Category: Covid-19

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Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism | Scientific Reports – Nature.com

June 4, 2024

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Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism | Scientific Reports - Nature.com

Watch: Fauci grilled by House Republicans over Covid-19 response – The Independent

June 4, 2024

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Watch again as House Republicans questioned Dr Anthony Fauci on his response to the Covid-19 pandemic and the origins of the virus on Monday, 3 June.

Lawmakers grilled the former head of the National Institute of Allergy and Infectious Diseases (NIAID) in his first congressional testimony in almost two years.

The GOP-led Select Subcommittee on the Coronavirus Pandemic have requested access to Dr Fauci's personal email and mobile phone records after obtaining information they say calls into question whether he may have attempted to keep some records away from the public eye.

Dr Fauci, who is appearing voluntarily, has declared he has "nothing to hide."

The 83-year-old served as NIAID Director from 1984 to 2022, overseeing research to treat diseases such as HIV and Aids, Ebola, Zika, and Covid-19.

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Watch: Fauci grilled by House Republicans over Covid-19 response - The Independent

Risk of death from COVID-19 lessens, but infection still can cause issues 3 years later Washington University School … – Washington University…

May 31, 2024

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Study also shows that patients hospitalized within 30 days after infection face 29% higher death risk in 3rd year compared with those not infected

New findings on long COVID by Washington University School of Medicine in St. Louis and the Veterans Affairs St. Louis Health Care system reveal that COVID-19 patients who were hospitalized within the first 30 days after infection face a 29% higher risk of death in the third year post-infection compared with people who have not had the virus. However, the three-year death risk marks a significant decline compared with such risk at previous time points post-infection. The study also shows that even people with mild COVID-19 still experienced new health problems related to the infection three years later.

New findings on long COVID long-term effects on health experienced by many who have had COVID-19 present a good-news, bad-news situation, according to a study at Washington University School of Medicine in St. Louis and the Veterans Affairs St. Louis Health Care system.

The bad news: COVID-19 patients who were hospitalized within the first 30 days after infection face a 29% higher risk of death in the third year compared with people who have not had the virus. However, the three-year death risk still marks a significant decline compared with such risk at the one- and two-year marks post-infection. The findings also show that even people with mild COVID-19 were still experiencing new health problems related to the infection three years later.

The good news: The increased risk of death diminishes significantly one year after a SARS-CoV-2 infection among people who were not hospitalized for the virus. This demographic accounts for most people who have had COVID-19.

The new research, published May 30 in Nature Medicine, tracked the viruss health effects in people three years after being infected with the original strain of COVID-19 in 2020. That year, about 20 million people tested positive for the virus in the U.S. The new study assessed the risk of death and 80 adverse health conditions in people three years after being diagnosed with COVID-19.

We arent sure why the viruss effects linger for so long, said senior author Ziyad Al-Aly, MD, a Washington University clinical epidemiologist and a global leader in long COVID research. Possibly it has to do with viral persistence, chronic inflammation, immune dysfunction or all the above. We tend to think of infections as mostly short-term illnesses with health effects that manifest around the time of infection. Our data challenges this notion. I feel COVID-19 continues to teach us and this is an important new lesson that a brief, seemingly innocuous or benign encounter with the virus can still lead to health problems years later.

Up to 10% of people infected with the virus experience long COVID, according to federal data.

Al-Alys prior research has documented COVID-19s damage to nearly every human organ, contributing to diseases and conditions affecting the lungs, heart, brain, and the bodys blood, musculoskeletal and gastrointestinal (GI) systems.

Such studies with longer follow-up are limited, said Al-Aly, a nephrologist who treats patients at the Washington University-affiliated John J. Cochran Veterans Hospital in midtown St. Louis. Addressing this knowledge gap is critical to enhance our understanding of long COVID and will help inform care for people suffering from long COVID.

Al-Aly and his team analyzed millions of de-identified medical records in a database maintained by the U.S. Department of Veterans Affairs, the nations largest integrated health-care system. The study included more than 114,000 veterans with mild COVID-19 who did not require hospitalization; more than 20,000 hospitalized COVID-19 patients; and 5.2 million veterans with no COVID-19 diagnosis. Patients were enrolled in the study from March 1, 2020, to Dec. 31, 2020, and followed for at least three years, until Dec. 31, 2023. Patients included people of diverse ages, races and sexes; statistical modeling ensured parity in representation.

In the third year after infection, COVID-19 patients who had been hospitalized experienced a 34% elevated health risk across all organ systems compared with people who did not have COVID. That number is down from a 182% increased risk one year after a COVID infection and a 57% risk two years after.

Among nonhospitalized patients, researchers found a 5% increased risk in suffering from long COVID in the third year after infection. This translates into 41 more health problems per 1,000 persons a small but not trivial burden. The long-term health effects in the third year primarily affected the GI, pulmonary and neurological systems. By comparison, the risk was increased by 23% one year after infection and increased by 16% two years after.

In the analysis, researchers also measured and compared the number of healthy life-years lost due to COVID-19. They found that among the nonhospitalized, at three years after infection, COVID-19 had contributed to 10 lost years of healthy life per 1,000 persons. By comparison, three years post-infection, those hospitalized for COVID-19 had experienced 90 lost years of healthy life per 1,000 persons.

For context, in the U.S., heart disease and cancer each cause about 50 lost years of healthy life per 1,000 persons, while stroke contributes to 10 lost years of healthy life per 1,000 persons.

That a mild SARS-CoV-2 infection can lead to new health problems three years down the road is a sobering finding, said Al-Aly, who is also director of the Clinical Epidemiology Center at the VA St. Louis Health Care System, and head of the research and development service. The problem is even worse for people with severe SARS-CoV-2 infection. It is very concerning that the burden of disease among hospitalized individuals is astronomically higher.

COVID-19 is a serious threat to the long-term health and well-being of people and it should not be trivialized, he said.

The extended trajectory for long COVID may change as researchers incorporate data from years beyond 2020. At that time, vaccines and antivirals had not been developed. Similarly, Al-Alys analysis does not consider subsequent variants such as omicron or delta.

Even three years out, you might have forgotten about COVID-19, but COVID hasnt forgotten about you, Al-Aly said. People might think theyre out of the woods, because they had the virus and did not experience health problems. But three years after infection, the virus could still be wreaking havoc and causing disease or illness in the gut, lungs or brain.

Cai M, Xie Y, Topol E, Al-Aly Z. Three-year outcomes of post-acute sequelae of COVID-19. Nature Medicine. May 30, 2024. DOI: https://doi.org/10.1038/s41591-024-02987-8.

This research was funded by the U.S. Department of Veterans Affairs.

