Mechanical response of human thoracic spine ligaments under quasi-static loading: An experimental study.

PURPOSE: This study aimed to investigate the geometrical and mechanical properties of human thoracic spine ligaments subjected to uniaxial quasi-static tensile test. METHODS: Four human thoracic spines, obtained through a body donation program, were utilized for the study. The anterior longitudinal ligament (ALL), posterior longitudinal ligament (PLL), capsular ligament (CL), ligamenta flava (LF), and the interspinous ligament and supraspinous ligament complex (ISL + SSL), were investigated. The samples underwent specimen preparation, including dissection, cleaning, and reinforcement, before being immersed in epoxy resin. Uniaxial tensile tests were performed using a custom-designed mechanical testing machine equipped with an environmental chamber (T = 36.6 °C; humidity 95%). Then, the obtained tensile curves were averaged preserving the characteristic regions of typical ligaments response. RESULTS: Geometrical and mechanical properties, such as initial length and width, failure load, and failure elongation, were measured. Analysis of variance (ANOVA) revealed significant differences among the ligaments for all investigated parameters. Pairwise comparisons using Tukey's post-hoc test indicated differences in initial length and width. ALL and PLL exhibited higher failure forces compared to CL and LF. ALL and ISL + SSL demonstrated biggest failure elongation. Comparisons with other studies showed variations in initial length, failure force, and failure elongation across different ligaments. The subsystem (Th1 - Th6 and Th7 - Th12) analysis revealed increases in initial length, width, failure force, and elongation for certain ligaments. CONCLUSIONS: Variations of both the geometric and mechanical properties of the ligaments were noticed, highlighting their unique characteristics and response to tensile force. Presented results extend very limited experimental data base of thoracic spine ligaments existing in the literature. The obtained geometrical and mechanical properties can help in the development of more precise human body models (HBMs).

Noninvasive monitoring in a patient with SAH diagnosis treated with Cerebrolysin - case report and review of the literature.

BACKGROUND: Subarachnoid hemorrhage (SAH) causes a high percentage of deaths and rehabilitation failures. Despite endovascular and surgery treatment algorithms, there is still no consensus on the guidelines for monitoring and neuroprotective treatment of patients. CASE REPORT: We report a case of a patient with SAH treated endovascularly. The patient was hospitalized in the intensive care unit and monitored using Near Infrared Spectroscopy (NIRS) and Optic Nerve Diameters Assessment (ONDS). CONCLUSIONS: Early and high-dose Cerebrolysin was used safely as neuroprotective treatment intravenously. The treatment using Cerebrolysin and additional monitoring was beneficial for the patient.

SOD1/Rag2 Mice with Low Copy Number of SOD1 Gene as a New Long-Living Immunodeficient Model of ALS.

The most recent research concerning amyotrophic lateral sclerosis (ALS) emphasizes the role of glia in disease development. Thus, one can suspect that the effective therapeutic strategy in treatment of ALS would be replacement of defective glia. One of the basic problems with human glial progenitors (hGRPs) replacement strategies is the time needed for the cells to become fully functional in vivo. The lifespan of most popular high copy number SOD1 mutant mice might be too short to acknowledge benefits of transplanted cells. We focused on developing immunodeficient rag2-/- model of ALS with lower number of transgene copies and longer lifespan. The obtained hSOD1/rag2 double mutant mice have been characterized. QPCR analysis revealed that copy number of hSOD1 transgene varied in our colony (4-8 copies). The difference in transgene copy number may be translated to significant impact on the lifespan. The death of long- and short-living hSOD1/rag2 mice is preceded by muscular weakness as early as one month before death. Importantly, based on magnetic resonance imaging we identified that mutant mice demonstrated abnormalities within the medullar motor nuclei. To conclude, we developed long-living double mutant hSOD1/rag2 mice, which could be a promising model for testing therapeutic utility of human stem cells.

Morphological changes of the vocal fold mucosa in hyperfunctional dysphonia diagnosed by psychoacoustic and videostroboscopic methods.

