Rasio Penutupan Luka pada Tikus Diabetes Diinduksi Streptozotocin dengan Perlakuan Dressing Tipe Pasif dan Interaktif (Penelitian Pendahuluan)

Deparaffinization is a stage before the staining process to remove/dissolve paraffin so that the absorption of color in tissue preparations is maximized. Deparaffinization is usually carried out using xylol and toluol. Xylol has toxic effects including acute neurotoxicity, heart and kidney damage, hepatotoxicity, fatal blood dyscrasias, skin erythema, dry skin, peeling skin, and also has a carcinogenic effect. The toxicity effect of olive oil is lower than that of xylol. Oils that have non-polar properties can remove the remaining paraffin contained in the tissue. The purpose of this study was to determine the microscopic appearance of the kidney tissue preparations of mice deparaffinized with olive oil on hematoxylin eosin (HE) staining. The type of research used is experimental research which is analyzed with a descriptive approach. The results of the assessment of preparations deparaffinized with xylol in 80 visual fields obtained 100% good preparations and preparations deparaffinized with olive oil in 80 visual fields obtained 0% poor preparations, 11.3% poor preparations, and 88.7% good preparation. So it can be said that better results are found in the microscopic picture of the kidney preparations of mice (Mus musculus) deparaffinized with xylol.

Isoliquiritigenin Alleviates Semen Strychni-Induced Neurotoxicity by Restoring the Metabolic Pathway of Neurotransmitters in Rats

Acute neurotoxicity of Semen Strychni can result in sudden death in epilepsy. The detoxification method and mechanism of Semen Strychni acute poisoning have not been clarified. This experiment focused on the mechanism of Semen Strychni neurotoxicity and the alleviation effects of isoliquiritigenin. The rats were intraperitoneally injected with Semen Strychni extract (125 mg/kg), followed by oral administration of isoliquiritigenin (50 mg/kg) for 7 days. FJ-B staining was used to evaluate the degree of injury on hippocampus neurons. The concentration of monoamines, amino acids, and choline neurotransmitters, the Dopamine (DA) and 5-hydroxytryptamine (5-HT) metabolic pathway in the hippocampus, cerebellum, striatum, prefrontal cortex, hypothalamus, serum, and plasma were detected by LC-MS/MS. The expression of neurotransmitter metabolic enzymes [catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO)] and neurotransmitter receptors [glutamate N-methyl-D-aspartic acid receptors (NMDARs) and gamma-aminobutyric acid type A receptor (GABRs)] were, respectively determined using ELISA and qRT-PCR. The results indicated that Semen Strychni induced neuronal degeneration in the hippocampal CA1 region. Meanwhile, Semen Strychni inhibited the mRNA expression of NMDAR1, NMDAR2A, NMDAR2B, GABRa1, GABRb2 and reduced the level of MAO, which disrupted the DA and 5-HT metabolic pathway. However, isoliquiritigenin reversed these effects. In summary, isoliquiritigenin showed alleviation effects on Semen Strychni-induced neurotoxicity, which could be attributed to restoring neurotransmitters metabolic pathway, most likely through the activation of NMDA receptors.

Microscopic Description of Mus Musculus Kidney Preparation Deparafinized with Olive Oil in Eosin (HE) Hematoxylin (HE) Staining

Deparaffinization is a stage before the staining process to remove/dissolve paraffin so that the absorption of color in tissue preparations is maximized. Deparaffinization is usually carried out using xylol and toluol. Xylol has toxic effects including acute neurotoxicity, heart and kidney damage, hepatotoxicity, fatal blood dyscrasias, skin erythema, dry skin, peeling skin, and also has a carcinogenic effect. The toxicity effect of olive oil is lower than that of xylol. Oils that have non-polar properties can remove the remaining paraffin contained in the tissue. The purpose of this study was to determine the microscopic appearance of the kidney tissue preparations of mice deparaffinized with olive oil on hematoxylin eosin (HE) staining. The type of research used is experimental research which is analyzed with a descriptive approach. The results of the assessment of preparations deparaffinized with xylol in 80 visual fields obtained 100% good preparations and preparations deparaffinized with olive oil in 80 visual fields obtained 0% poor preparations, 11.3% poor preparations, and 88.7% good preparation. So it can be said that better results are found in the microscopic picture of the kidney preparations of mice (Mus musculus) deparaffinized with xylol.

