Search

Summary Parasomnias and sleep‐related movement disorders (SRMD) are major causes of sleep disorders and may be drug induced. The objective of this study was to conduct a systematic review of the literature to examine the association between drug use and the occurrence of parasomnias and SRMD. Following Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines for reporting systematic reviews, we searched PubMed databases between January 2020 and June 2023. The searches retrieved 937 records, of which 174 publications were selected for full‐text screening and 73 drugs were identified. The most common drug‐induced parasomnias were nightmares and rapid eye movement (REM) sleep behaviour disorders and sleepwalking. In terms of drug‐induced SRMD, restless legs syndrome, periodic limb movement disorders (PLMD), and sleep‐related bruxism were most frequent. Medications that inhibit noradrenergic, serotonergic, or orexin transmission could induce REM sleep (e.g., nightmares). Regarding sleepwalking, dysregulation of serotoninergic neurone activity is implicated. Antipsychotics are mentioned, as well as medications involved in the gamma‐aminobutyric acid (GABA) pathway. A mechanism of desensitisation‐autoregulation of GABA receptors on serotoninergic neurones is a hypothesis. SRMD and PLMD could involve medications disrupting the dopamine pathway (e.g., antipsychotics or opioids). Opioids would act on mu receptors and increase dopamine release. The role of adenosine and iron is also hypothesised. Regarding bruxism, the hypotheses raised involve dysregulation of mesocortical pathway or a downregulation of nigrostriatal pathway, related to medications involving dopamine or serotonin. Parasomnias are rarely identified in drug product labels, likely due to the recent classification of their diagnoses. An analysis of pharmacovigilance data could be valuable to supplement existing literature data. [ABSTRACT FROM AUTHOR]

Background: A decrease in the regenerative capacity of age‐damaged liver tissue has been reported. Liver progenitor cells may play an important role in the regeneration of injured livers. In the present study we aimed to investigate improvements in the regenerative capacity of age‐damaged livers using chemically induced liver progenitors (CLiPs) derived from mature hepatocytes. Methods: Old (>90 weeks) and young (<20 weeks) mice underwent 70% hepatectomy, with or without trans‐splenic CLiP administration. The residual liver/bodyweight (LW/BW) ratio was measured on postoperative days 1 and 7, and changes in liver regeneration and histology were evaluated. Results: At 7 days post‐hepatectomy, LW/BW ratios were significantly better in CLiP‐treated old mice than in untreated old mice (p =.02). By contrast, no effect of CLiP transplantation was observed in young mice (p =.62). Immunofluorescence staining of liver tissue after CLiP administration showed an increase in Ki67‐positive cells (p <.01). Flow cytometry analysis of green fluorescent protein‐labeled CLiPs indicated that transplanted CLiPs differentiated into mature hepatocytes and were present in the recipient liver. Conclusions: CLiP transplantation appears to ameliorate the age‐related decline in liver regeneration in mice. [ABSTRACT FROM AUTHOR]

Abstract Background Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect of taxane treatment and can significantly affect patient quality of life. Currently, there are no effective treatments to alleviate symptoms of CIPN; thus, starting with prevention steps in high-risk patients is considered advantageous. However, for these prevention steps to be applicable to all patients, their side effects or accompanying discomforts should be minimal, and the intervention cost-effective. Compression therapy can be considered a prevention intervention, and using surgical gloves is feasible and cost-effective (approximately $0.6 per pair). Although previous studies on compression therapy using surgical gloves have reported decreased incidence of PN, these studies were non-randomized, limited to nab-paclitaxel treatment, and involved the use of small gloves, which may have caused discomfort. Therefore, this study aimed to assess the preventive effects of compression therapy using normal-sized surgical gloves on CIPN in patients treated with paclitaxel. Methods This clinical trial is designed to evaluate the preventive effects of compression therapy using surgical gloves on CIPN in women with stage II–III breast cancer who received paclitaxel chemotherapy for at least 12 weeks. This multicenter, randomized-controlled, open-label study will be conducted in six academic hospitals. Patients with medication or a medical history related to neuropathy or hand disease will be excluded. The primary outcome will be the preventive effect of compression therapy using surgical gloves, measured based on changes in the neurotoxicity component of the Functional Assessment of Cancer Therapy-Taxane questionnaire. Furthermore, we will assess the National Cancer Institute’s Common Terminology Criteria for Adverse Events grade of CIPN after 6 months. Notably, the estimated sample size, based on a p-value

Innate lymphoid cells (ILCs) have been shown to play essential roles in tumour immunity. Also, ILCs are involved in both homeostasis and inflammation. Evidence indicates that uncontrolled inflammatory response predisposes the intestine to colonic dysplasia and colorectal cancer (CRC). We investigated the frequency of three subsets of circulating ILCs in the early pathogenesis of colorectal carcinoma in the two distinct mouse models of colorectal cancer (CRC). We developed two mouse models representing the early pathogenic also reversible stages of CRC, including a chemically induced model, by administration of azoxymethane/dextran sulfate sodium (AOM/DSS), and an orthotopic mouse model, using the CT-26 cell line. Based on histopathological examinations, mice were divided into 3 groups including the dysplasia group (which consists of the chemically induced and the orthotopic induced), the chemically induced reparative change group, and a control group which was also considered in which mice were screened for stress originating from interventions and injections. Flow cytometry analysis was performed to evaluate the frequencies of ILC1, ILC2, and ILC3 in the peripheral blood of all studied mice. Altered composition of ILCs was observed in the peripheral blood of mice skewing toward ILC1s in the reparative change group compared to the control group (p value = 0.008); orthotopic-induced dysplasia and the chemically induced dysplasia groups did not differ significantly in terms of ILC subpopulations at the precancerous stages of colorectal dysplasia. A higher frequency of ILC1 in the chemically induced reparative change suggests a potentially anti-tumourigenic role participating in colorectal dysplasia. [ABSTRACT FROM AUTHOR]

