[Application and clinical efficacy of ultrasound debridement method in residual burn wounds].

Objective: To investigate the application and clinical efficacy of ultrasound debridement method in residual burn wounds. Methods: A retrospective cohort study was conducted. From August 2017 to August 2021, 64 patients with residual burn wounds who met the inclusion criteria were admitted to the 980th Hospital of the Joint Logistic Support Force of PLA. According to the debridement method adopted for the residual wounds, the patients were divided into ultrasound debridement group (34 cases, 22 males and 12 females, aged (31±13) years) and traditional debridement group (30 cases, 19 males and 11 females, aged (32±13) years). After the corresponding debridement, the wounds of patients in the two groups were selected for stamp skin grafting or large skin grafting according to the wound site and skin donor status. For unhealed wounds after stage Ⅰ surgery, secondary debridement and skin grafting were be performed, with the wound debridement methods in the 2 groups being the same as those of stage Ⅰ, respectively. On postoperative day 3, drug-sensitive test was used to detect the bacteria in the wound and the positive rate of bacteria was calculate. On postoperative day 7, the survival rate of skin slices in wound and the incidence of subcutaneous hematoma were calculated. At discharge, wound healing time and debridement times of patients were counted, and the secondary debridement rate was calculated. Data were statistically analyzed with independent sample t test or chi-square test. Results: On postoperative day 3, the wounds in ultrasound debridement group were infected with Staphylococcus aureus in 2 cases and Pseudomonas aeruginosa in 2 cases, and the wounds in traditional debridement group were infected with Staphylococcus aureus in 5 cases, Pseudomonas aeruginosa in 3 cases, Acinetobacter baumannii in 1 cases, Klebsiella pneumoniae in 1 cases, and Enterobacter cloacae in 1 cases. The positive rate of bacteria of wound in ultrasound debridement group was significantly lower than that in traditional debridement group (χ2=5.51, P<0.05). On postoperative day 7, the survival rate of skin grafts in ultrasound debridement group was (92±5) %, which was significantly higher than (84±10) % in traditional debridement group (χ2=6.78, P<0.01); the incidence of subcutaneous hematoma in ultrasound debridement group was 17.6% (6/34), which was significantly lower than 40.0%( 12/30) in traditional debridement group, χ2=3.94, P<0.05. At discharge, the wound healing time in ultrasound debridement group was (11.0±2.0) d, which was significantly shorter than (13.0±3.1) d in traditional debridement group (t=3.81, P<0.01); the secondary debridement rate of wounds in ultrasound debridement group was 2.9% (1/34), which was significantly lower than 20.0% (6/30) in traditional debridement group (χ2=4.76, P<0.05). Conclusions: Ultrasound debridement method can significantly reduce the bacterial load of residual burn wounds, reduce postoperative hematoma formation, and promote the survival of skin grafts to shorten the course of disease of patients.

Clinical and pathologic predictors of central lymph node metastasis in papillary thyroid microcarcinoma: a retrospective cohort study.

OBJECTIVE: To identify the clinical and pathological predictors of central lymph node metastasis (CLNM) in patients with clinically lymph node-negative papillary thyroid microcarcinoma (PTMC). MATERIALS AND METHODS: Data pertaining to 541 clinically lymph node-negative PTMC patients who underwent thyroid surgery at the Shanghai General Hospital between January 2010 and December 2013 were retrospectively analyzed. According to histopathological evidence of central lymph node involvement, patients were divided into central lymph node metastasis (CLNM)-positive and CLNM-negative groups; risk factors for CLNM were identified statistically. RESULTS: LNM was found in 148 (27.4%) patients. Gender (P = 0.002), age (P < 0.001), tumor size (P < 0.001), multifocality (P < 0.001), and extrathyroidal extension (P < 0.001) were significantly different between CLNM-positive and CLNM-negative groups. On multivariate analyses, male sex (odds ratio [OR] = 2.656), age <45 years (OR = 4.184), tumor size >0.575 cm (OR = 2.105), gross extrathyroidal extension (OR = 14.605) and multifocality (OR = 2.084) were independent risk factors for CLNM. Among patients who did not have any of these five risk factors, only 3.9% were found to have CLNM. CONCLUSIONS: A relatively high prevalence of CLNM was observed in patients with clinically lymph node-negative PTMC. CLNM was associated with male sex, younger age, larger tumor size, extrathyroidal extension and multifocal PTMC.

