Alkyl halides, super hydrogen production and the pathogenesis of pneumatosis cystoides coli

Background and aims-The colons of patients with pneumatosis cystoides coli produce excessive H-2. Exposure to alkyl halides could explain this. Six consecutive patients who had pneumatosis cystoides coli while taking chloral hydrate (1-5+ g/day) are reported. Patients 2 and 3 were investigated after they had ceased chloral hydrate treatment. One produced methane, the other did not. (Pneumatosis cystoides coli patients are non-methanogenic according to the literature.) Both had overnight fasting breath H-2 of less than 10 ppm. A literature review disclosed just one patient who was using chloral at the time of diagnosed pneumatosis cystoides coli, but an epidemic of the disease in workers exposed to trichloroethylene. Methods-(i) In vitro experiments with human faeces: chloral or closely related alkyl halides were added to anaerobic faecal cultures derived from four methane-producing and three non-methanogenic human subjects. H-2 and CH4 gases were measured. (ii) In vivo animal experiment: chloral hydrate was added to drinking water of four Wistar rats, and faecal HI compared with control rats. Results-Alkyl halides increased H-2 up to 900 times in methanogenic and 10 times in non-methanogenic faecal cultures. The K-i of chloral was 0.2 mM. Methanogenesis was inhibited in concert with the increase in net H-2. In the rat experiment, chloral hydrate increased H-2 10 times, but did not cause pneumatosis. Conclusions-Chloral and trichloroethylene are alkyl halides chemically similar to chloroform, a potent inhibitor of H-2 consumption by methanogens and acetogens. These bacteria are the most important H-2-consuming species in the colon. It is postulated that exposure to these alkyl halides increases net H-2 production, which sets the scene for counterperfusion supersaturation and the formation of gas cysts. In recent times, very low prescribing rates for chloral have caused primary pneumatosis cystoides to become extremely rare. As with primary pneumatosis, secondary pneumatosis cystoides, which occurs if there is small bowel bacterial overgrowth distal to a proximally located gut obstruction, is predicted by counterperfusion supersaturation. Inherent unsaturation due to metabolism of O-2 is a safety factor, which could explain why gas bubbles do not form more often in tissue with high H-2 tension.

The Australian mortality decline: all-cause mortality 1788-1990

This review describes the Australian decline in all-cause mortality, 1788-1990, and compares this with declines in Europe and North America. The period until the 1870s shows characteristic 'crisis mortality', attributable to epidemics of infectious disease. A decline in overall mortality is evident from 1880. A precipitous fall occurs in infant mortality from 1900, similar to that in European countries. Infant mortality continues downward during this century (except during the 1930s), with periods of accelerated decline during the 1940s (antibiotics) and early 1970s. Maternal mortality remains high until a precipitous fall in 1937 coinciding with the arrival of sulphonamide. Excess mortality due to the 1919 influenza epidemic is evident. Artefactual falls in mortality occur in 1930, and for men during the war of 1939-1945. Stagnation in overall mortality decline during the 1930s and 1945-1970 is evident for adult males, and during 1960-1970 for adult females. A decline in mortality is registered in both sexes from 1970, particularly in middle and older age groups, with narrowing of the sex differential. The mortality decline in Australia is broadly similar to those of the United Kingdom and several European countries, although an Australian advantage during last century and the first part of this century may have been due to less industrialisation, lower population density and better nutrition. Australia shows no war-related interruptions in the mortality decline. Australian mortality patterns from 1970 are also similar to those observed in North America and European countries (including the United Kingdom, but excluding Eastern Europe).