PURPOSE: The aim of the study was to provide a morphological assessment of the laryngeal mucosa in patients with hyperfunctional dysphonia diagnosed by psychoacoustic and videostroboscopic methods. MATERIAL AND METHODS: Forty patients with voice quality disorders of hyperfunctional dysphonia were recruited for participation in the study. The diagnosis of dysphonia was based on the Voice Rating Scale GRBAS, and endoscopic and stroboscopic assessment of the vocal folds. Acoustic assessment was carried out using following parameters: fundamental frequency, Jitter, Shimmer, Noise to Harmonic Rate and Yanagihara (YG) scale. In order to evaluate the morphology of the vocal fold mucosa transmission electron microscopy was performed using postoperative material obtained from the larynx. Results of clinical and morphological analysis were compared with the reference group. The morphological material was obtained from patients with hypopharyngeal cancer without pathological changes of the vocal folds. RESULTS: The psychoacoustic assessment using the perceptual GRBAS scale enables the appropriate diagnostics of hyperfunctional dysphonia, which was confirmed by evaluation of acoustic parameters and YG scale analysis. In 40 patients with voice quality disorders causing by hyperfunctional dysphonia, in morphological assessment of the laryngeal mucosa, 4 (10%) patients demonstrated the presence of oedema and signs of intensive dysphonia in psychoacoustic and stroboscopic examination. CONCLUSIONS: Oedema of the laryngeal mucosa confirmed by stroboscopic and ultramorphological examination may coexist with hyperfunctional dysphonia. The presence of the laryngeal oedema in patients with hyperfunctional dysphonia has the negative impact on voice quality in psychoacoustic assessment with the use of the GRBAS and YG scales.

The cumulative effect of nuclear factor-kappaB (NF-kappaB) inhibition and endothelins in early cerulein-induced acute pancreatitis in rats.

PURPOSE: To assess effects of NF-kappaB activation inhibitor (pyrrolidine dithiocarbamate--PDTC) alone or with endothelins (ET-1, ET-2, ET-3) in early course of cerulein-induced acute pancreatitis (AP) in rats. MATERIAL AND METHODS: After 4 h of AP in Wistar rats, treated with PDTC 10 or 40 mg/kg or with PDTC 10 mg/kg and ET-1, ET-2 or ET-3, 0.5 or 1.0 nmol/kg twice i.p. in 1 h interval, free active trypsin (FAT), total potential trypsin (TPT) and lipase in 12000 x g supernatants of pancreatic homogenates, plasma alpha-amylase and histological changes were assayed. %FAT/TPT was an index of trypsinogen activation. RESULTS: %FAT/TPT significantly increased to 12.42 +/- 2.14%, lipase to 5.51 +/- 0.84 U/mg protein and alpha-amylase to 28.5 +/- 5.61 U/mL in AP vs 1.96 +/- 0.31%, 1.29 +/- 0.11 U/mg and 5.80 +/- 1.38 U/ml in healthy control. Higher dose PDTC attenuated trypsinogen activation to 3.01 +/- 0.53% and alpha-amylase to 15.3 +/- 1.38. PDTC and ET-1 attenuated %FAT/TPT to 2.55 +/- 0.18% with lower and 2.34 +/- 0.44% with higher dose. ET-3 was less effective than ET-1: 6.76 +/- 0.46% with lower dose. Lower doses of ET-1 and ET-2 with PDTC, diminished lipase activity to 2.60 +/- 0.36 and 2.94 +/- 0.33. CONCLUSIONS: Cumulative attenuation of trypsinogen activation after lower dose of PDTC and ET-1 approximated the effect of higher dose of PDTC. Additional effect of ET-3 was weaker than ET-1, and ET-2 was ineffective in this respect. The combination of this NF-kappaB activation inhibitor and ET-1 could be beneficial in early course of edematous AP by attenuating of trypsinogen activation. However, it should be treated with caution because of some unfavorable effects on histological scores of pancreatic injury.

Effects of endothelin-1 or of its receptor A a selective antagonist, on histological and ultrastructural patterns in experimental acute pancreatitis in rats.

The role of endothelin-1 (ET-1) and of its receptor A (ETA) blockade in oedematous acute pancreatitis (AP) remains unclear. In 40 male Wistar rats with i.p. cerulein-induced AP, lasting 4 hours, ET-1 2x0.5 nmol/kg and 2x1.0 nmol/kg or selective ETA antagonist LU 302146, 10 mg/kg and 20 mg/kg was given i.p. simultaneously with cerulein. Histological and ultrastructural studies of pancreatic specimens were done. ET-1 decreased the inflammatory infiltration, but not the mean scores of necrosis and vacuolization in AP. The ultrastructural damage of acinar cells was less evident after ET-1 than in untreated AP. Selective ETA antagonist slightly aggravated the vacuolization and necrosis of acinar cells and some ultrastructural alterations in AP. In conclusion, ET-1, in contrast to selective ETA antagonist, exerts some protective effect in the early course of oedematous cerulein-induced acute pancreatitis in rats.

