Non-fatal opioid overdose, naloxone access, and naloxone training among people who recently used opioids or received opioid agonist treatment in Australia: The ETHOS Engage study.

BACKGROUND: Overdose is a major cause of morbidity and mortality among people who use opioids. Naloxone can reverse opioid overdoses and can be distributed and administered with minimal training. People with experience of overdose are a key population to target for overdose prevention strategies. This study aims to understand if factors associated with recent non-fatal opioid overdose are the same as factors associated with naloxone access and naloxone training in people who recently used opioids or received opioid agonist treatment (OAT). METHODS: ETHOS Engage is an observational study of people who inject drugs in Australia. Logistic regression models were used to estimate odds ratios for non-fatal opioid overdose, naloxone access and naloxone training. RESULTS: Between May 2018-September 2019, 1280 participants who recently used opioids or received OAT were enrolled (62% aged >40 years; 35% female, 80% receiving OAT, 62% injected drugs in the preceding month). Recent opioid overdose (preceding 12 months) was reported by 7% of participants, lifetime naloxone access by 17%, and lifetime naloxone training by 14%. Compared to people receiving OAT with no additional opioid use, recent opioid, benzodiazepine (preceding six months), and hazardous alcohol use was associated with recent opioid overdose (aOR 3.91; 95%CI: 1.68-9.10) and lifetime naloxone access (aOR 2.12; 95%CI 1.29-3.48). Among 91 people who reported recent overdose, 65% had never received take-home naloxone or naloxone training. CONCLUSIONS: Among people recently using opioids or receiving OAT, benzodiazepine and hazardous alcohol use is associated with non-fatal opioid overdose. Not all factors associated with non-fatal overdose correspond to factors associated with naloxone access. Naloxone access and training is low across all groups. Additional interventions are needed to scale up naloxone provision.

Use and perception of collars for companion cats in New Zealand.

AIMS: To investigate the use and utility of collars for companion cats in New Zealand, and to explore public perception of collar use. METHODS: An online questionnaire was distributed using emails and social media to members of the general public in New Zealand. The questionnaire collected details of respondents, cat ownership status, and responses to a number of questions regarding collar use in cats. RESULTS: A total of 511 responses were collected. Of these, 393/511 (76.9%) reported owning ≥1 cat at the time of the survey, and 141/393 (35.9%) stated that ≥1 of their cats wore collars and 211/393 (53.7%) had ≥1 of their cats micro-chipped. Of the respondents with a pet cat, 351/393 (89.3%) allowed their cats some outdoor access. Respondents mainly used collars for identification and to reduce predation. Reasons for not using collars included cat intolerance of collars, repeated collar loss and concern over collar safety. Differences were found between cat owners and non-owners regarding whether they agreed that cats were important for pest control (43 vs. 25%, p<0.001); that not all cats will tolerate collars (81 vs. 64%, p<0.001); that cats should be kept indoors at night (37 vs. 58%, p<0.001); or disagreed that well fed cats will not catch birds (60 vs. 70%, p=0.04); and disagreed that a cat without a collar was likely to be a stray (85 vs. 76%, p<0.001). Respondents most trusted veterinarians and the Society for the Prevention of Cruelty to Animals as sources of pet care information. CONCLUSIONS: Collar use within this sample of cat owners in New Zealand appeared to be low, with more using microchips for identification. The majority of cat owners in this study indicated their cats had some outdoor access, with collars being used for cat identification and to reduce hunting behaviour. Significant differences existed in opinions on cat management between cat owners and non-owners in this study. It should be noted that this preliminary exploration was based on a self-selected group of respondents and so results and conclusions cannot be extrapolated to the wider population. RELEVANCE: As the most trusted source of information about pet care, an enhanced understanding of cat ownership and management may be of use to veterinarians to promote responsible pet ownership and to develop national policies and practices to improve cat welfare.

Physiological responses in high-P subjects during active and passive coping.

