Reference interval establishment of full blood count extended research parameters in the multi-ethnic population of Malaysia.

Haematological cellular structures may be elucidated using automated full blood count (FBC) analysers such as Unicel DxH 800 via cell population data (CPD) analysis. The CPD values are generated by calculating volume, conductivity, and five types of scatter angles of individual cells which would form clusters or populations. This study considered 126 CPD parameter values of 1077 healthy Malaysian adults to develop reference intervals for each CPD parameter. The utility of the CPD reference interval established may range from understanding the normal haematological cellular structures to analysis of distinct cellular features related to the development of haematological disorders and malignancies.

[Analysis of silica dust detection results in workplace air of somewhere in enterprise].

Objective: To understand the occupational hazard and distribution of silica dust (free SiO(2)≥10%) in the workplace environment of the enterprises in Fengxian District, and to provide scientific basis for improving the working environment and protecting the physical and mental health of the workers. Methods: Individual sampling monitoring and on-site labor hygiene investigation were conducted on 421 workers involved in 87 silicon dust enterprises in the jurisdiction from 2014 to 2018, and measured concentration-time weighted average (C(TWA)) . Results: The results showed that the range of the C(TWA) was (0.021~17.000) mg/m(3), the median was 1.600 mg/m(3), and the qualified rate of 30.88%. The difference of total dust concentration was statistically significant in different years (Z=38.831, P<0.05) . The qualified rate of small-scale enterprises is higher than that of medium-scale enterprises (χ(2)=9.472, P<0.05) . The qualified rate of other domestic enterprises is higher than that of private enterprises and foreign enterprises (χ(2)=10.089, P<0.05) . The acceptance rate of metal products manufacturing is lower than that of general equipment manufacturing and other manufacturing enterprises (χ(2)=64.626, P<0.05) . The qualification rate of natural ventilation is higher than that of mechanical ventilation (χ(2)=6.278, P<0.05) . Conclusion: The enterprises involved in silicon production in Fengxian District need to further strengthen the production process reform and improve the ventilation and dust removal protection measures. Widely carry out the publicity of occupational disease prevention and control law, conduct targeted pre-job training, improve workers' awareness of self-protection, and protect the occupational health of workers in many ways.

Biological aerated filter treated textile washing wastewater for reuse after ozonation pre-treatment.

The combination of chemical and biological treatment processes is a promising technique to reduce refractory organics from wastewater. Ozonation can achieve high color removal, enhance biodegradability, and reduce the chemical oxygen demand (COD). The biological technique can further decrease COD of wastewater after ozonation as a pre-treatment. In this study the ozonizing-biological aerated filter processes were used to treat textile washing wastewater for reuse after conventional treatment. The result showed that when the influent qualities were COD about 80 mg/L, color 16 degree and turbidity about 8 NTU, using the combination processes with the dosages of ozone at 30-45 mg/L with the hydraulic retention time (HRT) of biological aerated filter (BAF) at 3-4 hours respectively, gave effluent qualities of COD less than 30 mg/L, color 2 degree and turbidity less than 1NTU. The cost of treatment was less than one yuan/t wastewater, and these processes could enable high quality washing water reuse in textile industry.

Lactate/glucose dynamics after rat fluid percussion brain injury.

Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Clinical studies have demonstrated a decline in extracellular fluid (ECF) glucose and an increase in lactate after TBI. In vitro studies suggest that this increase in lactate is mediated by increased glutamate and may provide a metabolic substrate for neurons, to aid in ionic restoration. This led us to hypothesize that high ECF lactate may be beneficial in recovery following TBI, where major ionic flux has been shown to occur. In this study, we measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before and after rat lateral fluid percussion brain injury (FPI; 2.06 +/- 0.13 atm) with and without IV lactate infusion (100 mM X 0.65 mL/h X 5 h) to test the hypothesis that arterial lactate can influence ECF lactate. Dialysate lactate increased within 10 min following FPI, with higher values in the lactate infusion group. Following FPI, the dialysate lactate increase was 238% with lactate infusion versus 171% increase with saline infusion. Dialysate glucose fell immediately following FPI, with a more severe decline in the saline group. The glucose decrease was 231% greater in the IV saline group. Furthermore, in the lactate infusion group, the dialysate glucose levels recovered to baseline levels by 4 h after injury, whereas they remained depressed through out the experiment, in the saline infusion group. We conclude that arterial lactate augmentation can increase brain dialysate lactate, and result in more rapid recovery of dialysate glucose after FPI. This may indicate a beneficial role for lactate, that may be potentially useful in the clinical situation, after TBI.

Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo.

The hypothesis has been advanced that the adrenal steroids dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) exert antiatherogenic and cardioprotective actions. Platelet activation has also been implicated in atherogenesis. To determine if DHEA and DHEAS affect platelet activation, the effects of these steroids on platelet aggregation were assessed both in vitro and in vivo. When DHEAS was added to pooled platelet-rich plasma before the addition of the agonist arachidonate, either the rate of platelet aggregation was slowed or aggregation was completely inhibited. Inhibition of platelet aggregation by DHEA was both dose- and time-dependent. Inhibition of platelet aggregation by DHEA was accompanied by reduced platelet thromboxane B2 (TxB2) production. Inhibition of platelet aggregation by DHEA was also demonstrated in vivo. In a randomized, double-blind trial, 10 normal men received either DHEA 300 mg (n = 5) or placebo capsule (n = 5) orally three times daily for 14 days. In one man in the DHEA group arachidonate-stimulated platelet aggregation was inhibited completely during DHEA administration, whereas in three other men in the DHEA group the rate of platelet aggregation was prolonged, and the sensitivity and responsiveness to agonist were reduced. None of the men in the placebo group manifested any change in platelet activity. These findings suggest that DHEA retards platelet aggregation in humans. Inhibition of platelet activity by DHEA may contribute to the putative antiatherogenic and cardioprotective effects of DHEA.

Brain lactate uptake increases at the site of impact after traumatic brain injury.

Although glucose is the main carbohydrate energy substrate for the normal brain, several studies published over the last 10 years now challenge this assumption. The activated brain increases its metabolism to meet increased energy demands by glycolysis after injury. In vitro studies now show that lactate alone can serve as an energy source to maintain synaptic function. In this study, we used 14C-lactate to test the hypothesis that blood lactate is acutely taken up by the injured brain, after fluid percussion injury (FPI) in the rat. 50 microCi radioactive lactate was injected i.v. immediately after FPI, in injured and sham rats. After 30 min, the brain was removed, frozen, and cut into 20 microm sections for autoradiography. Uptake of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain also took up the 14C-label. This increased concentration of radioactive lactate at the injury site suggests that the injured brain may use the lactate as an energy source.

Evidence for lactate uptake after rat fluid percussion brain injury.

UNLABELLED: Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. RESULTS: Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.

Etiological role of Alternaria alternata in human esophageal cancer.

In this paper, the mutagenicity and carcinogenicity of alternariol monomethyl ether (AME), alternariol (AOH), and their relevance to the etiology of human esophageal cancer were studied. These mycotoxins were produced by Alternaria alternata which was the main contaminating fungi isolated from the grain in Linxian County, an area with high incidence of esophageal cancer. This study demonstrated that: 1. AME and AOH might cause cell mutagenicity and transformation; 2. AME and AOH could combine with the DNA isolated from human fetal esophageal epithelium, activate the oncogens, c-H-ras and c-mys in it, and promote proliferation of human fetal esophageal epithelium in vitro; 3. squamous cell carcinoma of the fetal esophagus could be induced by AOH. According to the results of the studies of AME and AOH mentioned above, we consider that Alternaria alternata plays an important role in the etiology of human esophageal cancer.

The ischemia-selective KATP channel antagonist, 5-hydroxydecanoate, blocks ischemic preconditioning in the rat heart.

Although the KATP channel has been demonstrated to be involved in ischemic preconditioning (IPC) in most species, controversy still exists as to the role of this channel as a mediator of PC in the rat heart. Previously, the authors' laboratories have shown that glibenclamide blocks IPC in the intact rat heart, in a time-dependent manner; however, since glibenclamide has been shown to have non-selective effects unrelated to KATP channel blockade, a structurally dissimilar and ischemia-selective KATP channel blocker, 5-hydroxydecanoate (5-HD), was used to further elucidate the role of KATP channels in mediating IPC in the rat heart. Anesthetized, open-chested Sprague-Dawley rats were subjected to one of four protocols. In Group I, control (C), rats were subjected to 30 min of left coronary artery occlusion and 90 min of reperfusion. In Group II, IPC was elicited by 1 x 5 min occlusion followed by 10 min of reperfusion, prior to the 30 min occlusion and 90 min reperfusion periods, 5-HD (5 mg/kg, i.v.) was given 15 min prior to the 30 min occlusion period in non-preconditioned animals, or given 15 min prior to IPC (5-HD+IPC) (Groups III and IV, respectively). Infarct size (IS), as a percentage of the area at risk (AAR), was determined by triphenyltetrazolium staining. Ischemic preconditioning produced a marked reduction in infarct size (47.5 +/- 3.8% to 7.9 +/- 1.9%, *P < 0.01), which was completely abolished by 5-HD (50.5 +/- 2.6%). These data further suggest that the opening of KATP channels is an important component of IPC in the intact rat heart, similar to that observed in other species.