Activity of thyroid parafollicular (C) cells in rats with hyperthyroidism--preliminary ultrastructural investigations.

In the thyroid gland of mammals, except the basic follicular (F) cells, parafollicular (C) cells are detected. They belong to disperse neuroendocrine cells of the APUD system. Co-localisation of F and C cells in the thyroid gland is not accidental. It seems possible that there is an interaction between them, mediated by the peptidergic hormones. Calcitonin (CT) is proposed as an essential indicator of C cells. The role of C cells in the function of the thyroid gland has been not clarified till now, especially in hyperthyroid state. There are only a few data which document the ultrastructure of C cells in the physiological and pathological state. In the present study, the ultrastructure of thyroid C cells in an experimental model of hyperthyroidism was evaluated. Our preliminary study may confirm the functional interaction between follicular and parafollicular cells in the thyroid gland.

Assessment of connective tissue fibres in walls of allogenic arterial grafts preserved by the method of cold ischemia--a preliminary report.

The aim of the study was to evaluate microscopic changes in the wall structures of allogenic arterial grafts, preserved by the method of cold ischemia in relation to the storage period and to test the possibility of the storage period prolongation by allograft freezing at -70 degrees C. The middle layer ultrastructure is well preserved till 30 days from allograft harvesting, however, allograft freezing results in total destruction of elastic and collagen fibres in the arterial wall. An application of allogenic arterial grafts, preserved by the method of cold ischemia till 30 days from their harvesting, seems an efficient therapeutic method in the treatment of patients with synthetic vascular graft infection. Further prolongation of the storage period at -70 degrees C made the allograft useless for implantation.

The effect of endothelin-1, endothelin-2 and endothelin-3 in early cerulein-induced acute pancreatitis in rats.

PURPOSE: To assess the effect of endothelins: ET-1, ET-2 and ET-3 on trypsinogen activation, lipase activity and histological changes in the pancreas in early (4 hrs) cerulein acute pancreatitis (AP) in rats. MATERIAL AND METHODS: In 45 Wistar rats with cerulein induced AP (2 x 40 microg/kg i.p. at 1 hour interval, the effect of endothelins at the dose 2 x 0.5 or 2 x 1.0 nmol/kg i.p. was assessed vs untreated AP; 6 healthy rats were control (C). Free active trypsin (FAT), total potential trypsin after activation with enterokinase (TPT), lipase in 12000 xg supernatants of pancreatic homogenates and the plasma alpha-amylase were assayed. The %FAT/TPT was an index of trypsinogen activation. RESULTS: %FAT/TPT increased from 3.0 +/- 0.6 in C to 16.2 +/- 3.1 in AP (p < 0.01). ET-1 decreased this index to 4.8 +/- 1.1 after higher dose (p < 0.01); the effect of lower dose was insignificant. Attenuating effect of ET-2 was significant: 7.3 +/- 1.7 after higher dose (p < 0.05) and 6.1 +/- 0.9 after lower dose (p < 0.01). ET-3 diminished this index to 4.5 +/- 1.5 (p < 0.01) and to 6.3 +/- 2.2 (p < 0.05) respectively. Lipase activity in supernatant increased from 4.1 +/- 0.6 in C to 6.3 +/- 0.7 U/mg protein in untreated AP (p < 0.05) and plasma alpha-amylase from 7.0 +/- 0.6 in C to 25.9 +/- 4.3 U/ml in AP (p < 0.001), without essential changes in treated groups vs untreated AP. Higher doses of endothelins decreased inflammatory cell infiltration score in AP. CONCLUSIONS: The exogenous endothelins, especially ET-2 and ET-3 and to lesser extent ET-1 exerted some protective effect in early, edematous acute pancreatitis by the attenuation of trypsinogen activation and inflammatory cell infiltration in the pancreas.

Evaluation of morphological lesions in selected internal organs in lambs of Kamieniecka, Pomorska and Polish Blackheaded Mutton sheep and their crossbreeds.

