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Purpose Abutment screw loosening is a frequently encountered prosthetic complication in implant dentistry. Due to the detection of preload loss soon after initial torque application, abutment screw retightening 10 minutes after initial tightening has been recommended. The aim of this clinical study was to assess preload maintenance in the abutment screws of single posterior implants after 1 month of use by employing screw-cement-retained prostheses and a clinical assessing method, with the ultimate goal of helping to improve the clinical workflow of implant-based restorations. Materials and methods In total, 158 patients treated using three implant systems were divided randomly into two groups in which abutment screws were and were not retightened, respectively, approximately 10 minutes after initial torque application. Screw-cement-retained prostheses, which permitted the assessment of abutment screw preload maintenance and screw retightening after 1 month of use, were used. Preload loss at 1 month was defined as the failure to achieve the torque recommended for the abutment screws after 90-degree clockwise rotation of the screwdriver. The data were analyzed using binary logistic regression, with a significance level of P ≤ .05. Results No preload loss was detected 10 minutes after initial screw tightening. Preload loss was detected in 16 (10.13%) cases at 1 month after initial tightening, with no significant difference according to the implant system used, the presence or absence of retightening at 10 minutes after initial tightening, or implant position (premolar or molar). Conclusion Under the experimental conditions of this study, abutment screws in some bone-level, internal tapered-connection, platform-switching implant systems showed preload loss at 1 month after abutment placement for single posterior implant-based restorations, regardless of implant system or whether abutment screws had been retightened 10 minutes after abutment placement, or implant position (premolar or molar). It is necessary to retorque the abutment screws 1 month after initial torque. The screw-cement-retained prostheses used in this study permit abutment screw retightening at that time and have advantages over traditional methods.

Treatment history influences the outcomes of subsequent therapies in patients with relapsed or refractory multiple myeloma (RRMM) and needs to be considered when deciding which treatment to use next. To assess the relative merits of immunomodulatory (IMiD)-free treatments, a systematic literature review (SLR) was conducted to identify relevant randomized controlled trials in patients with RRMM. A network meta-analysis (NMA) was performed to assess various IMiD-free regimens, including bortezomib and dexamethasone (Vd)-based treatments, and to explore differences in patient outcomes. The SLR identified 52 articles, from which four trials were ultimately included in the base-case NMA. The NMA showed that daratumumab plus Vd (DVd) provided a significant advantage in prolonging progression-free survival. Similar trends were observed for overall survival and overall response. Across all outcomes, DVd had the highest probability of being the best treatment. These findings suggest that DVd may provide superior clinical outcomes for RRMM patients suitable for IMiD-free regimens.

Low permeability reservoirs need fracturing to obtain productivity. The damage of fracturing fluid to reservoir is an important factor affecting productivity. Obtaining reservoir sensitivity data is an important task for optimizing fracturing fluid. At present, data is still obtained from reservoir sensitivity experiments in China. This traditional method has relatively high veracity, but it costs a lot of manpower and it is often behind the project. Thus, a prediction model which BP neural network is put forward. The success rate is 100% when this method is applied to the two wells of changqing Oil field. The experimental result indicates that BP network, good prediction results can be obtained.

Aiming at problems of lack of theoretical research and existing resources, etc., in equipment’s combat resilience design for the chinese military, a new kind of equipment’s combat resilience design theory-TRIZ contradiction maters are used to describe the technical conflict in practical problem, the conflict resolving matrix is used to analysis problem, and the principle to solve the contradiction is given at last. This theory is strongly to solve the contradiction problem. For these reasons, the equipment’s combat resilience design process is proposed in this paper, and then taking the battlefield maintenance of radar phased array antenna as an example, this paper analyses the improvement design method to introduce the design of phased array antenna by using the TRIZ conflict matrix. The results show that, TRIZ conflict matrix can effectively guide the equipment’s combat resilience design, and can indicate the direction for the equipment’s combat resilience design to improve design efficiency.

