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PubMed1997

Functional methionine synthase deficiency due to cblG disorder: a report of two patients and a review.

Functional methionine synthase deficiency due to abnormal methylcobalamin metabolism causes megaloblastic anemia, moderate to severe developmental delay, lethargy, and anorexia in association with homocystinuria. Patients with this disorder of cobalamin metabolism can be classified into two separate groups, cblE or cblG, primarily on the basis of complementation analysis with cultured skin fibroblasts. We describe two unrelated boys, ages 3 and 5 years, with the cblG defect in methylcobalamin synthesis. Both children presented with severe developmental delay, lethargy, anorexia, and megaloblastic anemia. The diagnosis of homocystinuria was delayed in each case due to difficulties with detection of small amounts of homocystine in physiologic samples. The clinical course of cblG disease is favorably altered by treatment with intramuscular hydroxycobalamin. Megaloblastosis in the presence of adequate supplies of cobalamin and folate in the blood must alert the clinician to the possibility of functional methionine synthase deficiency and should prompt a careful search for associated biochemical hallmarks, including homocystinuria/emia.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2000

Analysis of messy longitudinal data from a randomized clinical trial. MRC Lung Cancer Working Party.

The randomized clinical trial, LU19, conducted by the Medical Research Council Lung Cancer Working Party, was designed to compare ACE (doxorubicin, cyclophosphamide and etoposide) chemotherapy plus G-CSF (granulocyte colony-stimulating factor) at 2-week intervals versus ACE chemotherapy alone at standard 3-week intervals in patients with small-cell lung cancer. This trial investigated whether more intensive administration of ACE would improve overall survival and affect the quality of life of patients. The report on overall survival and other outcome measures will be published in the Journal of Clinical Oncology. In this paper we focus on methods of analysing aspects of data reflecting quality of life. Twelve symptoms of lung cancer and its treatment - cough, haemoptysis, pain, nausea, vomiting, hoarse voice, sore mouth, rash, lethargy, lack of appetite, alopecia, and dysphagia - were scheduled to be assessed on seven occasions for the ACE arm and on eight occasions for the ACE+G-CSF arm by clinicians during the first 18 weeks of the treatment period. However, in practice the number of assessment forms completed per patient ranged from 1 to 9, and assessment time-points were very different from those planned. These 'messy' longitudinal data are explored by both a summary measure approach, in which experience of a symptom is summarized by a single value, and an extensive model-based statistical approach, which explicitly takes into account correlation within repeated measures. These analyses provide a clear picture of symptom comparisons between the two treatments. The application of various methods offers not only an approach to assessing the robustness of the results but also a basis for investigating reasons for inconsistency of results across methods. We conclude that except lethargy, which is worse in the ACE+G-CSF arm, all symptoms are similar across the two arms during the treatment period.

Amsacrine↗
PubMed1990

Function of vitamin B12 in the central nervous system as revealed by congenital defects.

The 13 cases of methylcobalamin (MeCbl) deficiency presenting in early infancy have all been developmentally delayed, and the majority have had seizures, hypotonia, lethargy, and microcephaly. The CNS injury appears to occur during the first 6 months of postnatal life. The same symptoms are seen in acquired cobalamin (Cbl) deficiency in the same age group. MRI performed at age 18-19 months and after 13-14 months of large amounts of Cbl, in two cases showed delayed myelination, most pronounced in the cerebrum. Isolated MeCbl deficiency is the consequence of cblE and G mutations where the lesion is of a single Cbl-dependent enzyme, the methyltransferase. One effect of a deficiency of MeCbl, and of the associated failure of the methionine synthase reaction, is, therefore, an impairment of myelination of the brain of the newborn. The slow, but usually incomplete, improvement in psychomotor status after years of treatment with Cbl may be related to the eventual myelination. However, the hypotonia, lethargy, and impaired responsiveness react to treatment with Cbl within 24-48 hours, which suggests an expression of MeCbl deficiency on the CNS distinct from the delayed myelination. Although there is much to be learned, it is now clear that a normally functioning Cbl-dependent methyl transferase is required for development and function of the human brain.

Amino Acid Metabolism, Inborn Errors↗
PubMed2005

Neonatal toxicity and transient neurodevelopmental deficits following prenatal exposure to lithium: Another clinical report and a review of the literature.

