Jerzy Kaulbersz was born on December 22nd
1891 in Kalisz in lawyer’s family, where he completed his elementary schooling
and the secondary school, but could not finish it because of the outbreak of
school strike in 1905 against strong russification involving the whole Russian
partition of Poland. From the early childhood, he was strongly advised at home
to learn foreign languages (Russian, German and French) and this helped him
in future academic education. He then left Kalisz and moved independently to
Jalta where he passed with distinction the final maturation examination. His
sister finished medical studies in Warsaw and later became professor and chairman
of Pediatric Clinic at Warsaw University, while his brother became a priest
and parson of All Saints Church in Warsaw.
After the completion of secondary education he moved to Germany to continue
his higher education in biology at Munich University, where in 1913 based on
his studies related to photoreception on arthropods entitled “Biological Observations
on Asellus aquaticus
” (1) he achieved the title of doctor of Phylosophiae
Naturalis (Ph.D.) in Freiburg and immediately started to study medicine. At
the outbreak of World War I (WWI) he returned to Austrian partition of Poland,
became mobilized to army working under supervision of Professor Otton Eilselsberg
in Vienna as medical help with paralysed patients as described by him in the
paper “The Electrical Excitability of the Nerves and Muscles in War Disabled
People with Spinal Cross Damage” published by G. Fischer, Jena (2). After the
WWI he completed medical education at the Jagiellonian University in Cracow,
receiving in 1920 the diploma of Doctor Medicinae Universalis (M.D.) and joined
Department of Physiology, being employed as assistant of Professor E. Maydell.
He prepared habilitation thesis in physiology in 1930 entitled „The Influence
of Vegetative Nervous System on Hydrogen Ion Concentration in Blood, Urine and
Digestive Juices” and published it in 1930 by Jagiellonian University Publishing
After Prof. Maydell’s death, he was appointed chairman of the Department of
Physiology in 1933 and then in 1934 he was nominated as Professor of Jagiellonian
University (Fig. 1
||Fig. 1. Professor Kaulbersz
in academic toga in front of lecture hall of Department of Physiology
as freshly nominated professor of Jagiellonian University and chairman
of Department of Physiology.
In general, J. Kaulbersz’s education and subsequent occupations could be divided
into three major periods:
1. Early years and education in Kalisz and Freiburg as described above;
2. Employment at the Department of Physiology of Jagiellonian University before WWII;
3. Work in Department of Physiology of Jagiellonian University Cracow after
WWII (Fig. 2
4. Work in Department of Physiology of Academy of Physical Education in Cracow
||Fig. 2. Prof. J. Kaulbersz
accompanied by first recruited assistants (from the left standing Dr R.
Bilski, Prof. J. Kaulbersz, Drs A. Oginski, T. Radecki and J. Bugajski,
sitting Dr J. Tasler) after his return from USA to Cracow in 1948 year.
In the second period of work at the Cracow Department of Physiology, Dr Kaulbersz, besides teaching medical physiology, was scientifically interested in the assessment of the role of nervous system in the regulation of gastric and pancreatic secretion as outlined in his habilitation thesis (3), confirming major I.P. Pavlov’s results (4) that vagal nerves activated in dogs by sham-feeding or by direct electrical excitation are important for the stimulation of both gastric and pancreatic secretion. His original finding was that the secretory response to central (sham-feeding) and peripheral electrical vagal excitation starts after the 4-7 min of latency period being followed by an increase in gastric acid and pancreatic protein secretion. This latency period was attributed by Jerzy Kaulbersz to the existence in vagal nerves of both inhibitory fibers (more sensitive) and excitatory fibers activated after longer excitation. Similar secretory reactions of the stomach and the pancreas to sham-feeding, were attributed by Kaulbersz to the excitation of stimulatory vagal fibers in these experiments on conscious dogs.
Major scientific achievements of Prof. J. Kaulbersz after his habilitation thesis included: A) Involvement of endocrine factors (pituitary, thyroid and gonads) in the control of gastric secretion in dogs (5-7); B) Effect of endocrine glands (pituitary, thyroid and gonads on the formation of Shay ulcerations and gastric secretion in rats (8, 9); C) Influence of inhibitory factors released from the intestines by fat, glucose and peptone on gastric secretion and healing of various types of experimental peptic ulcerations (10); D) Influence of gastric luminal environment on gastrin release (11); E) Gastric acid secretion after introduction of gastrin into the portal vein (12); F) Implication of bile in gastric secretion (13); G) Effects of various pharmacological agents (reserpine, neurotropic agents) and vagotomy on gastric secretion and peptic ulcerations (14); H) He combined action of cobalt and low atmospheric pressure on hematopoiesis (15); I) Gastric secretion following hypoxia and X-ray irradiation in cats (16); J) Isolation and purification of enterogastrone and urogastrone and their gastric inhibitory effects (17-20).