Background Can Background be changed from bold to normal text?: Chemically-induced liver progenitors (CLiPs) have promising applications in liver regenerative medicine. We aimed to clarify the efficacy of CLiPs for ameliorating fibrosis in a diet-induced nonalcoholic steatohepatitis rat model, since nonalcoholic fatty liver disease is currently recognized as the most common form of chronic liver disease in developed countries. Methods: Primary mature hepatocytes were isolated from 7-week-old male Wistar rats. To establish CLiPs, isolated hepatocytes were cultured in differentiation medium composed of Y-27632, A-83-01, and CHIR99021 (YAC medium). As an animal model that reproduces NASH pathophysiology, 6-week-old severe combined immunodeficient (SCID) mice were carefully selected and prepared and fed with choline-deficient, L-amino acid-defined, high-fat diet (HFD). After 12 weeks’ HFD feeding, the mice were assigned to continue HFD with or without the administration of rat CLiPs (HFD + CLiPs and HFD-CLiPs, respectively). Rat CLiPs were administered from the spleen. Hepatic fibrosis was semi-quantitatively evaluated according to histology. Liver parenchyma and blood samples were collected for biochemical analyses. Results: Rat CLiPs were positive for CK19 and EpCAM were successfully delivered to the liver. At 8 weeks after CLiPs transplantation, the HFD + CLiPs group showed significantly less positive staining than the HFD-CLiPs group. Alanine aminotransferase significantly improved in the HFD + CLiPs group, as demonstrated by Azan staining and αSMA immunostaining. RT qPCR showed that the liver expression of MMP2 and 9 tended to be higher in the HFD + CLiPs group. Conclusions: The anti-fibrotic effect of CLiPs was demonstrated in the immunodeficient NASH animal model and may have therapeutic applications in humans.

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect of taxane treatment and can significantly affect patient quality of life. Currently, there are no effective treatments to alleviate symptoms of CIPN; thus, starting with prevention steps in high-risk patients is considered advantageous. However, for these prevention steps to be applicable to all patients, their side effects or accompanying discomforts should be minimal, and the intervention cost-effective. Compression therapy can be considered a prevention intervention, and using surgical gloves is feasible and cost-effective (approximately $0.6 per pair). Although previous studies on compression therapy using surgical gloves have reported decreased incidence of PN, these studies were non-randomized, limited to nab-paclitaxel treatment, and involved the use of small gloves, which may have caused discomfort. Therefore, this study aimed to assess the preventive effects of compression therapy using normal-sized surgical gloves on CIPN in patients treated with paclitaxel. Methods: This clinical trial is designed to evaluate the preventive effects of compression therapy using surgical gloves on CIPN in women with stage II–III breast cancer who received paclitaxel chemotherapy for at least 12 weeks. This multicenter, randomized-controlled, open-label study will be conducted in six academic hospitals. Patients with medication or a medical history related to neuropathy or hand disease will be excluded. The primary outcome will be the preventive effect of compression therapy using surgical gloves, measured based on changes in the neurotoxicity component of the Functional Assessment of Cancer Therapy-Taxane questionnaire. Furthermore, we will assess the National Cancer Institute's Common Terminology Criteria for Adverse Events grade of CIPN after 6 months. Notably, the estimated sample size, based on a p-value < 0.025 and statistical power of 0.9, will consist of 104 patients (52 per group), accounting for a 10% sample loss. Discussion: This intervention can be easily implemented in clinical practice and may serve as a preventive strategy for CIPNs with strong patient adherence. If successful, this intervention could improve the quality of life and treatment adherence in patients receiving chemotherapy that can induce PN, extending beyond paclitaxel treatment alone. Trial registration: ClinicalTrials.gov, NCT05771974; Registered on March 16, 2023. [ABSTRACT FROM AUTHOR]

Obesity, classified as an epidemic by the WHO, is a disease that continues to grow worldwide. Obesity results from abnormal or excessive accumulation of fat and usually leads to the development of other associated diseases, such as type 2 diabetes, hypertension, cancer, cardiovascular diseases, among others. In vitro and in vivo models have been crucial for studying the underlying mechanisms of obesity, discovering new therapeutic targets, and developing and validating new pharmacological therapies against obesity. Preclinical animal models of obesity comprise a variety of species: invertebrates, fishes, and mammals. However, small rodents are the most widely used due to their cost-effectiveness, physiology, and easy genetic manipulation. The induction of obesity in rats or mice can be achieved by the occurrence of spontaneous single-gene mutations or polygenic mutations, by genetic modifications, by surgical or chemical induction, and by ingestion of hypercaloric diets. In this review, we describe some of the most commonly used murine models in obesity research.

BACKGROUND:Cerebral microhemorrhages (CMH) are commonly found in the aging brain. CMH are also the neuropathological substrate of cerebral microbleeds (CMB), demonstrated on brain MRI. Recent studies demonstrate the importance of systemic inflammation in CMH development, but the relationships among inflammation, aging, and CMH development are not well-defined. In the current study, we hypothesized that the pathogenesis of inflammation-induced CMH in mice differs by age. METHODS:We studied young (3 months, n = 20) and old (18 months, n = 25) C57BL/6 mice injected with low-dose lipopolysaccharide (LPS; 1 mg/kg, i.p.) or saline at 0, 6, and 24 h. Seven days after the first LPS/saline injection, brains were harvested, sectioned, and stained with hematoxylin and eosin (H&E) and Prussian blue (PB) to estimate acute/fresh and sub-acute CMH development, respectively. The relationships between microglial/macrophage activation (ionized calcium-binding adapter molecule-1), astrocyte activation (glial fibrillary acidic protein), blood-brain barrier (BBB) disruption (brain immunoglobulin G), aging, and CMH development were examined using immunohistochemistry. RESULTS:Aging alone did not increase spontaneous H&E-positive CMH development but significantly increased the number, size, and total area of LPS-induced H&E-positive CMH in mice. LPS- and saline-treated aged mice had significantly larger PB-positive CMH compared with young mice, but the total area of PB-positive CMH was increased only in LPS-treated aged mice. Aged mice had significantly increased microglial/macrophage activation, which correlated with H&E- and PB-positive CMH development. Aged mice treated with LPS had significantly increased astrocyte activation and BBB disruption compared with young LPS-treated mice. CONCLUSIONS:Aging makes the brain more susceptible to inflammation-induced CMH in mice, and this increase in CMH with aging is associated with microglial/macrophage activation.