I report the case of an infant girl who was exposed to lithium during gestation and her follow-up at the age of 1 year. She presented with transient neurodevelopmental deficits including lethargy, hypotonia, and poor oral feeding ability in the neonatal period. She required supportive treatment and made gradual improvement in neurologic functioning. On examination at the age of 1 year, physical findings and psychomotor development were normal. The English literature from 1978 to 2004 is reviewed. A total of 30 patients who were exposed to lithium during gestation with adequate clinical description were identified. A significant number of these babies presented with neurodevelopmental deficits and depressed neurological status including hypotonia, respiratory distress syndrome, cyanosis, lethargy, and weak suck and Moro reflexes in the neonatal period. The majority of these abnormalities resolved and most babies made full recovery. Other abnormalities were structural as well as functional involvement of the cardiovascular system, macrosomia, prematurity, jaundice, diabetes insipidus, and involvement of the thyroid gland. While the use of lithium during pregnancy does not appear to significantly increase the risk of congenital anomalies, it is frequently associated with perinatal complications and reversible neonatal toxicity. Suggested guidelines for appropriate monitoring of infants and breast-feeding of exposed babies are presented. In addition, prenatal surveillance of women with bipolar disorders who are being treated with lithium is briefly discussed.

Adult↗
PubMed1982

Valproate-induced hyperammonemia.

A patient with carbamyl phosphate synthetase deficiency had four episodes of hyperammonemia, up to 226 microM, associated with valproate (VPA) treatment. These were accompanied by vomiting, lethargy, and coma. A group of epileptic patients receiving VPA remained asymptomatic but had significantly higher mean plasma ammonium levels when compared to epileptic patients receiving other anticonvulsants: 33.6 +/- 1.9 (SEM) versus 23.6 +/- 1.5 microM. Thus, VPA caused symptomatic hyperammonemia in a patient with an impairment in urea synthesis and resulted in mildly elevated ammonium levels in epileptic patients. These data suggest that ammonium levels should be monitored in patients receiving VPA who exhibit signs of vomiting or lethargy.

Adolescent↗
PubMedDate not supplied

Visual evoked potentials in encephalopathy induced by galactosamine, ammonia, dimethyldisulfide, and octanoic acid.

Visual evoked potentials were utilized to examine the neuronal transmission changes provoked by galactosamine-induced hepatic encephalopathy and by administration in normal animals of toxins presumably involved in the pathogenesis of hepatic encepalopathy. Separate acute administrations of ammonia, dimethyldisulfide, and octanoic acid induced lethargy, convulsions in the case of the first two, and coma with visual-evoked potential patterns that never resembled the evoked potentials recorded in hepatic coma. By contrast, single and repeated administrations of the three above-mentioned toxins together at lower doses induced lethargy and coma with visual-evoked potential patterns similar to those observed in galactosamine-induced hepatic coma. These observations, together with previously published data, are consistent with the concept that the synergistic interaction of these toxins plays a significant role in the pathogenesis of hepatic encephalopathy.

Ammonia↗
PubMed2004

Isolation and characterization of pathogenic Vibrio alginolyticus from diseased cobia Rachycentron canadum.

Outbreaks of serious mortality among cultured juvenile cobia Rachycentron canadum L. (weighing 8-10 g) characterized by lethargy, dark skin and ascites in the peritoneal cavity while some fish possessing damaged eyes occurred in July and August of 2001 in Taiwan. Fifteen motile bacterial strains were isolated from head kidney and/or the ascites on tryptic soy agar supplemented with 1% NaCl (TSA1) and/or thiosulphate citrate bile salt (TCBS) sucrose agar plates during the two outbreaks. All the isolates were characterized and identified as Vibrio alginolyticus on the basis of biochemical characteristics, and comparisons with those of the reference strain V. alginolyticus ATCC 17749. The strain C3c01 (a representative of the 15 similar field isolates), was virulent to the cobia with an LD50 value of 3.28 x 10(4) colony forming units/g fish body weight. All the moribund/dead fish exhibited lethargy, dark skin and ascites in the peritoneal cavity as that observed in natural outbreaks. The same bacteria could be reisolated from kidney and the ascites of fish after bacterial challenge using TSA1 and TCBS plates. The results reveal that V. alginolyticus is an infectious agent of vibriosis in the cobia.