[Effect of CD40 knock out on cytotoxic effector function in CD8(+) T cell of mice with cigarette smoke-induced emphysema].

OBJECTIVE: To explore the effect of CD40 knock out on the cytotoxic function of CD8(+) T cell of mice with cigarette smoke-induced emphysema. METHODS: A total of 40 male C57 mice were divided into four groups according to the random number table, including CD40(+ /+) control group, CD40(+ /+) smoke-exposure group, CD40(-/-)control group, CD40(-/-)smoke-exposure group. The smoke-exposure groups were exposed to cigarette smoke for 24 weeks to establish emphysema model. Morphological changes were evaluated by linear intercepts. The percentages of CD8, perforin, granzyme B positive cells were evaluated by immunohistochemistry. The mRNA expressions of perforin, granzyme B, interleukin (IL) -27 were measured by fluorescent real time quantitative polymerase chain reaction (RT-PCR). The IL-27 cytokine level was tested by enzyme-linked immunosorbent assay (ELISA). RESULTS: The mean linear intercepts in CD40(+ /+) smoke-exposure group was significantly higher than CD40(+ /+) control group, CD40(-/-)control group, and CD40(-/-)smoke-exposure group [(37.2±3.6) vs (24.0±3.4), (22.5±2.4), (29.9±1.7) µm] (all P<0.05). CD40(-/-)smoke-exposure group was higher than CD40(+ /+) control group, CD40(-/-)control group (all P<0.05). The percentages of CD8 positive, perforin positive and granzyme B positive cells in CD40(+ /+) smoke-exposure group [(16.3±2.3)%, (11.4±2.1)%, (10.7±1.9)%] were significantly higher than CD40(+ /+) control group [(8.3±1.6)%, (5.1±1.2)%, (4.6±1.0)%], CD40(-/-)control group [ (6.4±1.5)%, (4.3±1.0)%, (4.2±1.0)%] and CD40(-/-)smoke-exposure group [(8.6±1.7)%, (5.6±1.3)%, (5.5±1.3)%] (all P<0.05). RT-PCR results showed that the mRNA expressions of perforin, granzyme B and IL-27 in CD40(+ /+) smoke-exposure group [(20.3±7.3), (18.3±12.3), (2.2±0.7)] were significantly higher than CD40(+ /+) control group [(9.4±4.8), (10.6±3.8), (1.3±0.6)], CD40(-/-)control group [ (8.1±3.1), (7.7±3.5), (1.1±0.5)] and CD40(-/-)smoke-exposure group [(12.9±6.2), (10.4±4.6), (1.5±0.4)] (all P<0.05). ELISA results showed that the level of IL-27 in CD40(+ /+) smoke-exposure group was significantly higher than CD40(+ /+) control group, CD40(-/-)control group and CD40(-/-)smoke-exposure group [(3 242±754) vs (1 627±710), (1 600±680), (1 850±583) ng/L] (all P<0.05). CONCLUSION: Knockout the CD40 gene can inhibit the cytotoxic effector function in CD8(+) T cells of mice with cigarette smoke-induced emphysema, and alleviate the degree of emphysema.

[Effect of CD40 on Foxp3(+) Treg cell in the lung of cigarette smoke exposure mice].