BackgroundCerebral microhemorrhages (CMH) are tiny deposits of blood degradation products in the brain and are pathological substrates of cerebral microbleeds. The existing CMH animal models are β-amyloid-, hypoxic brain injury-, or hypertension-induced. Recent evidence shows that CMH develop independently of hypoxic brain injury, hypertension, or amyloid deposition and CMH are associated with normal aging, sepsis, and neurodegenerative conditions. One common factor among the above pathologies is inflammation, and recent clinical studies show a link between systemic inflammation and CMH. Hence, we hypothesize that inflammation induces CMH development and thus, lipopolysaccharide (LPS)-induced CMH may be an appropriate model to study cerebral microbleeds.MethodsAdult C57BL/6 mice were injected with LPS (3 or 1 mg/kg, i.p.) or saline at 0, 6, and 24 h. At 2 or 7 days after the first injection, brains were harvested. Hematoxylin and eosin (H&E) and Prussian blue (PB) were used to stain fresh (acute) hemorrhages and hemosiderin (sub-acute) hemorrhages, respectively. Brain tissue ICAM-1, IgG, Iba1, and GFAP immunohistochemistry were used to examine endothelium activation, blood-brain barrier (BBB) disruption, and neuroinflammation. MRI and fluorescence microscopy were used to further confirm CMH development in this model.ResultsLPS-treated mice developed H&E-positive (at 2 days) and PB-positive (at 7 days) CMH. No surface and negligible H&E-positive CMH were observed in saline-treated mice (n = 12). LPS (3 mg/kg; n = 10) produced significantly higher number, size, and area of H&E-positive CMH at 2 days. LPS (1 mg/kg; n = 9) produced robust development of PB-positive CMH at 7 days, with significantly higher number and area compared with saline (n = 9)-treated mice. CMH showed the highest distribution in the cerebellum followed by the sub-cortex and cortex. LPS-induced CMH were predominantly adjacent to cerebral capillaries, and CMH load was associated with indices of brain endothelium activation, BBB disruption, and neuroinflammation. Fluorescence microscopy confirmed the extravasation of red blood cells into the brain parenchyma, and MRI demonstrated the presence of cerebral microbleeds.ConclusionsLPS produced rapid and robust development of H&E-positive (at 2 days) and PB-positive (at 7 days) CMH. The ease of development of both H&E- and PB-positive CMH makes the LPS-induced mouse model suitable to study inflammation-induced CMH.

Background: Bone cement implantation syndrome characteristically involves acute alterations in the function of respiratory and cardiovascular systems. We present a case report of cement reaction with unusual presentation, that is, hypoxia, hypertension and tachycardia. A 74-year-old hypertensive male on regular medications sustained a slip and fall, presented with a right intertrochanteric neck of femur fracture, now posted for cemented hemiarthroplasty. Intraoperatively, after applying bone cement, the patient developed sweating, dyspnoea, bilateral wheezing and tachypnoea and desaturation of up to 80%-84%. Respiratory symptoms were associated with tachycardia (140-160 bpm) and hypertension (220/110 mm Hg). The surgeon was alerted about the event, the patient was reassured, and respiration was assisted with positive pressure ventilation with supplementation of 100% oxygen., Discussion: Several mechanisms have been proposed, such as the toxic effect of systemically absorbed methyl methacrylate, exothermic reaction, fat and marrow embolism, high marrow pressure during cementing and anaphylactic reaction. The administration of adrenaline, which can worsen the clinical picture, is the mainstay in managing anaphylaxis., Conclusion: The association of hypertension and tachycardia with bone cement implantation syndrome, previously not reported, can have distinct pathomechanisms and cause a diagnostic and management dilemma., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Cerebral microbleeds are microscopic hemorrhages with deposits of blood products in the brain, which can be visualized with MRI and are implicated in cerebrovascular diseases. Hematoxylin and eosin (H&E) and Perl's Prussian blue are popular staining methods used to localize cerebral microbleeds in pathology. This paper compared these two staining techniques in a mouse model of cerebral microbleeds. We used lipopolysaccharide (LPS) to induce cerebral microhemorrhages. C57B6 mice were treated with LPS (5 mg/kg, i.p.) or vehicle at baseline and at 24 hr. The brains were extracted 48 hr after the first injection and adjacent coronal sections were stained with H&E and Prussian blue to compare the effectiveness of the two staining techniques. H&E-positive stains were increased with LPS treatment and were correlated with grossly visible microhemorrhages on the brain surface; Prussian blue-positive stains, by comparison, showed no significant increase with LPS treatment and did not correlate with either H&E-positive stains or surface microhemorrhages. H&E staining is thus a more reliable indicator of acute bleeding events induced by LPS in this model within a short time span.

Background: A decrease in the regenerative capacity of age-damaged liver tissue has been reported. Liver progenitor cells may play an important role in the regeneration of injured livers. In the present study we aimed to investigate improvements in the regenerative capacity of age-damaged livers using chemically induced liver progenitors (CLiPs) derived from mature hepatocytes., Methods: Old (>90 weeks) and young (<20 weeks) mice underwent 70% hepatectomy, with or without trans-splenic CLiP administration. The residual liver/bodyweight (LW/BW) ratio was measured on postoperative days 1 and 7, and changes in liver regeneration and histology were evaluated., Results: At 7 days post-hepatectomy, LW/BW ratios were significantly better in CLiP-treated old mice than in untreated old mice (p = .02). By contrast, no effect of CLiP transplantation was observed in young mice (p = .62). Immunofluorescence staining of liver tissue after CLiP administration showed an increase in Ki67-positive cells (p < .01). Flow cytometry analysis of green fluorescent protein-labeled CLiPs indicated that transplanted CLiPs differentiated into mature hepatocytes and were present in the recipient liver., Conclusions: CLiP transplantation appears to ameliorate the age-related decline in liver regeneration in mice., (© 2024 Japanese Society of Hepato‐Biliary‐Pancreatic Surgery.)

A 57-year-old man with a history of coronary artery disease and placement of an implantable cardioverter-defibrillator presented at our emergency room with an anterior ST-elevation myocardial infarction. Cardiac catheterization revealed an acutely occluded left main coronary artery, which was revascularized successfully with a bare-metal stent. Periprocedurally, the patient received aspirin, clopidogrel, unfractionated heparin, and eptifibatide. The patient was discharged a week later, but he returned to the emergency room the same day with recurrence of severe chest pain. Repeat cardiac catheterization revealed an acutely occluded stent, and the patient underwent repeat bare-metal stent placement and readministration of eptifibatide. On the next day, the patient's platelet count dropped acutely to less than 12,000/mm3. A test for heparin-induced thrombocytopenia antibody was negative. After discontinuation of eptifibatide, the patient's platelet count gradually returned to normal, and he was later discharged from the hospital with no complications. Eptifibatide-induced acute thrombocytopenia is a known but rare adverse effect. We review the handful of case reports in the medical literature, with emphasis on the prevalence, observed clinical course, and recently proposed physiologic mechanisms that probably are responsible for this phenomenon.