It should be emphasized that despite very difficult economic and political conditions
after WWII in Poland, Jerzy Kaulbersz was able to attend most of major international
physiological and gastroenterological congresses and to collaborate with his
former American colleagues in completion and publication of his papers in the
most prestigious journals such as American Journal of Physiology
(19, 20) without asking local authorities for permission
as it was requested by official regulations. This probably explains why Kaulbersz
despite of outstanding achievements in modern physiology was considered “unsuitable”
scientist for the election as member to Polish Academy of Sciences.
As mentioned before, the major studies of Prof. Kaulbersz and his co-workers were focused on the neuro-hormonal mechanisms of gastric and pancreatic secretion and the induction or healing of peptic ulcerations in animals.
The most elegant and comprehensive studies were carried out by Prof. Kaulbersz
with American co-workers (5-7) in surgical and physiological departments at
Wayne University College in Detroit, and prepared for the publication in American
in early 50th
after his return to Poland from USA. He was the only Polish physiologist awarded
honorary membership of American Physiological Society and received regularly
subscribed charge-free journals from this Society. As he was employed during
the WWII at the University of Wayne, he received regular income in dollars even
after return to Poland and this small amounts of “hard currency” allowed him
to attend scientific meetings abroad and pay for the reprints of the papers
published in foreign journals.
Using highly purified extracts of urine (urogastrone) and mucosa of the small
intestine (enterogastrone) prepared according to Gray’s techniques (17, 18),
Kaulbersz et al
. showed that the removal of the pituitary and adrenal
grands affected the inhibitory activities of these substances in dogs, suggesting
that the release and action of these potent natural gastric inhibitors may be
modified by major endocrine glands (Fig. 3
). The studies on enterogastrone
and urogastrone raised substantial international interest as following their
publication (19, 20) in prestigious journal such as Gastroenterology
numerous US pharmaceutical companies turned to us with the proposition of a
close collaboration regarding clinical application of these natural gastric
inhibitors in the treatment of peptic ulcer disease in humans but Polish regulations
at that time did not allowed for such collaborative studies. It is of interest
to mention that following our report of urogastrone as anti-secretory and antiulcer
agent, we received from Japan (Hitachi Chemical Company, Ibaraki, Japan) the
synthetic urogastrone that exhibited similar peptide structure and activity
similar to natural urine extract, being called urogastrone-epidermal growth
factor (URO/EGF). It was found in our hands to be highly effective gastric inhibitor
and ulcer healing promoting substance at least in rats with various ulcerations
such induced by stress, cold water immersion and immobilization, taurocholate
or ethanol application (21). These effects of URO/EGF were observed also after
oral application of this substance and found by our group to be mediated by
the stimulation of ornithine decarboxylase (ODC) activity and release of polyamines
such as spermine and putrescine as well as by increased generation of prostaglandin
E2. The antiulcer effects of URO/EGF could be reversed by the suppression of
the prostaglandin-cyclooxygenase activity with aspirin or ODC activity with
difluoro-methyl-ornithine (DFMO). Our further studies showed that urogastrone
is actually epidermal growth factor (EGF) secreted with urine (21).