KATP channels in rat heart: blockade of ischemic and acetylcholine-mediated preconditioning by glibenclamide.

The objective of this study was to examine if the opening of ATP-sensitive K+ (KATP) channels play an important role in ischemic preconditioning (PC) in the rat heart. A second goal was to test the role of acetylcholine (ACh) in mimicking PC and test if it could be blocked by KATP antagonist. Glibenclamide, a specific antagonist of the KATP channel, was given as two doses of 0.3 mg/kg each at 60 and 30 min before PC. Six groups of rats were subjected to ischemia and reperfusion (I/R) using these protocols: 1) control (I/R), 30-min ischemia followed by 90-min reperfusion (n = 6 rats); 2) preconditioned hearts given 5-min ischemia 10 min before I/R (n = 9 rats); 3) glibenclamide (0.3 mg/kg) treatment 60 and 30 min before PC (n = 13 rats); 4) glibenclamide treatment before I/R (n = 15 rats); 5) ACh infusion for 5 min (18 micrograms/ml) at a rate of 0.15 ml/min followed by equilibration for 10 min before I/R, n = 13 rats; and 6) glibenclamide treatment before ACh infusion followed by I/R (n = 11 rats). Preconditioning reduced the infarcted area (expressed as percent area at risk) from 42.0 +/- 4.4% in control to 8.7 +/- 6% (mean +/- SE, P < 0.05). Glibenclamide blocked the protection conferred by PC (39.1 +/- 4.5%, P < 0.05) without having a significant effect on control nonpreconditioned hearts. ACh infusion in lieu of PC also reduced infarct size to 25.0 +/- 5.63% (P < 0.05 compared with control), which was again blocked by glibenclamide (44.2 +/- 5.0%, P < 0.05). The data suggest that opening of KATP channels for ischemic and ACh-mediated preconditioning is also important in the rat heart.

Induction of 72-kDa heat shock protein does not produce second window of ischemic preconditioning in rat heart.

Ischemic preconditioning (PC) induces delayed phase of protection, known as the second window of protection (SWOP). We investigated this phenomenon in rat and correlated it with the expression of 72-kDa heat shock protein (HSP 72). Rats were preconditioned with 1, 2, and 3 cycles of 5-min left anterior descending artery occlusions, each separated by a 10-min reperfusion (PC x 1, PC x 2 and PC x 3, respectively). Another group of rats was preconditioned with heat shock (HS) by raising temperature to 42 degreesC for 15 min. Twenty-four hours later, rats were given sustained ischemia for 30 min and 90 min of reperfusion. Infarct sizes (%risk area) were 40.0 +/- 7.5, 37.6 +/- 5.6, and 47.6 +/- 2.4 (mean +/- SE) for PC x 1, PC x 2, and PC x 3 hearts, respectively, which were not different from the sham (49.9 +/- 3.9, P > 0.05). In contrast, infarct size was reduced from 47.5 +/- 3.8% in sham to 4.7 +/- 2.3% (P < 0.01) 24 h after HS. Additionally, early PC significantly reduced infarct size from 47.5 +/- 3.8% in controls to 6.0 +/- 1.2 and 5.0 +/- 1.1% with PC x 1 and PC x 3. Repeated PC cycles induced over a threefold increase in HSP 70 mRNA after 2 h compared with sham (P < 0.05). HSP 72, which increased 24 h after PC or HS, was not significantly different between the two PC stimuli. We conclude that PC does not induce SWOP in rat heart despite enhanced expression of HSP 72. In contrast, HS-induced delayed protection was associated with enhanced accumulation of HSP 72. It is possible that SWOP and HS have distinct mechanisms of protection that may not be exclusively related to HSP 72 expression.

Pharmacologic preconditioning with monophosphoryl lipid A is abolished by 5-hydroxydecanoate, a specific inhibitor of the K(ATP) channel.