Purpose: Naldemedine, an oral, peripherally acting μ-opioid receptor antagonist approved for the treatment of opioid-induced constipation (OIC), is renally excreted. This subgroup analysis integrated data from 3 Phase 3 trials (COMPOSE-1, COMPOSE-2, COMPOSE-3) to evaluate the safety and efficacy of naldemedine in patients with renal impairment (RI). Patients and Methods: Patients age 18– 80 years with chronic non-cancer pain (CNCP) and OIC received oral naldemedine 0.2 mg or placebo once daily. RI subgroups consisted of patients with normal function (baseline glomerular filtration rate ≥ 90 mL/min/1.73 m2), mild (≥ 60 to < 90 mL/min/1.73 m2), and moderate (≥ 30 to < 60 mL/min/1.73 m2) RI. Safety assessments based on ≤ 12 weeks of treatment from all 3 studies included incidence of treatment-emergent adverse events (TEAEs). Efficacy was based on the proportion of responders in COMPOSE-1 and COMPOSE-2 only, defined as ≥ 3 spontaneous bowel movements (SBMs)/week and a ≥ 1-SBM/week increase from baseline for ≥ 9 of 12 weeks and ≥ 3 of the last 4 weeks. Results: In total, 2328 patients were included in this analysis. The incidence of TEAEs was similar in the naldemedine and placebo groups (overall, 47.1% vs 45.6%; normal, 44.6% vs 43.6%; mild RI, 49.0% vs 44.7%; moderate RI, 46.6% vs 55.9%). GI-related TEAEs occurred more frequently in the naldemedine group versus placebo (overall, 21.8% vs 13.8%; normal, 21.6% vs 12.5%; mild RI, 22.6% vs 14.7%; moderate RI, 18.0% vs 14.2%). A significantly greater proportion of patients in the naldemedine 0.2 mg group were responders versus the placebo group (overall, 50.1% vs 34.1%, P< 0.0001; normal, 52.0% vs 39.3%; mild RI, 48.3% vs 30.3%; moderate RI, 52.5% vs 31.7%). Conclusion: This integrated analysis confirmed that OIC treatment with naldemedine 0.2 mg was generally well tolerated and effective in patients with CNCP and mild or moderate RI. Safety and efficacy results were consistent with the overall population. Clinicaltrials.gov Registration: COMPOSE-1: NCT01965158; COMPOSE-2: NCT01993940; COMPOSE-3: NCT01965652. [ABSTRACT FROM AUTHOR]

The definition of hyperprogressive disease (HPD) is controversial in the literature and has not been widely described in melanoma. The aim of this study was to determine whether the concept of HPD applies to patients treated for advanced melanoma, using a definition with a simple, reproducible criterion, and to determine whether it is possible to identify predictive factors for HPD. This was a retrospective analysis on a prospective cohort. The data were extracted from MelBase, a French prospective, multicentre cohort of adult patients with advanced melanoma. The patients, following informed consent, were treated prospectively with anti-PD1, ipilimumab+nivolumab, BRAF/MEKi, or chemotherapy, 1st line or thereafter. HPD was defined, within 3 months following the start of the treatment, with the help of a clinical and biological criterion using Response Evaluation Criteria in Solid Tumours, Eastern Cooperative Oncology Group Performance Score, and lactate dehydrogenase. The occurrence of HPD in the 4 groups was as follows (numbers of patients out of the total number): anti-PD1 98/1004 (10%), ipilumumab +nivolumab 19/327 (6%), targeted therapy 31/751 (4%), and chemotherapy 40/397 (10%). In the anti programmed cell death protein 1 (APD1) group, the relevant risk factors for HPD were: more than 3 metastatic sites (p = 0.03) and liver metastasis (p < 0.001). This data, thanks to relevant clinical and biological criteria feasible in daily practice, supports the presence of a subgroup whose disease deteriorates rapidly during mono-immunotherapy. Also observed with other treatments, HPD could be the consequence of a natural and aggressive evolution of the disease, alleviated by strong-acting treatments. • HPD can be defined with the help of a clinical and biological criteria. • HPD is linked to a poor prognosis of the disease. • In advanced melanoma approximately 10% of patients will meet the HPD criteria. • Risk factors for HPD can be identified for patients treated by APD1. [ABSTRACT FROM AUTHOR]

Introduction. Calcium channel blockers (CCBs) are commonly used agents in the treatment of hypertension as part of monotherapy or combination therapy. Peripheral edema is the most common side effect that requires discontinuation or replacement of treatment. Some studies in the literature have shown that long-acting dihydropyridine type CCBs lead chylous ascites in peritoneal dialysis patients. However, amlodipine-associated serous ascites cases are not available in the literature. Case Report. In this case report, we describe a rare case of amlodipine induced massive ascites in a 30-year-old male with renal transplantation. Conclusion. We aimed to create awareness that pharmacologic causes should be considered in cases of ascites of unknown aetiology. [ABSTRACT FROM AUTHOR]

Diabetes is an endocrine illness involving numerous physiological systems. To understand the intricated pathophysiology and disease progression in diabetes, small animals are still the most relevant model systems, despite the availability and progression in numerous invitro and insilico research methods in recent years. In general, experimental diabetes is instigated mainly due to the effectiveness of animal models in illuminating disease etiology. Most diabetes trials are conducted on rodents, while some research is conducted on larger animals. This review will discuss the methodology and mechanisms in detail for preparing diabetic animal models, considering the following important points. The exact pathophysiology of the disease may or may not be replicated in animal models, the correct induction doses must be given and the combination of different approaches for the models is recommended to get desired results.•Animal models are essential to understand diabetes etiology and pathophysiology.•Diabetic models can be developed in both rodents and non-rodents.•Chemically induced and genetic models of diabetes are widely used to study diabetes and diabetic complications., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors. Published by Elsevier B.V.)