Animals↗
PubMed1996

Subchronic toxicity of 4-vinylcyclohexene in rats and mice by inhalation exposure.

This study was conducted to evaluate the subchronic toxicity of 4-vinylcyclohexene (VCH). Male and female Sprague-Dawley rats and B6C3F1 mice were exposed by inhalation to VCH 6 hr/day, 5 days/week for 13 weeks. Rats were exposed to 0, 250, 1000, or 1500 ppm, and mice were exposed to 0, 50, 250, or 1000 ppm. In addition, another group of rats and mice was exposed to 1000 ppm butadiene so that a comparison could be made between the two compounds. Exposure to 1000 ppm VCH resulted in deaths of all male mice and 5/10 female mice on Test Days 11 or 12. Three additional female mice exposed to 1000 ppm VCH died prior to study completion. The most notable compound-related clinical sign was lethargy observed in the 1500 ppm VCH-exposed rats and 1000 ppm VCH-exposed mice. Male rats exposed to 1500 ppm VCH had significantly lower body weights compared to controls, and male and female rats in the 1500 ppm group had significantly lower body weight gains. None of the VCH-exposed animals or butadiene-exposed rats showed any compound-related hematological effects. However, mice exposed to 1000 ppm butadiene exhibited mild macrocytic anemia. Clinical chemistry evaluation and urinalysis showed no compound-related effects in rats exposed to either VCH or butadiene. Male and female rats exposed to 1000 or 1500 ppm VCH or 1000 ppm butadiene had increased absolute and/or relative liver weights, and male rats in these same exposure groups had increased relative kidney weights. Microscopically, increased accumulation of hyaline droplets was observed in the kidneys of male rats from all VCH exposure groups. Although compound-related, the droplets were not accompanied by cytotoxicity. In mice, the most notable adverse histopathological effect was ovarian atrophy in females exposed to 1000 ppm VCH or 1000 ppm butadiene. The atrophy was slightly more severe in the VCH-exposed females than in the butadiene-exposed females. There were no other compound-related pathological effects in male or female mice exposed to VCH. Additionally, butadiene-exposed male mice had decreased testicular weights, accompanied by slight testicular degeneration and atrophy. For VCH exposure, the no-observed-adverse-effect-level is 1000 ppm for rats based on lethargy and lowered body weights and 250 ppm for mice based on mortality and ovarian atrophy.

Administration, Inhalation↗
PubMed1990

Phase II study of N-methylformamide (N-MF) (NSC 3051) in patients with advanced epithelial ovarian cancer. A Gynecologic Oncology Group study.

Forty-four patients with advanced, measurable, epithelial carcinoma of the ovary were treated with 97 courses of N-methylformamide (N-MF) at doses ranging from 600-800 mg/m2, intravenously, daily for 5 days every 28 days. Forty-one patients had prior surgery and had received one prior chemotherapy regimen. Only seven patients had received any prior radiation therapy. All patients were Gynecologic Oncology Group (GOG) performance status 0, 1, or 2. Three partial responses were seen. Hematologic adverse effects were extremely rare as predicted by early clinical trials. One major toxicity was a syndrome consisting of some combination of myalgias, arthralgias, pleuritic pain, abdominal pain, peripheral neuropathy, anorexia, lethargy, and declining performance status (pain-lethargy syndrome) that was reversible with discontinuation of the drug. This adverse effect was as common a reason as hepatic toxicity for discontinuation of N-MF. As reported in previous studies with this drug, hepatic toxicity was also common, usually reversible, and also a cause for discontinuation of the drug. The low level of clinical activity and the unpleasant adverse effects in this population of patients with previously treated ovarian cancer makes it unlikely that this drug will play any significant role in treatment of epithelial ovarian cancer.

Adult↗
PubMed2001

A phase I study of paclitaxel and altretamine as second-line therapy to cisplatin regimens for ovarian cancer.