OBJECTIVE: To evaluate the effect of CD40 on Foxp3(+) Treg cell in the lung of cigarette smoke exposure mice. METHODS: According to the random number table, 20 wild type (WT) C57 BL/6 mice and 20 CD40(-/-)C57 BL/6 mice were randomly divided into two groups: WT control group, WT smoke-exposure group (24 weeks) and CD40(-/-) control group, CD40(-/-) smoke-exposure group (24 weeks) (n=10 each). Alveolar airspace enlargement was observed by HE staining. Morphological change was evaluated by mean linear intercepts (MLI). Immunohistochemical method was used to detect the quantity of Foxp3(+) cell in the lung. The mRNA expression of Foxp3 was measured by fluorescence quantitative real-time polymerase chain reaction (qRT-PCR). The protein level of Foxp3 was measured by Western blot. Interleukin (IL)-10 and IL-35 levels in the lung were tested by enzyme-linked immunosorbent assay (ELISA). RESULTS: The MLI in CD40(-/-) smoke-exposure group was significantly lower than the WT smoke-exposure group[(30.0±1.7) vs (37.3±3.7) µm], but higher than the CD40(-/-) control group[(23.2±2.5) µm], WT smoke-exposure group was significantly higher than the WT control group[(22.2±1.7) µm](all P<0.05). The percentage of Foxp3(+) cell in the lungs of CD40(-/-) smoke-exposure group was significantly higher than the WT smoke-exposure group and CD40(-/-) control group[(16.89±0.75)% vs (9.65±0.74)% and (13.58±0.51)%], WT smoke-exposure group was significantly lower than WT control group[(12.13±0.81)%](all P<0.05). In the lungs, Foxp3 mRNA and protein expression in CD40(-/-) smoke-exposure group were increased compared to WT-smoke-exposure group and CD40(-/-) control group, WT smoke-exposure group were decreased compared to WT control group (all P<0.05). In the lungs, the level of IL-10 in CD40(-/-) smoke-exposure group was higher than the WT smoke-exposure group and CD40(-/-) control group[(231±25) vs (80±31) and (183±29) ng/L], WT smoke-exposure group was lower than the WT control group[(192±37) ng/L](all P<0.05). The level of IL-35 in CD40(-/-) smoke-exposure group was higher than the CD40(-/-) control group, WT control group and WT smoke-exposure group[(208±29) vs (118±29) , (148±36), (137±37) ng/L, all P<0.05]. CONCLUSION: Knockout the CD40 gene can promote the differentiation of Foxp3(+) Treg cell in the lung of cigarette smoke exposure mice, indicating that blocking the CD40-CD40 ligand pathway may contribute to alleviate the smoking-induced pulmonary emphysema.

Equilibrium lines and barriers to phase transitions: the cubic diamond to beta-tin transition in Si from first principles.

The phase transition between the cubic diamond (cd) and beta-tin (ß-Sn) phases of Si under pressure and the region of interaction of the two phases are studied by first-principles total energy calculations. For a non-vibrating crystal we determine the pressure of the thermodynamic phase transition p(t) = 96 kbar, the Gibbs free energy barrier at p(t) of ΔG = 19.6 mRyd/atom that stabilizes the phases against a phase transition and the finite pressure range in which both phases are stable. We show that the phases in that pressure range are completely described by three equilibrium lines of states along which the structure, the total energy E, the hydrostatic pressure p that would stabilize the structure and the values of G all vary. Two equilibrium lines describe the two phases (denoted the ph-eq line, ph is cd or ß-Sn phase); a third line is a line of saddle points of G with respect to structure (denoted the sp-eq line) that forms a barrier of larger G against instability of the metastable ranges of the phase lines. An important conclusion is that the sp-eq line merges with the two ph-eq lines: one end of the sp-eq line merges with the cd-eq line at high pressure, the other end merges with the ß-Sn-eq line at low pressure. The mergers end the barrier protecting the metastable ranges of the two ph-eq lines, hence the lines go unstable beyond the mergers. The mergers thus simplify the phase diagram by providing a natural termination to the stable parts of all metastable ranges of the ph-eq lines. Although 96 kbar is lower than the experimental transition pressure, we note that phonon pressure raises the observed transition pressure.

Structure and stability under pressure of cubic and hexagonal diamond crystals of C, BN and Si from first principles.

Application has been made of first-principles total-energy band-structure theory to find the equilibrium states under constant pressure of the super-hard cubic diamond (cd) and hexagonal diamond (hd) structures of carbon (C), boron nitride (BN) and medium-hard silicon (Si). The absolute stability of the equilibrium state is found by determinations of the breakdown under pressure of several deformations of lattice parameters around the equilibrium state. The calculations show that the hd structures are much stronger than the cd structures. Thus the γ angle of the hd structure of both C and BN is stable for pressures greater than 20 Mbar while the γ angle of the cd structures breaks down at 13 and 11 Mbar respectively. Also the bulk moduli B of the hd structure of C and BN are substantially greater than the B values of the cd structure above 2 Mbar; the B values of hd structures of C and BN are 20% greater than cd structures at p = 20 Mbar. However the cd structures have greater stability relative to the hd structures as shown by a lower Gibbs free energy at pressures up to 20 Mbar. Comparison is made with the pressure dependences of the medium-hard crystals of Si in the same structures, which show notably different behavior.

