Anesthesia Infrastructure and Resources in Bangladesh.

BACKGROUND: Monitoring improvements in nationwide anesthesia capacity over time is critical to ensuring that population anesthesia needs are being met and identifying areas for targeted health systems interventions. Anesthesia resources in Bangladesh were previously measured using a cross-sectional nationwide hospital-based survey in 2012. No follow-up studies have been conducted since then. METHODS: A follow-up cross-sectional study was performed in 16 public hospitals; 8 of which are public district hospitals, and 8 are medical college (tertiary) hospitals in Bangladesh. A survey tool assessing hospital anesthesia capacity, developed by Vanderbilt University Medical Center, was utilized. Nationwide data were obtained from the Ministry of Health and Family Welfare and from the Bangladesh Society of Anaesthesiologists. Institutional Review Board approvals were obtained in the United States and Bangladesh, and informed consent was waived. RESULTS: Bangladesh has 952 anesthesiologists (0.58 anesthesiologists per 100,000 people), which represents a modest increase from 850 anesthesiologists in 2012. Significant improvements in electricity and clean water availability have occurred since the 2012 survey. Severe deficiencies in patient safety and monitoring equipment (eg, pulse oximetry, electrocardiography, blood pressure, anesthesia machines, and intubation materials) were noted, primarily at the district hospital level. CONCLUSIONS: Despite modest improvements in certain anesthesia metrics over the past several years, the public health care system in Bangladesh still suffers from substantial deficiencies in anesthesia care.

Age exaggerates proinflammatory cytokine signaling and truncates signal transducers and activators of transcription 3 signaling following ischemic stroke in the rat.

Neuroinflammation is associated with glial activation following a variety of brain injuries, including stroke. While activation of perilesional astrocytes and microglia following ischemic brain injury is well documented, the influence of age on these cellular responses after stroke is unclear. This study investigated the influence of advanced age on neuronal degeneration, neuroinflammation, and glial activation in female Sprague-Dawley rats after reversible embolic occlusion of the middle cerebral artery (MCAO). Results indicate that in comparison to young adult rats (3 months), aged rats (18 months) showed enhanced neuronal degeneration, altered microglial response, and a markedly increased expression of proinflammatory cytokines/chemokines following MCAO. In addition, the time-course for activation of signal transducers and activators of transcription 3 (STAT3), the signaling mechanism that regulates astrocyte reactivity, was truncated in the aged rats after MCAO. Moreover, the expression of suppressor of cytokine signaling 3 (SOCS3), which is associated with termination of astrogliosis, was enhanced as a function of age after MCAO. These findings are suggestive of an enhanced proinflammatory response and a truncated astroglial response as a function of advanced age following MCAO. These data provide further evidence of the prominent role played by age in the molecular and cellular responses to ischemic stroke and suggest that astrocytes may represent targets for future therapies aimed at improving stroke outcome.

CXCL13 expression in Chlamydia trachomatis infection of the female reproductive tract.

Chlamydia trachomatis is the most common cause of acute salpingitis worldwide. The socioeconomic impact of sexually transmitted infections (STI) caused by C. trachomatis is considerable. The purpose of this study was to investigate secretion of a unique chemokine, CXCL13, during the inflammatory process in human fallopian tube tissue in response to infection with C. trachomatis. We employed two models for our experiments: archived fallopian tube paraffin sections from known cases of salpingitis of unknown etiology and human fallopian tube organ culture established from fresh fallopian tube biopsies subsequently infected in vitro with C. trachomatis serovar E. We used immunohistochemistry, microarray analysis and cytometric bead array to study these specimens. In both models, we found that the fallopian tissue infected with C. trachomatis expressed CXCL13 and other characteristics of tertiary lymphoid tissue. In addition, we found that CXCL13 was expressed in multiple cell types, including endothelial cells, demonstrating a mechanism for the lymphoid aggregation seen in fallopian tube tissue during salpingitis and infection with C. trachomatis.

Inflammasomes bridge signaling between pathogen identification and the immune response.