About Washington University School of Medicine

WashU Medicine is a global leader in academic medicine, including biomedical research, patient care and educational programs with 2,900 faculty. Its National Institutes of Health (NIH) research funding portfolio is the second largest among U.S. medical schools and has grown 56% in the last seven years. Together with institutional investment, WashU Medicine commits well over $1 billion annually to basic and clinical research innovation and training. Its faculty practice is consistently within the top five in the country, with more than 1,900 faculty physicians practicing at 130 locations and who are also the medical staffs of Barnes-Jewish and St. Louis Childrens hospitals of BJC HealthCare. WashU Medicine has a storied history in MD/PhD training, recently dedicated $100 million to scholarships and curriculum renewal for its medical students, and is home to top-notch training programs in every medical subspecialty as well as physical therapy, occupational therapy, and audiology and communications sciences.

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Risk of death from COVID-19 lessens, but infection still can cause issues 3 years later Washington University School ... - Washington University...

A comprehensive analysis of COVID-19 nonlinear mathematical model by incorporating the environment and social … – Nature.com

May 29, 2024

In this section, we investigate the VL stability of matrix A defined in (16) to determine the global stability of the endemic equilibrium (E_{*}). The following definitions and preliminary lemmas are necessary prerequisites for this examination.

30,48,49,50. Consider a square matrix, denoted as M, endowed with the property of symmetry and positive (negative) definiteness. In this context, the matrix M is succinctly expressed as (M>0) or ((M<0)).

30,48,49,50. We write a matrix (A_{ntimes n}>0(A_{ntimes n}<0)) if (A_{ntimes n}) is symmetric positive (negative) definite.

30,48,49,50. If a positive diagonal matrix (H_{ntimes n}) exists, such that (HA+A^{T}H^{T}<0) then a non-singular matrix (A_{ntimes n}) is VL stable.

30,48,49,50. If a positive diagonal matrix (H_{ntimes n}) exists, such that (HA+A^{T}H^{T}<0) ((>0)) then, a non singular matrix (A_{ntimes n}) is diagonal stable.

The (2times 2) VL stable matrix is determined by the following lemma.

30,48,49,50. Let (B=begin{bmatrix} B_{11} &{} B_{12} \ B_{21} &{} B_{22}\ end{bmatrix}) is VL stable if and only if (B_{11}<0), (B_{22}<0), and (det (B)=B_{11}B_{22}-B_{12}B_{21}>0).

30,48,49,50. Consider the nonsingular (A_{ntimes n}=[A_{ij}]), where ((nge 2)), the positive diagonal matrix (C_{ntimes n}=textrm{diag}(C_{1},ldots , C_{n})), and (D=A^{-1}) such that

$$begin{aligned} {left{ begin{array}{ll} A_{nn}>0,\ widetilde{C}widetilde{A}+(widetilde{C}widetilde{A})^{T}>0,\ widetilde{C}widetilde{D}+(widetilde{C}widetilde{D})^{T}>0. end{array}right. } end{aligned}$$

Then, for (H_{n}>0), it ensures that the matrix expression (HA + A^{T}H^{T}) is positive definite.

We employ the same methodology used in51 to obtain the necessary outcomes for globally asymptotically.

If (R_{0}<1), the system (2) is globally asymptotically stable at ({E}_{0}=left( frac{b}{sigma },0,0,0,0,0 right)).

Taking the Lyapunov function corresponding to all dependent classes of the model

$$begin{aligned} L=m_1(S-S^*)+m_2(E-E^*)+m_3(I_S-I_S^*)+m_4(I_A-I_A^*)+m_5(R-R^*). end{aligned}$$

Taking derivative with respect to t yields

$$begin{aligned} L^prime =m_1S^prime +m_2E^prime +m_3I_S^prime +m_4I_A^prime +m_5R^prime . end{aligned}$$

After utilizing the values derived from system (2) and performing requisite calculations, we obtain:

$$begin{aligned} L ^prime =& ,m_{1}b+(m_2-m_1)frac{beta _{1}SP}{1+alpha _1P}+(m_2-m_1) frac{beta _2S(I_A+I_S)}{1+alpha _2(I_A+I_S)}+(m_1-m_2)varphi E+(m_4-m_2) upsilon E+(m_3-m_4)eta upsilon E\&+ (m_5-m_3)gamma _S I_S+(m_5-m_4)gamma _A I_A-m_1mu S-m_2mu E -m_3mu I_S-m_3delta I_S-m_4mu I_A-m_4delta I_A-m_5mu R. end{aligned}$$

Using (m_1=m_2=m_3=m_4=m_5=1) in the above equation gives

$$begin{aligned} L^prime= & , b-mu S-mu E-mu I_S-delta I_S-mu I_A-delta I_A-mu R\= & {} -left(mu N+delta (I_{A}+I_{S})-bright)<0. end{aligned}$$

Thus, the system (2) is globally asymptotically stable at (E_{0}), whenever (R_{0}<1). (square)

We propose the following Lyapunov function in order to prove the global stability at (E_{*}).

$$begin{aligned} L=m_1(S-S^*)^2+m_2(E-E^*)^2+m_3(I_S-I_S^*)^2+m_4(I_A-I_A^*)^2+m_5(R-R^*)^2+m_6(P-P^*)^2. end{aligned}$$

Here, (m_{1}), (m_{2}), (m_{3}), (w_{4}), (m_{5}), and (w_{6}) are non-negative constants. By taking the derivative of L with respect to time along the trajectories of the model (8), one has

$$begin{aligned} L^prime =2m_1(S-S^*)S^prime +2m_2(E-E^*)E^prime +2m_3(I_S-I_S^*)I_S^prime +2m_4(I_A-I_A^*)I_A^prime +2m_5(R-R^*)R^prime +2m_6(P-P^*)P^prime . end{aligned}$$

Here

$$begin{aligned}&2m_1(S-S^*)S^prime \&quad =2m_1(S-S^*)bigg{-frac{beta _{1}SP}{1+alpha _{1}P}-frac{beta _{2}S(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}+frac{beta _{1}S^*P^*}{1+alpha _{1}P^*}+ frac{beta _{2}S^*(I_A^*+I_S^*)}{1+alpha _{2}(I_A^*+I_S^*)}+varphi (R-R^*)-mu (S-S^*)bigg}\&quad =2m_1(S-S^*)bigg{-bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}bigg)S+bigg(frac{beta _{1}P^*}{1+alpha _{1}P^*}+ frac{beta _{2}(I_A^*+I_S^*)}{1+alpha _{2}(I_A^*+I_S^*)}bigg)S^*+varphi (R-R^*)-mu (S-S^*)bigg}\&quad =2m_1(S-S^*)bigg{-textbf{A}S+textbf{B}S^*+varphi (R-R^*)-mu (S-S^*)bigg}\&quad =2m_1(S-S^*)bigg{-textbf{A}S+textbf{A}S^*-textbf{A}S^*+textbf{B}S^*+varphi (R-R^*)-mu (S-S^*)bigg}\&quad =2m_1(S-S^*)bigg{-textbf{A}(S-S^*)-(textbf{A}-textbf{B})S^*+varphi (R-R^*)-mu (S-S^*)bigg}\&quad =2m_1(S-S^*)bigg{-(textbf{A}+mu )(S-S^*)-(textbf{A}-textbf{B})S^*+varphi (E-E^*)bigg}\&quad =2m_1(S-S^*)bigg{-bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}+mu bigg)(S-S^*) -frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}(P-P^*)\&qquad -frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_A-I_A^*) -frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_S-I_S^*)+varphi (R-R^*)bigg}\&quad =2m_1(S-S^*)bigg{-bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}+mu bigg)(S-S^*)+varphi (R-R^*)\&qquad -frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_S-I_S^*)-frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_A-I_A^*)\&qquad -frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}(P-P^*)bigg},\ end{aligned}$$

