{"id":90,"date":"2023-01-18T10:22:00","date_gmt":"2023-01-18T09:22:00","guid":{"rendered":"https:\/\/kurbel.org\/?page_id=90"},"modified":"2023-01-18T10:22:00","modified_gmt":"2023-01-18T09:22:00","slug":"reference-31-40","status":"publish","type":"page","link":"https:\/\/kurbel.org\/?page_id=90","title":{"rendered":"Reference 31-40"},"content":{"rendered":"\n<p><strong>Prof. Sven Kurbel MD, PhD \u2013 personal web pages<\/strong><br>Dept. of Physiology, Osijek Medical Faculty<br>J. Huttlera 4, 31000 Osijek, Croatia<br>e-mail: sven@jware.hr<\/p>\n\n\n\n<p><strong>31. Inertia of endocrine systems due to hormone binding to circulatory proteins.<br>Kurbel S, Zuci\u0107 D, Kurbel B, Gulam D, Gmajni\u0107 R, Krajina Z.<br>Med Hypotheses. 2003 Mar;60(3):430-8.<\/strong><\/p>\n\n\n\n<p>Osijek Medical Faculty, University of JJ Strossmayer, Croatia.<br>sven.kurbel@public.srce.hr<br>It is often presumed that the main role of hormone binding to albumins and<br>binding proteins (BPs) is to reduce oscillating levels of free hormone<br>molecules and to transport steroid hormones. This paper is an attempt to<br>define possible consequences of hormone molecules binding to carrier<br>proteins in circulation.Binding to albumins and BPs prevents exact and<br>quick control of hormone actions. Hormones without significant protein<br>binding govern vital and fast acting regulatory mechanisms (blood glucose<br>or calcium) in which any added inertia might be dangerous. In the<br>presented model, the added inertia for a partially bound hormone (H) is<br>defined as: H(bound)\/H(free). Values, calculated from the reported data,<br>range from 0.4 for GH to more than 2000 for T(4). In comparison to<br>albumins, high-affinity BPs make more stable reserve that would cover<br>periods of low or no hormone secretion. At the same time, hormone<br>molecules are taken away from the blood level control and thus might be<br>considered sequestrated.For hormones without protein binding, the<br>well-perfused areas of the body, or the areas with increased capillary<br>permeability, would be more exposed, making an uneven distribution among<br>target tissues. For the hormone that binds blood proteins, places of<br>secretion and tissue perfusion become unimportant, since the hormone is<br>being liberated anywhere in the circulation (i.e., for strongly bound<br>IGFs, IGF binding proteins do not just stabilize proinsulin actions of<br>IGF-1, but also make all parts of body to be under the same exposure to<br>liberated IGFs, an important feature to promote a symmetrical bone<br>growth).Estrogens are known to stimulate liver secretion of different BPs.<br>A possible explanation is that in the follicular phase there is a small<br>initial mass of granulosa cells, and it takes time to saturate free<br>estrogen carriers, before the normal free hormone level can be reached and<br>FSH secretion inhibited. Less inert peptide inhibin might suppress FSH<br>before free estrogens reach the required level. Without inhibin<br>suppression, an increased FSH level with an increased number of growing<br>follicles can be expected. Estrogens increased production of BPs augments<br>inertia of the estrogen loop and possibly modulates the FSH\/estrogen<br>negative feedback.<br>Publication Types:<br>Research Support, Non-U.S. Gov\u2019t<br>MeSH Terms:<br>Albumins\/metabolism<br>Animals<br>Endocrine System\/pathology\/*physiology<br>Estrogens\/metabolism<br>Growth Hormone\/metabolism<br>Hormones\/*metabolism<br>Humans<br>Models, Theoretical<br>Protein Binding<br>Substances:<br>0 (Albumins)<br>0 (Estrogens)<br>0 (Hormones)<br>9002-72-6 (Growth Hormone)<br>Publication Status: ppublish<br>PMID: 12581625 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>32. The osmotic gradient in kidney medulla: a retold story.<br>Kurbel S, Dodig K, Radi\u0107 R.<br>Adv Physiol Educ. 2002 Dec;26(1-4):278-81.