Microbial organisms express pathogen-associated molecular patterns (PAMPs) that can stimulate expression of proinflammatory mediators following ligation of pathogen recognition receptors. However, both commensal organisms and pathogens can express PAMPs. The immune system can distinguish between commensals and pathogens in part through secretion of the key inflammatory cytokines interleukin (IL)-1beta and IL-18. A PAMP such as lipopolysaccharide can induce production of intracellular pro-IL-1beta and pro-IL-18, but not their secretion. A second "danger signal", derived from host-cell molecules that are released from stressed or infected cells, or detected as a PAMP that is present in the cytosol, can stimulate assembly of an inflammasome that activates the protease caspase-1. Caspase-1, in turn, is responsible for processing and secretion of the mature IL-1beta and IL-18. Many diverse ligands leading to inflammasome activation have been identified, but the cell signaling pathways initiated by the ligands tend to converge on a small set of common mechanisms.

Administration of sesamol improved blood-brain barrier function in streptozotocin-induced diabetic rats.

Uncontrolled or poorly controlled blood glucose during diabetes is an important factor in worsened vascular function. While evidence suggests that hyperglycemia-induced oxidative stress plays a prominent role in development of microangiopathy of the retina, kidney, and nerves, the role oxidative stress plays on blood-brain barrier (BBB) function and structure has lagged behind. In this study, a natural antioxidant, sesamol, was administered to streptozotocin (STZ)-induced diabetic rats to examine the role that oxidative stress plays on BBB structure and function. Experiments were conducted at 56 days after STZ injection. Male Sprague-Dawley rats randomly were divided into four treatment groups CON--control; STZ--STZ-induced diabetes; CON + S--control + sesamol; STZ + S--STZ-induced diabetes + sesamol. Functional and structural changes to the BBB were measured by in situ brain perfusion and western blot analysis of changes in tight junction protein expression. Oxidative stress markers were visualized by fluorescent confocal microscopy and assayed by spectrophotometric analysis. Results demonstrated that the increased BBB permeability observed in STZ-induced diabetic rats was attenuated in STZ + S rats to levels observed in CON. Sesamol treatment reduced the negative impact of STZ-induced diabetes on tight junction protein expression in isolated cerebral microvessels. Oxidative stress markers were elevated in STZ as compared to CON. STZ + S displayed an improved antioxidant capacity which led to a reduced expression of superoxide and peroxynitrite and reduced lipid peroxidation. In conclusion, this study showed that sesamol treatment enhanced antioxidant capacity of the diabetic brain and led to decreased perturbation of hyperglycemia-induced changes in BBB structure and function.

Chlamydia trachomatis infection induces mucosal addressin cell adhesion molecule-1 and vascular cell adhesion molecule-1, providing an immunologic link between the fallopian tube and other mucosal tissues.

The development of a protective vaccine against the sexually transmitted disease caused by Chlamydia trachomatis may prevent complications associated with insidious infection. Vaccination via the vaginal route may not be practical, and other routes should be investigated. To this end, the adhesion molecules induced on the fallopian tube endothelium during infection with C. trachomatis were characterized. Adhesion molecules were identified in fallopian tube biopsy specimens cultured with 5 x 10(6) infection-forming units of C. trachomatis serovar E. Frozen sections were prepared from these tissues and were stained by immunohistochemical techniques. Infection with live, but not UV-inactivated, C. trachomatis induced a significant increase in levels of vascular cell adhesion molecule-1 and the mucosal addressin cell adhesion molecule-1 but not of other adhesion molecules. Therefore, infection with C. trachomatis induces adhesion molecules that are associated with other mucosal tissues and inflammatory sites, which suggests that mucosal routes of immunization may be effective.

Tetrahydrobiopterin levels regulate endothelial cell proliferation.

Vascular abnormalities, including altered angiogenesis, are major factors contributing to the morbidity and mortality of diabetes. We hypothesized that impaired angiogenesis in diabetes results from decreased tetrahydrobiopterin (BH4)-dependent synthesis of nitric oxide (NO) by endothelial cells (EC). To test this hypothesis, we utilized EC from spontaneously diabetic BB (BBd) and nondiabetes-prone BB (BBn) rats to investigate the link between BH4 and EC proliferation. There were significant decreases in the proliferation rate and expression of proliferating cell nuclear antigen in BBd versus BBn EC, with no evidence of apoptosis in either group. Sepiapterin (a precursor of BH4 via the salvage pathway) increased BH4 synthesis and enhanced proliferation of BBd EC. The stimulating effect of sepiapterin on EC proliferation was attenuated by NG-monomethyl-L-arginine, a NO synthase inhibitor. Reducing BH4 concentrations in BBn EC caused a decrease in proliferation, which was attenuated by a long-acting NO donor. Our results suggest that BH4 levels regulate proliferation of normal EC and that a BH4 deficiency impairs NO-dependent proliferation of BBd EC.