Investigations were carried out on 40 rams aged 50 days (n = 8), Kamieniecka (K), Pomorska (P) and Polish Blackheaded Mutton (PBM) breeds and their crossbreeds (K x PBM, P x PBM). Microscopic evaluation of the liver, kidneys, spleen and heart muscle in the rams as well as ultrastructural analyses of their liver and semitendinous muscle showed that retrogressive lesions, circulation disturbances, inflammation and progressive changes occurred respectively: frequently, occasionally, rarely. Internal organs, particularly liver and kidneys, of crossbred rams (K x PBM and P x PBM) were almost two times more affected with morphological lesions than purebred lambs (K and P). However, in the semitendinous muscle these differences were more vivid in the ultrastructural analysis than in the histopathological or macroscopic observations. Results suggest that breed growth-rate differences have effects on the pathomorphological pattern of the liver and kidneys in lambs. On the bases of this evaluation, it can also be emphasised that young PBM rams are less susceptible to morphological lesions than the K and P breeds.

Effects of the herbicide Roundup on the ultrastructural pattern of hepatocytes in carp (Cyprinus carpio).

Experimental studies were performed on healthy, 80-100 g carp (Cyprinus carpio). Fish were exposed by emersion in Roundup (205 mg of glyphosate/l or 410 mg of glyphosate/l) in concentrations of 40- to 20-fold lower than those used in practice. Electron microscopy revealed that the herbicide caused appearance of myelin-like structures in carp hepatocytes, swelling of mitochondria and disappearance of internal membrane of mitochondria in carp at both exposure concentrations. It means that Roundup was harmful to carp when used in applied concentrations. Results of these studies enhance our knowledge of ultrastructural pathomorphology of fish organs following exposure to Roundup.

Nitric oxide protects the ultrastructure of pancreatic acinar cells in the course of caerulein-induced acute pancreatitis.

Nitric oxide (NO) as a unique biological mediator that has been implicated in many physiological and pathophysiological processes may have a significant influence on the course of acute pancreatitis and the recovery process. The aim of the study was to evaluate the effect of a NO synthase inhibitor or a substrate for NO endogenous production on the ultrastructural features of the acinar cells in the course of caerulein-induced acute pancreatitis. Acute pancreatitis was induced in the rats by a supramaximal dose of caerulein. During acute pancreatitis induction, the rats were treated with L-arginine (the substrate for NO synthesis), NG-nitro-L-arginine (L-NNA, NO synthase inhibitor), L-arginine + L-NNA or saline. Light and electron microscopy examinations were performed in all groups after pancreatitis induction and additionally after 7 and 14 days of recovery. The study demonstrated that the NO synthase inhibitor given during pancreatitis induction in rats enhances the damage to the acinar cells, detected ultrastructurally, and increases the cellular inflammatory infiltration. In the later period, the considerable damage to the mitochondria and the changes in secretory compartment were observed, including dilated cisternae of Golgi apparatus, focal degranulation of rough endoplasmic reticulum, and reduced number of zymogen granules and condensing vacuoles. L-arginine reversed to some extent the deleterious effect of L-NNA, although when administered alone it had no apparent effect on the ultrastructure of pancreatic acinar cells compared with untreated animals. The obtained results indicate that the NO synthase inhibitor enhances the ultrastructural degenerative alterations in the pancreatic acinar cells in the course of caerulein-induced acute pancreatitis and confirm the protective role of endogenous nitric oxide in this disease.

Exocrine cell mitochondria of the rat pancreas after lead intoxication.

The aim of the study was to evaluate alterations in exocrine cell mitochondria of the rat pancreas after lead acetate intoxication. The experiment used 45 rats divided into 2 experimental groups receiving lead acetate to drink, of lead concentration 50 and 500 mg/dm3 (ppm), and a control group given tap water. The animals from the experimental group were decapitated after 2, 4, 6 and 8 weeks, 5 rats from the control group after 8 weeks of the experiment. Rats from experimental groups decapitated after 8 weeks had lead administration stopped after six weeks and then, for two weeks tap water was given. Pancreatic sections were examined with biochemical methods for the activity of cytochrome oxidase and succinic dehydrogenase. Ultrastructural and morphometric examinations were also performed. It was demonstrated that: a) exocrine cell mitochondria are particularly predisposed to lead effect, b) intoxication of rats with lower lead doses (50 ppm) causes reversible adaptative or compensatory changes in these organelles, c) intoxication of rats with higher lead doses (500 ppm) induces irreversible ultrastructural alterations in numerous mitochondria, including damage to inner and to outer mitochondrial membranes, d) structural changes in the mitochondria in the course of lead intoxication are the morphological expression of the impairment of metabolic processes, associated with the inhibited activity of the respiratory enzymes: succinic dehydrogenase and cytochrome oxidase.