||Fig. 3. First two papers related
to the isolation and gastric inhibitory activity of enterogastrone and
urogastrone published in Gastroenterology edited by M.I. Grossman
Another topic that was extensively studied under Jerzy Kaulbersz’s supervision
in collaboration with Janina Tasler and Andrzej Oginski (11), both active members
of the Department of Physiology. These studies concerned the mechanisms involved
in the release of gastrin, particularly the inhibitory effect of the acidification
of pyloric area on this release and gastric acid secretion. These studies were
carried out on conscious dogs equipped with double antral pouches, one perfused
with acid solution and another with meat extract and additionally with pouch
fashioned of fundic gland area (Heidenhain pouch) to monitor gastric acid secretion
). It was found that meat extract perfusing one antral pouch resulted
in the copious gastric acid secretion from the Heidenhain pouch due to the release
of gastrin and this effect was suppressed by acid perfusion of another pouch,
in the same dog, indicating that the same pyloric mucosa that is capable to
excite gastric acid secretion (via gastrin release) when perfused with meat
extract and may at the same time inhibit this secretion when perfused with HCl
solution possibly by direct acid suppressing effect on gastrin release from
the antral mucosa or indirectly by the release by acid of local inhibitor of
the gastrin release (Fig. 5
). Since acidification of the antral mucosa
in one antral pouch also inhibited acid secretion from the Heidenhain pouch
stimulated by the ethanol placed in the main stomach or by injection of exogenous
gastrin, it has been proposed that the antral mucosa may release both excitatory
(gastrin) and inhibitory (gastrone or antrogastrone) acting via endocrine pathway
to control acid secretion from the fundic mucosa (Fig. 6
). The results
of these experimental studies have been later confirmed by numerous investigators,
showing that, indeed, antral acidification causes local inhibition of gastrin
release but other substances such as antrogastrone, gastrin-inhibitory peptide
(GIP), vasoactive intestinal peptide (VIP) or somatostatin (SST) released by
D-cells placed neighbouring antral G-cells have been also considered to play
some role in „gastric acid autoregulation” (Fig. 7
4. Gastric inhibitory effects of enterogastrone originating from proximal
and distal intestine of hogs (left panel) and dogs (right panel) (19).
||Fig. 5. Inhibitory effect
of urogastrone originating from dogs with intact or removed adrenal glands
Some controversies regarding the mechanisms of gastrin release with the changes
in antral environment were finally elucidated when Gregory and Tracy (22, 23)
isolated and purified antral hormone (gastrin), showing that it exists in several
molecular forms such as “minigastrin” heptapeptide (G-7), “small gastrin” heptadecapeptide
(G-17), both sulphated gastrin I and unsulfated II and larger or ‘big” gastrin
(G-34). Further progeess in this story was made by Yalow and Berson (24) and
McGuigan and Trudeau (25), who accomplished radioimmunological determination
technique of plasma gastrin permitting the studies with various factors affecting
the release of this hormone from antral mucosa as well as from gastrinoma tumours.
Based on the studies of Debas et al
. (26), release of gastrin under physiological
conditions depends mainly upon the vagal activity and the luminal acidity as
it can be enhanced following antral distension e.g.
by food and blocked
almost completely by pretreatment with atropine and the low pH of antral. In
contrast, Thompson’s group (27, 28) proposed that the suppression of postprandial
gastrin release depends upon the action on G-cells of various hormones such
as gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP) and
secretin originating from the intestinal mucosa. According to our study gastric
acid secretion and mucosal blood flow can be suppressed by certain hormones
such as secretin and VIP (29). With the detailed characterization of the D-cells,
situated in close vicinity of the G-cells and releasing the most effective paracrine
inhibitor of gastrin release such as somatostatin (29), this hormonal substance
has been considered as major mediator of gastrin release by antral acidification
). At the beginning of this century, the enhanced gastrin release
and hipergastrinemia are believed to accompany the gastric infection with Helicobacter
pylori, which is now considered as the major pathogen of human stomach (30).
Studies in vitro
confirmed that epithelial AGS cells infected with H.
exhibit the oxidant-mediated activation of inflammatory signaling
and beta-carotene suppressed the expression of proinflammatory enzymes iNOS
and COX-2 (31).
||Fig. 6. Preparation of double
antral pouches (A&B) for studies of gastrin release and fundic (Heidenhain)
pouch (C) for recording of gastric acid secretion (adapted by permission
from Acta Physiol Pol (11)).
||Fig. 7. Heidenhain secretion
of acid in dogs with perfusion of antral pouch with meat extract plus
saline or HCl solution (upper panel) or meat extract without or with its
acidification (lower panel). (Adapted by permission from Acta Physiol
These studies required not only a variety of animal models, but also the supply of pure synthetic gut hormones and their measurements in plasma using specific radioimmunoassay’s and suitable equipments. They were purchased by funds obtained from the National Institute of Health, Bethesda, USA to support my research activity following my Postdoctoral Fellowship at UCLA, Los Angeles in 1964-66 under supervision of Dr M.I. Grossman, good friend of Prof. Jerzy Kaulbersz. By contacting me with Dr Grossman, Prof. Kaulbersz, already retired in Department of Physiology at Medical Academy on Cracow, could see with satisfaction that our Institute of Physiology could continue and progress in modern research in gastroenterological physiology, competing with other groups from technically more advanced countries than Poland.
