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Biomedical subjects

R K Puri

Publications and source records attributed to R K Puri.

At least 163 records · Page 9Linked to original sources
PubMed1991

Childhood morbidity and mortality in a large hospital over last four decades.

Pediatric statistics in a 50-year-old large hospital were analysed to find out any change in pediatric admission rate, morbidity and mortality and outcome of common disorders during the last four decades. Information was collected from four block years from each of the last four decades and compared. An increase of almost 250% in the total pediatric admissions as compared to an increase of 150% in total hospital admissions over last four decades suggest an increased awareness of maternal and child health by the community. The pediatric mortality excluding neonates has not shown a significant fall over the last four decades, being 14.6, 12.7 and 13.0% in 1955-1958, 1974-1977 and 1984-1987, respectively. Diarrheal disorders, pneumonia, tetanus and infections of central nervous system continue to remain the common causes of hospital admissions in children. The morbidity and mortality in these disorders, in general, have shown a significant decline though less appreciable in pyogenic meningitis, encephalitis and tetanus cases.

Brain Diseases↗
PubMed1991

Pediatric hypertension: clinical profile and etiology.

Thirty six symptomatic hospitalized hypertensive children were evaluated for clinical profile and etiology. They were divided into two groups of 23 and 13 patients, respectively of chronic persistent hypertension and acute transient hypertension. Headache, failure to thrive, dyspnea and edema were common clinical features. Renal parenchymal pathology was the commonest etiology in both groups with a tubulo-interstitial pathology being more common amongst chronic hypertensives and acute glomerulonephritis in acute transient hypertensives. Essential hypertension was uncommon, found in only two patients with chronic hypertension reflecting probably an asymptomatic status of most patients with essential hypertension.

Child↗
PubMed1990

IL-2-PE40 prevents the development of tumors in mice injected with IL-2 receptor expressing EL4 transfectant tumor cells.

A number of different immunotherapeutic reagents are currently being developed to target IL-2R for the treatment of leukemia, graft rejection, and certain autoimmune diseases. Previously, we have shown that IL-2-PE40, a chimeric protein composed of human IL-2 linked to the N-terminus of a truncated form of Pseudomonas exotoxin (PE), could effectively kill a variety of cell lines in vitro expressing either low, intermediate, or high affinity IL-2R. Here, we demonstrate that IL-2-PE40 can successfully retard or prevent the growth of a lethal ascites tumor or a solid tumor composed of EL4J murine thymoma cells transfected with the p55 murine IL-2R. The transfected line, EL4J-3.4, expresses 1,000 to 3,000 high affinity IL-2R. Survival extension in the ascites model was achieved by initiating treatment either after 4 to 6 h or within 5 days post-tumor injection in both athymic nude and C57BL/6 mice. Similarly, the growth of an aggressive s.c. solid tumor could also be inhibited. Extension of survival was not achieved either by using the truncated toxin alone not attached to IL-2 or by using an IL-2-PE40Asp553 mutant lacking a functional toxin. Survival extension was not caused by IL-2 activated NK or other host effector mechanisms as IL-2-PE40 was unable to prevent the receptor-negative EL4J parental line from forming a lethal ascites or a solid tumor. Thus, IL-2-PE40 is a potent, specific cytolytic reagent that may prove useful in the arsenal of anti-IL-2R immunotherapeutics.

ADP Ribose Transferases↗
PubMed1990

In vivo administration of interferon alpha and interleukin 2 induces proliferation of lymphoid cells in the organs of mice.

