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Biomedical subjects

J Marks

Publications and source records attributed to J Marks.

At least 307 records · Page 17Linked to original sources
PubMedDate not supplied

The correspondence between coronary heart disease mortality and risk factor prevalence among states in the United States, 1991-1992.

OBJECTIVE: This study aimed to examine the correspondence between seven established risk factors for coronary heart disease (CHD) and CHD mortality among the states in the United States. An ecologic analysis relating CHD risk factor prevalences to CHD mortality rates among 49 states was undertaken in 1991-1992. METHODS: Approximately 68,000 men and women ages 45-74 were randomly sampled and interviewed by telephone in surveys conducted in 49 states in 1991 and 1992. From these interviews, we estimated state-specific prevalences of smoking, overweight, physical inactivity, hypertension, elevated cholesterol, diabetes, and alcohol abstinence. These seven CHD risk factors were also combined to create a CHD risk index for each state. The main outcome measures were mortality rates from CHD (ICD9 codes 410.0-414.9) in each of 49 states in 1991-1992 for men and women ages 45-74. The analysis was based on multiple linear regression and Spearman's rank-order correlations between the CHD risk factor prevalences, the combined CHD risk index, and the CHD mortality rates among the 49 states. RESULTS: The prevalences of most of the CHD risk factors correlated with CHD mortality rates in the expected directions, and correlations were similar for men and women. The CHD risk index correlated strongly with CHD mortality for both men (r = 0.75) and women (r = 0.80). CONCLUSION: About 60% of the variance in CHD mortality between the states in the United States (56% for men and 64% for women) is attributable to differences between the states in the prevalences of seven established risk factors for CHD. As state health agencies prioritize resources for chronic disease prevention programs, they should consider the potential benefits of increased efforts to reduce the prevalences of modifiable CHD risk factors in their populations to reduce CHD mortality.

Aged↗
PubMedDate not supplied

Techniques of benzodiazepine withdrawal in clinical practice. A consensus workshop report.

This is a report of a consensus conference on the management of the benzodiazepine-dependent patient. While the focus is on patients who are already dependent, it is better to avoid dependence in therapeutic use by careful patient selection, low dose and short term administration. The management of dependence can normally be undertaken in general practice unless there are complicating factors, e.g. concomitant severe medical, psychiatric or social problems. Inpatient management is also preferable for those abusing drugs in the sociorecreational area. Withdrawal should be achieved by gradual dosage reduction over a period of several weeks. Support from the practitioner, family and friends is important to achieve good results. Since postwithdrawal problems occur, good clinician support is necessary over at least the next year. Despite the risk of dependence, it is stressed that benzodiazepines are valuable therapeutic agents for several psychiatric and physical disorders.

Anti-Anxiety Agents↗
PubMedDate not supplied

Aberrant splicing of the TSG101 tumor suppressor gene in human breast and ovarian cancers.

OBJECTIVE: To determine whether large deletions or other alterations in the putative tumor suppressor gene TSG101 play a role in the molecular pathogenesis of breast and ovarian cancers. METHODS: Expression of TSG101 transcripts was examined in breast and ovarian cancers using the reverse transcriptase-polymerase chain reaction (RT-PCR), and selected transcripts were sequenced. Southern blot analysis was performed to determine whether there were genomic deletions in the TSG101 gene, and Northern blot analysis was used to examine the relative abundance of various transcripts. RESULTS: All the cancerous and normal breast tissue examined expressed full length 1145 base pair (bp) TSG101 transcripts. Additional truncated transcripts were seen using the RT-PCR in 57 (64%) of 89 primary breast cancers, 1 (20%) of 5 breast cancer cell lines, 3 (50%) of 6 normal breast tissues, 16 (64%) of 25 primary ovarian cancers and 1 (33%) of 3 ovarian cancer cell lines. Only the primary breast (21%) and ovarian (24%) cancers had three or more truncated transcripts. None of the normal tissues or cell lines examined had more than two aberrant transcripts. DNA sequencing revealed that the most commonly expressed truncated transcript arises because of loss of 902 bp between codons 153 and 1055. Only full length TSG101 transcripts were seen on Northern blot analysis of breast cancer cell lines, however. There was no evidence of genomic deletions in the TSG101 gene on Southern blot analysis. CONCLUSION: Truncated TSG101 transcripts that probably represent splice variants are present in some breast and ovarian cancers, but there is no evidence to suggest that loss of this putative tumor suppressor gene plays a role in the molecular pathogenesis of these cancers.