The fact that gastrin and most of enterohormones and mediators expressed in
the gastrointestinal mucosa are delivered into the portal circulation and then
pass the liver, raised the question that hepatic modulation of these substances
may affect their activity at the target organ such as the stomach. The interest
in the liver modifying influence on gastric secretagogue resulted in numerous
studies such as that of Gregory in 1906 (32) showing that the ligation of portal
vein or transferring of portal blood into the large veins augmented gastric
secretory response to food ingestion, suggesting that the liver plays important
role in the modification of antral hormone released postprandially into the
portal circulation and its subsequent action on gastric secretion. Kaulbersz
and Bilski (12) were the first in Poland who showed that gastrin extract applied
in dogs into the femoral vein resulted in significantly higher acid output with
shorter latent period and longer duration of gastric secretion than those observed
after the administration of this gastrin preparation into the portal vein (Fig.
). The same authors (13) showed that bile injected intravenously inhibited
gastric acid secretion, whereas that applied intragastrically stimulated this
secretion revealing an important effect of hepatic secretion (bile) on gastric
secretory activity. The mechanism of this interaction between biliary and gastric
secretion has not been disclosed at that time.
||Fig. 8. Gastric acid outputs
from the Heidenhain pouch in dogs receiving injections of gastrin extract
and antral pouch perfused with saline (upper line) or acid solution (lower
lines). (Adapted by permission from Acta Physiol Pol (11)).
Kaulbersz and Bugajski (14) carried out the pharmacological type of studies using reserpine, serotonin, atropine, adrenaline in dogs with innervated and vagally denervated stomach. They confirmed that reserpine exerts a marked stimulatory influence on gastric secretion that can be abolished by the application of atropine or adrenaline and reduced by serotonin, suggesting the crucial role of autonomic, nerves in the control of gastric acid secretion. Radecki and Kaulbersz (33) documented the influence of psychotropic substances such as barbiturates (luminal), psychedrine, caffeine and strychnine on gastric secretion and the formation of gastric lesions in pylorus ligated rats. They observed an inhibitory influence of barbiturate on gastric ulcerogenesis and gastric acid secretion but no change in gastric secretion and gastric ulcers following the application of psychedrine, caffeine or strychnine. These studies had simply “practical” character as these substances were widely used in various clinical conditions, but it was not clear whether they affect gastric acid secretion and gastric ulcerogenesis. The results of this study were the first to clarify that the agents with inhibitory influence on the CNS such as barbiturate also suppress gastric secretion and prevent gastric lesion formation. Most interesting was the finding that the CNS excitatory agents such as caffeine, psychedrine or strychnine, unexpectedly, reduced rather than stimulated gastric secretion and gastric ulcerogenesis in rats.
||Fig. 9. Physiological and
pharmacological profile & regulation of gastric acid secretion.
Prof. Kaulbersz was highly interested in the effects of other environmental conditions such as X-ray irradiation and alteration in oxygen pressure on gastric secretion and ulcerogenesis. Together with A. Barylak and T. Radecki (16) they studied on cats maintained in low pressure chamber, the influence of strong X-irradiation in combination with hypoxia on the gastric secretion. It was found that hypoxia which by itself somewhat attenuated the gastric acid secretion induced by histamine in cats, while preventing the strong inhibitory action of X-irradiation on this secretion.
||Fig. 10. The volume and gastric
acid secretion in response to application of gastrin extract either to
femoral vein or to portal vein (Adapted from Kaulbersz and Bilski (12)).
Prof. Jerzy Kaulbersz was very interested in the physiological phenomena (physical activity, respiratory system and hematopoiesis) of adaptation of humans and animals to the climate of high mountains and hypoxia environments (34-37). He travelled to high mountains such as Mount Blanc in Alps or Cerro de Pasco in Peruvian Andes to investigate also on himself, the effects of hypoxia on hematopoiesis and to examine the limits of respiratory, circulatory and metabolic adaptation to lower atmospheric pressure. This particular aspect of Prof. Kaulbersz research activity was closely connected with the Department of Physiology in Physical Education Academy and will be the subject of separate discussion.
||Fig. 11. The birthday party
organized by prof. J. Kaulbersz for his coworkers in 1965.