$$begin{aligned}&2m_2(E-E^*)E^prime \&quad =2m_2(E-E^*)bigg{bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}bigg)S-bigg(frac{beta _{1}P^*}{1+alpha _{1}P^*}+ frac{beta _{2}(I_A^*+I_S^*)}{1+alpha _{2}(I_A^*+I_S^*)}bigg)S^*-(mu +upsilon )(E-E^*)bigg}\&quad =2m_2(E-E^*)bigg{textbf{A}S-textbf{B}S^*-(mu +upsilon )(E-E^*)bigg}\&quad =2m_2(E-E^*)bigg{textbf{A}S-textbf{A}S^*+textbf{A}S^*-textbf{B}S^*-(mu +upsilon )(E-E^*)bigg}\&quad =2m_2(E-E^*)bigg{textbf{A}(S-S^*)+(textbf{A}-textbf{B})S^*-(mu +upsilon )(E-E^*)bigg}\&quad =2m_2(E-E^*)bigg{bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}bigg)(S-S^*)+ frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}(P-P^*)\&qquad +frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_A-I_A^*) +frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_S-I_S^*)-(mu +upsilon )(E-E^*)bigg}\&quad =2m_2(E-E^*)bigg{bigg(frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}bigg)(S-S^*)-(mu +upsilon )(E-E^*)\&qquad +frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_S-I_S^*)+frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}(I_A-I_A^*)\&qquad +frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}(P-P^*)bigg},\&2m_3(I_S-I_S^*)I_S^prime =2m_3(I_S-I_S^*)bigg{eta upsilon (E-E^*)-(mu +delta +gamma _S+tau _{S})(I_S-I_S^*)bigg},\&2m_4(I_A-I_A^*)I_A^prime =2m_4(I_A-I_A^*)bigg{(1-eta )upsilon (E-E^*)-(mu +delta +gamma _A+tau _{A})(I_A-I_A^*)bigg},\&2m_5(R-R^*)R^prime =2m_5(R-R^*)bigg{gamma _A(I_A-I_A^*)+gamma _S(I_S-I_S^*)-(mu +varphi )(R-R^*)bigg}, quad textrm{and}\&2m_6(P-P^*)P^prime =2m_6(P-P^*)bigg{tau _A(I_A-I_A^*)+tau _S(I_S-I_S^*)-mu _P(P-P^*)bigg}. end{aligned}$$

Using these values in (L^prime), which implies that (L^prime =Z(MA+A^{T}M)Z^{T}.)

Here, (Z=[S-S^*, E-E^*, I_S-I_S^*, I_A-I_A^*, R-R^*, P-P^*]), (M={textbf{diag}}(m_1, m_2, m_3, m_4, m_5, m_6)), and

$$begin{aligned} A= & {} left( begin{array}{ccc} -frac{beta _{1}P}{1+alpha _{1}P}-frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}-mu &{} 0 &{} -frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}\ frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)} &{} -(mu +upsilon ) &{} frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}\ 0 &{} eta upsilon &{} -(mu +delta +gamma _S+tau _{S})\ 0 &{} (1-eta )upsilon &{} 0\ 0 &{} 0 &{} gamma _S\ 0 &{} 0 &{} tau _S\ end{array}right. nonumber \{} & {} left. begin{array}{ccc} -frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))} &{} varphi &{} -frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}\ frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))} &{} 0 &{} frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}\ 0 &{} 0 &{} 0\ -(mu +delta +gamma _A+tau _{A}) &{} 0 &{} 0\ gamma _A &{} -(mu +varphi ) &{} 0\ tau _A &{} 0 &{} -mu _P end{array}right) . end{aligned}$$

(16)

It is important to note that matrix (A_{(n-1)times (n-1)}) is derived from matrix A by removing its final row and column. In accordance with the works of Zahedi and Kargar48, Shao and Shateyi49, Masoumnezhad et al.50, Chien and Shateyi30, and Parsaei et al.29, we introduce a series of lemmas and theorems to examine the global stability of the EE at (E_{*}).

In order to make the calculation easier, we present the matrix (16) in more simplified form as given below:

$$begin{aligned} A=left( begin{array}{cccccc} -a &{} 0 &{} -b &{} -b &{} c &{} -d\ e &{} -f &{} b &{} b &{} 0 &{} d\ 0 &{} g &{} -h &{} 0 &{} 0 &{} 0\ 0 &{} i &{} 0 &{} -j &{} 0 &{} 0\ 0 &{} 0 &{} k &{} l &{} -m &{} 0\ 0 &{} 0 &{} n &{} p &{} 0 &{} -q\ end{array}right) . end{aligned}$$

(17)

Here, (a=frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}+mu), (b=frac{beta _{2}S^*}{(1+alpha _{2}(I_A+I_S))(1+alpha _{2}(I_A^*+I_S^*))}), (c=varphi), (d=frac{beta _{1}S^*}{(1+alpha _{1}P)(1+alpha _{1}P^*)}), (e=frac{beta _{1}P}{1+alpha _{1}P}+frac{beta _{2}(I_A+I_S)}{1+alpha _{2}(I_A+I_S)}), (f=(mu +upsilon )), (g=eta upsilon), (h=(mu +delta +gamma _S+tau _{S})), (i=(1-eta )upsilon), (j=(mu +delta +gamma _A+tau _{A})), (k=gamma _S), (l=gamma _A), (m=(mu +varphi )), (n=tau _S), (p=tau _A), and (q=mu _P).

It is important to note that all the parameters a,b,c,d,e,f,g,h,i,j,k,l,m,n,p, and q are positive. Throughout this paper, it is important to note that (a-e) and (-a+e) are always equal to (mu) and (-mu) respectively. Moreover, we conclude that all the diagonal elements (the negative values) of the matrix A are negative, which is a good sign for stability. We need to compute the eigenvalues to make a definitive conclusion for the global stability of (E_{*}). But finding the eigenvalues of the matrix A is quite time consuming. Therefore, we introduce a series of lemmas and theorems given below to examine whether all the eigenvalues of the matrix A have negative real parts or not?.

