Biomedical subjects

G Zajicek

Publications and source records attributed to G Zajicek.

At least 91 records · Page 5Linked to original sources

PubMed1986

Fetal activity in pregnancies complicated by systemic lupus erythematosus.

Fetal movements were assessed in 7 cases of systemic lupus erythematosus (SLE). The daily fetal movement count was lower than normal in 4 cases. Three patients with renal disease and raised blood pressure had decreased fetal movements until cessation and poor fetal outcome. Uncomplicated cases of SLE did not manifest cessation of fetal movement, and their fetal outcome was favorable. When a decrease in fetal movements becomes apparent and the condition is verified by other biophysical tests, the patient should be delivered provided the fetus is viable.

Female↗

PubMed1986

Resistance to cancer chemotherapy.

Human cancers are either refractory to chemotherapy, or acquire resistance to it. Although acquired resistance to chemotherapy is generally ascribed to the drug itself, it may be linked with the nature of neoplasia, since normal tissues e.g. gastrointestinal mucosa or bone marrow, do not seem to acquire resistance and their perpetuating sensitivity even undermines effective treatment. According to the theory presented herewith, chemotherapy ultimately fails since it is based on wrong premises. Cancer is regarded here as a metabolic deficiency, originating in stem cell destruction. Besides serving as tissue progenitors, stem cells are postulated to secrete a vital substance 'A' necessary for proper tissue function. Carcinogens interfere with 'A' production mainly by destroying stem cells, which the organism is incapable of fully replenishing, so that less 'A' is produced. This irreversible 'A' deficiency may be replenished solely by a substitute, or substance 'B', produced by a specialized organ, the neoplasm. Since carcinogens continue depleting additional stem cells, the deficiency worsens. In order to keep up with increasing demand the neoplasm has to proliferate more and more until it reaches a stage of decompensation when the harm inflicted by it outweighs its benefit. Stem cell depletion is regarded here as the common final pathway of carcinogens. The theory predicts that following a supply of 'A' producing stem cells or inactivated 'B' producing neoplastic stem cells, the tumor will regress. Tumor regression is achievable also by diminishing the demand for the missing metabolites, which may be accomplished by chemotherapy. 'A' and 'B' are consumed mainly by transitional cells. Upon their elimination the demand for 'A' declines and the tumor may wane. This is regarded here as the main role of chemotherapy in cancer, while its tumoricidal potency is indicated solely for repairing tumor induced function loss. It is proposed here that the good response to chemotherapy by Hodgkin's disease and seminoma is linked with their being partially infective. Both start as genuine smouldering infections turning later into neoplasms. While chemotherapy is adequate only during the infective phase, it is met with mounting resistance when applied during the neoplastic phase.

Antineoplastic Agents↗

PubMed1986

Cancer is a metabolic deficiency.

Cancer is regarded here as a metabolic deficiency originating in stem cell destruction. Tissue stem cells are postulated to secrete a vital substance 'A' necessary for proper tissue function. Carcinogens interfere with 'A' production mainly by destroying stem cells which the organism is incapable of fully replenishing so that less 'A' is produced. This irreversible 'A' deficiency may be compensated by a substitute, or substance 'B', produced by a specialized organ, the neoplasm. Since carcinogens continue depleting more and more stem cells, the deficiency worsens. In order to meet the increasing demand, the neoplasm proliferates more and more until reaching a stage of decompensation when the harm inflicted by it outweighs its benefit. Stem cell depletion is regarded here as the final common pathway for carcinogen action. The theory predicts that following a supply of 'A' producing stem cells or inactivated 'B' producing neoplastic stem cells, the tumor will regress.

Animals↗

PubMed1986

Fetal activity in premature rupture of membranes.

