The “Demon Plague” and Access to Care Among Asian Undocumented Immigrants Living with HIV Disease in New York City

Access to and utilization of care for HIV-positive Asians (A) and Pacific Islanders (PI) have been largely unaddressed despite the rising influx of immigrants from Asia and the Pacific to the United States and the growing HIV prevalence in these regions. This paper describes the cultural attitudes, behaviors, and perceptions that affect access to and utilization of care among Asian undocumented noncitizens living with HIV/AIDS (UNWHA) in New York City. Sixteen semistructured interviews with HIV-positive UNWHAs revealed that their access to care was influenced by community misperceptions of HIV transmission, discriminatory attitudes towards persons living with HIV, competing immigration related stressors, and difficulty navigating service systems. These findings underscore the importance of integrating HIV treatment with primary prevention and awareness of immigration-related stressors to ensure timely access to screening services and care among Asian UNWHAs.     

Toxicity associated with iron overload found in hemochromatosis: possible mechanism in a rat model.

Hemochromatosis is characterized by pathologic iron overload which often leads to various pathological conditions. The mechanism by which excess iron induces these conditions is not clearly understood. Using rats as the model, this investigation was conducted to explore the mechanism of toxicity associated with iron overload. Sprague-Dawley male rats were fed a 3% carbonyl iron-supplemented diet for eight weeks to achieve iron accumulation. Liver iron reached approximately 2 mg/g which is more than 16 times the control values (mean +/- SD, 0.12 +/- 0.02 mg/g, p < 0.001). Serum iron was consistently higher in the experimental rats (mg/L): 3.41 +/- 0.58 versus 1.89 +/- 0.18, p < 0.001. The high levels of iron accompanied enhanced oxidative damage in the hepatic nuclear DNA when 8-hydroxy-2'-deoxyguanosine (8-OHdG) was measured as a product of DNA oxidation. The levels of 8-OHdG in the experimental samples were significantly higher than the controls (8-OHdG X 10(-5)/dG): 4.22 +/- 1.82 versus 1.84 +/- 0.33, p < 0.05. The results of serum enzyme assays suggest that iron overload caused mild hepatocellular damage: alanine transaminase significantly increased; lactate dehydrogenase did not change; alkaline phosphatase decreased. Since the accumulation of 8-OHdG in the nuclear DNA is highly deleterious to cells, these data suggest oxidative damage in the nuclear DNA may be a critical factor in inducing diseases associated with iron overload.     

肠外营养对呼吸功能不全患者的影响

从加强医疗病房的重危患餐巾选取因呼吸衰竭而给予呼吸机支持的患者40例,随机分为A组20例进行肠外营养(parenteral nutrition,PN)治疗,B组20例未行PN治疗。对通气/换气功能各指标进行分析,结果两组患者的呼吸频率、pH、PaO_2、PaCO_2及HCO_3~-无明显差异;A组氧分压与吸入气氧浓度比值轻度降低,而肺泡-动脉氧压差及肺内分流明显升高。提示PN中的脂肪乳和高糖可能是导致呼吸功能改变的重要因素。     

Ⅰ期非小细胞肺癌淋巴结微转移规律的研究

目的探讨几个问题：（1）Ⅰ期非小细胞肺癌淋巴结微转移比率；（2）淋巴结微转移与肿瘤大小、病理类型、细胞分化程度、部位、分型、分期进行Logstic回归分析，确定影响微转移的主要因素；（3）探讨微转移的方式、顺序。方法对91例非小细胞肺癌清扫的肺门和隆突下淋巴结进行MCK（AEI／AE3）免疫组化标志检测微转移的存在。另外收集45例肺部良性病变手术时切除的肺门淋巴结45枚和Ⅱ期、Ⅲ期肺癌常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化（SP法）标志，分别作为阴性和阳性对照。结果45例肺部良性病变手术时切除的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阴性；Ⅱ期和Ⅲ期常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阳性。91例Ⅰ期非小细胞肺癌总的微转移率为49％（45／91）。结论Ⅰ期非小细胞肺癌淋巴结中存在微转移；Ⅰb期非小细胞肺癌微转移率明显高于Ⅰa期；有必要对Ⅰb期非小细胞肺癌进行术后化疗；肿瘤分期和分化程度是影响淋巴结微转移的主要因素；淋巴结微转移遵循肺门到纵隔的途径；腺癌存在跳跃式微转移。     

Poxvirus-based vaccine therapy for patients with advanced pancreatic cancer

Purpose  

An open-label Phase 1 study of recombinant prime-boost poxviruses targeting CEA and MUC-1 in patients with advanced pancreatic cancer was conducted to determine safety, tolerability and obtain preliminary data on immune response and survival.     

