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PubMed1987

Amsacrine evaluation.

Amsacrine, an antineoplastic agent currently undergoing clinical trials in the U.S., has been shown to be active against adult and pediatric leukemias, Hodgkin's disease, and non-Hodgkin's lymphomas. Amsacrine is highly bound to plasma proteins and is eliminated primarily via hepatic metabolism. Severe hepatic dysfunction will result in a decreased excretion rate of the drug. The primary side effect is a dose-related suppression of bone marrow function. Other reported toxic effects include mucositis, nausea, vomiting, cardiotoxicity, liver dysfunction, and alopecia. Despite these negative effects, amsacrine appears to have a role in the combination therapy of acute leukemias.

Adult↗

PubMed1991

Presence of adenosine deaminase on the surface of mononuclear blood cells: immunochemical localization using light and electron microscopy.

Adenosine deaminase, which is essential for lymphoid differentiation and function, has previously been considered to be a cytosolic enzyme. In this report we demonstrate that it can be found associated with the plasma membrane of lymphocytes. By means of immunological techniques using both light and electron microscopy, adenosine deaminase was localized on the external side of the plasma membrane of normal lymphocytes and monocytes. Since the enzyme expression differed depending on the type of cell examined, new hypotheses about the mechanisms involving purine metabolism in immune dysfunctions or immunodeficiency syndromes may be considered.

Adenosine Deaminase↗

PubMed2025

Gut microbiota: a hidden player in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects reproductive-aged women worldwide, causing hormonal imbalances and ovarian dysfunction. PCOS affects metabolic health and increases the risk of obesity, insulin resistance, and cardiovascular disease, in addition to infertility. This review delves deeper into the connections of gut microbiota with PCOS pathophysiology, particularly into its impact on hormone metabolism, obesity, inflammation, and insulin resistance by way of short-chain fatty acids, lipopolysaccharides, and gut-brain axis. Studies also show that changes in the metabolic processes and immune responses are seen in changes in the gut microbiota in PCOS subjects, such as changes in the Bacteroidetes and Firmicutes groups. Some bacteria, like Escherichia and Shigella, have been associated with dysbiosis in patients with PCOS, leading to systemic inflammation and changed hormone levels, which further worsen the clinical symptoms. Therapeutic interventions targeting the gut microbiota comprise probiotics, prebiotics, and fecal microbiota transplantation; these have potential to alleviate the symptoms of PCOS. Other precision microbiome-based therapies include postbiotics, and CRISPR-Cas9 genome editing, which are relatively new avenues toward precision treatment. This complex interlink of gut microbiota and PCOS pathophysiology will open the avenues for possible treatments for hormonal imbalances and metabolic problems that characterize these complex disorders. The review here focuses on the requirement of further studies to be able to elucidate the specific pathways relating gut microbiota dysregulation to PCOS and, thus, improve microbiome-based therapies for better clinical outcomes in affected individuals.

Humans↗

PubMed2003

Systemic effects and skin injury after experimental dermal exposure to monochloroacetic acid.

There have been many fatal occupational accidents of skin exposure to monochloroacetic acid (MCA). However, there have been no reports of dermatological findings and the lethal consequences have not yet been demonstrated. Therefore, harmful local and systemic effects were investigated after dermal exposure to MCA. A 0.5 mL aliquot of MCA solution (40% w/w) was applied to the abdominal skin of ten 10-week-old male SD rats under anesthesia. The exposure area (25 x 25 mm2) was 1.6% of the total surface area. The dose of MCA per area was 34.1 mg/cm2. Saline was similarly administered to 10 control rats. Histopathological findings after 10 min were observed by light microscopy. Blood samples were collected by exsanguinations from the carotid arteries after 4 h. Skin samples were collected 10 min after the initial exposure. Histological findings showed severe degeneration of collagen bundles in the epidermis and subcutaneous tissues. P(CO2), HCO(3)-, TCO2, BE and glucose levels were decreased in the MCA group. AST, m-AST, ALT, BUN, Cr, NH3, lactic acid, pyruvic acid, RBC, Hb, Hct, total protein and albumin were increased in the MCA group. The burn was determined to be a third-degree burn on the basis of the histopathological findings. The severe toxicity was probably a consequence of the rapid permeability. Biochemical parameters were a consequence of hepatocellular injuries, renal dysfunction, dysglyconeogenesis and dysfunction of ammonia metabolism. MCA reportedly enters the TCA cycle and inhibits aconitase. MCA metabolites also inhibit pyruvate carboxylase in the gluconeogenesis pathway. Therefore, the important serum biochemical abnormalities such as hypoglycemia and lactic acidosis should be monitored to find the acute systemic disorders.