Fetal movement (FM) counts by mothers with premature rupture of membranes (PROM) may be helpful in estimating fetal well being, provided FM assessment is not altered by the reduced amniotic fluid. It is possible that the decreased uterine volume restricts fetal movements, though the closer contact of the fetus to the uterine wall may enhance maternal perception of even weak FM. The present study compared maternally perceived FM in 41 cases of PROM to 120 uncomplicated pregnancies. No significant differences in FM counts were detected between the two groups at any of the gestational ages. Fetal movement counts by mothers with PROM, therefore, can assist fetal surveillance as is the case in pregnancies with intact membranes.

Female↗

PubMed1986

Fetal activity in pregnancies complicated by rheumatic heart disease.

Severe cardiac disease in pregnancy may be complicated by reduced placental perfusion and subsequent fetal deprivation. In the present study we have evaluated one fetal parameter that may thus be affected, namely fetal activity. The study group included patients with rheumatic heart disease: 36 women with mild and 5 with severe disease. Each counted fetal movements 3 times a day and from this the daily fetal movement recording was calculated. One hundred and twenty women with normal pregnancies were the controls. The mild cases had fetal activity which was similar to that of the controls. The severe cases had reduced fetal activity, which was significant statistically at 29 to 32 weeks of gestation. Three in the severe disease group had marked decrease of fetal movements on admission to hospital. A return to normal fetal activity was observed following improvement of the maternal cardiac state. As was previously suggested for other high and low risk pregnancies, the maternal perception and counting of fetal movements may aid the fetal surveillance of patients with rheumatic heart disease.

Female↗

PubMed1986

The streaming adrenal cortex: direct evidence of centripetal migration of adrenocytes by estimation of cell turnover rate.

Thirty adult male rats were injected with 0.5 microCi [3H]thymidine/g body weight (specific activity 5 Ci/mmol) and killed, in groups of five, 1 h and 14, 30, 60, 90 and 120 days after injection. The displacement of labelled adrenocytes with time was estimated in autoradiograms of adrenal sections. The radial distance of the labelled cell from the capsule was measured with an eyepiece micrometer and expressed in cell location units, i.e. the number of cells separating the labelled cell from the capsule. One hour after labelling, 95% of labelled cells were confined to the outer quarter of the cortex. During the following days, adrenocytes were displaced inwardly, approaching the medulla at a velocity of 0.24 locations/day. They traversed the three cortex zones, reaching the medulla after 104 days. The three adrenal zones represent three differentiation states of the adrenocyte. When young, the adrenocyte secretes aldosterone, after leaving the glomerulosa it produces corticosteroids and on reaching the reticularis it produces sex hormones. The adrenal cortex is a cell renewal system made of two compartments. A progenitor compartment extending between locations 1 and 15, and a functional compartment, covering locations 16-64. The first compartment produces 0.47 cells daily, which enter the second. Half of them die on their way while the rest are eliminated in the reticular zone. The cell stream is nourished by a subcapsular stem cell.

Adrenal Cortex↗

PubMed1985

Odontoblast turnover in the impeded and unimpeded rat incisor derived from computerized histomorphometry.

A computerized histomorphometric method was devised to estimate the kinetics of odontoblast turnover and dentinogenesis in rat incisors. The method was applied to two groups of rats: one group with lower incisors in impeded eruption and another group with the left lower incisor in the unimpeded state. The teeth were divided into six equal segments, from which consecutive ground sections were obtained. The distance of each ground section from the posterior border of the alveolar bone was calculated. Each section was magnified, traced, and the tracings fed into a computer by a sonic digitizer. The perimeters and areas of dentine and pulp in each ground section were calculated by the computer. The mean odontoblast density along the predentine was evaluated from histological sections taken both from the same tooth segments and from teeth sectioned midsagittally. These served for the estimation of the predentine area occupied by the average odontoblast. In the impeded group, this area was 11% larger than in the unimpeded one. Outer dimensions of teeth, namely the circumference of the dentine, the labiolingual width, and the mesiolateral width remained constant and equal for both groups. Daily rates of dentine apposition were computed and were found to vary according to the age of the odontoblasts. Odontoblasts of impeded teeth started to secrete matrix at a rate of 17 microns/day, which increased slightly to 19 microns/day and later declined to 7 microns/day on the 38th day. Dentine production of unimpeded odontoblasts, on the other hand, started at a rate of 16 microns/day and gradually increased to 34 microns/day on the 17th day.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

The streaming submandibular gland.