The matrix (A_{6times 6}) defined in (17) is VL stable.

Obviously (-A_{66}>0). Consider (C=-widetilde{A}) be a (5times 5) matrix that is produced by eliminating the final row and column (-A). Utilizing Lemma 4.2, we can demonstrate the diagonal stability of matrices (C=-widetilde{A}) and (mathbb{C}=-widetilde{A^{-1}}). Let examine the matrix (C=-widetilde{A}) and (mathbb{C}=-widetilde{A^{-1}}), from (17) we obtain

$$begin{aligned} C=left( begin{array}{ccccc} a &{} 0 &{} b &{} b &{} -c\ -e &{} f &{} -b &{} -b &{} 0\ 0 &{} -g &{} h &{} 0 &{} 0\ 0 &{} -i &{} 0 &{} j &{} 0\ 0 &{} 0 &{} -k &{} -l &{} m end{array}right) , quad textrm{and}quad ,mathbb{C}=frac{1}{det (-A)}left( begin{array}{ccccc} mathbf{{c}_{11}} &{} mathbf{c_{12}} &{} mathbf{c_{13}} &{} mathbf{c_{14}} &{} mathbf{c_{15}}\ mathbf{{c}_{21}} &{} mathbf{c_{22}} &{} mathbf{c_{23}} &{} mathbf{c_{24}} &{} mathbf{c_{25}}\ mathbf{{c}_{31}} &{} mathbf{c_{32}} &{} mathbf{c_{33}} &{} mathbf{c_{34}} &{} mathbf{c_{35}}\ mathbf{{c}_{41}} &{} mathbf{c_{42}} &{} mathbf{c_{43}} &{} mathbf{c_{44}} &{} mathbf{c_{45}}\ mathbf{{c}_{51}} &{} mathbf{c_{52}} &{} mathbf{c_{53}} &{} mathbf{c_{54}} &{} mathbf{c_{55}}\ end{array}right) . end{aligned}$$

Here

$$begin{aligned} det (-A)=-d (a - e) m (g j n +h i p) - left(c e (g j k +h i l) + (b (a - e) h i + (b (a - e) g - a f h) j) mright) q<0, end{aligned}$$

and

$$begin{aligned} mathbf{c_{11}}= & {} -mleft(d g j n + d h i p + b h i q + b g j q - f h j qright),\ mathbf{c_{12}}= & {} -d m (g j n + h i p) + left(c (g j k + h i l) - b (h i + g j) mright) q,\ mathbf{c_{13}}= & {} -f j m (d n + b q) + c left(d i (l n - k p) + (f j k + b i (-k + l)) qright),\ mathbf{c_{14}}= & {} -f h m (d p + b q) + c left(d g (-l n + k p) + (b g (k - l) + f h l) qright),\ mathbf{c_{15}}= & {} -c left(d g j n + d h i p + b h i q + b g j q - f h j qright),\ mathbf{c_{21}}= & {} e h j m q, quad mathbf{c_{22}}=a h j m q,\ mathbf{c_{23}}= & {} d (a - e) j m n + j left(c e k + b (a - e) mright) q,\ mathbf{c_{24}}= & {} d (a - e) h m p + h left(c e l + b (a - e) mright) q,\ mathbf{c_{25}}= & {} c e h j q,quad mathbf{c_{31}}=e g j m q,\ mathbf{c_{32}}= & {} a g j m q,\ mathbf{c_{33}}= & {} -a m left(d i p + b i q - f j qright) + e i left(d m p - c l q + b m qright),\ mathbf{c_{34}}= & {} d (a - e) g m p + g left(c e l + b (a - e) mright) q,\ mathbf{c_{35}}= & {} c e g j q,quad mathbf{c_{41}}=e h i m q,quad mathbf{c_{42}}=a h i m q,\ mathbf{c_{43}}= & {} d (a - e) i m n + i left(c e k + b (a - e) mright) q,\ mathbf{c_{44}}= & {} -a m left(d g n + b g q - f h qright) + e g left(d m n - c k q + b m qright),\ mathbf{c_{45}}= & {} c e h i q,\ mathbf{c_{51}}= & {} e left(g j k + h i lright) q,\ mathbf{c_{52}}= & {} a left(g j k + h i lright) q, \ mathbf{c_{53}}= & {} d (a - e) i (l n - k p) + left(b e i (k - l) + a (f j k + b i (-k + l))right) q,\ mathbf{c_{54}}= & {} d (-a + e) g (l n - k p) + left(b e g (-k + l) + a (b g (k - l) + f h l)right) q,\ mathbf{c_{55}}= & {} d (-a + e) (g j n + h i p) + left(b (-a + e) h i + left(-a b g + b e g + a f hright) jright) q. end{aligned}$$

Since

$$begin{aligned} det (-A)=-d (a - e) m (g j n +h i p) - left(c e (g j k +h i l) + left(b (a - e) h i + (b (a - e) g - a f h) jright) mright) q<0, end{aligned}$$

and

$$begin{aligned} mathbf{c_{55}}=d (-a + e) (g j n + h i p) + left(b (-a + e) h i + ((-a + e)b g + a f h) jright) q. end{aligned}$$

Therefore

$$begin{aligned} mathbb{C}_{55}=frac{-left(mu (d g j n + d h i p + b h i q + b g j q) - a f h j qright)}{-mu m (d g j n + d h i p + b h i q + b g j q)-(c e (g j k + h i l) - a f h j m) q}, end{aligned}$$

which implies that

$$begin{aligned} mathbb{C}_{55}=frac{mu left(d g j n + d h i p + b h i q + b g j qright) - a f h j q}{mu m left(d g j n + d h i p + b h i q + b g j qright)+left(c e (g j k + h i l) - a f h j mright) q}>0. end{aligned}$$

Using the information provided in Lemma 4.2, we assert and demonstrate that (C=-widetilde{A}) and (mathbb{C}=-widetilde{A^{-1}}) exhibit diagonal stability, thereby establishing the VL stability of the matrix A. (square)

In accordance with Theorem 4.6, the matrix (C=-widetilde{A}) is affirmed to possess diagonal stability.