Accidents, Occupational↗

PubMed2001

Phase I trial of 72-hour continuous infusion UCN-01 in patients with refractory neoplasms.

PURPOSE: To define the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of the novel protein kinase inhibitor, UCN-01 (7-hydroxystaurosporine), administered as a 72-hour continuous intravenous infusion (CIV). PATIENTS AND METHODS: Forty-seven patients with refractory neoplasms received UCN-01 during this phase I trial. Total, free plasma, and salivary concentrations were determined; the latter were used to address the influence of plasma protein binding on peripheral tissue distribution. The phosphorylation state of the protein kinase C (PKC) substrate alpha-adducin and the abrogation of DNA damage checkpoint also were assessed. RESULTS: The recommended phase II dose of UCN-01 as a 72-hour CIV is 42.5 mg/m(2)/d for 3 days. Avid plasma protein binding of UCN-01, as measured during the trial, dictated a change in dose escalation and administration schedules. Therefore, nine patients received drug on the initial 2-week schedule, and 38 received drug on the recommended 4-week schedule. DLTs at 53 mg/m(2)/d for 3 days included hyperglycemia with resultant metabolic acidosis, pulmonary dysfunction, nausea, vomiting, and hypotension. Pharmacokinetic determinations at the recommended dose of 42.5 mg/m(2)/d for 3 days included mean total plasma concentration of 36.4 microM (terminal elimination half-life range, 447 to 1176 hours), steady-state volume of distribution of 9.3 to 14.2 L, and clearances of 0.005 to 0.033 L/h. The mean total salivary concentration was 111 nmol/L of UCN-01. One partial response was observed in a patient with melanoma, and one protracted period ( > 2.5 years) of disease stability was observed in a patient with alk-positive anaplastic large-cell lymphoma. Preliminary evidence suggests UCN-01 modulation of both PKC substrate phosphorylation and the DNA damage-related G(2) checkpoint. CONCLUSION: UCN-01 can be administered safely as an initial 72-hour CIV with subsequent monthly doses administered as 36-hour infusions.

Adult↗

PubMed2006

Optimizing therapy of seizures in patients with renal or hepatic dysfunction.

Patients with epilepsy may suffer from renal or hepatic diseases that interfere with their antiepileptic drug (AED) treatment. Furthermore, such diseases may themselves cause seizures. Reduced renal function and hypoalbuminemia lead to accumulation of renally excreted AEDs, such as gabapentin, vigabatrin, topiramate, levetiracetam, and phenytoin. Valproate, lamotrigine, and benzodiazepines are less affected. Low protein-bound AEDs are extensively removed by hemodialysis and supplemental doses are required for dialysis patients. Uremia and related conditions, including intracranial hemorrhage, glucose and electrolyte imbalances, and concomitant drug use, can cause seizures, as can dialysis encephalopathy, primary cerebral lymphoma, fungal infections, and immunosuppressant toxicity in renal transplant recipients. Hepatic dysfunction reduces enzymatic metabolism of AEDs and causes hypoalbuminemia. Gabapentin, topiramate, and levetiracetam are preferred in these conditions, whereas conversely valproate and felbamate are potentially hepatotoxic and should be avoided. Seizures related to hepatic encephalopathy are controlled by oral lactulose or neomycin. Porphyria sufferers may benefit from gabapentin, oxcarbazepine, or levetiracetam. Seizures in Wilson's disease may derive from d-penicillamine-induced pyridoxine deficiency. Effective treatment of seizures in renal and hepatic diseases requires attention to changes in AED pharmacokinetics and adequate care of the underlying illnesses. Monitoring of free drug concentrations is a valuable aid to therapy.

Anticonvulsants↗

PubMed2002

Fomepizole as an antidote for ethylene glycol poisoning.