publisher‐imprint‐name Springer volume‐issue‐count 1 issue‐article‐count 0 issue‐toc‐levels 0 issue‐pricelist‐year 2018 issue‐copyright‐holder The Author(s) issue‐copyright‐year 2018 article‐contains‐esm No article‐numbering‐style Unnumbered article‐registration‐date‐year 2018 article‐registration‐date‐month 10 article‐registration‐date‐day 31 article‐toc‐levels 0 toc‐levels 0 volume‐type Regular journal‐product ArchiveJournal numbering‐style Unnumbered article‐grants‐type OpenChoice metadata‐grant OpenAccess abstract‐grant OpenAccess bodypdf‐grant OpenAccess bodyhtml‐grant OpenAccess bibliography‐grant OpenAccess esm‐grant OpenAccess online‐first false pdf‐file‐reference BodyRef/PDF/40169_2018_Article_215.pdf target‐type OnlinePDF issue‐type Regular article‐type ReviewPaper journal‐subject‐primary Medicine & Public Health journal‐subject‐secondary Medicine/Public Health, general journal‐subject‐collection Medicine open‐access true --> Osteoarthritis (OA) is one of the most common chronic conditions in the world today. It results in breakdown of cartilage in joints and causes the patient to experience intense pain and even disability. The pathophysiology of OA is not fully understood; therefore, there is currently no cure for OA. Many researchers are investigating the pathophysiology of the disease and attempting to develop methods to alleviate the symptoms or cure the OA entirely using animal models. Most studies on OA use animal models; this is necessary as the disease develops very slowly in humans and presents differently in each patient. This makes it difficult to effectively study the progression of osteoarthritis. Animal models can be spontaneous, in which OA naturally occurs in the animal. Genetic modifications can be used to make the mice more susceptible to developing OA. Osteoarthritis can also be induced via surgery, chemical injections, or non‐invasive trauma. This review aims to describe animal models of inducing osteoarthritis with a focus on the models used on mice and their advantages and disadvantages that each model presents. [ABSTRACT FROM AUTHOR]

Background: Closed reduction of dislocations or surgical procedures conducted under locoregional anesthesia are sometimes interfered or even precluded by the muscular tone present in an awake patient with spontaneous breathing. In these clinical conditions the administration of a subanesthetic dose of rocuronium can allow for these procedures to be completed, without losing spontaneous breathing. Objective: To describe our fi rst experiences employing subanesthetic doses of rocuronium in awake patients. Methods: chart review of patients treated with subanesthetic doses of rocuronium in awake patients with spontaneous breathing. Results: 16 treatments were performed on 15 patients to enable completing closed reduction of dislocations or surgery procedures under locoregional anesthesia. The degree of muscular relaxation needed to complete the procedures was attained in all cases, even though a second dose was needed in fi ve patients; one of the prosthesis dislocated could not be reduced due to mechanical problems. Final doses of rocuronium ranged between 4 and 10 mg for absolute values or between 0.05 and 0.10 mg/kg for weight-related doses. Undesired adverse effects (diplopia, metallic taste) were scarce and transient, and well tolerated by the patients. Conclusion: Administration of subanesthetic doses of rocuronium may be a useful alternative in clinical conditions where a brief degree of muscular relaxation is needed. [ABSTRACT FROM AUTHOR]

Pyogenic granuloma (PG) is a benign non-neoplastic mucocutaneous lesion. It is a reactional response to constant minor trauma and might be related to hormonal changes. In the mouth, PG is manifested as a sessile or pedunculated, resilient, erythematous, exophytic and painful papule or nodule with a smooth or lobulated surface that bleeds easily. PG preferentially affects the gingiva, but may also occur on the lips, tongue, oral mucosa and palate. The most common treatment is surgical excision. This paper describes a mucocutaneous PG on the upper lip, analyzing the clinical characteristics and discussing the features that distinguish this lesion from other similar oral mucosa lesions. The diagnosis of oral lesions is complex and leads the dentist to consider distinct lesions with different diagnostic methods. This case report with a 4 year-follow-up calls the attention to the uncommon mucocutaneous labial location of PG and to the fact that surgical excision is the safest method for diagnosis and treatment of PG of the lip, even when involving the mucosa and skin

Hepatic angiosarcoma is a rare primary tumor of the liver with a mesenchymal origin. Diagnosis is difficult because clinical manifestations and imaging studies are inconclusive. In many cases a diagnosis is obtained during necropsy, not being apparent during the course of disease. It is associated with several risk factors, but these contribute to explaining only a few of all reported cases. When clinical manifestations begin progression is often fast, and possibilities for curative treatment are limited. We report two cases of hepatic angiosarcoma. In the first one, our patient had an insidious initial course, and then suddenly presented with hepatic failure followed by acute respiratory distress. A diagnosis was reached during necropsy. In the second case, we initiated the study of a chronic liver disease using fine-needle aspiration biopsy, which showed findings suggestive of hepatic angiosarcoma. In the following weeks the patient started on a torpid clinic course, and died from multiple organ failure.El angiosarcoma hepático es una neoplasia de estirpe mesenquimal de baja frecuencia y difícil diagnóstico por su forma inespecífica de manifestarse clínica y radiológicamente. Tanto es así que muchos diagnósticos se obtienen mediante necropsia, no siendo posible poner de manifiesto la enfermedad durante su curso. Se asocia a diferentes agentes etiológicos, pero en la mayoría de los casos no es posible establecer una exposición concreta a ninguno de ellos. Cuando comienza a manifestarse, la evolución suele ser rápida y las opciones de tratamiento curativo son escasas. Presentamos en nuestro trabajo dos casos de angiosarcoma hepático. En el primero, el paciente sufre en principio una evolución insidiosa, presentando al fin, y de forma abrupta, un cuadro de insuficiencia hepática seguido de distrés respiratorio, falleciendo por este motivo. El diagnóstico se alcanza en la necropsia. En el segundo caso se inicia un estudio de hepatopatía en el cual se indica una PAAF. Esta es informada como hallazgos compatibles con angiosarcoma hepático. El paciente presenta en las semanas ulteriores una evolución tórpida, falleciendo en fracaso multiorgánico.

