Hipoksia sistemik kronik tidak menimbulkan peningkatan konsentrasi MDA otak sementara dalam plasma terjadi peningkatan yang tidak bermakna konsentrasi MDA plasma. Induksi hipoksia sistemik meningkatkan aktivitas spesifik enzim AChE pada jaringan otak dan meningkatkan kadar GFAP jaringan otak secara bermakna. Sedangkan pada plasma tidak terjadi peningkatan kadar GFAP. Pada induksi hipoksia sistemik ini belum terjadi kerusakan oksidatif. Peningkatan aktivitas spesifik AChE dan kadar GFAP merupakan mekanisme adaptasi otak untuk mencegah terjadinya kerusakan karena hipoksia.

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Chronic systemic hypoxia induced hypoxia in the brain region thus brain cells produce energy by anaerobic metabolism. Anaerobic metabolism cause depletion in ATP synthesis. ATP depletion stimulates alterations on calcium ion in the sitoplasma of neuronal cells through the overstimulation of glutamate receptor. Alterations in intracellular calcium ions stimulates ACh release in neuronal cells. Hypoxia increased free radicals level in the cell, thus increased MDA as the final product of lipid peroxidation by free radicals. Due to respond the brain damage, astrocyte produces more spesific sitosceletal protein called GFAP.

The aim of the study was to analyze the effects of chronic systemic hypoxia in brain damage by measuring the MDA level in brain tissue compared to plasma, spesific activity of AChE in the brain tissue and GFAP level in the brain tissue compared to plasma. Twenty-five male Spraque Dawley rats were subjected to systemic hypoxia by placing them in the hypoxic chamber supplied 8-10% of O2 for 0, 1, 3, 5, and 7 days, respectively. Cortex and hipocampus of brain tissue and blood plasma were used as the sample. MDA levels were measured using Will?s methode. AChE spesific activity was measured using RANDOX Butyrylcholinesterase Colorimetric Methode. GFAP was analyzed using Rat GFAP ELISA kit by CUSABIO.

This study demonstrates that MDA level didn't increase during induced hypoxic systemic in the brain tissue, meanwhile there's no significance increased of MDA levels in plasma. There's significance increased of AChE spesific activity during induced hypoxic systemic in the brain tissue. This study also demonstrates significance increased in brain tissue's GFAP level but not in the plasma during induced systemic hypoxia. We conclude that there?s no oxydative damage in the brain tissue during this induced systemic hypoxia. The increased in AChE spesific activity and GFAP levels showed an adaptive mechanism to protect the brain tissue from hypoxic insult."