Twenty female young adult rats were injected with tritiated thymidine (3HTdR). The animals were then killed in groups of five, at the following times: 1 hour, and 4, 16, and 23 days. Autoradiograms of sections through the submandibular gland were prepared, and the location of labelled cells in relationship to tubuli and acini was recorded. The different tubular and acinar cross sections could be distinguished by their cell number. Narrow tubuli had fewer nuclei than the wider ones. The nuclear number of a cross section was defined as its class and the location of a labelled epithelial cell was expressed in relationship to the class where it was found. The location of a labelled stromal cell was determined by the class of its neighboring tubular or acinar cross sections. The mean cell numbers of intercalated, granular, and striated duct cross sections were, respectively, 4.7, 10.5, and 10.2, while the average cell content of acini was 4.7 cells. One hour after labelling most labelled tubular epithelial and stromal cells were found in tubular cross sections (or low tubular classes), while in the acini, labelled epithelial and stromal cells were found mainly in wider cross sections (or higher acinar classes). Within the next 23 days labelled tubular cells and stroma proceeded into higher classes, while labelled acinar epithelium and stroma cells were displaced into narrower cross sections (or lower classes). The displaced tubular epithelium and stroma covered daily 0.26 classes. At this velocity the cell will reach the highest tubular class in 62 days and the estimated maximal tubular cell life span is 62 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Effect of misoprostol and cimetidine on gastric cell turnover.

The effects of misoprostol 200 micrograms q.i.d. and cimetidine 300 mg q.i.d. on gastric cell turnover were investigated in duodenal ulcer patients before and after four weeks of therapy. Endoscopic biopsies were incubated with 3H-thymidine. Glandular column length (number of cells per column) and the number of labelled cells per column were determined by autoradiography. There were no significant treatment effects on column length of the gastric pits of either the antrum or fundus. However, misoprostol and cimetidine had opposing effects on cell turnover. Misoprostol significantly decreased the number of labelled cells in antral (P less than 0.01) and fundic (P less than 0.001) gastric pits. However, cimetidine significantly increased (P less than 0.01) the number of labelled cells in antral and fundic columns. The increased gastric cell turnover caused by cimetidine may contribute to its activity in peptic ulcer disease. The decreased cell turnover induced by misoprostol does not appear to be a mechanism responsible for its well-established cytoprotective activity.

Adult↗

PubMed1985

Compensatory proliferative response of the rat submandibular salivary gland to unilateral extirpation.

The present experiment was conducted in order to identify the progenitor compartment of the submandibular salivary gland (SSG) and to explore the proliferative activity of this gland in response to unilateral extirpation. Left submandibular and retrolingual glands were extirpated in 30 rats (B.W. 200 +/- 12 g). The rats were killed 0, 1, 2, 3, 5 and 7 days after surgery. Five intact rats served as controls. The animals were given intraperitoneal injections of 3HTdR (0.5 microCi/grB. W) 1 h before they were killed. The contralateral SSG's were subjected to routine histological procedures and embedded in glycol methacrylate. Selected sections (2 micron thickness) were processed for autoradiography. In each gland, labelled and unlabelled nuclei were counted in 50 random microscopic fields and sorted according to their parenchymal histomorphological features and "nuclear class" (number of nuclei/cross section/feature). In the control glands the total labelling index (LI) was 0.18%; during acute compensatory stimulation, however, the total LI reached a maximum of 0.86% on day 3 after surgery. suggesting that the SSG, which normally undergoes a slow turnover, is capable of elevated proliferation in response to a stimulus. In both normal and stimulated glands, the LI was higher in the intercalated ducts (1.1%-5.85%) than in the granular ducts (0.17%-0.93%) and acini (0.05%-0.36%). This consistency of LI ratio between the various histomorphological features in the normal and experimental glands indicates that the glandular progenitor compartment is located in the intercalated ducts, which supply cells to both the ductal system and acini.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Effect of misoprostol and cimetidine on gastric cell labeling index.

