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PubMed1983

Inclusive fitness, altruism and family adaptation.

An integrative model of family functioning is put forward using a sociobiological framework. Three key sociobiological concepts that have a relevance to family interaction are inclusive fitness, altruism, and a struggle for status. The term 'inclusive fitness' encompasses the parents' own fitness and that of their kith and kin. Altruism refers to how parents promote the survival of their progeny and extended family. The struggle for status refers to a struggle for power and prestige. According to the author's hypothesis 'inclusive fitness' exerts its influence through the struggle for status which in turn influences the degree of altruism and the level of 'family adaptation'. The parents' level of inclusive fitness largely determines the level of family adaptation which in turn influences the growth and individuation of the next generation. A common negative outcome of failure in the struggle for status and power is a displacement of the struggle for power into a family context. Failure in a struggle for status between peer group members would in a pretechnological society probably have reflected a relative lack of fitness. Failure in the struggle for status is likely to generate maladaptive cycles in the family which will lower the inclusive fitness of the parents. A concept of ideal family functioning is derived from sociobiology and specifically related to a high inclusive fitness in the parents. The author argues that sociobiological concepts can contribute to the development of an integrative theory of family behaviour. The clinical implications of this model are explored.

Adaptation, Psychological↗

PubMedDate not supplied

Microvillous inclusion disease: report of a case with atypical features.

Microvillous inclusion disease is a rare lethal disorder characterized by intractable, severe, watery diarrhea beginning in early infancy. The underlying defect is thought to be an autosomal recessive genetic abnormality resulting in defective brush-border assembly and differentiation. Normally, this diagnosis is easily established through the electron microscopic demonstration of characteristic microvilli-lined inclusions lying within the apical cytoplasm of surface enterocytes. In a small number of patients appearing to have microvillous inclusion disease it has not proven possible to demonstrate the typical inclusions. The existence of another entity, termed intestinal microvillous dystrophy, has been proposed to account for such occurrences. This assertion was founded in large part upon the observation that the few subjects studied all displayed a slightly atypical clinical presentation. The case now being presented exhibited the morphologic features ascribed to intestinal microvillous dystrophy but had a clinical presentation that was entirely typical of microvillous inclusion disease. It serves thus to conceptually unite intestinal microvillous dystrophy with microvillous inclusion disease.

Colon↗

PubMed1992

Isolation and renaturation of bio-active proteins expressed in Escherichia coli as inclusion bodies.

Over-expression of recombinant proteins in Escherichia coli often results in the formation of insoluble and inactive material as inclusion bodies. Within the last years specific methods and strategies have been developed to produce bio-active proteins from these inclusion bodies. These methods include (i) isolation and purification of inclusion bodies, (ii) solubilization and reduction of the insoluble material, and (iii) renaturation of the proteins including formation of native disulphide bonds. Inclusion bodies are isolated from E. coli cells after desintegration of cells by mechanic forces. Due to their stability, inclusion bodies may be purified by washing with detergent solutions or low concentrations of denaturant. High concentrations of urea and guanidine hydrochloride are used in combination with reducing reagents such as 2-mercaptoethanol or dithiothreitol to reduce and solubilize proteins from inclusion bodies. After purification of solubilized materials, proteins are renatured and native disulphide bonds are formed by either air oxidation or glutathione reoxidation starting from reduced material, or by disulphide interchange starting from mixed disulphides containing peptides. Final yield of renatured proteins is raised by low concentrations of proteins and by adding low concentrations of denaturant during renaturation.

Animals↗

PubMed2004

[Studies on the preparation technology of beta-cyclodextrin inclusion compound for chuanxiong volatile oil extracted with CO2 supercritical fluid].

OBJECTIVE: To explore the preparation technology of beta-cyclodextrin inclusion compound for chuanxiong volatile oil. METHOD: Orthogonal test was used to evaluate the influence of the 4 factors, including the proportion of volatile oil to beta-cyclodextrin, the mode of mixing, inclusion temperature and mixing time. RESULT: The best inclusion condition is the proportion of volatile oil to beta-cyclodextrin 1:9, the mode of mixing grinding, inclusion temperature 60 degrees C and inclusion time 90 min. CONCLUSION: The best inclusion technology of chuanxiong volatile oil is confirmed.