PURPOSE: The efficacy and pharmacokinetics of paclitaxel when combined with altretamine for ovarian cancer were studied. METHODS: A group of 30 patients, whose only chemotherapy was one or more cisplatin-based non-paclitaxel-containing regimens and whose ovarian cancer failed to respond or had relapsed within 6 months of their last platinum regimen, received paclitaxel as a 3-h intravenous infusion and altretamine given orally in four divided doses daily for 14 days repeated every 28 days. Doses were escalated from paclitaxel/altretamine 135/150 mg/m2 to 250/300 mg/m2 in cohorts of three patients. RESULTS: The dose-limiting toxicities at 250/300 mg/m2 were WHO grade 3 myalgias and arthralgias in two patients and grade 3 lethargy, stomach cramps, peripheral neuropathy and vomiting in single patients. Considering all dose levels in cycle 1, 16 patients had grade 3 or 4 neutropenia but there was only one episode of febrile neutropenia. Other grade 3 toxicities were vomiting in four patients, myalgias in three, peripheral neuropathy in two and lethargy in two. Grade 3 alopecia occurred in 23 patients. Three patients achieved a complete response and 12 achieved a partial response for an overall objective response rate of 50%. Responses occurred at all dose levels of 175/150 mg/m2 and higher. The median freedom from progression was 35 weeks, with a median survival of 55 weeks. Altretamine did not alter the pharmacokinetics of paclitaxel and there were no consistent differences in paclitaxel pharmacokinetic parameters or toxicities between course 1 and 2. No dose-response relationships were evident above paclitaxel/altretamine 175/150 mg/m2. CONCLUSION: Paclitaxel and altretamine can be safely combined and with a high response rate in relapsed ovarian cancer, justifying further studies with this combination.

Administration, Oral↗
PubMed2005

Sudden death in children due to intracranial mass lesion.

STUDY OBJECTIVE: Intracranial causes of sudden and unexpected death in children are uncommon and are usually due to trauma, epilepsy or to catastrophic haemorrhage associated with neoplasms or vascular malformations. We sought to review the presenting symptoms and signs of intracranial mass lesions that led to sudden death to guide clinicians in early identification of these potentially treatable conditions. METHODS: All cases of sudden unexpected death attributed to intracranial mass lesion that occurred from 1996 to 2002 at the Oxford Radcliffe Hospitals, NHS Trust, were reviewed. RESULTS: During the study period, six children, aged between 10 weeks and 12 years, died suddenly with intracranial mass lesions other than haematomas. All of them were unsuspected of having a neurological disease prior to death. All patients were found to have an intracranial mass lesion. There were colloid cyst (n=2), glioblastoma multiform (n=1), primitive neuro-ectodermal tumour (n=1), pyogenic abscess (n=1) and histologically unverified tumour (n=1). Presenting features included headache and vomiting in four cases, vomiting longer than 1 week in three and lethargy in four cases. Three patients were misdiagnosed with viral illness. CONCLUSION: The case series highlights a life-threatening but misleading presentation of intracranial mass lesions. The diagnosis of viral illness should be made cautiously when headache and vomiting occur in the absence of focal complaints. A history of vomiting exceeding a few days duration warrants further investigation. Persistent lethargy should be considered a neurological rather than a non-specific clinical sign.

Brain Diseases↗
PubMed1986

Absent postprandial duodenal motility in a child with cystic fibrosis. Correction of the symptoms and manometric abnormality with cisapride.

A 19-mo-old boy with cystic fibrosis presented with a lifelong history of feeding problems and constipation, and an 8-mo history of episodes of repeated retching, diaphoresis, dehydration, and somnolence after eating. Tests of esophageal motility and gastric emptying of a 5% glucose meal were normal. Antroduodenal pressure recordings during fasting demonstrated the presence of all phases of the interdigestive motor complex. After consumption of a 240-ml complex liquid meal, however, the contractile pattern that generally accompanies eating was absent and gastric emptying was markedly delayed. When bethanechol or metoclopramide was given 10 min before the complex liquid meal, there was a paucity of contractile activity, gastric emptying was slow, and symptoms of lethargy, diaphoresis, and retching were present. When cisapride was given, there was frequent irregular contractile activity, faster gastric emptying, and no symptoms of lethargy. During the past year treatment with cisapride has been a requirement in order to prevent recurrence of the symptoms. Antroduodenal pressure studies proved helpful in the identification of a treatable manometric abnormality that was associated with symptoms of delayed gastric emptying.

Bethanechol↗
PubMed1976

Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys.

