J B Weiss

1.3k total citations
36 papers, 1.0k citations indexed

About

J B Weiss is a scholar working on Molecular Biology, Rheumatology and Cancer Research. According to data from OpenAlex, J B Weiss has authored 36 papers receiving a total of 1.0k indexed citations (citations by other indexed papers that have themselves been cited), including 20 papers in Molecular Biology, 9 papers in Rheumatology and 8 papers in Cancer Research. Recurrent topics in J B Weiss's work include Angiogenesis and VEGF in Cancer (16 papers), Protease and Inhibitor Mechanisms (7 papers) and Cell Adhesion Molecules Research (7 papers). J B Weiss is often cited by papers focused on Angiogenesis and VEGF in Cancer (16 papers), Protease and Inhibitor Mechanisms (7 papers) and Cell Adhesion Molecules Research (7 papers). J B Weiss collaborates with scholars based in United Kingdom, United States and Mexico. J B Weiss's co-authors include Robert A. Brown, B. McLaughlin, M. Bhushan, C.E.M. Griffiths, P. J. Phillips, S. Kumar, Sabry Ayad, C. R. Hill, A Garner and M. D. Brown and has published in prestigious journals such as Biochemical Journal, Journal of Cell Science and Journal of Applied Physiology.

In The Last Decade

J B Weiss

35 papers receiving 979 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
J B Weiss United Kingdom 19 486 204 180 169 157 36 1.0k
Laurie Pukac United States 14 840 1.7× 105 0.5× 185 1.0× 166 1.0× 157 1.0× 21 1.4k
B. R. Olsen United States 12 548 1.1× 339 1.7× 192 1.1× 234 1.4× 135 0.9× 16 1.0k
Velidi H. Rao United States 21 530 1.1× 143 0.7× 534 3.0× 387 2.3× 288 1.8× 53 1.5k
T Tsukada Japan 14 464 1.0× 69 0.3× 188 1.0× 66 0.4× 327 2.1× 21 889
Suzanne Spong United States 11 729 1.5× 59 0.3× 204 1.1× 194 1.1× 307 2.0× 12 1.4k
R Berthier France 15 763 1.6× 40 0.2× 128 0.7× 246 1.5× 173 1.1× 41 1.5k
Kadir Demircan Türkiye 17 463 1.0× 153 0.8× 295 1.6× 138 0.8× 165 1.1× 53 1.0k
Claudia Qiao Lin United States 7 623 1.3× 49 0.2× 205 1.1× 213 1.3× 217 1.4× 8 1.0k
A Zambonin-Zallone Italy 11 945 1.9× 359 1.8× 161 0.9× 362 2.1× 399 2.5× 12 1.4k
K Rubin Sweden 8 380 0.8× 35 0.2× 86 0.5× 143 0.8× 158 1.0× 8 850

Countries citing papers authored by J B Weiss

Since Specialization
Citations

This map shows the geographic impact of J B Weiss's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by J B Weiss with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites J B Weiss more than expected).

Fields of papers citing papers by J B Weiss

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by J B Weiss. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by J B Weiss. The network helps show where J B Weiss may publish in the future.