<\/strong><\/p>\n\n\n\n<p>Department of Physiology, Osijek Medical Faculty, 31000 Osijek, Croatia.<br>sven.kurbel@public.srce.hr<br>This article is an attempt to simplify lecturing about the osmotic<br>gradient in the kidney medulla. In the model presented, the kidneys are<br>described as a limited space with a positive interstitial hydrostatic<br>pressure. Traffic of water, sodium, and urea is described in levels (or<br>horizons) of different osmolarity, governed by osmotic forces and positive<br>interstitial pressure. In this way, actions of the countercurrent<br>multiplier in nephron tubules and of the countercurrent exchanger in vasa<br>recta are integrated in each horizon. We hope that this approach can help<br>students to better accept conventional presentations in their textbooks.<br>Publication Types:<br>Research Support, Non-U.S. Gov\u2019t<br>MeSH Terms:<br>Humans<br>Kidney Medulla\/*metabolism<br>Osmosis<br>Physiology\/*education<br>*Teaching<br>Publication Status: ppublish<br>PMID: 12443999 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<br>Free at producer site<\/p>\n\n\n\n<p><strong>33. Amoxycillin, clarithromycin and either sucralfate or pantoprazole for eradication of Helicobacter pylori in duodenal ulcer (a randomized<br>controlled trial).<br>Vcev A, Vceva A, Kurbel S, Takac B, Stimac D, Ivandi\u0107 A, Ostoji\u0107 R, Barbir<br>A, Hovat D, Mihaljevi\u0107 S.<br>Wien Klin Wochenschr. 2001 Dec 17;113(23-24):939-41.<\/strong><\/p>\n\n\n\n<p>Internal Clinic, Clinical Hospital Osijek. btakac@gmx.net<br>BACKGROUND: Sucralfate enhances the anti-Helicobacter pylori activity of<br>antimicrobials and has an inhibitory effect on H. pylori. AIM: To evaluate<br>the efficacy and safety of one-week sucralfate-based eradication therapy<br>for H. pylori infection in patients with duodenal ulcers, compared with<br>treatment based on pantoprazole, in a randomized controlled multicenter<br>study. METHODS: One hundred and twenty patients with active duodenal<br>ulcers and H. pylori infection were treated with amoxycillin 1 g b.d. plus<br>clarithromycin 500 mg b.d. for the first 7 days. Patients were randomly<br>assigned to receive either sucralfate 1 g t.d.s. for 4 weeks (SAC group; n<br>= 60) or pantoprazole (PAC group; n = 60) 40 mg b.d. for the first 7 days<br>and 40 mg o.d. for the next 3 weeks. The patient\u2019s H. pylori status was<br>determined by a urease test and histological investigation before the<br>treatment, and again 4 weeks after cessation of all medication. RESULTS:<br>One hundred and eleven patients completed the study. H. pylori infection<br>was eradicated in 76.4% (42\/55) of patients in the SAC group (ITT<br>analysis: 70%, 95% CI: 58-80%) vs. 85.7% (48\/56) of patients in the PAC<br>group (ITT analysis: 80%, 95% CI: 70-89) (N.S.). All ulcers had healed.<br>There were no significant differences between the two regimens regarding<br>the occurrence of adverse effects. CONCLUSION: Our study shows that<br>one-week triple therapy with amoxycillin, clarithromycin and either<br>pantoprazole or sucralfate are effective regimens to cure H. pylori<br>infection in patients with duodenal ulcer.<br>Publication Types:<br>Clinical Trial<br>Comparative Study<br>Randomized Controlled Trial<br>MeSH Terms:<br>2-Pyridinylmethylsulfinylbenzimidazoles<br>Adult<br>Aged<br>Amoxicillin\/*administration &amp; dosage\/adverse effects<br>Benzimidazoles\/*administration &amp; dosage\/adverse effects<br>Clarithromycin\/*administration &amp; dosage\/adverse effects<br>Drug Therapy, Combination<br>Duodenal Ulcer\/diagnosis\/*drug therapy<br>Duodenoscopy<br>Female<br>Follow-Up Studies<br>Helicobacter Infections\/diagnosis\/*drug therapy<br>Helicobacter pylori\/*drug effects<br>Humans<br>Male<br>Middle Aged<br>Omeprazole\/analogs &amp; derivatives<br>Sucralfate\/*administration &amp; dosage\/adverse effects<br>Sulfoxides\/*administration &amp; dosage\/adverse effects<br>Substances:<br>0 (2-Pyridinylmethylsulfinylbenzimidazoles)<br>0 (Benzimidazoles)<br>0 (Sulfoxides)<br>102625-70-7 (pantoprazole)<br>26787-78-0 (Amoxicillin)<br>54182-58-0 (Sucralfate)<br>73590-58-6 (Omeprazole)<br>81103-11-9 (Clarithromycin)<br>Publication Status: ppublish<br>PMID: 11802510 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>34. Model of interstitial pressure as a result of cyclical changes in the<br>capillary wall fluid transport.