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Biomedical subjects

D Rastogi

Publications and source records attributed to D Rastogi.

6 recordsLinked to original sources

T-helper type 2 polarization among asthmatics during and following pregnancy.

BACKGROUND: Asthma is the most common medical condition during pregnancy. While increased production of T helper cytokines has been reported to occur in both asthma and pregnancy, the effect of T-helper type 2 (Th2) polarization on asthma symptoms during pregnancy has not been well-characterized. OBJECTIVE: We hypothesized that systemic Th2 cytokine and chemokine polarization occurs among asthmatics to a greater extent during their pregnancy, and is associated with more severe asthma and increased Th2 polarization in the newborn. METHODS: Fifty-six pregnant asthmatics were recruited from prenatal clinics affiliated with New York Presbyterian Hospital. Systemic production of interleukin-4, interferon-gamma, eotaxin and IP10 were measured by intracytoplasmic staining or ELISA at recruitment, peripartum and post-partum, and in the cord blood. The frequency of asthma symptoms was measured by questionnaires and compared with Th biomarkers. RESULTS: The chemokine ratio (IP10/eotaxin) declined over the course of pregnancy (from 3.3 +/- 1.3 to 1.4 +/- 0.2, P = 0.016), but IP10 and eotaxin increased post-partum. The decrease in the chemokine ratio was associated with more frequent asthma symptoms. A non-significant trend towards decreased interferon-gamma and increased interleukin-4 production was detected. Cord blood eotaxin levels correlated with maternal levels (r = 0.35, P = 0.03). Other peripartum biomarkers were not associated with Th2 polarization nor with subsequent respiratory symptoms in the newborn. CONCLUSION: IP10/eotaxin declined over the course of pregnancy and was associated with worse asthma symptoms. Alterations of Th1/Th2 chemokine balance during pregnancy may identify women prone to more severe asthma during pregnancy.

Adult↗

Host-bacterial interactions in the initiation of inflammation.

The respiratory epithelium provides both a physical and an immunological barrier to inhaled pathogens. In the normal host, innate defences prevent bacteria from activating inflammation by providing efficient muco-ciliary clearance and antimicrobial activity. Bacteria that persist in the airway lumen, as in cystic fibrosis, activate both the professional immune cells in the respiratory mucosa as well as the more abundant airway epithelial cells. As most of the bacteria become entrapped in airway mucin, shed bacterial products such as pili, flagella, peptidoglycan and lipopolysaccharide from lysed bacteria are likely to be the stimuli most important in activating epithelial signalling. The airway cells respond briskly to bacterial components through several signalling systems which activate epithelial expression of pro-inflammatory cytokines and chemokines. These signals recruit neutrophils to the airways where they eliminate the contaminating bacteria causing inflammation and the ensuing clinical signs of infection.

Bacteria↗

Leukemoid reaction in extremely low-birth-weight infants.

The objective of this paper was to determine the incidence of leukemoid reaction and to evaluate its relationship with maternal and neonatal factors in extremely low-birth-weight (ELBW) infants. The design a case-controlled retrospective study of all live-born ELBW infants (<1000 g) over a period of 2 years, from July 1994 to June 1996. A total of 60 preterm infants were born during the study period, and are included in this report. The infants who demonstrated leukemoid reaction formed the study group, while the remainder formed the control group. Leukemoid reaction was defined as a white blood cell (WBC) count > or = 50,000/mm3. The relationship between maternal and neonatal variables and WBC counts was studied. Nine of the 60 infants studied demonstrated counts >50,000/mm3, with an incidence of 15%. There was no significant association demonstrated between maternal or neonatal variables and leukemoid reaction. Patients with leukemoid reaction had a better overall survival. Leukemoid reaction in ELBW infants is a rare and recently documented phenomenon. In our study the incidence was 15%. Although many factors have been postulated as a cause of this phenomenon, we could not demonstrate any relationship between these factors and high WBC counts, including sepsis and the use of antenatal steroids, the two most likely variables. It was interesting to note that the infants who were able to mount a leukemoid response had a better chance of survival than those who did not.

Analysis of Variance↗

Pseudohypoparathyroidism-Albright hereditary osteodystrophy.

A 13 year old girl with short stature, and retarded mental growth with coarse facies and deranged thyroid function test was initially suspected as a case of hypothyroidism and was started on thyroxine. Lack of response to treatment and on further investigations it was diagnosed as a case of pseudohypoparathyroidism. High index of suspicion and careful evaluation is important to diagnose such an entity.

Adolescent↗

Development of thermotolerance in CHO cells: modification by procaine.

We have tested the reported ability of procaine to inhibit the induction and the development of thermotolerance in Chinese hamster ovary cells. Thermotolerance was induced either by hyperthermia alone (10 min, 45 degrees C) or by combining hyperthermia and procaine (5 min, 45 degrees C + 10 mM procaine) with heating times adjusted to yield similar cell survival after the conditioning treatments. Both the kinetics of thermotolerance development in fresh medium without procaine and the magnitude of thermotolerance 6 h after heat conditioning were similar for the two treatment groups. Development of thermotolerance in the presence of procaine was tested by adding the drug at 5 or 10 mM to culture medium between, but not during two fractionated heat treatments. Thermotolerance development was observed even in the presence of 10 mM procaine, but only if cell survival was corrected for the 37 degrees C-procaine toxicity. Complete survival curves of cells incubated for 6 h at 37 degrees C in 7.5 mM procaine between heat conditioning and test heating showed a D0 that was only 35 per cent lower than that of thermotolerant controls. The data are consistent with the reported sensitization to heat killing by procaine, but show that thermotolerance induction and development were only minimally perturbed by procaine.

Animals↗

Uncoupling of oxidative phosphorylation does not induce thermotolerance in cultured Chinese hamster cells.

Two uncouplers of oxidative phosphorylation, 2,4-dinitrophenol (DNP) and carbonyl cyanide m-chlorophenylhydrazone (CCCP), were tested for their ability to modify the survival of cultured Chinese hamster ovary (CHO) and Chinese hamster V79 cells treated with hyperthermia. The uncouplers were used under conditions that inhibit oxidative ATP synthesis, as judged from measurements of cellular ATP levels. Incubation of CHO cells in glucose-free Hanks' balanced salt solution (HBSS) containing 1 mM DNP for 1 h at 37 degrees C followed by reincubation at 37 degrees C in complete growth medium for 3 or 16 h, showed no substantial changes in the 45 degrees C heat survival curve as compared to heated cells not exposed to DNP. Thus, DNP treatment of CHO cells did not induce thermotolerance. Carbonyl cyanide m-chlorophenylhydrazone (CCCP), tested under similar experimental conditions, did alter cellular heat resistance. The major change in the 45 degrees C survival curve of CHO cells pretreated with CCCP was an increase in the width of the shoulder: the Dq value increased from 14 min to 24 min, for the control and CCCP-treated cells respectively. The D0 value did not change appreciably. In contrast, heat-induced thermotolerance (10 min, 45 degrees C + 16 h, 37 degrees C) was characterized primarily by an increase in the D0 parameter from 4 min (unheated cells) to 17 min. Similar results were observed with CCCP-treated V79 cells. The data demonstrate that heat resistance induced by 1.2 microM CCCP was manifest as an increased cellular capacity to accumulate and/or repair hyperthermia damage, rather than an induction of thermotolerance, and that this effect probably was not related to the action of CCCP as an uncoupler of oxidative phosphorylation.

2,4-Dinitrophenol↗