As (C_{55}>0), using Lemma 4.2, we must demonstrate the diagonal stability of the reduced matrix (D=widetilde{C}) and its inverse (mathbb{D}=widetilde{C^{-1}}) to complete the proof. Thus the matrix D can be obtained from the matrix C given in Theorem 4.6, we have

$$begin{aligned} D=left( begin{array}{cccc} a &{} 0 &{} b &{} b\ -e &{} f &{} -b &{} -b\ 0 &{} -g &{} h &{} 0\ 0 &{} -i &{} 0 &{} j end{array}right) , quad textrm{and}quad ,,mathbb{D}=frac{1}{det (C)}left( begin{array}{cccc} mathbf{d_{11}} &{} mathbf{d_{12}} &{} mathbf{d_{13}} &{} mathbf{d_{14}}\ mathbf{d_{21}} &{} mathbf{d_{22}} &{} mathbf{d_{23}} &{} mathbf{d_{24}}\ mathbf{d_{31}} &{} mathbf{d_{32}} &{} mathbf{d_{33}} &{} mathbf{d_{34}}\ mathbf{d_{41}} &{} mathbf{d_{42}} &{} mathbf{d_{43}} &{} mathbf{d_{44}} end{array}right) , end{aligned}$$

here

$$begin{aligned} det (C)=-c e (g j k + h i l) + left(b (-a + e) h i + ((-a + e)b g + a f h) jright) m<0, end{aligned}$$

and

$$begin{aligned} mathbf{d_{11}}= & {} -(b h i + b g j - f h j) m,\ mathbf{d_{12}}= & {} c (g j k + h i l) - b (h i + g j) m,\ mathbf{d_{13}}= & {} c f j k - b left(c i (k - l) + f j mright), \ mathbf{d_{14}}= & {} b c g (k - l) + f h (c l - b m),\ mathbf{d_{21}}= & {} e h j m, mathbf{d_{22}}=a h j m,\ mathbf{d_{23}}= & {} j left(c e k + b (a - e) mright),\ mathbf{d_{24}}= & {} h left(c e l + b (a - e) mright),\ mathbf{d_{31}}= & {} e g j m, mathbf{d_{32}}=a g j m,\ mathbf{d_{33}}= & {} -c e i l + left((-a + e)b i + a f jright) m,\ mathbf{d_{34}}= & {} g left(c e l + b (a - e) mright),\ mathbf{d_{41}}= & {} e h i m, mathbf{d_{42}}=a h i m,\ mathbf{d_{43}}= & {} i left(c e k + b (a - e) mright),\ mathbf{d_{44}}= & {} -c e g k + left((-a + e)b g + a f hright) m. end{aligned}$$

Since

$$begin{aligned} det (C)=-c e (g j k + h i l) + left(b (-a + e) h i + left((-a + e) b g + a f hright) jright) m, end{aligned}$$

and

$$begin{aligned} mathbf{d_{44}}=-c e g k + left((-a + e)b g + a f hright) m. end{aligned}$$

Therefore

$$begin{aligned} mathbb{D}_{44}=frac{c e g k +mu b g m - a f h m}{ce(gjk+hil)+bmu (hi+gj)m-afhjm}>0. end{aligned}$$

(square)

The matrix (mathbb{C}=-widetilde{A^{-1}}) defined in Theorem 4.6 is diagonal stable.

Consider the matrix (mathbb{C}) in 4.6, we see that (mathbb{C}_{55}>0), Using Lemma 4.2, we must demonstrate that the modified matrix (E=widetilde{mathbb{C}}) and its inverse (mathbb{E}=widetilde{mathbb{C}^{-1}}) exhibit diagonal stability. This establishes the completion of the proof. Thus the matrix D can be obtained from the matrix (mathbb{C}) given in Theorem 4.6, we have

$$begin{aligned} E=frac{1}{det (-A)}left( begin{array}{cccc} mathbf{{c}_{11}} &{} mathbf{c_{12}} &{} mathbf{c_{13}} &{} mathbf{c_{14}}\ mathbf{{c}_{21}} &{} mathbf{c_{22}} &{} mathbf{c_{23}} &{} mathbf{c_{24}}\ mathbf{{c}_{31}} &{} mathbf{c_{32}} &{} mathbf{c_{33}} &{} mathbf{c_{34}}\ mathbf{{c}_{41}} &{} mathbf{c_{42}} &{} mathbf{c_{43}} &{} mathbf{c_{44}}\ end{array}right) ,,quad textrm{and}quad ,mathbb{E}=frac{1}{det (mathbb{C})}left( begin{array}{cccc} mathbf{{e}_{11}} &{} mathbf{e_{12}} &{} mathbf{e_{13}} &{} mathbf{e_{14}}\ mathbf{{e}_{21}} &{} mathbf{e_{22}} &{} mathbf{e_{23}} &{} mathbf{e_{24}}\ mathbf{{e}_{31}} &{} mathbf{e_{32}} &{} mathbf{e_{33}} &{} mathbf{e_{34}}\ mathbf{{e}_{41}} &{} mathbf{e_{42}} &{} mathbf{e_{43}} &{} mathbf{e_{44}}\ end{array}right) . end{aligned}$$

Here

$$begin{aligned} det (mathbb{C})&=frac{qell ^{4}}{det (-A)}<0, end{aligned}$$

and

$$begin{aligned} mathbf{e_{11}}= & {} -a qell ^{3}, mathbf{e_{12}}=0, mathbf{e_{13}}=-(d n + b q)ell ^{3},\ mathbf{e_{14}}= & {} -(d p + b q)ell ^{3}, mathbf{e_{21}}=e qell ^{3}, mathbf{e_{22}}=-f qell ^{3},\ mathbf{e_{23}}= & {} (d n + b q)ell ^{3}, mathbf{e_{24}}=(d p + b q)ell ^{3}, mathbf{e_{31}}=0,\ mathbf{e_{32}}= & {} g q ell ^{3}, mathbf{e_{33}}=-h qell ^{3}, mathbf{e_{34}}=0, mathbf{e_{41}}=0,\ mathbf{e_{42}}= & {} i qell ^{3}, mathbf{e_{43}}=0, mathbf{e_{44}}=-j qell ^{3}. end{aligned}$$

Here

$$begin{aligned} ell =left[d (a - e) m (g j n + h i p) + left{c e (g j k + h i l) + left(b (a - e) h i + (b (a - e) g - a f h) jright) mright} qright] end{aligned}$$

Since

$$begin{aligned} det (mathbb{C})&=frac{qell ^{4}}{det (-A)}, end{aligned}$$

and

$$begin{aligned} mathbf{e_{44}}=-j q ell ^{3}. end{aligned}$$

Therefore

$$begin{aligned} mathbb{E}_{44}=frac{-j}{det (-A)ell }>0, end{aligned}$$

where (det (-A)<0) and (ell >0). (square)

The matrix D, as described in Lemma 4.3 and denoted by (widetilde{C}), exhibits diagonal stability.