Elasticity in crystals under pressure.

The elastic behavior and stability of elemental crystals are studied in the neighborhood of a stable equilibrium state, also called a phase, at finite pressure p. It is shown that two kinds of elastic constants are needed to describe elasticity under pressure. One set, designated as c(ij),i,j = 1-6, determines stability or lack of it; another set, designated as c(ij)(p), describes the linear relation between small additional stresses and strains added to the crystal in equilibrium at p. The stress-strain coefficients c(ij)(p) differ from previous formulations of the stress-strain relations by Barron and Klein (1965 Proc. Phys. Soc. 85 523) and Wallace (1972 Thermodynamics of Crystals (New York: Wiley)), who give c(ij) as stress-strain coefficients. Hence we were led to verify the use of the c(ij)(p) using a first-principles numerical calculation example for face centered cubic Al at 1500 kbar. The Gibbs free energy G of the crystal under pressure is shown to provide both a simple definition of equilibrium and an efficient way to calculate all the elastic constants of a general crystal. A computer program finds stable phases by making jumps in structure from an arbitrary initial structure; the jumps converge to minima of G with respect to the structure. In the calculation, 21 elastic constants are evaluated from a special set of G values and the 6 × 6 elastic constant matrix is tested for stability.

Equilibrium lines and crystal phases under pressure.

A crystal phase in equilibrium under changing pressure traces out a line in structure space where each point corresponds to a structure. Along that equilibrium line the structure and all static properties describe the static behavior of the phase, including two sets of elastic constants and the bulk modulus. We discuss and illustrate the calculation of the equilibrium line and the properties from both the Gibbs free energy and the internal energy. We show that the bulk modulus, which gives a stress to strain ratio along the equilibrium line, has a universal relation independent of pressure to that set of elastic constants which control the stability, but not to the set of elastic constants appearing in the stress-strain relations at constant pressure.

Phases of Ca from first principles.

Structures and properties of many of the phases of Ca under pressure are calculated from first principles by a systematic procedure that minimizes total energy E with respect to structure under the constraint of constant volume V. The minima of E are followed on successive sweeps of lattice parameters for 11 of 14 Bravais symmetries for one-atom-per-cell structures. The structures include the four orthorhombic phases. Also included are the hexagonal close-packed and cubic diamond phases with two atoms per primitive cell. No uniquely orthorhombic phases are found; all one-atom orthorhombic phases over a mega-bar pressure range are identical to higher-symmetry phases. The simple cubic phase is shown to be stable where it is the ground state. The number of distinct one-atom phases reduces to five plus the two two-atom phases. For each of these phases the Gibbs free energy at pressure p, G(p), is calculated for a non-vibrating lattice; the functions G(p) give the ground state at each p, the relative stabilities of all phases and the thermodynamic phase transition pressures for all phase transitions over a several-megabar range.

Phases of vanadium under pressure investigated from first principles.

The existence and stability under pressure of three phases of vanadium are calculated from first principles. The phases are one body-centered cubic (bcc) and two rhombohedral phases (rh(u) and rh(l)), which have greater and lower α values than the primitive bcc rhombohedral cell. The bcc phase is shown in two ways to become unstable at 0.65 Mbar, in agreement with an observed phase transition, but in disagreement with previous higher estimates. The rh phases exist when the bcc phase is unstable, but the bcc phase stabilizes again at 3 Mbar, and the rh phases disappear. At 1.15 Mbar the rh(u) phase becomes and remains unstable and the rh(l) phase becomes the ground state up to 3 Mbar, where the rh(l) phase disappears and the bcc phase takes over. The theory gives four phase transitions among the phases over the pressure range from 0 to 3 Mbar; two of them are bcc to rh(u)-a low pressure (0.3 Mbar) thermodynamic transition found from Gibbs free energies being equal (not observed) and a higher pressure (0.65 Mbar) instability transition when the bcc phase becomes unstable (observed).

Altered expression of tumor suppressors p16 and Rb in gastric carcinogenesis.