Background: Subclinical doses of propofol produce anterograde amnesia, characterized by an early failure of memory consolidation. It is unknown how propofol affects the amygdala-dependent emotional memory system, which modulates consolidation in the hippocampus in response to emotional arousal and neurohumoral stress. We present an event-related functional magnetic resonance imaging study of the effects of propofol on the emotional memory system in human subjects.Methods: Thirty-five healthy subjects were randomized to receive propofol, at an estimated brain concentration of 0.90 μg ml(-1), or placebo. During drug infusion, emotionally arousing and neutral images were presented in a continuous recognition task, while blood-oxygen-level-dependent activation responses were acquired. After a drug-free interval of 2 h, subsequent memory for successfully encoded items was assessed. Imaging analysis was performed using statistical parametric mapping and behavioural analysis using signal detection models.Results: Propofol had no effect on the stereotypical amygdalar response to emotional arousal, but caused marked suppression of the hippocampal response. Propofol caused memory performance to become uncoupled from amygdalar activation, but it remained correlated with activation in the posterior hippocampus, which decreased in proportion to amnesia.Conclusions: Propofol is relatively ineffective at suppressing amygdalar activation at sedative doses, but abolishes emotional modulation and causes amnesia via mechanisms that commonly involve hyporesponsiveness of the hippocampus. These findings raise the possibility that amygdala-dependent fear systems may remain intact even when a patient has diminished memory of events. This may be of clinical importance in the perioperative development of fear-based psychopathologies, such as post-traumatic stress disorder.Clinical Trial Registration: NCT00504894. [ABSTRACT FROM AUTHOR]

Objective. To analyze the effect of various fluoride formulations in commercially available agents on working properties of various nickel-titanium orthodontic wires. Materials and methods. Uncoated (NiTi), rhodium coated (RhNiTi) and nitrified (NNiTi) wires were immersed to dH2O, MiPaste, Elmex and Mirafluor for 1 h. Unloading slope characteristics (average force, bending action of the force and average plateau length) and the percentage of useable constant force during unloading were observed. Surface roughness ( Ra) was measured. SEM and EDS were used for observation of the surface. Results. NiTi had decreased loading and unloading elastic modulus ( E) and yield strength (YS) after immersion to MIPaste and Mirafluor. The unloading YS decreased in the RhNiTi by the MIPaste. The loading and unloading YS of the NNiTi increased in Elmex and increased average plateau force. RhNiTi showed higher average plateau length and the percentage of useful constant force during unloading in Mirafluor and the average plateau force lowered after immersion to MIPaste. The unloading slope characteristics for NiTi were affected by all three prophylactic agents, mostly by Mirafluor, and produced significantly lower forces during both loading and unloading, similarly to the NNiTi wires. The RhNiTi had the lowest forces during both loading and unloading in MIPaste. All results were at significance; p < 0.05. Difference in Ra was observed for RhNiTi after immersion to the MI Paste ( p < 0.001; η2 = 0.761). Conclusion. The NiTi and NNiTi wires lose less working force when combined with Elmex. The RhNiTi improve their working properties with Mirafluor and deteriorate when combined with MiPaste. [ABSTRACT FROM AUTHOR]

The anode-free lithium metal battery is considered to be an excellent candidate for the new generation energy storage system because of its higher energy density and safety than the traditional lithium metal battery. However, the continuous generation of SEI or isolated Li hinders its practical application. In general, the isolated Li is considered electrochemically inactive because it loses electrical connection with the current collector. Here we show an abnormal phenomenon that the lost capacity appears to be recovered after cycles when the isolated Li reconnects with a deposited Li metal layer. The isolated Li reconnection is ascribed to the chemical induction of the block copolymer coating. The migration of Li + is affected by the electron delocalization and the electron cloud density of the polymer, which determine the conversion direction of Li + . Based on the mechanism, we propose a strategy to slow down the capacity decay of the anode-free lithium metal battery.

Chemically-induced liver progenitors (CLiPs) have promising applications in liver regenerative medicine. We aimed to clarify the efficacy of CLiPs for ameliorating fibrosis in a diet-induced nonalcoholic steatohepatitis rat model, since nonalcoholic fatty liver disease is currently recognized as the most common form of chronic liver disease in developed countries., Methods: Primary mature hepatocytes were isolated from 7-week-old male Wistar rats. To establish CLiPs, isolated hepatocytes were cultured in differentiation medium composed of Y-27632, A-83-01, and CHIR99021 (YAC medium). As an animal model that reproduces NASH pathophysiology, 6-week-old severe combined immunodeficient (SCID) mice were carefully selected and prepared and fed with choline-deficient, L-amino acid-defined, high-fat diet (HFD). After 12 weeks' HFD feeding, the mice were assigned to continue HFD with or without the administration of rat CLiPs (HFD + CLiPs and HFD-CLiPs, respectively). Rat CLiPs were administered from the spleen. Hepatic fibrosis was semi-quantitatively evaluated according to histology. Liver parenchyma and blood samples were collected for biochemical analyses., Results: Rat CLiPs were positive for CK19 and EpCAM were successfully delivered to the liver. At 8 weeks after CLiPs transplantation, the HFD + CLiPs group showed significantly less positive staining than the HFD-CLiPs group. Alanine aminotransferase significantly improved in the HFD + CLiPs group, as demonstrated by Azan staining and αSMA immunostaining. RT qPCR showed that the liver expression of MMP2 and 9 tended to be higher in the HFD + CLiPs group., Conclusions: The anti-fibrotic effect of CLiPs was demonstrated in the immunodeficient NASH animal model and may have therapeutic applications in humans., Competing Interests: The authors declare no conflicts of interest in association with the present study., (© 2022 The Japanese Society for Regenerative Medicine. Production and hosting by Elsevier B.V.)

Background: Diabetes is a major threat to public health in the United States and worldwide. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. Objective: We assessed the epidemiologic literature for evidence of associations between persistent organic pollutants (POPs) and type 2 diabetes. Methods: Using a PubMed search and reference lists from relevant studies or review articles, we identified 72 epidemiological studies that investigated associations of persistent organic pollutants (POPs) with diabetes. We evaluated these studies for consistency, strengths and weaknesses of study design (including power and statistical methods), clinical diagnosis, exposure assessment, study population characteristics, and identification of data gaps and areas for future research. Conclusions: Heterogeneity of the studies precluded conducting a meta-analysis, but the overall evidence is sufficient for a positive association of some organochlorine POPs with type 2 diabetes. Collectively, these data are not sufficient to establish causality. Initial data mining revealed that the strongest positive correlation of diabetes with POPs occurred with organochlorine compounds, such as trans-nonachlor, dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCBs), and dioxins and dioxin-like chemicals. There is less indication of an association between other nonorganochlorine POPs, such as perfluoroalkyl acids and brominated compounds, and type 2 diabetes. Experimental data are needed to confirm the causality of these POPs, which will shed new light on the pathogenesis of diabetes. This new information should be considered by governmental bodies involved in the regulation of environmental contaminants. INSET: CORRECTION. [ABSTRACT FROM AUTHOR]