The Australian mortality decline: cause-specific mortality 1907-1990

This review describes the changes in composition of mortality by major attributed cause during the Australian mortality decline this century. The principal categories employed were: infectious diseases, nonrheumatic cardiovascular disease, external causes, cancer,'other' causes and ill-defined conditions. The data were age-adjusted. Besides registration problems (which also affect all-cause mortality) artefacts due to changes in diagnostic designation and coding-are evident. The most obvious trends over the period are the decline in infectious disease mortality (half the decline 1907-1990 occurs before 1949), and the epidemic of circulatory disease mortality which appears to commence around 1930, peaks during the 1950s and 1960s, and declines from 1970 to 1990 (to a rate half that at the peak). Mortality for cancer remains static for females after 1907, but increases steadily for males, reaching a plateau in the mid-1980s (owing to trends in lung cancer); trends in cancers of individual sites are diverse. External cause mortality declines after 1970. The decline in total mortality to 1930 is associated with decline in infection and 'other' causes, Stagnation of mortality decline in 1930-1940 and 1946-1970 for males is a consequence of contemporaneous movements in opposite directions of infection mortality (decrease) and circulatory disease and cancer mortality (increase). In females, declines in infections and 'other' causes of death exceed the increase in circulatory disease mortality until 1960, then stability in all major causes of death to 1970. The overall mortality decline since 1970 is a consequence of a reduction in circulatory disease,'other' cause, external cause and infection mortality, despite the increase in cancer mortality (for males).

Effects of cyanide on coral photosynthesis: implications for identifying the cause of coral bleaching and for assessing the environmental effects of cyanide fishing

Modulated chlorophyll fluorescence techniques were used to examine the effects of cyanide (NaCN) from cyanide fishing on photosynthesis of the symbiotic algae (zooxanthellae) located within the tissues of the zooxanthellate hard coral Plesiastrea versipora. Incubating corals for 3 h in a cyanide concentration of >10(-5) M NaCN under a saturating light intensity (photosynthetically active radiation [PAR] intensity of 250 mu mol quanta m(-2) s(-1)) caused a long-term decrease in the ratio of variable to maximal fluorescence (dark-adapted F-v/F-m). The effect of cyanide on dark-adapted F-v/F-m was Light dependent; thus F-v/F-m only decreased in corals exposed to 10(-4) M NaCN for 3 h under PAR of 250 mu mol quanta m(-2) s(-1). In corals where dark-adapted F-v/F-m was significantly lowered by cyanide exposure, we observed significant loss of zooxanthellae from the tissues. causing the corals to discolour (bleach). To further examine the light-dependent effect of cyanide and its relation to loss of zooxanthellae, corals were exposed to 10-4 M NaCN or seawater only (control), either in darkness or under 250 mu mol quanta m(-2) s(-1). ill significant decrease in dark-adapted F-v/F-m and loss of zooxanthellae only occurred in corals exposed to cyanide in the light. These results suggest cyanide causes the dissociation of the symbiosis (bleaching) by affecting photosynthesis of the zooxanthellae. Quenching analysis using the saturation-pulse technique revealed the development of high levels of non-photochemical quenching in cyanide-exposed coral. This result is consistent with the known property of cyanide as an inhibitor of the dark reactions of the Calvin cycle, specifically as an inhibitor of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco). Therefore, chronic photoinhibition and an impairment of photosynthesis of zooxanthellae provides an important 'signal' to examine the environmental effects of cyanide fishing during controlled releases in situ.

Effects of habitat modification in mangroves on the structure of mollusc and crab assemblages

