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PubMed1992

The early and late processing of lysosomal enzymes: proteolysis and compartmentation.

Lysosomal enzymes are subjected to a number of modifications including carbohydrate restructuring and proteolytic maturation. Some of these reactions support lysosomal targeting, others are necessary for activation or keeping the enzyme inactive before being segregated, while still others may be adventitious. The non-segregated fraction of the enzyme is secreted and can be isolated from the medium. It is considered that the secreted lysosomal enzymes fulfill certain physiological and pathophysiological roles. By comparing the secreted and the intracellular enzymes it is possible to distinguish between the reactions that occur before and after the segregation. In this review the reactions that may influence the segregation are referred to as the early processing and those characteristic for the enzymes isolated from lysosomal compartments as the late processing. The early processing is characterized mainly by modifications of carbohydrate side chains. In the late processing, proteolytic fragmentation represents the most conspicuous changes. The review focuses on the compartmentation of the reactions and the proteolytic fragmentation of lysosomal enzyme precursors. While a plethora of proteolytic reactions are involved, our knowledge of the proteinases responsible for the particular maturation reactions remains very limited. The review points also to work with cells from patients affected with lysosomal storage disorders, which contributed to our understanding of the lysosomal apparatus.

Animals↗

PubMed1996

Insect hormones in vertebrates: anabolic effects of 20-hydroxyecdysone in Japanese quail.

Ecdysteroids are hormones controlling cell proliferation, growth and the developmental cycles of insects and other invertebrates. They are occasionally present in various unrelated plants for no apparent reason; no phytohormonal function has yet been identified. In certain cases, ecdysteroids are accumulated to high levels in leaves, roots or seeds. Some ecdysteroid-containing plants have been known as medicinal plants for centuries. One of them, Leuzea carthamoides Iljin (Asteraceae), growing in Central Asia, contains 0.4% ecdysteroid in dry roots and 2% in seeds. A pharmacological preparation from this plant, "Ecdisten', is already available as a commercial preparation for its anabolic, tonic and other effects, for medical use (review). It remained problematic, however, whether ecdysteroids were truly responsible for these effects, because Leuzea contains a number of other biologically active compounds in addition to ecdysteroids. We extracted and purified ecdysteroids from the seeds of Leuzea. With 6 g of 96% 20-hydroxyecdysone (20E), we made a large-scale feeding assay with Japanese quail to find out whether ecdysteroid alone could duplicate the anabolic effects of the seeds. We found that the 96% ecdysteroid increased the mass of the developing quails in a dose-dependent manner, with the rate of increase proportional to the ecdysteroid content in the seeds; there was a 115% increase in living mass with 100 mg kg-1 of pure 20E compared with 109.5% increase with 100-180 mg kg-1 20E equivalents in the seeds. We conclude that the plethora of growth-promoting, vitamin-like effects induced in vertebrates by Leuzea is mediated by ecdysteroids.

Animals↗

PubMedDate not supplied

Burn depth: a review.

Despite the plethora of technologic advances, the most common technique for diagnosing burn depth remains the clinical assessment of an experienced burn surgeon. It is clear that this assessment is accurate for very deep and very shallow burns. But since clinical judgment is not precise in telling whether a dermal burn will heal in 3 weeks, efforts to develop a burn depth indicator are certainly warranted to accurately determine which dermal burns to excise and graft. This review summarizes the considerable literature in which a variety of techniques to determine burn depth have been used.

Animals↗

PubMed1990

Sexually transmitted diseases of the colon, rectum, and anus. The challenge of the nineties.