Colorectal cancer is a heterogeneous disease that afflicts a large number of people in the USA. The use of animal models has the potential to increase our understanding of carcinogenesis, tumor biology, and the impact of specific molecular events on colon biology. In addition, animal models with features of specific human colorectal cancers can be used to test strategies for cancer prevention and treatment. In this review, we provide an overview of the mechanisms driving human cancer, we discuss the approaches one can take to model colon cancer in animals, and we describe a number of specific animal models that have been developed for the study of colon cancer. We believe that there are many valuable animal models to study various aspects of human colorectal cancer. However, opportunities for improving upon these models exist. [ABSTRACT FROM AUTHOR]

Background: DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms) or reaction to drugs with eosinophilia and systemic symptoms is a serious drug reaction associated with the use of aromatic anticonvulsants and allopurinol. At least 44 drugs have been associated with DRESS. The aim was to present the case of a patient with DRESS syndrome associated with phenytoin. Clinical case: a 20 years old woman, with a history of seizures since childhood, presented generalised tonic-clonic seizures for the last three months. Therefore, she began treatment with 100 mg of phenytoin, administered orally, every 8 hours. Three weeks later, she developed fever up to 42 degrees, papules in the hands extending to trunk and extremities, generalized rubicund, pruritus, pain while urinating, adding hyperoxia, dysphagia and dry cough. Consequently, she went to the emergency room. Discussion: the diagnosis is clinical and it is set according to the criteria of the scale of RegiSCAR. As the initial manifestations are unspecific, the diagnosis and treatment could be delayed. The importance of recognizing this syndrome is an early treatment to get better prognostics. The mortality is up to 10 %. [ABSTRACT FROM AUTHOR]

Objectives: Several case reports of lupus-like syndrome suggest that statins could have triggered the development of this rare autoimmune disease. However, data on the association between statin use and lupus-like syndrome are scarce. We assessed whether there was an association between statin use and the occurrence of lupus-like syndrome. Methods: A case/noncase study based on individual case safety reports listed in the World Health Organization global individual case safety reports database (VigiBase) was conducted. According to World Health Organization adverse reaction terminology, cases were defined as reports of lupus-like syndrome. Each case was matched with 5 noncases by age, gender, and time of reporting. Use of statins was classified according to the Anatomical Therapeutic Chemical classification code system. Covariates, ie, use of corticosteroids, immunosuppressive drugs, nonsteroidal anti-inflammatory drugs, antidepressants, antiepileptics, proton pump inhibitors, and cardiovascular drugs, were determined. Multivariate logistic regression was used to calculate the reporting odds ratios with 95% confidence intervals. Results: We identified 3362 reports of lupus-like syndrome as cases and 27,092 reports of other adverse drug reactions as noncases. Statins were more frequently reported as suspected drug in cases (3.2%) than in noncases (1.5%). After adjustment for several covariates, statins were associated with the reporting of lupus-like syndrome (reporting odds ratios 2.01; 95% confidence intervals 1.61-2.51). Conclusions: We found an association between reporting of statins and lupus-like syndrome. Further studies are needed to confirm this finding in more detail and establish causality. [Copyright &y& Elsevier]

Anti-angiogenic targeted therapies are now major tools in the management of solid tumors. Briefly, one can distinguish between monoclonal antibodies such as bevacizumab directed against vascular endothelial growth factor (VEGF) and small molecules such as those targeted against receptors with tyrosine-kinase activity. Soon after they were marketed, these drugs showed cardiovascular toxicities, such as hypertension, left ventricular systolic dysfunction, heart failure and conduction abnormalities. The most frequent cardiovascular side effect of targeted therapies is hypertension, but the most life-threatening is QT prolongation with its risk of torsade de pointe and sudden cardiac death. Since the incidence of different types of cardiovascular side effects following targeted therapies varies across studies-and despite the fact that several meta-analyses attempted to summarize available information-those side effects are still not well identified. In addition, their reversibility is not precisely known. This review aims to present and discuss the various cardiovascular toxicities of anti-angiogenic targeted therapies for cancer. [ABSTRACT FROM AUTHOR]

A large number of drugs have been implicated in causing depression by case reports and case series. For a few specific drugs, the association has subsequently been confirmed by appropriately designed studies. In other instances, a lack of substantiating evidence has lead to a gradual disappearance of concern about a potential association. The benzodiazepines represent a deviation from this pattern: they are widely believed to cause depression, but there is a lack of evidence to substantiate this claim. In DSM-IV, there is a category of mood disorder for drug-induced depression (substance-induced mood disorder), and the text of the manual specifically refers to benzodiazepines as a potential cause. Despite the apparently entrenched nature of this belief, there continues to be a lack of credible evidence that benzodiazepines can cause depression as a side effect. [ABSTRACT FROM AUTHOR]

Introduction: Exposure to cancer and its treatments, including chemotherapy and radiotherapy, may result in late adverse effects including endocrine dysfunction. Endocrine disorders are the most commonly reported long-term complications of cancer treatment, especially by adult survivors of childhood cancers. This review will explore the endocrinologic adverse effects from non-endocrine cancer therapies.Methods: Searches including various Internet-based medical search engines such as PubMed, Medline Plus, and Google Scholar were conducted for published articles.Results: One hundred sixty-nine journal articles met the inclusion criteria. They included case reports, systematic analyses, and cohort reports. Endocrine disorders including hypothalamus dysfunction, hypopituitarism, syndrome of inappropriate anti-diuretic hormone secretion, diabetes insipidus, growth hormone disorders, hyperprolactinemia, gonadotropin deficiency, serum thyroid hormone-binding protein abnormalities, hypothyroidism, hyperthyroidism, hypomagnesium, hypocalcemia, hyperparathyroidism, hyperparathyroidism, adrenal dysfunction, gonadal dysfunction, hypertriglyceridemia, hypercholesterolemia, diabetes mellitus, and glycosuria were identified and their association with cancer therapies were outlined.Discussion/conclusions: The journal articles have highlighted the association of cancer therapies, including chemotherapy and radiotherapy, with endocrine dysfunction. Some of the dysfunctions were more often experienced than others. Especially in patients treated with radiotherapy, some endocrinologic disorders were progressive in nature.Implications For Cancer Survivors: Recognition and awareness of endocrine sequelae of cancer treatments may permit for early detection and appropriate follow-up care for cancer survivors, thus improving their overall health and quality of life. [ABSTRACT FROM AUTHOR]