Enhancing release of peptide YY after near-total proctocolectomy: jejunal pouch vs. ileal pouch-distal rectal anastomosis.

Reconstructing the enteric tract after near-total proctocolectomy by interposing a jejunal pouch between the distal ileum and the distal rectum slows small intestinal transit and decreases the number of stools per day compared to a conventional ileal pouch-distal rectal reconstruction. Our hypothesis was that the jejunal pouch operation brings about these results by protecting the ability of the ileal mucosa to secrete peptide YY, thus augmenting the hormonal ileal brake on small intestinal transit and decreasing the stool frequency. In five jejunal pouch dogs and five ileal pouch dogs, more than 6 months after the operation, serum peptide YY concentrations were determined before and at 30-minute intervals for 180 minutes after a standard meal. Fasting serum concentrations of peptide YY, measured by radioimmunoassay, were greater in jejunal pouch dogs (mean +/- SEM, 1340 +/- 143 pg/ml) than in ileal pouch dogs (804 +/- 52 pg/ml; P < 0.01). Postprandial peptide YY concentrations in jejunal pouch dogs were also greater at 30 minutes (jejunal pouch = 1524 +/- 131 pg/ml, ileal pouch = 913 +/- 67 pg/ml; P = 0.01) and 60 minutes after the meal (jejunal pouch = 1723 +/- 250 pg/ml, ileal pouch = 1001 +/- 70 pg/ml; P = 0.05) and peaked sooner (jejunal pouch = 81 +/- 17 minutes, ileal pouch = 147 +/- 12 minutes; P = 0.01). We concluded that the jejunal pouch operation results in greater ileal fasting and postprandial secretion of peptide YY than the ileal pouch operation. The greater release may account, in part, for the slower small bowel transit and decreased number of stools after the jejunal pouch operation.

Chlamydia trachomatis infection does not enhance local cellular immunity against concurrent Candida vaginal infection.

Although Th1-type cell-mediated immunity (CMI) is the predominant host defense mechanism against mucosal Candida albicans infection, CMI against a vaginal C. albicans infection in mice is limited at the vaginal mucosa despite a strong Candida-specific Th1-type response in the draining lymph nodes. In contrast, Th1-type CMI is highly effective against an experimental Chlamydia trachomatis genital tract infection. This study demonstrated through two independent designs that a concurrent Candida and Chlamydia infection could not accelerate or modulate the anti-Candida CMI response. Together, these results suggest that host responses to these genital tract infections are independent and not influenced by the presence of the other.

Development of dendritic cells in culture from human and murine thymic precursor cells.

The earliest T-precursor population in the adult murine thymus can give rise to dendritic cells (DC) in culture if stimulated with a cocktail of cytokines that includes interleukin (IL)-3, but not with cytokine mixes based on granulocyte-macrophage colony stimulating factor (GM-CSF), normally used to generate myeloid-derived DC. This and other evidence led to the proposal that two different lineages of DC exist, one lymphoid-related and the other myeloid-related. To determine whether this selective response to cytokines was restricted to murine DC, early human thymic T-precursors were isolated and their capacity to generate DC in response to various cytokines directly compared to their murine counterparts. In contrast to cultures of murine thymic precursors, CD34+CD1a- lineage marker negative (Lin-) precursor cells from the human thymus proliferated and generated DC with both the IL-3-containing cytokine mix lacking GM-CSF and with GM-CSF based cytokine mixes. These CD34+CD1a-Lin- human precursor cells also gave rise to NK cells under appropriate culture conditions, but produced no granulocyte, monocyte, eosinophil, megakaryocyte or erythroid cells in standard soft-agar colony-forming cell assays. Thus, although apparently lymphoid-restricted, the human thymic DC precursors responded to the myeloid factor GM-CSF as well as to the cytokines selective for murine lymphoid-related DC.

Characteristics and evolution of extraintestinal manifestations associated with ulcerative colitis after proctocolectomy.

