Summary (text)
Abstract (text)
Hematopoietic stem cells do not repair the infarcted mouse heart.
Recent reports suggest that hematopoietic stem cells (HSC) can transdifferentiate into cardiomyoctes and contribute to myocardial regeneration after injury. This concept has recently been challenged by studies in which bone-marrow (BM)-derived cells do not acquire a cardiac phenotype after direct injection into ischemic myocardium.
In this study, we analyzed the effect of increased circulating adult BM cells by stimulation with stem cell factor (SCF; 200 microg/kg/d for 7 days) and granulocyte-colony stimulating factor (G-CSF, 50 microg/kg/d for 7 days) or by peripheral delivery of isolated adult BM cells on morphological and hemodynamic parameters of mouse hearts 6 weeks after induction of chronic myocardial infarction (MI). All animals were splenectomized to prevent sequestration of BM cells 2 weeks prior to the induction of MI. Cytokine treatment was initiated either 3 days prior to or 6 h after MI. Isolated, either whole or by magnetic beads lineage-depleted BM cells were injected via a tail vein 6 h after MI.
Left and right ventricular (LV and RV) function revealed no improvement in any treatment group when compared to untreated MI animals at baseline resting conditions as well as after stimulation with norepinephrine (NE; 1, 5, 10, 25, 50, and 100 ng bolus i.v. in 10 microl each) as measured by catherization with ultraminiature 1.4 F tip pressure transducers 6 weeks after MI. Moreover, there was no sign of myocardial regeneration in histological or gene expression analyses.
Mobilization or i.v. injection of BM cells do not have a measurable effect on cardiac regeneration.
[Pubmed - MEDLINE]
Full Text Sources
检索记录[]
丁香园旗下网站用程序模拟键盘和鼠标键盘
在Windows大行其道的今天，windows界面程序受到广大用户的欢迎。对这些程序的操作不外乎两种，键盘输入控制和鼠标输入控制。有时，对于繁杂的，或重复性的操作，我们能否通过编制程序来代替手工输入，而用程序来模拟键盘及鼠标的输入呢？答案是肯定的。这主要是通过两个API函数来实现的。 　　
　　下面以Delphi为例来介绍一下如何实现这两个功能。模拟键盘我们用Keybd_event这个api函数，模拟鼠标按键用mouse_event函数。大家不用担心，在delphi里调用api函数是很方便的事。 　　
　　先介绍一下Keybd_event函数。Keybd_event能触发一个按键事件，也就是说回产生一个WM_KEYDOWN或WM_KEYUP消息。当然也可以用产生这两个消息来模拟按键，但是没有直接用这个函数方便。Keybd_event共有四个参数，第一个为按键的虚拟键值，如回车键为vk_return,　tab键为vk_tab。第二个参数为扫描码，一般不用设置，用0代替就行。第三个参数为选项标志，如果为keydown则置0即可，如果为keyup则设成“KEYEVENTF_KEYUP”，第四个参数一般也是置0即可。用如下代码即可实现模拟按下i键，其中的$49表示i键的虚拟键值： keybd_event($49,0,0,0);
                                                      keybd_event($49,0,KEYEVENTF_KEYUP,0); ... 　　
　　mouse_event最好配合setcursorpos(x,y)函数一起使用，与Keybd_event类似，mouse_event有五个参数，第一个为选项标志，为MOUSEEVENTF_LEFTDOWN时表示左键按下，为MOUSEEVENTF_LEFTUP表示左键松开，向系统发送相应消息。第二三个参数分别表示x,y相对位置，一般可设为0,0,第四五个参数并不重要，一般也可设为0,0。若要得到Keybd_event和mouse_event函数的更详细的用法，可以查阅msdn或delphi帮助。下面是关于mouse_event的示例代码：
　setcursorpos(20,132);
   mouse_event(MOUSEEVENTF_LEFTDOWN,0,0,0,0);
   mouse_event(MOUSEEVENTF_LEFTUP,0,0,0,0);
   mouse_event(MOUSEEVENTF_LEFTDOWN,0,0,0,0);
   mouse_event(MOUSEEVENTF_LEFTUP,0,0,0,0); ...