There have been relatively few studies of the psychophysiological correlates of Eysenck's dimension of psychoticism (P) and those which do not exist report findings which cannot be readily integrated to isolate a distinctive physiological basis of P. The present study investigated differences between subjects scoring high and low on the P scale of the Eysenck Personality Questionnaire (EPQ) in relation to sympathetic and parasympathetic arousal following aversive stimulation. An active-passive coping paradigm using an aversive tone was selected to elicit responses and cardiovascular measures (heart period, heart period variance, T-wave amplitude) and a skin conductance measure (event-related skin conductance) were obtained. The findings show that differences between high- and low-P subjects are specific to the coping condition. Under active coping, high-P subjects exhibited greater sympathetic arousal following the aversive tone than low-P subjects. There was no significant difference between the high-P and low-P subjects on any physiological variable under the passive coping condition. It is suggested that if there is differential functioning of the divisions of the autonomic nervous system in subjects differing in P, that these differences may only manifest themselves under specific situations.

Risk of chromosomal abnormalities, with emphasis on live-born offspring of young mothers.

In a large public urban hospital obstetrics service with > 123,000 deliveries in a 10-year period (1980-89), the frequencies (0.12%) of any type of chromosomal abnormality and of trisomy syndromes were analyzed for maternal age-related risk, by logistic regression. Focusing on very young gravidas, we found that in the study period there were 9,332 births (7.5% of all deliveries) to mothers < or = 16 years old. Estimated risks of chromosomal abnormalities among offspring associated with very young maternal age (9-16 years) were similar to those age-associated risks of mothers 20-29 years old. Risks of chromosomal abnormalities increase with advancing maternal age and are independent of ethnicity.

Alginate, small bowel sterol excretion, and absorption of nutrients in ileostomy subjects.

The effect of alginate on ileostomy excretion of sterols and nutrients was investigated in six ileostomy subjects fed a constant low-fiber diet with or without supplementation with 7.5 g sodium alginate. A mean of 95% of uronic acids derived from the sodium alginate was recovered in the ileostomy contents. Supplementation with alginate increased fat excretion by 140% and decreased bile acids excretion by 12%. Sodium and potassium excretion were significantly increased whereas starch and nitrogen excretion were unchanged. Five of six subjects showed a decreased apparent absorption of iron and manganese with alginate, which, however, was not statistically significant. Absorption of phosphorus, calcium, magnesium, and zinc were unchanged. Almost no digestion of sodium alginate occurs in the stomach and small intestine. The increased fatty acids excretion may be explained by the binding or trapping of fatty acids in the gel matrix formed by alginate, which may also cause a reduced bile flow.

Methotrexate and reproduction in men: case report and recommendations.

Methotrexate has been used in the treatment of recalcitrant psoriasis for more than 35 years. We examined the significance of impaired spermatogenesis in a young man undergoing methotrexate treatment for severe psoriasis with associated arthritis. A medical geneticist was consulted and a review of the literature was performed. Genetic abnormalities that could lead to mutagenesis include chromosomal abnormalities and single-gene mutations. These aspects are considered and recommendations are made for counseling men undergoing methotrexate therapy so that risks and options can be considered.

Ataxia and a cerebellar defect in the exencephaly-prone SELH/Bc mouse stock.

SELH/Bc inbred mice have an abnormal mechanism of anterior neural tube closure and 10-20% of embryos have a lethal neural tube closure defect, exencephaly. Our previous studies have focused on this multifactorial threshold trait. However, SELH mice are also characterized by another trait that also shows non-Mendelian transmission ratios, an ataxia recognized in juvenile and adult mice. Here we report our first genetic and morphological studies of the ataxia trait. Recent pedigree records for the SELH colony showed that 7% of the 467 weaned progeny from normal breeding pairs were ataxic; 17 of the 20 pairs produced ataxic progeny. This result was statistically consistent with the hypothesis that all SELH mice have the ataxic genotype, which is expressed in only 7% of them. Genetic studies of an outcross to a normal strain and the subsequent F2 and testcross of the F2 were also done. The results were consistent with a one or two gene locus cause of liability to ataxia in SELH mice. The genetic correlation between exencephaly production and ataxia production for a sample of nine F2 males was 0.35, as expected if both traits are caused by the same genes, but was not statistically significant. In another approach, we examined the morphology of brains from normal and ataxic adult SELH mice. All 20 brains from non-ataxic SELH mice were morphologically normal. In all 18 brains from ataxic SELH mice the cerebellum was abnormal, lacking the vermis, and characterized by a midline fissure. This phenotype in mice has previously been known in Mendelian mutants at the Wnt-1 locus.(ABSTRACT TRUNCATED AT 250 WORDS)

Complementary duplication and deletion of 17 (pcen----p11.2): a family with a supernumerary chromosome comprised of an interstitially deleted segment.