We sought to determine the role of opening of adenosine triphosphate (ATP)-sensitive potassium channel (K(ATP) channel) in monophosphoryl lipid A (MLA)-induced myocardial protection after ischemia/reperfusion (I/R) in rabbit. We used 5-hydroxydecanoate (5-HD), an ischemia-selective inhibitor of K(ATP) channel, to block MLA-stimulated cardiac protection. Four groups of rabbits were studied: group I, MLA-vehicle; group II, MLA; group III, MLA + 5-HD; and group IV, 5-HD only. MLA (35 microg/kg, i.v.) or vehicle were given 24 h before I/R. 5-HD (5 mg/kg) was given 15 min before ischemia. All rabbits underwent 30-min coronary occlusion, followed by 3-h reperfusion. Area at risk was delineated by injection of Evan's blue, and infarct size was determined by tetrazolium staining. Pretreatment with MLA reduced infarct size (percentage of area at risk) from 40+/-8.6% to 15.1+/-1.5%. The infarct size increased to 51.9+/-5.8% with 5-HD in MLA-treated rabbits. 5-HD did not alter infarct size significantly when given in vehicle-treated control rabbits. These data suggest that MLA exerts its protective effect through activation of K(ATP) channel.

Dissociation of heat shock proteins expression with ischemic tolerance by whole body hyperthermia in rat heart.

Heat shock (HS) results in the expression of heat shock proteins (hsp) and confers tolerance against subsequent ischemic injury. We examined the extent of myocardial protection in vivo, and determined the level of hsp expression induced by HS as a function of time. Anesthetized rats were subjected to HS by raising core temperature to 42 degrees C for 15 min and they were then allowed to recover from 2 to 30 h (n = 8-11 for each time point). At the appropriate time, animals were subjected to 30 min of ischemia via ligation of the LAD, followed by 90 min of reperfusion. Infarct size was determined by tetrazolium staining and hsp expression was assessed by Western blots. Following ischemia/reperfusion, the infarct sizes (% risk area) were 51.3 +/- 3.7, 41.0 +/- 7.7, 48.0 +/- 6.9 after 2, 4 and 12 h of HS, which were not significantly different from 39.2 +/- 2.75 in non heat-shocked animals (P > 0.05). In contrast, the infarct size was reduced significantly to 11.0 +/- 3.1% in 24 h HS group (P < 0.01 v non-heat-shocked control, 2, 4 and 12 h HS groups), but increased back to 40.0 +/- 3.2% (P < 0.01) by 30 h after HS. No major significant differences in the mean arterial blood pressure, heart rate or rate pressure product was observed between different groups. The synthesis of 72- and 27-kD hsp in HS groups was rapid, reaching > 80% of maximum within 4 h of initial insult and peaked by 12 h, whereas the protective effect of HS was absent at these time points. We conclude that ischemic tolerance afforded by HS cannot be solely explained on the basis of hsp expression, and may be dependent on factors such as post-translational modifications, translocation of hsps or some other as yet unidentified factors.

Role of protein kinase C and 72 kDa heat shock protein in ischemic tolerance following heat stress in the rat heart.

Heat stress (HS) and the subsequent expression of 72 kDa heat shock protein (HSP 72) has been shown to enhance post-ischemic functional recovery and reduce infarct size. Because the synthesis of heat shock proteins involves activation of heat shock transcription factors through phosphorylation, we hypothesized that inhibition of protein kinase C (PKC) would block HS mediated protection and expression of HSP 72 in the heart. Five groups of rats were studied (1) Sham anesthetized, (2) HS group--animals were heat shocked by raising the whole body core temperature to 42 degrees C for 15 min, (3) Vehicle group--HS rats treated with 50% DMSO in saline, (4) PKC inhibitor-treated group--specific PKC antagonist, chelerythrine chloride (5 mg/kg, i.p) given 30 min prior to HS and (5) Vehicle treated control--non-HS rats treated with vehicle prior to ischemia/reperfusion. Hearts were subjected to 30 min of regional ischemia and 90 min of reperfusion 24 h after HS. Risk area was delineated by injection of 10% Evan's blue and infarct size determined using computer morphometry of tetrazolium stained sections. Infarct size (% area at risk) reduced significantly from 49.4 +/- 2.3% (n = 7) in sham to 10.0 +/- 2.5% (p < 0.01) and 9.1 +/- 3.0% in HS and vehicle treated HS groups respectively (p < 0.05) Treatment with chelerythrine prior to HS increased infarct size to 49.4 +/- 2.3% (p < 0.05). Infarct size in chelerythrine-treated non-HS ischemic/reperfused heart was 40.7 +/- 5.4%, which did not differ significantly from vehicle-treated sham group. Western blot analysis demonstrated marked increase in HSP 72 in HS groups (with or without vehicle treatment) and pretreatment with chelerythrine chloride failed to inhibit the expression of HSP 72. The results suggest that HS-induced ischemic tolerance is mediated via PKC pathway and this protection does not appear to be directly related to the expression of HSP 72 in rat heart.