OBJECTIVE: To assess the use of fomepizole in the treatment of ethylene glycol poisoning in the absence of hemodialysis. DATA SOURCES: A MEDLINE search (1966-May 2001) of English-language literature pertaining to the use of fomepizole in ethylene glycol poisoning was performed. Key search terms included fomepizole, ethylene glycol poisoning, and hemodialysis. References cited in those articles were also evaluated. DATA SYNTHESIS: Results from a number of case reports and a prospective trial suggest that fomepizole is a safe and effective antidote in the treatment of ethylene glycol poisoning. CONCLUSIONS: Case reports and 1 prospective trial have shown that, in the absence of both renal dysfunction and significant metabolic acidosis, the use of fomepizole should obviate the need for hemodialysis. However, the decision to add hemodialysis in the treatment of ethylene glycol poisoning based on plasma ethylene glycol concentrations is still debatable. A randomized, controlled trial is needed to determine the exact criteria for adding hemodialysis.

Acid-Base Imbalance↗

PubMed2006

Current schizophrenia drugs: efficacy and side effects.

Over the course of the past decade, the acceptance of several second-generation antipsychotics (SGAs) as effective medication for the treatment of schizophrenia has led to some changes. SGAs have a lower risk of inducing extrapyramidal side effects and tardive dyskinesia compared with first-generation antipsychotics, and have been said to be more successful in long-term treatment and tolerability. They also significantly improve the quality of life of schizophrenic patients. However, during treatment with SGAs other adverse effects can occur, such as weight gain, metabolic changes, sexual dysfunction and QTc-prolongation, significantly affecting the patient's physical health. Consequently, these side effects might be the reason that a high proportion of patients discontinue treatment with SGAs. Thus, from the authors' view, optimising individualised treatment implies increasing the efficacy of current schizophrenia drugs. This can be achieved by finding clinical or pharmacogenetic predictors for the most appropriate drug or drug combination, and by improving side-effect management in combination with non-pharmacological interventions in order to increase patients' quality of life and treatment compliance, possibly resulting in a better long-term outcome.

Antipsychotic Agents↗

PubMed2002

Modulation of the peroxisomal gene expression pattern by dehydroepiandrosterone and vitamin D: therapeutic implications.

Peroxisomes are ubiquitous organelles required for several metabolic functions. Their dysfunction is responsible for a group of human inherited disorders. In the search for endogenous factors regulating the peroxisomal compartment in normal liver, we treated female rats with dehydroepiandrosterone (DHEA) and 25-hydroxycholecalciferol for 1 and 6 days. Relative transcription levels of 39 selected genes were evaluated by real-time quantitative RT-PCR analysis. Catalase (peroxisomal marker)-specific activity was assayed in total liver homogenate and peroxisomes were visualized by catalase localization. DHEA induced peroxisome proliferation and raised catalase specific activity. Expression levels of 16 (of which 11 were peroxisomal) genes were altered. Pex 11, acyl-CoA oxidase,l - andd -multifunctional enzyme, thiolase 1, phytanoyl-CoA hydroxylase, 70 kDa peroxisomal membrane protein and very long chain acyl-CoA synthetase were upregulated, three others were downregulated. Vitamin D caused downregulation of six genes. Administration of vitamin D to peroxisomal disorder patients may be contraindicated. The adrenocortical hormone DHEA is a potential natural regulator of the peroxisomal compartment. Its therapeutic use in X-linked adrenoleukodystrophy, some other beta-oxidation defects and classical Refsum should be considered.

Animals↗

PubMed2025

Impaired natural killer cell maturation in lung adenocarcinoma driven by FABP4 and SPON2 downregulation through disrupted lipid metabolism.