上面的代码表示鼠标的双击，若要表示单击，用两个mouse_event即可(一次放下，一次松开)。 　
　注意，不管是模拟键盘还是鼠标事件，都要注意还原，即按完键要松开，一个keydown对应一个keyup；鼠标单击　完也要松开， 不然可能影响程序的功能。 　　
　　　好了，希望本文能让你对模拟键盘和鼠标按键有个初步的了解，如果想更深入的了解其中的奥妙，可以查阅详实的msdn在线帮助，并多多动手实践。
解决锁定键盘鼠标的方法
如果你不需要屏蔽Ctrl+Alt+Del组合键,可以使用低级键盘钩子(WH_KEYBOARD_LL)与低级鼠标钩子(WH_MOUSE_LL),这两种消息钩子的好处是不需要放在动态链接库中就可以作全局钩子,将键盘消息与鼠标消息截获.
unit uHookKeyAndM
{ 该单元利用WH_KEYBOARD_LL与WH_MOUSE_LL两种类型的钩子分别截获键盘消息与鼠标消息}
{ 由于这里只是需要将消息屏蔽,故只需对钩子函数的返回结果设为1即可. }
{ 提供两个函数StartHookKeyMouse与StopHookKeyMouse两个函数. }
Windows, Messages, SysU
WH_KEYBOARD_LL =13;
WH_MOUSE_LL =14;
procedure StartHookKeyM
procedure StopHookKeyM
implementation
hhkLowLevelKybd:HHook=0;
hhkLowLevelMouse:HHook=0;
function LowLevelKeyboardProc(nCode:I WParam:WPARAM; LParam:LPARAM):LRESULT;
Result:=1;
if nCode&&0 then Result:=CallNextHookEx(0,nCode,WParam,LParam);
function LowLevelMouseProc(nCode:I WParam:WPARAM; LParam:LPARAM):LRESULT;
Result:=1;
if nCode&&0 then Result:=CallNextHookEx(0,nCode,WParam,LParam);
procedure StartHookKeyM
if hhkLowLevelKybd = 0 then
hhkLowLevelKybd := SetWindowsHookEx(WH_KEYBOARD_LL, LowLevelKeyboardProc, Hinstance, 0);
if hhkLowLevelMouse = 0 then
hhkLowLevelMouse:=SetWindowsHookEx(WH_MOUSE_LL,LowlevelMouseProc,HInstance,0);
procedure StopHookKeyM
if hhkLowLevelKybd && 0 then
UnhookWindowsHookEx(hhkLowLevelKybd);
hhkLowLevelKybd:=0;
if hhkLowLevelMouse && 0 then
UnHookWindowsHookEx(hhkLowLevelMouse);
hhkLowLevelMouse:=0;
initialization
hhkLowLevelKybd:=0;
hhkLowLevelMouse:=0;
finalization
if hhkLowLevelKybd && 0 then UnhookWindowsHookEx(hhkLowLevelKybd);
if hhkLowLevelMouse && 0 then UnhookWindowsHookEx(hhkLowLevelMouse);
来自：conworld, 时间： 16:06:31, ID：2996263
高手终于出现了，谢谢
你的方法确实实现了锁定鼠标，但是我想达到的效果是：
1.锁定键盘
2.鼠标只能在我的程序窗口中操作
来自：smokingroom, 时间： 17:01:12, ID：2996381
要求2(鼠标只能在我的程序窗口中操作)的实现:
修改LowLevelMouseProc过程如下:
PMSLLHOOKSTRUCT=^MSLLHOOKSTRUCT;
MSLLHOOKSTRUCT = record
mouseData:DWORD;
flags:DWORD;
time:DWORD;
dwExtraInfo:DWORD;
MouseRect:TR //这是你需要限制的Mouse活动范围.
function LowLevelMouseProc(nCode:I WParam:WPARAM; LParam:LPARAM):LRESULT;
p:PMSLLHOOKSTRUCT;
Result:=0;
if nCode=HC_ACTION then
p:=PMSLLHOOKSTRUCT(LParam);
if (p.pt.X & MouseRect.Left) or (p.pt.X & MouseRect.Right) or
(p.pt.Y & MouseRect.Top) or (p.pt.Y & MouseRect.Bottom) then
Result:=1;
if nCode&&0 then Result:=CallNextHookEx(0,nCode,WParam,LParam);
附取得MouseRect的代码,假定你的主窗体体为MainFrm
MouseRect:=MainFrm.ClientR
MouseRect.TopLeft:=MainFrm.ClientToScreen(MouseRect.TopLeft);
MouseRect.BottomRight:=MainFrm.ClientToScreen(MouseRect.BottomRight);
另在Result:=1之前加多一个ClipCursor(@MouseRect)效果会更好,可以有效解决当按下Ctrl+Alt+Del后将Mouse移出窗体后,Mouse失效的情况.
if (p.pt.X & MouseRect.Left) or (p.pt.X & MouseRect.Right) or
(p.pt.Y & MouseRect.Top) or (p.pt.Y & MouseRect.Bottom) then
ClipCursor(@MouseRect)
Result:=1;
阅读(...) 评论()Summary (text)
Abstract (text)
The fall of biological maturation promoting factor (MPF) and histone H1 kinase activity during anaphase and telophase in mouse oocytes.