We have previously shown that interleukin 2 (IL-2) synergizes with interferon alpha (IFN-alpha) in mediating the regression of established pulmonary and hepatic metastases and the reduction of intradermal tumor in various murine tumor models. To understand the mechanism of synergy, we have examined lymphoid cell proliferation in various organs of mice in response to IL-2 and IFN-alpha administration. We have utilized a technique for labeling newly synthesized DNA in vivo with 5-[125I]iodo-2'-deoxyuridine to examine proliferation of endogenous cells in response to IL-2 and IL-2 plus IFN-alpha. A proliferation index was calculated by dividing cpm in the tissues treated with cytokines by cpm obtained in corresponding tissues of control mice. After 4 days of IL-2 administration, a significant uptake of 5-[125I]iodo-2'-deoxyuridine was observed in the lungs, liver, kidneys, and spleen (proliferation index of 13, 10.3, 3.6, and 3.2, respectively). IFN-alpha alone mediated very little incorporation of radiolabel but when administered in combination with IL-2 a reduction of IL-2-induced proliferation was seen on day 4. For example 19,272 +/- 4,556 cpm (mean +/- SE) were obtained in the liver of IL-2-treated mice, compared to 8,103 +/- 2,111 cpm in livers of IL-2 plus IFN-alpha-treated mice (P less than 0.05). Similar inhibition of IL-2-induced proliferation was observed in the lungs, kidneys, and spleen. In contrast, on days 7 or 8, higher uptake of radiolabel was obtained in IFN-alpha plus IL-2-treated lungs, liver, and kidneys, compared to organs of mice treated with IL-2 alone or IFN-alpha alone. A proliferation index of 30.5, 9.8, and 10 was obtained in the lungs, liver, and kidneys of IL-2- plus IFN-alpha-treated animals, compared to 9.6, 3.6, and 5.5 in the corresponding organs of IL-2-treated mice. The effects of IFN-alpha on IL-2-induced proliferation was dose dependent; very low dosages of IFN-alpha (1,000 units/dose) were able to cause the inhibition of proliferation at 3 days of therapy and increase at 7 days of therapy. Continued proliferation of cells was observed in most organs when IL-2 plus IFN-alpha was injected for 9 consecutive days. Pretreatment irradiation of mice at 500 rad largely eliminated the proliferative response to IL-2 as well as to IFN-alpha plus IL-2 at both 3 and 7 days. Histological studies of lungs receiving cytokine therapy for 3 and 7 days corroborated the results of the 5-[125I]iodo-2'-deoxyuridine incorporation assay. At day 3 a significant infiltration of lymphoid cells was seen in IL-2-treated lungs, whereas little or no lymphocytic infiltration was observed in IL-2- plus IFN-alpha-treated lungs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Expression of high-affinity IL-4 receptors on murine tumour infiltrating lymphocytes and their up-regulation by IL-2.

Since interleukin-2 (IL-2) and IL-4 act in concert to support the development of cytotoxic T lymphocytes (CTL) and the generation of antigen-specific tumour infiltrating lymphocytes (TIL), we investigated the interaction of these cytokines with an established TIL line. TIL proliferated in an additive fashion in response to suboptimal concentrations of IL-2 and various concentrations of IL-4. TIL possessed high-affinity IL-4 receptors whether cultured in recombinant IL-2 (rIL-2) or rIL-4, but cells cultured in rIL-2 had higher numbers of IL-4 receptors than cells cultured in rIL-4. When TIL were cultured in increasing concentrations of rIL-2, a dose-dependent enhancement in IL-4 receptor number was observed. The maximum induction of IL-4 receptor expression was achieved by 4 hr of incubation with rIL-2 and was completely blocked by cycloheximide. Other cytokines, such as rIL-1, recombinant tumour necrosis factor (rTNF), recombinant interferon-alpha (rIFN-alpha) and rIFN-gamma, had no effect on IL-4 receptor number. rIL-2 also up-regulated IL-4 receptors on CTLL-2, a murine CTL line. These data indicate that high-affinity IL-4 receptors exist on murine TIL and they can be up-regulated by IL-2. Our observation that IL-2 up-regulates IL-4 receptor may help explain the additive effects of these lymphokines on the proliferation of TIL and other cell lines. It may also help explain their co-operative effects on the generation of antigen-specific TIL and the differentiation of CTL.

Animals↗
PubMed1990

Empyema in infancy and childhood.

A study of 108 cases of empyema during 18 months period showed the incidence of empyema to be 2.17%. Staph. aureus (17.6%) was the common causative organism. Response to a combination of cloxacillin and gentamicin was better than that of crystalline penicillin and gentamicin. Only 30.3% cases needed intercostal drainage for more than 2 weeks. Almost 43% cases could be discharged by 3-4 weeks after hospitalisation and 38.1% by 30-57 days. The mortality rate was 12.1%. Among the survivors, excluding 8 children who left against medical advice, all had complete recovery excepting one child in whom AFB was isolated and who developed bronchiectasis and recurrent hemoptysis, inspite of antituberculous treatment. Age of the child, antibiotic combination given and nutritional status appear to be the main factors influencing the recovery and prognosis.