BACKGROUND: Although natural killer (NK) cells play a crucial role in antitumor immunity, the metabolic changes driving their dysfunction in lung adenocarcinoma remain poorly understood. This study investigates how these metabolic modifications impact NK cell function within the lung adenocarcinoma microenvironment. METHODS: A total of 13 pairs of lung adenocarcinoma samples were obtained from The Cancer Genome Atlas. Differential gene expression, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and single-cell metabolic quantification analyses were used to characterize the transcriptomic, pathway, and metabolic signatures of NK cells. The developmental trajectory was reconstructed via pseudotime analysis. The fatty acid-binding protein 4 (FABP4) and spondin2 (SPON2) expression was examined using immunofluorescence (IF) and immunohistochemistry (IHC) in patients with lung adenocarcinoma. In NK cells with FABP4 downregulation, FABP4 function was analyzed using antibody-independent cell-mediated cytotoxicity assays, flow cytometry (FCM), and liquid chromatography-mass spectrometry. RESULTS: The number of NK cells was significantly decreased in the lung adenocarcinoma microenvironment. FABP4 and SPON2 expression was significantly lower in NK cells within tumor tissues than in the adjacent tissues. FABP4 expression was significantly lower in tumor tissues than in the adjacent tissues, whereas no significant difference in SPON2 expression was observed. The cytotoxic function of NK cells with decreased FABP4 levels was impaired. Non-targeted lipid metabolism analysis indicated that differentially expressed lipids in NK cells with low FABP4 levels were functionally enriched in the glycerophospholipid metabolism pathway compared to those in normal NK cells. CONCLUSIONS: The study findings present new evidence showing that low FABP4 and SPON2 gene expression may impair NK cell maturity by affecting lipid metabolism in lung adenocarcinoma. These results provide a new perspective on restoring immune function in patients with lung cancer.

FABP4↗

PubMed1990

Direct approach to arteriovenous malformations in functional areas of the cerebral hemisphere.

The natural history of patients with arteriovenous malformations (AVM's) suggests that serious morbidity associated with AVM's in functional areas is likely to be much greater than in silent areas. Various modes of treatment of AVM's in functional areas, including direct surgical intervention, embolization, and irradiation, have been considered to carry high risks. The authors advocate direct surgical intervention to these AVM's via a microsurgical technique based on knowledge of the hemodynamic anatomy of AVM's. The technique is designed to circumscribe the AVM without removing any surrounding cortical tissue or white matter and to preserve microcirculation in the functional area. Controlled hypotension (mean arterial blood pressure 40 to 60 mm Hg) is appropriate to enhance the safety of surgical procedures without causing metabolic and electrophysiological dysfunction. Another means to prevent neurological complications is multi-staged resection of larger AVM's, which permits obliteration compartment by compartment. This technique has the advantage of maintaining circulatory sufficiency in the functional area. There was no mortality among 56 patients who underwent the surgical procedure described. Of those, 55 patients resumed their preoperative occupation and one patient became self-sufficient.

Adolescent↗

PubMed1984

Effect of estrogen on lipoprotein lipase activity and cytoplasmic progestin binding sites in lean and obese Zucker rats.

Injections of 5 micrograms estradiol benzoate (EB) for 5 days resulted in decreases in the rate of body weight gain in both lean (Fafa) and obese (fafa) Zucker rats. EB administration also resulted in significant induction of cytoplasmic progestin binding sites in both hypothalamic-preoptic area (H-POA) and adipose tissues from rats of both genotypes. However, EB treatment significantly decreased lipoprotein lipase (LPL) activity in adipose tissue from lean, but not obese, Zucker rats and the same treatment increased LPL activity in the uteri from lean, but not obese, Zucker rats. The data are discussed in terms of the metabolic and reproductive dysfunctions observed in the genetically obese rat.

Adipose Tissue↗

PubMed2006

Intracerebral streptozotocin model of type 3 diabetes: relevance to sporadic Alzheimer's disease.