The effect of antecedent acute ethanol ingestion on the pancreas ultrastructure in taurocholate pancreatitis in rats.

The rat pancreas ultrastructure was examined 6, 12, and 18 h after (1) taurocholate-induced acute pancreatitis and after (2) pancreatitis preceded 6 h earlier by intragastric acute 40% ethanol ingestion (5 g/kg b.w.). Pancreatic specific trypsin activity and plasma alpha-amylase were assayed at the same time intervals. The antecedent acute ethanol ingestion resulted in the evident aggravation of pancreas ultrastructural alterations. Acute pancreatitis preceded by ethanol resulted in the increase of zymogen granules number, RER channels were more irregularly distributed, autophagosomes were more abundant and degeneration of mitochondria was more advanced when compared to acute pancreatitis without ethanol ingestion. Tryptic activity increased to higher degree in all pancreatitis groups preceded by ethanol, but this difference was statistically significant (P < 0.01) only after 18 h. These morphological (but not biochemical) differences progressed 12 h after pancreatitis induction. After 18 h of acute pancreatitis the number of zymogen granules decreased in previously alcoholized rats, but tryptic activity remained twofold higher that in animals not given ethanol. Other signs of cellular impairment were still more prominent in alcoholized rats. The obtained results suggest that even single acute ethanol abuse prior to acute pancreatitis does aggravate the morphological and biochemical lesions observed in this disease with possible negative consequences for the prognosis.

The liver ultrastructure in caerulein and taurocholate acute pancreatitis in the rats.

The purpose of the study was to compare the morphological alterations of the liver in two models of acute pancreatitis: caerulein-induced (edematous) and taurocholate-induced (necro haemorrhagic one). The experiments were performed on 24 male, Wistar rats, weighing 240-260 g. In group I (n = 8) the supramaximal stimulation with i.v. caerulein (5 micrograms/kg/h) during 12 h was applied (C-AP). Control animals (group II, n = 4) received i.v. saline (C-C). In group III (n = 8) 5% sodium taurocholate (0.2 ml/min) was injected into the bile-pancreatic duct during sterile laparotomy (T-AP). In group IV (n = 4) animals were sham operated (T-C). The specimens of the liver were excised after decapitation of rats at 12 h after beginning of caerulein infusion or intraductal injection of sodium taurocholate. The light and electron microscopy was performed. The marked hepatic lesion were found in both variants of experimental pancreatitis, however they were far more advanced in taurocholate pancreatitis. In light microscopy the dispersed foci of colliquative necrosis, degeneration of hepatocytes, swelling of Kupffer cells predominated in taurocholate pancreatitis. The glycogen deposits were depleted but lipid droplets were increased in size and number. The swelling of mitochondria, degeneration of their matrix and cristae, increase of autophagocytosis and numerous lysosomes, the lesions of sinusoids with increased activity of phagocytic cells were more evident in taurocholate pancreatitis--(more severe model of the disease). These findings document severe injury to the liver in acute pancreatitis depending on the severity of inflammatory process in pancreas. They also suggest that the liver could be not only passive target of pancreatogenic noxa in acute pancreatitis, but it could be also a defensive barrier against spreading of injuring agents on other system. This role seems to be especially evident in more severe form--taurocholate induced pancreatitis.

The effect of beta-thia-iminoprostacyclin in taurocholate acute pancreatitis in rats: the role of antecedent acute ethanol abuse.