<br>Kurbel S, Kurbel B, Belovari T, Mari\u0107 S, Steiner R, Boz\u00ed\u0107 D.<br>Med Hypotheses. 2001 Aug;57(2):161-6.<\/strong><\/p>\n\n\n\n<p>Osijek Medical Faculty, University JJ Strossmayer, 31000 Osijek, Croatia.<br>sven.kurbel@public.srce.hr<br>Reported interstitial pressures range from -8 to +6 mm Hg in different<br>tissues and from &lt;-20 mm Hg in burned tissue or more than +30 mm Hg in<br>tumors. We have tried to link interstitial pressure to the here proposed<br>cyclical changes in the fluid transport across the capillary wall.In the<br>presented model interstitial pressure is considered as an average of<br>pressures in numerous pericapillary spaces. A single pericapillary<br>pressure is a dynamic difference between the net outward (hydraulic<br>pressure+interstitial colloid osmotic pressure) and inward (plasma colloid<br>oncotic pressure) forces. Hence, dominating net outward forces would<br>result in a positive pericapillary interstitial pressure, while stronger<br>inward forces would produce negative pressures in the pericapillary space.<br>All interruptions of blood flow leave some blood in capillaries with a<br>normal oncotic pressure and no hydrostatic pressure that might act as a<br>strong absorber of interstitial fluid until the blood flow is<br>reestablished.Model assumptions for the systemic circulation capillaries<br>include (a) precapillary sphincters can almost entirely stop the capillary<br>flow, (b) only a minority of sphincters are normally open in the tissue,<br>and (c) hydrostatic pressures in unperfused capillaries are similar to the<br>pressures at their venous ends.The key proposal is that capillaries with<br>closed precapillary sphincters along their entire length have low<br>hydrostatic pressure of 10 to 15 mm Hg. This pressure cannot force<br>filtration, so these capillaries reabsorb interstitial fluid from the<br>pericapillary space along their entire length. In the open capillaries,<br>hydrostatic pressure filtrates fluid to the pericapillary space along most<br>of their length. Fluid enters, moves some 20 or 30 micrometers away and<br>back to be reabsorbed at the same point. Closed periods are periods of<br>intense fluid reabsorption, while the short open periods refill the space<br>with fresh fluid. It can be calculated that subcutaneous tissue<br>interstitial pressure values might develop if the closed periods are 1.14<br>to 2.66 times longer than the open periods. Positive interstitial<br>pressures observed in some organs might develop if open periods are longer<br>than the closed periods.High interstitial colloid pressure in lungs makes<br>both perfused and unperfused capillaries absorptive, resulting in more<br>negative values of lung interstitial pressure. The same model is used to<br>explain interstitial pressure values in tumors, burned tissue and<br>intestinal villi.<br>Copyright 2001 Harcourt Publishers Ltd.<\/p>\n\n\n\n<p>MeSH Terms:<br>*Blood Pressure<br>Capillaries\/*physiology<br>Endothelium, Vascular<br>*Models, Biological<br>Publication Status: ppublish<br>PMID: 11461165 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>35. A model of the gastric gland ejection cycle: low ejection fractions<br>require reduction of the glandular dead space.<br>Kurbel S, Kurbel B, Dmitrovi\u0107 B, Vcev A.<br>J Theor Biol. 2001 Jun 7;210(3):337-43.<\/strong><\/p>\n\n\n\n<p>Osijek Medical Faculty, University JJ Strossmayer, Osijek, Croatia.