Acute Disease ; Adult ; Brain Diseases ; chemically induced ; Carbon Disulfide ; poisoning ; Humans ; Male ; Occupational Diseases ; chemically induced

Adult ; Brain Diseases ; chemically induced ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Male ; Middle Aged ; Occupational Diseases ; chemically induced

Adolescent ; Adult ; Brain Diseases ; chemically induced ; therapy ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Male

Toxic leucoencephalopathy (TLE) is a rare neurological complication of heroin abuse. 'Chasing the dragon' is an inhalational mode of heroin abuse that originated in Southeast Asia. Intriguingly, no cases of TLE have been reported from this region, although the inhalational mode of heroin abuse is common. We herein report the case of a middle-aged man with a history of polysubstance abuse who presented with progressive neurological symptoms and progressed to an uncommunicative state. While the initial impression was that of iatrogenic parkinsonism, diffuse leucoencephalopathy with sparing of the cerebellum was noted on magnetic resonance imaging. In view of his history of inhalational heroin abuse close to the onset of the neurological symptoms, a diagnosis of TLE was made. No clinical improvement was noted with administration of a dopaminergic agent. This is the first known case of delayed TLE following heroin inhalation from Southeast Asia with the unusual feature of cerebellar sparing.
Administration, Inhalation ; Brain ; pathology ; Disease Progression ; Heroin ; administration & dosage ; Heroin Dependence ; complications ; Humans ; Leukoencephalopathies ; chemically induced ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; Singapore

OBJECTIVETo develop the organophosphate-induced delayed neuropathy (OPIDN) hen model with 2,4,6-trimethylbenzoyl phenylphosphonate (TOCP), and observe the change of pathology and investigate the alterations of microtubulin associated protein 2 (MAP2).

METHODS48 adult hens were randomly divided into four groups, including three experimental groups and control group (n = 12 each group). The hens in three experimental groups were treated with TOCP by gavage at single dosages of 250, 500 and 750 mg/kg respectively while the control hens received an equivalent volume of corn oil by gavage. All hens were sacrificed after 21 days of treatment. Half hens in each group were dissected for HE examination and myelin straining of brain, spinal cord and sciatic nerve while brains of another half hens were dissected for the determination of MAP2 by western blotting.

RESULTSThe delayed neurotoxicity symptoms of hens both in 500 and 750 mg/kg groups were consistently observed. The pathological changes of brain, spinal cord and sciatic nerve in 500 and 750 mg/kg groups showed nerve cells difference necrosis, increased cytoplasm basophilia, microglia proliferation, mono-nuclear and lymphocyte infiltration, myelin sheath extensive up to part of them disaggregation deletion. Compared with the control group, at 500 and 750 mg/kg respectively the increase of MAP2 was 25% and 23% (P < 0.01 and P < 0.05).

CONCLUSIONSThe histopathologic changes of OPIDN caused by TOCP have dose-response relationship. The changes of MAP2 in nervous system may contribute to the occurrence and development of TOCP induced delayed neurotoxicity.

Animals ; Brain ; metabolism ; pathology ; Chickens ; Female ; Microtubule-Associated Proteins ; metabolism ; Nervous System Diseases ; chemically induced ; metabolism ; pathology ; Organophosphates ; toxicity

Appropriate selection and measurement of lead biomarkers of exposure are critically important for health care management purposes, public health decision making, and primary prevention synthesis. Lead is one of the neurotoxicants that seems to be involved in the etiology of psychologies. Biomarkers are generally classified into three groups: biomarkers of exposure, effect, and susceptibility.The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer's disease, Parkinsons disease, and schizophrenia. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children and adults.
Alzheimer Disease ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Animals ; Behavior ; drug effects ; Biomarkers ; metabolism ; Brain ; metabolism ; pathology ; physiopathology ; Brain Diseases ; chemically induced ; pathology ; physiopathology ; Environmental Exposure ; adverse effects ; Humans ; Lead ; pharmacokinetics ; toxicity ; Lead Poisoning ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Neurotoxicity Syndromes ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Parkinson Disease, Secondary ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Schizophrenia ; chemically induced ; metabolism ; pathology ; physiopathology

Gefitinib is regarded as a relatively safe agent for the treatment of an advanced non-small cell lung cancer (NSCLC). Pulmonary toxicity such as interstitial lung disease associated with gefitinib is uncommon with an estimated all time incidence around 1% worldwide. Moreover, a case of gefitinib associated with pulmonary cystic changes has not been reported yet. In this report we present a case of progressive multiple air cystic changes in both lungs in a patient with NSCLC and intrapulmonary metastases who underwent a gefitinib therapy.
Antineoplastic Agents/*adverse effects ; Brain Neoplasms/secondary ; Carcinoma, Non-Small-Cell Lung/*drug therapy/secondary ; Cysts/*chemically induced ; Female ; Humans ; Lung/pathology ; Lung Diseases/*chemically induced ; Lung Diseases, Interstitial ; Lung Neoplasms/*drug therapy ; Middle Aged ; Quinazolines/*adverse effects

OBJECTIVETo explore the relationship between excitatory amino acids (EAAs) and acute in toxicated encephalopathy induced by 1,2-dichloroethane (1,2-DCE).