Studies indicate that immune responses after trauma-hemorrhage are significantly depressed in males compared with enhanced immune responses in females under such conditions. Although androgen depletion in male mice by castration before soft tissue trauma and hemorrhagic shock prevents the depression of cell-mediated immunity, the underlying mechanism responsible for this remains unclear. Because the thymus is the primary location of T-cell lymphopoiesis and thymocytes express a large number of androgen receptors, we investigated whether differences in thymic apoptosis might contribute to the divergent immune response in males versus females after trauma-hemorrhage. To study this, male and female C3H/HeN mice were subjected to sham operation or soft tissue trauma (laparotomy) and hemorrhagic shock followed by fluid resuscitation. Animals were killed 72 h thereafter and thymocytes were isolated. Thymocyte interleukin 3 (IL-3) release was significantly suppressed in males, but not females, after trauma-hemorrhage. A parallel increase in thymic apoptosis that was primarily in the CD8+ thymocyte subset was observed in the males. Furthermore, In vitro treatment of thymocytes with 5α-dihydrotestosterone (DHT) increased the rate of apoptosis and decreased IL-3 release in a dose-dependent manner. Thus, the gender-dependent dimorphic immune response after trauma-hemorrhage may be in part due to an androgen-induced increase in thymic apoptosis in males under such conditions.

Sepsis is reported to induce an increase in the rate of apoptosis (Ao), in immature lymphoid cells residing in hematopoietic tissues such as the thymus and bone marrow. Alternatively, secondary lymphoid tissue, such as the spleen exhibit little innate (unstimulated) Ao. However, it is unknown whether or not polymicrobial sepsis has any effects on the frequency of Aoin mucosal lymphoid tissue and what, if any, are the functional consequences of such a change. To assess this, Peyer's patch cells were harvested from C3H/HeN (endotoxin-sensitive) mice killed 12 or 24 hours after the onset of polymicrobial sepsis (cecal ligation and puncture [CLP]). The results indicate that the percentage of cells that were Ao+ as determined by flow cytometry were markedly increased at 24 hours, but not at 12 hours post-CLP. This correlates well with evidence of increased DNA fragmentation as well as histological changes observed both at a light and transmission electron microscopic level of the Peyer's patch Ao. Phenotypically, these changes were restricted to the B220+ (B-cell) population that also exhibited a marked increase of Fas/Apo-1 antigen expression. The functional consequence of this increased apoptosis appears to be associated with the endogenous stimulation (activation) of IgA production by mucosal B lymphocytes and increased nuclear c-Rel expression. Furthermore, we found that Peyer's patch lymphocytes isolated from C3H/HeJ-Faslgld(endotoxin-tolerant/Fas ligand- [FasL] deficient) as opposed to C3H/HeJ (endotoxin-tolerant) inbred mice did not exhibit increased Ao after CLP. These findings indicate that increased B-cell Ao appears to be a FasL-Fas antigen-mediated process, but is not due to endotoxin sensitivity. In conclusion, we speculate that the increased Fas-associated apoptosis detected in mucosal B cells (as opposed to splenic or bone marrow B cells) may be due to increased luminal antigens other than endotoxin, released due to gut barrier integrity breakdown during sepsis.

Although intestinal mucosal immune dysfunction occurs after trauma and hemorrhage and appears to contribute to infectious complications, the mechanism is not known. In this regard, the inappropriate induction of immune cell apoptosis may contribute to the immune dysfunction following trauma and hemorrhage. To study this, we examined Peyer's patch cells for evidence of apoptosis and changes in Fas protein expression, as well as alterations in the relative lymphocyte subpopulations after trauma and hemorrhagic shock. Male C3H/HeN mice underwent sham operation, trauma (i.e., laparotomy), hemorrhagic shock (mean arterial blood pressure of 35 +/- 5 mmHg for 90 min, followed by adequate crystalloid resuscitation), or trauma plus hemorrhage. Peyer's patch cells were isolated at 24 and 72 hr after the procedure. The percentage of apoptotic cells, Fas protein expression, and cell percentage of phenotype were determined by flow cytometry. The results indicate that trauma alone induced no significant change in the measured parameters. However, (i) there were a significant decrease in total viable cell yield and an increased apoptosis in Peyer's patch cells at 24 and 72 hr following hemorrhage or trauma plus hemorrhage; (ii) the increased apoptosis in Peyer's patch was predominantly in cells of the B-cell lineage; (iii) the increased apoptosis was associated with an elevated Fas expression. In conclusion, hemorrhage alone or trauma plus hemorrhage can induce increased apoptosis in Peyer's patch cells, which is associated with the increased Fas expression. Thus, apoptotic involution may play an important role in the depression of intestinal mucosal immune function after trauma and hemorrhagic shock.

