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All Journal Indonesian Journal Health Science and Medicine
Sadiq, Dina H.
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Health Professions Medicine & Pharmacology Public Health Veterinary

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Why Cancer Cells Crave Sugar: A Review: Mengapa Sel Kanker Sangat Membutuhkan Gula: Sebuah Ulasan Sadiq, Dina H.
Indonesian Journal on Health Science and Medicine Vol. 2 No. 1 (2025): July
Publisher : Universitas Muhammadiyah Sidoarjo

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21070/ijhsm.v2i1.139

Abstract

In addition to causing weight gain, eating too much sugar raises the risk of obesity and diabetes, both of which raise the chance of cancer. It turns out that while eating sugar does not always cause cancer, it can cause the disease because of the way it affects your waist. Sugar is necessary for cancer cells to survive, not to proliferate and divide. Although this sugar is absorbed by all bodily tissues, it is more readily absorbed by tissues with higher energy requirements, such as cancer cells. Because of this, some people have concluded that sugar accelerates the growth of cancer cells. "I'd be shocked if cutting back on sugar didn't help lower the risk of cancer," she says. "High-fructose corn syrup, which is found in soft drinks, sweetened teas, sports drinks, and processed meals, as well as in candy, cookies, ice cream, and sweetened breakfast cereal, should be avoided. Highlights: Excess sugar raises obesity and diabetes risk, increasing cancer risk. Cancer cells absorb more sugar due to higher energy needs. Avoid high-fructose corn syrup in processed and sugary foods. Keywords: cancer, cells, crave, sugar
Evaluation of Cortisol and Heat Shock Proteins in Rabbits Under Cadmium-Induced Stress and Chelation Therapy: Evaluasi Kortisol dan Protein Kejut Panas pada Kelinci yang Mengalami Stres yang Diinduksi Kadmium dan Terapi Khelasi Sadiq, Dina H.; Hussein, Diyar Mohammad
Indonesian Journal on Health Science and Medicine Vol. 2 No. 1 (2025): July
Publisher : Universitas Muhammadiyah Sidoarjo

Show Abstract | Download Original | Original Source | Check in Google Scholar

Abstract

Background: Cadmium (Cd) exposure poses a significant environmental and occupational health concern, as it induces oxidative stress and disrupts cellular homeostasis. This study investigated the cadmium-induced stress response by examining its effects on cortisol and heat shock protein expression in rabbits, as well as the potential use of chelation therapy. Methods: Thirty-six New Zealand White rabbits were randomly divided into four groups (n=9) - control, cadmium exposure group (5 mg/kg CdCl₂ for 28 days), chelation therapy group (cadmium exposure and DMSA treatment at 50 mg/kg for 14 days), and DMSA group only. Serum cortisol levels were measured using an enzyme-linked immunosorbent assay (ELISA) method. The expression levels of heat shock protein 70 (HSP70) and HSP90 were evaluated using Western blot on liver and kidney tissue. Results: Cadmium exposure increased serum cortisol (48.3 ± 6.2 ng/mL vs. 22.1 ± 3.4 ng/mL in controls, p<0.001). Cadmium exposure also increased HSP70 and HSP90 in liver (3-fold and 2.8-fold, respectively) and kidney (2.9-fold and 2.5-fold, respectively) tissues. Furthermore, chelation therapy with DMSA reduced serum cortisol to 31.7 ± 4.8 ng/mL (p < 0.01) and somewhat reversed heat shock protein levels. Conclusion: Cadmium exposure is a significant source of physiological stress in rabbits, as evidenced by increased serum cortisol levels and post-exposure expression of heat shock protein (HSP). DMSA chelation therapy has therapeutic effects for reducing cadmium-induced stress response, and shows potential value as a treatment plan for cadmium poisoning patients.Highlight : Cadmium exposure significantly elevates cortisol and heat shock proteins, indicating systemic and cellular stress in rabbits. DMSA chelation therapy partially reduces these stress markers, showing potential as a treatment for cadmium poisoning. The correlation between cortisol and HSP expression suggests integrated biomarkers can assess cadmium-induced stress effectively. Keywords : Cadmium Toxicity, Cortisol, Heat Shock Proteins, Chelation Therapy, DMSA
Mice's Liver, Kidney, and Suprarenal Gland Histogenesis Mus Musculus Sadiq, Dina H.
Indonesian Journal on Health Science and Medicine Vol. 1 No. 2 (2024): October
Publisher : Universitas Muhammadiyah Sidoarjo

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21070/ijhsm.v2i2.286

Abstract

This work used histological and histochemical methods to look at how the mice's liver, kidney, and suprarenal glands develop after birth. Therefore, using mice in scientific research is permissible. The experiment used thirty-two samples of the liver, kidney, and suprarenal gland of mice, eight at each age (one day, seven days, fourteen days, and twenty-one days). A thin capsule encased the liver on the first day of life; a thicker capsule encased it after 14 to 21 days. Hepatocytes made up the parenchyma, and a central vein encircled them. The parenchyma was further split by the sinusoids, and Next to the endothelial cells that encircled the hepatic sinusoids were protruding Kupffer cells. The liver measurements change with aging. Cortical, midcortical, and juxtamedullary renal corpuscles are distinguished by their increasing diameter with age. Distal convoluted tubules are shorter than the longest convoluted tubules, which are the proximal ones. Furthermore, Henle loops were short at one-day and adult ages but long at other ages. Highlights: Postnatal development of liver, kidney, and adrenal glands showed significant age-dependent structural changes in mice. Renal corpuscles increased in diameter with age, while Henle loops were short at 1 day and adulthood but elongated at intermediate stages. Histochemical analysis revealed well-developed basement membranes and tubular structures, indicating progressive organ maturation.
Co-Authors Hussein, Diyar Mohammad