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Biomedical subjects

H Jonas

Publications and source records attributed to H Jonas.

16 recordsLinked to original sources
PubMed1999

Associations between alcohol related hospital admissions and alcohol consumption in Victoria: influence of socio-demographic factors.

OBJECTIVE: To examine the cross-sectional ecologic associations between apparent per-capita alcohol consumption, alcohol-related hospital admission rates, and the distributions of socio-demographic factors for people residing in 76 Local Government Areas (LGAs) in Victoria, during the 1995-1996 fiscal year. METHOD: Visitor-adjusted per-capita alcohol consumption was obtained from wholesale sales data from the Liquor Licensing Commission Victoria. Alcohol-related hospital admission rates were extracted from the Victorian Inpatient Minimum Dataset, and adjusted by the appropriate aetiologic fractions. Summary socio-demographic measures were derived from the 1996 Census. Their associations were analysed using multiple linear regression. RESULTS: Per-capita alcohol consumption ranged from 4 to 14 litres absolute alcohol/year and alcohol-related hospital admission rates ranged from 5 to 25 per 10,000 residents/year (external-cause diagnoses) and 8-37 per 10,000 residents/year (disease diagnoses). Higher levels of per-capita consumption were associated with higher admission rates (r = 0.45 for external cause diagnoses, r = 0.66 for disease diagnoses, and r = 0.70 for all diagnoses), each per-capita increase of one litre/year corresponding to increased admission rates of 0.6, 1.5 and 2.1 per 10,000 person-years, respectively. Further adjustments by summary socio-demographic measures reduced, but did not modify, the associations between per-capita consumption and admission rates. CONCLUSIONS AND IMPLICATIONS: Summary measures of sales-based per-capita alcohol consumption and socio-demographic environments may provide useful indicators of alcohol-related morbidity in Victorian communities.

Alcohol Drinking↗
PubMed1985

Pericardial meshing: an effective method for prevention of pericardial adhesions and epicardial reaction after cardiac operations.

Cardiac reoperations, particularly for coronary revascularization, are becoming more frequent and carry increased risk of damage to the heart during resternotomy. We experimentally evaluated a pericardial meshing technique to facilitate primary pericardial closure. In 18 mongrel dogs, an 8 by 5 cm pericardial flap was fashioned through a left thoracotomy. A standardized procedure for induction of pericardial adhesions was carried out in all animals. Animals were divided into three groups of six animals each: Group I (control)--the pericardial flap was primarily resutured; Group II--the flap was meshed and then resutured; and Group III--the flap was replaced by a pericardial substitute. Animals were put to death 8 weeks postoperatively and the pericardial space was examined for adhesions and epicardial reaction. The extent of adhesions and epicardial reaction was graded as: 0--none; 1--minimal; 2--moderate; and 3--severe. Both in Group I and Group III severe pericardial adhesions (grade 2-3) and epicardial reactions (grade 2-3) were formed, which obscured the underlying coronary anatomy. In Group II pericardial adhesions and epicardial reactions were none to minimal (grade 0-1) and the underlying coronary anatomy was not obscured. The meshed pericardium was completely regenerated by normal pericardium within several weeks. This study demonstrates that pericardial meshing facilitates primary tension-free pericardial closure. Free drainage of intrapericardial blood is achieved. A complete anatomic layer between heart and sternum is restored. Pericardial meshing is superior to the pericardial substitutes examined, as adhesions and epicardial reactions are significantly reduced, and the coronary anatomy is readily identifiable.

Animals↗
PubMed1978

The effect of intra-amniotic prostaglandin F2alpha on anterior pituitary hormone release during midtrimester abortion.

The effect of intra-amniotic administration of prostaglandin F2alpha (PGF2alpha) on pituitary hormone release was studied in women undergoing midtrimester abortion. Serum prolactin (PRL), growth hormone (GH), thyrotropin (TSH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured prior to and at 15-minute intervals for 2 hours following intra-amniotic administration of 40 gm of urea alone, 20 mg of PGF2alpha and 40 gm of urea, or an equal volume of normal saline. Serum PRL levels were significantly higher at sampling times from 15 through 120 minutes when both PGF2alpha and urea were administered than after saline or urea alone. The elevation in serum GH following PGF2alpha and urea was not significantly greater than for urea alone. The GH response in the women receiving normal saline was significantly less than for the two groups of women receiving the abortifacients. These results indicate that the GH response was related to the stress effects of the abortifacients. There was no difference in the TSH, LH, and FSH responses for the three groups. These results suggest that PGF2alpha selectively causes pituitary release of PRL in women during midtrimester pregnancy.

Abortion, Induced↗
PubMed1978

Pituitary response to LHRH in midtrimester pregnancy.

The effects of lutenizing hormone releasing hormone (LHRH) on serum luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), thyroid stimulating hormone (TSH), and growth hormone (GH) were studied in 10 women in the second trimester of pregnancy. Serum LH was measured using the LHbeta-RIA, with the anti-betaLH serum being preabsorbed with purified hCG. This assay was unaffected by hCG levels up to 500 IU/ml. Basal serum levels of LH was undetectable and basal FSH levels were low in these 10 women. No release of LH or FSH was observed after administration of 100 microgram of LHRH. However, there was a statistically significant rise in PRL from mean basal levels of 139.9 ng/ml to a mean peak level of 159.0 ng/ml at 30 minutes after LHRH administration. Both TSH and GH displayed small elevations at 15 minutes after LHRH administration; however, these elevations were not significant because of the wide range in responses. The results of this study indicate that gonadotropin release is inhibited during the second trimester of pregnancy. Finally, it appears that pregnancy is a condition in which LHRH administration results in a nonspecific release of several hormones.

Adult↗