METHODSSD rats were randomly divided into 7 groups: 1 control group, 3 exposure (5.0, 10.0, 20.0 g/m(3)) groups and 3 duration (2, 4, 6 h after 10.0 g/m(3) exposure) groups. Rats were exposed to 1,2-DCE for 12 h by continual static inhalation. Water content of cerebral cortex and medulla was measured by wet-dry method; The contents of glutamate (Glu), aspartate (Asp), glycine (Gly) and gamma-aminobutyric acid (GABA) in brain tissues were determined by high performance liquid chromatography (HPLC).

RESULTSWater content of cerebral cortex in 3 exposure groups (76.10% +/- 1.41%, 76.45% +/- 0.75%, 79.95% +/- 1.45% respectively) were higher than that of control group (74.22% +/- 1.77%, P < 0.05, P < 0.01). That of medulla was increased significantly merely at 20.0 g/m(3) (71.77% +/- 3.07%, P < 0.05). Water content of cortex in 3 duration groups (79.36% +/- 2.10%, 79.48% +/- 1.21%, 80.64% +/- 1.93% respectively) were higher than that of 10.0 g/m(3) instant exposure group (P < 0.05). The content of Asp [(4.83 +/- 0.35) micro mol/g, (7.17 +/- 0.40) micro mol/g, (10.52 +/- 0.39) micro mol/g], Glu [(23.86 +/- 0.62) micro mol/g, (31.21 +/- 2.50) micro mol/g, (28.23 +/- 1.58) micro mol/g] and Gly [(5.59 +/- 1.01) micro mol/g, (6.06 +/- 0.83) micro mol/g, (7.26 +/- 1.34) micro mol/g] in exposure groups were higher than those of corresponding control groups [(3.72 +/- 0.48) micro mol/g, (21.09 +/- 1.20) micro mol/g, (3.83 +/- 0.44) micro mol/g, P < 0.05, P < 0.01]. Compared to 10.0 g/m(3) instant group, Asp content was increased at 2, 4, 6 h (P < 0.01), Glu content at 2, 4 h (P < 0.05), and peak value of Glu appeared at 4 h [(35.40 +/- 2.40) micro mol/g] while Gly content was significantly decreased (P < 0.01). GABA did not show evident changes in both exposure or duration groups (P > 0.05).

CONCLUSIONEAAs appears to be related with the development of acute intoxicated encephalopathy induced by 1,2-DCE, and its damage to neuron might be one of the mechanisms of brain edema.

Acute Disease ; Animals ; Body Water ; metabolism ; Brain Chemistry ; drug effects ; Brain Diseases ; chemically induced ; Ethylene Dichlorides ; poisoning ; Excitatory Amino Acids ; analysis ; Female ; Male ; Rats ; Rats, Sprague-Dawley

Acute Disease ; Adult ; Aged ; Blood-Brain Barrier ; physiopathology ; Brain Diseases ; blood ; chemically induced ; Carbon Monoxide Poisoning ; complications ; Female ; Humans ; Interleukin-6 ; blood ; Male ; Middle Aged

Numerous studies have demonstrated the clinical activity of temozolomide, a second-generation alkylating agent, against malignant brain tumors, however, its activity has not been reported in an Asian population. This study analyzed the efficacy and toxicity of temozolomide in 25 adult patients with recurrent or progressive malignant gliomas after surgery and standard radiation therapy with or without chemotherapy, enrolled in our institution since July 2000. Sixteen patients had glioblastoma multiforme (GBM), six with anaplastic astrocytoma, and three with anaplastic oligodendroglioma. Of the 25 patients, 3 (12%) achieved a complete response (CR), 8 (32%) achieved a partial response (PR), 6 (24%) had stable disease (SD), and 8 (32%) had progressive disease (PD). Two patients achieved a CR, 4 patients achieved a PR, 3 patients had SD and 7 patients had PD in GBM, and 1 patient achieved a CR, 4 patients achieved a PR, 3 patients had SD, 1 patient had PD in the non-GBM patients. Median progression free survival was 8 weeks in GBM and 22 weeks in the non-GBM patients. The median overall survival of each group was 17 weeks and 28 weeks. Temozolomide demonstrated moderate activity in recurrent and progressive malignant gliomas without serious toxicity.
Vomiting/chemically induced ; Treatment Outcome ; Survival Analysis ; Neoplasm Recurrence, Local ; Nausea/chemically induced ; Middle Aged ; Male ; Magnetic Resonance Imaging ; Liver Diseases/chemically induced ; Leukopenia/chemically induced ; Humans ; Glioma/*drug therapy/radiotherapy/surgery ; Female ; Drug Administration Schedule ; Dacarbazine/administration & dosage/adverse effects/*analogs & derivatives/therapeutic use ; Combined Modality Therapy ; Brain Neoplasms/*drug therapy/radiotherapy/surgery ; Brain/drug effects/pathology ; Antineoplastic Agents, Alkylating/administration & dosage/adverse effects/therapeutic use ; Adult ; Adolescent ; Administration, Oral