Abstract: Prinzmetal’s angina is a condition characterized by chest pain, transient ST elevation, and negative biochemical markers of myocardial cell necrosis. We describe a case of chemically-induced “silent” ST segment elevation related to Atenolol overdose in a patient without coronary artery stenosis. We conclude that the cause for the transient myocardial ischemia is coronary vasospasm, precipitated by beta-blocker overdose. [Copyright &y& Elsevier]

Background: Propofol injection pain is a well-known problem in pediatric anesthesia. Premixture of lidocaine with propofol although effective does not abolish injection pain in all children. Promising results have been reported with pretreatment of the vein with ketamine. The purpose of this prospective, double-blind randomized, clinical trial with active control was to evaluate the efficacy of premixing propofol with ketamine in the prevention of injection pain in children. Methods: After ethics committee and parental approval and children’s assent, 116 children, aged 1–12 years, were randomly allocated to receive an IV induction dose of admixture of racemic ketamine 0.5 mg·ml−1 (ketamine group) or lidocaine 1 mg·ml−1 in propofol 10 mg·ml−1 (lidocaine group). The outcome measures were signs and symptoms of injection pain (primary outcome: the incidence of injection pain), hemodynamic and respiratory parameters, and adverse effects during anesthesia induction (secondary outcomes). Results: Patients’ characteristics were similar in the two groups. Fewer children (13/58) in the lidocaine group than in the ketamine group (26/58) (mean difference 23%, 95% CI for difference 6–40%, P = 0.018) developed pain on injection of propofol. There were no differences in hemodynamic parameters between the two groups. One child in the lidocaine group developed laryngospasm, but no other adverse events were recorded. Conclusions: Injection pain was twice as common with ketamine–propofol admixture than with lidocaine–propofol admixture. [ABSTRACT FROM AUTHOR]

A 17-year-old boy with acute lymphoblastic leukemia developed acute renal failure within 48 h of an intravenous high-dose methotrexate (5 g/m 2 ) infusion. His renal function returned to baseline 14 days later with supportive care, folinic acid rescue, and urinary alkalinization. A retrospective review revealed that the patient had been exposed to iopamidol, an intravenous contrast medium, on the day prior to the commencement of methotrexate treatment. Methotrexate-associated nephropathy is a rare complication in pediatric oncology, and a review of the literature suggests that exposure to nephrotoxic agents may be a significant but perhaps underrecognized risk factor for its development. [ABSTRACT FROM AUTHOR]

Chlorine is a widely used industrial chemical. Individuals can be exposed to chlorine through transportation accidents, industrial exposures or misuse of domestic cleaners. While most exposed individuals recover normal pulmonary function, chlorine can cause a variety of lung injuries including pulmonary edema, restrictive lung disease, and obstructive disease, including Reactive Airways Dysfunction Syndrome. Residual effects of chlorine exposure are a function of intensity of exposure, minute ventilation during exposure, and host characteristics such as cigarette smoking and atopy. This monograph will summarize uses of chlorine, the potential for accidents, the mechanism of chlorine toxicity in the lung, and review acute and chronic effects of chlorine exposure on the lung, as well as systemic effects of massive chlorine exposure. [ABSTRACT FROM AUTHOR]

Spontaneously occurring and chemically induced pheochromocytomas are rare in mice. That the mouse pheochromocytoma is a more appropriate animal model than that of the rat for study of human medullary adrenal tumors has been suggested. The expression of phenylethanolamine-N-methyltransferase (PNMT), the enzyme responsible for production of epinephrine from norepinephrine, is common to both mouse and human pheochromocytomas. This investigation assessed the expression of the immunohistochemical markers PNMT, tyrosine hydroxylase (TH), and chromogranin A (CGA) in spontaneously occurring and chemically induced pheochromocytomas in the B6C3F1 mouse. Spontaneous tumors were derived from control animals from 10 different studies and the pheochromocytomas from treated groups from 4 different studies. All tumors were positive for maximal TH expression. A highly significant difference in PNMT expression ( p<0.01) occurred between spontaneously occurring pheochromocytomas classified as benign or “malignant” by the criteria of toxicologic pathology. Chemically induced tumors showed intermediate PNMT staining. A marked reduction in CGA expression occurred in pheochromocytomas induced by technical grade pentachlorophenol, compared to the other three chemicals and the spontaneously occurring tumors. These findings suggest that immunohistochemistry is a reliable tool in investigating the functional capabilities of pheochromocytomas in mice. PNMT expression is a tightly regulated component of the chromaffin cell phenotype and appears to be readily lost in mouse pheochromocytomas, particularly those with aggressive characteristics. [ABSTRACT FROM AUTHOR]

Background: Propofol has been widely used in general anesthesia. Although it is also often used in pediatric anesthesia, there has been only limited scientific evidence on the use of propofol in children up to 3 years.Methods: A prospective, randomized, double-blind, therapeutic equivalence study comparing two propofol 1% emulsions (Propofol 1% Fresenius vs. Diprivan 1%) was performed in 60 patients scheduled for routine surgery or for diagnostic laparoscopic procedures requiring anesthesia. To guarantee comparability of age distribution between the two groups, a stratified randomization with patients younger than 12 months of age in a low age group and with patients aged 12 months to 3 years in a high age group was used. The average propofol induction dose and the average propofol infusion dose were analyzed to prove equivalence. The side-effects profile was analyzed to compare the safety profiles of the two propofol formulations in this study.Results: There were no differences in baseline characteristics between the two treatment groups of high and low age. Medications used for induction and maintenance of anesthesia, and side-effects profiles were comparable, as were the average propofol dose for induction of anesthesia (range of the mean dose 4.0-4.2 mg/kg) and for maintenance of anesthesia (range of the mean dose in the first hour 8.74-9.42 mg x kg(-1) x h(-1)).Conclusions: The two 1% propofol formulations were equally effective in our patient population of infants and young children between 1 month and 3 years of age. No differences between the two propofol formulations were found with regard to the circulatory reaction, lipid metabolism, dosages, and recovery profile in the studied age groups. [ABSTRACT FROM AUTHOR]