AIMS: Describe the characteristics of extraintestinal manifestations complicating ulcerative colitis present preoperatively and determine their evolution after surgery. METHODS: Between 1976 and 1986, 281 patients with ulcerative colitis exhibiting one or more extraintestinal manifestations (EIM) before either IPAA (n = 147), Brooke ileostomy (n = 71), Kock pouch (n = 48) or ileorectostomy (n = 15) were assessed retrospectively. The clinical evolution of each manifestation was classified as having disappeared, improved, remained unchanged or aggravated postoperatively. An efficacy index was designed to assess the ratio of the number of cases cured or improved over the number of cases unchanged or aggravated. The relationship between EIM and gender, age, duration of disease and the type of surgery was also ascertained. RESULTS: 433 EIM were observed in 281 patients. The most common were arthralgias of the large joints (n = 146), of the sacroiliac joint (n = 59) and the small joints (n = 51). In comparison to patients without EIM having received the same operation during the same period of time, EIM were seen more often in women, younger patients, than those with longer duration of disease and the ileoanal anastomosis group. 60% had only one EIM at a time. Based on the efficacy index, thromboembolic accidents and erythema nodosum were the most commonly cured or improved. Ocular manifestations and primary sclerosing cholangitis were unaffected. The other EIM responded favorably but variably with improvement in two thirds of patients. The presence of a rectal remnant (IRA) or ileal reservoir did not affect the evolution of the EIM. CONCLUSIONS: Thromboembolic complications which are life-threatening, erythema nodosum and arthralgia of the small and large joints which impair quality of life, benefited the most from proctocolectomy. Those conditions may be considered preoperatively when making the decision for surgery.

Dendritic cells derived from multiple myeloma patients efficiently internalize different classes of myeloma protein.

Myeloma protein is a unique tumor antigen that can be used to devise tumor-specific vaccination strategies. As dendritic cells (DCs) are extremely potent at inducing T-cell responses, clinical protocols have been designed using myeloma protein-pulsed DCs to elicit anti-tumor cell responses in vivo. To optimize antigen pulsing of DCs, we investigated mechanisms of antigen uptake and evaluated various laboratory parameters including class of myeloma protein, antigen exposure time, and DC maturational stage.DCs were generated by culturing peripheral blood stem cells from myeloma patients in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). Myeloma proteins were labeled with fluorescein isothiocyanate (FITC) and internalization of protein by DCs was measured by flow cytometry.IgG, IgA, and free-kappa light chain myeloma proteins were all rapidly internalized by DCs in a time-dependent fashion. Maturation of DCs with tumor necrosis factor-alpha (TNF-alpha) resulted in diminished uptake. Endocytosis of myeloma protein by DCs was primarily mediated by fluid-phase macropinocytosis based on morphology, nonsaturable uptake kinetics, and sensitivity to drugs that inhibit membrane ruffling. Pulse-chase experiments revealed that the majority of internalized myeloma protein disappeared within 4 hours but was retained in the presence of chloroquine, indicating antigen processing had occurred. Cultured DCs from myeloma patients are functional and can efficiently endocytose different classes of myeloma protein by the mechanism of macropinocytosis. This demonstrates the feasibility of using all classes of myeloma protein for producing DC vaccines, and defines culture conditions for optimizing antigen loading of DCs for induction of anti-myeloma responses.

Bile acid absorption after near-total proctocolectomy in dogs: ileal pouch vs. jejunal pouch-distal rectal anastomosis.

Bile acid malabsorption is often present in patients after near-total proctocolectomy and ileal pouch-anal canal anastomosis, suggesting ileal dysfunction. Experiments were performed in dogs to compare bile acid absorption after a modified procedure, in which a jejunal pouch was interposed between the terminal ileum and the distal rectum, with that after a conventional ileal pouch operation. Fecal bile acid output (equivalent to hepatic bile acid biosynthesis) and composition were determined by gas chromatography/mass spectrometry in five jejunal pouch dogs and in five ileal pouch dogs more than 6 months after operation. Fecal bile acid output in the jejunal pouch dogs (mean +/- standard deviation) was 215 +/- 59 mg/day (10.1 +/- 2.7 mg/kg-day), a value similar to that obtained in the ileal pouch dogs (261 +/- 46 mg/day [12.8 +/- 3.1 mg/kg-day]; P >0.05). These values were also similar to those reported by others for healthy unoperated dogs, indicating that increased bile acid biosynthesis occurring in response to bile acid malabsorption was not present. Fecal bile acids in pouch dogs were completely deconjugated and extensively 7-dehydroxylated (jejunal pouch = 90.4% dehydroxylated; ileal pouch = 88.6% +/- 6.6% dehydroxylated) and consisted predominantly of deoxycholic acid derivatives. We conclude that when either a jejunal pouch or an ileal pouch is used as a rectal substitute in dogs, an anaerobic pouch flora develops that efficiently deconjugates and dehydroxylates bile acids, rendering them membrane permeable. The resultant passive absorption of unconjugated bile acids appears to compensate for any loss of active ileal absorption of conjugated bile acids, and bile acid malabsorption does not occur.