The cascade of Alzheimer's disease (AD) neurodegeneration is associated with persistent oxidative stress, mitochondrial dysfunction, impaired energy metabolism, and activation of pro-death signaling pathways. More recently, studies with human postmortem brain tissue linked many of the characteristic molecular and pathological features of AD to reduced expression of the insulin and insulin-like growth factor (IGF) genes and their corresponding receptors. We now demonstrate using an in vivo model of intracerebral Streptozotocin (ic-STZ), that chemical depletion of insulin and IGF signaling mechanisms combined with oxidative injury is sufficient to cause AD-type neurodegeneration. The ic-STZ-injected rats did not have elevated blood glucose levels, and pancreatic architecture and insulin immunoreactivity were similar to control, yet their brains were reduced in size and exhibited neurodegeneration associated with cell loss, gliosis, and increased immunoreactivity for p53, active glycogen synthase kinase 3beta, phospho-tau, ubiquitin, and amyloid-beta. Real time quantitative RT-PCR studies demonstrated that the ic-STZ-treated brains had significantly reduced expression of genes corresponding to neurons, oligodendroglia, and choline acetyltransferase, and increased expression of genes encoding glial fibrillary acidic protein, microglia-specific proteins, acetylcholinesterase, tau, and amyloid precursor protein. These abnormalities were associated reduced expression of genes encoding insulin, IGF-II, insulin receptor, IGF-I receptor, and insulin receptor substrate-1, and reduced ligand binding to the insulin and IGF-II receptors. These results demonstrate that many of the characteristic features of AD-type neurodegeneration can be produced experimentally by selectively impairing insulin/IGF functions together with increasing oxidative stress, and support our hypothesis that AD represents a neuro-endocrine disorder associated with brain-specific perturbations in insulin and IGF signaling mechanisms, i.e. Type 3 diabetes.

Alzheimer Disease↗

PubMed2000

Environmental medicine, part one: the human burden of environmental toxins and their common health effects.

Chemical compounds ubiquitous in our food, air, and water are now found in every person. The bioaccumulation of these compounds in some individuals can lead to a variety of metabolic and systemic dysfunctions, and in some cases outright disease states. The systems most affected by these xenobiotic compounds include the immune, neurological, and endocrine systems. Toxicity in these systems can lead to immune dysfunction, autoimmunity, asthma, allergies, cancers, cognitive deficit, mood changes, neurological illnesses, changes in libido, reproductive dysfunction, and glucose dysregulation. Chemicals and their effects on these systems are reviewed in this article. Subsequent articles in this series will focus on therapeutic regimens to combat the toxic effects of these and other compounds.

Endocrine System↗

PubMed1998

[Cyclic vomiting syndrome in children].

Cyclic vomiting syndrome in children is a manifestation of various etiologies, including gastroenterological and renal disorders, central and autonomic nervous system abnormalities, as well as metabolic and endocrine dysfunction. Frequently no organic cause is found. Personality profiles of children with cyclic vomiting reveal perfectionism, competitiveness, and aggressive behavior. Vomiting attacks have been induced by anxiety and excitement in patients with cyclic vomiting. We describe an 8-year-old girl with cyclic vomiting, frequently associated with occipital headaches, photophobia or dizziness. Psychiatric evaluation indicated a generalized anxiety disorder.

Anxiety Disorders↗

PubMed1975

[Artificial hyperventilation in head injury. I. Spontaneous hyperventilation and assisted ventilation (author's transl)].

The present study was desined to clarify the roles of artificial hyperventilation in management of the patients with cerebral injury. Here reported is the first part of the serial studies and concerned with general informations about hyperventilation. The measurements of PaCO2, minute ventilation volume (VE), dead space (VD), tidal volume (VT), cardiac output (by dye dilution method), oxygen consumption (by Fick' principle) and oxygen equilibrium were performed in the patients suffering from acute, severe head injury. And the effect of assisted ventilation on them were investigated (using pressure-limited respirator). 1. There was a common finding that marked and sustained increase in VE, VA (alveolar ventilation), and decrease in PaCO2 existed during the first week of injury. 97% of both VE and VA were above normal and mean value of PaCO2 was 29-33 mmHg. The syndrome of spontaneous hyperventilation was evidently more prominent in the nonsurvived group of patients. It was noteworthy that increased VE (or VA) was dependent neither on VD or pulmonary dysfunction nor on metabolic acidosis of arterial blood. The relation of VA to base excess in head injury was well contrasted to that of acute CO poisoning. 2. Assisted ventilation resulted in increased VT and decreased respiratory rate, and little change in VE. Consequently, PaCO2 changed only from 33.0 to 29.4 mmHg as a mean of entire series of patients. But when the influence affected by hypoxemic drive was subsided, a significant reduction of PaCO2 was disclosed following assisted ventilation. The assisted ventilation with pure oxygen was also associated with reduced cardiac output (from 6.0l/min to 5.3l/min), though the oxygen consumption changed variedly among the patients. 3. The fact was confirmed that both hypocapnea and alkalosis produced the left-sised shift of oxygen dissociation curve, decrease in P50 (P02 at 50% saturation of oxygen), and in addition, narrowed arterio-mixed venous oxygen difference. The changes of artero-mixed venous oxygen saturation difference which were calculated at 100 mmHg of PaO2 and 40mmHg of mixed venous PO2 were in a linear fashion with those of P50. Apart from the problems on injured brain, the beneficial and non-beneficial effects of hyperventilation were further discussed. The availability and inidcation of artificial hyperventilation should be precisely evaluated later, in a comprehensive manner with the subsequent studies (Part 2 and 3) on cerebral metabolism and intracranial pressure.