It is clear that (D_{44}>0). By applying Lemma 4.2, our task is to demonstrate the diagonal stability of the reduced matrix (F=widetilde{D}) and its inverse (mathbb{F}=widetilde{D^{-1}}), thereby completing the proof. Thus from Lemma 4.3, we have

$$begin{aligned} F=left( begin{array}{ccc} a &{} 0 &{} b\ -e &{} f &{} -b\ 0 &{} -g &{} h end{array}right) , quad textrm{and}quad ,,mathbb{F}=frac{1}{det ({D})}left( begin{array}{ccc} mathbf{f_{11}} &{} mathbf{f_{12}} &{} mathbf{f_{13}}\ mathbf{f_{21}} &{} mathbf{f_{22}} &{} mathbf{f_{23}}\ mathbf{f_{31}} &{} mathbf{f_{32}} &{} mathbf{f_{33}} end{array}right) . end{aligned}$$

Here

$$begin{aligned} det (D)=b (-a + e) h i + left((-a + e)b g + a f hright) j>0 (textrm{see} textrm{Proposition} 4.1 (iii)), end{aligned}$$

and (mathbf{f_{11}}=f h j - b (h i + g j)>0 (textrm{see} textrm{Proposition} 4.1 (iv))), (mathbf{f_{12}}=-b (h i + g j)), (mathbf{f_{13}}=b f j), (mathbf{f_{21}}=e h j), (mathbf{f_{22}}=a h j), (mathbf{f_{23}}=b (a - e) j), (mathbf{f_{31}}=e g j), (mathbf{f_{32}}=a g j), (mathbf{f_{33}}=(-a + e) b i + a f j>0 (textrm{see} textrm{Proposition} 4.1 (v))).

Since (det (D)>0), and (mathbf{f_{33}}>0), therefore (mathbb{F}_{33}>0). (square)

The matrix (mathbb{D}), as defined in Lemma 4.3 denoted by (widetilde{C^{-1}}), exhibits diagonal stability.

It is obvious that (mathbb{D}_{44}>0), by employing Lemma 4.2, our task is to demonstrate the diagonal stability of a modified matrix (G=widetilde{mathbb{D}}) and its inverse (mathbb{G}=widetilde{mathbb{D}^{-1}}). This verification serves as the completion of the proof. Thus from Lemma 4.3, we have

$$begin{aligned} G=frac{1}{det (C)}left( begin{array}{ccc} mathbf{d_{11}} &{} mathbf{d_{12}} &{} mathbf{d_{13}}\ mathbf{d_{21}} &{} mathbf{d_{22}} &{} mathbf{d_{23}}\ mathbf{d_{31}} &{} mathbf{d_{32}} &{} mathbf{d_{33}} end{array}right) , quad textrm{and}quad ,mathbb{G}=frac{1}{det (mathbb{D})}left( begin{array}{ccc} mathbf{g_{11}} &{} mathbf{g_{12}} &{} mathbf{g_{13}}\ mathbf{g_{21}} &{} mathbf{g_{22}} &{} mathbf{g_{23}}\ mathbf{g_{31}} &{} mathbf{g_{32}} &{} mathbf{g_{33}} end{array}right) . end{aligned}$$

Here

$$begin{aligned} det (mathbb{D})&=frac{-mell _{1}^{3}}{det (C)}>0, end{aligned}$$

and

$$begin{aligned} mathbf{g_{11}}= & a mell _{1}^{2}, mathbf{g_{12}}=0, mathbf{g_{13}}=-(c k - b m)ell _{1}^{2}, mathbf{g_{21}}=-e mell _{1}^{2}, mathbf{g_{22}}=f mell _{1}^{2}, ,mathbf{g_{23}}= & {} -b mell _{1}^{2}, mathbf{g_{31}}=0, mathbf{g_{32}}=-g mell _{1}^{2}, mathbf{g_{33}}=h mell _{1}^{2}. end{aligned}$$

Here

$$begin{aligned} ell _{1}=left[c e (g j k + h i l) + left{b (a - e) h i + left(b (a - e) g - a f hright) jright} mright] end{aligned}$$

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May 29, 2024

New data from the RECOVERY trial show that women who contracted COVID-19 during pregnancy had a lower risk of developing long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), than other women, according to a study in eClinicalMedicine.

The retrospective study from the National Institutes of Health (NIH) Researching COVID to Enhance Recovery (RECOVER) trial included women ages 18 to 49 years with lab-confirmed SARS-CoV-2 infection from March 2020 through June 2022 seen in 19 US health systems.

PASC was defined as symptoms identified 30 to 180 days postSARS-CoV-2 infection. A total of 83,915 women with COVID-19 acquired outside of pregnancy and 5,397 women with COVID-19 acquired during pregnancy were compared and included in the final analysis.

The authors said this was the first study to compare long-COVID outcomes through the lens of pregnancy.

Overall, the authors found that non-pregnant women were older and had more comorbidities than pregnant women with COVID-19, which may have contributed to the findings that non-pregnant women were significantly more at risk for developing long COVID than were pregnant women.

Pregnant women had an incidence of PASC of 25.5% compared to 33.9% non-pregnant women, an adjusted hazard ratio (aHR) of 0.85 (95% confidence interval [CI], 0.80 to 0.91).

The cumulative incidence of PASC in the 180 days following the incident infection date was 30.8 per 100 people among those with COVID acquired during pregnancy compared with 35.8 per 100 people among those with COVID acquired outside of pregnancy, the authors said.

For pregnant women with COVID-19, the average gestational week at infection was 34 weeks, and the average week of delivery was 39 weeks. Hispanic women made up 27.8% of pregnant women with COVID, compared to 14.3% of non-pregnant women with COVID.

SARS-CoV-2 infection acquired during pregnancy compared with acquired outside of pregnancy was associated with a higher incidence of abnormal heartbeat, abdominal pain, and thromboembolism,

"SARS-CoV-2 infection acquired during pregnancy compared with acquired outside of pregnancy was associated with a higher incidence of abnormal heartbeat, abdominal pain, and thromboembolism," the authors wrote. Pregnant women with COVID were also more likely to be hospitalized during the acute phase of infection compared to non-pregnant women.

Non-pregnant women, however, were more likely to experience joint pain, sleep disorders, cognitive problems, difficulty breathing, brain dysfunction, hair loss, acute pharyngitis (throat infection), malnutrition, malaise and fatigue, and chest pain if they developed long COVID.

"The current findings further our understanding of PASC after acquiring SARS-CoV-2 infection in pregnancy to inform patient counseling and direct future research. Further prospective study is necessary to confirm these findings," the authors concluded.

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Pregnant women with COVID-19 may be at lower risk for long COVID - University of Minnesota Twin Cities

Reminder for IPRC Webinar "Treating Post-COVID-19 Conditions in Children" on May 30 – RCPA

May 29, 2024

Thursday, May 30, 2024 12:00 pm 1:00 pm EDT; 11:00 am 12:00 pm CDT; 10:00 am 11:00 am MDT; 9:00 am 10:00 am PDT Register

Laura Malone, MD, PhD

Dr. Laura Malone is the director of the Pediatric Post-COVID-19 Rehabilitation Clinicat Kennedy Krieger Institute.She is alsoa physician scientist in Kennedy Kriegers Center for Movement Studies and an assistant professor of Neurology and Physical Medicine and Rehabilitation at the Johns Hopkins University School of Medicine.

