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The Journal of Society Medicine (JSOCMED)
Published by PT. CoinReads Media Prima
ISSN : -     EISSN : 29645565     DOI : https://doi.org/10.47353/jsocmed.v2i1
Core Subject : Health, Science,
Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience
The Journal of Society Medicine (JSOCMED) | ISSN (e): 2964-5565 is a leading voice in the Indonesia and internationally for medicine and healthcare. Published continuously, JSOCMED features scholarly comment and clinical research. JSOCMED is editorially independent from and its The Editor-in-Chief (EIC) is Prof. dr. Aznan Lelo, PhD, SpFK. JSOCMED offers many attractive features for authors, including free online access to all research articles, online publication ahead of print, and online responses to articles published as Quick Comments. In addition, as befitting a publication of the Journal of Society Medicine, JSOCMED implements best practice in scientific publishing with an open peer review process, declarations of competing interests and funding, full requirements for patient consent and ethical review, and statements of guarantorship, contributorship, and provenance.
Arjuna Subject : Kedokteran - Kedokteran (Lain-Lain)
Articles 5 Documents
 1 
Search results for , issue "Vol. 2 No. 2 (2023): February" : 5 Documents clear
Weaning Difficulty in Patient with End Stage Renal Disease Acute with Respiratory Failure due to Pulmonary Edema and Pneumonia Bangun, Primta; Suwarman, Suwarman
Journal of Society Medicine Vol. 2 No. 2 (2023): February
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (365.731 KB) | DOI: 10.47353/jsocmed.v2i2.29

Abstract

Introduction: End Stage Renal Disease (ESRD) 5D patient have potential to respiratory failure due to excess fluid, thus increasing the incidence of repeated hospital admissions. Deaths were reported in about 15%– 30% cases, where 50%–60% of patients needed respiratory support with mechanical ventilation. About 30%– 40% of patients had complications in the weaning process from mechanical ventilation. Prolonged mechanical ventilation increased mortality and morbidity, the length of stay periods and costs. Case Report: This case report will discuss the difficult weaning from mechanical ventilation in patients with ESRD 5D who have respiratory failure due to edema pulmonary and pneumonia who were hospitalized at the Intensive Care Unit (ICU) of Hasan Sadikin Hospital - Bandung for 20 days Conclusion: Weaning difficulty due to accumulation positive fluid balance during hospitalization lead to longer use of mechanical ventilation and pulmonary infection get heavier. A positive cumulative fluid balance could be one factor of weaning difficulty
Prolotherapy in Chronic Coccydynia Edlin; Sinaga, Mual Kristian
Journal of Society Medicine Vol. 2 No. 2 (2023): February
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v2i2.61

Abstract

Introduction: Coccydynia, or coccygodynia, is pain in the tailbone or coccyx area. Despite identifying chronic coccyx pain happened hundreds of years ago, its treatment can be difficult and sometimes controversial due to the multifactorial nature of coccyx pain. Many physiological and psychological factors contribute to its etiology. Most cases of coccydynia resolve within weeks to months with or without conservative treatment, but for some patients, the pain could be chronic and bothersome. Cases: This report describes a patient who experienced a traumatic fall from a height, causing chronic coccyx pain. Coccyx pain is local and does not radiate, usually gets worse when changing from sitting to standing or vice versa. This makes it difficult for patients to carry out their usual activities. After taking pain medications regularly for years, the pain does not improve. Conclusion: Prolotherapy is an injection therapy for chronic musculoskeletal injuries, including coccydynia. Injection prolotherapy aims to tighten and strengthen weak or lax tendons, ligaments, or joint capsules through the multiplication and activation of fibroblasts. The main principle is the injection of small amounts of irritant solution into the painful ligament and tendon insertions as well as in the adjacent joint space over several treatment sessions. This technique has been shown to reduce patient pain by approximately 50% of initial pain after the first session of prolotherapy. It is hoped that the repetition of this session will further reduce and even eliminate the chronic pain that the patient has been suffering.
Role of Glucagon in The Metabolic Response: Review Tona, Azwar Iwan; Syukri, Maimun
Journal of Society Medicine Vol. 2 No. 2 (2023): February
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.47353/jsocmed.v2i2.62