Mechanisms producing hypertriglyceridemia during bacterial sepsis have not been well defined. In this study lipid disposal mechanisms were assessed in 76 infected and 19 control male rhesus monkeys by the ability to dispose of triglycerides after: (1) oral lipid loading; (2) intravenous lipid loading; and (3) by lipolytic enzyme activity tests as measured by postheparin lipolytic activity (PHLA). Studies were performed both before and 48 hr after intravenous inoculation with either Salmonella typhimurium or Diplococcus pneumoniae when illness was uniformly severe and fasting serum triglyceride elevations were increased maximally. S. typhimurium-infected monkeys demonstrated significant fasting hypertriglyceridemia (p is less than 0.001), reduced clearance of orally and intravenously administered lipid and markedly reduced PHLA. During this gram-negative sepsis, mild lethargy, slight diarrhea, and a 2% mortality were observed. During D. pneumoniae sepsis, average fasting triglyceride concentrations were slightly, but not significantly elevated. While oral lipid clearance was impaired, intravenous lipid clearance was unimpaired, and PHLA was slightly reduced. Marked lethargy, agitation, and a 20% mortality were present during this gram-positive infection. Results of this study support the concept that an impairment of lipid disposal mechanisms, particularly during gram-negative sepsis with S. typhimurium, may significantly contribute to the observed hypertriglyceridemia.

Administration, Oral↗
PubMed1987

Toxicity of N-methyl-2-pyrrolidone (NMP): teratogenic, subchronic, and two-year inhalation studies.

Pregnant rats were exposed to N-methyl-2-pyrrolidone (NMP) at atmospheric concentrations of 0.1 and 0.36 mg/liter for 6 hr/day on Days 6 through 15 of gestation. Except for sporadic lethargy and irregular respiration in several rats the first 3 days of exposure, there were neither abnormal clinical signs nor pathological lesions in the maternal rats. Exposure did not affect either the outcome of pregnancy or embryonal growth rate. No abnormal development was detected in the vital organs and skeletons of the fetuses. Rats were exposed to an aerosol-vapor mixture of NMP at concentrations of 0, 0.1, 0.5, and 1.0 mg/liter for 6 hr/day, 5 days/week for 4 weeks. At 0.1 and 0.5 mg/liter exposure levels, rats did not show any significant clinical signs or pathological lesions. However, lethargy, respiratory difficulty, and excessive mortality were found in rats exposed to 1.0 mg/liter. These rats had focal pneumonia, bone marrow hypoplasia, and atrophy of lymphoid tissue in the spleen and thymus. These lesions were reversible in surviving rats following 2 weeks of recovery. Increases in the relative and absolute numbers of neutrophils were observed during exposure at 1.0 mg/liter, but returned to normal limits after 2 weeks of recovery. Rats were exposed to vapor of NMP at concentrations of 0, 0.04, or 0.4 mg/liter for 6 hr/day, 5 days/week for 2 years. Male rats at 0.4 mg/liter showed slightly reduced mean body weight. No life-shortening toxic or carcinogenic effects were observed in rats exposed for 2 years to 0.04 or 0.4 mg/liter of NMP.

Administration, Inhalation↗
PubMed1991

Acute and subchronic toxicity studies with detirelix, a luteinizing hormone-releasing hormone antagonist, in the rat and monkey.

Acute (single dose), 2-week, and 3-month toxicology studies were conducted with detirelix, a luteinizing hormone-releasing hormone (LHRH) antagonist, in rats and cynomolgus monkeys. Acute studies were conducted by intravenous and subcutaneous injection. Subchronic studies were conducted by daily subcutaneous injection. Clinical signs after a single intravenous dose included lethargy, edema, cyanosis, pallor, and red ears in rats at greater than or equal to 0.3 mg/kg and lethargy and facial flushing in monkeys at greater than or equal to 0.5 mg/kg. In subchronic studies, detirelix at greater than or equal to 0.4 mg/kg/day (rats) and at greater than or equal to 0.2 mg/kg/day (monkeys) produced atrophy of the reproductive organs, inhibition of ovulation and spermatogenesis, decreased body weight gain in male rats and monkeys, and increased body weight gain in female rats. In the rat, morbidity and/or mortality occurred throughout the treatment phase at a subcutaneous dose of greater than or equal to 2.0 mg/kg/day. In both species, the time to recovery of normal reproductive organ morphology and function was directly related to dose. Exogenous testosterone decreased the severity of reproductive and body weight effects in male rats. In conclusion, the acute effects of detirelix were consistent with peripheral vasodilation. Subchronic effects were associated with inhibition of pituitary gonadotropic and gonadal hormone secretion.