<br>sven.kurbel@public.srce.hr<br>This paper was inspired by the reported results of authors from Uppsala<br>and Lund that gastric glands in rats rhythmically contract 3-7 cycles per<br>minute and develop luminal pressures more than 10 mmHg. To ensure that<br>pepsinogen is not retained in the acid-rich section of the gland, ejection<br>fractions would need to be more than 50% of the gland volume. We have<br>tried to calculate the ejection fraction of such contractions. Dimensions<br>of human gastric glands were measured on the fresh frozen samples of<br>macroscopically and histologically normal gastric mucosa. In total, 18<br>specimens (from nine persons) were measured under the microscope. The<br>density of glands was 135 +\/- 11 (mean +\/- S.D.) glands per mm( 2) of<br>gastric mucosa. A typical gastric gland is a tubular structure 1.2 +\/-<br>0.22 mm long and 0.03-0.05 mm wide. We have used 1 mm for length and 0.03<br>mm for the gland diameter to calculate that each gland approximates a<br>volume of 707 pl, suggesting that the total glandular volume for 15<br>million glands reaches 10.6 ml. Further calculations based on one to five<br>contractions per minute on an average and on the total volume of gastric<br>glands of 10 ml showed that only ejection fractions less than 10% deliver<br>daily volumes less than 3 l. The presented model of the gastric gland<br>activity is based on the idea that the low ejection fractions require a<br>reduction of the glandular dead space. The reduced luminal pressure during<br>the gland relaxation might cause backflux of hydrophobic viscoelastic<br>mucus through the gland aperture. Repeated glandular contractions and<br>relaxations would move the mucus all the way to the gland bottom, filling<br>the gland cavity below the neck with an axial semisolid mucous cylinder.<br>This filling would reduce the gland dead space. During contractions, the<br>gland would eject mainly the peripheral, the more liquid part of its<br>content. The decreasing luminal pressure in the relaxing gland would pull<br>the outlet mucus inside, protecting gland apertures from the gastric<br>juice.<br>Copyright 2001 Academic Press.<\/p>\n\n\n\n<p>MeSH Terms:<br>Bicarbonates\/*metabolism<br>Gastric Mucosa\/anatomy &amp; histology\/*secretion<br>Humans<br>Hydrogen-Ion Concentration<br>Ion Transport<br>Models, Biological<br>Mucus\/*secretion<br>Substances:<br>0 (Bicarbonates)<br>Publication Status: ppublish<br>PMID: 11397134 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>36. A model of hydraulic interactions in liver parenchyma as forces behind<br>the intrahepatic bile flow.<br>Kurbel S, Kurbel B, Dmitrovic B, Wagner J.<br>Med Hypotheses. 2001 May;56(5):599-603.<\/strong><\/p>\n\n\n\n<p>Physiology, Osijek Medical Faculty, University JJ Strossmayer, Osijek,<br>Croatia. sven.kurbel@public.srce.hr<br>The small diameters of bile canaliculi and interlobular bile ducts make it<br>hard to attribute the bile flow solely to the process of secretion. In the<br>model liver within its capsule is considered a limited space in which<br>volume expansions of one part are possible only through the shrinking of<br>other parts. The liver capsule allows only very slow volume changes. The<br>rate of blood flow through the sinusoides is governed by the<br>Poisseuill-Hagen law. The model is based on a concept of circulatory liver<br>units. A unit would contain a group of acini sharing the same conditions<br>of arterial flow. We can imagine them as an acinar group behind the last<br>pressure reducer on one arterial branch. Acini from neighboring units<br>compose liver lobules and drain through the same central venule. One<br>lobule can contain acini from several neighboring circulatory units. The<br>perfusion cycle in one unit begins with a transient tide in the arterial<br>flow, governed by local mediators. Corresponding acini expand, grabbing<br>the space by compressing their neighbors in the same lobules. Vascular<br>resistance is reduced in dilated and increased in compressed acini. Portal<br>blood flows through the dilated acini, bypassing the compressed neighbors.