Cell fusions have been used to determine the biological activity of the MPF complex in murine oocytes during their progression through anaphase and telophase to metaphase II. Oocytes (1) at metaphase I, (2) during the anaphase-telophase transition, or (3) at metaphase II were fused to germinal vesicle-staged (immature) oocytes. The hybrids were cultured for 1 h in the presence of db cAMP before fixation and nuclear evaluation. Metaphase I oocytes invariably induced germinal vesicle breakdown (GVBD) in the immature partner. By contrast, anaphase/telophase oocytes never induced GVBD in immature oocytes. The capacity to induce GVBD reappears after the formation of the second metaphase plate. In a second study, histone H1 kinase activity was measured during mouse oocyte maturation in single oocytes. H1 kinase activity was low in GV oocytes, increased sharply at MI, declined during anaphase and telophase and increased again at MII. After egg activation, H1 kinase activity was reduced to basal levels. These results provide direct evidence that a drop in activity of MPF in murine oocytes occurs concomitantly with the exit from metaphase I; MPF activity remains low until the cell re-enters metaphase.
PMID: 1323308 [Pubmed - MEDLINE]
Full Text Sources
检索记录[]
丁香园旗下网站Summary (text)
Abstract (text)
Gender influences [Ca(2+)](i) during metabolic inhibition in myocytes overexpressing the Na(+)-Ca(2+) exchanger.
The Na(+)-Ca(2+) exchanger (NCX) may contribute to Ca(2+) overload and injury in ischemic cardiomyocytes. Recently, NCX overexpression was reported to increase ischemia/reperfusion injury in male and oophorectomized female but not in female mice. We therefore measured the effects of gender and estrogen on [Ca(2+)](i) and [Na(+)](i) during metabolic inhibition (MI) in myocytes from wild-type (WT) and transgenic (TG) mice overexpressing NCX.
Flow cytometry was used with fluo 3 for [Ca(2+)](i) and sodium green for [Na(+)](i) measurements. Male TG mouse myocytes had higher [Ca(2+)](i) after 30 minutes of MI (1086+/-160 nmol/L, n=8) than male WT (688+/-104 nmol/L, n=9, P=0.01). The increase in [Ca(2+)](i) during MI induced by NCX overexpression in female myocytes was not significant, however (TG 552+/-62 nmol/L, n=9; WT 426+/-44 nmol/L, n=7). The magnitude of rise in [Ca(2+)](i) during MI was greater in male than female myocytes. KB-R7943, an NCX inhibitor, abolished the effect of NCX overexpression but did not totally eliminate the effect of gender on [Ca(2+)](i) during MI. NCX current density and basal Na(+) pump function were not influenced by gender. The rise in [Na(+)](i) during MI was greater in male than in female myocytes. Estrogen attenuated the increase in [Ca(2+)](i) and [Na(+)](i) in male myocytes during MI and abolished the gender difference in [Na(+)](i) during MI.
Increased expression of NCX results in a more marked rise in [Ca(2+)](i) during MI in male than in female mouse myocytes. This gender difference appears to be mediated in part by an inhibitory effect of estrogen on the rise in [Na(+)](i), an NCX modifier, during MI.
[Pubmed - MEDLINE]
Full Text Sources
检索记录[]
丁香园旗下网站Summary (text)
Abstract (text)
Macrophage migration inhibition-activity after implantation of methylcholanthrene-induced sarcoma, Ehrlich ascites cancer or mouse ascites hepatoma-134 cancer cells in mice.
Cells from methylcholanthrene-induced tumor (MC-tumor), Ehrlich ascites cancer or mouse ascites hepatoma (MH-134) were subcutaneously implanted in dorsal area of mice to examine the specific cell mediated immunity following implantation. The migration index (MI) of lymphocytes was determined at various time periods after cell transplantation. The MI-activity increased under all three implantations, reached maximum at a certain period, decreased gradually and disappeared. The maximum MI-activity coincided with the proliferation period of the implanted tumor cells. This peak occurred on the tenth postimplantation day with MC-tumors, on the fifth day with Ehrlich ascites cancer and on the sixth day with MH-134 cancer. In lymphoid tissues of animals with MC-tumor and Ehrlich ascites cancer, strong MI-activity appeared early in the regional axillary lymph nodes, while weak activity was observed consistently in the distant mesenterial lymph nodes. The MI-activity of the splenic lymphoid cells resembled the axillary lymph nodes cell activity. The MI-activity of venous blood lymphoid cells was parallel to the average value of lymphoid cells of the spleen and axillary and mesenterial lymph nodes.
PMID: 184687 [Pubmed - MEDLINE]
Full Text Sources
检索记录[]
丁香园旗下网站