Animals↗
PubMed1985

Pediatric carbon monoxide toxicity.

We report a series of 28 pediatric carbon monoxide exposures. Sixteen patients (57%) were judged to have potentially toxic carboxyhemeglobin (COHb) levels (greater than 15%). In this group the range of COHb blood levels was 16.7% to 44.0% (mean = 26.5%). An unusually high incidence of syncope (56.3%, 9/16) and lethargy (68.7%, 11/16) was observed. Every patient with a COHb level greater than or equal to 24% experienced syncope; a marked departure from published adult values. Lethargy was reported at a mean COHb concentration of 25.9%. All patients with levels over 25% COHb, neurologic findings, acidosis, or syncope were considered candidates for hyperbaric oxygen therapy (HBOT). No morbidity from HBOT was encountered. Eighty-nine percent (25/28) of the patients are reportedly doing well, with no late sequelae identified. Delayed neurologic sequelae in three patients include chronic headaches, memory difficulties, or decline in school performance.

Adolescent↗
PubMedDate not supplied

Five-year multicenter retrospective review of cyclobenzaprine toxicity.

Cyclobenzaprine (CBP) has a cyclic structure similar to amitriptyline. In overdose, CBP has been suggested to produce the cardiovascular and neurologic toxicity found with the cyclic antidepressants. To examine this possibility, a retrospective chart review of all cases of CBP exposure reported to five regional poison centers was performed for the years 1989-93. There were a total of 750 charts identified for CBP exposure, of which 523 had data sufficient for evaluation. There were 121 polydrug ingestions leaving 402 pure CBP ingestions. Ages ranged from 7 mo to 77 yrs, with a mean of 20 yrs; 26% were 6 yrs or less. Females comprised 63% of the patient group. No deaths occurred. Dysrhythmias beyond sinus tachycardia were infrequent, and none were life-threatening. No seizures occurred. Common effects were lethargy, sinus tachycardia, and agitation, and both hypertension and hypotension were seen. All symptomatic cases with a known time of ingestion were symptomatic within 4 h of ingestion. Doses ingested ranged from 5-1000 mg, with a mean of 133 mg. Asymptomatic and symptomatic patients had a mean dose ingested of 45 mg and 183 mg, respectively. Treatment was primarily gastrointestinal (GI) decontamination and supportive care. Other therapies required were mechanical ventilation, dopamine, fluid bolus, sedation, and foley catheter. Symptoms requiring treatment beyond GI decontamination did not occur with ingestions less than 100 mg. In conclusion, cyclobenzaprine does not appear to produce the life-threatening cardiovascular or neurologic effects of the cyclic antidepressants in doses less than 1 g. Lethargy and anticholinergic effects are prominent, though serious toxicity is infrequent.

Adolescent↗
PubMedDate not supplied

Repetitive behaviors in autism: relationships with associated clinical features.

Relationships between repetitive behaviors (RBs) and associated clinical features (i.e., cognitive and adaptive functioning levels, sleep problems, medication use, and other behavioral problems) were examined in two groups (High nonverbal IQ > or = 97 versus Low nonverbal IQ < or = 56) of children with autism spectrum disorders (n = 14; mean age = 10 years, 7 months). For the group as a whole, nonverbal cognitive ability (NVIQ) (as measured by the Leiter-R), adaptive functioning level, the presence of sleep problems, and three scales of the Aberrant Behavior Checklist (ABC) (Irritability, Lethargy, and Hyperactivity) were highly correlated with total RB scores on the Repetitive Behavior Scale-Revised (RBS-R). After controlling for NVIQ, adaptive level, sleep problems, and two scales of the ABC (Irritability and Lethargy) were not significantly associated with RB scores. However, there remained a significant positive correlation between the presence of RBs and the Hyperactivity scale of the ABC. Parent ratings of their stress levels and the presence of RBs in their children were highly correlated. The relationship between RBs and associated clinical features in autism is complex and future studies should control for cognitive ability when examining the direct and indirect relationships of these variables with RBs.

Adaptation, Psychological↗