During the past two decades, an explosive growth in both the prevalence and types of sexually transmitted diseases has occurred. Up to 55 percent of homosexual men with anorectal complaints have gonorrhea; 80 percent of the patients with syphilis are homosexuals. Chlamydia is found in 15 percent of asymptomatic homosexual men, and up to one third of homosexuals have active anorectal herpes simplex virus. In addition, a host of parasites, bacterial, viral, and protozoan are all rampant in the homosexual population. Furthermore, the global epidemic of AIDS has produced a plethora of colorectal manifestations. Acute cytomegalovirus ileocolitis is the most common indication for emergency abdominal surgery in the homosexual AIDS population. Along with cryptosporidia and isospora, the patient may present to the colorectal surgeon with bloody diarrhea and weight loss before the diagnosis of human immunodeficiency virus (HIV) disease. Other patients may present with colorectal Kaposi's sarcoma or anorectal lymphoma, and consequently will be found to have seropositivity for HIV. However, in addition to these protean manifestations, one third of patients with AIDS consult the colorectal surgeon with either condylomata acuminata, anorectal sepsis, or proctitis before the diagnosis of HIV disease. Although aggressive anorectal surgery is associated with reasonable surgical results in some asymptomatic HIV positive patients, the same procedures in AIDS (symptomatic HIV positive) patients will often be met with disastrous results. It is incumbent upon the surgeon, therefore, to recognize the manifestations of HIV disease and diagnose these conditions accordingly.

Acquired Immunodeficiency Syndrome↗

PubMed1996

cAMP inhibits bud growth in a yeast strain compromised for Ca2+ influx into the Golgi.

Biochemical and physiological studies have implicated cAMP and cAMP-dependent protein kinase (PKA) in a plethora of essential cellular processes. Here we show that yeast cells partially depleted of PKA activity (due to a tpkw mutation) and bearing a lesion in a Golgi-localized Ca2+ pump (Pmr1), arrest division with a small bud. The bud morphology of the arrested tpk1w pmr1 mutant cells is characteristic of cells in S phase; however, the terminal phenotype of processes such as DNA replication and nuclear division suggests arrest at the G2/M boundary. This small bud, G2-arrest phenotype is similar to that of strains with a defect in cell wall biosynthesis (pkc1) or membrane biogenesis (och1); however, the biochemical defect may be different since the tpk1w pmr1 double mutants retain viability. The growth defect of the tpk1w pmr1 mutant can be alleviated by preventing the increase in cellular cAMP levels that is known to be associated with a decrease in PKA activity, or by supplementing the medium with millimolar amounts of Ca2+. Although the biochemical consequences of this increase in cAMP concentration are not known, the small-bud phenotype of the double mutant and the known protein processing defect of the pmr1 lesion suggest that the localization or function of some membrane component might be compromised and susceptible to perturbations in cellular cAMP levels. One candidate for such a protein is the cAMP-binding membrane ectoprotein recently described in yeast.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1993

Linkage studies of psychiatric disorders.

Linkage analysis has been successful in identifying the genetic basis of numerous Mendelian diseases. These successes were due in part to the rapid developments in molecular biology, which have yielded a plethora of informative genetic markers. Although there is strong evidence that the manifestation of schizophrenia and bipolar affective disorders is controlled by genes, no evidence for linkage has been established. For psychiatric disorders, the most important limiting factor is likely to be the lack of single loci with very large effects that occur with any relevant frequency. The difficulties of linkage studies in psychiatric disorders are discussed with reference to non-psychiatric genetic diseases for which linkage to genetic markers has been successful. Recommendations for collecting information to clarify the patterns of transmission of the psychiatric disorders are described.

Genetic Linkage↗

PubMed1996

Pathological anatomy in the teaching of rheumatology.

Whereas rheumatology regroups nosological entities, its teaching must be partly based on a presentation of the corresponding anatomopathological aspects which in fact are various patchworks made up of elementary, generally nonspecific lesions of osteoarticular pathology. Such an approach will provide an objective guideline between the needs of the practitioner (who often thinks in terms of morphology through radiological images) and the plethora of modern basic data. Thus the methods can be adapted to the needs of various audiences (medical students, specialists in training, paramedical personnel) and to every material and financial possibilities. In all cases it must be integrated with clinical and radiological lectures, based on macroscopic and radiological correlations and complemented, as far as possible, with appropriate histological images.

