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We introduce a novel method to derandomize the learning with errors (LWE) problem by generating deterministic yet sufficiently independent LWE instances that are constructed by using linear regression models, which are generated via (wireless) communication errors. We also introduce star-specific key-homomorphic (SSKH) pseudorandom functions (PRFs), which are defined by the respective sets of parties that construct them. We use our derandomized variant of LWE to construct a SSKH PRF family. The sets of parties constructing SSKH PRFs are arranged as star graphs with possibly shared vertices, i.e., the pairs of sets may have non-empty intersections. We reduce the security of our SSKH PRF family to the hardness of LWE. To establish the maximum number of SSKH PRFs that can be constructed -- by a set of parties -- in the presence of passive/active and external/internal adversaries, we prove several bounds on the size of maximally cover-free at most $t$-intersecting $k$-uniform family of sets $\mathcal{H}$, where the three properties are defined as: (i) $k$-uniform: $\forall A \in \mathcal{H}: |A| = k$, (ii) at most $t$-intersecting: $\forall A, B \in \mathcal{H}, B \neq A: |A \cap B| \leq t$, (iii) maximally cover-free: $\forall A \in \mathcal{H}: A \not\subseteq \bigcup\limits_{\substack{B \in \mathcal{H} \\ B \neq A}} B$. For the same purpose, we define and compute the mutual information between different linear regression hypotheses that are generated from overlapping training datasets., Comment: This is the preprint of a paper published in IEEE Access, vol. 11, pp. 73235-73267, 2023

Conditional disclosure of secrets (CDS) allows multiple parties to reveal a secret to a third party if and only if some pre-decided condition is satisfied. In this work, we bolster the privacy guarantees of CDS by introducing function-private CDS wherein the pre-decided condition is never revealed to the third party. We also derive a function secret sharing scheme from our function-private CDS solution. The second problem that we consider concerns threshold distributed point functions, which allow one to split a point function such that at least a threshold number of shares are required to evaluate it at any given input. We consider a setting wherein a point function is split among a set of parties such that multiple evaluations do not leak non-negligible information about it. Finally, we present a provably optimal procedure to perform threshold function secret sharing of any polynomial in a finite field., Comment: The is the full version of the paper that will appear in Cryptology and Network Security (CANS), 2021

Secret sharing allows distributing a secret among several parties such that only authorized subsets, specified by an access structure, can reconstruct the secret. Sehrawat and Desmedt (COCOON 2020) introduced hidden access structures, that remain secret until some authorized subset of parties collaborate. However, their scheme assumes semi-honest parties and supports only restricted access structures. We address these shortcomings by constructing an access structure hiding verifiable secret sharing scheme that supports all monotone access structures. It is the first secret sharing scheme to support cheater identification and share verifiability in malicious-majority settings. The verification procedure of our scheme incurs no communication overhead. As the building blocks of our scheme, we introduce and construct: (i) a set-system with $> \exp\left(c\frac{2(\log h)^2}{(\log\log h)}\right)+2\exp\left(c\frac{(\log h)^2}{(\log\log h)}\right)$ subsets of a set of $h$ elements. Our set-system, $\mathcal{H}$, is defined over $\mathbb{Z}_m$, where $m$ is a non-prime-power. The size of each set in $\mathcal{H}$ is divisible by $m$ but the sizes of their pairwise intersections are not, unless one set is a subset of another, (ii) a new variant of the learning with errors (LWE) problem, called PRIM-LWE, wherein the secret matrix is sampled such that its determinant is a generator of $\mathbb{Z}_q^*$, where $q$ is the LWE modulus. The security of our scheme relies on the hardness of the LWE problem, and its share size is $$(1+ o(1)) \dfrac{2^{\ell}}{\sqrt{\pi \ell/2}}(2 q^{\varrho + 0.5} + \sqrt{q} + \mathrm{\Theta}(h)),$$ where $\varrho \leq 1$ is a constant and $\ell$ is the total number of parties. We also provide directions for future work to reduce the share size to \[\leq \dfrac{1}{3} \left( (1+ o(1)) \dfrac{2^{\ell}}{\sqrt{\pi \ell/2}}(2 q^{\varrho + 0.5} + 2\sqrt{q}) \right).\], Comment: Final version published in Theoretical Computer Science, 2021, volume 886, pp. 106-138