<br>The cycle ends when the portal tide slowly diminishes and acinar volume is<br>back on the interphase value until the new perfusion cycle is started in<br>another circulatory unit. Each cycle probably takes minutes to complete.<br>Increased pressures both in dilated and in compressed acini force the bile<br>to move from acinar canalicules. Both up and down changes in acinar volume<br>might force the acinar biliary flow. In cases of arterial<br>vasoconstriction, increased activity of vasoactive substances would keep<br>most of the circulatory units in the interphase and increased liver<br>resistance can be expected. Liver fibrosis makes all acini to be of fixed<br>volume and result in increased resistance. Because of that, low pressure<br>portal flow would be more compromised, as reported. In livers without<br>arterial blood flow, although some slow changes in the portal flows can be<br>expected, acinar volume changes should be reduced. In acute liver injury,<br>enlarged hepatocytes would diminish sinusoidal diameter and increase<br>acinar resistance. In liver tumors, areas of neovascularization with<br>reduced resistance would divert the arterial flow from the normal tissue,<br>while in the compressed perifocal areas, increased vascular resistance<br>should diminish mainly the portal flow.<br>Copyright 2001 Harcourt Publishers Ltd.<\/p>\n\n\n\n<p>MeSH Terms:<br>Bile\/*secretion<br>Bile Ducts, Intrahepatic\/*physiology\/secretion<br>Blood<br>Liver\/*physiology<br>Publication Status: ppublish<br>PMID: 11388774 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>37. Intracranial infection after missile brain wound: 15 war cases.<br>He\u0107imovi\u0107 I, Dmitrovi\u0107 B, Kurbel S, Blagus G, Vranes J, Rukovanjski M.<br>Zentralbl Neurochir. 2000;61(2):95-102.<\/strong><\/p>\n\n\n\n<p>Division of Neurosurgery, University Hospital Osijek, Osijek University<br>Medicine School.<br>OBJECTIVES: The present study describes 15 cases of intracranial<br>infections developed in a group of in patients with missile brain wound<br>(MBW), during the war in Croatia in the region of East Slavonia. METHOD:<br>The retrospective study included 88 MBW casualties. There were 11 females<br>and 77 males aged 2-80 years. The projectile penetration of the cranial<br>dura was confirmed and the presence of intracranially retained foreign<br>bodies was evaluated with computerized tomography (CT) in all the<br>patients. The wounded were treated according to the modern recommendations<br>of neurotrauma care. However, we extracted only accessible bone\/metallic<br>fragments during intracranial debridement. All intracranial infections<br>were documented by cultures, CT, surgery or autopsy. The mean follow-up<br>period of wounded with intracranial infections was 2.4 years (range, 10<br>days to 7 years). RESULTS: Intracranial infection developed in 14 patients<br>(17%) as \u201cearly intracranial infections\u201d. Among 14\/15 cases, infection<br>developed within the first 8 weeks, and in 1 case 5 months after wounding.<br>We recorded 4 cases of isolated bacterial meningitis, whereas in 9 cases<br>brain abscess had developed. In 6 cases brain abscess was associated with<br>concomitant meningitis and epidural empyema. Local cerebritis developed in<br>one case, as well as subdural empyema with the concomitant meningitis in<br>one case. There were 8 deaths in total of 15 cases. Glasgow Outcome Score<br>3 was observed in 2 and good outcome in 5\/15 cases. The infectious<br>organisms were isolated in 8 cases. Gram-positive bacteria were found in<br>12 different specimens. Gram-negative bacteria were found in 9 specimens.<br>The most frequently isolated organism was Staphylococcus aureus.<br>beta-hemolytic streptococcal and clostridial infections were not observed.