Prediction of retention in micellar electrokinetic chromatography from solute structure. 1. Sodium dodecyl sulfate micelles.

Like other chromatographic techniques, retention factor, k, in micellar electrokinetic chromatography (MEKC) is directly related to solute partition coefficient and the chromatographic phase ratio as k = Kphi. Unlike conventional chromatography, however, the phase ratio and partition coefficient can be accurately determined in MEKC for a given micellar pseudostationary phase. This means that retention factor in MEKC can be predicted for solutes with known micelle-water partition coefficients without any prior experimentation. In this paper, the use of this simple relationship for prediction of retention behavior in MEKC is examined. The principle of additivity of functional group contribution to partitioning is used to calculate the micelle-water partition coefficient, Kmw, for SDS micellar pseudophase. The micellar substituent constants for 20 functional groups (training set) were determined. Using these substituent constants, the Kmw and retention factors for a group of 80 neutral solutes (test set) were predicted. The linear plot of predicted versus observed log k had an R2 = 0.97 and a slope equal to 1.01. It is shown that the retention times (thus chromatograms) in MEKC can be predicted from the calculated retention factors after only one initial experiment to measure teo and t(mc) under the experimental conditions.

Glucosamine inhibits inducible nitric oxide synthesis.

Glucosamine is widely used in Europe for treatment of arthritis in humans. Based on recent findings that excess production of nitric oxide (NO) by inducible NO synthase (iNOS) mediates the pathogenesis of arthritis, we hypothesized that glucosamine may inhibit NO synthesis. To test this hypothesis, we used an in vivo rat model of lipopolysaccharide (LPS)-induced inflammation. Intravenous administration of d-glucosamine (0.5 mmol/kg) 6 h before, at the time of, and 6 h after intraperitoneal LPS injection (1 mg/kg) decreased urinary excretion of nitrate by 31 and 48%, respectively, at days 1 and 2 post LPS administration. When cultured macrophages were treated with LPS (1 microg/ml) to induce iNOS expression, addition of 0.1, 0.5, 1, and 2 mM d-glucosamine decreased NO production by 18, 38, 60, and 89%, respectively. Glucosamine had no effect on cellular arginine, NADPH or tetrahydrobiopterin concentrations, but dose-dependently suppressed iNOS protein expression. Similar decreases in iNOS protein occurred in spleen, lung, and peritoneal macrophages of glucosamine-treated rats. These studies demonstrate that glucosamine is a novel inhibitor of inducible NO synthesis via inhibition of iNOS protein expression, and provide a biochemical basis for the use of glucosamine in treating chronic inflammatory diseases such as arthritis.

Modulation of tumor angiogenesis by stem cell factor.

Mast cells accumulate within solid tumors and can release many angiogenic factors, suggesting that they may modulate vascularization of tumors. Stem cell factor (SCF) stimulates mast cell migration, proliferation, and degranulation and therefore may influence mast cell behavior within tumors. We investigated the contribution of SCF to tumor angiogenesis by manipulating its level in mammary tumors. Sense or antisense cDNA fragments of rat SCF were ligated into an episomal expression vector. Ethylnitrosourea-induced rat mammary tumor cell lines were transfected with vector containing either control (no insert, C-P), sense (S-P), or antisense (AS-P) SCF DNA. The functional nature of the transfectants was confirmed by measuring SCF in cell lysates and conditioned media. Immunohistochemical analysis of the tumors induced in Berlin-Druckrey rats by these transfected cells demonstrated that mast cell number and microvascular density were significantly higher in S-P tumors and significantly lower in AS-P tumors, compared with C-P tumors. The expression of von Willebrand factor, an endothelial cell marker, showed a similar pattern. AS-P tumors were significantly smaller than either C-P or S-P tumors. These data suggest that SCF modulates tumor growth and angiogenesis via the involvement of mast cells.

Characterization of the binding site for a novel class of noncompetitive alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonists.