The promoting effect of acute ethanol (E) abuse and protective effect of prostaglandin derivatives in acute pancreatitis (AP) remain obscure. The aim of this study was to assess the effect of previous intake of high-dose E on trypsinogen (Tn) activation and labilization of pancreatic lysosomal membranes (PLM), in taurocholate AP in rats, considering treatment with stable beta-thia-iminoprostacyclin (T). In 60 male Wistar rats taurocholate AP was induced or a sham operation was performed. Half of them received 40% E (5 g/kg body weight), 6 h earlier. T (0.3 mg/kg body weight i.g.) was applied before E or before the induction of AP. Free active (FAT) and total potential (TPT) trypsin, free (F) and total (T) cathepsin B, phospholipase A2 (PLA2), and lipase (L) activities were assayed. Percentage FAT/TPT was an index of Tn activation and fractional free (% F/T) activity of cathepsin B was an index of PLM fragility. FAT increased after 12 h of AP, and in E rats this increase was even more evident. Pretreatment and treatment with T partly prevented this increase, however, this effect was abolished or limited in rats previously given E-the changes were not effected by T. PLA2 and L activities in AP were not diminished after T. The promoting effect of acute E abuse prior to AP could be dependent on augmented activation of Tn and labilization of PLM. The protective effect of T seems to be dependent on the decrease in Tn activation in pancreatitic tissue. The potential therapeutic effect of this drug in AP could be limited by previous acute E intake, as evidenced by differences in histopathological changes.

Does antecedent ethanol intake affect course of taurocholate pancreatitis in rats?

The pathogenic role of acute ethanol abuse in acute pancreatitis (AP) is still obscure. The aim of the study was to evaluate the effect of antecedent intake of a high dose of 40% ethanol (5 g/kg body wt.), on trypsinogen activation, pancreatic lysosomal membrane labilization, and activities of phospholipase A2 and lipase in taurocholate AP in rats. In 80 male Wistar rats, AP or sham operation (SO) was produced 6 hr after intragastric saline (S) or ethanol (E) administration, and animals were sacrificed after 6, 12, and 18 hr. Free active trypsin (FAT) and total potential trypsin (TPT) were assayed in the pancreatic homogenate. Percentage free activity (%F/T) of cathepsin B was determined as an index of lysosomal membrane fragility. The most evident activation of trypsin occured at 6 hr AP (11.6% of TPT in S group and 16.4% in E group). Antecedent ethanol increased FAT 18 hr after SO from 0.105 +/- 0.048 microg/g protein to 0.258 +/- 0.054 and AP lasting 18 hr from 0.331 +/- 0.072 to 0.695 +/- 0.110. The %F/T of cathepsin B was highest at 18 hr of AP, suggesting maximal labilization of lysosomal membranes at this time. This labilization occurred earlier (at 12 hr of AP) in E group. The increasing effect of antecedent E on lipolytic enzymes was evident after 6 hr of AP. In conclusion, the antecedent intake of high dose of ethanol significantly promoted the conversion of trypsinogen to trypsin in taurocholate acute pancreatitis, whereas its additional effect toward labilization of pancreatic lysosomal membranes and the increase of lipolytic enzymes activities was less evident. Therefore, the promoting impact of acute ethanol intake in the development of acute pancreatitis could be mainly dependent on its increasing effect on trypsinogen activation.

Ultrastructural evaluation of microcirculatory vessels in rheumatoid synovial membrane.

Since morphological lesions in microcirculatory vessels are often difficult to be found in the light microscope, the electron microscope investigations were performed on the synovial membrane biopsy specimens from 70 patients with rheumatoid arthritis (RA). Most common lesions referred to venules, capillaries and arterioles were swelling and proliferation of endothelial cells, adherence of lymphocytes, monocytes and neutrofiles to the endothelium, their margination and diapedesis. Also destructive changes in the endothelial cells, basement membrane thickening due to their multiplication and microthrombi were observed. Platelet aggregates, fibrin, fragments of desintegrated cells and deposits of granulofibrillary substance corresponding to fibrinoid necrosis were frequently seen. In 7 patients, lesions of this kind were found only in electronograms. It can be assumed that the evaluation of ultrastructural changes in the microcirculatory vessels may be of great significance as a complementary diagnostic examination in future determination of RA progression and further prognostication.

Intermediate cells in chronic pancreatitis--ultrastructural observations.

Ultrastructural evaluation of the pancreas resected due to advanced chronic pancreatitis revealed the presence of numerous intermediate cells exhibiting both the morphologic features of the exocrine-acinar cell and those of the endocrine cell of Langerhans'islets in 3 out of 5 cases examined. The analysis of ultrastructural pictures showed a predominance of acinar-alpha, beta cells, although acinar-alpha and acinar-beta cells were also found. The role of an increases in the number of intermediate cells in chronic pancreatitis is not clear and requires further investigations.