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All Journal Kertha Negara : Journal Ilmu Hukum Folia Medica Indonesiana Jurnal NERS Jurnal Farmasi Klinik Indonesia Journal Of Vocational Health Studies Qanun Medika - Medical Journal Faculty of Medicine Muhammadiyah Surabaya Jurnal Ilmu Kefarmasian Indonesia Majalah Patologi Indonesia Darmabakti Cendekia: Journal of Community Service and Engagements Majalah Biomorfologi (Biomorphology Journal) Jurnal Psikiatri Surabaya (Surabaya Psychiatry Journal) Jurnal Syntax Transformation Indian Journal of Forensic Medicine & Toxicology Jurnal Kesehatan Tambusai Pharmaceutical Sciences and Research (PSR) Jurnal Pengabdian Masyarakat Bhinneka Sewagati Jurnal Pengabdian Masyarakat Bangsa Journal of Clinical Microbiology and Infectious Diseases

Imam Susilo

Departemen Patologi Anatomi, Fakultas Kedokteran Universitas Airlangga RSUD Dr. Soetomo, Jl. Mayjen. Prof. Dr. Moestopo No. 47 Surabaya, Indonesia

Author-ID : 396487

Agriculture, Biological Sciences & Forestry Arts Humanities Biochemistry, Genetics & Molecular Biology Civil Engineering, Building, Construction & Architecture Computer Science & IT Dentistry Economics, Econometrics & Finance Education Energy Engineering Environmental Science Health Professions Immunology & microbiology Industrial & Manufacturing Engineering Languange, Linguistic, Communication & Media Law, Crime, Criminology & Criminal Justice Mathematics Medicine & Pharmacology Neuroscience Nursing Physics Public Health Social Sciences Other

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Expressions of β-Tryptase and Chymase in Lung Mast Cells due to Anaphylactic Shock through Histopathological Appearance at Different Post-Mortem Intervals Biqisthi Ari Putra; Imam Susilo; Ahmad Yudianto
Folia Medica Indonesiana Vol. 59 No. 1 (2023): March
Publisher : Universitas Airlangga

Highlights: The post-mortem interval is related to tryptase and chymase expressions in anaphylactic shock incidence Forensic experts can utilize tryptase and chymase as markers of anaphylactic (non-anaphylactoid) shock that occurs in the lungs. Abstract: Anaphylactic shock is a hypersensitivity response, a commonly type I hypersensitivity involving immunoglobulin E (IgE). It is caused by an antigen-antibody reaction that occurs immediately after a sensitive antigen enters the circulation. Anaphylactic shock is a clinical manifestation of anaphylaxis that is distributive shock, characterized by hypotension due to sudden blood vessel vasodilation and accompanied by a collapse in blood circulation that can result in death. β-tryptase and mast cell chymase expressions in the lungs of histopathological specimens that had experienced anaphylactic shock were examined at different post-mortem intervals in this study. A completely randomized design (CRD) method was employed by collecting lung samples every three hours within 24 hours of death, and then preparing histopathological and immunohistochemical preparations. The mast cell tryptase and chymase expressions were counted and summed up in each field of view, and the average was calculated to represent each field of view. The univariate analysis yielded p-values of 0.008 at the 15-hour post-mortem interval, and 0.002 at the 12-hour post-mortem interval. It was concluded that tryptase and chymase can be utilized as markers of anaphylactic (non-anaphylactoid) shock in the lungs.

NEUROGENIC MODULATION BY NEUROKININ-1 RECEPTOR ANTAGONIST, CP-96,345 TO INHIBIT RHEUMATOID ARTHRITIS DEVELOPMENT IN ADJUVANT INDUCED ARTHRITIS RAT MODEL Wirasasmita, Yuyun; Rahmadi, Mahardian; Susilo, Imam; Khotib, Junaidi
Folia Medica Indonesiana Vol. 52 No. 2 (2016): APRIL - JUNE 2016
Publisher : Universitas Airlangga

Rheumatoid arthritis (RA) is a chronic form of persistent inflammation. Meanwhile, Substance P is the most associated neuropeptide in neurogenic inflammation and hyperalgesia commonly found in chronic pain. Substance P act by binding to neurokinin-1 receptor. The present study was conducted to evaluate the effect of neurokinin-1 receptor antagonist (CP-96,345) on Adjuvant Induced Arthritis rat model, induced by Complete Freund's Adjuvant (CFA). The objective is to attenuate neurogenic inflammation which in turn will increase the latency time of hyperalgesia response, decreases neurokinin-1 receptor expression, and inhibits the development of RA in AIA rat model. Rats were intra-articularly injected with CFA 1 hour after the administration of CP-96,345 either by 0.63 µg/gr; 1.25 µg/gr; or 2.5 µg/gr also intra-articularly. Caliper measurements and hot-plate test were performed on day 0, 3, 5, 7, 9, 11, and day 13. Expression of neurokinin-1 receptor in joint tissue were evaluated by immunohistochemistry, and RA progress in joint tissue were observed hystopathologically. CP-96,345 at 2.5 µg/gr significantly increases the latency of hyperalgesia response time on CFA induced rats (p=0.044) and decreased the neurokinin-1 receptor expression in joint tissue (p=0.029) compared to CFA induced rats. There was no significant difference for caliper measurements and RA progress between CFA incduced rats and treated group. Conclusively, CP-96,345 increases the latency of hyperalgesia response time and decreases the NK-1 receptor expression in rat joint but could not inhibit RA progression.