Anti-Bacterial Agents↗
PubMed1989

Decrease in interleukin 2-induced vascular leakage in the lungs of mice by administration of recombinant interleukin 1 alpha in vivo.

The administration of interleukin 2 (IL-2) to mice and humans is limited by the induction of a dose-dependent increase in vascular permeability causing a vascular leak syndrome (VLS). We have investigated the impact of the injection of recombinant interleukin 1 alpha (IL-1 alpha) on the VLS induced by IL-2 by measuring the extravasation of 125I-albumin into tissues and by assessing wet and dry lung weights. IL-1 alpha alone did not induce any significant extravasation of radiolabeled albumin. IL-2 alone, however, caused a significant increase in the extravasation compared to control lungs. IL-1 alpha injection along with IL-2 significantly reduced the IL-2-induced extravasation of radiolabeled albumin [9,886 +/- 533 (SEM) cpm were observed in IL-2 and IL-1 alpha-treated lungs compared to 14,172 +/- 2,628 cpm in lungs treated with IL-2 alone (P less than 0.02)]. IFN-alpha in combination with IL-2 produced more severe vascular leakage than caused by IL-2 alone. IL-1 alpha also significantly decreased (P less than 0.05) the vascular permeability induced by the combination of IFN-alpha and IL-2. We observed 44,811 +/- 13,131 cpm in IFN-alpha- and IL-2-treated lungs compared to 18,350 +/- 2,622 cpm in IFN-alpha-, IL-2-, and IL-1 alpha-treated lungs. The IL-2- and IFN-alpha-induced increase in lung water weight was also reduced significantly by the addition of IL-1 alpha. The decrease in vascular leakage was dependent on the dose and timing of IL-1 alpha administered. When recombinant IL-1 alpha was given as a single i.p. injection, 24 h before the injection of IL-2 (or Hanks' balanced salt solution) or IL-2 and IFN-alpha no abrogation of the VLS was observed. Although IL-1 alpha decreased VLS significantly in mice treated with IFN-alpha and IL-2 the survival of mice was not improved by the simultaneous administration of IL-1 alpha. Histologically, treatment with IFN-alpha and IL-2 produced marked perivascular and intraalveolar edema which was completely eliminated by the addition of IL-1 alpha. However, some perivascular edema in IL-1 alpha-treated mice remained which was equivalent to that caused by IL-2 alone. Treatment of MCA-106 induced pulmonary metastases was enhanced by the administration of IFN-alpha and IL-2 together.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Combined effects of interferon alpha and interleukin 2 on the induction of a vascular leak syndrome in mice.

Immunotherapy with interleukin 2 (IL-2) alone or in combination with lymphokine-activated killer cells can mediate tumor regression in mice and in man. Further dose escalation of IL-2 along with lymphokine-activated killer cells has been prevented by the development of a vascular leak syndrome produced by IL-2. Because we have found that interferon alpha (IFN-alpha) or tumor necrosis factor (TNF-alpha) has synergistic antitumor effects when administered together with IL-2, we have tested the vascular leakage induced by these lymphokine combinations. We used a murine model to quantify vascular leakage by measuring the extravasation of 125I-albumin from the intravascular space as well as the wet and dry lung weights after treatment with different cytokines. Cytokines (or Hanks balanced salt solution) were administered to C57BL/6 mice and 4 h after the last injection the vascular leak was quantified. IFN-alpha alone did not cause extravasation of radiolabel or increase in wet lung weights, though when given in combination with IL-2, significantly greater extravasation (P less than 0.01) as well as increase in lung water weights (P less than 0.05) was observed compared to the response in mice treated with IL-2 alone. IFN-alpha in combination with IL-2 induced significant vascular leakage earlier than the response induced by IL-2 alone. For example treatment with IFN-alpha and IL-2 induced accumulation of 14,674 +/- 605 cpm in the lungs at day 1 while IL-2 alone induced 12,340 +/- 251 cpm. The degree of vascular leakage was highly related to the dose of IFN-alpha administered along with IL-2 and increased vascular leak syndrome was evident even at low doses (5000 units) of IFN-alpha. Immunosuppression of mice by pretreatment irradiation (500 rad) markedly decreased the development of vascular leak syndrome induced by IL-2 and IFN-alpha. Interestingly IFN-gamma and TNF-alpha did not induce vascular leakage in the lungs when given alone, and did not add or synergize with IL-2 in causing the syndrome. Thus the administration of IFN-alpha in combination with IL-2 produces a dose-limiting vascular leakage that is more severe than that caused by IL-2 alone, and may be mediated, directly or indirectly by host radiosensitive cells.

