中国海上风电并网容量突破千万千瓦

记者: 刘羊旸 . . . . . . . . .

从国家能源局获悉，截至2021年4月底，中国海上风电并网容量达到1042万千瓦。

国家能源局有关负责人表示，近年来，我国海上风电建设成效显著。今年1月至4月，我国海上风电发电量为99.4亿千瓦时。

据行业统计，我国海上风电年平均利用小时数约2500小时，比陆上风电年平均利用小时数高出约500小时。

据介绍，2021年，全国风电、光伏发电量占全社会用电量的比重将达到11%左右，后续逐年提高。

Source : 新华网

How COVID Upended a Century of Patterns in U.S. Deaths

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Denise Lu wrote . . . . . . . . .

The U.S. death rate in 2020 was the highest above normal since the early 1900s — even surpassing the calamity of the 1918 flu pandemic.

A surge in deaths from the Covid-19 pandemic created the largest gap between the actual and expected death rate in 2020 — what epidemiologists call “excess deaths,” or deaths above normal.

Aside from fatalities directly attributed to Covid-19, some excess deaths last year were most likely undercounts of the virus or misdiagnoses, or indirectly related to the pandemic otherwise. Preliminary federal data show that overdose deaths have also surged during the pandemic.

A New York Times analysis of U.S. death patterns for the past century shows how much 2020 deviated from the norm.

A shift in a downward trend

Since the 1918 pandemic, the country’s death rate has fallen steadily. But last year, the Covid-19 pandemic interrupted that trend, in spite of a century of improvements in medicine and public health.

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In the first half of the 20th century, deaths were mainly dominated by infectious diseases. As medical advancements increased life expectancy, death rates also started to smooth out in the 1950s, and the mortality rate in recent decades — driven largely by chronic diseases — had continued to decline.

In 2020, however, the United States saw the largest single-year surge in the death rate since federal statistics became available. The rate increased 16 percent from 2019, even more than the 12 percent jump during the 1918 flu pandemic.

Largest increases in death rate since 1910

A striking single-year uptick

In 2020, a record 3.4 million people died in the United States. Over the last century, the total number of deaths naturally rose as the population grew. Even amid this continual rise, however, the sharp uptick last year stands out.

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Combined with deaths in the first few months of this year, Covid-19 has now claimed more than half a million lives in the United States. The total number of Covid-19 deaths so far is on track to surpass the toll of the 1918 pandemic, which killed an estimated 675,000 nationwide.

According to the Centers for Disease Control and Prevention, about 10 percent of the deaths last year can be directly attributed to Covid-19, which overtook other leading causes of death — like chronic lower respiratory diseases and unintentional injuries, such as car accidents and overdose deaths — to become the third biggest killer, after heart disease and cancer.

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Source : The New York Times

Where Africa’s Startup Activity Is Concentrated

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Source : Statista

巨額經濟紓困計劃的利弊

作者: 謝國生 . . . . . . . . .

針對2019冠狀病毒病大流行危機，繼美國國會2020年先後通過總值2.3萬億和9000億美元的紓困法案，今年3月，總統拜登又簽署總值1.9萬億美元的「美國救援計劃法案」，共佔美國本地生產總值（GDP）的24%，數目之大，就連2009年為應付金融危機推出的8000億美元經濟刺激方案，也顯得相形見絀。

提振經濟不易

據紐約聯邦儲備銀行對消費者支出的調查【表】，綜觀三輪紓困措施，美國消費者平均會將35.2%的援助金用作償還債務，38.4%作為儲蓄，用作消費的只佔26.5%。2020年美國信用卡債務減少近830億美元，跌幅佔全國信用卡債務12%。儘管2021年1月消費支出按月增長2.4%，為7個月來最大增幅，但同期個人收入已增長10.1%，可見該國消費還未回到疫前水平，世紀一遇的疫災令消費者趨向謹慎。

更有甚者，1.9萬億美元紓困方案或為經濟帶來長期損失。其主要爭議之一是方案將減低產出缺口（output gap，亦即潛在GDP與實際出現GDP之差），並可能引發通脹壓力。美國前財長薩默斯（Lawrence Summers）認為，全球金融海嘯後，美國在2009至2019年這10年間，經濟復甦步伐為第二次大戰以來最慢。他最近又在《華盛頓郵報》撰文，指正當美國經濟預期快速增長，而消費需求仍未復元，私人儲蓄更大量過剩之際，9000億和1.9萬億美元的兩項刺激經濟計劃實在過於龐大。另一邊廂，拜登政府則顯然主張刺激經濟力度愈猛愈好。