Education, Medical↗

PubMed1993

Electrophysiological, biochemical and behavioral evidence for 5-HT2 and 5-HT3 mediated control of dopaminergic function.

Several lines of evidence have suggested a link between serotonergic and dopaminergic systems in the brain. The interpretation of much of these early data needs careful reevaluation in light of the recent understanding of the plethora of serotonin receptor subtypes, their distribution in the brain and the new findings with more selective serotonin antagonists. Electrophysiological, biochemical and behavioral evidence obtained using highly selective antagonists of the 5-HT2 or 5-HT3 receptor subtypes, MDL 100,907 or MDL 73,147EF, respectively, supports the thesis that serotonin modulates the dopaminergic system. This modulation is most evident when the dopaminergic system has been activated.

Animals↗

PubMed1997

Nitric oxide signaling in invertebrates.

Nitric oxide (NO) is an unconventional neurotransmitter and neuromodulator molecule that is increasingly found to have important signaling functions in animals from nematodes to mammals. NO signaling mechanisms in the past were identified largely through experiments on mammals, after the discovery of NO's vasodilatory functions. The use of gene knock out mice has been particularly important in revealing the functions of the several isoforms of nitric oxide synthase (NOS), the enzyme that produces NO. Recent studies have revealed rich diversity in NO signaling. In addition to the well-established pathway in which NO activates guanylyl cyclase and cGMP production, redox mechanisms involving protein nitrosylation are important contributors to modulation of neurotransmitter release and reception. NO signaling studies in invertebrates are now generating a wealth of comparative information. Invertebrate NOS isoforms have been identified in insects and molluscs, and the conserved and variable amino acid sequences evaluated. Calcium-calmodulin dependence and cofactor requirements are conserved. NADPH diaphorase studies show that NOS is found in echinoderms, coelenterates, nematodes, annelids, insects, crustaceans and molluscs. Accumulating evidence reveals that NO is used as an orthograde transmitter and cotransmitter, and as a modulator of conventional transmitter release. NO appears to be used in diverse animals for certain neuronal functions, such as chemosensory signaling, learning, and development, suggesting that these NO functions have been conserved during evolution. The discovery of NO's diverse and unconventional signaling functions has stimulated a plethora of enthusiastic investigations into its uses. We can anticipate the discovery of many more interesting and some surprising NO signaling functions.

Animals↗

PubMed1991

Bioactions of 5-hydroxyicosatetraenoate and its interaction with platelet-activating factor.

In a variety of stimulated cells, platelet-activating factor (PAF) and numerous arachidonate derivatives are co-products that form as a consequence of receptor-mediated phospholipid mobilization. These lipid co-products produce a plethora of biological effects in a wide variety of cell systems. Furthermore, they often have a fascinating although less widely appreciated, interaction. 5-HETE, at submicromolar concentrations, exerts relatively few direct bioactions. It does, however, potently (16-160 nM) raise cytosolic free calcium [Ca2+]i and augment PAF-induced responses in human polymorphonuclear neutrophils (PMN) by as much as 100- to 1000-fold. 5-HETE acts on PMN by a structurally specific, stereospecific and pertussis toxin-inhibitable mechanism. In addition, PMN exposed to 5-HETE exhibit homologous but not heterologous desensitization. These findings suggest that 5-HETE, like PAF, may bind to its own specific plasmalemmal receptors to exert its unique set of bioactions. However, further investigation is required to demonstrate any putative 5-HETE receptors. Other potential mechanisms of 5-HETE-induced bioactions together with the possible effects of 5-HETE on PAF transduction mechanisms are also discussed.

Animals↗

PubMedDate not supplied

The S-R information stream: where's the filter?