AIM: To determine whether expression of the tumor suppressors p16 and Rb is altered in gastric carcinoma. METHODS: Mucosal biopsies were endoscopically obtained from patients with superficial gastritis (n = 12), atrophic gastritis (n = 15), atypical hyperplasia (n = 20) and gastric cancer (n = 40). Upon obtainment, all samples were immediately fixed with 10% buffered formalin, embedded in paraffin, and sectioned serially. Protein expression of p16 and Rb was detected by immunohistochemistry (ABC method). RESULTS: The gastric epithelium samples showed various degrees of nuclear immunostaining for p16 and Rb according to the different stage of lesion. Progressive pathology of the lesions was associated with a decreasing trend in positive immunostaining for p16 protein (83.3% > 73.3% > 30.0% > 27.5%) but an increasing trend for Rb protein (25.0% > 46.7% > 60.0% > 67.5%). A negative correlation was found between these two parameters and gastric cancer. Correlation analysis of the 40 cases of gastric cancer identified a negative correlation for 20 of the cases. When positive (n = 9) and negative tissues (n = 11) were compared, a statistically significant difference was found (50.0%, 22.5%, 27.5%) (P < 0.05). CONCLUSION: Abnormal expression of p16 and Rb may play an important role in gastric carcinogenesis.

p53 protein accumulation and gene mutations in multifocal esophageal precancerous lesions from symptom free subjects in a high incidence area for esophageal carcinoma in Henan, China.

BACKGROUND: Multifocal occurrence of precancerous lesions of the esophagus has been observed among individuals in a high incidence area for esophageal carcinoma in Henan Province, China. Results from recent studies suggest that p53 protein accumulation and mutation occur early in the pathogenesis of esophageal carcinoma. Discordant p53 gene mutations have been observed in invasive carcinoma and preinvasive lesions from a patient with esophageal carcinoma. The p53 alterations in the multifocal precancerous lesions from symptom-free subjects, however, have not been investigated. METHOD: Two biopsy samples, one each from the middle-third and the lower-third of the esophagus, from each subject, were taken from 55 symptom-free subjects in a high incidence area for esophageal cancer in Huixian, Henan Province, China. p53 protein accumulation and p53 gene mutation were analyzed in the multifocal esophageal precancerous lesions from these subjects. RESULTS: Histopathologic examination showed that among the 110 biopsies, 20 had dysplasia, 72 had basal cell hyperplasia, and 18 had normal epithelia. Concurrent lesions at the middle- and lower-third biopsy occurred in 2 subjects with dysplasia (2 of 55 subjects, 4%) and 26 subjects with basal cell hyperplasia (26 of 55 subjects, 47%). Analysis by immunohistochemistry showed high concurrent rates of p53 protein accumulation (51 of 55 subjects, 93%). p53 sequence analysis of 32 samples from 16 subjects identified missense mutations in 5. In one subject, there were three different mutations in the middle-third biopsy (codon 161, GCC-->GAC) and the lower-third biopsy (codon 159, GCC-->CCC). A single mutation was detected in the other four subjects in either the middle- or lower-third biopsy. CONCLUSIONS: The present findings indicate that p53 protein accumulation and mutations occur in the early stages of human esophageal carcinogenesis. Independent somatic mutations of the p53 tumor suppressor gene and protein accumulation in different regions of the esophageal "field" might be key molecular events in multifocal esophageal carcinogenesis.

Changes in p53 and cyclin D1 protein levels and cell proliferation in different stages of human esophageal and gastric-cardia carcinogenesis.

The objective of this study was to quantify the changes in p53 and cyclin D1 protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high-risk population in Henan, China. Immunoreactivity of p53, cyclin D1 and proliferating-cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53-immunostaining-positive cells was low in normal epithelia, slightly increased in basal-cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10-fold), and further increased in squamous-cell carcinoma (SCC) (40-fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin D1-immunostaining-positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53-positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53-positive cells was very low, much lower than that of PCNA-positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53-positive cells from CAG to DYS was more dramatic (100-fold). From DYS to adenocarcinoma (AC), the p53-positive and the PCNA-positive cells increased 4-fold. On the other hand, the number of cyclin D1-positive cells did not increase in pre-cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre-cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric-cardia cancers, which frequently occur together in many high-incidence areas.