Carbon Dioxide↗

PubMed2005

[Study of diffusion of muscone in different inclusion complexes and liposome through mouse (correction of rat) skin in vitro].

OBJECTIVE: To compare the penetrating rate of muscone in different inclusion complexes and liposome. METHOD: The transdermal effect of muscone in different inclusion complexes and liposome was studied comparatively on mouse [corrected] skin with 40% EtOH as the absorption solution and with an improved Franz diffuse cell. RESULT: Among the different inclusion complexes and liposome, the penetrating rate of muscone in the HP-beta-cyclodextrin inclusion and the liposome were higher than muscone, and that of muscone in the beta-cyclodextrin inclusion is the lowest. CONCLUSION: The HP-beta-cyclodextrin inclusion and the liposome can hence the muscone transdermal speed.

2-Hydroxypropyl-beta-cyclodextrin↗

PubMed2006

[Study on the characterizations of beta-cyclodextrin-benzoylferrocene-thiosemicarbazone inclusion complex and micro-environmental effects].

Inclusion complex of benzoylferrocene-thiosemicarbazone (TBF) with beta-cyclodextrin (beta-CD) was prepared by using kneading method. Continuous variation plot proved that 2:3 (TBF: beta-CD) inclusion complex has been formed. The characterizations of the inclusion complex were studied by UV, FTIR and X-ray diffractometry. By using the data of UV spectroscopy, the binding constant of the inclusion compound was estimated to be 5.04 x 10(13) (L4 x (mol)(-4)), and its change in absorption with time was studied. The stability of inclusion is obviously greater than the guest molecule. Furthermore, the influences of different solvents and pH on the UV spectra of TBF and beta-CD-TBF were discussed respectively. The results show that different micro-environments have apparently different effects on electric spectra of guest and inclusion complexes.

English Abstract↗

PubMed2006

[Study on the inclusion behavior of p-sulphonatocalix[4]arene with acridine by spectrofluorometric titrations].

p-sulphonatocalix[4] arene (1) was prepared according to the literature, and spectrofluorometric titrations were performed to investigate the inclusion behavior of (1) and acridine in citrate buffer solution (pH 5.92, 0.1 mol x L(-1)) at different temperatures. It was found that in definite concentration range, the emission peak of acridine exhibited a slight red shift and th fluorescence intensity decreased when (1) was added. They form stable host-guest complex, and the stoichiometry of the inclusion complex is 1 : 1. The stability constants of the inclusion complex at 15.0 degrees C, 20.0, 25.0 and 30.0 degrees C were determined as 3.08 x 10(5), 4.45 x 10(4), 2.58 x 10(4) and 8.90 x 10(3), respectively. The thermodynamic parameters of inclusion process, deltaG, deltaH and deltaS, were determined. The experimental results indicated that the inclusion process was an exothermic and enthalpy-driven process. It was found that the stability constants descended when temperature rose. The most probable pattern of the inclusion complex between (1) and acridine was proposed as: acridine partially goes into the cavity of (1), and the protonated N atom and the negatively charged sulphonyl group bond firmly owing to strong electrostatic interaction. With the main contribution of electrostatic interaction and the assistance of Van de Waals and hydrophobic interaction, the host and the guest molecules form 1 : 1 supramolecular complex.

English Abstract↗

PubMed1987

Morphologic study of inclusions in tissues from pigs inoculated with cytomegalovirus.

Six 5-day-old gnotobiotic pigs inoculated intranasally with the J-1 strain of porcine cytomegalovirus (PCMV) were euthanatized within 9 to 18 days after inoculation. All pigs developed a subclinical form of PCMV infection and had characteristic intranuclear inclusions in all tissues. Morphologically, 2 types of inclusions were observed. One was a small herpetic intranuclear inclusion in reticuloendothelial cells, which contained a few nucleocapsids in the nucleus. The other was a typical cytomegalic intranuclear inclusion in macrophages in the lungs and in tubuloalveolar gland cells in the nasal mucosa. Inclusions contained many nucleocapsides in the nucleus and a large number of enveloped viral particles in the cytoplasm. The distribution of the specific immunofluorescent antigen of PCMV was coincident with the presence of herpetic and cytomegalic inclusions.

Animals↗

PubMed1996

An intron splicing enhancer containing a G-rich repeat facilitates inclusion of a vertebrate micro-exon.