Base Sequence↗
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Sequence organization and genomic complexity of primate theta 1 globin gene, a novel alpha-globin-like gene.

The alpha-like and beta-like globin genes have provided a paradigm for the study of molecular evolution and regulation of multigene families in eukaryotes. The human alpha-globin gene cluster, which is on chromosome 16 (ref. 1), consists of six genes arranged in the order 5'-zeta(embryonic)-psi zeta-psi alpha 2-psi alpha 1-alpha 2(adult)-alpha 1(adult)-3'. DNA sequencing data have demonstrated that zeta (ref. 6) and alpha 2 (or alpha 1, refs 7-9) are the embryonic and adult genes, respectively, while psi zeta (ref. 6), psi alpha 2 (ref. 5) psi alpha 1 (ref. 10) are all inactive pseudogenes. Restriction mapping analysis has shown that the structure of this locus in several anthropoid primates is nearly identical to that of the human. Recently, we have isolated the adult alpha-globin gene region from orang-utan, olive baboon and rhesus macaque by molecular cloning. We report here the complete nucleotide sequence of a gene located immediately downstream from the adult alpha 1-globin gene of the orang-utan, along with its flanking DNA. We designate this gene as theta 1, and show that it contains the essential sequence elements required for an expressive gene. The putative polypeptide is 141 amino acids long, identical to that of the alpha- or zeta-globin, but its predicted amino-acid sequence is nearly as different from the orang-utan alpha-globin (55 differences) as the human zeta-globin is from the human alpha-globin (59 differences), suggesting an ancient history for the theta 1-globin gene. Results of blot hybridization experiments using the cloned orang-utan theta 1 gene sequence as probe demonstrate a similar alpha 2-alpha 1-theta 1 linkage map existing in the human genome. Furthermore, multiple copies of sequences homologous to the theta 1 gene are detected in both human and orang-utan. These results cast a new light on the primate alpha-globin gene family, and have intriguing implications for the existence of previously unreported, functional globin-like gene(s) in the primate genomes.

Amino Acid Sequence↗
PubMedDate not supplied

Evidence that the recently discovered theta 1-globin gene is functional in higher primates.

A new subfamily of the alpha-globin-like family has recently been identified in higher primates, rabbit, galago and possibly the horse. One member of this subfamily, theta 1, is downstream from the adult alpha 1-globin gene. In orang-utan, but not in rabbit or galago, the theta 1-gene appears to be structurally intact, suggesting that it may be functional in this species. The orang-utan theta 1-gene possesses initiation and termination codons, and the predicted polypeptide differs from the orang-utan alpha 1-globin by 55 amino acids. The upstream promoter boxes CCAAT and ATA are present, although approximately 150 base pairs (bp) farther upstream than in the alpha 1-gene. This structural difference in the promoter between the orang-utan theta 1- and alpha 1-genes has led Proudfoot to speculate that the theta 1-gene may be inactive. We have now cloned the theta 1- and alpha 1-globin genes from the olive baboon, and have compared their sequences with those of orang-utan. The unique promoter structure of the orang-utan theta 1-gene is highly conserved in baboon, although the orang-utan and baboon diverged nearly 30 million years ago. The coding sequences of the two theta 1-genes differ by only 6.3% with 22 out of 27 nucleotide substitutions being codon third position silent changes. These data support the view that the theta 1-gene has been functional in the baboon, orang-utan, and by implication, in man. We also estimate that the duplication event generating the theta 1- and alpha-globin-like subfamilies may have occurred as much as 260 million years ago.

Amino Acid Sequence↗