This short and incomplete overview of achievements of Kaulbersz and his associates
in experimental gastroenterological research placed him in the highest level
and top rank scientists comparable to those in developed countries such as USA.
With its over 200 papers, predominantly written in English and published in
prestigious American and European journals and presented in numerous congresses
in Europe and America, Prof. Kaulbersz should be undoubtedly considered as leader
in experimental gastrointestinal physiology in Poland. He was the only honorary
Member of American Physiological Association in Poland and at the same time
he kept friendly personal relation with I.P. Pavlov in St. Petersburg. I had
a chance to follow some of Prof. Kaulbersz routes in USA and Europe, where he
was considered and well-respected by the top world gastroenterologists and physiologists
such as Dr A. C. Ivy (Chicago IIl), Dr M.I. Grossman (Los Angeles, LA), Dr L.
Dragstedt (Gainsville, FL), Dr C.F. Code (Rochester MN), Dr R.A. Glass GB (New
York), Dr R.A. Gregory (Liverpool, UK), Dr A. Robert (Kalamazoo MI), and many
others to be a leading world physiological gastroenterologist. An outstanding
research activity of Prof. Kaulbersz was partly due to the fact that he actually
lived in the small room in the Department Physiology so he could spend most
of the time and attention to control the ongoing experimental studies on various
species being undisturbed by family. He used to make rounds twice daily in the
morning to lecture on physiology to medical students and then afternoon to discuss
with students their laboratory work and with his co-workers the ongoing experimental
research and preparation of papers for he next national or international meetings
of physiology or gastroenterology. Despite of enormous capacity to work, Prof.
Kaulbersz had a time to spend with his co-workers relaxing time and always invited
them for his birthday party, which he prepared by himself and considered as
"holy" tradition (Fig. 9
||Fig. 12. Ceremony of Diploma
of Doctor Honoris Causa assigned to prof. Kaulbersz by the Rector of Academy
of Medicine in Cracow in 1974.
- Kaulbersz GJ. Biological Observations on Asellus aquaticus. Jena , Gustav Fischer, 1913.
- Kaulbersz GJ. The Electrical Excitability of the Nerves and Muscles in War Disabled People with Spinal Cross Damage. Jena, Gustav Fischer, 1918.
- Kaulbersz J. On the Influence of Vegetative Nervous System on Hydrogen ion Concentration in Blood, Urine and Digestive Juices, Krakow, Jagiellonian University Publications 1930.
- Pavlov IP. The Work of the Digestive Glands. W.H. Thompson (transl.). London, Griffin, 1910.
- Kaulbersz J, Patterson TL, Sandweiss DJ. Further experiments on effects of urine extracts from hypophysectomized dogs on gastric secretion. Am J Physiol 1954; 176: 388-392.
- Kaulbersz J, Patterson TL, Sandweiss DJ, Saltzstein HC. The effect of urine extract from thyroidectomized dogs on gastric secretion. Rev Gastroenterol 1949; 16: 257-259.
- Kaulbersz J, Patterson TL, Sandweiss DJ. The effect of urine extract from ooephorectomized dogs on gastric secretion. Rev Gastroenterol 1949; 16: 254-256.
- Konturek S, Radecki T, Kaulbersz J. Shay ulcer in hypophysectomized rats. Acta Physiol Pol 1958; 9: 601-606.
- Radecki T, Konturek S, Kaulbersz J. Effect of thyroid, adrenal and gonad extirpation on gastric ulcer formation and secretion in rats. Acta Physiol Pol 1963; 14: 29-35.
- Radecki T, Konturek S, Kaulbersz J. Studies on the effect of fat as well as of glucose, sodium chloride and peptone solutions on gastrin motility in rats. Acta Physiol Pol 1970; 21: 410-417.
- Kaulbersz J, Tasler J, Oginski A. Mechanism of the inhibitory effect of the pyloric area acidification on gastric secretion. Acta Physiol Pol 1972; 13: 409-417.
- Kaulbersz J, Bilski R. Gastric secretion after introduction of gastrin into the portal vein. 2nd World Congress of Gastroenterology, Munich 1962; 2: 75-79.
- Kaulbersz J, Bilski R. The effect of bile applied intragastrically and intravenously on gastric secretion. Acta Physiol Pol 1954; 54: 57-70.