The average length of a vertebrate axon is approximately 130 nt. Decreasing the size of an internal axon to less than 51 nt induces axon skipping, implying a minimal size for exons. A few constitutively included internal exons, however, are extremely small. To investigate if such micro-exons require special mechanisms for their inclusion, we studied the sequences necessary for inclusion of a 6-nt axon from chicken cardiac troponin T (cTNT). In vivo, the cTNT micro-exon was not included in mRNA unless accompanied by a 134-nt sequence located next to the micro-exon in the downstream intron. Increasing the length of the micro-exon alleviated the requirement for the intron element, indicating that the lack of inclusion of the micro-exon in the absence of a facilitating sequence was due to its small size, rather than suboptimal splice sites. The intron element contained six copies of a G-rich 7-nt sequence. Multimers of the repeat supported exon inclusion, indicating that the repeat sequence is an important part of the intron element. The entire intron element activated inclusion of a heterologous 7-nt exon, suggesting that the intron element is a general enhancer for the splicing of micro-exons. In vitro, the intron element and the repeated sequence facilitated splicing of a heterologous exon. Because of the ability of the cTNT intron element to facilitate the splicing of heterologous exons, we have termed the element an intron splicing enhancer (ISE). Interestingly, the ISE demonstrated position independence in that it facilitated inclusion of the heterologous micro-exon when placed either upstream or downstream of the micro-exon. In vitro, the ISE or copies of the ISE G-rich repeat stimulated splicing of an adjacent intron. The ISE thus becomes one of only a few characterized ISEs containing a G-rich repeat and the first to work both upstream and downstream of a target axon.

3T3 Cells↗

PubMed1997

Attitudes toward the use of gender-inclusive language among residency trainees. The McMaster Residency Training Program Directors.

OBJECTIVE: To explore postgraduate medical trainees' attitudes toward the use of gender-inclusive language. DESIGN: Self-administered questionnaire. SETTING: Seven residency training programs at McMaster University, Hamilton, Ont., from July 1993 to June 1994. PARTICIPANTS: Of 225 residents in the programs, 186 responded to the survey, for a response rate of 82.7%. Men and women were equally represented among the respondents. OUTCOME MEASURES: Categorization of attitudes about the use of language as gender-inclusive or gender-exclusive; characteristics predicting a gender-inclusive attitude. RESULTS: Factor analysis and Cronbach's alpha (0.90) supported the existence of a construct related to attitudes about language use, the poles of which were categorized as gender-inclusive and gender-exclusive. The authors classified residents with respect to their attitudes to language use from their responses to the questionnaire. In univariate analyses, sex, residency program and country of graduation significantly predicted a gender-inclusive attitude (p < 0.01). Only the first 2 variables were significant in a multivariate model; residency program explained 18% of the variance and sex 3%. Residents in obstetrics and gynecology and psychiatry had the most gender-inclusive attitudes, whereas residents in surgery and anesthesia had the most gender-exclusive attitudes. CONCLUSIONS: Residents' values are reflected in the language they choose to use. Language use may provide an index of underlying attitudes that may create hostile environments for female trainees.

Adult↗

PubMed1993

Biotin-containing intranuclear inclusions in endometrial glands during gestation and puerperium.

Intranuclear inclusions sometimes are observed in endometrial glands, especially during puerperium, and superficially they resemble those from herpesvirus-infected cells. To study the significance of the inclusions, endometrial and placental tissue from 215 subjects, including 69 pregnancy-associated samples, were examined. With screening by peroxidase-labeled avidin alone, followed by the peroxidase reaction, only pregnancy-related endometrium (in 32 cases) demonstrated reactivity in the intranuclear inclusions. These intranuclear inclusions demonstrated positive immunostaining for biotin using the peroxidase-antiperoxidase method in all but six cases, whereas there was no reaction for Herpes simplex in any of the cases. The endometrial tissues of the 32 cases were obtained from the 16th gestational week to the 37th postpartum day. Although the histogenesis of these intranuclear inclusions has not been clarified, they should not be mistaken for those in endometrial cells infected by herpesvirus because of intranuclear biotin and a false-positive histochemical reaction in the avidin-biotin-peroxidase complex method.

Biotin↗

PubMed1985

Inclusions in equine cytologic specimens.