Pavlovian conditioning procedures, in which events such as tastes, lights, and sounds become predictors of food, water, and shocks, have been used for studying the role of the information filter in the selection of conditioned responses. Different models posit the filter at different locations in the S-R stream, but most models suggest either a pre-encoding filter, in which much information is discarded at an early stage of processing, or a post-encoding filter, in which the information is stored but not subsequently expressed in behavior. A selective review of the literature on cue-competition effects reveals a plethora of phenomena that support a post-encoding, but not a pre-encoding filter in Pavlovian processes.

Animals↗

PubMed1990

Chronic lung disease in the sleep apnea syndrome.

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.

Humans↗

PubMed2004

Genetics of deafness in India.

Linkage analysis in families with hereditary hearing loss have revealed a plethora of chromosomal locations linked to deafness reflecting the extreme heterogeneity of the disorder. 40 of the genes contained within these loci have been mapped lending an insight into the diverse molecules operating in the inner ear and the remarkable complexity of the cellular and molecular processes involved in the transucdation of sound in the auditory system. Among this diversity, Connexin 26 has been found to be the most common cause of deafness the world around. The authors review here the prevalence of this gene in the Indian population as found in their study, together with other deafness genes segregating non-syndromic deafness, accounting for approximately 40% of all cases. This indicates there are several more to be identified yet. Knowledge of the genetic cause of deafness in our families is important for accurate genetic counseling and early diagnosis for timely intervention and treatment options.

Connexin 26↗

PubMedDate not supplied

Inhibition by metals of X-ray and ultraviolet-induced DNA repair in human cells.

A number of metals have been shown to be involved in the etiology of animal and human neoplasms. The molecular mechanisms have not yet been determined, but the observed plethora of genetic effects observed following treatment of mammalian cells with metals clearly indicates the possibility that metals can exert their effects at least partially at the level of DNA metabolism. Several studies have suggested that metal treatment may inhibit normal DNA repair processes in procaryotic and eucaryotic cells but a systematic study of this question has not previously been conducted. The present study surveyed the ability of 15 metal salts to interfere with repair of X-ray or UV-induced DNA damage in HeLa cells. Hg+(+), As++(+), Cu+(+), Ni+(+), Co+(+), and Cd+(+) were shown to inhibit the excision of pyrimidine dimers from DNA and to do so in a dose-dependent fashion. Inhibition of repair by only Ni+(+) and Co+(+) resulted in the accumulation of long-lived DNA strand breaks suggestive of a block in the gap-filling stage of repair. Ability to inhibit repair was not correlated with cytotoxicity. X-ray repair was sensitive to Hg+(+), Ni+(+), As++(+), Ga+(+), Zn+(+), and Mo(VI). All inhibitory metals inhibited closure of single strand DNA breaks. Ga+(+) appeared, in addition, to inhibit a later step involving chromatin reconstitution. These findings support the notion that interference of DNA repair processes may be a consequence of exposure of mammalian cells to certain metals. This may be a factor in the etiology of metal-associated carcinogenesis.

Cells↗

PubMed2006

Polycythemia as the first manifestation of Cushing's disease.

A 39-yr-old man presented to our hospital with unexplained erythrocytosis and hypertension. His follow-up for erythrocytosis had begun 2 yr earlier in another hospital and he had been diagnosed with polycythemia rubra vera. On admission to our hospital he was hypertensive (165/95 mmHg) and, except for the presence of moon-like face and facial plethora, his physical examination was normal. His hemoglobin concentration was 19.2 g/dl, and hematocrit was 58.9% with an increased red blood cell mass of 58 ml/kg as measured by radioisotope (Cr51). Blood film, other hematological indices except for elevated leukocyte alkaline phosphatase score, arterial gas analysis, and examination of aspirated bone marrow were all normal. An abdominal ultrasonography showed no evidence of splenomegaly. A diagnosis of probable secondary erythrocytosis was made. Early-morning serum cortisol and 24-h urinary free cortisol concentration as well as serum ACTH were high. Serum cortisol was not suppressed by low-dose dexamethasone, but suppressed by high-dose dexamethasone. Pituitary magnetic resonance imaging showed no lesion. After inferior petrosal sinus sampling suggesting right-central ACTH secretion, the patient underwent transnasal-transsphenoidal pituitary adenomectomy. Both hypercortisolemia and erythrocytosis regressed completely after the adenomectomy. After the operation, the patient's hemoglobin concentration and hematocrit decreased steadily, and 1 month post-adenomectomy his hemoglobin is 14.9 g/dl and hematocrit 44.8%. Thus, Cushing's syndrome should be a routine part of evaluation of unexplained polycythemia.