<br>Among the 15 patients with intracranial infection, just one did not have<br>intracranially retained bone and\/or metallic fragments. However, among the<br>73 head injuries without intracranial infections only 10 did not have<br>retained fragments. CSF fistula and\/or dehiscence developed in 13\/15<br>patients with intracranial infection. In 67\/73 wounded without<br>intracranial infections, wound complications were not registered.<br>CONCLUSIONS: The liberal use of post-contrast CT of the brain within the<br>first 2 months after injury, especially if performed early in the clinical<br>course, can lead to a prompt diagnosis of most of \u201cearly intracranial<br>infections\u201d. The surgical procedures in order to prevent wound CSF<br>fistula\/dehiscence development are absolutely necessary. The immediate<br>scalp and dural wound repair in case of wound complications are absolutely<br>indicated and if needed, the procedures can be repeated. However, it seems<br>that retained fragments are not responsible for an increased rate of<br>intracranial infection.<br>MeSH Terms:<br>Adolescent<br>Adult<br>Brain Abscess\/*etiology\/physiopathology<br>Brain Diseases\/*microbiology<br>Brain Injuries\/*complications<br>Croatia<br>Female<br>Fever<br>*Foreign Bodies<br>Glasgow Coma Scale<br>Gram-Negative Bacterial Infections\/etiology<br>Gram-Positive Bacterial Infections\/etiology<br>Humans<br>Male<br>Middle Aged<br>Retrospective Studies<br>*War<br>Wound Infection\/*diagnosis\/physiopathology<br>Wounds, Gunshot\/*complications\/physiopathology<br>Publication Status: ppublish<br>PMID: 10986758 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>38. Cancer incidences in the digestive tube: is cobalamin a small intestine<br>cytoprotector?<br>Kurbel S, Kovacic D, Radic R, Drenjancevic I, Glavina K, Ivandic A.<br>Med Hypotheses. 2000 Mar;54(3):412-6.<\/strong><\/p>\n\n\n\n<p>Physiology, University \u2018JJ Strossmayer\u2019, Osijek Medical Faculty, Osijek,<br>Croatia. sven.kurbel@public.srce.hr<br>Malignancies are common in the digestive tube, although with unequal<br>distribution among segments. The aim of this paper was to compare<br>available interpretations of the low cancer incidence in the small bowel<br>and high in the large bowel. Supposed mechanisms include relatively small<br>bacterial population, large secretion of liquid and rapid transit in the<br>small bowel. Small bowel mucosa is the main absorptive part of the<br>digestive tube with absorption rates for various nutrients so high that<br>they can even be considered as clearances from the intestinal content.<br>Consequently, these nutrients are not present in the large bowel. An<br>alternative explanation is that an absorbable protective substance from<br>the intraluminal content, might protect the mucosa from malignant<br>transformations. It can be speculated that if there are any cytoprotective<br>substances in the digested food their effect would be expressed mostly in<br>the absorptive small intestine, leaving the large bowel mucosa<br>unprotected. Vitamin B12 might be a possible candidate for this role.<br>Cobalamin molecules are initially bound to haptocorrin (Hc) in the<br>stomach, but in the small intestine B12 is transferred to intrinsic factor<br>(IF) after the action of pancreatic trypsin on Hc. Cobalamin-IF complexes<br>are absorbed in the terminal ileum leaving only a small fraction of B12 to<br>enter the large bowel. We have tried to summarize available data regarding<br>cancer incidences in digestive tube, segmental length and transit times of<br>tube content. Cancer density is calculated as incidence per length and<br>transit speed as length per transit time. Cancer incidences for seven<br>intestinal segments were considered low if they were below one case per<br>100 000 inhabitants annually, while the low cancer density meant less than<br>six cases per 100 000 inhabitants per metre. For instance, transverse<br>colon was