Co-authorship network of co-authors of J B Weiss

This figure shows the co-authorship network connecting the top 25 collaborators of J B Weiss. A scholar is included among the top collaborators of J B Weiss based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with J B Weiss. J B Weiss is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Bhushan, M., B. McLaughlin, J B Weiss, & C.E.M. Griffiths. (1999). Levels of endothelial cell stimulating angiogenesis factor and vascular endothelial growth factor are elevated in psoriasis. British Journal of Dermatology. 141(6). 1054–1060. 159 indexed citations
2.
Weiss, J B & B. McLaughlin. (1998). Molecules in focus Endothelial cell stimulating angiogenesis factor. The International Journal of Biochemistry & Cell Biology. 30(4). 423–427. 2 indexed citations
3.
Egginton, Stuart, et al.. (1998). Capillary growth in relation to blood flow and performance in overloaded rat skeletal muscle. Journal of Applied Physiology. 85(6). 2025–2032. 95 indexed citations
4.
Kurdy, Nasser, et al.. (1996). Endothelial stimulating angiogenic factor in early fracture healing. Injury. 27(2). 143–145. 19 indexed citations
6.
Weiss, J B, et al.. (1994). ENDOTHELIAL CELL STIMULATING ANGIOGENESIS FACTOR—A NEW BIOLOGICAL MARKER FOR DISEASE ACTIVITY IN ANKYLOSING SPONDYLITIS?. Lara D. Veeken. 33(4). 332–335. 10 indexed citations
7.
Taylor, Carol M., B. McLaughlin, J B Weiss, & N.G. Maroudas. (1992). Concentrations of endothelial-cell-stimulating angiogenesis factor, a major component of human uterine angiogenesis factor, in human and bovine embryonic tissues and decidua. Reproduction. 94(2). 445–449. 10 indexed citations
8.
Odedra, Rajesh & J B Weiss. (1991). Low molecular weight angiogenesis factors. Pharmacology & Therapeutics. 49(1-2). 111–124. 25 indexed citations
9.
Taylor, Carol M., et al.. (1991). Matrix Integrity and the Control of Angiogenesis. International Journal of Radiation Biology. 60(1-2). 61–64. 8 indexed citations
10.
Taylor, Carol M., et al.. (1991). Raised levels of latent collagenase activating angiogenesis factor (ESAF) are present in actively growing human intracranial tumours. British Journal of Cancer. 64(1). 164–168. 12 indexed citations
11.
Cooper, RG, et al.. (1991). Elevated endothelial-cell-stimulating angiogenic factor activity in rodent glycolytic skeletal muscles. Clinical Science. 81(2). 267–270. 6 indexed citations
12.
Taylor, Carol, B. McLaughlin, J B Weiss, & Issar Smith. (1988). Bovine and human pineal glands contain substantial quantities of endothelial cell stimulating angiogenic factor. Journal of Neural Transmission. 71(1). 79–84. 13 indexed citations
13.
Weiss, J B. (1987). Rheumatology. An Annual Review. Vol. 10. Connective Tissue: Biological and Clinical Aspects. Annals of the Rheumatic Diseases. 46(7). 568–568. 1 indexed citations
14.
Murphy, John F., et al.. (1986). Comparison of urinary glycosaminoglycan excretion in rheumatoid arthritis, osteoarthritis, myocardial infarction, and controls.. Annals of the Rheumatic Diseases. 45(2). 162–166. 8 indexed citations
15.
Hill, C. R., et al.. (1983). Angiogenic factor in vitreous from diabetic retinopathy. Cellular and Molecular Life Sciences. 39(6). 583–585. 24 indexed citations
16.
Rajapakse, C. N. A., et al.. (1983). Increased bone metabolism in rheumatoid arthritis as measured by the whole-body retention of 99Tcm methylene diphosphonate.. Annals of the Rheumatic Diseases. 42(2). 138–141. 12 indexed citations
17.
Braidman, Isobel, David C. Anderson, Carolyn Jones, & J B Weiss. (1983). Separation of two bone cell populations from fetal rat calvaria and a study of their responses to parathyroid hormone and calcitonin. Journal of Endocrinology. 99(3). 387–399. 13 indexed citations
18.
Morgan, K, et al.. (1983). 1 Alpha 2 alpha 3 alpha collagen is arthritogenic.. Annals of the Rheumatic Diseases. 42(6). 680–683. 34 indexed citations
19.
Weiss, J B, et al.. (1970). Evidence for the role of terminal regions of tropocollagen in fibrillogenesis: specific enzymic degradation studies. Biochemical Journal. 117(2). 22P–22P. 2 indexed citations
20.
Weiss, J B, et al.. (1969). Spatial recognition of methionine in the tropocollagen macromolecule. Biochemical Journal. 112(1). 11P.1–11P.1. 1 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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