Expression of hematopoietic progenitor cell associated antigen CD34 in chronic myeloid leukemia.

The expression of progenitor cell associated antigen CD34 was investigated in cells from 28 patients with chronic myeloid leukemia (CML). The CD34 positivity varied from 0-26% in patients with chronic phases CML (n = 17); from 6-64% in patients with accelerated phase CML (n = 4); and from 27-97% in the patients with blastic crisis of CML (n = 8). The difference in CD34 positivity between chronic (mean 10.1 +/- 2.3%), accelerated (37.7 +/- 13.3%) and blastic (58.0 +/- 7.3%) phases of CML is statistically significant (p less than 0.05), however, the number of patients studied, especially in accelerated and blastic phases is very small. There was no difference in the CD34 positivity of the cells in the peripheral blood and in the bone marrow. CD34 positivity was higher in patients with chronic phase CML at diagnosis (untreated patients) than in those who were studied during treatment. The possible importance of serially studying CD34 positivity in patients with CML is discussed in the paper.     

Primary pulmonary non-Hodgkin's lymphoma: a report of four cases

Four cases of primary non-Hodgkin's lymphoma of the lung are described. Two cases had low and two intermediate grade lymphoma at the time of diagnosis. The patient who had disease for long duration and received pulmonary radiotherapy developed intractable chest infection and died six months after diagnosis; the three patients having short history of disease and treated with surgery and/or chemotherapy have been doing well for 4 to 77 months after the diagnosis. It is concluded that diagnosis of primary pulmonary lymphoma should be suspected in patients with nodular or interstitial lung disease and bronchoalveolar lavage with aspiration cytology should be done to make an early diagnosis.     

A STUDY OF NEUROKININS AND OTHER OEDEMA-INDUCING MEDIATORS AND MECHANISMS IN THERMAL INJURY

1. Mechanisms involved in the plasma extravasation observed following thermal injury of rat dorsal skin were investigated. 2. Heat applied to the dorsal skin of anaesthetized rats by a temperature-controlled skin heater (1 cm diameter) for 5 min induced temperature-dependent plasma protein extravasation a. 48–48.5°C, measured for up to 4 h following initiation of heat. 3. A tachykini. NK₁ receptor antagonist (SR140333), a bradykinin B₂ receptor antagonist (HOE 140) and a cyclooxygenase inhibitor (indomethacin), when given as cotreatments prior to the selected measurement period, markedly suppressed oedema formation observed over 0–1 h (P < 0.05) but not that observed over 3–4 h after injury. 4. These results indicate that although neurokinins, bradykinin and cyclo-oxygenase products may be important for the early response to thermal injury, they do not appear to play an important role in the ongoing oedem. response. 5. Neutrophils accumulate at the inflammatory site by 4h after thermal injury. Therefore, the effect of depletion of circulating neutrophils by a rat anti-neutrophil antiserum on oedema formation over the 0–4 h period was investigated. The results show that oedema formation was similar in control and antineutrophil-treated rats. 6. In conclusion, the data from the present study indicate that neuropeptides as well as other vasoactive mediators play a role in the acute plasma extravasation observed after thermal injury, but not in the ongoing inflammatory injury. Neutrophils, despite their presence at sites of thermal injury, do not appear to be involved in mediating the oedema formation observed up to 4 h after thermal injury.     

肠脂垂炎:急腹症的鉴别诊断

肠脂垂为沿结肠带两侧分布的许多小突起,长度0.5-5.0cm,     

Tight glycemic control in the ICU - is the earth flat?

Tight glycemic control in the ICU has been shown to reduce mortality in some but not all prospective randomized control trials. Confounding the interpretation of these studies are differences in how the control was achieved and underlying incidence of hypoglycemia, which can be expected to be affected by the introduction of continuous glucose monitoring (CGM). In this issue of Critical Care, a consensus panel provides a list of the research priorities they believe are needed for CGM to become routine practice in the ICU. We reflect on these recommendations and consider the implications for using CGM today.Continuous glucose control in the ICU: report of a 2013 Round Table meeting, published in this issue of Critical Care[1], summarizes the discussion and recommendations of a round table meeting on the management of blood glucose levels in the ICU. The self-selected panel of authors recommends eight areas where it believes research is needed, beginning with head-to-head comparisons of different continuous glucose monitoring (CGM) devices and ending with randomized controlled studies validating closed-loop insulin delivery.Appropriately, the recommendations focus on what is needed to advance CGM into the ICU and do not address whether tight glycemic control is beneficial or what the appropriate target range should be. Nonetheless, the answers to these questions will impact the importance of the recommendations. Of the prospective randomized controlled studies performed to date, many have failed to show a clinical benefit to tight glycemic control (TGC) - including our own study in children less than 3 years of age following cardiac surgery [2]. Our current study assessing the possible benefit of TGC in hyperglycemic critically ill children with cardiovascular and/or respiratory failure ({"type":"clinical-trial","attrs":{"text":"NCT01565941","term_id":"NCT01565941"}}NCT01565941) seeks to answer the question whether control in the target range 80 to 110 mg/dL results in better outcomes than control in the 150 to 180 mg/dL target range. Clearly, if the 80 to 110 mg/dL range proves beneficial, the need to introduce CGM into the ICU will be paramount as this target range is difficult to achieve without increasing the incidence of hypoglycemia. This may be less important if the 150 to 180 mg/dL range is shown to be equally effective. It is possible that TGC with CGM will reduce glucose variability irrespective of the target range, and the panel’s recommendations appropriately call for study of the effect of different treatment algorithms on this metric. However, it should be noted that the evidence the authors cite supporting the importance of glycemic variability [3] is based on retrospective analysis, which cannot be used to infer causality.Still, the question remains as to how best to manage glucose levels in critically ill patients today. Putting aside whether control in a low target range is better than in a higher range, or whether a reduction in glucose variability per se improves clinical outcomes, there are low and high glucose levels that would be treated today in virtually every ICU. Every effort needs to be made to avoid these ends of the spectrum. To this end, one might ask whether CGM devices should be used in the ICU now. One can correctly infer from the recommendations that there have been no head-to-head comparisons of different CGM devices, and that the trends reported have also not been validated. Likewise, investigators who have established insulin protocols at their institutions might ask whether the protocols need to be re-evaluated given the marked differences in insulin recommendations noted by Wilson and colleagues [4] in work highlighted by the consensus panel. Our own review of TGC protocols concurs with that of Wilson and colleagues [4] in that we also noted substantive differences among the existing protocols [5]; however, we concluded that virtually all the protocols could be expected to achieve and maintain their desired target glucose ranges and each could be reasonably expected to benefit from the use of CGM devices.