2019至2020年，美國GDP下降了3.5%，遠低於大多數經濟學家在疫情爆發時的預測。考慮到2020年下半年強勁的經濟增長，GDP的產出缺口估計約為GDP的4%。薩默斯和其他經濟學家並無否定需要更多財政刺激措施，但須考慮數額、時機和性質等因素。在疫後經濟繼續復甦的大前提下，1.9萬億美元的方案已佔美國GDP的9%，遠超出了4%的產出缺口。事實上，高於4%的增長就可能導致經濟過熱，引發通脹壓力。

提防通脹隱憂

聯儲局在2020年8月調整通脹政策，把過往2%的長遠通脹目標，由上限改為平均數值，亦即通脹率可在2%水平上下調節。至於有關維持此一平均通脹目標的具體時段，聯儲局則未有任何行政上的方針。

聯儲局近期似乎已經擺脫了對通脹的擔憂。2021年3月，聯儲局將本年經濟增長預測從去年12月的4.2%上調至6.5%，並將通脹預期上調至2.2%，失業率則從5%下調至4.5%；同時預測2022年經濟增長達3.3%、通脹率2%、失業率3.9%。由於近10年美國的勞動力參與率偏低，故此聯儲局也不太顧慮失業率下降導致工資上漲。

鑑於估計經濟快速復甦，即使2021年通脹加速，聯儲局仍不打算收緊貨幣政策，並計劃直至2024年將利率目標維持在近零水平；主要論點是會導致長期通脹緊縮的因素，例如人口老齡化、技術創新和全球化等，仍在發揮作用。該局主席鮑威爾在國會作證時表示，他並不擔心近期長期債券收益率上升，指出這類債券的表現似乎反映出市場對經濟前景日益樂觀。

但與此同時，M2貨幣供應量由2010至2019年期間，每年以5.8%增長，自2020年2月以來，則已飆升27%至4.2萬億美元。這是1943年以來貨幣供應量的最大增幅，主因是聯儲局資產負債表規模增加3.3萬億美元。目前的M2貨幣供應速度仍然處於歷史性低水平，但如果貨幣供應速度加快，則會導致通脹上升。

部分商品的通貨膨脹亦正加劇。疫情令生產能力降低，工廠難以交付貨物，供應鏈投入價格因原材料短缺、運輸成本上升和商品價格攀升而上揚，導致今年1月生產者價格指數（Producer Price Index，簡稱PPI）按月上升1.3%，2月上升0.5%，3月上升1%，至4月又上漲了1.3%，將12個月的增幅推高至5%，為10年來增幅之冠。企業亦逐漸通過向消費者提高價格，以收回增加的成本。因應需求驅動而供應緊張的經濟往往引發通貨膨脹。

赤字預算作風

商界及金融市場普遍認為疫情不可能於短期內完全消失，但專業投資者當前所憂慮的市場風險並非疫情，而是通貨膨脹。債券投資者恐怕債券價格下跌，而不分青紅皂白拋售債券，導致美國10年期國債收益率在近期暴漲。雖然是次債券危機並未如2013年債券恐慌時嚴重；當年美國10年期國債收益率在大概短短4個月內就已攀升到1.2%，債券增長速度更為劇烈，反觀目前國債收益率升至1.37%，則歷時近7個月。

在疫災或會重燃的陰影下，美國股市亦在聯儲局4月貨幣政策會議紀錄發布後大幅下跌，恐慌指數一度飆升20%。聯儲局部分官員似乎已準備在經濟復甦加快速度下，考慮改變貨幣政策，調整資產購買的步伐。

對於近年來背負廉價債務借款人，尤其是主權政府和企業而言，高利率都將構成負擔。2020年，各國政府因刺激經濟而增加的財政債務達16.3萬億美元，增幅為20%。同年美國政府的公共債務亦上升3萬億美元以上，佔GDP的120%，若包括第三輪的1.9萬億美元方案，GDP佔比更達130%，為二戰後的最高水平（二戰以來的75年間，美國政府有63年出現預算赤字）。

長遠而言，美國難免因債務負擔沉重的趨勢而引起經濟隱憂。國會預算辦公室預計，至2051年，單是聯邦政府的債務將倍增至GDP的202%。自疫症爆發以來，該國企業承擔的新債務共1.5萬億美元。2020年，基於房屋按揭、學生和汽車貸款增加，美國家庭債務增長2.9%至14.6萬億美元。可幸的是利率低企，借款人的償債能力尚見強勁。

面對頗大的利率和通脹風險，關鍵在於通脹上升屬暫時性、周期性抑或結構性。雖然通脹趨升足以令債務貶值，可用較便宜的美元還債，但高利率卻會增加借款人及企業的再融資成本，並削弱其融資能力，對經濟前景自然構成威脅。

2008年全球金融危機後及當前疫症大流行後的經濟復甦都有賴央行長期保持低利率政策，但通貨膨脹帶來的高利率卻會窒礙復甦。為應對冠狀病毒病造成的經濟災難，美國政府被迫推出史上最大規模的紓困方案。方案雖對重啟經濟能收一時之效，但債務上升、公共財政惡化，以及通脹壓力等長期後遺症，絕對不容忽視。

Source : HKU

Researchers Identify Proteins That Predict Future Dementia, Alzheimer’s Risk

The development of dementia, often from Alzheimer’s disease, late in life is associated with abnormal blood levels of dozens of proteins up to five years earlier, according to a new study led by researchers at the Johns Hopkins Bloomberg School of Public Health. Most of these proteins were not known to be linked to dementia before, suggesting new targets for prevention therapies.