Although the thymus is an important organ in the ontogeny of T lymphocytes, little is known about the effects of hemorrhage and/or trauma on this organ. The objective of this study was to determine whether trauma–hemorrhage induces increased thymic apoptosis and, if so, which mediators may be involved. Male C3H/HeN mice underwent either sham operation, hemorrhagic shock (mean artery blood pressure of 35 ± 5 mmHg for 90 min, followed by blood and fluid resuscitation), fracture of the right tibia, or fracture plus hemorrhage, respectively. At 3 days after the procedure, total viable thymocyte yield, thymocyte apoptosis (flow cytometry), thymus-derived IL-3 (bioassay), and GM-CSF (ELISA) were determined. The results demonstrate that fracture alone induces no significant change in the parameters measured. However, (i) there was a significant decrease in total viable thymocyte yield and an increase in thymocyte apoptosis following hemorrhage or fracture plus hemorrhage; (ii) thymocyte IL-3 release was significantly reduced after hemorrhage as well as fracture plus hemorrhage; (iii) thymus-derived GM-CSF was significantly increased after fracture plus hemorrhage, but not with hemorrhage alone. In conclusion, severe hemorrhage alone or coupled with fracture can induce thymus atrophy via apoptosis. In addition, the decreased IL-3 release suggests that apoptotic thymic involution may be due to the lack of growth factor support. Such dyshomeostasis may contribute to inappropriate/inadequate T cell maturation leading to host immune suppression following trauma–hemorrhage. Increased thymus-derived GM-CSF might be in part responsible for the systemic inflammatory response following trauma–hemorrhage.

Recently immunotherapy for gastrointestinal tumor has rapidly developed, and has improved the effect of cancer comprehensive treatment as an adjunctive therapy in combination with surgery, chemotherapy, and radiation therapy. Adoptive transfer of immune cells is an important treatment method for advanced gastric cancer. In this paper, we reviewed the application of adoptive transfer therapy for advanced gastric cancer in the perioperative period and propose a new model for immunotherapy of advanced gastric cancer based on our experience and the results of clinical experiment.

To investigate the clinical characteristics, 3-month outcome and predictive factors in the very elderly patients with ischemic stroke.A total of 305 acute ischemic patients aged 65 years and over were enrolled in the study. They were divided into two subgroups by age: 80 years old and over (n = 78), 65 - 79 years old (n = 227). The clinical outcome was assessed by the modified Rankin Scale (mRS) on (90 ± 7) days after stroke, and categorized as good (scoring 0 - 2) or poor (scoring 3 - 6) outcome.Significantly lower BMI [(23.62 ± 4.92) kg/m(2) vs (25.08 ± 3.69) kg/m(2), P = 0.005], lower frequency of dyslipidemia (56.41% vs 71.13%, P = 0.006) and alcohol intake (0% vs 6.61%, P = 0.043) were found in the very elderly group. The rates of poor functional outcome in the ≥ 80 years group and the 65 - 79 years old group were 56.41% (44/76) and 41.40% (94/224) respectively, with a P value of 0.015. Multivariate logistic regression analysis showed that higher National Institute of Health stroke scale (NIHSS) total score (OR 1.48, 95%CI 1.19 - 1.83) and lower albumin level (OR 0.73, 95%CI 0.55 - 0.95) were associated with poor outcome in ≥ 80 year old, whereas higher NIHSS total score (OR 1.38, 95%CI 1.24 - 1.53) and complications during hospital stay (OR 2.58, 95%CI 1.07 - 6.19) were predictive factors in the 65 - 79 years old group.Our study suggests that NIHSS scores, albumin level and complications during hospitalization are useful predictive factors for the short-term poor functional outcome in the patients of ≥ 65 years old and ≥ 80 years old patients have a worse prognosis.