Secret sharing provides a means to distribute shares of a secret such that any authorized subset of shares, specified by an access structure, can be pooled together to recompute the secret. The standard secret sharing model requires public access structures, which violates privacy and facilitates the adversary by revealing high-value targets. In this paper, we address this shortcoming by introducing \emph{hidden access structures}, which remain secret until some authorized subset of parties collaborate. The central piece of this work is the construction of a set-system $\mathcal{H}$ with strictly greater than $\exp\left(c \dfrac{1.5 (\log h)^2}{\log \log h}\right)$ subsets of a set of $h$ elements. Our set-system $\mathcal{H}$ is defined over $\mathbb{Z}_m$, where $m$ is a non-prime-power, such that the size of each set in $\mathcal{H}$ is divisible by $m$ but the sizes of their pairwise intersections are not divisible by $m$, unless one set is a subset of another. We derive a vector family $\mathcal{V}$ from $\mathcal{H}$ such that superset-subset relationships in $\mathcal{H}$ are represented by inner products in $\mathcal{V}$. We use $\mathcal{V}$ to "encode" the access structures and thereby develop the first \emph{access structure hiding} secret sharing scheme. For a setting with $\ell$ parties, our scheme supports $2^{\binom{\ell}{\ell/2+1}}$ out of the $2^{2^{\ell - O(\log \ell)}}$ total monotone access structures, and its maximum share size for any access structures is $(1+ o(1)) \dfrac{2^{\ell+1}}{\sqrt{\pi \ell/2}}$. The scheme assumes semi-honest polynomial-time parties, and its security relies on the Generalized Diffie-Hellman assumption., Comment: This is the full version of the paper that appears in D. Kim et al. (Eds.): COCOON 2020 (The 26th International Computing and Combinatorics Conference), LNCS 12273, pp. 246-261. This version contains tighter bounds on the maximum share size, and the total number of access structures supported

Anonymity is a desirable feature for vehicle-to-vehicle (V2V) communications, but it conflicts with other requirements such as non-repudiation and revocation. Existing, pseudonym-based V2V communications schemes rely on certificate generation and signature verification. These schemes require cumbersome key management, frequent updating of certificate chains and other costly procedures such as cryptographic pairings. In this paper, we present novel V2V communications schemes, that provide authentication, authorization, anonymity, non-repudiation, replay protection, pseudonym revocation, and forward secrecy without relying on traditional certificate generation and signature verification. Security and privacy of our schemes rely on hard problems in number theory. Furthermore, our schemes guarantee security and privacy in the presence of subsets of colluding malicious parties, provided that the cardinality of such sets is below a fixed threshold., Comment: This is the full version of the paper that appeared in 2017 IEEE Vehicular Networking Conference (VNC), pp. 139-146. DOI: 10.1109/VNC.2017.8275624

We define a pseudorandom function (PRF) $F: \mathcal{K} \times \mathcal{X} \rightarrow \mathcal{Y}$ to be bi-homomorphic when it is fully Key homomorphic and partially Input Homomorphic (KIH), i.e., given $F(k_1, x_1)$ and $F(k_2, x_2)$, there is an efficient algorithm to compute $F(k_1 \oplus k_2, x_1 \ominus x_2)$, where $\oplus$ and $\ominus$ are (binary) group operations. The homomorphism on the input is restricted to a fixed subset of the input bits, i.e., $\ominus$ operates on some pre-decided $m$-out-of-$n$ bits, where $|x_1| = |x_2| = n$, and the remaining $n-m$ bits are identical in both inputs. In addition, the output length, $\ell$, of the operator $\ominus$ is not fixed and is defined as $n \leq \ell \leq 2n$, hence leading to Homomorphically induced Variable input Length (HVL) as $n \leq |x_1 \ominus x_2| \leq 2n$. We present a learning with errors (LWE) based construction for a HVL-KIH-PRF family. Our construction is inspired by the key homomorphic PRF construction due to Banerjee and Peikert (Crypto 2014). An updatable encryption scheme allows rotations of the encryption key, i.e., moving existing ciphertexts from old to new key. These updates are carried out via \emph{update tokens}, which can be used by an untrusted party since the update procedure does not involve decryption of the ciphertext. We use our novel PRF family to construct an updatable encryption scheme, named QPC-UE-UU, which is quantum-safe, post-compromise secure and supports unidirectional ciphertext updates, i.e., the update tokens can be used to perform ciphertext updates but they cannot be used to undo already completed updates. Our PRF family also leads to the first left/right key homomorphic constrained-PRF family with HVL., Comment: This is the full version of the paper that appears in Cryptology and Network Security 2019, LNCS, Springer, Volume 11829, pp. 3-23