Adult↗

PubMed2005

A six month mitotane course induced sustained correction of hypercortisolism in a young woman with PPNAD and Carney complex.

A low-dose mitotane (MT) regimen was evaluated as a pharmacological approach for correcting the severe hypercortisolism in a young woman affected by Carney complex (CNC) and primary pigmented nodular adrenocortical disease (PPNAD). In the first 12 week period, the MT daily dose was progressively increased from 0.5 to 4.0 g/day. This dosage was maintained for an additional 16 weeks (cumulative dose 602 g, plasma MT maximum level 12 microg/ml), and then stopped because of sustained signs of hypoadrenalism requiring prednisone replacement. Complete regression of seborrhea, acne, and plethora was observed after 8 weeks of treatment (cumulative dose 95 g). Regular menses returned after 13 weeks (cumulative dose 197 g, plasma MT 8 microg/ml). Profound decrease of both serum cortisol (from 615 to 220 nmol/l) and urinary free cortisol (UFC) values (from 1498 to 477 nmol/day) was noted after 16 weeks of treatment (cumulative dose 314 g, plasma MT 8 microg/ml). MT treatment was associated with mild gastric discomfort and reversible increase of cholesterol plasma levels. Low serum cortisol and UFC were still observed 41 weeks after MT was discontinued (plasma MT 0.2 microg/ml). Our report demonstrates that low dose MT treatment may be a safe and effective modality for a sustained correction of hypercortisolism by PPNAD in subjects with CNC waiting for surgery.

Adrenal Cortex Diseases↗

PubMed1998

Molecular mechanisms of programmed cell death.

Programmed cell death and apoptosis have now been recognised as biological phenomena which are of fundamental importance to the integrity of organisms. What may have evolved as an altruistic defence against pathogen invasion in simple organisms is now a major regulatory mechanism in the development and maintenance of multi-cellular organisms. The classically defined morphological characteristics of apoptosis are now accompanied by a plethora of information regarding common biochemical and genetic mediators of programmed cell death. It is apparent that life and death decisions are taken by individual cells based on their interpretation of physiological signals, or their own self-assessment of internal damage. The knowledge that cell death is a genetically regulated process has highlighted an inherent potential for manipulation and offered new avenues for research into several diseases, and also productivity improvements in the biotechnology industry. This relatively "new frontier" in cell science has undoubtedly widened our perspectives and may provide novel strategies to expedite both medical and biotechnological research.

Animals↗

PubMed2000

Biosynthesis of cobalamin (vitamin B12): a bacterial conundrum.

The biosynthesis of cobalamin (vitamin B12) is described, revealing how the concerted action of around 30 enzyme-mediated steps results in the synthesis of one of Nature's most structurally complex 'small molecules'. The plethora of genome sequences has meant that bacteria capable of cobalamin synthesis can be easily identified and their biosynthetic genes compared. Whereas only a few years ago cobalamin synthesis was thought to occur by one of two routes, there are apparently a number of variations on these two pathways, where the major differences seem to be concerned with the process of ring contraction. A comparison of what is currently known about these pathways is presented. Finally, the process of cobalt chelation is discussed and the structure/function of the cobalt chelatase associated with the oxygen-independent pathway (CbiK) is described.

Aminolevulinic Acid↗