The findings are based on new analyses of blood samples of over ten thousand middle-aged and elderly people—samples that were taken and stored during large-scale studies decades ago as part of an ongoing study. The researchers linked abnormal blood levels of 38 proteins to higher risks of developing Alzheimers within five years. Of those 38 proteins, 16 appeared to predict Alzheimer’s risk two decades in advance.

Although most of these risk markers may be only incidental byproducts of the slow disease process that leads to Alzheimer’s, the analysis pointed to high levels of one protein, SVEP1, as a likely causal contributor to that disease process.

The study was published in Nature Aging.

“This is the most comprehensive analysis of its kind to date, and it sheds light on multiple biological pathways that are connected to Alzheimer’s,” says study senior author Josef Coresh, MD, PhD, MHS, George W. Comstock Professor in the Department of Epidemiology at the Bloomberg School. “Some of these proteins we uncovered are just indicators that disease might occur, but a subset may be causally relevant, which is exciting because it raises the possibility of targeting these proteins with future treatments.”

More than six million Americans are estimated to have Alzheimer’s, the most common type of dementia, an irreversible fatal condition that leads to loss of cognitive and physical function. Despite decades of intensive study, there are no treatments that can slow the disease process, let alone stop or reverse it. Scientists widely assume that the best time to treat Alzheimer’s is before dementia symptoms develop.

Efforts to gauge people’s Alzheimer’s risk before dementia arises have focused mainly on the two most obvious features of Alzheimer’s brain pathology: clumps of amyloid beta protein known as plaques, and tangles of tau protein. Scientists have shown that brain imaging of plaques, and blood or cerebrospinal fluid levels of amyloid beta or tau, have some value in predicting Alzheimer’s years in advance.

But humans have tens of thousands of other distinct proteins in their cells and blood, and techniques for measuring many of these from a single, small blood sample have advanced in recent years. Would a more comprehensive analysis using such techniques reveal other harbingers of Alzheimer’s? That’s the question Coresh and colleagues sought to answer in this new study.

The researchers’ initial analysis covered blood samples taken during 2011–13 from more than 4,800 late-middle-aged participants in the Atherosclerosis Risk in Communities (ARIC) study, a large epidemiological study of heart disease-related risk factors and outcomes that has been running in four U.S. communities since 1985. Collaborating researchers at a laboratory technology company called SomaLogic used a technology they recently developed, SomaScan, to record levels of nearly 5,000 distinct proteins in the banked ARIC samples.

The researchers analyzed the results and found 38 proteins whose abnormal levels were significantly associated with a higher risk of developing Alzheimer’s in the five years following the blood draw.

They then used SomaScan to measure protein levels from more than 11,000 blood samples taken from much younger ARIC participants in 1993–95. They found that abnormal levels of 16 of the 38 previously identified proteins were associated with the development of Alzheimer’s in the nearly two decades between that blood draw and a follow-up clinical evaluation in 2011–13.

To verify these findings in a different patient population, the scientists reviewed the results of an earlier SomaScan of blood samples taken in 2002–06 during an Icelandic study. That study had assayed proteins including 13 of the 16 proteins identified in the ARIC analyses. Of those 13 proteins, six were again associated with Alzheimer’s risk over a roughly 10-year follow-up period.

In a further statistical analysis, the researchers compared the identified proteins with data from past studies of genetic links to Alzheimer’s. The comparison suggested strongly that one of the identified proteins, SVEP1, is not just an incidental marker of Alzheimer’s risk but is involved in triggering or driving the disease.

SVEP1 is a protein whose normal functions remain somewhat mysterious, although in a study published earlier this year it was linked to the thickened artery condition, atherosclerosis, which underlies heart attacks and strokes.

Other proteins associated with Alzheimer’s risk in the new study included several key immune proteins—which is consistent with decades of findings linking Alzheimer’s to abnormally intense immune activity in the brain.

The researchers plan to continue using techniques like SomaScan to analyze proteins in banked blood samples from long-term studies to identify potential Alzheimer’s-triggering pathways—a potential strategy to suggest new approaches for Alzheimer’s treatments.

The scientists have also been studying how protein levels in the ARIC samples are linked to other diseases such as vascular (blood vessel-related) disease in the brain, heart and the kidney.

Source: Johns Hopkins Bloomberg School of Public Health