To investigate the migration and distribution of CTL (cytotoxic T lymphocyte) and CIK (cytokine-induced killer) cells in gastric tumor model.Subcutaneous gastric tumor model was established by BGC-823 cancer cells in nude mice. Both CTL and CIK cells were labeled with 99Tc(m) directly and then inoculated into nude mice with subcutaneous tumor by intravenous injection separately. Three mice of each group were evaluated by single-photon emission computerized tomography (SPECT) at 1 h, 6 h and 24 h post-inoculation. After SPECT imaging, 3 mice in each group were sacrificed and got samples of the tumor, liver, spleen, kidney, lung, intestine, etc. The tissue samples were weighed and radioactivity was determined with a well-type scintillation counter. The accumulation of labeled CTL and CIK cells in tissues were expressed as %ID/g (percentage activity of injection dose per gram of tissue) and T/NT (tumor/non-tumor) values were analyzed.The tracing of both cells in SPECT showed a clear migration path away from the injection point to solid tumor, and can be detected in all organs and tissues such as liver, spleen, kidney, lung and intestine, etc not long after injection. The %ID/g peak values of CTL in organs from the highest to the lowest were as follows: tumor (7.79 +/- 0.46), liver (4.12 +/- 0.51), intestine (2.71 +/- 0.16), kidney (1.44 +/- 0.25), spleen (1.24 +/- 0.12), kidney (1.12 +/- 0.11), and all the T/NTs were above 1. The %ID/g peak values of CIK cells in organs from the highest to the lowest were as follows: liver (6.64 +/- 0.67), tumor (5.47 +/- 0.87), intestine (3.55 +/- 0.23), kidney (2.34 +/- 0.41), spleen (1.45 +/- 0.17), lung (1.27 +/- 0.21), and T/NTs1 except for liver. After injection, the %ID/g values of tumor in CTL group were 2.35 +/- 0.28 (1 h), 4.58 +/- 0.52 (6 h) and 7.79 +/- 0.46 (24 h) respectively while the %ID/g values of tumor in CIK group 2.23 +/- 0.46 (1 h), 3.25 +/- 0.70 (6 h) and 5.47 +/- 0.87 (24 h) respectively. At 24 h point, the %ID/g of CTL in tumor was much higher than CIK cells (P0.05).The definite directional tumor-targeting capacity of CTL and CIK cells in tumor-bearing nude mice is promising.

To construct implantable engineered liver tissue (ELT) using type I collagen gel as scaffold.Type I collagen was obtained from the tail of a rat. Hepatocytes were collected from a Sprague-Dawley rat, mixed with liquid type I collagen and Dulbecco's modified Eagle's medium to create hepatocyte/collagen gel construct. The construct was inoculated in a 96-well plate. 0, 3, 5, 7, 9, 11, 13, and 15 days after the inoculation the viability of hepatocytes in vitro was measured by MTT assay. Phase contrast microscopy was used to observe the morphology of the hepatocyte/collagen gel construct. Three SD rats underwent injection of the hepatocyte/collagen gel construct into the subcutaneous space. One week later the implant was taken out. The morphology was conducted by routine H.E. staining and immunohistochemical staining. The morphology and function of hepatocytes was investigated by inverted microscopy, routine H.E. staining and immunohistochemical staining. The constructs were also implanted into subcutaneous space, and the differentiation of hepatocytes and the formation of engineered liver tissue were observed by routine H.E. staining and immunohistochemical staining.Phase contrast microscopy showed that the hepatocytes were distributed evenly in the construct and remained round-shape throughout the in vitro culture. MTT assay demonstrated that the high viability of hepatocytes (87%) was maintained up to 7 days, and then decreased gradually. Albumin, the specific marker of hepatocytes remained positive by immunohistochemical staining after 15-day culture. One week after implantation into subcutaneous space, the implanted hepatocytes retained its hepatocyte-specific morphology, i.e. round shape, large nuclear/cytoplasm ratio as well as binuclear cells, and formed small engineered liver tissue containing blood vessels within and surrounding the tissue.A novel approach to construct implantable engineered liver tissue using collagen gel as scaffold for growth and differentiation of hepatocytes has been dev eloped. This technique is an attractive tool for the development of liver tissue engineering.