The effect of misoprostol and cimetidine on gastric cell turnover was studied. Endoscopic biopsy specimens of fundic and antral mucosa were obtained from duodenal ulcer patients before and after 4 wk of therapy with cimetidine 1.2 g/day or misoprostol 800 micrograms/day. Biopsy specimens were incubated with [3H]thymidine. Glandular column length and number of labeled cells were determined after autoradiography. There was no significant difference in column length of antral or fundic glands before or after therapy with cimetidine and misoprostol. The number of antral and fundic labeled cells was significantly decreased after misoprostol treatment (3.6 +/- 0.3 and 4.6 +/- 0.4, mean +/- SE), as opposed to their respective number before therapy (6.9 +/- 0.5 and 8.3 +/- 0.8) (p less than 0.01). On the other hand, after treatment with cimetidine, the number of antral and fundic labeled cells was significantly higher (11.8 +/- 0.9 and 7.5 +/- 1.0, respectively) as compared with their number before therapy (5.7 +/- 0.5 and 5.6 +/- 0.6, respectively). The decreased gastric cell turnover induced by misoprostol indicates that the trophic effect of prostanoids on gastric mucosa is not due to an increase in cellular kinetics. The increased gastric cell turnover induced by cimetidine may contribute to its therapeutic effect in peptic ulcer disease.

Adult↗

PubMed1985

Congenital neoplasia--a stem cell pathology.

The theory presented herewith provides a unified explanation for neoplasia and teratogenesis, both regarded here as stem cell disorders. Proliferating cells in the organism form two mutually exclusive classes, immortal stem cells and transitional cells whose life span is limited. Any lasting change in the organism e.g. tissue differentiation or neoplasia, is determined by stem cells. Congenital as well as adult neoplasms exhibit three key features: maturation arrest, stem cell pool expansion and increased cell turnover and they progress through the following states: dysplasia, neoplasia in situ, benign stage (e.g. polyp) and overt neoplasia. The neoplasm is regarded here as an organ with a purpose intended to supply the organism with a missing substance. Besides serving as tissue progenitors, stem cells are postulated here to secrete a substance 'A' necessary for a proper tissue function. Carcinogens interfere with the substance production mainly by depleting stem cells so that less 'A' is produced. The capacity of the adult to replenish the depleted stem cells is limited, and the missing substance has to be formed by an alternative way i.e. by Neoplasia. The 'A' substitute formed by the neoplasm denominated as 'B' is however less efficient than 'A'. Neoplastic growth thus depends upon the relative abundance of substances 'A' and 'B'. Since in the growing organism, stem cells multiply, some of the missing 'A' is replenished by them and the neoplasm may regress.

Embryonal Carcinoma Stem Cells↗

PubMed1985

Inflammation initiates cancer by depleting stem cells.

According to the theory presented herewith, neoplasia results solely from stem cell depletion. Besides serving as tissue progenitors, stem cells are postulated to secrete a vital substance 'A' necessary for proper tissue function. Carcinogens interfere with 'A' production mainly by destroying stem cells and since the latter are not replenished, less 'A' is produced. In order to repair the deficiency, the organism grows a special organ, the neoplasm, dedicated to produce a substitute, denominated here as substance 'B'. Since carcinogens continue depleting stem cells, the neoplasm has to grow more and more in order to keep up with the demand, until reaching a stage of decompensation when the harm inflicted by it is greater than its benefit. Any stem cell depleting substance or process e.g. ablation, chemotherapy and inflammation, is regarded here as a carcinogen. Even animal tumor viruses are postulated here to exert their harm mainly by depleting stem cells. Protracted inflammation e.g. ulcerative colitis or cystic mastopathy, hits stem cells and is followed therefore by neoplasia. Age specific incidence rates of such pathologies resemble precursor-successor curves of tracer kinetics. The precursor inflammation hits young adults, while its successive neoplasia is more prevalent in older individuals. Although most age specific curves of adult cancers are unimodal, at least five are bimodal, resembling precursor-successor curves. These are: Hodgkin's disease, seminoma, nasopharyngeal and retroperitoneal tumors and cancer of bone and joints. It is suggested here that these age specific curves are mixtures of two pathologies, an inflammatory, which is prevalent in young persons, followed by neoplasia.