The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor is an ionotropic glutamate receptor that mediates fast excitatory synaptic transmission throughout the central nervous system. In addition to the glutamate binding site, allosteric modulatory sites on the receptor are inferred from the ability of synthetic compounds to affect channel function without interaction with the glutamate binding site. We have identified a novel class of potent, noncompetitive AMPA receptor antagonists typified by CP-465, 022 and CP-526,427. The latter compound was radiolabeled and used to elucidate the pharmacology of one allosteric modulatory site. [(3)H]CP-526,427 labels a single binding site in rat forebrain membranes with a K(d) value of 3.3 nM and a B(max) of 7.0 pmol/mg of protein. The [(3)H]CP-526,427 binding site does not seem to interact directly with the glutamate binding site but overlaps with that for another class of AMPA receptor antagonists, the 2,3-benzodiazepines. This binding site is distinct from that for the antagonist Evans blue and for several classes of compounds that modulate AMPA receptor desensitization. These results indicate the existence of at least two physically distinct allosteric sites on the AMPA receptor through which channel activity or desensitization is modulated.

Expression of mucosal homing receptor alpha4beta7 is associated with enhanced migration to the Chlamydia-infected murine genital mucosa in vivo.

The CD4 T helper cell type 1 (Th1) response is essential for the resolution of chlamydial genital infection in mice. However, not all Th1 clones are equally protective in eradicating the infection. Since oral immunization regimens produce protective immunity, we evaluated the role of the mucosa-associated homing receptor, alpha4beta7, in trafficking to the genital mucosa. Using a panel of CD4, Th1 cell lines and clones, we compared the lymphocyte homing patterns of a Chlamydia-specific, protective clone (P-MoPn), a nonprotective clone (N-MoPn), and a keyhole limpet hemocyanin (KLH)-specific cell line (KLH-1). T cells were labeled with the fluorescent dye PKH-26, adoptively transferred into Chlamydia-infected mice, and monitored at different time points throughout the course of a genital infection. We found that clones P-MoPn and N-MoPn migrated to similar extents to the genital tract and in significantly greater numbers than the KLH-specific T-cell line. Both clones and the KLH-1 line expressed similar levels of the adhesion molecules alpha4, beta1, CD44, and CD11a. However, clones P-MoPn and N-MoPn expressed higher levels of the mucosal homing receptor, alpha4beta7. Also, clones P-MoPn and N-MoPn but not the KLH-1 line migrated to the mesenteric lymph node, suggesting a mucosal recirculation pattern. Moreover, blocking alpha4beta7 adhesion interaction in vivo significantly reduced the recruitment of P-MoPn but not KLH-1 to the genital tract. These findings show that the mucosal homing receptor alpha4beta7 is utilized by a subset of CD4 cells during migration to the Chlamydia-infected genital tract.

Characterization of lymphocyte response in the female genital tract during ascending Chlamydial genital infection in the guinea pig model.

It is well known that pathology caused by chlamydial infection is associated closely with the host response to the organism and that both innate and adaptive host responses contribute to tissue damage. While it is likely that the organism itself initiates the acute inflammatory response by eliciting cytokine and chemokine production from the host cell, the adaptive response is the result of activation of the cell-mediated immune response. While there are several studies describing the nature of the pathologic response in primate, guinea pig, and murine models, there is less information on the kinetics of the CD4 and CD8 response following primary and challenge infections. In this study, we have quantified by flow cytometry the mononuclear cell response to genital infection with the agent of guinea pig inclusion conjunctivitis in the cervix, endometrium, and oviducts at various times following a primary intravaginal infection and after a challenge infection. Tissues from individual animals were assessed for cells expressing CD4, CD8, or Mac-1 and for B cells. Peak responses of each subset occurred 10 to 14 days after a primary infection. The number of Mac-1-expressing cells in each tissue site was found to be dependent on the size of the inoculating dose of chlamydiae. The responses of each cell type were generally stronger in the cervix than in the upper genital tract. In contrast to the murine model but consistent with the primate models, there were equal numbers of CD4 and CD8 cells present in the infiltrates. Twenty-one days after challenge infection, which was performed 50 days after the primary infection, there was a significant increase in the number of CD4, CD8, and B cells in the oviduct compared to the number of these cells at the same time after a primary infection, providing clear cellular evidence for a cell-mediated immune pathologic response.

Collodion baby: a case report.

A case report of a collodion baby born in a community hospital who was diagnosed, stabilized, and transferred for dermatologic management is presented. Differential diagnosis based on cornification disorder phenotypes is outlined. The initial stabilization, management, and nursing considerations of the infant with impaired barrier function of the skin are outlined.