considered as a high cancer incidence place (2.15 cases), with<br>low cancer density (4.3 cases\/m). Transit speed more than 0.3 metre\/hour<br>was associated with low cancer incidences (accuracy 0.85) and low cancer<br>density segments (accuracy 1.00). Cobalamin availability showed similar<br>distribution, available in low incidence segments and unavailable in high<br>incidence segments. Experimental studies are needed to quantify B12<br>availability in the large bowel and to determine whether small amounts of<br>B12-IF or, perhaps, B12-haptocorrin complexes are absorbed by the small<br>bowel mucosa. Without that, no cytoprotective effects of B12 in the<br>digestive tube can be expected.<br>Copyright 2000 Harcourt Publishers Ltd.<\/p>\n\n\n\n<p>MeSH Terms:<br>Anticarcinogenic Agents\/*pharmacology<br>Digestive System Neoplasms\/*epidemiology\/*prevention &amp; control<br>Humans<br>Incidence<br>Intestine, Small\/*pathology<br>Vitamin B 12\/*pharmacology<br>Substances:<br>0 (Anticarcinogenic Agents)<br>68-19-9 (Vitamin B 12)<br>Publication Status: ppublish<br>PMID: 10783476 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>39. Histochemical changes in the rectal mucosa of diabetic patients with<br>and without diarrhea or constipation.<br>Ivandi\u0107 A, Prpic-Krizevac I, Dmitrovi\u0107 B, Vcev A, Kurbel S, Peljhan V, Bacun T.<br>Wien Klin Wochenschr. 2000 Jan 14;112(1):21-6.<\/strong><\/p>\n\n\n\n<p>Department of Internal Medicine, Osijek University Hospital, Croatia.<br>Sixty-four diabetic patients, 35 with diarrhea, 15 with constipation and<br>14 without stool problems, and forty healthy subjects, were subjected to<br>rectosigmoidoscopy. During rectosigmoidoscopy, rectal biopsy specimens for<br>histological and histochemical analysis were obtained. Histological<br>findings of nonspecific colitis in 25 out of 64 diabetic patients were<br>uniformly distributed among the three groups (p = 0.959). However, the<br>finding was slightly more common in diabetic patients than in controls<br>(eight out of 40 control subjects, p = 0.043). A positive PAS reaction was<br>observed in 30 out of 64 diabetic patients and was also uniformly<br>distributed among the three groups (p = 0.508), but was significantly more<br>common among diabetic patients than controls (three out of 40, p &lt; 0.001).<br>A positive reaction to cholesterol was found in 46 out of 64 diabetic<br>patients, also uniformly distributed among the three groups (p = 0.773).<br>It was significantly more common in diabetic patients than in controls<br>(nine out of 40, p &lt; 0.001). Reactions of the rectal mucosa histological<br>specimens to glycogen and triglycerides were negative, both in diabetic<br>patients and in controls. In conclusion, it appears that stool problems<br>among our diabetic patients were not related to the positivity of PAS or<br>to the positive cholesterol reaction in the rectal mucosa histological<br>specimens. Since positive findings of both reactions were more common in<br>specimens taken from diabetic patients than in controls, positive<br>reactions might be related to metabolic disturbances in diabetic patients.<br>MeSH Terms:<br>Adult<br>Aged<br>Biopsy<br>Cholesterol\/metabolism<br>Colitis\/pathology<br>Constipation\/pathology<br>Diabetes Mellitus, Type 1\/*pathology<br>Diabetes Mellitus, Type 2\/*pathology<br>Diarrhea\/pathology<br>Female<br>Humans<br>Intestinal Mucosa\/*pathology<br>Male<br>Middle Aged<br>Rectum\/*pathology<br>Sigmoidoscopy<br>Substances:<br>57-88-5 (Cholesterol)<br>Publication Status: ppublish<br>PMID: 10689736 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n\n\n\n<p><strong>40. Minoxidil and male-pattern alopecia: a potential role for a local<br>regulator of sebum secretion with vasoconstrictive effects?<br>Kurbel S, Kurbel B, Zani\u0107-Matani\u0107 D.<br>Med Hypotheses. 1999 Nov;53(5):402-6.<\/strong><\/p>\n\n\n\n<p>Department of Physiology, Osijek Clinical Hospital, Croatia.