Animals↗
PubMed1989

Poliomyelitis: 20 years--the Pondicherry experience.

During a 20-year period, 12,830 cases of acute poliomyelitis in children (aged 1 month-12 years) were seen in a South Indian teaching hospital (Pondicherry). Almost three-quarters (72.4%) of children were below the age of 2 years. The median age at onset of poliomyelitis shifted from 19.5 months (in the period 1968-1977) to 11 months (in the years 1978-1987). After 1981, epidemic peaks were noted every third year. 66.3% of cases had not received even a single dose of oral polio vaccine and 14.7% cases were vaccine failures (in the years 1983-1987). Provocation of poliomyelitis occurred in 66% of children and usually followed intragluteal injections associated with treatment of non-specific fevers. The overall mortality was 2.13%, the major cause of death being respiratory failure (60%). Polio virus type 1 was the major isolate among selected cases studied during 1983-1987. The risk factors identified in our study are lack of immunization and administration of intramuscular injections during the pre-paralytic phase. Ensuring early administration of multiple doses of oral polio vaccine to infants and avoiding intramuscular injections in young febrile children are important measures for the control of poliomyelitis--a continuing problem in Southern India.

Age Factors↗
PubMed1989

Robinow syndrome.

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Abnormalities, Multiple↗
PubMed1989

Domperidone.

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Child↗
PubMed1988

Increased vascular permeability in organs mediated by the systemic administration of lymphokine-activated killer cells and recombinant interleukin-2 in mice.

Significant tumor regressions in mice with established carcinomas, sarcomas, and melanomas and in humans with advanced cancers have been observed following immunotherapy with lymphokine-activated killer (LAK) cells and recombinant interleukin-2 (IL-2). However, dose escalations of LAK cells and IL-2 have been prevented by the development of a vascular leak syndrome (VLS). Although IL-2 alone can produce this VLS, we investigated the role of transferred LAK cells, generated by the incubation of syngeneic splenocytes in IL-2, in mediating this phenomenon. We used a murine model to quantitate the vascular leak by measuring the extravasation of iv injected 125I-bovine serum albumin. A permeability index (PI) was calculated by dividing the mean cpm of tissues from treated mice by those from control animals. The systemic transfer of LAK cells and IL-2 produced a significantly greater extravasation of albumin in the lungs, liver, and kidneys than after Hanks' balanced salt solution, IL-2, or LAK cells alone (in the lungs, for example, PI = 4.7, 1.4, and 1.6 after LAK cells and IL-2, LAK cells alone, and IL-2 alone, respectively). To eliminate the contribution to the leak by host lymphocytes, we irradiated mice before cell transfer. As compared to controls, LAK cells and IL-2 resulted in higher extravasation in the lungs, liver, kidneys, and spleen. However, a similar vascular leak was not observed in the lungs, liver, and kidneys after treatment with IL-2 plus fresh or cultured (without IL-2) splenocytes. Moreover, the combination of IL-2 excipient and LAK cells or IL-2 and irradiated LAK cells did not produce a fluid leak. The development of the VLS by LAK cells was directly related to the dose of concurrently administered IL-2 and the number of injected cells. Depletion of Thy 1.2-positive lymphocytes using antibody and complement prior to generating the LAK cells used in adoptive transfer did not abrogate the VLS in any of the organs tested. Similarly, depletion of L3T4 and Lyt-2 positive cells in vivo using monoclonal antibodies prior to harvesting spleens for generation of LAK cells also had no impact on the VLS. In contrast, in vitro treatment of LAK precursor cells with antibody to asialo-GM-1 plus complement completely eliminated the VLS when the depleted cells were cultured in IL-2 and subsequently transferred.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