A sister and brother were investigated because both were developmentally delayed although they had somewhat different physical anomalies. The girl was found to have an interstitial deletion of chromosome 17. Her karyotype was 46,XX,del(17) (pter----p11.2::cen----qter). Her brother had normal chromosomes in peripheral lymphocytes. Cytogenetic investigation of the mother showed the presence of the same deletion as in her daughter and a small supernumerary chromosome. The supernumerary chromosome appeared to contain the material deleted from the short arm of 17 since the mother's phenotype was normal. Study of skin fibroblasts in her son showed that he was mosaic for a normal cell line and one that contained the extra small chromosome; thus, he had mosaic partial trisomy 17(cen----p11.2). The origin of the centromere and telomere(s) of the small supernumerary chromosome in this family presents an interesting problem.

Congenital cataracts in mother, sister, and son of a patient with Hallermann-Streiff syndrome: coincidence or clue?

The son of a patient with Hallermann-Streiff Syndrome (HSS) was found to have congenital cataracts, but no other findings of the syndrome. Similar findings were reported in the patient's mother and sister. The significance of this observation is uncertain.

Verification of the fetal valproate syndrome phenotype.

We have evaluated 19 children who were exposed to valproic acid (VPA) in utero to look for manifestations of a fetal valproate syndrome (FVS), as proposed by Di Liberti et al. [1984]. We found no consistent alterations of pre- or postnatal growth with exposure to VPA monotherapy. Postnatal growth deficiency and microcephaly were present however, in two thirds of children exposed to VPA in combination with other anticonvulsants. Developmental delay or neurologic abnormality was found in 71% of those exposed to VPA monotherapy, and in 90% of those exposed to VPA and other anticonvulsants. Craniofacial anomalies, which can be seen with other anticonvulsant exposures, including midface hypoplasia, short nose with a broad and/or flat bridge, epicanthal folds, minor abnormalities of the ear, philtrum or lip, and micrognathia were also found in infants whose mothers used VPA. Prominent metopic ridge and outer orbital ridge deficiency or bifrontal narrowing and certain major anomalies such as tracheomalacia, talipes equinovarus (with intact spine) and lumbosacral meningomyelocele seem to be peculiar to infants with VPA exposure. Other defects such as urogenital anomalies, inguinal or umbilical hernias, and minor digital anomalies that are common to other prenatal anticonvulsant exposures are also occasionally found in those exposed to VPA. Heart defects have been found in infants exposed to nearly every class of anticonvulsant although the types of defects associated with maternal VPA use may be clarified when classified by pathogenetic mechanism. Our findings overall are in agreement with the report of Di Liberti et al. [1984].

del(20p) with manifestations of arteriohepatic dysplasia.

A small-for-gestational age white female infant was noted to have multiple minor anomalies and severe jejunal stenosis. Mild peripheral pulmonic stenosis, skeletal anomalies, and cholestasis with paucity of intrahepatic bile ducts were observed, and she was diagnosed as having arteriohepatic dysplasia. Chromosome analysis of peripheral blood leukocytes showed a 46,XX,del(20)(p11.2) chromosome constitution.

Further delineation of Weaver syndrome.

Seven new cases of Weaver syndrome are described, including the first reported case in an adult. Overgrowth is usually but not always present. The combination of characteristic facies and developmental delay, with the peculiar radiographic findings of accelerated dysharmonic osseous maturation and splaying of the distal long bones, is diagnostic of Weaver syndrome.

Anatomic correlates of ultrasonographic prenatal diagnosis.

In utero sonographic diagnoses from forty-five malformed infants were correlated with their autopsy findings. Fifty-two malformations were diagnosed prenatally in 42 of the patients but 90 additional malformations were not. Nine sonographically diagnosed abnormalities were not confirmed at autopsy. Factors compromising sonographic diagnosis included: limited examinations, small fetal size, timing of examination, oligohydramnios, fetal position, nature of the malformation and unfamiliarity of the ultrasonographer with specific malformation syndromes. In utero ultrasonography is an invaluable tool of diagnosing congenital malformations but has limitations.