THE POTENCY OF ALPHA LIPOIC ACID AS ANTI INFLAMMATORY ON THE COMPLETE FREUND'S ADJUVANT-INDUCED RHEUMATOID ARTHRITIS IN RAT MODEL Megawati, Selvi; Rahmadi, Mahardian; Susilo, Imam; Khotib, Junaidi
Folia Medica Indonesiana Vol. 52 No. 2 (2016): APRIL - JUNE 2016
Publisher : Universitas Airlangga

Rheumatoid arthritis (RA) is an autoimmune diseases which is characterized by chronic inflammation of the synovial tissue in joints. This research was designed to investigate the effect of alpha lipoic acid as antioxidant on rats with complete freund's adjuvant (CFA)-induced RA by intra articular injection of complete freund's adjuvant (CFA). ALA was administered orally once a day for 7 days at 30, 60 and 120 mg doses a week after CFA injection. The severity of arthritis was evaluated by joint diameter and latency time on thermal stimulation. Joint diameter and latency time on thermal stimulation will measured on day 0, 3, 5, 7, 10, 12 and 14. Measurement of malondialdehyde (MDA) level in plasma was performed using thiobarbituric acid (TBA) method to assess lipid peroxidation. Histology of joint was examined by microscope following hematoxylin-eosin staining. The result showed that treatment with ALA at 30 mg and 60 mg significantly decreased the joint diameter compared to CFA group (p=0.003; p=0.001 respectively) and rat's latency time on thermal stimulation was also significantly increased compared to CFA group (p=0.015; p=0.026 respectively). Measurement of MDA in CFA group and ALA group had no significant difference. Histological staining indicated that the recovery of the synovial membranes of joint in ALA group had no effect. Results indicated that ALA has the effect to suppress the development of inflammation in RA but not through oxidative stress pathway.

THE MECHANISM OF ALPHA LIPOIC ACID ON REDUCING THE MDA LEVEL AND MCP-1 EXPRESSION IN ENDOTHELIAL DYSFUNCTION OF HYPERCHOLESTEROLEMIA RAT (Rattus norvegicus) MODEL Sari, Dewi Perwito; Susilo, Imam; Khotib, Junaidi
Folia Medica Indonesiana Vol. 52 No. 3 (2016): JULY - SEPTEMBER 2016
Publisher : Universitas Airlangga

Endothelial dysfunction is an initial condition of atherosclerosis and other vascular diseases where one of the risk factors is hypercholesterolemia. Blood cholesterol levels is associated with an increase in the production of reactive oxygen species (ROS). The increasing of ROS production can cause increased oxidative stress which in turn resulting in endothelial dysfunction. Alpha lipoic acid (ALA) is one of the antioxidant compound that has been developed and studied. In this study we found that the use of ALA in Rattus norvegicus rats signifficantly lower the total cholesterol levels at dose 60 mg/kgBW (p=0.020). ALA also inhibit the expression of Monocyte Chemoattractant Protein-1 (MCP-1) at dose 60 mg/kgBW (p=0.044) and reduces the formation of Malondialdehyde (MDA) at dose 120 mg/kgBW (p=0.009), which is the initial stage of the atherogenic development and prognosis of events, thus, ALA can reduce the risk of further damage to the endothelium.

Co-Authors . Heriyawati Abdurahman Abdurrahman Abdurrahman Abdurrahman Adhi Dharma Wibawa, Adhi Dharma Ahmad Yudianto Alphania Rahniayu Anny Setijo Rahaju, Anny Setijo Ardiansyah Ariani, Grace Aziz, Nahdah Aulia Bambang Purwanto Betty Agustina Tambunan Biqisthi Ari Putra Christrijogo Soemartono Waloejo Deshinta Fitrianti Syahida Dwinka Syafira Eljatin DYAH FAUZIAH, DYAH Eko Budi Koendhori, Eko Budi Fadli, Sonny Fajrin, Fifteen A. Ferdinant Martinus Djawa Fifteen A. Fajrin Fifteen Aprila Fajrin Fitriani, Fatimah Nur Fransiska Maria Christianty Furaidah, Erna Gondo Mastutik Hanum, Safa Salsabila Hartawan, M. Wildan Nabalah Haykal, Muhammad Nazhif Hedianto, Tri Hendrarto, Bagus Adjie Dwi Heriyawati, Heriyawati Hidayah, Rizka Nurul I Ketut Suardita Ilmiah, Khafidhotul Indriani, Ratri Dwi Indriastuti, Endah Junaidi Khotib Karimah, Azimatul Karimah, Rumman Khaerana, A. Insyirah KUSUMASTUTI, ETTY HARY Mahardian Rahmadi ManikRetno Wahyunitisari Megawati, Selvi Muhammad Al-Farouq Yufiro Akbar Nahdah Aulia Aziz Nila Kurniasari Nina Mardiana Njoto, Edwin Nugroho Pamungkas, Yuri Parlindungan, Putra Gelar Prananda S. Airlangga Putra, Bilqisthi Ari Putra, Gumilar Fardhani Ami Putri Alief Siswanto Putri, Atina Irani Wira Putri, Naomi Lesmana Qonitatillah, Ana Rahmanto, Ilham Raihan Akbar Muhammad Rangkuti, Rahmah Yasinta Rejeki, Purwo Sri Ridhoi, Ahmad Ridholia, Ridholia S.Pd. M Kes I Ketut Sudiana . Safitri, Cahyani Tiara Sakina Sakina Sakina, Sakina Sandi Ardiya Rasitullah Sari, Aditya Sita Sari, Dewi Perwito Semedi, Bambang Pujo Setya Wijoyo, Dhia Lintang Sjahjenny Mustokoweni, Sjahjenny Suharjono, Suharjono, Suharjono Sundari Indah Wiyasihati Syulthoni, Zain Budi Targanski, Constantia Lidwina Utariani, Arie Wahyunitisari, Manik Retno Wardhani, Puspa Willy Sandhika Wirasasmita, Yuyun Wiratama, Priangga Adi Zavita Anwar

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