To study differentiation of human bone marrow-derived mesenchymal stem cells (BDMSC) into blood vessel endothelial cells for ideal cell origin of complex organ tissue engineering vascularization and injured tissue repairing by cell transplantation.After different days of induction with vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in 3D fibrin-gels and matrigel, BDMSC and angiogenesis were determined by the utilization of morphological observation, tissue section and CD34, CD31, vascular endothelial growth factor receptor-1 (VEGFR-1, Flt-1), VEGFR-2 (Flk-1), and vWF that were special for blood vessel endothelial cells.After 3D-cultured and induced with VEGF and bFGF in vitro in fibrin-gels and matrigel for 3-21 days, BDMSC expressed CD34, CD31, Flt-1, Flk-1, and vWF came into vessel-like configuration.VEGF, bFGF as well as Flt-1 and Flk-1, expressed by BDMSC, may form a feasible microenviroment after induction and play an important role during processes of blood vessel endothelial cell differentiation and vessel-like configuration forming of BDMSC. Mesenchymal stem cells may be applied to tissue engineering vascularization and injured tissue repairing by cell transplantation.

Biodegradable stents have advantages for the treatment of benign and malignant biliary stricture, especially eliminating the need for stent removal. In our present work, helical poly-l-lactic acids (PLLA) stent was fabricated and evaluated in vivo and in vitro. For in vivo study, bile duct injury canine models were made by transection of common bile ducts. Duct to duct anastomosis was done with helical PLLA biodegradable stents. Scanning electron microscopy (SEM) and histopathology were performed after three months. For In vitro study, sludge attachment assessment was performed. Polyethylene (PE) and PLLA membranes were immersed in human bile for two months. The samples were taken out and characterized by SEM. Self-expanding property of the helical stent was tested in 37 degrees Celsius water. The results demonstrate that the biodegradable stent had not only good biocompatibility, but also self-clearing effect to clear the attached sludge away. The self-expanding property facilitated stent implantation and also suggested possibility to be implanted endoscopically.

To study the early and late changes in mRNA expression in macrophages in response to lipopolysaccharide (LPS) with a cDNA microarray approach using the Clontech Atlas microarray.mRNA was isolated from unstimulated control and LPS stimulated murine peritoneal macrophages at 2 hours and 24 hours poststimulation, converted to (33)P radiolabeled cDNA, and hybridized to mouse array membranes.In macrophages being stimulated for 2 hours, 69 out of 1 176 genes were found to differ by over 3-fold compared with the control. Among them 44 genes were up-regulated and 25 genes were down-regulated. In macrophages stimulated for 24 hours, 11 genes were up-regulated and 26 genes were down-regulated compared with the control. Only 8 genes were identified both at 2 hours and at 24 hours poststimulation. The expressions of many genes encoding transcription factor, cytokines, cell signaling modulators and apoptosis associated proteins were found to have changed. Some genes that were not previously linked to this model, such as bric-a-brac (BTB) and cap-n-collar(CNC) homology 1(BACH1), early growth response protein 2 (EGR2), E47 interaction protein 1 (EIP1), Ngfi-A binding protein 2 (NAB2), myeloblastosis oncogene-like protein (MYBL2), neurofibromatosis 1 (NF1), ciliarry neurotropic factor (CNTF) and semaphorin 4A (Sema4A).This study has allowed us to identify genes that may potentially be regulated by LPS at early and late phase in macrophages. These may contribute to better understanding of the mechanism underlying LPS or bacteria induced inflammatory and immune response following infection and trauma.