ATP-sensitive potassium channel mediates delayed ischemic protection by heat stress in rabbit heart.

Heat shock protects against myocardial ischemia-reperfusion injury possibly via increased expression of heat shock proteins. The direct evidence of heat shock protein protection in vivo remains circumstantial, and no other new mechanism of protection has been proposed. Recent studies suggest that opening of ATP-sensitive K+ channels (KATP channels) plays an important role in ischemic preconditioning; however, it is not known whether this channel is also important in delayed protection conferred by heat shock. Anesthetized rabbits underwent heat shock treatment by raising core temperature to 42 degrees C for 15 min. Twenty-four hours later, the animals were reanesthetized and subjected to regional ischemia-reperfusion. The specific KATP channel blockers glibenclamide (0.3 mg/kg i.p.) and sodium 5-hydroxydecanoate (5HD; 5 mg/kg i.v.) were used to block the channel function. The drugs were administered at two different times, either pre-heat stress or preischemia. Infarct size was determined by triphenyltetrazolium chloride staining. The 72-kDa heat shock protein (HSP 72) was measured by Western blots. Our results show that heat shock produced a marked reduction in infarct size (39.4 +/- 8.1 to 14.3 +/- 2.5% of risk area, P < 0.05). Glibenclamide and 5HD completely abolished heat shock-induced reduction in infarct size (42.3 +/- 0.32 and 33.7 +/- 4.8%) when given before ischemia-reperfusion; however, these antagonists failed to block protection when administered before the onset of heat shock. Furthermore, the enhanced expression of HSP 72 in heat shock groups was not diminished by glibenclamide or 5HD, suggesting a lack of a direct role of this protein in conferring cardiac protection by heat shock. The complete blockade of cardiac protection by glibenclamide and 5HD strongly suggests that opening of this channel is a very important component of heat shock-induced ischemic protection in rabbit hearts.

Delayed preconditioning of cultured adult rat cardiac myocytes: role of 70- and 90-kDa heat stress proteins.

We investigated the protective effect of heat stress and metabolic preconditioning in cultured adult rat cardiac myocytes and correlated this effect with induction of heat shock proteins (HSP). Myocytes were preconditioned with sublethal heat shock or metabolic preconditioning for 30 min. Twenty hours later, preconditioned myocytes were subjected to lethal heat shock (46 degrees C for 2 h) or ischemia by incubation in ischemic buffer for 2 h. Cellular injury index was reduced from 69 +/- 4.0% in lethally heat-shocked cells to 27.0 +/- 1.6% with heat shock preconditioning (mean +/- SE; P < 0.01) and 19.0 +/- 3.0% with metabolic preconditioning (P < 0.01). Cellular injury index was 81.0 +/- 1.0% in ischemic myocytes and was reduced to 25.9 +/- 2.7 and 21.4 +/- 2.6% in heat shock- and metabolic-preconditioned myocytes, respectively (P < 0.01). A significant cross-tolerance of myocytes against lethal injury was observed with the two preconditioning methods. Western blot analysis revealed 3.3- and 2.5-fold increases in HSP 90 and 500- and 15-fold increases in HSP 70 with heat shock and metabolic preconditioning, respectively. HSP 27 expression remained unaltered relative to control cells. We conclude that heat shock and metabolic preconditioning induce delayed tolerance against lethal injuries in adult cardiac myocytes with elevated levels of HSP 70 and HSP 90.

Induction of mutagenesis and transformation by the extract of Alternaria alternata isolated from grains in Linxian, China.

Alternaria alternata is commonly found in the grain in areas of high incidence of oesophageal cancer and is a suspected cancer-causing factor in Linxian, China. In this study, this fungus was isolated from corn in Linxian and cultured. The extract of this fungus was shown to induce 6-thioguanine-resistant mutants in V79 cells and cause transformation of NIH/3T3 mouse fibroblast cells. Metabolic activation does not seem to be required for these activities. The mutagenic and transforming activities of the extract of A. alternata suggest that this fungus may be a factor in the etiology of oesophageal cancer in Linxian.