Sternal malformation/vascular dysplasia association.

Sternal defects associated with superficial craniofacial vascular lesions are rare. We report on two additional patients with a sternal cleft and cutaneous, craniofacial hemangiomata to emphasize that this unusual combination of findings represents a recognizable sternal malformation/vascular dysplasia association. In addition, internal vascular lesions were also identified in these individuals, in one instance involving the upper respiratory tract and in the other the viscera. Although the pathogenesis of these findings is unclear, an early disturbance affecting midline mesodermal structures leading to lack of complete fusion of lateral sternal bands and overlying cutaneous tissue, or deficient formation of a proposed medioventral unpaired structure which may be involved in the formation of the sternum, and persistence and proliferation of midline angioblastic tissue may be possible mechanisms during the sixth to ninth gestational weeks. To date, all but one of the 15 known cases have been sporadic and no teratogen has been identified as a cause for these clinical manifestations. The presence of this association should signal the need to search for potentially life-threatening internal hemangiomata.

A "new" lethal multiple congenital anomaly syndrome: joint contractures, cerebellar hypoplasia, renal hypoplasia, urogenital anomalies, tongue cysts, shortness of limbs, eye abnormalities, defects of the heart, gallbladder agenesis, and ear malformations.

Three cases of a lethal malformation syndrome with severe visceral anomalies were seen in two families and include one pair of sibs. The predominating external manifestations are mesomelic dwarfism, micrognathia, V-shaped upper lip, microglossia, thick alveolar ridges, ambiguous genitalia, webbed neck, highly arched palate, clubfeet, fused fontanelles, inclusion cysts of the tongue, four-finger creases, digital anomalies, apparently low-set ears, widely spaced nipples, and dislocated thighs and forearms. The internal findings include oligopapillary renal hypoplasia, severe congenital heart defect, cerebellar hypoplasia, pulmonary hypoplasia, hypoplastic larynx, and hypoplastic gallbladder. Other findings from the two autopsies and one clinical investigation not documented in all three patients include unilobar lungs, hydrocephalus, cataracts, microphthalmia, polydactyly, islet cell hyperplasia, suprapubic skin crease, urethral anomalies, and a decreased number of turns of the cochlea. The hypoplasia seen in the several affected organs is similar to the disordered development seen in experimental models of branching epithelial morphogenesis in which mesenchymal-epithelial interaction has been disrupted.

Etiologic heterogeneity of fetal hydrocephalus diagnosed by ultrasound.

Increased use of fetal ultrasound imaging by obstetricians has led to an increased rate of in utero detection of fetal malformations. Eight patients referred for level II sonography for confirmation of suspected fetal hydrocephalus were found to have affected fetuses. Examination of the resulting fetuses and infants revealed remarkable etiologic heterogeneity for the hydrocephalus. The risk for recurrence of hydrocephalus and other malformations in future offspring of these mothers varies from negligible to 25%. This experience emphasizes that there are many causes of fetal hydrocephalus and that careful diagnostic studies must be performed on any fetus or infant found to have hydrocephalus, so that accurate genetic counseling can be provided to the family.

Genetic heterogeneity in spondyloepiphyseal dysplasia congenita.

Two unrelated infants seen for evaluation of short stature at 14 and 27 months, respectively, had clinical and radiographic findings consistent with the diagnosis of spondyloepiphyseal dysplasia congenita (SED congenita). No other anomalies were noted. Both sets of parents were normal, both family histories were unremarkable, and neither couple was consanguineous. Both families were counseled that SED congenita is an autosomal dominant disorder and that sporadic cases probably result from new mutations; a low recurrence risk was given. Both families subsequently produced a second affected child. Our experiences suggest that genocopies of autosomal dominant SED congenita exist that are clinically and radiographically indistinguishable, at least within the first 3 years. Autosomal recessive inheritance seems most likely, although alternative explanations are possible. Genetic heterogeneity should be considered when providing genetic counseling for sporadic SED congenita in young children.