Recent studies suggest that increased lymphocyte apoptosis (Ao) detected in peripheral blood T cells from burn patients appears to contribute to decreased lymphocyte immunoresponsiveness. However, while it is known that sepsis induces a marked depression in the splenocyte immune response (i.e. decreased interleukin-2, interferon-gamma production and proliferation) in response to the T-cell mitogen concanavalin A (Con A), it is unknown whether this depression is associated with an increase in inducible Ao and if so, which mediators control this process. To assess this, splenocytes were harvested from mice at 24 hr (a period associated with decreased Con A response) after the onset of polymicrobial sepsis [caecal ligation and puncture (CLP)] or sham-CLP (Sham) and then stimulated with 2.5 microg Con A/ml (24 hr). Septic mouse splenocytes stimulated with Con A, while not showing a change in their phenotypic make-up, did exhibit a marked increase in the percentage of splenocyte that were Ao+ which was associated with altered cytokine release. This appears to be due to an increase in the percentage of Ao+ cells in the CD4+ CD8- population and was associated with enhanced Fas antigen expression as well as an increase in mRNA for the Fas-FasL gene family. To determine if the changes in Ao are due to either endotoxin (a product of Gram-negative bacteria seen in CLP mice) or the expression of Fas ligand (FasL; a mediator of activation-induced lymphocyte Ao), a second set of studies examining Con A-inducible Ao was performed with splenocytes harvested from septic endotoxin-tolerant C3H/HeJ and the FasL-deficient C3H/HeJ-Fasl gld mice. The results show that increased splenocyte Ao detected following CLP is due to a FasL-mediated process and not to endotoxin. Thus the inadvertent up-regulation of FasL-mediated splenocyte Ao may contribute to the depression of splenocyte immune responses seen during polymicrobial sepsis.

Background; Apoptosis (A o ) is a normal constitutive process that seems to have pathological effects in diseases of immune deficiency and autoimmune disorders, as well as in certain lymphoid tissues during sepsis. Little is known about this process in mucosal lymphoid tissue, such as intestinal intraepithelial lymphocytes (IELs). Objectives: To determine whether sepsis induces increased A o in small intestinal IEL, whether this was associated with functional changes in cytokine gene expression in the IEL, and which mediators control this process and their impact on the survival of the mouse with sepsis. Design: Male C3H/HeN (endotoxin-sensitive), C3H/ HeJ (endotoxin-tolerant), and C3H/HeJ-FasL gld (endotoxin-tolerant/Fas ligand [FasL]-deficient) mice were subjected to sepsis (cecal ligation and puncture [CLP]) and IELs were harvested at 4 (early) or 24 hours (late sepsis). Alterations in the cell phenotype and A o (TUNEL [terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick-end labeling] assay) were determined by 3-color now cytometry. Cytokine gene expression was assessed by multiprobe RNase protection assay. Results: At 4 hours after CLP, only the frequency of IEL which was CD8 + decreased markedly. By 24 hours after CLP, the number of CD8 + and CD4 + cells decreased while the proportion of double-negative cells showed a marked increase when compared with sham-controls. The percentage of A o positive in CD8 + and CD4 + double-positive and double-negative cells increased markedly 24 hours after CLP concomitant with a significant (P