Endoscopic Nd:YAG laser therapy in patients with early superficial carcinoma of the esophagus and the gastric cardia.

A group of 33 patients, 27 with early superficial esophageal cancer and six with early superficial carcinoma of the gastric cardia, were treated with endoscopic neodymium:yttrium aluminum garnet (Nd:YAG) laser from April 1989 to March 1993. Of the 33 patients, in 32 (97%) the disappearance of the cancer cells was noted. They were treated 1-6 times (average 2.6) with laser irradiation. No serious complications, such as perforation, occurred in the series. Twenty-two patients were followed up for 24-55 months. A negative biopsy was recorded in 16 (72.7%) of the 22 patients; the other six (27.3%) cases were found to have recurrent early cancer during the follow-up period from the 36th to the 40th months, and were treated with supplementary endoscopic therapy or surgical resection. It is suggested that endoscopic Nd: YAG laser may be a safe and effective therapy for early carcinoma of the esophagus and the gastric cardia, when the risks of surgery are too high or the patient has refused surgical resection.

[The role of TNF-alpha in the growth and differentiation of U937 cells induced by PMA and IFN-gamma].

The effects of PMA and IFN-gamma on regulation of growth and differentiation of human monoblastic leukemic cell U937 were examined. U937 cells were stimulated by different concentrations of PMA and IFN-gamma respectively and NBT reduction assay was used to detect the differentiation of the cells. The results showed that both PMA and IFN-gamma dose-dependently induced differentiation of U937 cells into mature macrophage-like cells. The data also revealed a time-course response in the differentiation induction. Moreover, the U937 cell growth was significantly inhibited by the treatment of PMA and IFN-gamma. These results suggest that PMA and IFN-gamma coupled the regulation of U937 cell growth and differentiation. It was found that tumor necrosis factor-alpha (TNF-alpha) was expressed by the stimulated U937 cells. The specific monoclonal antibody against TNF-alpha diminished the effects of PMA and IFN-gamma on the growth and differentiation of U937 cells. Thus the endogenous TNF-alpha may involved in the mechanism of the effects of PMA and IFN-gamma on the differentiation of U937 cells. The regulatory action of the endogenous TNF-alpha on U937 cells was not due to its cytotoxic effect.

Accumulation of p53 protein in human esophageal precancerous lesions: a possible early biomarker for carcinogenesis.

The level of p53 protein was determined immunohistochemically in normal tissues and tissues with different severities of lesions (basal cell hyperplasia, dysplasia, carcinoma in situ, and carcinoma) from surgically resected human esophagi and esophageal biopsies of symptom-free subjects. The samples were from an area with high esophageal cancer incidence in northern China (Linxian and Huixian in the Henan province). Tissue sections were incubated with p53 antibodies for immunostaining. Conventional hematoxylin and eosin stain was also used. In surgically resected esophageal specimens, elevated p53 protein levels were found in the cell nuclei in tissues with precancerous and cancerous lesions. From basal cell hyperplasia to dysplasia to carcinoma in situ, the p53 immunostain-positive cells increased in number, and their distribution had roughly the same pattern as that of the proliferating cells. However, positive stain was not observed in the dividing basal cells of the normal epithelium of the surgically resected tissues. A similar pattern of immunostaining was observed in the abnormal tissues of the biopsy samples from the symptom-free subjects. An intriguing observation is that some p53 immunostain-positive cells were observed in 3 of 6 cases of histologically normal epithelia of biopsy samples. Only the papillary immunostaining pattern was observed in these three "normal" cases. Although the molecular basis for such positive stain remains to be investigated, it is possible that p53 protein accumulation occurs early in the pathogenesis of esophageal cancer and that p53 mutation is closely associated with the initiation of this cancer. The accumulation of p53 protein may be a promising early biomarker for identifying high-risk subjects for esophageal cancer.

A randomized double-blind intervention study on the effect of calcium supplementation on esophageal precancerous lesions in a high-risk population in China.