Acute neurotoxicity of acetaminophen in chicks

Acetaminophen is a non-steroidal drug used as an anti-inflammatory, analgesic and antipyretic in humans and animals. In chicks, neurotoxicity associated with acetaminophen has not been fully elucidated. The aim of this study was to identify the neurobehavioral, biochemical and histopathological effects of acetaminophen in 7 day-old broiler chicks. The acute LD50 of acetaminophen was estimated by the up- and- down method, and then the influence of acetaminophen on the open field activity and tonic immobility test was recorded. The behavioral signs and toxicity scores were recorded. The liver enzymes, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were estimated. Histopathology of the brain and liver were performed. The acetaminophen LD50 value in chicks was 1077 mg/kg, intramuscularly. Acetaminophen reduced the general locomotive activity of the chicks, measured in the open- field arena, as a result of a significant rise in latency in moving from the central square, and a reduction in the numbers of lines crossed as well as reduction in the vocalization score compared to the control. Intramuscular injections of acetaminophen at doses of 500 and 1000 mg/kg induced signs of toxicosis, such as head dropping, closed eyelids, immobility, loss of vocalization, and recumbency, followed by death. Histopathological examination of the brain showed the presence of congestion of blood vessels, vasogenic edema and necrosis of Purkinje cells. Degenerative changes and liver enzyme function showed liver dysfunction. Our results show behavioral, biochemical and histopathological data demonstrating that acetaminophen at high doses produced acute neurotoxicity in chicks.

Effect of Methyl Ethyl Ketone (MEK) Organic Solvent Exposure on Incidence of Neurotoxicity in Shoe Manufacturing Workers

Background: Shoe manufacturing factory workers in developing countries are daily exposed to complex mixtures of organic solvents. Chemical exposure occurs through inhalation / respiration and skin which can affect many physiological systems. The main chemical exposure to organic solvents in shoe manufacturing comes from the process of gluing and cleaning process by using organic solvents on footwear in the assembling section. Methyl ethyl ketone is one type of organic solvent which, when entering into the body through inhalation routes can cause irritation of the nose, throat, lungs and chest becomes congested. Acute neurotoxicity is a collection of symptoms in the central nervous system (central nervous system depression, psychomotor disorders, narcosis, drowsiness, headache, dizziness, dyspepsia, and nausea). Method: The research design was a prospective cohort research consisting of 45 people for each high MEK exposed group and low exposed to MEK. Data collection was done by interview, physical examination, MEK level measurement of pre-shift urine and end-shift work, and filling out questionnaires Form Acute symptoms rating questionnaire at the beginning of work shift (07.00), 2 hours after work (09.00), break (12.00), 2 hours after break (15.00), and end of work shift (16.00). Result: The incidence of acute neurotoxicity symptoms in the MEK-high exposed group based on the Acute Symptoms questionnaire was 51.1%. Age factor with symptoms of acute neurotoxicity in workers at PT. X with p value = 0.432, gender factor with p value = 0.162, education factor with p value = 0.897, nutritional status factor with p value = 0.865, alcohol habit factor with p value = 0.181, coffee drinking habit factor with p value = 0.265, and smoking habit factor with p value = 0.968, work duration factor with symptoms of acute neurotoxicity at worker in PT. X with p value = 0.533, and the use factor of personal protective equipment (PPE) with p value = 0.470. In this research, symptoms of acute neurotoxicity were dominant are fatigue (80%), headache (77.8%), nausea (71.1%), dizziness (66.7%), and feeling of intoxication (53.3%). Conclusion: There are no subject and occupational factors that have a significant effect to the symptoms of acute neurotoxicity. Conducting isolation of other work areas for workers exposed to chemicals that because of high potential to harm other workers in the vicinity. Reassessing the hazard risk of using MEK substitutes with other chemicals that are of lower risk or replace with water-based solvents. Provide PPE eligible to all workers exposed to chemicals and workers around them. A PPE fit test is used for workers to feel comfortable while wearing it, giving strict sanctions to workers who do not consistently use personal protective equipment.

A Comparison of the Neuroprotective and Reactivating Efficacy of a Novel Bispyridinium Oxime K870 with Commonly Used Pralidoxime and the Oxime HI-6 in Tabun-Poisoned Rats

Aim: The comparison of neuroprotective and central reactivating effects of the oxime K870 in combination with atropine with the efficacy of standard antidotal treatment in tabun-poisoned rats. Methods: The neuroprotective effects of antidotal treatment were determined in rats poisoned with tabun at a sublethal dose using a functional observational battery 2 h and 24 h after tabun administration, the tabun-induced brain damage was investigated by the histopathological evaluation and central reactivating effects of oximes was evaluated by the determination of acetylcholinesterase activity in the brain using a standard spectrophotometric method. Results: The central reactivating efficacy of a newly developed oxime K870 roughly corresponds to the central reactivating efficacy of pralidoxime while the ability of the oxime HI-6 to reactivate tabun-inhibited acetylcholinesterase in the brain was negligible. The ability of the oxime K870 to decrease tabun-induced acute neurotoxicity was slightly higher than that of pralidoxime and similar to the oxime HI-6. These results roughly correspond to the histopathological evaluation of tabun-induced brain damage. Conclusion: The newly synthesized oxime K870 is not a suitable replacement for commonly used oximes in the antidotal treatment of acute tabun poisonings because its neuroprotective efficacy is only slightly higher or similar compared to studied currently used oximes.