Adolescent↗

PubMed1985

The estimation of host-resistance in cancer.

From the third year after its clinical diagnosis and onward the cancer hazard rate continuously declines. This phenomenon is common to all cancers irrespective of stage, and far less pronounced in other chronic diseases. It is so typical of cancer as to be regarded as a "law of the improving chances of the cancer patient". Although the cancer hazard rate itself is higher than in most other chronic diseases, it always declines while in other chronic diseases it rises. Two kinds of processes operate in cancer: a noxa and host resistance. Throughout cancer progression the organism maintains a delicate equilibrium with the noxa, only its reserves are continuously depleted and when exhausted the noxa overpowers the host's resistance and the patient dies. The hazard rate is inversely proportional to the patient's reserve. Its decline indicates that the host resists the noxa better and better, since however his reserves are limited, he ultimatelly succumbs to it. This phenomenon also shapes cancer age specific incidence and mortality rates. From the age of 15 years and onward the curves ascend in an exponential fashion, gradually tapering off, which is viewed here as a token of a mounting resistance of the organism to the carcinogenic noxa. Host resistance operates also during tumor growth, accounting for the Gompertzian shape of its growth curve. The growth rate of most human tumors progressively decreases and is therefore best described by the Gompertz function which initially rises in an exponential fashion and gradually tapers off. Tumor size and growth rate indirectly reflect the host's condition or reserve. The two tumor attributes are related to the hazard rate in the following manner: Tumor size is proportional to the hazard rate, indicating host reserve. Tumor growth rate is proportional to the hazard rate change, indicating host resistance. Both indicators may be estimated independently and applied to the assessment of the host's reserve and resistance during cancer progression.

Adolescent↗

PubMed1985

The streaming liver.

Twenty male adult rats weighing 200 g were injected with tritiated thymidine (3HTdR). The animals were then killed in groups of five, at the following times: 1 h, 1, 3 and 5 weeks. Autoradiograms of sections through the liver were prepared. The distances between labelled cells and the portal space rim were measured. One hour after labelling most labelled cells were confined to a region extending from the portal space rim up to a distance of 700 micron, which roughly corresponds to Rappaport's hepatic acinus zones-1 and -2. Throughout the experiment lasting 5 weeks labelled cells entered zone-3 and advanced toward the terminal hepatic vein. Hepatocytes travelled at a daily velocity of 1.44 micron, covering daily 0.324% of the acinus diameter. During the experiment acinus size did not change appreciably. The estimated mean hepatocyte cell cycle time was 37 days and its life expectation, 201 days. These experiments show that the liver is essentially a slowly renewing cell population. Hepatocytes nascent at the portal space gradually stream toward the terminal hepatic vein where they are probably eliminated by apoptosis. Their journey lasts 201 days. Since hepatocytes are glued together with tight junctions, all have to advance toward their terminal hepatic veins en masse. During their voyage, they traverse the three acinus zones, and since in each they produce different enzymes, each zone represents a differentiation state of the advancing cell. It is suggested further that the streaming hepatocyte carries with it its nerve supply and is accompanied by sinusoidal endothelium and Kupffer cells.

Animals↗

PubMed1985

Results of therapy in adult acute nonlymphoblastic leukemia: experience in Jerusalem, Israel, during 1975-1982.