Dr. Malone has a PhD in Biomedical Engineering from Johns Hopkins University and her medical degree from the University of North Carolina. She completed her pediatric neurology residency at Johns Hopkins School of Medicine. Dr. Malones clinical practice focuses on the neurological care of children with perinatal stroke, other brain injuries, and long COVID. Her research focuses on understanding complex pediatric disorders and on improving outcomes using mechanistic neurorehabilitation approaches. Regarding COVID-19, Dr. Malone investigates clinical phenotypes of children with persistent symptoms after COVID-19infection and investigates factors and mechanisms that promote good recovery.

Objectives: At the end of this session, the learner will:

Audience: This webinar is intended for all interested members of the rehabilitation team.

Level: Intermediate

Certificate of Attendance: Certificates of attendance are available for all attendees. No CEs are provided for this course.

Complimentary webinars are a benefit of membership in IPRC/RCPA. Registration fee for non-members is $179. Not a member yet?Consider joining today.

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Reminder for IPRC Webinar "Treating Post-COVID-19 Conditions in Children" on May 30 - RCPA

The Impact of COVID-19 on Asthma Diagnosis, Health Care Utilization – AJMC.com Managed Markets Network

May 29, 2024

Two posters presented at the American Thoracic Society (ATS) 2024 International Conference found that asthma can be diagnosed after COVID-19 like other respiratory viral infections, and that the pandemic exerted a substantial influence on health care utilization for serious asthma outcomes.

Man holding paper model of lungs | Elena - stock.adobe.com

The first poster was based on a retrospective study that analyzed medical records of patients with respiratory symptoms between January 2022 and March 2023, to compare the clinical features and final diagnoses of these patients.1

The study categorized patients as those with recent COVID-19 and those without, assessing clinical features, final diagnoses, and pulmonary function tests. A total of 3,168 patients were included in the study, in which 842 (26.58%) had recent COVID-19 and 2,326 (73.42%) did not.

Patients in the COVID-19 group were more often female (61.6%) and had a significantly lower mean (SD) age (53.45 [17.12] years vs 60 [16.95] years; P < .001) than patients in the nonCOVID-19 group. Additionally, 632 (19.95%) patients were clinically diagnosed with asthma, with 150 (17.8%) in the COVID-19 group and 482 (20.7%) in the non-COVID-19 group, showing no statistical significance (P = .07).

Furthermore, the researchers found no significant difference in forced expiratory volume per 1 second (FEV1) based on COVID-19 status among patients with asthma, while subacute cough was significantly more prevalent in the COVID-19 group (45.7% vs 1.7%; P < .001).

Therefore, the researchers believe that asthma can be diagnosed after COVID-19 in a similar manner to other respiratory viral infections, and that the incidence of asthma diagnosis post-COVID-19 did not significantly differ from patients without a history of COVID-19 infection.

The second poster aimed to examine the impact of the COVID-19 pandemic on health care utilization for pediatric patients with asthma.2

The study included electronic health record (EHR) data encompassing more than 13,000 patients, more than 32,000 records, more than 8700 emergency visits, and more than 4000 hospitalizations for asthma. From this data, the researchers identified 2347 individuals with an index visit1165 pre-pandemic, 289 during the pandemic, and 893 post-pandemic. The mean age of patients was 6.4 (4.4) years, and 40.4% were female. Additionally, 50.8% of patients were White, 41.5% were Black, and 7.7% identified as other race(s).

Times to the next emergency visit were much shorter during the pandemic (253 days) and post-pandemic (101 days) compared with the pre-pandemic (276.5 days), as well as median times to next hospitalization, with 338.5 days during the pandemic, 120 days post-pandemic, and 437 days pre-pandemic, respectively.

Additionally, Black patients had faster median emergency visit returns than White patients both before and during the pandemic but had longer median times post-pandemic. The researchers noted that the effect of the pandemic on emergency visits and hospitalizations tended to be different among groups. Furthermore, the time-to-emergency visit was more pronounced in White patients compared with Black patients (P < .0001).

Therefore, the researchers believe the findings suggest the COVID-19 pandemic had substantial influence on health care utilization for severe asthma outcomes in children, and that these effects have been endured for an extended period.

References

1. Hur G, Chang S, Sim J, et al. Clinical presentation and diagnosis of respiratory symptoms during the COVID-19 pandemic. Abstract presented at: American Thoracic Society International Conference; May 17-22, 2024; San Diego, CA. Accessed May 28, 2024. https://www.abstractsonline.com/pp8/#!/11007/presentation/9405

2. Forno E, Bo N, Liu J, et al. EHR-based survival analysis to examine the impact of the COVID-19 pandemic on severe asthma outcomes in pediatrics. Abstract presented at: American Thoracic Society International Conference; May 17-22, 2024; San Diego, CA. Accessed May 28, 2024. https://www.abstractsonline.com/pp8/#!/11007/presentation/4513

Continued here:

The Impact of COVID-19 on Asthma Diagnosis, Health Care Utilization - AJMC.com Managed Markets Network

COVID-19 cases on the rise in Hawaii – Big Island Now

May 29, 2024

Just when you think its safe to go back into the grocery store, department store, restaurant, etc., etc., etc., of course a nasty respiratory illness has to come along and complicate your plans.

The culprit this time? You might have guessed it: COVID-19.

Yes, the scourge that made everyones lives that much more difficult beginning in 2020 is again on the rise in Hawaii.

COVID-19 is at the yellow, or medium activity level, meaning the virus is circulating at higher levels throughout the state than would be expected based on historic trends, and continuing to increase.

In Hawaii County, there were 129 new cases reported the week of May 14-20, the most recent data available. The Big Island is seeing a weekly average of 14 new cases a day.

The state saw an additional 659 new COVID cases reported the same week, with an weekly average of 71 new cases a day.

Case numbers are still updated once a week.

A rundown of the other counties for the week of May 14-20 shows:

Cases of the flu and respiratory syncytial virus, or RSV, remain at green statewide, or low activity levels.

Overall acute respiratory disease is at the medium level throughout the islands.

The latest levels of respiratory diseases and levels of infection come from the states new Repiratory Disease Dashboard.

The website was developed by the state Health Departments Disease Outbreak Control Division and provides an at-a-glance snapshot of respiratory disease activity statewide, including COVID-19.

The dashboard addresses not only COVID-19 but other acute respiratory illnesses such as influenza, or the flu, and RSV. Respiratory diseases occur year-round in the islands.

The new Respiratory Disease Dashboard provides, in one place, a summary of what is happening with several major respiratory viruses that contribute to respiratory disease in Hawaii, said State Epidemiologist Sarah Kemble This helps people make informed decisions about their health.

The dashboard shows that COVID testing positivity is higher than expected and climbing, Kemble added, with emergency room visits and hospital admissions increasing.

Based on this information, I would recommend checking whether youve had the 2023-24 COVID-19 vaccine, and if not, or if youre eligible for a repeat dose, go get it today, she said.

Dashboard trends show COVID remains a health concern, and the public should take reasonable precautions to avoid getting sick. Among them:

Additional strategies for reducing the spread of COVID and other respiratory disease can be found on the state Health Departments website.