Inclusions and cellular changes were seen in cytologic specimens from 1 healthy horse, 6 horses hospitalized because of respiratory problems, and 1 horse hospitalized because of colic and hepatitis. Two bronchial aspirates contained detached ciliated cytoplasmic tufts and cytoplasmic inclusions characteristic of the specific degenerative process called ciliocytophthoria. These changes and inclusions resembled those seen in bronchial aspirates from human beings with parainfluenza virus infection. Four bronchial aspirates and 2 serous fluid specimens had nuclear inclusions resembling those seen in a variety of specimens from human beings with herpetic infections. The abnormalities and inclusions were similar to changes seen in cell monolayer and suspension cultures infected with equine herpesvirus type 1.

Animals↗

PubMed2001

Inclusion body myositis mimicking motor neuron disease.

OBJECTIVE: To describe the clinical and electrophysiologic features of patients with inclusion body myositis that was misinterpreted as motor neuron disease. PATIENTS AND METHODS: We retrospectively retrieved the medical records of 70 patients with a pathologic diagnosis of inclusion body myositis. From this group, we selected those who had been first diagnosed as having motor neuron disease or amyotrophic lateral sclerosis. We reviewed the clinical, electrophysiologic, laboratory, and morphologic studies. RESULTS: Nine (13%) of 70 patients with inclusion body myositis had been diagnosed as having motor neuron disease. Six of the 9 patients had asymmetric weakness; in 4 the distal arm muscles were affected. Eight patients had finger flexor weakness. Tendon reflexes were preserved in weak limbs in 6, hyperactive in 2, and absent in 1. Four patients had dysphagia. Fasciculation was seen in 2 patients. None had definite upper motor neuron signs or muscle cramps. Routine electromyographic studies showed fibrillation potentials and positive sharp waves in all 9. Fasciculation potentials were seen in 7 and long-duration polyphasic motor unit potentials were seen in 8. There was no evidence of a myogenic disorder in these 9 patients. Muscle biopsy was done because of slow progression or prominent weakness of the finger flexors and was diagnostic of inclusion body myositis. A quantitative electromyogram was myopathic in 4 of the 5 patients studied. CONCLUSIONS: Inclusion body myositis may mimic motor neuron disease. Muscle biopsy and quantitative electromyographic analysis are indicated in patients with atypical motor neuron disease, especially those with slow progression or early and disproportionate weakness of the finger flexors.

Aged↗

PubMed1992

Management of dysphagia in inclusion body myositis.

Inclusion body myositis is an inflammatory myopathy in which dysphagia has been considered a rare finding. However, recent literature finds dysphagia an increasingly common symptom as more cases of inclusion body myositis are identified. Unlike some inflammatory myopathic disorders, inclusion body myositis is resistant to treatment with corticosteroids, and therefore, the otolaryngologist may be consulted regarding surgical options for relief of dysphagia. A patient is described in whom severe progressive dysphagia associated with inclusion body myositis developed. Impaired pharyngeal wall motion and cricopharyngeal achalasia were demonstrated by videofluoroscopic evaluation, and the patient was successfully treated by cricopharyngeal myotomy. The pathophysiologic nature of inclusion body myositis and the mechanisms of cervical dysphagia in the inflammatory myopathies are reviewed.

Aged↗

PubMed2000

Neuronal intranuclear inclusion disease and juvenile parkinsonism.

Juvenile parkinsonism (onset age <20 yrs) is uncommon and few cases with neuropathologic confirmation have been reported. We present the case of a 17-year-old boy who presented with asymmetric arm tremor and bulbar symptoms. His paternal great aunt had parkinsonism with onset at age 22 years. Examination revealed parkinsonism in the absence of additional neurologic signs except for delayed pupillary responses to light. He responded well to levodopa but developed motor fluctuations and disabling dyskinesias after 3 years of treatment. Following attempted withdrawal of levodopa at age 24 years, he developed severe aspiration pneumonia complicated by cardiorepiratory arrests and he died 6 months later. At autopsy, the dominant histologic feature was wide-spread neuronal hyaline intranuclear inclusions. Neuronal depletion was observed in the substantia nigra, locus ceruleus, and, to a lesser extent, in the frontal cortex, and inclusions were particularly prominent in these areas. Inclusions were immunoreactive for ubiquitin and were typical of those seen in neuronal intranuclear inclusion disease (NIID), a rare, multisytem neurodegenerative disease. NIID should be considered in the differential diagnosis of juvenile parkinsonism. A link between NIID and hereditary neurodegenerative disorders characterized by expanded polyglutamine tracts is supported by the similar appearance of intranuclear inclusions in both conditions and by a family history in some cases of NIID.