- Kaulbersz J, Bugajski J. Studies on the mechanism of action of reserpine on gastric secretion. Acta Physiol Pol 1967; 18: 411-422.
- Kaulbersz J, Taler J, Bugajski J. The combined action of cobalt and low atmospheric pressure on hematopoiesis. Acta Biol Crac 1962, 5: 95-107.
- Kaulbersz J, Barylak A, Radecki T. Gastric secretion in cats after intensive irradiation connected with previous and simultaneous hypoxia. Acta Physiol Pol 1954; 15: 71-73.
- Gray JS, Bradley WB, Ivy A. On the preparation and biological assay of enterogastrone. Am J Physiol 1937; 118: 463-467.
- Gray JS, Culmer CU, Wieczorowski E, Adkinson JI. Preparation of pyrogen-free urogastrone. Proc Soc Exp Biol N Y 1940; 43: 225-230.
- Kaulbersz J. Konturek S. Comparison of enterogastrone derived from various sections of the intestine. Gastroenterology 1962; 43: 457-462.
- Konturek S, Kaulbersz J. Effect of urogastrone from adrenalectomized dogs on gastric secretion. Gastroenterology 1963; 44: 801-804.
- Konturek SJ, Brzozowski T, Dembinski A. Gastric protective and ulcer healing action of epidermal growth factor. In Advances in Drug Therapy of Gastrointestinal Ulcerations. A. Garner, B.J.R. Whittle (eds). Chichester, John Wiley and Sons, 1989, pp. 262-273.
- Gregory RA, Tracy HJ. The constitution and properties of two gastrins extracted from hog antral mucosa: I. The isolation of two gastrins from hog antral mucosa. II. The properties of two gastrins isolated from hog antral mucosa Gut 1964; 5: 103-117.
- Gregory RA, Tracy JJ. Isolation of two “big gastrins” from Zollinger-Ellison tumor tissue. Lancet 1972; 2: 797-799.
- Yalow RS, Berson SA. Further studies on the nature of immunoreactive gastrin in human plasma. Gastroenterology 1871; 60: 203-214.
- McGuigan JE. Production and characterization of specific antibodies to gastrin with no cross-reacivity with cholecystokinin-pancreaozymin. Am J Med Sci 1970; 260: 139-149.
- Debas HT, Walsh JH, Grossman MI. Mechanisms of release of antral gastrin. In Gastrointestinal Hormones, JC. Thompson (ed.). Univ. Texas Press, 1975, pp. 425-436.
- Villar HV, Fender HR, Rayford PL, Ramus I, Thompson JC. Inhibition of gastrin release by GIP and VIP. In Gastrointestinal Hormones, J.C. Thompson (ed.). Univ. Texas Press, 1975, pp. 467-474.
- Becker HD, Reeder DD, Thompson JC. Vagal control of gastrin release. In Gastrointestinal Hormones, J.C. Thompson (ed.). Univ. Texas Press, 1975, pp. 437-446.
- Dockray GJ. Peptide control systems of the gut as therapeutic targets. In Advances in Drug Therapy of Gastrointestinal Ulceration. A. Garner, B.J.R. Whittle (eds.). Chichester, John Wiley and Sons, 1988, pp. 231-248.
- Konturek PC, Konturek SJ, Brzozowski T. Helicobacter pylori infection in gastric cancerogenesis. J Physiol Pharmacol 2009; 60: 3-21.
- Jang SH, Lim JW, Kim H. Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells. J Physiol Pharmacol 2009; 60(Suppl 7): 131-137.
- Gregory RA. Gastric secretory responses after portal venous ligation. J Physiol (London) 1906, 144: 123-137.
- Radecki T, Kaulbersz J. The influence of factors modifying the excitability of the c1ntral nervpus system on experimental peptic ulcers in rats. Acta Physiol Pol 1955; 56: 13-18.
- Kaulbersz J. Recherches sur resistance des erytrocytes. Bulletin International de l’Academie Polonaise des Sciences et des Lettres 1932; 261-292.
- Kaulbersz J. Resistance of erythrocytes and the reticulocyte count at high mountains. Medycyna Doswiadczalna i Spoleczna 1934; 18: 1-39.
- Kaulbersz J. Blood under the influence of climatic changes. Acta Biol Exp 1939: 13: 118-132.
- Kaulbersz J. The limits of physical effort in the light of physiology of exercise. Ann Rev 1971; 10: 85-92.