Studies indicate that lymphoid tissue (e.g., thymus, bone marrow, and Peyer's patches) shows evidence of increase apoptosis (Ao, a form of nonnecrotic cell death) during sepsis. However, it is not known if mucosal lymphoid tissue, such as lamina propria (LP), also shows evidence of increased Ao and if so, is this associated with functional changes, i.e., cytokine gene expression in the LP. To examine this, male C3H/HeN mice were subjected to cecal ligation and puncture (CLP) and lamina propria mononuclear cells (LPMC) were harvested at 4 h (early sepsis) or 24 h (late sepsis). Alterations in the cell phenotype as well as Ao (Tunel assay) were determined by three-color flow cytometry. Cytokine gene expression was assessed by multiprobe RNase protection assay. Sham LPMC preparations were found to be 34.4 +/- 2.4% B220(+) (B-cells), while 12.4 +/- 2.1% were CD8(+) (cytotoxic T-cells), 22.0 +/- 0.8% were CD4(+) (helper T-cells), and 6.4 +/- 0.7% were F4/80(+) (macrophages). The frequency of B220(+) (9%* upward arrow) and CD8 (6%* upward arrow) populations increased markedly at 4 h after CLP; however, this increase was not seen at 24 h. The percentage of Ao+ in CD8(+), B220(+), and F4/80(+) cells increased markedly at both 4 and 24 h. CD4(+) cells showed a marked increase in Ao only at 24 h after CLP. When LPMC mRNA expression was examined, a significant increase in IL-2, -10, and -15 gene expression was observed only at 24 h but not 4 h after CLP. Thus, the early phenotypic changes associated with increased Ao may be a reflection of localized immune cell activation in early sepsis contributing to the increased cytokine gene expression seen in late sepsis. This localized activation may contribute to gastrointestinal inflammation and/or immune dysfunction in sepsis.

Background: Although hemorrhage or trauma (laparotomy) alone in mice produces a marked immunosuppression for 3 to 4 days and trauma plus hemorrhage produces immune depression for 5 days after resuscitation, it remains unknown when the immune functions return to normal after trauma-hemorrhage and whether lymphocyte and macrophage functions are similarly affected by trauma-hemorrhage. Methods: Male C3H/HeN mice underwent either sham operation, trauma (laparotomy), hemorrhagic shock (mean arterial blood pressure of 35 ± 5 mm Hg for 60 minutes, followed by fluid resuscitation), or trauma plus hemorrhage. Plasma, splenocytes, splenic macrophages, and peritoneal macrophages were harvested at 7 or 10 days after the operation. Plasma and macrophage tumor necrosis factor, interleukin (IL)-6, and splenocyte IL-2 and IL-3 release were determined by bioassay, and splenocyte proliferation was measured by [ 3 H]thymidine incorporation. Results: Splenocyte proliferation, splenocyte lymphokine release, and splenic and peritoneal macrophage cytokine release were still markedly decreased in the trauma-hemorrhage group compared with other groups at 7 days but returned to normal by day 10. Tumor necrosis factor and IL-6 levels, however, were not detectable in plasma of any groups at 7 or 10 days after operation. Conclusion: The results indicate that a more severe and prolonged immunodepression occurs after combined trauma and hemorrhage than after trauma or hemorrhage alone.

AIM: To investigate the role of cytokine gene expression in organ damage at different tissue sites during sepsis. METHODS: Male NIH mice were subjected to cecal ligation and puncture (CLP) or sham operation (Sham). Pro-inflammatory cytokine (TNFα, IL-1β and IL-6) and anti-inflammatory cytokine (IL-4) gene expression in the liver and lung tissue were assessed by RT-PCR. The permeability of microvascular and water content in the lungs and liver were also examined. RESULTS: Significant increase in TNFα, IL-1β and IL-6 gene expression was observed at 3 and 12 h after CLP both in the liver and lungs (P < 0.01).The level of IL-4 gene expression was not changed after CLP in the lungs, but increased at 12 h after CLP (P < 0.01) in the liver tissue. Both the liver and lungs showed a significant increase in microcirculatory permeability at 12 h after CLP(P < 0.01), and the increase in the lungs was higher than that in the liver. The water mass fractions in the liver (P < 0.05) and lungs (P < 0.01) were increased after CLP, and the increase in the lungs happened earlier and more severely than that in the liver. CONCLUSION: The inflammatory response in the liver and lungs was different during sepsis. At the early stage of sepsis, pro-inflammatory reaction dominates both in the liver and lungs. But at the later stage of sepsis, induction of compensatory anti-inflammatory response was seen in the liver but not in the lungs. This difference in situ activity may contribute to the different vulnerability of organ damage during sepsis. The strategy of systemic administration of anti-inflammatory drugs to sepsis should be reconsidered.