The abundance and species richness of mollusc and crab assemblages were examined in a subtropical mangrove forest in Moreton Bay, Queensland, Australia, which has been disturbed and damaged by the construction of a wooden boardwalk and a path. Sections of the forest immediately adjacent to the boardwalk and path were compared with reference areas to determine whether changes to the small-scale structural complexity within the forest affected the benthic fauna. The disturbed area was characterised by having 65-80% fewer pneumatophores, significantly fewer species and individuals of molluscs, but significantly more species and individuals of crabs than the reference areas. The abundance of mangrove pneumatophores and the attached epiphytic algae were manipulated at two sites to determine whether observed differences in these features could account for the differences in the assemblage of molluscs in the disturbed area of the forest compared with reference areas. Five experimental treatments were used: undisturbed controls, pneumatophore removals (abundance reduced by ca. 65%), epiphytic algal removals (algae removed from ca. 65% of pneumatophores), pneumatophore disturbance controls and algal disturbance controls. The experimental reduction of the abundance of mangrove pneumatophores and the associated epiphytic algae led to significant declines (by as much as 83%) in the number of molluscs utilising the substratum in the modified plots. There was no significant difference in the abundance of molluscs in the pneumatophore and algal removal plots suggesting any effect was primarily related to removal of the epiphytic algae from the surface of the pneumatophores. The responses by the biota to the changes in the physical environment demonstrate that even relatively small-scale modifications to the physical structure of subtropical mangrove forests can lead to significant effects on the diversity and abundance of macrobenthic organisms in these habitats. Such modifications have the potential to cause cascading effects at higher trophic levels with a deterioration in the value of these habitats as nursery and feeding grounds. Future efforts at conservation of these estuarine environments must focus on the prevention or reduction of modifications to the physical structure and integrity of the system, rather than just on the prevention of loss of entire patches of habitat. (C) 2000 Elsevier Science B.V. All rights reserved.

Mothers' mental illness and child behavior problems: Cause-effect association or observation bias

Objective: A number, of studies have consistently found that a mother's mental health (particularly her level of depression) is a strong predictor of mental health problems experienced by her child(ren). However, the validity of this finding is in doubt because the majority of these studies have relied on maternal reports as indicators of children's behavior. Method: This prospective, longitudinal study examines data an the mental health of the mother from prior to the birth of her child to when the child reaches 14 years of age. Child behavior is measured at 14 years of age using reports from mother and child. Mother and child responses are compared to provide an indication of the possible magnitude of maternal observation bias in the reporting of child behavior problems. Results: Anxious and/or depressed mothers tend to report more cases of child behavior problems than do their mentally healthy counterparts or children themselves. Differences between mothers and youths In reporting behavior problems appear to be related to the mothers' mental health. Conclusions: Current maternal mental health impairment appears to have a substantial effect on the reporting of child behavior problems by the mother, thereby raising questions about the validity of reports of child behavior by persons who are currently emotionally distressed.

Perturbed upper limb movements cause short-latency postural responses in trunk muscles

Addition of a load to a moving upper limb produces a perturbation of the trunk due to transmission of mechanical forces. This experiment investigated the postural response of the trunk muscles in relation to unexpected limb loading. Subjects performed rapid, bilateral shoulder flexion in response to a stimulus. In one third of trials, an unexpected load was added bilaterally to the upper limbs in the first third of the movement. Trunk muscle electromyography, intra-abdominal pressure and upper limb and trunk motion were measured. A short-latency response of the erector spinae and transversus abdominis muscles occurred similar to 50 ms after the onset of the limb perturbation that resulted from addition of the load early in the movement and was coincident with the onset of the observed perturbation at the trunk. The results provide evidence of initiation of a complex postural response of the trunk muscles that is consistent with mediation by afferent input from a site distant to the lumbar spine, which may include afferents of the upper limb.

Interaction of RTD-1, a cyclic antimicrobial defensin from Rhesus macaque leukocytes, and its open chain analogue with membrane mimics

In contrast to other mammalian defensins, rhesus theta defensin-1 (RTD-1) is composed of just 18 amino acids with the backbone cyclized through peptide bonds. Antibacterial activities of both the native cyclic peptide and a linear form were examined, showing that the cyclic form was 3-fold more active than the open chain analogue, oRTD-1, although both peptides adopt very similar structures in water. It was suggested that the additional charges at the termini of oRTD-1 are the cause for its lower antimicrobial activity. Therefore, we studied the interaction of both peptides with membrane mimics composed of zwitterionic (PC) and negatively charged (PG) phospholipids, major lipid components of erythrocyte and bacterial cell membranes, respectively. Microcalorimetry showed that RTD-1 and oRTD-1 did not affect the phase behavior of PC liposomes, while in PG liposomes both peptides induced new phase transitions above the chain melting transition of the lipid. The shape and fraction differed between both peptides, depending also on their concentration, which will be discussed in terms of their antimicrobial activity.