Abstract

Historically, glucagon is the counter-regulatory hormone of insulin. Glucagon secretion is induced by fasting conditions or hypoglycaemia to increase glucose levels. Glucagon is the dominant product of alpha cells in the islet and was first identified in 1923 during an attempt to purify insulin, where it was identified as a contaminant hyperglycaemia factor. Further research determined that the hyperglycaemic action of glucagon is mediated by increased hepatic glycogenolysis and gluconeogenesis to increase endogenous glucose production. Insulin and glucagon as opposing hormones work together for glycaemic control. Diabetic hyperglycaemia is caused by increased impaired insulin action and inappropriately elevated glucagon levels. This review summarizes an important function of glucagon is its role as a regulator of glucose homeostasis. Increased plasma glucagon levels lead to increased hepatic glucose production. The balance between insulin and glucagon is responsible for maintaining euglycaemia conditions. In conditions of hypoglycaemia, increased glucagon secretion leads to increased hepatic glucose production through a number of cellular mechanisms including suppression of glycogenesis and glycolysis and stimulation of glycogenolysis and gluconeogenesis
What is the function of Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 in pain processes? Hamdi, Tasrif
Journal of Society Medicine Vol. 2 No. 2 (2023): February
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v2i2.63

Abstract

At the cellular level, the pathophysiology of neuropathic pain can be divided into two parts. The first is the early phase (several days) and the second is the late phase (ranging from weeks to months and years). Cancer cell growth in the periphery will cause nerve damage in the periphery and prolonged pain will cause changes in nerve transmission processes in the periphery and centre. This underlies the occurrence of peripheral neuropathic pain. Damage to peripheral nerve tissue will trigger peripheral sensitisation and then central sensitisation. After peripheral nerve cell damage (including axon damage), schwan cells will release MMP-9, initiating macrophage cell infiltration. Then there will be degradation of myelin basic protein. The presence of damaged axons will cause an increase in the number of sodium channels and hyperexcitability of ectopic signals from afferent nerve fibres. The result is a continuous action potential that eventually contributes to central sensitisation characterised by hyperalgesia and allodynia. This review summarizes that neuropathic pain occurs through hyperexcitability (hypersensitisation) of nerve cells is IL-1β, MMP-9 in the early phase, MMP-2 in the late phase and finally microglia and astrocyte cells.
Diagnosis of Tuberculosis infection in HIV: A Review Wahyudi, Hendra
Journal of Society Medicine Vol. 2 No. 2 (2023): February
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v2i2.64

Abstract

The high prevalence and increasing incidence of HIV has adversely affected the control of several endemic diseases, including tuberculosis (TB). In HIV there is a progressive decrease in CD4 T cells which is associated with progressive damage to immunity, in the form of a severe decrease in digestive tract lymphoid cells, erythrocyte apoptosis, increased permeability of the digestive tract and finally massive CD4 T cell destruction. HIV will attempt to enter target cells (dendrite cells, macrophage cells), which are cells capable of expressing CD4 T cell receptors and express chemokine coreceptors (CCR5 or CXCR4) on the surface of CD4 T cells. HIV utilises CXCR4 to destroy CD4 T cells at acute onset, resulting in a decrease in CD4 T cell numbers. The condition of decreased CD4 T cell count in HIV will also be aggravated by the presence of TB co-infection. CD4 T cells contribute to controlling Mycobacterium tuberculosis. The adaptation of Mycobacterium tuberculosis in HIV patients can also weaken the cytokine immunity of interfor-γ, interleukin-10 patients in HIV infection. HIV-1 induces a decrease in CD4+ levels and the development of active tuberculosis. This review summarizes that Mycobacterium tuberculosis has an important component, Lipoarabinomannan (LAM), which has a broad ability to inhibit the influence of immunoregulators, thereby suppressing the proliferation of T lymphocytes, inhibiting macrophage activation and neutralising the influence of free radicals. Decreased immune status and nutritional status due to Mycobacterium tuberculosis can accelerate the course of HIV infection towards AIDS.

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