You can visit the new Respiratory Disease Dashboard here.

Continued here:

COVID-19 cases on the rise in Hawaii - Big Island Now

What Is Asymptomatic COVID-19 and Are You Contagious? – Health Essentials

May 29, 2024

The emergence of COVID-19 and its slow integration into our daily lives has impacted everybody. But that impact hasnt been the same across the board. One reason? The physical experience of being sick with COVID-19 can vary wildly from person to person. Contracting COVID-19 is deadly for some, while others dont get so much as a sniffle. How exactly is that possible?

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Were learning more about COVID-19 every day. And theres so much information out there that it can be hard to keep up. We asked infectious disease specialist Donald Dumford, MD, to bring us up to date on asymptomatic COVID-19. He details the ongoing research on the topic and explains how we can use what we know to navigate our new normal in a smart, safe way.

Simply put, the word asymptomatic means being sick without having symptoms. No fever, no cough, no body aches, no fatigue. Nothing. Your bodys actively battling a disease and in some cases spreading it without you even realizing youre unwell.

Its called being an asymptomatic carrier. Asymptomatic carriage isnt something that happens with all diseases, but it does happen with COVID-19. And it happens quite a bit. Dr. Dumford says its one of the reasons the virus proved impossible to contain and why it transitioned from an isolated outbreak to a global pandemic so quickly.

Dr. Dumford notes that its common to confuse asymptomatic COVID-19 with pre-symptomatic COVID-19, so lets clarify these terms.

As we mentioned, an asymptomatic person goes through the whole course of their illness without developing symptoms. They may never even realize they were sick. The term pre-symptomatic meanwhile, refers to whats called an incubation period. Thats the time between getting infected and showing symptoms of an illness.

All viruses, including COVID-19, have an incubation period. In many cases, its when the virus is most contagious. While they are two different things, being pre-symptomatic and being asymptomatic are both tricky from a disease prevention standpoint because in both cases, a person can pass the virus on to other people without realizing theyre doing it.

Asymptomatic COVID-19 is quite common. Scientists think that at least 20% of all people infected with COVID-19 never have symptoms. Meanwhile, because COVID-19 reinfection is common and many of us have established some immunity to the virus its not unusual to experience both symptomatic and asymptomatic COVID-19 infections over the course of ones life.

At this stage in the pandemic, whether or not having COVID-19 will make you feel sick is, at least partially, a game of chance. But theres a growing body of evidence indicating that some of us are playing with loaded dice.

Studies indicate that children and adolescents may be more likely to have an asymptomatic infection than adults. Research also suggests that a lack of COVID-19 symptoms may sometimes be determined by genetics. That would make sense because we already know that some people are genetically predisposed to developing critical cases of COVID-19 pneumonia. These two branches of COVID-19-related research may one day help us limit the severity of symptoms in people who are prone to severe complications.

Dr. Dumford explains that not having symptoms of COVID-19 doesnt mean you cant infect other people. And the people you infect have the same risk of having symptoms that you did.

In other words, the virus youre passing on isnt different. Whats different is how your body responds.

Given that so many people with COVID show minimal to no symptoms, the possibility of exposure is present virtually every day, Dr. Dumford says. That makes preventive measures all the more important, especially if you or somebody you love is vulnerable to severe complications from COVID.

The U.S. Centers for Disease Control and Prevention (CDC) announced significant changes in COVID-19 isolation guidance on March 1, 2024. Their new policy says that isolation should be determined on the basis of clinical symptoms. That means you can end your isolation as soon as:

You see where this is going: People with asymptomatic COVID-19 infections now arent required to isolate at all. Its still encouraged to wear a well-fitting mask for the five days after coming out of isolation. If you dont have to isolate at all, Dr. Dumford says you should still strongly consider masking in public for five days after youre diagnosed.

Asymptomatic COVID-19 cases have always slipped through the net to a certain extent, even at the height of the pandemic. But in the past, many people had to submit to regular testing to attend work or school. Required testing is much rarer nowadays and many people are no longer able to isolate for five days without facing professional or academic consequences. The pandemic isnt over, but it sometimes feels like it is.

What does all this mean in practical terms?

Theres one other thing to be aware of: While its rare, some people with asymptomatic COVID-19 do go on to develop long COVID. In other words, they develop symptoms days, weeks or months after the virus resolves. And those symptoms continue for months or, in some cases, years.

Approximately 20% of individuals infected with COVID-19 are asymptomatic. That means they dont have any symptoms and may never even know they were sick. Thats a problem from a public health standpoint because the person who had COVID-19 is still contagious and can unknowingly spread the virus to other people. Its also reason #418 that staying up to date on your COVID-19 vaccines is so important.

If you know that you have an asymptomatic case of COVID-19, be sure that you wear a mask and practice social distancing if youre going to be around other people. Isolation guidelines are changing as the virus becomes part of our everyday lives, but your responsibility to protect others from infection isnt.

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What Is Asymptomatic COVID-19 and Are You Contagious? - Health Essentials

Hawaii Health Departments new Respiratory Disease Dashboard shows increasing COVID-19 activity – Maui Now

May 29, 2024

May 28, 2024, 4:15 PM HST

Playing in :00

COVID-19 activity is on the rise, according to a new Respiratory Disease Activity dashboard released by the Hawaii State Department of Health (DOH).

The dashboard, developed by the DOH Disease Outbreak Control Division(DOCD), provides an at-a-glance snapshot of current respiratory disease activity statewide, including COVID-19. The dashboard addresses not only COVID-19, but other acute respiratory illnesses, including influenza (flu) and respiratory syncytial virus (RSV).Respiratory diseases occur year-roundin Hawaii.

Currently, COVID-19 is at the yellow, or medium activity level, meaning the virus is circulating at higher levels than would be expected based on historic trends. COVID-19 activity is also increasing. Flu and RSV remain at green, or low activity levels. Overall acute respiratory disease is at the medium level.

The new Respiratory Disease dashboard provides, in one place, a summary of what is happening with several major respiratory viruses that contribute to respiratory disease in Hawaii. This helps people make informed decisions about their health, said State Epidemiologist Sarah Kemble. This week, the dashboard shows that COVID-19 test positivity is higher than expected and climbing, and that ED (emergency department) visits and hospital admissions for COVID-19 are also going up. Based on this information, I would recommend checking whether youve had the 2023-24 COVID-19 vaccine, and if not, or if youre eligible for a repeat dose, go get it today.

Current dashboard trends show that COVID-19 remains a health concern, and the public should take reasonable precautions to avoid getting sick. Among them:

Additional strategies for reducing COVID-19 and other respiratory disease spread can be found athealth.hawaii.gov/docd.

Visit the new dashboardhere.

See more here:

Hawaii Health Departments new Respiratory Disease Dashboard shows increasing COVID-19 activity - Maui Now

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