荆芥连翘汤对促进皮肤溃疡愈合的影响

目的 观察荆芥连翘汤对小鼠皮肤溃疡的治疗作用。方法 建立小鼠皮肤创伤和烫伤两种皮肤溃疡模型．比较荆芥连翘汤以及rhEGF的用药组和自身对照组小鼠皮肤溃疡面积，用昆微镜观察溃疡面炎症细胞浸润情况。结果 和自身对照组相比，荆芥连翘汤可明显缩小小鼠皮肤溃疡面积（P〈0．001），同时炎症细胞浸润显著减少（P〈0．001）；荆芥连翘汤用药组疗效显著优于rhEGF用药组。结论 荆芥连翘汤可明显促进小鼠皮肤溃疡的愈合。     

The effects of plantago-mucilage A from the seeds ofPlantago asiatica on the immune responses in ICR mice

Effects of plantago-mucilage A (P-MA) on the immune responses were studied in ICR mice. Mice were divided into 4 groups (10 mice/group), and P-MA at doses of 7, 21 and 63 mg/kg were orally administered to mice once a day for 21 consecutive days. Mice were immunized and challenged with sheep red blood cells (SRBC). P-MA at 63 mg/kg/day significantly increased the body weight gain and the relative weights of spleen and thymus, as compared with those in controls. However, there were no significant effects on liver weight due to P-MA treatment. Plaque forming cells (PFC) and hemagglutination (HA) titers to SRBC were significantly enhanced in mice dosed at 21 and 63 mg/kg/day P-MA, as compared with those in controls. Delayed-type hypersensitivity (DTH) reaction to SRBC, phagocyte activity and circulating leukocyte were also significantly increased in mice dosed at 63 mg/kg/day P-MA. These results demonstrate that P-MA markedly enhances both humoral immune and allergic reaction to SRBC at concentrations which don’t act on the relative weight of liver.     

Simple measurement of spinal cord evoked potential: a valuable data source in the rat spinal cord injury model.

Measurement of spinal cord evoked potentials (SCEPs) is proposed as a means of predicting locomotion outcome in the rat spinal cord injury (SCI) model. Using 55 rats, three reproducible peak waves (waves I, II and III) were observed during stimulation at the C7 level with recording at the L1 epidural space. Hemisection at the T13 level showed three wave loss patterns: wave III loss only, loss of both wave II and III, and loss of all three waves. Defining an ideal SCI model as establishment of stable monoparesis or paraparesis, all animals in the wave II-III loss group showed favorable results. Histological data and electrophysiological properties allowed reasonable assumptions of wave origin: wave I from extrapyramidal tracts, wave II from the ventral corticospinal tract, and wave III from the dorsal corticospinal tract. Complete destruction of pyramidal tracts in both dorsal and ventral fibers was essential for long-term impairment of locomotion.     

A phenytoin-sensitive cationic current participates in generating the afterdepolarization and burst afterdischarge in rat neocortical pyramidal cells

We report here on the ionic mechanisms underlying the depolarizing afterpotential (DAP) in neocortical pyramidal cells, with special interest in those underlying the burst afterdischarge. Injections of short depolarizing current pulses under whole-cell current clamp with a CsCl-based internal medium generated, in most pyramidal cells, a single action potential with a plateau phase (plateau-AP), followed by a slowly decaying DAP both in the absence and presence of TTX. Under voltage-clamp, the same cells displayed a slow tail current (tail-I) at the offset of depolarization. When intracellular free Ca²⁺ was chelated with 10 mm BAPTA or when extracellular Ca²⁺ was replaced with equimolar Ba²⁺, neither the slow DAP nor the slow tail-I was observed. Extracellular application of Co²⁺ or Cd²⁺ reduced Ca²⁺ currents and the slow tail-I. Cation substitution experiments revealed that the channel generating the slow tail-I was permeable to K⁺ and Cs⁺ more than to Na⁺ (P_K≈P_Cs > P_Na > P_NMDG≈P_TEA). The cationic slow tail-I was not reduced by applying antagonists of the metabotropic glutamate receptor (MCPG, 1 mm ) and the muscarinic receptor (atropine, 1–10 μm ). Thus, the slow DAP was produced by activation of the cationic channel whose gating is solely dependent on [Ca²⁺]_i. An increase in [K⁺]_o from 3 to 6 or 9 mm enhanced the slow DAP, and resulted in a generation of burst afterdischarges. An anticonvulsant, phenytoin (PT; 1–10 μm ) suppressed the slow DAP while enhancing the plateau-AP in the presence of TTX, most likely by blocking the cationic channel.