Adolescent↗

PubMed2002

Accumulation of 14-3-3 proteins in glial cytoplasmic inclusions in multiple system atrophy.

Glial cytoplasmic inclusions are the pathological hallmark of multiple system atrophy. However, the molecular mechanisms underlying the formation of glial cytoplasmic inclusions remain unclear. Alpha-synuclein, a major component of glial cytoplasmic inclusions, has the ability to interact with 14-3-3 proteins, which mediate several types of signal transduction pathways. To elucidate the role of these 14-3-3 proteins in patients with multiple system atrophy, we performed immunohistochemical studies on 14-3-3 in brain tissue specimens from 7 control subjects and from 15 patients with multiple system atrophy. In both control and multiple system atrophy cases, 14-3-3 immunoreactivity was observed mainly in the neuronal somata and proximal processes, as well as the nerve fibers. Even in the severely affected regions of patients with multiple system atrophy, 14-3-3 immunoreactivity generally was spared in the surviving neurons, some of which were strongly immunolabeled. In addition, numerous glial cytoplasmic inclusions were intensely immunostained, and neuronal cytoplasmic inclusions and dystrophic neurites were also immunoreactive for 14-3-3. Our results suggest that an aberrant accumulation of 14-3-3 proteins may occur in brains affected by multiple system atrophy, and that 14-3-3 proteins may be associated with the pathogenesis of multiple system atrophy.

14-3-3 Proteins↗

PubMed2003

Ribonuclear inclusions in skeletal muscle in myotonic dystrophy types 1 and 2.

Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are caused by genomic expansions of CTG or CCTG repeats. When transcribed, these mutations give rise to repeat expansion RNAs that form nuclear inclusions and compromise the function of myonuclei. Here, we have used in situ hybridization and immunofluorescence to compare DM1 and DM2 and search for proteins that associate with the RNA nuclear (ribonuclear) inclusions. Although muscle disease is generally more severe in DM1, the ribonuclear inclusions were 8- to 13-fold more intense in DM2, implying greater amounts of repeat expansion RNA. Expression of repeat expansion RNA in myoblasts has been implicated in the pathogenesis of congenital DM1. However, we found that repeat expansion RNA is also expressed in myoblasts in DM2, a disorder that has not been associated with a congenital phenotype. Of 10 putative CUG binding proteins tested for colocalization with mutant RNA, only proteins in the muscleblind family were recruited into ribonuclear inclusions. Previous studies have shown activation of the protein kinase, PKR, by expanded CUG repeats in vitro. However, breeding experiments utilizing PKR knockout mice indicate that this kinase is not required for disease pathogenesis in a transgenic mouse model of DM1. We conclude that ribonuclear inclusions are a key feature of the muscle pathology in DM and that sequestration of muscleblind proteins may have a direct role in the disease process.

Animals↗

PubMed1984

Neurofilament subunit--related proteins in neuronal intranuclear inclusions.

Well-preserved nuclei were isolated from the brain of a patient with neuronal intranuclear inclusion disease ( NIID ). The inclusions in situ stained for proteins and, by immunohistochemical techniques, for the 200K and 68K components of the neurofilament protein triplet but were negative for the 145K neurofilament protein. At the electron microscopic level the inclusions were seen to consist of straight, randomly arranged tubular filaments 8.5 to 9.5 nm in diameter. They were resistant to extraction with hot buffer containing sodium dodecyl sulfate (SDS) and 2-mercaptoethanol, indicating that the proteins of NIID inclusions are probably cross-linked by covalent bonds other than disulfide. This feature is also exhibited by the paired helical filaments occurring in brain in Alzheimer's disease. No major differences were found in the polypeptide composition of nuclei in NIID and control nuclei resolved by SDS-polyacrylamide gel electrophoresis. The inclusions isolated from SDS-extracted nuclei were shown by immunohistochemical techniques to stain for all three neurofilament subunits, indicating that 145K -related antigenic sites were uncovered during the extraction procedure.

Aged↗