Biomedical subjects
Publications and source records attributed to M Hertzberg.
The concurrent problems of bleeding placenta praevia and thromboembolism present a difficult management problem. We present a case of pulmonary embolism successfully treated with low molecular weight heparin in a woman with a major grade placenta praevia, who required emergency operative delivery.
Factor X circulates as a serine protease which is converted to the active form at the point of convergence of the intrinsic and extrinsic coagulation pathways. Subsequently, the enzymatic species, factor Xa, is involved in macromolecular complex formation with its cofactor factor Va, a phospholipid surface and calcium to convert prothrombin into thrombin. The gene encoding factor X shares a number of structural and organisational features in common with the other vitamin K-dependent coagulation proteins, suggesting that they have evolved from a common ancestral gene. Each of the exons encoding these proteins can be considered as a module coding for a homologous domain in each protein. These structural domains in factor X are responsible for specific functional properties including gamma-carboxylase recognition, calcium binding, phospholipid surface interaction, as well as cofactor and substrate binding. Studies of recombinant proteins and proteolytic fragments continue to provide significant insight into structure-function relationships of the protein modules within factor X.
A total of 630 haplotypes for the phenylalanine hydroxylase (PAH) gene locus were established in five groups of Polynesians comprising Samoans, Tongans, Cook Islanders, Maori, and Niueans. Considerable genetic continuity was demonstrated between these widely dispersed populations, since three common haplotypes (4, 1, and 7) constituted over 95% of alleles. A control group of individuals from Southeast Asia shared the same major haplotypes, 4, 1, and 7, with Polynesians. These data provide further support for the theories of genetic homogeneity and of Asian affinities of the Polynesian precursor populations. The absence of severe phenylketonuria (PKU) in both Polynesians and Southeast Asians is consistent with the lack of PAH haplotypes 2 and 3, on which the severe PKU mutants have arisen among Caucasians.
One hundred fifty Polynesians from five different island groups (Samoans, Maoris, Niueans, Cook Islanders, and Tongans) were surveyed for the presence of an Asian-specific length mutation of mitochondrial (mt) DNA by using enzymatic amplification with thermostable Taq DNA polymerase. Ninety-three percent of Polynesians exhibited this 9-bp deletion, including 100% of Samoans, Maoris, and Niueans. The same deletion was also found in 8% of Tolais from New Britain and in 14% of coastal New Guineans. A deletion frequency of 82% in Fijians confirmed their ethnic affinity to Polynesians. In contrast, the deletion was absent in 30 New Guinea highlanders and 31 Australian aborigines, the only exception being an aborigine who also had the Southeast Asian triplicated zeta-globin gene rearrangement in his nuclear DNA. These data support the theories claiming that an independent group of pre-Polynesian ancestors who colonized into the Pacific were ultimately derived from east Asia.
Globin gene mapping data enable Polynesians to be divided into three distinct groups: (i) Maoris, Cook Islanders, (ii) Tongans, Samoans, (iii) Niue Islanders. Unusual RFLPs detected by the restriction enzymes Apa I and Bgl II are found in Polynesians. A high frequency of alpha-thalassemia in this population is explained by genetic drift and a founder effect.
Twenty-five Israeli combat veterans fulfilling DSM-III criteria for posttraumatic stress disorder (PTSD) participated in an open, prospective trial of phenelzine sulfate administration (median daily dose, 60 mg; range, 30 to 90 mg); three patients withdrew early due to side effects. Treatment was continued for at least four weeks in 22 cases and thereafter for as long as it was felt to be of benefit. Therapeutic efficacy was rated using a new PTSD scale, the Hamilton Depression Scale, and the Hamilton Anxiety Scale administered at four weekly intervals. Six patients completed four to eight weeks of phenelzine treatment; seven patients, nine to 13 weeks; and nine patients, 14 to 18 weeks. Comparison of mean prediscontinuation scores with pretreatment ratings showed, at best, only small (23% to 38%) differences (on the PTSD and Hamilton Anxiety scales) in the group treated for nine to 13 weeks. Two patients with a concurrent diagnosis of panic disorder and two with a concurrent diagnosis of dysthymic disorder were the most improved symptomatically but fell short of clinically significant remission. Although statistically significant improvement was observed on seven of the 12 items of the PTSD scale, sleep disturbance was the only symptom showing a clinically impressive change. These results only partially support previous positive reports of phenelzine treatment of PTSD.
Dopamine-Beta-Hydroxylase (D.B.H.)-activity was measured in the plasma of untreated Parkinsonian patients, after tretment with L-dopa and 2-Bromo-alpha-ergocriptine. The findings were compared to the D.B.H.-activity of a matched healthy control group. After L-dopa loading D.B.H.-activity decreased in the Parkinsonian patients by 27.6 +/- 3.1% compared to 16.2 +/- 3.3% (p less than 0.02) in the control group. After 2-Bromo-alpha-ergocriptine laoding the decrease in D.B.H.-activity was 32.6 +/- 4.4% in the parkinsonian patients, and 158 +/- 4.9% (p less than 0.02) in the control group. This reduced D.H.B.-activity after L-dopa loading may reflect an impairment, in the Parkinsonian patients' ability to metaoblize L-dopa. The reduced D.B.H.-activity after treatment with 2-Bromo-alpha-ergocriptine may be explained by a pronounced antagonistic influence of 2-Bromo-alpha-ergocriptine on the presynaptic dopamine receptors, suggesting that presynaptic dopaminergic receptors are involved in Parkinson's disease.
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The present state of knowledge is reviewed concisely in terms of the experimental methods used, the effect of apparatus size, accuracy of data, methods of data presentation, and the sensitivity of the limits to initial temperature and pressure. The heat of combustion per mole of gas mixture at the lean limit is a reliable thermochemical criterion for the flammability of organic fuels with comparable reactivities. The limit calorific value for the heavy paraffins is 11.5 +/- 0.1 kcal mole -1. However, kinetic effects strongly influence this value. Highly reactive fuels (hydrogen, acetylene) require lower energy contents, whereas less reactive fuels (ammonia) require higher values. Hydrogen-starved fuels (carbon monoxide, cyanogen) show marked anomalies and are sensitive to impurities that can provide H-atom chain carriers. These kinetic effects are reflected in the experimentally measurable burning velocity of the fuel. This parameter is a key ingredient in the theory of flammable limits, which is briefly sketched. Five competing processes dissipate power from the combustion wave and quench it at some characteristic limit velocity. The prevalent consensus that the limits are controlled by natural convection is clearly demonstrated, and the complex interplay of kinetics and thermochemistry follows logically therefrom.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.