Brain Injuries↗

PubMed2001

Toward an understanding of violence: neurobehavioral aspects of unwarranted physical aggression: Aspen Neurobehavioral Conference consensus statement.

OBJECTIVE: Violence is a global problem that poses a major challenge to individuals and society. This document is a consensus statement on neurobehavioral aspects of violence as one approach to its understanding and control. BACKGROUND: This consensus group was convened under the auspices of the Aspen Neurobehavioral Conference, an annual consensus conference devoted to the understanding of issues related to mind and brain. The conference is supported by the Brain Injury Association and by individual philanthropic contributions. Participants were selected by conference organizers to represent leading opinion in neurology, neuropsychology, psychiatry, trauma surgery, nursing, evolutionary psychology, medical ethics, and law. METHODS: A literature review of the role of the brain in violent behavior was conducted and combined with expert opinion from the group. The major goal was to survey this field so as to identify major areas of interest that could be targeted for further research. Additional review was secured from the other attendees at the Aspen Neurobehavioral Conference. RESULTS: The group met in the spring of 1998 and 1999 for two 5-day sessions, between which individual assignments were carried out. The consensus statement was prepared after the second meeting, and agreement on the statement was reached by participants after final review of the document. CONCLUSIONS: Violence can result from brain dysfunction, although social and evolutionary factors also contribute. Study of the neurobehavioral aspects of violence, particularly frontal lobe dysfunction, altered serotonin metabolism, and the influence of heredity, promises to lead to a deeper understanding of the causes and solution of this urgent problem.

Adult↗

PubMed2002

[Acute coronary syndromes in patients treated with HIV protease inhibitors].

INTRODUCTION: Cardiovascular complications occurring in patients infected by the human immunodeficient virus (HIV) have considerably changed since the appearance, in April 1996, of highly active antiretroviral tri-therapy (HAART), associating reverse transcriptase and protease HIV-1 inhibitors. The spectacular efficacy of anti-proteases has led to the almost complete disappearance of these opportunistic complications. However, in May 1998, acute coronary accidents were reported in the literature, thus questioning the possible responsibility of antiprotease treatment in the occurrence of accelerated atheroma. METHOD: We report a series of 8 seropositive patients in whom an acute coronary event had occurred between February 1997 and February 1999. RESULTS: The patients were young and all exhibited cardiovascular risk factors (smoking, dyslipidemia) and were treated with HIV-1 protease inhibitors. Six patients presented myocardial infarction, one patient unstable angina and one patient effort angina. COMMENTS: A rise in triglycerides was observed principally on ingestion of ritonavir and a rise in cholesterol and LDL-cholesterol with all the antiprotease agents. Glucose intolerance was observed with indinavir. The occurrence of acute coronary events appeared to be related to antiprotease treatment (at the origin of metabolic disorders, endothelial dysfunction...), although it was impossible to say whether the antiprotease agents were responsible for the early atheroma or whether they simply contributed to the event. The coronary lesions were characterized by their number (single artery) and their topography (proximal or median). Nelfinavir may carry less cardiovascular risks than the other antiproteases. Mean term prognosis was relatively good, after therapeutic adjustment (change in antiprotease, strategic measures against cardiovascular risk factors, introduction of anti-anginal treatment...). CONCLUSION: Larger and longer studies would help to specify the role of antiproteases in the occurrence of early coronary events. Rigorous monitoring (lipid and glucose measurements, tests to search for myocardial infarction,..) together with the development of new antiretroviral molecules would reduce the number of coronary events in this type of patient.

Adult↗