<br>sven.kurbel@public.srce.hr<br>Regulation of the hair cycle takes place at the pilo-sebaceous unit with<br>the sebaceous gland as a sex hormone-dependent part. Although minoxidil<br>stimulates proliferation of follicular cells and activation of<br>prostaglandin endoperoxide synthase-1, it was suggested that other<br>mechanisms, such as an increase in the local blood flow, might mediate the<br>drug effect on hair growth. If that is the case, it is possible that<br>minoxidil counteracts some vasoconstrictive mediator of male-pattern<br>alopecia. This hypothetical vasoconstrictive mediator X would have to meet<br>some criteria: (I) vasoconstriction both in the general circulation and in<br>the hair-growing skin; (II) local vasoconstrictive activity in the hair<br>growing skin should be related to the circulating testosterone level;<br>(III) only an increase in the local mediator X activity causes<br>male-pattern alopecia, since hypertensive patients are not balder than<br>expected. The sebaceous gland is a possible place of the mediator X<br>secretion since it is a sex-hormone-dependent part of the pilo-sebaceous<br>unit. ET-1 might be a suitable candidate for the mediator X, since male<br>hormones raise ET-1 plasma levels and female hormones lower them. The<br>speculation presented here is that ET-1, beside vasoconstriction in the<br>general circulation, might also regulate the sebum secretion, by<br>triggering contractions of the myoepithelial cells. This hypothetical<br>mechanism would normally remain confined to the sebaceous gland. During<br>puberty, sex hormones stimulate growth of sebaceous glands in both sexes.<br>In women hypertrophied sebaceous glands under estrogen control would not<br>increase its ET-1 content, while in men, testosterone would increase ET-1<br>secretion that might affect the neighboring arterioles. Induced<br>vasoconstriction might reduce the hair growth and promote hair loss. If<br>ET-1 plays the described role, then an ET-1 antagonist, i.e. bosentane,<br>should also have some hair-growing properties.<br>MeSH Terms:<br>Alopecia\/blood\/*drug therapy<br>Endothelin-1\/pharmacology<br>Estrogens\/blood<br>Humans<br>Male<br>Minoxidil\/pharmacology\/*therapeutic use<br>Models, Theoretical<br>Sebum\/*secretion<br>Testosterone\/blood<br>Vasoconstriction\/drug effects<br>Vasodilator Agents\/pharmacology\/*therapeutic use<br>Substances:<br>0 (Endothelin-1)<br>0 (Estrogens)<br>0 (Vasodilator Agents)<br>38304-91-5 (Minoxidil)<br>58-22-0 (Testosterone)<br>Publication Status: ppublish<br>PMID: 10616041 [PubMed \u2013 indexed for MEDLINE]<br>From PubMed<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Prof. Sven Kurbel MD, PhD \u2013 personal web pagesDept. of Physiology, Osijek Medical FacultyJ. Huttlera 4, 31000 Osijek, Croatiae-mail: sven@jware.hr 31. Inertia of endocrine systems due to hormone binding to circulatory proteins.Kurbel S, Zuci\u0107 D, Kurbel B, Gulam D, Gmajni\u0107 R, Krajina Z.Med Hypotheses. 2003 Mar;60(3):430-8. Osijek Medical Faculty, University of JJ Strossmayer, Croatia.sven.kurbel@public.srce.hrIt is often presumed that the main role of hormone binding to albumins andbinding proteins (BPs) is to reduce oscillating levels of free hormonemolecules and to transport&hellip;<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-90","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/pages\/90","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/kurbel.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=90"}],"version-history":[{"count":1,"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/pages\/90\/revisions"}],"predecessor-version":[{"id":91,"href":"https:\/\/kurbel.org\/index.php?rest_route=\/wp\/v2\/pages\/90\/revisions\/91"}],"wp:attachment":[{"href":"https:\/\/kurbel.org\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=90"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}