78 previously untreated patients (aged 16-82 years) with acute nonlymphoblastic leukemia received intensive chemotherapy for induction of remission. In 64 patients, the combination used consisted of daunomycin and cytosine arabinoside with or without 6-thioguanine. The overall remission rate was 59 and 87% for those who received what was considered as adequate therapy. Patients who achieved remission received maintenance and, in part, late intensification. The median duration of remission was 9 months. The median survival of the patients who attained remission was 24 months, compared to 15 months for the entire patient group and 3 months for patients who failed to achieve remission. Age had no effect on the rate and duration of the remission obtained but the median survival was significantly longer in patients below the age of 50 years.

Adolescent↗

PubMed1984

On the maturation rate of the neutrophil.

Fifty-three maturing bone marrow cells of the granulocyte cell series stained with Giemsa stain and magnified 1,000 times were scanned by a "computerized microscope" consisting of a LSI-11/23 microprocessor and a black-and-white video camera attached to a "frame grabber ." Each sampled cell was digitized into 70 X 70 pixels, each pixel representing 0.04 micron of the real image. The pixel gray values ranged between 0 and 255. Zero stood for white, 255 represented black, while the numbers in between stood for the various shades of gray. The cells represented six different stages of granulocytic maturation: myeloblast, promyelocyte, myelocyte, metamyelocyte , band form, and polymorphonuclear granulocyte. A discriminant analysis program selected 19 features best distinguishing between the six different cell types and computed five canonical discriminant functions defining a Space in which maturation was studied. In the Space, distance between two cells serves as a measure of similarity. The closer two cells are, the more similar they are and vice versa. This measure was applied here to express the degree of similarity between the neutrophil maturation classes, and since they represent states in the neutrophil life history, it is applicable also as a yardstick for the quantitation of differentiation. In the Space, the life history of a cell is represented by a trajectory originating in the myeloblast and terminating in the granulocyte state. Displacement along the trajectory represents cell maturation that is expressed relatively to the least differentiated state of the myeloblast. The further a cell from this state the more mature it is. The same yardstick also serves for differentiation rate estimates represented in the Space by displacement velocities that are derived from the known "transit times" of a cell in each state. The methodology is also applied for cell production estimates. Unlike other "computerized microscopes" serving for cell classification, the instrument described in this study is primarily a cell-comparator providing a precise measure of similarity between any two cells.

Bone Marrow Cells↗

PubMed1984

Neoplasia--a stem cell pathology.

Cell proliferation in the organism is accompanied by cell displacement. Proliferating tissues exhibit three key characteristics: a site of origin of the stem cell, a tissue radius along which all constituents except the stem cell are displaced and a periphery where cells are eliminated. The tissue thus consists of two cell types: Stem and transitional. Since only the first resides permanently in the tissue any lasting change observed in the tissue is directed by the stem cell. Each stem cell division results in two cell types: one replacing the parent cell to remain a stem cell, while the other originates an outward displaced transitional cell clone whose life span is limited. In the normal state, the stem cell pool is constant, although its replenishment capacity is limited. Neoplasia is regarded here as a purposeful tissue alteration originating in a stem cell change manifested by: Aneuploidy, maturation arrest, stem cell pool enlargement and increasing cell turnover. Stem cells are assumed to secrete a substance 'A' necessary for a proper tissue function, whose production is impeded by carcinogens, mainly by stem cell depletion. Since however stem cell replenishment is limited, the organism grows a specialized organ, the neoplasm, producing a less efficient substitute for 'A', denominated here as substance 'B'. Neoplastic growth is indirectly dependent upon the abundance of substance 'A', the supply of which should be followed by a reduction of neoplastic mass. Neoplasia is thus viewed here as a protective function directed by the stem cell and linked with "oncogenes". Each determined stem cell is harbouring a specific oncogene and exhibits a typical neoplasm. Since the theory predicts that neoplastic growth indirectly depends upon the abundance of substance 'A', it may be tested by investigating the effect of substance 'A' producing stem cells upon the growing neoplasm. Their supply to the organism should be followed by a reduction of the neoplastic mass.

Aneuploidy↗