To determine whether dietary calcium supplementation affects esophageal precancerous lesions, 200 subjects with esophageal lesions in a high-risk area for esophageal cancer in China (Huixian, Henan) were randomly divided into 2 groups (100 subjects/group). Subjects in one group received an oral supplementation of calcium carbonate tablets (1200 mg of calcium daily), and subjects in the other group received placebo pills for 11 months. At the entry and the end of the trial, esophagoscopy was performed, and 2 or 3 biopsy specimens were taken from the middle and lower thirds of the esophagus and from macroscopic lesions, if any, of each subject for histopathology and cell proliferation analysis with deoxythymidine labeling. In comparison to normal epithelium, increased proliferative compartment size was observed in epithelia with hyperplasia or dysplasia. After the intervention, the percentage of individuals with "normal epithelium," "basal cell hyperplasia," "basal cell hyperplasia II," and "basal cell hyperplasia III and dysplasia" were 44, 31, 13, and 11% in the calcium group and 35, 39, 17, and 6% in the placebo group, respectively. The labeling index was 0.046 in the calcium group and 0.044 in the placebo group. After the intervention, the labeling index in basal cell layers 1 to 5, the major zone of cell proliferation, fell 38% in the calcium group and 44% in the placebo group from before the intervention. Therefore, in this study, calcium supplementation was not shown to have beneficial effects in alleviating precancerous lesions and abnormal cell proliferation patterns.

Prevalence survey of precancerous lesions of the oesophagus in a high-risk population for oesophageal cancer in France.

The prevalence of precancerous lesions of the oesophagus and their association with alcohol drinking, tobacco smoking and some dietary factors were examined in an endoscopic survey carried out in Lower Normandy, France, a high-risk area for oesophageal cancer. The study included 134 male volunteers of 35-64 years of age. In 124 of the volunteers oesophageal biopsies were evaluable. At histology, the prevalence of chronic oesophagitis, epithelial atrophy and dysplasia was 63%, 1.6% and 4.8%, respectively. The prevalence of these precancerous lesions was significantly associated with cigarette smoking and frequent consumption of butter.

[IL-2 potentiates the IL-3 production by ConA activated mouse splenic T cells].

In addition to the regulation of T cell growth, IL-2 exerts effects on the induction of certain lymphokines. We show here that IL-2 synergizes with 5 micrograms/ml of ConA to promote the production of IL-3 in mouse splenic T cell cultures. IL-3 was measured as CFU-GEMM-inducing activity on mouse bone marrow progenitor cells in the supernatant of the stimulated mouse splenic T cells (TCM). The resting T cells produced no CFU-GEMM-inducing activity, but could be induced to produce low level of CFU-GEMM-inducing activity in the presence of ConA. In vitro exposure to IL-2 markedly increased CFU-GEMM-inducing activity production (nearly up to 8-fold) by the ConA-activated T cells. Optimal stimulation was observed when 80 u/ml IL-2 was used for 48 h incubation. Anti-mouse IL-3 monoclonal antibody inhibited the CFU-GEMM inducing activity of TCM. Moreover, the TCM stimulated the proliferation of IL-3 dependent cell line FDC-P1. We also show that IL-2 and ConA-treated T cells expressed high level of IL-3 mRNA through dot blot analysis. These results confirmed the nature of CFU-GEMM-inducing activity of TCM as IL-3. The capacity of IL-2 to promote the production of IL-3 may represent an important mechanism by which it mediate the communication between the immune and hematopoietic systems.

Epidemiological study of precursor lesions of oesophageal cancer among young persons in Huixian, China.

A total of 538 subjects (354 males, 184 females) were investigated in a high-risk area for oesophageal cancer in China to provide large-scale data on the prevalence of chronic oesophagitis among persons below 25 years of age. The survey included an oesophagoscopy with guided biopsies and cytology, a physical examination, an interview and collection of a 10-ml blood sample and overnight urine. Histologically confirmed oesophagitis was found in 43.5% of male and 35.6% of female subjects. Mild and moderate oesophagitis was associated positively with consumption of burning hot beverages, family history of oesophageal cancer, frequent consumption of cottonseed oil, cigarette smoking, a clinical diagnosis of oral leukoplakia and seborrhoeic dermatitis; negative associations were seen with frequent consumption of fresh fruit, meat and eggs. A significantly higher level of urinary nitrate was found in the diseased group, but no difference was seen with regard to any of the N-nitrosamino acids measured.