“Kernicterus” due to hyperbilirubinemia is one of main cause of irreversible brain damage in low and middle income countries. Deaths due to “kernicterus” are ranked within the top 3 causes of neonatal death in African countries. Neonates experiencing permanent or temporary absence or reduced activity of Uridine diphosphate-glucuronosyl-transferase A1 (UGT1A1) enzyme present increased levels of total unconjugated bilirubin (UCB) in the blood. When the bilirubin binding capacity of serum albumin is saturated, this results in the increase in the free fraction of bilirubin (Bf). The excess of Bf is accumulated in lipid-rich tissues such as the brain, where it may reach toxic levels causing bilirubin-induced encephalopathy in jaundiced newborns and patients with Crigler-Najjar syndrome Type I, leading to kernicterus if not promptly treated. Bilirubin causes severe neurological dysfunction by affecting several different cellular pathways such as, induction of oxidative stress, endoplasmic reticulum (ER) stress, autophagy, neuroinflammation and DNA damage. The work done in this thesis focus on the DNA damaging effect of bilirubin on neuronal (SH SY 5Y) and non-neuronal (HeLa) cells and the effect of bilirubin on the different double stranded break (DSB) repair pathways was investigated using HeLa DR GFP and HeLa cell lines. Bilirubin exposure led to time-dependent increase in DNA damage in neuronal cells. Treatment with the anti-oxidant N-acetylcysteine (NAC) caused a dose-dependent decrease in DNA damage, suggesting a key role of oxidative stress in bilirubin-induced DNA damage. In the second part of this work, I studied the effect of bilirubin on different DSB repair pathways using HeLa cell lines. Treatment with bilirubin modulated Homologous Recombination (HR) in a time-dependent manner. In fact, treatment with different doses of bilirubin led to a dose-dependent increase in HR. Bilirubin-induced increase in HR was reversed by addition of NAC, suggesting the important

“Kernicterus” due to hyperbilirubinemia is one of main cause of irreversible brain damage in low and middle income countries. Deaths due to “kernicterus” are ranked within the top 3 causes of neonatal death in African countries. Neonates experiencing permanent or temporary absence or reduced activity of Uridine diphosphate-glucuronosyl-transferase A1 (UGT1A1) enzyme present increased levels of total unconjugated bilirubin (UCB) in the blood. When the bilirubin binding capacity of serum albumin is saturated, this results in the increase in the free fraction of bilirubin (Bf). The excess of Bf is accumulated in lipid-rich tissues such as the brain, where it may reach toxic levels causing bilirubin-induced encephalopathy in jaundiced newborns and patients with Crigler-Najjar syndrome Type I, leading to kernicterus if not promptly treated. Bilirubin causes severe neurological dysfunction by affecting several different cellular pathways such as, induction of oxidative stress, endoplasmic reticulum (ER) stress, autophagy, neuroinflammation and DNA damage. The work done in this thesis focus on the DNA damaging effect of bilirubin on neuronal (SH SY 5Y) and non-neuronal (HeLa) cells and the effect of bilirubin on the different double stranded break (DSB) repair pathways was investigated using HeLa DR GFP and HeLa cell lines. Bilirubin exposure led to time-dependent increase in DNA damage in neuronal cells. Treatment with the anti-oxidant N-acetylcysteine (NAC) caused a dose-dependent decrease in DNA damage, suggesting a key role of oxidative stress in bilirubin-induced DNA damage. In the second part of this work, I studied the effect of bilirubin on different DSB repair pathways using HeLa cell lines. Treatment with bilirubin modulated Homologous Recombination (HR) in a time-dependent manner. In fact, treatment with different doses of bilirubin led to a dose-dependent increase in HR. Bilirubin-induced increase in HR was reversed by addition of NAC, suggesting the important